Step 3 Q-Bank Part 1

Management of an Ectopic Pregnancy

-*Hemodynamically stable* Pts w/ suspected ectopic pregnancy (first-trimester vaginal bleeding + absence of intrauterine pregnancy) should undergo eval with *pelvic U/S & a β-hCG level* -An *early INTRAuterine pregnancy can be visualized by U/S when the β-hCG LEVEL IS >3,500 IU/L!!!* -E.g. Pelvic U/S can show an *empty uterus (i.e. thin endometrial stripe) and a Complex Adnexal Mass ==> DX of ECTOPIC PREGNANCY* (mass contains a fetal pole w/ cardiac activity) -SX of Ectopic: Usu occur *6-8wks after LMP w/ Vaginal Bleeding* but sometimes also *lower abdo pain & amenorrhea*; *unilateral pelvic pain*; can be *ASX p/w incidental mass on U/S* -*MC location for Ectopic is the Ampulla of FT*; other implantation sites incl *ovary, abdomen, & cornual region of uterus* -*RF* for Ectopic: *Prior ectopic pregnancy, Hx of pelvic surgery (e.g. appendectomy), Tobacco use, Pelvic Inflam DZ, Infertility, & IVF* -*TX* is either *Medical (e.g. Methotrexate, a folic acid antagonist) or Surgical Management*, depending on **hemodynamic status & contraindications to methotrexate* -Methotrexate is PREFERRD bc it's AS Effective as surgery W/O risks of surgery -*Methotrexate is CONTRAINDICATED* in pts w/ *HEPATIC DZ or RENAL DZ* (e.g. *diabetic nephropathy* in T1DM) *d/t decreased clearance & slower drug metabolism increasing risk for methotrexate toxicity and its assoc complications* (e.g. *Acute respiratory distress syndrome, bowel ischemia, bone marrow myelosuppression, pulm fibrosis, Hepatotoxicity, Nephrotoxicity*) -Other *contraindications to Methotrexate incl Peptic Ulcer DZ, Immunodeficiency, Active Pulmonary DZ, & BREASTFEEDING* -Additionally, *methotrexate is NOT recommended in pts w/ RUPTURED Ectopic* (e.g. *free fluid in posterior cul-de-sac*) *or who have a High Likelihood of TX Failure (e.g. fetal cardiac activity, β-hCG >5,000 IU/L)* -Pts w/ contraindications to methotrexate require *immediate surgical management (e.g. laparoscopy & salpingectomy)* Note: Mifepristone (an antiprogestin) & Misoprostol (a prostaglandin) are medical management options for abortions, not ectopics

How does a fluid bolus help to diagnose Hepatorenal Syndrome?

-*Hepatorenal Syndrome is a common cause of Acute Renal Failure in Cirrhotic pts, but is a Dx of Exclusion - abnormal LFTs, Incr BUN/Cr* -In Hepatorenal syndrome. the urinary sediment is usu benign -An *U/S* should be done to excl urinary obstruction -*Spontaneous bacterial peritonitis (SBP) is a freq precipitant of hepatorenal syndrome and as such, paracentesis is required* -- For a *DX of SBP, need ≥250 WBCs/mm3 in ascitic fluid* -Pts w/ *cirrhosis* develop *decreased peripheral vascular resistance 2º to Splanchnic Vasodilation* --> *Decreased renal perfusion of Hepatorenal Syndrome* -A *VOLUME CHALLENGE* would be the next appropriate step to *CONFIRM a DX of Hepatorenal Syndrome* -*A FAILURE To Respond (blood pressure Incr) would be Consistent With Hepatorenal Syndrome*; the fluid bolus is needed to confirm that the renal failure isn't secondary to intravascular volume depletion* -TX: A *combination of Octreotide + Midodrine OR Norepinephrine only can be used if the pt's renal failure does not respond to fluids* -*Albumin should be continued for ≥2-3d*

Pemphigoid Gestationis

(previously called *Herpes Gestationis*) -An *AUTOIMMUNE DZ* that typically *presents in the Second or Third trimester* with *ABDOMINAL PRURITUS that PRECEDES a truncal rash* -The characteristic rash of *Pemphigoid Gestationis begins as Periumbilical, urticarial papules & plaques that develop into vesicles & bullae* -The *rash begins at the umbilicus and spreads over the entire body but SPARES the mucous membranes* -DX is Clinical, but skin biopsy can confirm -*TX* goal is *sx control, relieving pruritus & limiting bullae formation* -*TX*: *Mid-potency to High-potency Topical Corticosteroids* (e.g. *TRIAMCINOLONE*) -*Antihistamines (e.g. loratadine, cetirizine)* can also be added for *pruritus relief* -If *Unresponsive to topical* corticosteroids, may need *Systemic Corticosteroids (e.g. Prednisone)* or, rarely, *immunosuppressants* (e.g. *cyclosporine, azathioprine*) -*Intractable Dz* may be an *indication for early-term delivery* -*Obstetric Complications* incl *prematurity, FGR, & Neonatal Pemphigoid Gestationis* -*Sx typically resolve spontaneously after delivery*, but pts are at *risk of recurrence w/ subsequent pregnancies*

Polymorphic Eruption of Pregnancy

(previously called *Pruritic Urticarial Papules & Plaques of Pregnancy) -Typically p/w in the *Third trimester or during Postpartum period* -P/w *pruritic, erythematous papules that begin WITHIN Abdominal Striae* and often *spread to the extremities* -The face, palms, soles, & periumbilical regions are SPARED

Indications for prophylactic administration of anti-D immunoglobulin for RhD-negative patients**

**Antepartum PPX is NOT indicated if the father is RhD negative* • At 28-32 wks gestation • <72hrs after delivery of RhD-positive infant • <72hrs after spontaneous abortion • Ectopic pregnancy • Threatened abortion • Hydatidiform mole • Chorionic villus sampling, amniocentesis • Abdominal trauma • 2nd & 3rd trimester bleeding • External cephalic version

What is the *% risk likelihood of acute hepatitis B progressing to chronic hepatitis B infection*?

*5% or less!* The risk of developing sx in acute HBV infection progressively increases w/ age d/t enhanced immune response to the virus. Consequently, the *risk of progression from acute to chronic HBV infection DECREASES with age*. The *progression rate for perinatally-acquired infection is 90% d/t increased immune tolerance*. Pts infected at age 1-5 have a 20-50% progression rate to chronic HBV infection. But *for adults, the progression rate is <5%* NOTE: *Hepatitis C has a much higher risk of progression to chronic infection (~75-85%)*. The acute phase is often mild or ASX, and pts are typically DX by serology in later stages of the illness. *Similarly to HBV infection, the severity of acute Sx in HCV infection is inversely proportional to the risk of chronic infection.*

Which medications *decrease mortality in heart failure* pts?

*ACE Inhibitors or Angiotensin II Receptor Blockers (ARBS), β-Blockers* (Except in acute decompensated HF!!), and *Spironolactone decrease mortality* -Thiazide or Loop diuretics are used mainly for symptomatic relief -Hydralazine with Nitrate therapy improves both symptoms and mortality in some pts

What is the most common cause of *hemoptysis*?

*ACUTE BRONCHITIS* -*Antibiotics are generally NOT recommended for management of Acute Bronchitis in otherwise healthy pts* as *most [COPD/obstructive airway dz] exacerbations* are of *viral etiology* -HOWEVER, guidelines DO *recommend Antibiotic Therapy for pts who have a COPD Exacerbation with any TWO of the following features*: • *Increased sputum purulence* (e.g. cough productive of green-yellow sputum) • *Increased sputum volume* • *INCR DYSPNEA* -Should also *give ABX* for those requiring *mechanical ventilation*

POOR PROGNOSTIC INDICATORS OF PSGN

*ADULT age of onset, ESP those with a preexisting HX of CKD* as well as those with *Preexisting kidney disease, Metabolic syndrome, and Diabetes* are all poor prognostic indicators in PSGN -PSGN, complication of *Grp A Strep (Strep pyogenes) infection (either impetigo or pharyngitis)* which *presents 2-4 weeks after infxn* -PSGN is d/t *formation of Ag-Ab immune complexes, deposited along glomerular basement membrane* causing *activation of complement & inflam* --> *NEPHRITIC SYNDROME* -Clinical features incl: *gross hematuria, HTN, edema (periorbital or generalized)* -UA shows *RBCs & RBC casts, mild proteinuria* -Serum studies show *Incr Cr, Positive Antistreptococcal Antibodies (e.g. Antistreptolysin O), and LOW C3 Complement levels* (d/t consumption) -PSGN is MC in *children age 5-12yo* and has *excellent prognosis in this age group*, with most achieving complete normalization of renal fxn -However, *up to 40% of ADULTS Dx w/ PSGN develop CKD* and *Persistent HTN, Recurrent Proteinuria*, and *10% progress to ESRD*

What factors predispose someone to *digoxin toxicity?*

*AE* of Digoxin: *Cholinergic effects (N/V/D), Blurry Yellow Vision, Arrhythmias, AV Block* -Can lead to *Hyperkalemia --> Indicates POOR Prognosis* *Factors Predisposing to TOXICITY*: ● *Renal Failure* (Decr excretion) ● *Hypokalemia* (Permissive for Digoxin binding at K+-binding sites on Na+/K+-ATPase) ● *Drugs that displace Digoxin from tissue-binding sites* ● *DECR Clearance of Digoxin d/t VERAPAMIL, AMIODARONE, & QUINIDINE* (Inhibited renal tubular secretion of digoxin, increases serum levels of digoxin); Also *Spironolactone*! *Antidote: Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+.*

What aged pts should be vaccinated against HPV?

*ALL Female & Male pts age 11-26yo* (INCL those w/ a hx of genital warts, abnormal Pap cytology, or positive HPV DNA test) -To decrease the risk for HPV transmission and HPV-related cancers in men and women -Vaccination in boys contributes to *herd immunity* against cervical cancer in women Note: Pts aged *26-45yo* can *STILL receive the vaccine*, but its *effectiveness may be Decreased d/t an increased likelihood of prior HPV exposure from previous sexual partners* -NOT indicated in pregnancy

What is the best initial diagnostic test when diagnosing Pernicious Anemia?

*ANTI-INTRINSIC FACTOR AUTO-ANTIBODIES MEASUREMENT is FIRST-LINE* -- 50-84% sensitivity and almost *100% specificity* (anti-parietal cell antibodies are much LESS Specific) *Schilling Test* is a classic diagnostic test for pernicious anemia that uses *radiolabeled cobalamin* - but it is more cumbersome than anti-IF antibody testing, so it is *used as the Second-Line Test if the anti-IF test is negative*

What disease is characterized by *ANTIMITOCHONDRIAL Antibodies*?

*ANTIMITOCHONDRIAL ANTIBODIES are Sensitive & Specific for PRIMARY BILIARY CIRRHOSIS*

Which cardiac arrhythmias are pts with *hypertrophic cardiomyopathy (HCM)* at increased risk for?

*ATRIAL FIBRILLATION* -The increased risk is d/t *left ventricular diastolic dysfunction* --> *Left atrial enlargement*, creating a substrate for A-fib. -*Thromboembolic Stroke related to A-fib* is an *Imp cause of M&M in HCM* pts *VENTRICULAR TACHYCARDIA* -The increased risk is d/t *myocardial disarray & fibrosis*, as well as *chronic myocardial ischemia resulting from myocardial oxygen supply-demand mismatch* -*Sustained ventricular tachycardia* is the typical *cause of Sudden Cardiac Death, the MCC of mortality in HCM* -*Periodic AMBULATORY ECG MONITORING (e.g. 24hr Holter monitoring)* is *indicated in HCM pts* so that arrhythmic complications can be promptly recognized -This monitoring is esp imp in those w/ SX suggestive of *paroxysmal arrhythmia*, like in a pt w/ *intermittent palpitations* -*Evidence of A-fib on EKG monitoring warrants the initiation of chronic anticoagulation,* and *evidence of ventricular tachycardia* (e.g. *bursts of nonsustained ventricular tachycardia*) *may warrant placement of an Implantable Cardioverter Defibrillator*

Calculation for Absolute risk increase

*Absolute risk increase (ARI)* is the *difference in risk of an outcome (e.g. death/complications) between an exposed group and a nonexposed group* *ARI = Risk-e - Risk-ue*

What skin conditions is insulin resistance associated with?

*Acanthosis Nigricans* and *Multiple Skin Tags!* Skin tags aka acrochordons are benign outgrowths of normal skin, pedunculated, skin-colored papules, usu in areas of friction - axilla, neck, under-boob, inguinal Note: Skin tags also occur more freq w/ age -Skin tags assoc with obesity, insulin resistance, overt diabetes, and metabolic syndrome; also occurs more freq in pregnancy and pts w/ colonic polyps -Clinical Dx for skin tags, no TX required, but can do snip excision or cryosurgery

First-line pharmacotherapy for *dementia-related cognitive impairment*?

*Acetylcholinesterase inhibitors* - *Donepezil, Rivastigmine, Galantamine* NMDA-r antagonist, *Memantine*, is another med shown to be modestly beneficial for symptomatic management of mod-severe dementia Note: No meds are disease-modifying; only used for symptomatic tx

What is *TX w/ 100% Oxygen* used in?

*Acute TX of Cluster Headaches* -Which cause *Unilateral ipsilateral autonomic symptoms, like lacrimation, rhinorrhea, and excruciating periorbital pain & conjunctival injection* -Acute TX also involves *sumatriptan* -*PPX w/ VERAPAMIL*

Acute Sickle Hepatic Crisis in Pregnancy

*Acute pain episodes more common during pregnancy*, esp w/ *increasing gestational age and in postpartum period*!! -Can get *acute sickle hepatic crisis* triggered by persistent N/V causing dehydration, which causes *intra & extravascular hemolysis (e.g. jaundice, scleral icterus, anemia), hepatic sinusoid vaso-occlusion causing hepatic tissue ischemia & infarction (e.g. RUQ pain, elevated transaminases) and systemic inflammation (fever)* -Repetitive episodes assoc w/ *Increased Fetal (e.g. growth restriction, preterm birth) & Maternal (e.g. preeclampsia, placental abruption) Morbidity* -Management incl addressing vaso-occlusive triggers, analgesia (e.g. opioids), IV fluids for hydration, and possible venous thrombosis prophylaxis -Acute sickle hepatic crisis is *self-limited* and usually *resolves in <2wks*

Drugs associated with photosensitivity

*Amiodarone* Diuretics (thiazides [esp *Hydrochlorothiazide*] + loops [furosemide]) ?Methotrexate Oral and topical retinoids Fluoroquinolones St. John's Wort Sulfa Antibiotics/*Sulfonamides (Sulfamethoxazole, Sulfisoxazole, Sulfadiazine)* ?Tacrolimus *Tetracyclines (esp Doxycycline)* Voriconazole Chlorpromazine Psoralens Simeprevir *5-FU* *Acetazolamide* TX of photosensitivity rash includes discontinuation of the sulfa drug, use of sunscreen, & avoidance of sun exposure

TX for most intrapartum intraamniotic infections?

*Ampicillin + Gentamicin*

How do you stop an *acute episode of anterior epistaxis if direct nostril compression, topical vasoconstriction, and cauterization fail*?

*Anterior nasal packing( (e.g. *bacitracin-covered sponge*)

Anthracycline-related Cardiotoxicity

*Anthracyclines (DOXORUBICIN)* can cause *acute cardiotoxicity* in the form of *MYOCARDITIS & VENTRICULAR ARRHYTHMIA* -Would not expect to see cardiac arrest being preceded by sine wave pattern (widened QRS complexes) characteristically seen in severe hyperkalemia (which is seen Tumor Lysis Syndrome)

Presentation difference b/w gastric and duodenal ulcers?

*Duodenal Ulcers*: -Temporary improvement of epigastric pain after small meals is typical -Worsening SX @Night *Gastric Ulcers*: -Pain exacerbation after meals occurs Note: Surveillance endoscopy is indicated to confirm healing of Gastric ulcers, w have a HIGH risk for malignancy, but this risk is LOW for Duodenal and no surveillance endoscopy is needed

RF for C. difficile-associated diarrhea?

*Antibiotic Use* -ABX disrupt the barrier fxn of normal colonic flora -*Fluoroquinolones, Clindamycin, & Broad-Spectrum Penicillins/Cephalosporins* are *most likely* to be implicated *Gastric Acid Suppression* -C. diff spores are *acid-resistant* -But *PPIs and H2-blockers alter colonic microbiome and incr risk for C. diff proliferation* *Hospitalization* -*Nosocomial Exposure* accounts for *most C. diff transmissions* *Advanced Age, ≥65yo* -Older individuals often have *diminished colonic immunity* and *greater exposure to ABX, PPIs, & hospital environments* Note: Probiotic-rich yogurt or other Probiotics have NOT been proven for primary or secondary prevention of C. diff infection (insufficient evidence)

Treatment of early neurosyphilis

*Aqueous crystalline penicillin G* P/w HA, confusion, & cranial neuropathies; may cause meningitis CSF lymph count 200-400

Which autoimmune conditions are assoc w/ type 1 diabetes mellitus?

*Autoimmune thyroiditis and Celiac disease!!* *Type 1 DM*: T-cell-mediated destruction of pancreatic islet β cells *Autoimmune thyroiditis*: Screen for this using *anti-thyroglobulin & anti-thyroid peroxidase antibodies* when make the diagnosis of Type 1 DM. Asses *TSH levels q1-2yrs* as soon as glycemic control achieved. *Celiac disease*: 5% of T1DM pts develop celiac dz, usu in first few years after dx. Screen with *anti-tissue transglutaminase IgA antibodies* and *IgA levels* to exclude false-negative antibody testing in those with IgA deficiency. This should be done at time of diagnosis of T1DM and again several years later. Less likely, but T1DM pts may also develop *Addison disease, autoimmune gastritis, or vitiligo*

Inheritance Patterns: -Autosomal dominant -Autosomal recessive -X-linked dominant -X-linked recessive -Mitochondrial

*Autosomal Dominant* -*Affect 50% of all children born to an Affected Parent* -The *dz appears* in *Consecutive Generations* and *father to son transmission is common* *Autosomal Recessive* -*Affects ~25% of all children with TWO Carrier Parents* -*Offspring* of a *Single Affected Parent* are *CARRIERS* for, but *DO NOT HAVE* the disorder -As a result, *dz freq Skips Generations* *X-Linked Dominant* -*All Female children of Affected Males HAVE the condition* *X-Linked Recessive* -*Male Offspring of a Female Carrier typically have a 50% chance of being Affected*, *whereas Female Offspring have a 50% chance of being Carriers* *Mitochondrial* -*Maternally-Inherited* -The condition is *passed from the Affected Mom to Male & Female Offspring* -HOWEVER, *male offspring do NOT further transmit the condition*

Marfan Syndrome

*Autosomal dominant* characterized by a *defect* in the connective tissue glycoprotein, *fibrillin-1*, on the *FBN1 gene on Ch. 15*, affecting the skeleton, heart, & eyes -*Findings*: Tall & slender w/ long extremities; Incr Arm:Height ratio; Pectus carinatum (more specific) or pectus excavatum; joint hypermobility; Long, tapering fingers & toes (arachnodactyly); Flat feet; Kyphosis &/or Scoliosis; Cystic medial necrosis of aorta; Aortic incompetence & dissecting aortic aneurysms; Floppy mitral valve; Lens Subluxation up & out (Ectopia lentis) seen on slit-lamp exam -Most concerning comorbidity is *aortic root dz*; aortic root dilation occurs in majority and can lead to life-threatening *aortic dissection*; therefore, *echo* is performed at time of DX and *annually* to monitor progression -A *β-blocker* is usu given to *decr myocardial contractility & reduce stress on aortic wall* -If aortic root diameter is significantly/rapidly enlarging, surgical replacement considered -No intellectual disability

Homocystinuria

*Autosomal recessive* due to *cystathionine synthase deficiency* or *decr affinity of cystathionine synthase for pyridoxal phosphate[vit B6]* or *methionine synthase (homocysteine methyltransferase) deficiency* -All forms result in *excess homocysteine* leading to: • Incr *homocysteine in urine* • Osteoporosis • *Marfanoid* habitus • Ocular changes (*myopia, ectopia lentis /down & in/*) • Cardiovascular effects (*thrombosis, venous thromboembolism, atherosclerosis -> Stroke & MI*) • Kyphosis • *Intellectual disability*

Use of which medication is especially known to *increase the result of fall injury in elderly* pts?

*BENZODIAZEPINES* -Benzos, e.g. Lorazepam, is *strongly assoc w/ risk of falls [and subsequent fractures] and increased mortality in older pts* -*Intermediate- (alprazolam, lorazepam) and long-acting (diazepam, clonazepam) agents and higher doses* increase this risk even further by *contributing to impaired balance and decreased mental alertness* Other RF assoc w/ increased falls incl *advanced age, female sex, hx of a fall, use of other psychotropic meds (e.g. antipsychotics, antidepressants), cognitive impairment, lower extremity weakness, balance problems, & arthritis*

Is Barrett Esophagus benign or premalignant?

*Barrett Esophagus* is a *PREMALIGNANT condition* that can *progress to dysplasia and ultimately Esophageal Adenocarcinoma* -HOWEVER, the overall *risk for malignant transformation is LOW* in Barrett Esophagus (*0.3-0.5% per year*) -Barretts occurs in *10-15% of pts w/ chronic GERD (i.e. >5-10yrs)*; risk factors incl Older age (>50yo), tobacco use, and male sex -Barretts pts should receive *periodic surveillance endoscopy w/ biopsy* to *monitor for dysplastic changes* -*Endoscopic Ablation* is ONLY indicated for those WITH *dysplastic changes*, d/t a /higher risk for malignant transformation/ (*4-8% per year for high-grade dysplasia*) -TX: *Lifelong proton pump inhibitor therapy is required* to prevent acid-induced esophageal injury and reduce the risk for malignant transformation

Benefits vs Risks/Complications of Neonatal Circumcision

*Benefits*: • *Significant DECR (~10 fold) in UTIs within first year of life* • *Prevention of pathologic phimosis* (i.e. foreskin constriction preventing retraction) and *Modest Reduction in Risk of Penile Cancer* (likely d/t reduction in phimosis, which is a RF) • *Reduction in certain penile inflammatory disorders* (e.g. *balanitis*) • *Reduction in Risk of acquiring SOME STIs* (e.g. *HPV*) *and HIV* through penile-vaginal sex (does NOT protect against gonorrhea or chlamydia) *Risks/Complications* -*Infection, inadequate skin removal, urethral injury* -BUT COMPLICATION RATE IS <1%

Is breastfeeding safe when pts are taking antiepileptic drugs?

*Breastfeeding is ENCOURAGED in women w/ epilepsy bc the Benefits of Breastfeeding OUTWEIGH the risks for exposure of the infant to antiepileptic drugs* -Studies show that *neurodevelopmental outcomes in breastfed infants are either better than or no different from those who are not breastfed* -*ALL AEDs are excr into breast milk in variable amounts* - estimated that ethosuximide reaches 90% of its plasma concentration in milk, whereas valproate reaches 1-10%

What are *garlic preparations* often used to tx?

*Hypercholesterolemia* is sometimes TX w/ *GARLIC PREPARATIONS*; however, there is *limited data for its efficacy*. *Fish Oil supplementation* can be effective in the *TX of Refractory Hypertriglyceridemia*

Brugada Syndrome & Congenital Long QT Syndrome

*Brugada Syndrome* -Assoc w/ *incr risk of sudden cardiac death* -(Autosomal dominant -Most commonly d/t *loss of function mutation of Na+ channels* -*EKG: Pseudoright bundle branch block & ST-segment elevations in leads V1-V3* -*TX*: *Prevent sudden cardiac death with Implantable Cardioverter-Defibrillator (ICD)* *Congenital Long QT Syndrome* -Also assoc w/ *incr risk of sudden cardiac death* -Caused by *mutations of KCNQ1* --> *Loss of function mutation of K+ channels (affects repolarization)* -Includes: • *Romano-Ward syndrome*—autosomal *dominant*, pure cardiac phenotype (*no deafness*). • *Jervell and Lange-Nielsen syndrome*— autosomal *recessive, sensorineural deafness* -*EKG: QTc >450 msec in men >470 msec in women* -*TX*: *Prevent sudden cardiac death with Implantable Cardioverter-Defibrillator (ICD)*

Which study design is best when investigating an outbreak of an acute infectious disease?

*CASE-CONTROL STUDIES* -A *case-control study* design *explores the assoc b/w exposure and dz, can be conducted when the # of affected individuals is small, and generally allows for quick localization f the outbreak source* -Subjects who developed the disease are CASES and should be questioned about their recent exposures; Unaffected subjects are CONTROLS to reflect the exposure experience of the general population -*If CASES are more likely to be exposed than Controls (i.e. Statistically Significant Odds Ratio >1), then an ASSOC B/W DZ & EXPOSURE can be Established* Note: *Correlational studies* attempt to *measure assoc b/w multiple variables and are generally conducted by natural observation, surveying, or archival research*; they help *develop but not test hypotheses* Note: *Cross-sectional studies* BEGIN with *risk factor/exposure status* and THEN *compare Disease Prevalence (at a certain point in time) to provide a SNAPSHOT*; they are helpful in determining prevalence rather than investigating outbreaks or etiologies

What is the *TX of choice for Insomnia*?

*CBT* is the preferred *initial* therapy for insomnia Elderly pts have INCR risk for AE of Hypnotic meds, incl daytime sedation, cognitive impairment, delirium, night wandering, agitation, balance problems, falls, & fractures If meds are necessary, they should be Rx w/ caution and in the smallest possible dose

Which *SSRI* treats *BOTH Depression && associated Insomnia*?

*CITALOPRAM* Pts w/ insomnia should be evaluated for depression! If DX of depression is made, TX w/ an antidepressant rather than a hypnotic

Pneumonias in Immunocompromised: CMV Pneumonia Legionella Pneumonia Pneumocystis Pneumonia Streptococcus Pneumonia

*CMV Pneumonia* -Usu causes *fever, cough, dyspnea, & DIFFUSE ground-glass opacities (not a nodular infiltrate, like in pulmonary aspergillosis)* -*CMV PPX w/ valganciclovir* *Legionella Pneumonia* -Causes *cough, chest pain, hemoptysis, & Nodular pulmonary infiltrate (although a LOBAR or INTERSTITIAL infiltrate is MC) -Pts usu have *HIGH fever & GI Sx (N/V/D) PRIOR to the onset of Pulmonary Sx* -*Legionella PPX w/ Levofloxacin* *Pneumocystis Pneumonia* -Common infxn in pts w/ *recent stem cell transplantation* and usu manifests with *DIFFUSE Interstitial pulmonary infiltrates & FULMINANT Respiratory Failure* -*PCP PPX w/ TMP-SMX* *Strep Pneumonia* -*MC bacterial cause of PNA but is usu assoc w/ a LOBAR (not a nodular) pulmonary infiltrate* -Less likely to occur in the setting of *PPX Levofloxacin*

What is the first diagnostic test to do in a pt with iron deficiency anemia (microcytic, fatigue) and a positive fecal occult blood test (i.e. heme-positive stool on guaiac)?

*COLONOSCOPY* is the FIRST INITIAL TEST CHOICE! (with official iron studies) MCC of Iron deficiency anemia in USA is blood loss - and in *Male pts >50yo with IDA?* *Colon cancer needs to be ruled out first*

*First-line TX* for pts w/ *symptomatic leiomyomas (fibroids)* who wish to *preserve fertility*?

*COMBINED ESTROGEN/PROGESTIN CONTRACEPTIVES* (e.g. *Pills, Patch, Vaginal Ring*) *and* *PROGESTIN-RELEASING IUDs* (which *decr uterine bleeding by inducing endometrial atrophy* and *reducing leiomyoma size*) Note: *Copper-containing IUDs* are effective, long-acting, reversible contraceptives, but a *common AE of copper IUDs is INCR menstrual bleeding* which can lead to *worsened anemia*; Plus, copper IUDs *don't decr leiomyoma size or decr thickness of endometrial lining* Can also use *GnRH Agonists* (e.g. *Leuprolide*) can be used to *temporarily TX heavy menstrual bleeding caused by estrogen-dependent fibroids* - HOWEVER, *usefulness is limited d/t decr bone mineral density w/ prolonged use & sx recurrence after tx completion*; continuous GnRH admin initially leads to incr FSH & Estrogen release with HPO axis stimulation [and unchanged GnRH levels] causing incr endometrial proliferation & incr menstrual bleeding, but then w/ prolonged use, exogenous GnRH agonists cause desensitization and downregulation of pituitary GnRH-receptors, leading to reduced FSH & Estrogen levels, and inhibition of Endogenous GnRH release ==> Resulting in Hypogonadotropic Hypogonadism, causing decr fibroid size and decr menstrual bleeding)

What is the *MOST EFFECTIVE Method of Emergency Contraception*? (includes all options of OCPs, IUDs, etc.)

*COPPER-CONTAINING IUD or 52mg PROGESTIN-RELEASING IUD* is the *MOST EFFECTIVE method of emergency contraception (>99% effective)* -An *IUD can be placed within 5 days of unprotected intercourse* and *prevents pregnancy by interfering w/ sperm function, delaying ovulation, and preventing fertilization & implantation* -HOWEVER, *IUD placement is CONTRAINDICATED in the setting of Acute Cervicitis* (e.g. pt w/ yellow vaginal discharge, friable cervix that bleeds easily on contact, & multiple PMN leukocytes seen on microscopy of discharge) Note: *Emergency OCPs (levonorgestrel = Plan B; ulipristal = Ella) prevent pregnancy by DELAYING OVULATION*. The *Efficacy of Ulipristal does NOT decrease with time*, *as is the case with levonorgestrel (Plan B) and combined hormonal contraceptives* Note: *OCPs w/ Progesterone Doses EQUIVALENT to Levonorgestrel (Plan B)* can be used as a *form of emergency contraception*. HOWEVER, *OCPs are Less Effective than Ulipristal and have more AE (N/V) when used in Emergency Contraception Doses* Note: An *etonogestrel subcutaneous implant* is a *long-acting, reversible contraceptive*; it is *NOT* a form of emergency contraception.

Child with recurrent respiratory infections, bronchiectasis (chronic productive cough), constipation, and failure to thrive (weight loss)?

*CYSTIC FIBROSIS* Autosomal recessive mutation affecting the CF transmembrane conductance regulator gene impairs chloride transport, resulting in abnormally thick secretions -Viscous secretions in lungs -> mucus plugging --> hyperinflation from chronic obstruction and bronchiectasis -Thick intestinal secretions -> GI tract dehydrated, constipation-prone -Mucus blocks pancreatic ducts -> impairs pancreatic enzyme secretion --> Malabsorption, Failure to Thrive, & CF-related diabetes *SWEAT CHLORIDE TEST IS GOLD STANDARD FOR DIAGNOSIS OF CF! TWO ELEVATED SWEAT CHLORIDE LEVELS IN A SYMPTOMATIC PT IS DIAGNOSTIC*

Acute Interstitial Nephritis

*Causes* -Medications ~75% of cases (e.g. antibiotics [*ciprofloxacin, ceftriaxone*, β-lactams], NSAIDs, PPIs) -Rheumatologic dz (e.g. SLE, Sjogren syndrome, sarcoidosis) -Infections (e.g. Legionella, tuberculosis, CMV) *Clinical Features* -New med exposure -*AKI* (*oliguria* [urine output ≤0.3 mL/kg/hr], *incr serum Cr*) -Arthralgias, malaise, rash -Classic *triad* of *fever, skin rash, & eosinophilia RARELY present* *DX* -Clinical presentation; clinical dx w/o bx -Urinalysis: *WBCs & WBC casts ± mild RBCs & proteinuria* (*Pyuria* is WBC in urine, is highly suggestive of AIN!!) -Peripheral eosinophilia ± urine eosinophils - ±Renal biopsy showing *tubulointerstitial inflam & edema* *Management of AIN* -*Prompt Discontinue offending agent* or Treat underlying condition & *serial monitoring of renal fxn studies* for spontaneous AIN resolution -*Systemic glucocorticoids* (for those who don't improve quickly or who have significant renal failure) -Supportive *hemodialysis* if needed -AIN involves *antigen hypersensitivity that causes inflam within the renal interstitium and tubules*, resulting in *tubular accumulation of WBCs (i.e. pyuria, WBC casts)*, and often *mild proteinuria &/or hematuria d/t tubular damage*

How to Tx Radial Head Subluxation (Nursemaid's Elbow)?

*Child (6mo-5yo) p/w refusal to move arm immediately after forearm pulled or arms swung, holding arm close to body w/ forearm pronated and elbow extended* *X-ray NOT NEEDED if classic Hx & PE findings* *TX w/ REDUCTION BY FOREARM HYPERPRONATION or SUPINATION/FLEXION*

Classification of Angina

*Classic* -Typical location (e.g. substernal), quality, & duration -Provoked by exercise or emotional stress -Relieved by rest or nitroglycerin *Atypical* -2 of the 3 characteristics of classic angina *Nonanginal* -<2 of the 3 characteristics of classic angina

IgA Nephropathy aka Berger Disease

*Clinical Features* -Onset: Spontaneous or several days after URI or GI infection -*Episodic gross hematuria* (isolated or recurrent) - ± flank pain, low-grade fever, *incr blood pressure* -ASX, microscopic hematuria can occur *Lab Findings* -Urinalysis: *protein, blood, RBCs, RBC casts* -*Normal serum C3 & C4* complement -Incr serum creatinine *Diagnosis* -Usu clinical -Confirmed by kidney bx; *mesangial IgA deposition of IgA-based immune complex deposits* *Prognosis/Risk Factors* -Often /self-resolves/ -*ESRD* in some (50%) pts: • RF: *Incr creatinine, Incr BP (>140/90), Persistent proteinuria (>1g/d; greatest RF)* • Slowly progressive (>10yrs)

What is the MC complication of acute diverticulitis?

*Colonic Abscess!* occurring in 15-55% of cases -SX of colonic abscess resemble uncomplicated diverticulitis, but often don't improve w/ conservative management -*Confirm Diverticular Abscess w/ REPEAT Abdo CT, as a localized fluid collection* -Most abscesses need *percutaneous drainage & IV ABX*, followed by *consideration for elective partial colectomy several weeks later*

Medial Medullary Syndrome

*Contralateral hemiparalysis and ipsilateral CN XII palsy (tongue deviation towards the lesion)*

What are common causes of *decreased vision in Elderly pts (esp >75yo)?*

*Cortical CATARACTS & ~ASSOCIATED~ AGE-RELATED MACULAR DEGENERATION (AMD)* 40% prevalence of cataracts in this age group, and associated AMD is 20% -*Cataracts* represent *slow, progressive opacification of the lens, progressing to painLESS blurry vision w/ generally intact visual fields* -*Age-related Macular Degeneration* refers to *degeneration of the central portion of the retina* (?d/t chronic inflam or infxn), leading to *Loss of CENTRAL vision* -Early changes are ASX but can progress to *difficulty reading, scotomas, or needing brighter light for visualization* -*Drusen (cellular debris)* may be visible in *early stages (Dry AMD)* -With *WET AMD (choroidal neovascularization),* the *presentation* can be *more acute* -*Visual loss related to AMD may be IRREVERSIBLE, unlike that related to Cataracts* -Pts with cataracts should be thoroughly evaluated for the severity of AMD, as they may not benefit from cataract surgery alone (e.g. lens extraction); *AMD Management* (e.g. *oral eye vitamin, potential intravitreal therapy if wet AMD*) may be warranted -Cataract surgery may also increase the risk of AMD progression (possibly bc the opacified lens provided some protection from AMD); therefore, decisions about cataract surgery in AMD pts should be based on an assessment of the potential gain from lens extraction (cataract surgery)

What sx do you expect in a pt with a posterior communicating artery aneurysm?

*Cranial Nerve III (Oculomotor N) Palsy* -PCom A can cause a *subarachnoid hemorrhage* - pt p/w *sudden-onset HA, nausea, & nuchal rigidity* characteristically -CN III Palsy presents with *ptosis & anisocoria* (unequally sized pupils) -PCom-compression --> Ipsilateral CN III palsy --> *Mydriasis* ("blown pupil"); may also see *ptosis, down & out eye*

*Cryptorchidism*

*Cryptorchidism = An Undescended Testicle, p/w an Empty Hemiscrotum and Palpable Tesicle in Inguinal Canal* -*Normal testicular descent* from intraabdominal space thru inguinal canal *occurs at 28wks gestation* -- Any interruption results in an Undescended Testis -*Natural course of cryptorchidism in most pts is Spontaneous Descent of Undescended Testis during the first FEW MONTHS of life* -HOWEVER, *those w/ an undescended testis AT AGE 6MO are Referred for ORCHIOPEXY, BC Spontaneous Descent is Very UNLIKELY after this age!!* -The *purpose of Orhiopexy is to REDUCE the RISK for MALIGNANCY & INFERTILITY*: ● *Malignancy*: Pts w/ a *hx of cryptorchidism* are at *INCR risk for a Testicular Germ Cell Tumor (e.g. Seminoma)*, which can *involve the ipsilateral or contralateral (i.e. the normally descended) testis*. If an undescended testis is bilateral or intraabdominal, the risk for testicular cancer is even greater! *Although orchiopexy decreases the rate of malignant transformation, the Risk REMAINS Higher than that of the general population, even despite surgery*. HOWEVER, *fixation of the testis in the scrotum (i.e. orchiopexy) enables easier detection of testicular masses on exam* ● *Infertility*: Bc the *seminiferous tubules & Sertoli cells are temperature-sensitive and prone to heat damage, the lower body temp in the scrotum is ideal for sperm production*. Testicles OUTSIDE the scrotum are *at risk for atrophy & necrosis of the seminiferous tubules*, resulting in *reduced quality & quantity of sperm & DECR Fertility*. Bc the *duration of cryptorchidism usu correlates w/ the degree of subfertility, EARLY Orchiopexy (BEFORE AGE 1YO) is Recommended to Help Preserve Fertility Potential*

Are there any vitamins or supplements that exist that reduce the risk of dementia?

*NO* -To date, there is no conclusive evidence that any vitamins or dietary supplements are effective in preventing dementia -Vitamin E is NOT recommended for the prevention of Alzheimer disease in healthy adults, but has shown modest benefit in pts w/ mild to moderate AD -Omega-3 fatty acids can help decr cardiovascular risk factors for dementia, and may reduce the risk of death from coronary heart disease; However, RCTs have NOT demonstrated a direct impact on preventing dementia

Which disease are Gottron's papules associated with?

*DERMATOMYOSITIS!* *Gottron's papules* are red/purple papules or plaques, typically involving the dorsal and radial surfaces of the metacarpophalangeal joints, proximal interphalangeal joints, and proximal phalanx -*DX of Dermatomyositis based on Clinical Findings (proximal symmetrical myopathy, elevated creatine protein kinase, incr aldolase, incr LDH) and SEROLOGIC tests (Positive Antinuclear Antibody [ANA] in 80% as a Screening test; Confirmatory test incl myositis-specific Ab - e.g. anti-Jo, anti-Mi2)* -*Muscle and Skin biopsies* only if *uncertain DX* -Dermatomyositis is assoc w/ *extramuscular findings* incl *INTERSTITIAL LUNG DZ, Dysphagia, & Myocarditis* -- Perform a *CXR to screen for ILD if no pulm sx present* -In pts *with respiratory Sx and those w/ Abnormal CXR Findings* --> *CT CHEST & PFTs (pulm fxn testing) Recommended!* -Though dermatomyositis may *occur alone*, it is *also often seen as a PARANEOPLASTIC SYNDROME OF MALIGNANCY, which may be detected before, after , or with the skin and muscle sx* • A pt w/ Gottron papules, difficulty getting up from a chair, malaise, wt loss, & low-grade fever should raise suspicion for malignancy! -*ALL pts* with *Newly-DX Dermatomyositis* should *undergo Age-Appropriate Cancer Screening* -The *most common assoc cancers w/ dermatomyositis incl Adenocarcinoma of the Cervix, Ovaries, Lung, Pancreas, Bladder, & Stomach* -Dermatomyositis secondary to malignancy may resolve entirely once the cancer has been successfully treated

What does impaired ability to dorsiflex the foot indicate?

*Damage to the DEEP Peroneal Nerve* causing *foot drop* -Commonly caused by *compression of or injury to the Common Peroneal Nerve at the lateral neck of the fibula* -In addition to *impaired ankle dorsiflexion (footdrop) and toe extension*, affected pts typically have *PARESTHESIA and/or sensory loss over the LATERAL Lower Leg and DORSAL Foot*

Neonatal Polycythemia

*Definition* -*Hematocrit >65% in full-term infants* -Hb >22 g/dL -Seen at 2-3hrs of life *Causes* -*Incr erythropoiesis* from *intrauterine hypoxia*: maternal diabetes, HTN, smoking; intrauterine growth restriction -Erythrocyte transfusion: delayed cord clamping, twin-twin transfusion -Genetic/metabolic dz: hypo/hyperthyroidism, genetic trisomy (13, 18, 21) *Clinical Presentation* -ASX (most common) -*Ruddy skin* w/ generalized erythema -*Hypoglycemia, hyperbilirubinemia* -Resp distress, cyanosis, apnea -Irritability, jitteriness -Abdominal distension *TX* -ASX pts can be observed clinically, bc usu resolves in first 24hrs of life, but those w/ clinical sx need tx -*IVF, Glucose* (first-line) -*Partial exchange transfusion* if first-line tx didn't work (consists of withdrawing blood from the infant and infusing normal saline) *Complications of UNTX Polycythemia* -*Hypoglycemia, hyperbilirubinemia* -*Hyperviscosity* -*Hypoperfusion, tissue hypoxia* -All d/t incr RBC volume -Untx, worsening polycythemia will p/w plethora, *lethargy*, irritability, drowsiness, poor feeding, abdo distension, & *hypotonia* -Respiratory compromise can occur, causing *apnea or cyanosis* -*Metabolic derangements* (low glucose, elevated bilirubin) There can be variability in measurements with capillary samples (e.g. heel prick) versus peripheral blood. *If Hct >65% on heel prick, confirm elevated hematocrit by rechecking a sample from peripheral venous blood which is more reliable*, unaffected by changes in temp & blood flow, & often up to 15% lower than a capillary sample

Vasa Previa

*Definition* -Fetal vessels overlying/in close proximity the cervix (cervical os) surrounded by thin fetal membranes (instead of thick, gelatinous, protective Wharton's jelly), which can result in vessel rupture and exsanguination/fetal death -Typically DX on fetal anatomy U/S at 18-20wks gestation *Risk Factors* -Placenta previa (placental attachment to lower uterine segment over/close to internal cervical os) -Multiple gestations -In vitro fertilization -Succenturiate placental lobe (smaller accessory lobe) *Clinical Presentation* -*PainLESS vaginal bleeding (minimal & transient) w/ Rupture of Membranes or Contractions* (/primarily reflects fetal blood loss from a torn fetal vessel/) -*FHR abnormalities* (e.g. *bradycardia <110bpm*, sinusoidal pattern) -*Fetal exsanguination & demise* (hypotension from fetal bleeding leads to fetal HR abnormalities and *rapid fetal exsanguination & demise*) *Management* -*EMERGENCY C-SECTION* -If identified in 2nd trimester, pts would require 3rd trimester inpt management w/ early C-section delivery at 34-35wks (i.e. prior to onset of contractions or ROM)

Delirium definition

*Delirium*: A *reversible, acute confusional state involving fluctuating levels of consciousness & inattention* -Most commonly seen in *elderly pts w/ medical illness*

Dementia definition

*Dementia*: Involves an *irreversible, global deterioration in cognitive abilities & functioning*, which *freq incl short-term memory problems, impaired communication skills, & a decline in activities of daily living*

Who makes health care decisions in Adult pts w/ Intellectual Disability?

*Designated Guardian* after the pt is ≥18yo if the adult child's disability is severe enough to impair global decision making capacity, or ability to communicate -Usu its the *parents* who *pursue guardianship to continue making decisions* for their child with ID; but if they do NOT, then *the pt becomes their own guardian* (Guardianship laws vary by state) -Need to first determine guardianship status for adult pts w/ intellectual disability! It should be clarified early in the medical relationship to facilitate decision making -Adults w/ ID should be assessed for *capacity* first when making their own health care decisions, if they don't have a guardian

What is desmopressin used to treat?

*Desmopressin (DDAVP)& is an *ADH analog* used to TX: - *CENTRAL Diabetes Insipidus* -*von Willebrand disease* (desmopressin releases vWF stored in endothelium) -*Sleep Enuresis* (bedwetting ≥2x/wk for ≥3mo in kids >5yo) (*desmopressin decreases nocturnal urine production*; AE uncommon, but can cause *dilutional hyponatremia* if drink a lot before bed) -*Hemophilia A* (Factor 8 Deficiency; give desmopressin & factor 8 concentrate)

What test do you use to confirm DX of Shingles?

*Direct fluorescent antibody testing for VZV* can confirm shingles, which usu p/w *erythematous papules progressing to grouped vesicles in a dermatomal distribution*

What is *DIVERSION* when it comes to medication misuse?

*Diversion* involves *transferring medication from the pt to another individual*

What medications are used to treat prolactinomas?

*Dopamine AGONISTS (e.g. cabergoline, bromocriptine)* which help to *decr the size and secretion of prolactin from the adenoma* If these don't work, can do *surgery*

What is *phantom pain*?

-*Phantom Pain refers to PERCEIVED PAIN in an extremity following amputation* -It is *caused by AFFERENT pain fibers that previously served the affected limb*

What is the most serious complication of thrombolysis? (e.g. w/ tissue plasminogen activator, alteplase/reteplase)

*EARLY INTRACRANIAL HEMORRHAGE*, occurring in ~5-8% of pts. -When *ICH is suspected* (like when pt *suddenly develops neurologic deterioration, new/worsening headache, N/V, or a sudden incr in BP*), *OBTAIN REPEAT HEAD IMAGING IMMEDIATELY* (e.g. *noncontrast CT*) -If hemorrhage is confirmed, *Reversal Agents are given promptly* (thrombolysis-related ICH has mortality rate of 50-60%) -- *Reversal agents should contain FIBRINOGEN or INCR FIBRINOGEN* (e.g. *CRYOPRECIPITATE, ANTIFIBRINOLYTICS*), thereby *counteracting the effect of tissue plasminogen activator which decr fibrinogen by activating the fibrinolytic pathway* *Cryoprecipitate* - *Quick* onset of action, Contains *Factor 8, vWF, & Fibrinogen*; it *replaces fibrinogen & activates the intrinsic pathway* *Antifibrinolytics* (e.g. *Aminocaproic acid, Tranexamic acid*) - *Prevent Fibrinolysis* by *competitively inhibiting the conversion of plasminogen to plasmin*; they *indirectly increase fibrinogen* Admin of Additional Reversal Agents depends on pt's medication HX: -For those taking *anticoagulation therapy* (e.g. *warfarin, direct oral anticoagulants*), *FFP or Protein Complex Concentrate (PCC)* may be given bc *both activate the coagulation cascade* -For those taking *direct factor Xa inhibitors* (e.g. *rivaroxaban, apixaban*), *reversal with Andexanet Alfa (recombinant modified factor Xa)*, which *binds & sequesters the Xa inhibitor* -For those who *recently received heparin* (e.g. for DVT PPX), *Protamine Sulfate* is recommended

Best tx for pregnant pt with severe depression with psychotic features, and active suicidal thoughts?

*ELECTROCONVULSIVE THERAPY* -*Highly effective TX for unipolar or bipolar depression* in pts with *psychotic features or persistent suicidality* or who require *rapid treatment response* (e.g. *severe neurovegetative sx, nutritional depletion, refusal to eat/drink*) -*ECT IS SAFE DURING PREGNANCY!!!*

Calcium, phosphorus, and PTH levels in *Secondary Hyperparathyroidism 2/2 CKD*

*ELEVATED PTH* (moderately) *ELEVATED SERUM PHOSPHORUS* (inorganic) *LOW/LOW-NORMAL SERUM CALCIUM* -Secondary Hyperparathyroidism is triggered by a Low/low-normal serum Calcium level caused by the following: ● *DECR Renal Phosphate Excr*: The resulting *hyperphosphatemia* leads to *formation of Calcium-Phosphate complexes in the bloodstream* (i.e. *PO4 binds free Ca2+*) ● *DECR formation of ACTIVE Vitamin D (1,25-Dihydroxyvitamin D)*: The *failing kidneys* are *less able to convert vitamin D3 (what is usu measured by the lab) to active 1,25-Dihydroxyvitamin D,* leading to *DECR intestinal absorption, renal reabsorption, & bone mobilization of Calcium* contributing to the *Low serum Ca2+* -*PTH acts to Incr Serum Ca2+* (thru effects on bone, kidneys, & intestines) *but despite persistent PTH elevation, it cannot overcome the disruption caused by the failing kidneys* -One of the major consequences is *CKD-Mineral Bone Disorder (e.g. Renal Osteodystrophy!!)* -*Persistent PTH elevation causes ongoing INCR Bone Turnover* --suggested by *Elevated ALP*-- which can *lead to Osteitis Fibrosa Cystica,* a form of Renal Osteodystrophy *characterized by reduced bone mineralization, marrow fibrosis, & increased fracture risk* -Bc *Hyperphosphatemia* (e.g. *d/t decr renal excr*) plays a prominent role in *2° HyperPTH, Initial TX is w/ DIETARY PHOSPHATE RESTRICTION,* which *reduces the risk of CKD-mineral bone disorder* --If *phosphorus remains elevated,* *NON-Calcium-Containing Phosphate Binders* (e.g. *Sevelamer*) are then *added* -*OVERTREATMENT* (i.e. *Excessive PTH Suppression*) can *INCR the Risk of Adynamic Bone DZ* (another form of Renal Osteodystrophy), which is *characterized by low bone turnover*

What agents should be given to a female patient who experienced *sexual assault*? I.e. *Empiric Postexposure Prophylaxis for Sexual Assault*

*Emergency Contraception* - e.g. *Copper-containing or Progestin-releasing IUD (>99%, most effective), or *if have a contraindication to IUD placement* (e.g. ongoing *acute cervicitis*), with *Ulipristal, which can be taken up to 5-days after unprotected sex* *Doxycycline* - for *Chlamydia* *Ceftriaxone* - for *Gonorrhea* *Metronidazole* - for *Trichomonas* *Tenofovir-Emtricitabine with Raltegravir* - for *HIV*; give *PEP within 72hrs of assault, esp if evidence of genital trauma, anal intercourse, or multiple assailants* d/t *incr risk of HIV transmission* *Hepatitis B Vaccine ± Hepatitis B Immunoglobulin* - for *HBV, depending on vaccination status* (not indicated for recently completed vaccination). *In NON-immune pts, hepatitis B vaccination is administered after exposure; Hepatitis B Immunoglobulin is added IF the assailant may be Hep B-Positive* Note: *Current guidelines say that PEP for Syphilis with Penicillin is NOT recommended. Serologic Testing for syphilis is recommended @initial eval, and repeat serologies are obtained @6wks & @3mo*

What malignancy is assoc w/ untreated Celiac Disease?

*Enteropathy-Associated T-cell Lymphoma (EATL)* -EATL is an *aggressive hematologic malignancy* that primarily *affects the JEJUNUM* -Manifestations typically *begin w/ abdo pain and B-symptoms (wt loss, fatigue, fever)* -*Bowel obstruction, bowel perforation, & GI bleeding* are common as the dz progresses (pt p/w *worsening mid-abdo pain, abdo cramps, & black stools, positive for occult blood*) -Most EATL pts *present late in dz course* when *curative options are limited* -- bc of this, *prognosis is POOR w/ median survival of 10mo*

What is and which organism causes Erythrasma?

*Erythrasma* is a *superficial* skin infection affecting *intertriginous* areas, forming *well-defined erythematous patches or thin plaques w/ fine wrinkling* in the *groin, axillae, inframammary region, or umbilicus* -Can be caused by *Corynebacterium minutissimum*, a *gram positive bacillus* found in normal skin flora

Which organisms can cause Hemolytic Uremic Syndrome?

*Escherichia coli serotype O157:H7* AND *Shigella dysenteriae* (very small inoculum required; acid stable so resistant to gastric acid) Shiga toxin (enterotoxin) causes HUS - triad of *anemia, thrombocytopenia, & AKI d/t microthrombi* forming on damaged endothelium --> *Mechanical Hemolysis w/ Schistocytes on PBS*, *Platelet consumption*, and *Decr renal blood flow* *E. coli O157:H7* -*Uncomplicated* --> *NO ABX TX!!!* (Incr HUS risk if give ABX) *Shigella dysenteriae*: -*Uncomplicated* --> TX w/ ABX (*Ceftriaxone* preferred, or Cipro [but avoid cipro in kids]) -*Complicated (i.e. causing HUS)* --> *Supportive TX, ± PRBC/PLT transfusions; NO ABX!!!* (Can lead to further release of Shiga toxin if given)

How to manage exercise-induced hypoglycemia in a type 1 diabetics?

*Hypoglycemic episodes during exercise in Type 1 Diabetics* can be *managed by decreasing the insulin dose (e.g. reducing NPH basal insulin), eating before exercising, and avoiding injections of insulin in the exercising limbs* *Type 1 Diabetics do NOT have endogenous insulin production and require Basal Insulin, by injection of twice-daily NPH or once-daily injection of Glargine Insulin at bedtime* *NPH* is an *intermediate-acting insulin with peak actions after 4-6hrs of injection*, and its *effects can last up to 16-18hrs*

How does GFR change with age?

*Estimated GFR begins to decline by 8-10 mL/min per decade starting @40-50yo* *Age-related loss of renal function* is *considered NORMAL* and warrants *NO ADDITIONAL Diagnostic Studies or Treatment* -This *age-related Decr in Renal FXN is NOT typically accompanied by a significant rise in Cr, bc Cr is derived from muscle tissue*, which *decr in mass with age (i.e. sarcopenia)* NOTE: Pts taking *ACE Inhibitors (Lisinopril)* cause a *slight & usu temporary reduction in GFR soon after initiation* via *alterations in the glomerular blood flow, but a continued decline in GFR over the years would not be expected* - i.e. *decreases GFR by preventing constriction of efferent arterioles* (also causes Incr Renin d/t loss of negative feedback, and prevents inactivation of bradykinin, a potent vasodilator)

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

*Etiologies* -CNS disturbance (e.g. stroke, hemorrhage, trauma) -Medications (e.g. *carbamazepine, cyclophosphamide, SSRIs, valproic acid, NSAIDs*) -*Lung DZ* (e.g. *pneumonia*) -Ectopic ADH secretion (e.g. *small cell lung CA*) -Pain &/or Nausea *Clinical Features* -*Mild/moderate hyponatremia* --> Nausea, forgetfulness -*Severe hyponatremia* --> Seizures, Coma -*Euvolemia* (e.g. moist mucous membranes, no edema, no JVD) (*excessive free water retention; euvolemic hyponatremia with continued urinary Na+ secretion*) *Lab Findings* -*Hyponatremia* -*Serum osmolality <275 (i.e. /hypotonic/)* -*Urine osmolality >100* -*Urine Sodium >40mEq/L* (elevated urine osmolality & urine sodium are considered classic for SIADH) *Urine Osmolality > Serum Osmolality* *Management* -*Fluid restriction* (first-line) ± salt tablets -IV Hypertonic (3%) saline for severe hyponatremia -Diuretics -Conivaptan, tolvaptan, demeclocycline Note: Increased urine osmolality during water deprivation during water deprivation test indicates */psychogenic polydipsia/*

What is the most common cause of *inherited or hereditary thrombophilia* causing *multiple episodes of venous thromboembolism*?

*FACTOR V LEIDEN* (Autosomal Dominant) -Accounts for 40-50% of inherited thrombophilias (esp in Caucasians) and predispose pts to the dev of venous thromboembolism -Involves production of a mutant factor V that is resistant to degradation by activated protein C -Complications incl DVT, cerebral vein thromboses, and recurrent pregnancy loss

False Positive Rate False Negative Rate

*FPR = 1 - SPECIFICITY* *FPR = 1 - (TN / [TN + FP]) *FNR = 1 - SENSITIVITY* *FNR = 1 - (TP/[TP+FN])* *Sensitivity = True Positive Rate = TP / (TP + FN) = 1 - False Neg Rate* *Specificity = True Negative Rate = TN / (TN + FP) = 1 - False Pos Rate*

Turner Syndrome

*Female, 45,XO* - *SHORT STATURE & HYPOGONADISM* -*Short stature* (associated with SHOX gene, *preventable with growth hormone therapy*), *ovarian dysgenesis (streak ovary), broad chest with widely spaced nipples*, *bicuspid aortic valve, coarctation of the aorta (femoral < brachial pulse), lymphatic defects (result in webbed neck or cystic hygroma; lymphedema in feet, hands), horseshoe kidney, high-arched palate, shortened 4th metacarpals. Visual & hearing deficits* -*Incr predisposition for autoimmune endocrinopathy* (esp *Primary Hypothyroidism*) -*Most common cause of 1° amenorrhea!!*. -No Barr body. -Menopause before menarche. -*DECR Estrogen leads to INCR LH & FSH*. -Sex chromosome (X, or rarely Y) loss often due to *nondisjunction during meiosis or mitosis* -Meiosis errors usually occur in paternal gametes --> sperm missing the sex chromosome. -Mitosis errors occur after zygote formation --> loss of sex chromosome in some but not all cells --> mosaic karyotype (eg. 45,X/46XX) - which is assoc w/ incr risk for gonadoblastoma (remove streak gonads in mosaic pts). (!) As soon as Diagnose Turners, MUST do an *ECHO* to look for *Cardiac Defects, incl Coarctation of Aorta, Bicuspid Aortic Valve, Mitral Valve Prolapse, & Hypoplastic Heart*. Additionally, also require *visual & hearing assessment, Renal U/S, & TSH level measurement*

Triad for Infectious Mononucleosis?

*Fever, diffuse bilateral cervical LAD, & exudative pharyngitis* Sometimes the spleen is enlarged.

What kind of testing is required in a pt of *28wks gestation*?

*For Physiologic Anemia*: -At 24-28wks gestation, all pregnant women should undergo screening for anemia w/ an *H&H or CBC*, which can then be compared to results from initial prenatal visit -Physiologic anemia occurs in most pregnancies 2º to an *expanding plasma volume* that is disproportionate to the incr in RBC mass -Iron requirements incr in pregnancy -*TX of Physiologic Anemia is w/ IRON supplementation* *For Gestational Diabetes Mellitus*: -Gestational diabetes screening is also performed at 24-28wks d/t the *rise in human placental lactogen (hPL)*, a hormone secr by placenta that increases fetal glucose supply by inducing maternal insulin resistance!! -If positive 50g 1hr glucose challenge test, then must undergo a subsequent confirmatory 100g 3hr glucose tolerance test prior to DX of GDM *For Antibody Screening*: -*Rh(D)- Negative* women should undergo antibody screening and receive an anti-D immune globulin injection Note: Just bc a pregnant pt has severe headaches and LE edema, which are often assoc w/ preeclampsia, if her BP is normal, the DX of preeclampsia is excluded. If she had HTN then next step in evaluation is a 24hr urine collection for protein

How to TX *Group A Strep Pyogenes Pharyngitis*?

*GAS pharyngitis, occurs at age 5-15, and p/w abrupt fever, sore throat, & malaise in the ABSENCE of URI sx (e.g. cough, rhinorrhea, congestion).* PE classically shows *tonsillar exudates, tender anterior cervical LAD, & palatal petechiae*. *DX confirmed w/ throat culture (preferred) or rapid antigen testing PRIOR to initiation of ABX* *ORAL PENICILLIN/AMOXICILLIN x10-DAYS* is the *TX of choice* for streptococcal pharyngitis. If penicillin-allergic, tx with *cephalosporin (mild rxn) or 5-d course of azithromycin/clindamycin (anaphylaxis to penicillin).* -The *BENEFITS of ABX Therapy Incl:* 1. *DECR SX severity & duration* 2. *Prevention of spread* to close contacts 3. *Prevention of suppurative complications* (e.g. peritonsillar abscess, cervical lymphadenitis) 4. *PREVENTION OF ACUTE RHEUMATIC FEVER* (NOT PSGN glomerulonephritis!) -10d course of PO penicillin will ensure full eradication of bacterial carriage and to prevent rheumatic fever -*Daily long-term prophylactic ABX are indicated for pts with a HX of Rheumatic Fever to prevent recurrence of the disease* Note: PSGN occurs 1-3wks after a cutaneous or pharyngitis streptococcal infection. Unclear if ABX are preventive for PSGN the way they are for Rheumatic fever. Note: If pts cannot tolerate PO penicillin, then can do a *SIngle dose of INTRAMUSCULAR PENICILLIN* which is *bactericidal for up to a month*

Can an acute pulmonary embolism p/w a fever?

*YES, in ~15% of cases* *Fever defined as Temp ≥38.3ºC (101º F)* -Although fever often indicates presence of infxn, there are numerous other causes of fever - incl rheumatologic disease, malignancy, medications, and acute PE

GERD Management and when to do an Endoscopy?

*GERD* is characterized by *Substernal Burning and Regurgitation* (e.g. sour taste in mouth) d/t *inappropriate relaxation of the lower esophageal sphincter, allowing retrograde flow of gastric contents into esophagus and mouth* and is *assoc w/ conditions that incr sphincter laxity* (e.g. *obesity, pregnancy*) -In pts with *Frequent GERD Sx* (*>2x/wk*) that interfere with life, *GERD is TX with [a TRIAL of] acid-suppressing PPI therapy* (e.g. *Omeprazole*); they *do NOT need to H. pylori testing* -*PPIs inhibit hydrogen-potassium ATPase*, present on the *parietal cells* of the stomach, *suppressing acid prodn & improving heartburn sx* -Evaluation with *Upper GI Endoscopy* is *only indicated in GERD pts w/ ALARM FEATURES* (e.g. *Dysphagia, Odynophagia, Weight Loss, Anemia*) and it can be considered in pts who have *Longstanding SX (>5-10yrs),* which is a *RF for intestinal metaplasia of the esophagus (Barrett's)* Note: Presence of bacterial infection with *H. PYLORI* should be *assessed* in pts with *DYSPEPSIA,* which is *Characterized by EPIGASTRIC BURNING & SX of Bloating, Nausea, or Early Satiety.* *There is NO ROLE for H. pylori testing in GERD!!*

What type of neoplasm results from the *malignant transformation of chorionic villi or trophoblast*?

*GESTATIONAL TROPHOBLASTIC NEOPLASIA* -*Choriocarcinoma* is the most aggressive form of GTN, and metastasis to the lungs, vagina, CNS, or liver often occurs (p/w abnormal vaginal bleeding) -Although GTN is *typically a sequela of a hydatidiform mole*, it *can follow any type of pregnancy*, including a normal term delivery, spontaneous abortion, or ectopic pregnancy (maternal age >40yo incr risk) -Initial eval for suspected GTN incl *quantitative β-hCG; thyroid, renal, & hepatic fxn panels; pelvic U/S; & CXR* TX: *Chemotherapy (typically Methotrexate) & Hysterectomy* -*After TX, β-hCG levels monitored as a marker for disease remission or progression*

What herbal supplements are often used to treat *osteoarthritis*?

*GLUCOSAMINE & CHONDROITIN* -However, *limited* studies demonstrating their clinical benefit

What makes a *good screening* test?

*HIGH SENSITIVITY, which helps to rule OUT the disease*, *giving as few false-negative results* as possible - *decr # of false-negs* -Furthermore, the *high sensitivity increases the negative predictive value (NPV)* of the test: *NPV=TN/(TN+FN)* *HIGH SENSITIVITY TESTS USED FOR SCREENING, LOW FALSE NEGATIVE RATE*

Lab Abnormalities in Tumor Lysis Syndrome?

*HYPERPHOSPHATEMIA* *HYPOCALCEMIA* *HYPERURICEMIA* *HYPERKALEMIA* *ELEVATED CR/BUN indicating ACUTE KIDNEY INJURY* -TLS involves *excessive release of intracellular contents*, incl *potassium, phosphate, & purine nucleic acids* from *dying malignant cells* -Phosphate binds free Ca2+, causing *hypocalcemia* and the purine nucleic acids are *metabolized into uric acid causing elevation of uric acid* -TLS MC occurs *following initiation of chemo* in pts w/ high tumor burden, but *can also occur spontaneously* in *malignancies w/ rapid cell turnover (e.g. Non-Hodgkin lymphoma, acute leukemia)* -*AKI in TLS results from Precipitation of Calcium-Phosphate (radiopaque, wedge-shaped prisms) & Uric Acid (radiolucent, rhomboid/rosettes) Kidney Stones*, leading to *Renal Tubular Obstruction* -Additionally, *elevated uric acid reduces nitric oxide levels* --> *causing Renal Vasoconstriction & localized inflam, facilitating both ischemic & inflammatory renal injury* -Optimal *TX of AKI d/t TLS is w/ Aggressive IV Hydration PLUS uric acid-reducing therapy w/ RASBURICASE (urate oxidase analogue)* -*Rasburicase is preferred to Allopurinol or Febuxostat (xanthine oxidase inhibitors) bc Rasburicase metabolizes existing elevated uric acid levels that have accumulated, rather than simply preventing the production of additional uric acid* Note: Rasburicase is *contraindicated in G6PD deficiency* d/t *risk of methemoglobinemia (oxidized iron, Fe3+, doesn't bind O2, but binds cyanide; tx w/ methylene blue & vitamin C) & Hemolysis*

Which electrolyte abnormality can lead to *hyperactive deep tendon reflexes*?

*HYPOCALCEMIA* *Hypocalcemia* can occur *during or immediately after surgery*, esp in pts undergoing *major surgery & Requiring Extensive (multiple) RBC Transfusions* -Usu hypocalcemia occurs d/t *volume expansion & hypoalbuminemia* and is therefore *ASX*; HOWEVER, sometimes manifests as *HYPERACTIVE DEEP TENDON REFLEXES (may be the initial manifestation of hypocalcemia), MUSCLE CRAMPS, & RARELY, CONVULSIONS* -The etiology of *hypocalcemia w/ massive blood transfusion* is related to the *large amounts of CITRATE used to Anticoagulate the blood*; the *citrate chelates (binds) w/ calcium, leading to hypocalcemia* -*HYPOmagnesemia* may *mimic hypocalcemia* BUT is assoc w/ *heavy alcohol use, prolonged nasogastric suction or diarrhea, and diuretic use* -*Mild HYPERmagnesemia results in DECR DTRs; Severe HYPERmagnesemia causes LOSS of DTRs & Muscle Paralysis*, thereby leading to *Flaccid Quadriplegia, DECR Respiration, & Eventual APNEA*

Which muscles does actively flexing the knee against resistance allow assessment of?

*Hamstring muscles* -*Injury to the hamstrings (e.g. tear)* typically causes *pain, swelling, bruising, & tenderness in the posterior aspect of the thigh*

When should you hospitalize a pt with Anorexia Nervosa?

*Hemodynamic Instability* -HR <40 bpm -BP <80/60 or Light-headed feeling/syncope from severe dehydration -Orthostatic changes (decr in SBP ≥20 and in DBP ≥10 with standing) -Hypothermia *Arrhythmia (low K & Mg), Severe Bradycardia, Acute Food Refusal, BMI <15, Electrolyte Derangements (decr serum PO4, K, Mg, & Thiamine), & Suicidality/Psychosis* *Refeeding Syndrome* - potentially fatal complication of nutritional rehabilitation in underweight pts w/ chronic poor oral intake -*Congestive HF can dev* from a *weak, atrophic heart that cannot handle fluid & electrolyte shifts* -- also dev *pulmonary & peripheral edema* -*Phosphate, Potassium, Magnesium, & Thiamine are rapidly depleted in anorexia and need replacement (oral phosphate preferred to IV, fix hypophosphatemia before starting feeds!) -^Electrolytes should be monitored closely while caloric intake is increased incrementally *Once medically stabilized*, mainstay *TX for Anorexia is Psychotherapy (CBT) & Nutritional Rehabilitation*

Cocaine Intoxication & Withdrawal

*Intoxication* -*Impaired judgment, pupil DILATION, hallucinations (incl tactile), paranoid ideations, angina, sudden cardiac death* -Chronic use may lead to *perforated nasal septum* d/t vasoconstriction & resulting ischemic necrosis -TX: alpha-blockers, benzodiazepines (beta-blockers are NOT recommended) *Withdrawal* -Acute onset of depression w/ pronounced fatigue following a period of increased energy -Abrupt cessation is usu followed by a "crash" which can induce *severe depression w/ suicidal ideation and psychomotor slowing* with milder sx that resolve in 1-2wks (withdrawal involves mostly psychological sx rather than physical) -Common sx incl: *depression, fatigue, hypersomnia, increased dreaming, hyperphagia, impaired concentration, & intense drug craving* -Physical sx are minor and rarely require tx

How should you treat a pt with pulmonary embolism that causes right ventricular dysfunction and hemodynamic instability requiring vasopressor support?

*Hemodynamic instability* is the /most important indication/ for *THROMBOLYSIS* in PE patients, which can be administered via *systemic infusion or catheter-directed therapy* -Other relative *indications for thrombolysis* incl *severe right ventricular dysfunction, large clot burden, and evidence of free, right-sided cardiac thrombus* *Contraindications to Thrombolytic TX in PE* include: *Intracranial neoplasm or prior hemorrhage; cerebrovascular abnormalities; active bleeding; & recent cranial trauma*.--These pts should be considered for *surgical or catheter-directed embolectomy* Receive *Thrombolysis* IF *Pulm Embolism W/ Hypotension (SBP <90) AND LOW-Bleeding risk* Receive *Embolectomy* (percutaneous or surgical) IF *Shock likely to cause death within hours* OR *Failed Thrombolysis* (*or Thrombolysis Contraindicated*) *W/ Persistent Hypotension* Note: Although most PE pts should be started on *anticoagulation (e.g. heparin)*, those w/ *hemodynamic instability should have AC HELD until after thrombolytic therapy to minimize bleeding risk*

How to diagnose suspected pulmonary embolism in a hemodynamically stable pt vs. an unstable pt?

*Hemodynamically STABLE* -Determine pretest probability: • If High --> Confirmation Testing w/ CT Angiography or V/Q scan --> PE diagnosed or excluded • If Low/Intermediate --> D-dimer Screen --> If Negative, then PE excluded; If Positive D-dimer --> Confirm w/ CT Angio or V/Q --> PE diagnosed or excluded *Hemodynamically UNSTABLE* -*Assess right ventricle function* with an *emergent TTE* • If *Echo* shows *New Dysfunction (i.e. RV dilation or RV hypokinesis indicating reduced systolic function)* --> *Presumed Massive PE* --> *TX w/ Empiric Thrombolysis (Fibrinolysis)* (e.g. tPA thrombolytics like alteplase, reteplase, streptokinase, tenecteplase) • If *Echo shows Normal* results --> *Evaluate for other causes of shock*

What is HELLP syndrome assoc with pregnancy?

*Hemolysis, Elevated LFTs, Low Platelet count (≤100,000)* -A *variant of preeclampsia, occurring >20wks gestation* but *can occur in the postpartum period too!!* Clinical: *N/V, RUQ pain, Headache & Visual changes, HTN* Labs: *Microangiopathic hemolytic anemia; Elevated LFTs; Thrombocytopenia; ± Proteinuria* *TX: Delivery; Magnesium Sulfate for seizure ppx; Antihypertensives (e.g. hydralazine); supportive care, serial lab evals* *Complications*: *Abruptio placentae; Subcapsular liver hematoma; Acute renal failure; Pulmonary edema; DIC* Note: In HELLP and Preeclampsia, *IV antihypertensives (e.g. Labetalol, Hydralazine) are indicated for ACUTE control of BP ≥ 160/110*

HELLP Syndrome

*Hemolysis, Elevated Liver enzymes, & Low Platelets (≤100,000)* -HELLP syndrome, a variant of preeclampsia, typically occurs at *>20wks gestation* but can also occur during the *postpartum period* -Presenting signs & sx of HELLP syndrome incl: Malaise, *HA*, Visual Changes, N/V, *Epigastric/RUQ Pain*, *HTN*, & Proteinuria -HELLP pts are *at risk for seizures*; *MAGNESIUM SULFATE* is the first-line therapy for *Seizure PPX* -Other complications of HELLP Syndrome incl: Abruptio Placentae, DIC, Renal Failure, Pulmonary Edema, & Hepatic Hematoma -For this reason, TX also incl supportive care, serial laboratory evaluations, and (for pts who are still pregnant) delivery Note: In HELLP syndrome && Preeclampsia, IV Antihypertensives (e.g. Labetalol, Hydralazine) are typically indicated for acute control of BP ≥160/110 Note: Plasma Exchange is indicated when HELLP syndrome is complicated by fulminant hepatic disease (e.g. AST >2,000) and there is NO assoc HTN.

How does herpes simplex & primary varicella infections present?

*Herpes Simplex* infections typically p/w as *multiple vesicular & ulcerative lesions on mucosal surfaces*; *Primary herpes simplex* typically p/w *prodromal sx* (e.g. fever, malaise, HA) and *lesions are accompanied by lymphadenopathy*; *TX w/ Oral Acyclovir* *Primary Varicella* infections typically present as a *pruritic, generalized, rash composed of successive crops of macules that progress into red papules and crusted pustules*; *Prodromal sx* assoc w/ varicella infection incl *fever, anorexia, & pharyngitis*; *TX w/ Oral Acyclovir*

Occupational HIV Postexposure Prophylaxis

*High-Risk Contact (PPX Recommended!)* -Exposure of: *Mucous membrane, nonintact skin*, or *percutaneous* (*needlestick*) exposure -Exposure to: *Blood, semen, vaginal secr, any body fluid w/ visible blood* (CSF, pleural/pericardial, synovial, peritoneal, amniotic fluid have uncertain risk) *Low-Risk* Contact (PPX *NOT* Recommended) -Exposure to urine, feces, nasal secr, saliva, tears (no visible blood) *Timing* -Initiate *urgently* - preferably within the *first few hrs* -*Continue for 4 WEEKS* *Regimen* -TX with *≥3-drug regimen* recommended • Two nucleotide/nucleoside reverse transcriptase inhibitors (e.g. *tenofovir, emtricitabine*) PLUS -Integrase strand transfer inhibitor (e.g. *raltegravir/elvitegravir/dolutegravir*), protease inhibitor (~navir drugs), or a nonnucleoside reverse transcriptase inhibitor (delaviridine/efavirenz/nevirapine)

What's the MCC of non-PTH-dependent hypercalcemia?

*Humoral hypercalcemia of malignancy (HHM)* which is d/t *secr of PTH-related protein (PTHrp, which also binds PTH receptors)* -Hypercalcemia in primary hyperPTH is usu Mild (<12mg/dL) and often ASX, whereas *HHM is typically more acute & severe hypercalcemia with suppressed PTH (<20pg/mL)* -*Renal dysfunction* may occur d/t *dehydration from polyuria & vomiting* and *hypercalcemia-induced vasoconstriction of intrarenal blood vessels* -Other causes of *cancer-assoc hypercalcemia* incl *overproduction of 1,25-dihydroxyvitamin D* (*certain lymphomas*) and *bony metastases* (e.g. *multiple myeloma*) -Though HHM usu seen in pts w/ known malignancy, *hypercalcemia may be the presenting feature of the malignancy* -*HHM is often seen in Advanced Malignancy & confers a POOR Prognosis*

Complications of Multiple Myeloma

*Hypercalcemia* -Can be ASX or SX (e.g. anorexia, nausea, polyuria, constipation, weakness, confusion) -TX w/ hydration & dexamethasone (mild), bisphosphonates (mod-severe) *Renal Insufficiency* -Usu d/t *light-chain cast nephropathy* or *deposition dz* -Can be acute or gradual -Eventual *normocytic anemia* d/t kidney damage -May require *plasmapheresis* or *dialysis* *Infections (e.g. PNA, UTI)* -Highest risk in first 3-4mo of therapy -Vaccines, PPX ABX during TX to help prevent *Skeletal Lesions* -Usu present w/ *bone pain or pathologic fracture* -*Bisphosphonates* for prevention *Hyperviscosity Syndrome* -*Nasal or oral bleeding, blurry vision, neurologic sx (e.g. confusion, HA), heart failure* d/t IgM pentamers -Severe cases p/w somnolence, coma, seizures -*Plasmapheresis* for symptomatic pts -Usu arises in the setting of *excess monoclonal IgM prodn* usu in *Waldenstrom Macroglobulinemia, but ~0.5% of MM generate monoclonal IgM* *Thrombosis* -Incr risk of *Arterial* (stroke/TIA, MI) *& Venous Thrombosis*

Whipple's Triad of Hypoglycemia?

*Low blood glucose level, <60 mg/dL* *Sx of Hypoglycemia* *Symptomatic Relief w/ Admin of Glucose* The presence of Whipple's triad is strongly suggestive of true hypoglycemia

Complications of Donor Nephrectomy

*IMMEDIATE Risks* -Risks are primarily those typical of surgical procedures, such as DVT and hospital-acquired infections -Overall surgical mortality rate is very low at 3.1/10,000 donors. *LONG-TERM Risks* -Long-term risk are also quite low -Although there is an immediate decrease in net GFR following donor nephrectomy, compensatory hypertrophy in the remaining kidney largely replaces lost renal fxn -As a result, there is NO increased risk of ESRD in kidney donors!!! -Overall mortality in kidney donors is also similar to that of the general population -*Kidney donation* is, however, assoc w/ an *increased risk of gestational complications in female donors of childbearing age* -These complications incl: Fetal Loss, Preeclampsia, Gestational Diabetes, & Gestational HTN -It is generally recommended that women complete their planned childbearing prior to kidney donation -However, this is not an absolute contraindication to donation, and it is possible for women who have not completed childbearing to proceed with the procedure if they are appropriately informed of the risks.

How do you increase statistical power?

*INCREASE THE SAMPLE SIZE! Increasing the sample size will be needed to Increase the Power of the study so as to detect a smaller effect size (difference between groups)* *Sample size* is *related to Statistical Power*, which is the *ability to detect a significant effect in a study* (e.g. difference between groups), *when an effect really exists* -Generally, *larger sample sizes have higher statistical power than smaller* sample sizes -However, *sample size & statistical power* are affected by a number of parameters, including the *magnitude of the expected effect size* (*size of expected difference between the groups*) and the *level of statistical significance adopted* in the study

Which epidemiological parameters do NOT change with prevalence? I.e. Are INDEPENDENT of disease prevalence? Which parameters are DEPENDENT of disease prevalence?

*INDEPENDENT of Disease PREVALENCE* -Sensitivity -Specificity -Likelihood ratio *DEPENDENT on Disease PREVALENCE* -Positive predictive value (PPV= TP/(TP+FP); varies directly with prevalence (i.e. higher prevalence, high PPV) -Negative predictive value (NPV = TN/ (TN+FN); varies indirectly with prevalence (i.e. higher prevalence, low NPV)

What treatment should be given to patients with cirrhosis with concern for variceal hemorrhage?

*IV OCTREOTIDE* -Initiate *after stabilizing* the pt (*intubation, IV fluids, type & cross*), *while awaiting endoscopic therapy (for confirmation)* -Octreotide is thought to decr the elevated portal venous pressure that causes variceal formation and may stop the hemorrhage

Medical Management of Anaphylaxis

*Immediate Management*: -*EPINEPHRINE* (MOST IMPORTANT!) • *IM preferred*, may be *repeated up to 3 doses* • *IV in severe/refractory* cases -*IV crystalloid fluids & Trendelenburg* positioning for *hypotension* -*Albuterol* for *bronchospasm* -*Early intubation* for *upper airway obstruction* *Adjunctive Management*: -*H1/H2 antihistamines* (e.g. H1, diphenhydramine, hydroxyzine, loratadine; H2, famotidine, cimetidine, ranitidine) • *Glucocorticoids* • *Glucagon* for pts on *beta-blockers (reversal)* • Hospital admission for severe initial presentation (e.g. shock) or Ongoing SX despite TX

Lupus Nephritis

*Immune complexes* containing *anti-dsDNA antibodies within the glomeruli* of SLE pts

What does *Saw Palmetto possibly increase the risk for*?

*Increased Bleeding Risk!* *Use saw palmetto cautiously in pts undergoing surgery* d/t *possible incr. risk of perioperative bleeding*, likely *d/t platelet dysfunction*

What happens when you *conduct multiple independent hypothesis tests without proper adjustment to the alpha level*?

*Increases the rate of type 1 errors* -- meaning that *when evaluating multiple secondary endpoints, there is a higher probability of erroneously finding a statistically significant result with one of these endpoints* (e.g. (higher likelihood of type 1 error*) *due to chance alone*. This phenomenon is known as the *multiplicity*, or *multiple testing, problem* -In general, the *rate of type 1 error will increase depending on the alpha level for individual tests and the number of independent tests* -For example, the rate of type 1 error in a study attempting to evaluate 5 secondary endpoints would be ~23%, whereas the classically accepted value is usu set ≤5% (statistically significant p-value) -Statistical techniques can be used to account for the multiple testing problem (e.g. the α level or p-value is sometimes adjusted)

Latent Tuberculosis

*Induration of 5mm: Risk Factors* -*HIV* infection -Recent contact w/ TB-infected pt -Pt w/ *fibrotic changes* on CXR suggestive of prior TB -Organ transplant recipient -Immunocompromise *Induration of 10mm: RF* -Recent immigration from high prevalence country -Injection drug user -Residents and employees of high-risk settings (prisons, homeless shelters, healthcare facilities) -Children <4yo *Induration of 15mm: RF* -No known risk factor Note: Induration from prior BCG vaccine rarely exceeds 15mm, and significantly decreases 15yrs after it is received. *Interferon gamma release assays can be used to distinguish a true positive tuberculin skin test from prior BCG vaccination.* -Treatment for Latent TB is still indicated since the infection can become reactivated if the pt were to become immunocompromised. -The regimen of choice for *TX of Latent TB* is *Isoniazid for 9mo* Note: Rifampin for 4mo is an alternative TX for Latent TB, but the combination of rifampin w/ isoniazid is not recommended.

Routine Prenatal Lab Testing

*Initial prenatal visit* -Rh(D) type & antibody screen -Hb/Hct, MCV, ferritin -Rubella & varicella immunity -Urine cx -Urine dipstick for protein -Chlamydia PCR (if risk factors present) -Pap test (if screening indicated) *24-48 wks* -Hb/Hct for anemia, CBC -Antibody screen if Rh(D)-Negative -1hr 50-g Glucose Challenge Test for Gestational Diabetes (d/t rise in human placental lactogen secr by placenta that increases fetal glucose supply by inducing maternal insulin resistance) *36-38 wks* -Group B Streptococcus (agalactiae) rectovaginal culture

When should a COPD Exacerbation be managed as an *INPATIENT?*

*Inpatient management of COPD Exacerbation* is *indicated only for those* who *FAIL Outpatient therapy* or who have *Severe SX (e.g. rapidly worsening dyspnea, worsening hypoxia/hypoxemia, AMS, FEV1 <50% than predicted)*

Are herbal preparations regulated by governmental agencies?

*NO!* Herbal preparations are generally classified as food or dietary supplements, enabling manufacturers to avoid the same scientific scrutiny that prescription drugs receive as they are readied for market

Pramipexole, Bromocriptine: MOA

-*Pramipexole & Bromocriptine directly activate dopamine receptors in the brain* without need for metabolism to its active form (unlike with Levodopa) -Used in progressive dopamine deficiency, *PARKINSON DZ*

What is the tx for nodulocystic acne or mutlidrug-refractory acne?

*Isotretinoin* is a highly effective oral tx for *nodulocystic acne, acne that has failed other topical/oral therapy, & acne that leads to Scarring* -Acne may initially flare up and subsequently improve within first few wks of therapy w/ isotretinoin -*One course of tx over 4-6mo period* usu provides a permanent improvement in acne -Isotretinoin use is limited d/t AE, esp *teratogenicity* (e.g. spontaneous abortion, congenital malformations) -*Female pts of childbearing potential, regardless of sexual activity, must have TWO NEGATIVE Pregnancy Tests prior to starting therapy* -And those who ARE sexually active, must use *TWO Concurrent Contraception Methods* (e.g. *OCPs & condoms*) *a MONTH Before, During, and After tx* Note: Isotretinoin in Male sexual partner is NOT assoc w teratogenicity (minimal amount of drug excr in semen) Other AE: Dry skin and mucous membranes, myalgias. Bc of *incr risk for AE (e.g. pseudotumor cerebri w/ concomitant tetracycline [doxycycline] use), other systemic tx for acne must be DISCONTINUED when initiating isotretinoin therapy*

How do you diagnose Turner syndrome?

*KARYOTYPE CHROMOSOME ANALYSIS* is DIAGNOSTIC -Turner Syndrome results from *complete or partial absence of an X-Ch, due to a RANDOM ERROR in cell division* called *NONDISJUNCTION*. -Turner syndrome is considered a *SPORADIC EVENT*, so the *likelihood of recurrence in subsequent pregnancies is similar to that of the general population* (*it is NOT inherited!!!*) *Dx suspected d/t short stature alone, or delayed thelarche and primary amenorrhea in adolescence* (d/t *ovary dysgenesis*) -Can have *horseshoe kidney* (causing *obstructive nephropathy, 2/2 vesicoureteral reflux -> freq UTIs*) Turner pts have *normal intelligence usually*, but should be monitored for incr risk of learning disabilities. Turner assoc with webbed neck and congenital lymphedema

What is *kava kava* used for?

*KAVA KAVA* is an herbal prep that may help with sx of *anxiety and insomnia* ---however its use is NOY recommended d/t potential *Risk of Severe Liver Toxicity*

What is the most common chromosomal cause of *male infertility*?

*KLINEFELTER SYNDROME (47, XXY)* -Physical exam findings incl *gynecomastia & cryptorchidism*

Kawasaki DZ - Quick Overview

*Kawasaki* Dz is a *vasculitis characterized by ≥5d of Fever PLUS ≥4 Clinical Criteria (b/l nonexudative Conjunctivitis, Mucosal Changes [oral mucositis, strawberry tongue], cervical LAD >1.5cm [0.6cm], Rash [polymorphous -> desquamating], Extremity changes [hand-foot changes-edema, erythema)* -Usu *Asian kids <4yo* -May dev *coronary artery aneurysms, thrombosis, or rupture* --> which *can cause DEATH* -*TX: IVIG + ASPIRIN*

Which vertebral level does the cremasteric reflex correspond to?

*L1-L2 level of spinal cord!* L1-L2 is also responsible for *hip flexion & adduction* Note: Cremasteric reflex can be diminished or lost secondary to *diabetic autonomic neuropathy* (as well as *erectile dysfunction, diminished testicular sensation, bladder dysfunction, & inability to masturbate*)

L5 Radiculopathy S1 Radiculopathy

*L5 Radiculopathy* -Can cause *decreased sensation of the lateral thigh* but also causes *sensory loss over the lateral shin & dorsal foot* -Muscle *weakness of foot dorsiflexion & inversion (tibialis anterior), foot eversion (peroneus), toe extension ( *S1 Radiculopathy* -Affects *sensation over the posterior thigh & posterolateral calf* -BOTH L5 & S1 Radiculopathies are usu accompanied by *low back pain that radiates into the leg, && weakness of supplied muscles is often present*

Which vertebral level does dorsiflexion & plantar flexion correspond to?

*L5-S2 region of spinal cord!*

Length-time bias vs. Lead-time bias

*LENGTH-TIME BIAS* -Seen with *screening tests* -Occurs when the *survival benefits of a screening test are overestimated/overstated d/t the detection of a disproportionate amount of pts w/ SLOWLY Progressive, BENIGN Cases* -These pts tend to be asymptomatic for a longer time, making it more likely that they will be diagnosed based on screening tests rather than clinical symptoms of the [slowly-progressive] disease *LEAD-TIME BIAS* -Another common bias seen with *screening tests* -Occurs when *a test diagnoses a disease earlier* and *as a result, the time from diagnosis until death APPEARS Prolonged - even though there is actually NO improvement in survival*

Which factors are most assoc *requests for euthanasia & physician-assisted suicide*?

*LOSS OF AUTONOMY* *LOSS OF CONTROL OF THE DYING PROCESS* *LOSS OF DIGNITY* *LOSS OF ABILITY TO ENGAGE IN PLEASURABLE ACTIVITIES* *FEAR OF FUTURE SUFFERING* [rather than actual pain in the moment]

Lactose Intolerance presentation vs Irritable Bowel Syndrome presentation

*Lactose Intolerance* -*Chronic watery, LARGE-volume diarrhea, flatulence, & bloating* after meals d/t malabsorption (no abdo pain) -Adult onset, presenting in 20-40yo -Deficiency/reduced activity of lactase on small intestine brush border (lactose --> glucose & galactose normally) -SX occur as the *osmotic load* of undigested carbs pass through intestines, drawing water into lumen, & decr transit time -Colonic bacteria also ferment lactose, creating short-chain fatty acids & hydrogen gas --> Bloating & flatulence -Can do lactose breath hydrogen test *Irritable Bowel Syndrome* -Results from poorly-understood alterations in GI motility -Pts usu have *recurrent abdominal pain and changes in bowel habits* (e.g. *SMALL- to moderate-volume diarrhea*)

What are latent errors? What are heuristics?

*Latent errors are System-Level Factors* (e.g. *inefficient protocols*) *that cause adverse events* *Heuristics* are *mental shortcuts* -*Availability heuristic* or is a type of cognitive bias that helps us make fast, sometimes incorrect, assessments. It involves relying on info that quickly comes to mind or is most readily available

What cardiac manifestations may reflect changes of long-standing hypertension?

*Left ventricular hypertrophy!!* -Displaced point of maximal impulse down & to the left -On EKG can see LVH w/ nonspecific ST-T wave changes

CREST Syndrome

*Limited scleroderma*—*LIMITED skin involvement* confined to *fingers and face*. Also with *CREST syndrome*: *C*alcinosis cutis, anti-*C*entromere antibody, *R*aynaud phenomenon, *E*sophageal dysmotility, *S*clerodactyly, and *T*elangiectasia. More benign clinical course.

Can lithium be used during pregnancy?

*Lithium* is used to *TX BIPOLAR MANIA and DEPRESSION* Though *Lithium is assoc w/ a slightly Incr risk of cardiac malformation (EBSTEIN ANOMALY)*, *Lithium CAN be used during Pregnancy* in pts with *SEVERE Bipolar illness*

MEN Syndromes - Quick Overview

*MEN1*: Pituitary adenoma (also vision defects), Parathyroid hyperplasia/adenoma (hyperparathyroidism w/ hypercalcemia, incr PTH, polyuria, kidney stones, decr bone density), Pancreatic tumors (esp gastrinomas, leading to recurrent peptic ulcers). May also be assoc w/ multiple cutaneous lipomas too. *MEN2A*: Parathyroid hyperplasia, Medullary Thyroid Carcinoma (screen for incr calcitonin), Pheochromocytoma (screen with plasma metanephrines) *MEN2B*: Mucosal neuromas, Marfanoid body habitus, Medullary Thyroid Carcinoma (screen for incr calcitonin), Pheochromocytoma (screen with plasma metanephrines)

Which imaging modality has the highest sensitivity for diagnosing osteomyelitis?

*MRI* > 3-phase bone scan > Tagged WBC scan > Probe-to-bone test or Visible bone > Plain x-rays *MRI w/ contrast* of the foot is the diagnostic test with the greatest sensitivity and a *high negative predictive value* for the diagnosis or exclusion of osteomyelitis of the foot

Beck triad of Cardiac Tamponade

*MUFFLED HEART SOUNDS* *DISTENDED NECK VEINS* *HYPOTENSION* Other findings: -*Elevated HR* -*Pulsus Paradoxus* - Decr systolic BP by >10 mmHg during inspiration -EKG shows *low voltage QRS complexes* and *electrical alternans* (d/t swinging movement of heart by large effusion, causing compression of the heart) -Equilibration of diastolic pressures in all 4 chambers

What is the most common/important factor in *predisposing elderly pts* to an *increased incidence of adverse drug reactions*?

*MULTIPLE MEDICATION USE* -Pts >65yo take an average of 2-6 prescribed drugs and 1-3 non-prescribed drugs daily -These pts are at an *increased risk preoperatively for anesthetic and operative drug reactions* -Most common meds assoc w/ adverse drug rxns incl *anti-psychotics, anti-hypertensives, sedatives, diuretics, NSAIDs, corticosteroids, & digoxin* Note: Age itself does not incr risk of a perioperative adverse drug rxn

What is mannitol used for?

*Mannitol* is an *osmotic agent used to tx elevated ICP* caused by trauma, intracranial hemorrhage, CNS tumors, and stroke.

What *maternal and fetal complications* have an *INCR risk* in *Adolescent (≤19yo) Pregnancies*?

*Maternal Complications* -Hydatidiform Mole -Preeclampsia -Anemia -Operative Vaginal Delivery -Postpartum Depression *Fetal Complications* -Gastroschisis -Omphalocele -Preterm Birth/Delivery -Low Birth Weight -Perinatal Death/Mortality ^likely underlying etiologies for *preterm labor in teen moms* are *Inadequate Nutrition & Physiologic Immaturity* (teen moms require even higher daily caloric,calcium, & iron requirements) *Adolescents who deliver preterm do NOT appear to be at increased risk for preterm delivery in subsequent pregnancies beyond their teenage years*

What are meta-analyses used for?

*Meta-analysis* is an epidemiologic tool used to *INCR the POWER of a Study (i.e. INCR its ability to detect associations, if such associations exist) by POOLING DATA FROM SEVERAL STUDIES* -When a single study has a *very small sample size* and the outcome of the study is *rare*, it is *difficult* for the study to find *statistically significant associations, even when real and valid associations exist* -^In such cases, *meta-analysis can be used to INCR the Sample Size, thereby INCREASING the POWER of the analysis* -The *Major DISADVANTAGE of Meta-Analysis* is that it incl *concomitant "pooling" of the biases & limitations of individual studies into one analysis* -The *Major ADVANTAGES of Meta-Analysis* include the *Increased Statistical Power and Robustness for estimating associations*, which usu outweigh the limitations of this epidemiological tool

Alcohol Withdrawal Syndrome

*Mild Withdrawal - 6-24hrs since last drink* -Anxiety, insomnia, tremors, diaphoresis, palpitations, GI upset, intact orientation *Seizures - 12-48hrs since last drink* -Single seizure or multiple generalized tonic-clonic *Alcoholic Hallucinosis - 12-48hrs since last drink* -Visual/auditory/tactile; intact orientation; /stable/ vitals *Delirium Tremens - 48-96hrs since last drink* -Confusion, agitation, fever, tachycardia, HTN, diaphoresis, hallucinations TX Alcohol Withdrawal with *BENZODIAZEPINES*. If the pt has significant liver dz, *lorazepam* is the preferred agent d/t its intermediate half-life, lack of active metabolites, and availability in IV form (can also give oxazepam & temezepam if have liver dz). Note: Chlordiazepoxide & Diazepam are /long/-duration benzos metabolized by phase 1 cyto-P450 oxidation into active metabolites & would confer serious risk of toxic accumulation in liver dysfunction pts

What is *MISUSE* when it comes to medications?

*Misuse* consists of *taking higher doses to achieve euphoric effects alone or in combination w/ illicit drugs* and is more commonly seen w/ intermediate-release preparations

When is the right time to perform a myringotomy and place tympanostomy tubes?

*Myringotomy* is a procedure to create a hole in the ear drum to allow fluid that is trapped in the middle ear to drain out, using *tympanostomy tubes* -If pts experience *persistent treatment failure, has persistent effusion for >3mo, or ≥3 episodes of Acute Otitis Media in 6mo, or ≥4 episodes in 1yr*, consider these interventions

Does pregnancy alter NAAT results for gonorrhea or chlamydia? (e.g. false positives)

*NAAT* is the preferred test for diagnosing C. trachomatis and N. gonorrhoeae d/t its *high sensitivity & high specificity* NAAT false-positive and false-negative results are *RARE* and Pregnancy does NOT alter NAAT test performance!

Major Differences B/W Neurofibromatosis 1 & 2

*NF1* -Mutation in *NF1 tumor suppressor gene on Ch 17* that codes for *neurofibromin*, a negative regulator of RAS -*Autosomal dominant*, 100% penetrance -*Café-au-lait spots (HYPERpigmented), cutaneous neurofibromas, optic gliomas, pheochromocytomas, Lisch nodules (pigmented iris hamartomas), axillary freckling* *NF2* -Mutation in *NF2 tumor suppressor gene on Ch 22* -*Autosomal dominant* -*Bilateral acoustic schwannomas /neuromas (b/l deafness), juvenile cataracts, meningiomas, & ependymomas, and HYPOpigmented café-au-lait spots*

NNT formula

*NNT = 1/ARR* ARR = Absolute risk reduction ARR = Control rate - Treatment rate

Is Wolff-Parkinson-White syndrome a common cause of Sudden Cardiac Death?

*NO!! WPW is an UNCOMMON cause of SCD!* -*Resting EKG* characteristically show *a short PR interval with slurred upstroke & widening of the QRS complex (delta-wave)* -MC type of *ventricular preexcitation syndrome* -*Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses rate-slowing AV node* --> *Ventricles partially depolarize earlier than expected* --> *Characteristic delta wave w/ Widened QRS complex & shortened PR interval* -May result in *Reentry circuit* --> *Supraventricular tachycardia (SVT)* -*TX*: *Procainamide* -Avoid AV nodal blocking drugs (adenosine, diltiazem, verapamil, β-blockers, digitalis)

Basal Cell Carcinoma - 3 main Subtypes

*NODULAR BCC* ~80% of cases! MC subtype! -*Shiny, pearly, skin-colored nodule with TELANGIECTASIS* -*ROLLED (Raised) BORDER and ULCERATION* often present *SUPERFICIAL BCC* Second MC type! -P/w *Pink or Red Macules, patches, or thin plaques*, sometimes with *Atrophic-appearing centers* and *peripheral small, pearly papules* *MORPHEAFORM/INFILTRATIVE BCC* Least common type! -P/w *pale, scar-like indentations* -The *classic morphology of Nodular BCC* may be *easily recognizable,* BUT *atypical presentations occur frequently* -Although a lesion can have an *irregular shape* and *lack the typical pearly surface,* an *older, fair-skinned* pt with an *ulcerated lesion with raised/rolled borders* is consistent with *BCC* -In general, any *CHRONIC (>3WKS), NON-Healing, ULCERATED lesions suggest MALIGNANCY and warrant BIOPSY*

Management of Heart Failure: Order of Therapy

*NYHA Class I* -No limits w/ physical activity -TX: ACEI/ARB *NYHA Class II* -Slight limitation w/ physical activity -Ordinary activity causes fatigue, palpitations, or dyspnea -TX: ACEI/ARB PLUS: • Diuretics • Beta blockers w/ EF ≤40% once euvolemic • Spironolactone if EF <30% w/ stable renal fxn & K+ • Defibrillators for EF ≤30% *NYHA Class III* -Marked Limitation w/ physical activity -Less than ordinary activity causes fatigue, palpitations, or dyspnea -TX: Same as before PLUS: • Isosorbide Dinitrate ± Hydralazine if African American • Digoxin if symptomatic w/ Spironolactone • Cardiac Resynchronization therapy if QRS >150 msec *NYHA Class IV* -Unable to carry out any physical activity w/o symptoms -Can have symptoms at rest -TX: Same as before PLUS: • Transplant/Ventricular assist device evaluation

Near-Miss Events Sentinel Events Nonpreventable Adverse Events Preventable Adverse Events

*Near-Miss Events* -*Preventable* errors that are *caught before they ultimately harm the pt* -e.g. Drug prescribed to the wrong pt, but the nurse catches the error prior to drug administration *Sentinel Events* -*Preventable* errors that *cause significant or irreversible pt harm* and that *signify a clear deviation from standards of care & possible negligence* (e.g. wrong-side surgery) *or serious system flaws* (e.g. serious drug rxn in a pt w/ a documented allergy to the drug) *Nonpreventable Adverse Events* -*Complications of TX* that *may occur despite appropriate medical practice consistent with current standards of care* *Preventable Adverse Events* -Occur from *personnel error* or *failure to follow standards of care*

What drugs are used to *TX Hypertension in Pregnancy*?

*Nifedipine, methyldopa, labetalol, hydralazine*

Preferred Antiarrhythmic Therapy for Atrial Fibrillation Pts

*No CAD or Structural Heart Dz* -Flecainide (class IC) -Propafenone (class IC) *Left Ventricular Hypertrophy* -(Class IC antiarrhythmics contraindicated in LVH) -Dronedarone (class III) -Amiodarone (class III) *CAD W/O Heart Failure* -Sotalol (class III) -Dronedarone (class III) *Heart Failure* (LV systolic dysfxn w/ EF<35%) -Amiodarone (class III) -Dofetilide (class III) *Recurrent SX Refractory to Medication* -Radiofrequency ablation

What is the primary and secondary intervention used in preventing esophageal variceal hemorrhage?

*Nonselective beta blockers (propranolol & nadolol)* PRIMARY: In pts w/ no prior bleeding episodes but with known esophageal varices SECONDARY: Known varices & prior bleeding *Best used in combination with endoscopic surveillance and band ligation*

Osteoarthritis vs Reactive Arthritis vs Rheumatoid Arthritis

*OSTEOARTHRITIS* -MCC a *Slowly Progressive Arthropathy affecting the Weight-bearing joints of the lower extremities and Interphalangeal joints of the hands* -*Synovial fluid analysis* is *typically BLAND, w/ <2,000 cells/mm3, <50% neutrophils, and NO crystals* *REACTIVE ARTHRITIS* -P/w *acute symmetric arthritis* and typically *follows a GI or GU infection* -Classic triad: "can't see, pee, or bend my knee" • *Conjunctivitis, Urethritis, Arthritis* -Associated with *infections by Shigella, Campylobacter, E coli, Salmonella, Chlamydia, Yersinia* *RHEUMATOID ARTHRITIS* -*Autoimmune*, can cause a *variety of joint manifestations*, although the *Proximal Interphalangeal, Metacarpophalangeal, & Wrist Joints are most commonly affected* -*Morning STIFFNESS IS PROLONGED, >1HR* -Can cause an *Inflammatory Synovial Fluid Effusion, but crystals are NOT present* -Inflammation induces formation of *pannus (proliferative granulation tissue), which erodes articular cartilage & bone* -*Positive Rheumatoid Factor (IgM Antibody that targets IgG Fc region in 80%), Positive Anti-Cyclic Citrullinated Peptide (Anti-CCP +) Antibody is more specific to RA* -*Pain, swelling, & morning stiffness >1hr, Improving W/ USE* -*SYMMETRIC JOINT INVOLVEMENT* -*Systemic Sx (fever, fatigue, wt loss) & Extraarticular Manifestations common*

What is the most appropriate measure of association between exposure and disease in case-control studies?

*Odds Ratio* is a measure of association b/w exposure and disease in case-control studies. Participants initially identified based on their *disease status* (i.e. cases have dz, controls don't); The frequency of exposure is subsequently compared between cases and controls OR represents the odds of exposure among cases relative to controls *OR = 1.0 (null value)* --> odds of exposure among cases is same as odds of exposure among controls; therefore, *exposure is NOT assoc w/ dz* *OR ≠ 1.0* --> odds of exposure among cases are lower (OR<1) or higher (OR>1) than among controls; therefore *exposure IS assoc w/ dz* OR is sometimes described as the odds of dz among exposed pts relative to nonexposed pts *Null value is always OR = 1*

Which tx for inflammatory acne vulgaris can cause significant photosensitivity? And how to manage?

*Oral Doxycycline (tetracycline antbiotic)* Meds used to tx inflammatory acne incl benzoyl peroxide, topical retinoids, and topical/oral abx -The most common agent that causes significant photosensitivity is *doxycycline (dose-dependent!)* - can also occur w/ other tetracyclines (e.g. minocycline), benzoyl peroxide, and retinoids -Photosensitivity Presentation: Ranges from a mildly erythematous rash, to blistering that develops minutes to hours after skin is exposed to sunlight (exaggerated sunburn!) -Prevention incl avoiding direct sunlight and using sunscreen -Bc doxycycline photosensitivity is *dose-dependent*, nonacute management incl *decreasing the dosage or discontinuation* -TX of *minor* burns w/ intact epidermis is *supportive*, incl symptomatic relief of pain & pruritus (e.g. cool compress, aloe vera) -*NSAIDs (e.g. ibuprofen)* can reduce pain and erythema and minimize damage to the epidermis if given right after sun exposure -Systemic antihistamines (diphenhydramine) used for pruritus -Severe sunburns require hospitalization, IVF & IV Analgesia, & wound care

Cross-Sectional Study

-Generally a type of *observational study* in which a *specific population or group is studied at one specific point in time, therefore providing a cross section of the group at that particular time point*

TX of Osteopenia & Osteoporosis

*Osteopenia = DXA T-score -1.0 to -2.5* *Osteoporosis = DXA T-score -2.5 or less* -*ALL osteopenia & osteoporosis pts* should be *counseled to Exercise Regularly, Incr Dietary Intake of Vitamin D & Calcium, and Refrain from Smoking or Consuming Excessive Alcohol (>2 drinks/day for women)* -*Antiresorptive therapy (e.g. Bisphosphonates) are indicated in the following*: • *Osteopenia & High 10yr Osteoporotic Fracture Risk* (i.e. *probability of major osteoporotic fracture ≥20% or hip fracture ≥3%*) calculated using a *FRAX risk calculator*; potential risks of pharmacologic tx (e.g. osteonecrosis or atypical fractures for bisphosphonates) are outweighed by the benefits for fracture risk reduction • *Confirmed Osteoporosis* by either *DXA result (i.e. T-score ≤ -2.5) OR Hx of Fragility Fracture*

What is the Most Reliable method for verifying Endotracheal Tube (ETT) Placement in the Trachea rather than the esophagus?

*PERSISTENT CAPNOGRAPHIC WAVEFORM W/ VENTILATION* -*Capnography* (quantitative waveform or colorimetric analysis) is a *noninvasive technique to measure [CO2] in Exhaled Breath* -- It is the *most reliable method for verifying Proper ETT Placement in the Trachea!* -Clinical findings, incl *auscultation of breath sounds over both lung fields, chest wall rise w/ assisted ventilation, visualization of ETT passing through the vocal cords, and fogging of the ETT on exhalation are NOT reliable indicators of correct placement*

What are pts w/ PMS/PMDD at increased risk for?

*PMS/PMDD* are characterized by *somatic* (e.g. *bloating, breast tenderness*) *and affective* (e.g. *depression, anxiety, anger, irritability*) *assoc w/ menstrual cycle* -Bc pts with PMS/PMDD experience *dysregulation of the serotonergic system*, they may also have a *predisposition for Primary Mood & Anxiety Disorders* (e.g. *Major Depressive Disorder*) that are also characterized by *serotonergic dysfunction* -Estimated that lifetime risk of a mood or anxiety disorder in PMS pts approaches 80% and is elevated in the years before and after PMS sx occur

What is the strongest risk factor for *stent thrombosis after coronary stent placement*? What complication can occur if stent thrombosed?

*POOR ADHERENCE TO DUAL ANTIPLATELET THERAPY (Low dose Aspirin + P2Y12-receptor blocker, Clopidogrel/ Prasugrel/ Ticagrelor) following stent placement* -*DAPT = Baby Aspirin + Clopidogrel* -*DAPT is recommended for a minimum of 3-6 months following placement of a coronary stent to reduce the risk of stent thrombosis* - therefore pts should be *aggressively screened & counseled for medication adherence to reduce the risk of stent thrombosis* *Stent Thrombosis (leading to abrupt vessel occlusion)* is an uncommon, but *potentially fatal*, *complication of coronary artery stenting*, with *most events (i.e. Myocardial Infarction or DEATH) occurring WITHIN 30 DAYS of stent placement* -*Total thrombotic occlusion* of the stented artery is typical, leading to *transmural (i.e. ST elevation) myocardial infarction* (e.g. *chest pain, nausea*) that is often *complicated by Cardiogenic Shock* (e.g. *hypotension, cool extremities*) *or Sudden Cardiac Death* Note: *Inferior wall MI* is commonly complicated by *bradycardia*, d/t heightened vagal tone/sensitivity as well as *impaired blood supply from the Right Coronary A [in most pts] to the Sinoatrial & Atrioventricular Nodes*

What is the MCC of small intestinal obstruction in pts with a hx of abdominal/pelvic surgery?

*POSTOPERATIVE ADHESIONS* Less common causes of SBO incl hernia, neoplasm, volvulus, intussusception, & stricture formation in pts w/ IBD

What does chlamydia in pregnancy incr the risk for? (i.e. pregnancy complications of chlamydia)

*PRETERM PRELABOR RUPTURE OF MEMBRANES, PRETERM LABOR, & POSTPARTUM ENDOMETRITIS* d/t untreated, undertreated, or recurrent chlamydial [ascending] infection -*Vertical transmission* via contact b/w fetus and infected maternal discharge during delivery can result in complications, incl *neonatal pneumonia & neonatal conjunctivitis* *Nonpregnant* pts w/ Chlamydia are TX w/ *Doxycycline monotherapy* Since doxy is a potential teratogen, *pregnant pts tx w/ AZITHROMYCIN* and all sexual partners are tx to prevent reinfection. Pts advised to abstain from sex for 7d following the completion of tx. Pts TX for an STI during pregnancy should be *retested a month after completing treatment to ensure cure* Pts with an STI dx early in pregnancy are also *retested in third trimester, prior to delivery*

Is PCOS best TX w/ a copper-containing or progestin-containing IUD?

*PROGESTIN-CONTAINING IUD* -PCOS pts have *irregular menses (anovulation), androgen excess (acne, hirsutism), & polycystic ovaries on U/S* -*Chronic anovulation* --> *Unopposed Estrogen EXCESS* --> *Uncontrolled Endometrial Proliferation & INCR Risk for Endometrial Hyperplasia & Cancer* -Usu *OCPs are first-line* (provides predictable menstrual cycle & regular progestin exposure to counteract the effects of endometrial estrogen stimulation) -Women who aren't candidates for OCPs (forgetfulness, contraindications to estrogen) can be offered a *PROGESTIN-CONTAINING IUD* -- A *long-acting* contraceptive that *provides endometrial protection* by *thinning the endometrium and reversing hyperplasia* Note: *Copper-containing IUDs do NOT protect the endometrium, not helpful in PCOS*. And they usu increase menstrual bleeding & cramping.

What is Proportionality and Justice? (Ethical principles in medicine)

*PROPORTIONALITY* -*Ensure that methods used to achieve a worthwhile goal are necessary, appropriate, and Not excessive* -Considers whether a TX goal is sufficiently worthwhile and whether a medical intervention for achieving that goal is proportional in terms of potential harm and achievable benefit -Proportional interventions are *necessary, appropriate, & not excessive* *JUSTICE* -*Equally distribute healthcare resources and provide fair & equitable treatment*

Pt with bilateral cataracts, basal ganglia calcifications, with hyperphosphatemia, & elevated PTH. What is the most likely diagnosis?

*PSEUDOHYPOPARATHYROIDISM* -Cataracts and basal ganglia calcs are signs of *CHRONIC HYPOCALCEMIA* (does not occur with acutely deranged calcium levels)

Inadequate TX of Appendicitis increases the risk for which complication?

*PYLEPHLEBITIS* - *infective suppurative thrombosis of the portal vein* and is a rare complication of *intra-abdominal infection* -*Pylephlebitis, an infective suppurative portal vein thrombosis*, is a rare but devastating complication of *untreated appendicitis or other intra-abdominal or pelvic infections* (e.g. *diverticulitis*) -The portal venous system drains most of the GI tract; infections assoc w/ GI tract can lead to *localized thrombophlebitis* that can *extend to the portal vein* -Clinical Features of pylephlebitis incl an *acute or chronic onset of fever, RUQ pain, jaundice, & hepatomegaly* -Lab eval shows *Incr ALP & GGT*; Imaging (e.g. *Abdo CT, Ultrasound*) reveals *thrombus* -*POLYMICROBIAL BACTEREMIA* is common -TX incl *prolonged broad-spectrum ABX (e.g. vancomycin and piperacillin/tazobactam) to prevent complications*, incl *bowel ischemia, portal HTN, & hepatic abscess*

How does bone pain caused by metastatic disease usually feel for patients?

*Pain from bone metastasis is typically DULL and ACHING or boring in character,* and *Symptoms usu occur AT NIGHT* Pts w/ bone mets often have *Unremarkable Physical Exams and Plain (Normal) X-rays* -- so usu need additional imaging studies -Imaging modalities in skeletal metastasis are dependent on whether lesions are primarily Osteolytic, Osteoblastic, or Mixed ● *Primarily OsteoLYTIC Mets*: (e.g. *multiple myeloma*) Poorly visible on Radioisotope (Technetium-99 MDP) bone scans (as labeled technetium is preferentially taken up in areas of NEW bone formation). *Plain X-RAYS & PET-CT* are *more effective* ● *Primarily OsteoBLASTIC Mets*: (e.g. *prostate cancer*) *Easily seen on Radioisotope (Technetium-99 MDP) Bone Scans* ● *MIXED Lytic/Blastic Mets*: (e.g. *breast cancer*) Usu seen on *Radioisotope bone scans*, but *PET CT* may be helpful in some cases

Post-Intensive Care Syndrome

*Pathophysiology & RF* -RF: *ICU delirium, ARDS, prolonged mechanical ventilation* -Pathophys: *CNS hypoxia*, neuroinflammation & metabolic disruption *Clinical Features* -*Psychiatric*: >50% w/ major *depression* (e.g. dysphoria, flat affect, psychomotor retardation, irritability, sleep disturbances) and/or *PTSD* (dx can occur within 5yrs of ICU stay; sleep disturbances in first few wks common) -*Neurocognitive*: *Attention/memory deficits* persisting for *several years*, reduced executive function & processing speed -*Physical*: >50% with *reduced mobility & functional independence* requiring daily assistance for months to years; usu need outpatient physical therapy; mild global weakness may persist, but most pts are able to walk independently again *Management Implications* -Prevention: *Early therapy participation* (PT/OT even when intubated) -Treatment: Multidisciplinary post-ICU clinic; Pharmacotherapy for psychiatric sx -Prognosis: Set realistic recovery expectations during GOC discussions; Most require *additional home care & never return to work*; major *negative impacts on quality of life*

Which ABX meds are generally safe in pregnancy?

*Penicillins* (e.g. *amoxicillin, ampicillin, amox-clav*) *Cephalosporins* (e.g. *cephalexin* [first-gen], *ceftriaxone* [third-gen], *cefaclor* [second gen]) -Note: Ceftriaxone should be avoided late in pregnancy, bc it can cause kernicterus *Clindamycin* -Covers gram-positive and anaerobic bacteria (e.g. Bacteroides, Clostridium perfringens) and anaerobic infections above he diaphragm (metronidazole covers below the diaphragm) *Macrolides* (e.g. *azithromycin, clarithromycin, erythromycin*)

*Elevated calcitonin levels* in pt with *Medullary thyroid CA following total thyroidectomy* -- best next step?

*Persistently elevated calcitonin indicates residual METASTATIC Medullary thyroid cancer disease* *CT SCAN OF NECK & CHEST ± High-resolution U/S of Neck is recommended as the next step to look for metastatic dz* -Surgical resection should be performed if a resectable lesion(s) is found -If no lesion found, then an Abdo CT & Bone Scan may be required -- I-111 Octreotide or PET scan may be helpful if CT scans are negative despite the elevated calcitonin levels

What test to confirm DX of Tinea infections?

*Potassium hydroxide staining of skin sample* can DX Tinea infections by showing the *characteristic segmented hyphae and arthrospores* -Tinea infections usu present as *pruritic, erythematous, circular, & scaly lesions w/ central clearing*

Of these options below, which values are *prevalence dependent*? • Negative predictive value • Positive predictive value • Sensitivity • Specificity

*Predictive values* (*PPV & NPV*) are affected by *prevalence* of the condition being studied *Sensitivity and specificity are INDEPENDENT of Prevalence* *PPV & NPV are DEPENDENT on Prevalence*

Acute Mesenteric Ischemia

*Presentation* -Rapid/*Acute* onset of *periumbilical* pain (often /severe/); N/V -*Pain out of proportion to exam findings* (i.e. mild tenderness to abdo palpation, no guarding, soft, not really distended) -Hematochezia (late complication) -Note: *Chronic mesenteric ischemia* p/w cramping abdo pain after eating *Risk Factors* -*Atherosclerosis* (acute or chronic) -*Embolic source* (thrombus, cardiac vegetation) -*Hypercoagulable* disorders -*Hypovolemia* state d/t trauma, hemodialysis -*Recent myocardial infarctions*, arrhythmias, or heart failure (incr risk d/t ease of formation of ventricular thrombi & potential for poor perfusion) *Lab Findings* -Leukocytosis -*Elevated amylase* (reflecting intraabdominal inflam) & phosphate levels -*Metabolic acidosis* (d/t *elevated lactate*) *Diagnosis* -*CT abdo angiography (preferred)* or MR Angiography if pt has contrast allergy -Mesenteric angiography if dx unclear *Complications* -If untx, can cause bowel infarction, sepsis, & death

Lab Characteristics for the following: Pseudohypoparathyroidism True Hypoparathyroidism Vitamin D Deficiency Hyperphosphatemia Primary Hyperparathyroidism Secondary Hyperparathyroidism Tertiary Hyperparathyroidism

*Pseudohypoparathyroidism* -DECR Ca2+, INCR PO4, INCR PTH; Incr ALP *TRUE Hypoparathyroidism* -DECR Ca2+, INCR PO4, DECR PTH; Decr Vit D *Vitamin D Deficiency* -DECR Ca2+, DECR PO4, INCR PTH; Incr ALP, Decr Vit D *Hyperphosphatemia* (usu d/t seizure, tumor lysis, acute renal failure) -Acutely DECR Ca2+, INCR PO4, INCR PTH; Incr ALP, Decr Vit D *Primary Hyperparathyroidism* (Adenoma/Hyperplasia) -INCR Ca2+, DECR PO4, INCR PTH *Secondary Hyperparathyroidism* (CKD) -DECR Ca2+, INCR PO4, INCR PTH; Incr ALP, N/Decr Vit D *Tertiary Hyperparathyroidism* (Refractory/Autonomous 2/2 CKD) -INCR Ca2+, DECR PO4, REALLY HIGH PTH

Pulmonary Complications of Polymyositis

*Pulmonary Complications*: *interstitial lung disease (ILD)*, *infection* (d/t immunosuppressive therapy), *drug-induced pneumonitis* (e.g. methotrexate pneumonitis), and *respiratory muscle weakness* -ILD is esp common in pts w/ *positive anti-Jo-1 Ab* and can be identified on *high-resolution CT imaging* as *ground-glass opacities, reticular changes, honeycombing, or patchy consolidation* -*Pulmonary fxn tests* should be done to *distinguish ILD from resp muscle weakness* and will show *decr vital capacity, total lung capacity, & diffusing capacity* -Initial management of ILD in polymyositis pts is similar to tx of the underlying polymyositis - with *systemic glucocorticoids & corticosteroid-sparing agents*, but note that ILD may progress despite tx, even if myopathic features improve

What is *saw palmetto* most commonly used to tx?

*SAW PALMETTO* is a popular herbal prep most often *used by men to TX benign prostatic hyperplasia* -Its use has NOT been shown to significantly improve urinary sx or flow measures -It also does not appear to affect PSA levels or prostate size -*Generally well-tolerated* but may cause *mild side effects* (*GI discomfort*, HA, dizziness); less frequent AE incl HTN, cholestatic hepatitis, & pancreatitis NOTE: Should be *used cautiously in pts undergoing surgery* d/t *possible Incr risk of perioperative BLEEDING*

Manifestations of Sarcoidosis

*Pulmonary*: Bilateral hilar adenopathy; Interstitial infiltrates *Cutaneous*: Papular, nodular, or plaquelike lesions; Erythema nodosum *Ophthalmologic*: Anterior uveitis (iridocyclitis or iritis); Posterior uveitis; Keratoconjunctivities sicca *Reticuloendothelial*: Peripheral LAD (~40%); Hepatomegaly (~20%); Splenomegaly *Musculoskeletal*: Acute polyarthritis (esp ankles); Chronic arthritis *Cardiovascular*: Atrioventricular block; Dilated/restrictive cardiomyopathy *CNS/Endocrine*: Facial nerve palsy; Central diabetes insipidus; Hypercalcemia *Lofgren Syndrome*: Erythema nodosum, Hilar adenopathy, Migratory polyarthralgias, Fever Note: Extrapulmonary manifestations (~30% of cases) can be the presenting sx instead of lung sx, and are almost always accompanied by *significant fatigue* -Screening for suspected cases begins with *CXR bc >90% will have bilateral hilar or mediastinal LAD*

Acute Cervicitis

*Purulent Cervical Discharge + Cervical Friability* -Other Sx incl: *Intermenstrual &/or Postcoital Spotting, Dysuria, & Dyspareunia* -- HOWEVER, Women are *Often ASX* -*NAAT testing* is *indicated for ALL pts w/ Suspected Cervicitis to CONFIRM Infection*; HOWEVER,*TX is given EMPIRICALLY* based on Exam alone and does NOT need to wait for results -*Empiric TX* allows for *earlier symptomatic relief* and *decreases risk for transmission to sexual partners* -A *delay in TX* increases the *risk for ascending infection* (e.g. *Pelvic inflam dz*) and *long-term sequelae* (e.g. *tubal scarring, infertility*) -*First-line Empiric TX is DUAL Therapy w/ CEFTRIAXONE + DOXYCYCLINE*, which provides *coverage* against the *2 MC pathogens, Chlamydia trachomatis & Neisseria gonorrhoeae* -The pt's *sexual partner(s) should also be empirically TX* -To *Prevent Reinfection,* the *pt and her partner(s) should Abstain from Sex for ONE WEEK After Completion of TX* -For pts *with an IUD who dev Acute Cervicitis or Pelvic Inflam DZ, IUD Removal does NOT improve clinical outcomes* and therefore is *NOT indicated* -HOWEVER, *IUD Removal* can be *considered in a pt* whose *condition does NOT improve with ABX*

Middle-aged adult pt w/ long smoking hx, erythrocytosis (elevated hemoglobin, high-normal hematocrit), and hematuria (UA w/ moderate blood, elevated RBCs, but no casts) should raise suspicion for what?

*RENAL CELL CARCINOMA!* Major RF for RCC incl *cigarette smoking, obesity, & HTN* -Pts can have flank pain, hematuria, & palpable abdo mass (but this presentation is rare) Next step, *abdominal CT*

In which condition of childhood is *costochondral junction enlargement* usu seen?

*RICKETS/OSTEOMALACIA* d/t *VITAMIN D DEFICIENCY* -Defective mineralization of osteoid (osteomalacia) or cartilaginous growth plates (rickets, only in children) -X-rays show *osteopenia and pseudofractures in osteomalacia*, and *epiphyseal widening and metaphyseal cupping/fraying in rickets*. -Children with rickets have *pathologic bow legs (genu varum)* (bows OUT), as well as *beadlike costochondral junctions (rachitic rosary), craniotabes (soft skull).* Decr vitamin D --> Decr serum Ca --> Incr PTH secretion --> Decr serum PO4 Hyperactivity of Osteoblasts --> Incr ALP

Which is the most common *VIRAL cause of traveler's diarrhea*?

*ROTAVIRUS!* -Manifests w/ vomiting, *nonbloody* diarrhea, & fever (but generally, *bacterial etiologies are far more common*)

Relative Risk formula

*RR = (risk of outcome in exposed) / (risk of outcome in unexposed)* *RR = (# those w/ dz & exposed / total # exposed) / (# those w/ dz & no exposure / total # with no exposure)* *RR = 1* --> NO assoc b/w exposure & disease *RR >1* --> Exposure IS assoc with INCR Dz occurrence (*exposure is DETRIMENTAL*) *RR <1* --> Exposure is assoc with DECR Dz occurrence (*exposure is PROTECTIVE*) Typically used in *cohort* studies to look at the risk of developing a dz in the exposed group versus in the unexposed group and dividing the two

How old do you have to be to begin receiving the flu vaccine?

*Recommended for all those ≥6mo of age* -Flu vaccine is *inactivated and contains no live virus*, so it is *safe for immunocompromised pts, pregnant women, to household contacts of pregnant* -Note: The flu vaccine contains a /small amount of egg protein/, but those with anaphylaxis to egg can receive the vaccine as an outpt or inpt. *Since anaphylaxis after vaccines is RARE (<1.5 per 1 million vaccines), egg allergy (personal or FHX) is NOT a contraindication*

Altering Warfarin Dose based on concurrent medications d/t interactions that lead to over- or under-anticoagulation and increased bleeding risk (± change in PT)

*Reduce Warfarin Dose by 25-50%* (to compensate for the increase in serum warfarin concentration) *After Initiating*: -*AMIODARONE!!* -Metronidazole, Fluoroquinolones *Increase Warfarin Dose* (to compensate decreased warfarin effect by enhanced metabolism &/or decr in serum concentration of warfarin) *If Initiating*: -*RIFAMPIN, Phenobarbital, OCPs*

What is relative risk a measure of association of?

*Relative Risk* is a measure of association *based on risk/incidence* and is used in *cohort studies and experimental designs*, in which participants are initially selected based on *exposure status* (i.e. exposed or nonexposed to risk factor or treatment) and then followed over time to assess development of disease Compare to case-control studies, where cases (already have the dz), so case-control studies cannot calculate and compare the risk/incidence of disease b/w the case and control groups. Instead, they compare the odds of exposure to a RF between cases and controls

Drugs commonly used to tx Tuberculosis

*Rifampin* -MOA: Inhibition of bacterial DNA-dependent RNA polymerase -AE: GI effects, rash, red-orange body fluids, cytopenias *Isoniazid* -MOA: Inhibition of mycolic acid synthesis -AE: Neurotoxicity (give vit B6/pyridoxine!!), Hepatotoxicity *Pyrazinamide* -MOA: Unclear -AE: Hepatotoxicity, Hyperuricemia *Ethambutol* -MOA: Inhibition of arabinosyl transferase (?) -AE: Optic Neuropathy

Iron Deficiency Anemia in Children

*Risk Factors* -Prematurity -Lead exposure -Age <1: Delayed introduction of solids (i.e. exclusively breastfeeding beyond 6mo); Cow's, soy, or goat's milk -Age >1: More than 24oz/day of cow's milk; <3 servings/day of iron-rich foods *Diagnosis* -Screening hemoglobin at age 1yr -Hemoglobin <11, decr MCV, incr RDW *Treatment*: Empiric trial of iron supplementation Note: If pts w/ FHx of hemoglobinopathies, must order *hemoglobin electrophoresis*. The presence of HbA & HbS in a 60:40 ratio is consistent with sickle cell train, which is generally ASX and not a cause of anemia and microcytosis

Which vertebral level does anal sphincter tone correspond to?

*S2-S4 region of spinal cord!*

What is the *Triple Drug Therapy for HIV PPX (Postexposure Prophylactic Antiretroviral Therapy, PEP)*?

*TENOFOVIR-EMTRICITABONE W/ RALTEGRAVIR* *PEP CONTINUED FOR 4 WEEKS!*

DDX of Travel-Associated Diarrhea

*SHORT-Term Illnesses* -*Rotavirus & Norovirus*: brief illness; vomiting common -*ETEC & EPEC*: contaminated food & drinking water -*Campylobacter*: prominent abdo pain, "pseudoappendicitis," bloody diarrhea -*Salmonella*: frequent fever -*Shigella*: fever, bloody diarrhea, & abdo pain *LONG-Term Illnesses (>2wks)* -*Cryptosporidium, Cystoisospora, Microsporidia spp*: chronic illness in immunosuppressed pts -*Cyclospora*: prolonged, relapsed infection -*Giardia*: common in wilderness & rural USA, Asx pts may continue to shed organism for months (fatty, stinky stools)

Which disease processes are assoc with increased risk for osteonecrosis (AKA avascular necrosis or Osteochondritis Dissecans)

*SLE Sickle cell disease Antiphospholipid antibody syndrome Chronic renal insufficiency Hemodialysis Trauma Gaucher's disease HIV infection S/p Renal transplantation Caisson's disease* (Acute decompression syndrome (Caisson's disease) is an acute neurological emergency in divers. It is caused due to release of nitrogen gas bubbles that impinge the blood vessels of the spinal cord and brain and result in severe neurodeficit) *At highest risk are SLE pts on chronic high-dose corticosteroid therapy (>15-20 mg/d)* *DIAGNOSE WITH MRI>>>> x-ray plain films* *Goal of therapy of Osteonecrosis is to preserve the native joint for as long as possible* -Main modalities of TX incl: *Conservative therapy, Core decompression, Osteotomy, & Joint replacement (stage 4, flattening femoral head w/ joint space narrowing)*

Standardized Mortality Ratio (SMR) Calculation & Definition

*SMR = Observed # of Deaths / Expected # of Deaths* -*Standardized mortality ratio is represents an adjusted measure of overall mortality & is calculated by dividing the number of deaths in the population of interest, by the expected number of deaths in a standard reference population*; it is typically used in *occupational epidemiology* -The expected # of deaths is calculated based on age-specific rates of death in a standard reference population e.g. An SMR of 1.75 indicates that the observed # of deaths among miners (population of interest) was 1.75x (or 75%) HIGHER than would be expected if these miners had the same death rate as the standard population.

What is the most common neural tube defect?

*SPINA BIFIDA AKA MYELOMENINGOCELE* -Defect of lower vertebral column, *exposes spinal cord & meninges* (skin thin/absent covering) -Caused by *failure to close caudal neuropore* properly during fetal development -Most d/t *folate deficiency during pregnancy*, other RF: *pregestational diabetes, maternal obesity*, maternal fever in first trimester, genetics -*INCR AFP levels on maternal screening is suspicious for Neural Tube Defect*; *DX Confirmed on Prenatal U/S* -After birth, cover spina bifida in moist, sterile dressing and plastic wrap to prevent infection and heat loss. Then Urgent Surgical Repair, which results in *Hydrocephalus* requiring a *ventriculoperitoneal shunt* in >50% of infants -*Despite surgical repair, Motor, Sensory, & Autonomic Fxns BELOW the level of Spina Bifida/Myelomeningocele are usu affected* -*NEUROGENIC BLADDER*, p/w *urinary retention/incontinence, recurrent UTIs, & potential renal dysfunction*, is *almost UNIVERSAL* -TX w/ *clean intermittent catheterization* to relieve pressure on upper urinary tract and helps prevent urinary stasis -*NEUROGENIC BOWEL* is also common, and scheduled regimen of *laxatives, suppositories, & enemas* is recommended to *Tx Constipation*

TX of Obsessive Compulsive Disorder?

*SSRIs* (e.g. *fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, escitalopram*) and the *TCA, Clomipramine* is also effective (SSRIs preferred over Clomipramine d/t better AE profile) High doses & prolonged therapeutic trials is needed, and gradual up-titration is necessary to enhance tolerability. Note: SSRIs are also used as first-line agents in TX of Premature Ejaculation d/t their potential AE to cause delayed ejaculation *Exposure & Response Prevention therapy*, a specific form of cognitive behavioral therapy, is considered *first-line psychotherapy* for OCD -involves gradual and repetitive exposure to anxiety-provoking stimuli that produce obsessional thoughts, followed by prevention of performing the assoc compulsion/ritual. Through the process of *habituation*, in which anxiety levels subside over time, OCD sx are reduced

What is *St. John's wort* used for?

*ST. JOHN'S WORT* is frequently used to tx *depression* -- however, *inconsistent evidence to support its efficacy*

What is the most common cause of [nonpurulent] cellulitis?

*STREPTOCOCCUS PYOGENES* (GROUP A STREP) Nonpurulent cellulitis involves the *deep dermis or subcutaneous fat* and presents w/ *tenderness and warm erythema with flat, ill-defined borders* -Infection usu develops *after a break in the skin* (e.g. insect bite) -*Indolent* course, w/ increasing size and systemic sx developing after several days -NO fluctuance or purulent drainage -*TX*: Systemic ABX with *CEPHALEXIN FOR ≥5days* (tx as outpt) Note: Staph aureus is a less common cause of nonpurulent cellulitis, but is the most common isolated pathogen in skin abscesses

Types of Urinary Incontinence

*STRESS* -Leakage with coughing, sneezing, laughing, lifting, incr intra-abdominal pressure d/t outlet incompetence (urethral hypermobility or intrinsic sphincteric deficiency) -TX: Lifestyle modification, Kegels, pessary, urethral sling surgery *URGE* -Sudden, overwhelming, or frequent need to urinate d/t overactive bladder (detrusor muscle instability) -TX: Lifestyle modification, Kegels, Bladder training (timed voiding), Antimuscarinic medications (e.g. Oxybutynin) *OVERFLOW* -Constant dribbling of urine, incomplete bladder emptying d/e detrusor underactivity or outlet obstruction leading to leak w/ overfilling -Increased post-void residual urine (urinary retention) on catheterization or ultrasound -TX: Intermittent catheterization, relieve of obstruction (e.g. α-blockers for BPH), correct underlying etiology

Which popular herbal remedies are assoc. w/ *Incr. risk of Bleeding*?

*Saw Palmetto Ginkgo Biloba Ginseng Garlic*

Sensitivity Specificity False Negative Rate False Positive Rate Positive Predictive Value Accuracy

*Sensitivity*: Ability to correctly identify disease in a pt with disease; TP/(TP+FN) *False Negative Rate*: Complement of sensitivity, indicating the rate of negative test results in positive pts; FNR= 1 - Sensitivity *Tests with HIGH Sensitivity have LOW FNRs (i.e. low rate of negative results in positive pts)* *Tests that have LOW Specificity have HIGHER FPRs* *Specificity*: Ability to correctly identify absence of disease in a pt without the disease; TN/(TN+FP) *False Positive Rate*: Complement of specificity, indicating the rate of positive results in negative pts; FPR = 1 - Specificity -The *Accuracy* of a diagnostic test is the *probability that it correctly identifies positive disease* *Accuracy = (TP+TN)/ (TP+TN+FP+FN)* -The *Positive Predictive Value* of a diagnostic test is the *probability that a person with a positive test actually has the disease* *PPV = TP/(TP+FP)*

Serum Sickness-Like Syndrome

*Serum Sickness (SS)* is an *Immune complex-mediated hypersensitivity rxn (Type 3) that occurs when circulating antibodies combine with antigen in the blood & tissues, and overload normal clearance mechanisms* --> *Activates complement & causes Disease* -A minority of *Acute Hepatitis B infection develop an SS-LIKE Syndrome* that is *attributed to complement activation by circulating immune complexes composed of Hep B surface antigen* -Characterized by *fever, polyarthritis, & dermatitis* -Pts also freq report *fatigue or malaise* -Rash is variable, and can incl *urticaria or maculopapular or petechial patterns* -SS-like syndrome usu dev during the *prodromal, preicteric phase of acute infection* and *resolves w/ onset of jaundice* -Other *extrahepatic manifestations of HBV infection caused by circulating immune complexes* include *Polyarteritis Nodosa & Glomerulonephritis (usu Membrane Nephropathy, less often MPGN)*

What are the first steps in evaluating *thyroid nodules*?

*Serum TSH levels and Thyroid Ultrasound* -Pts w/ thyroid nodules should be evaluated for *risk of malignancy* (e.g. FHX, Radiation exposure in childhood, Cervical LAD), *compressive sx* (e.g. hoarseness, difficulty swallowing), & *functional status* (e.g. eu-, hyper-, or hypothyroid) -Pts w/ *suspicious U/S findings* (e.g. *large size, hypoechoic, microcalcifications, internal vascularity*) *or cancer RF* should *undergo FNA w/ cytology of nodule* -Pts w/ *normal or elevated TSH have a Higher risk of malignancy* & should be considered for FNA based on U/S -*Low TSH levels suggest a hyperfunctioning nodule*, which has a *Lower Risk of Malignancy* and should be *evaluated w/ thyroid scintigraphy (Radionuclide Thyroid Scan)* -- a "hot" nodule (incr isotope uptake in nodule w/ decr uptake surrounding) is rarely malignant and may be TX as benign hyperthyroidism

How is HPV transmitted?

*Sexually* transmitted infection! -Spread by *skin-to-skin contact* -*Condoms offer partial protection*, but do not cover the entire genital area, so HPV can STILL be transmitted

Wolff-Parkinson-White (WPW) Syndrome - Quick Findings on EKG What drug is contraindicated in WPW pts?

*Short PR interval* *Wide QRS complex* *Delta waves* -*Administration of ADENOSINE* (*given for regular, narrow-complex tachycardia*, QRS duration 90msec) can *PROVOKE A-FIB W/ RAPID CONDUCTION via the Accessory Pathway,* which can *Degenerate into VENTRICULAR FIBRILLATION*, causing *loss of consciousness and requiring Defibrillation* THEREFORE - *ADENOSINE SHOULD BE AVOIDED IN WPW SYNDROME pts*

Chronic Pancreatitis

*Significant weight loss + bulky, foul-smelling (requiring multiple flushes) stools* is c/w *Fat Malabsorption & Steatorrhea* -*Abdo pain accompanied by fat malabsorption* should *raise suspicion for Chronic Pancreatitis, ESP in pts w/ Hx of heavy alcohol intake* and multiple prior hospitalizations for abdo pain -Chronic Pancreatitis tends to cause *Epigastric abdo pain that radiates to the back* and can be *relieved by sitting up or leaning forward*, positions that move the inflamed pancreas away from other organs -*CP pain* can be *episodic or continuous,* and may be *exacerbated by meals* -Unlike in Acute Pancreatitis, which can be diagnosed in the appropriate setting by elevations in serum lipase or amylase, *chronic pancreatitis does NOT regularly result in lab abnormalities in lipase or amylase* -Consequently, a *Magnetic Resonance Cholangiopancreatography (MRCP)* of the abdomen would be the best test -*Pancreatic calcifications* are the *hallmark of CP*; *Pancreatic enlargement, pancreatic duct dilation, & pseudocysts* may also be seen -MRCP has higher sensitivity & specificity for CP compared to X-rays or U/S; *Abdo CT* is an acceptable alternative -After confirming DX, *First-line TX is Lifestyle & Dietary Modification (eating small, low-fat meals, fat-soluble vitamin supplementation), Alcohol & Tobacco Cessation ± Pancreatic Enzyme supplementation* if significant exocrine insufficiency (low fecal elastase-1 levels) to help improve the sx of abdo pain & malabsorption -For pts who don't achieve adequate relief after initial measures, can try *nonopioid analgesics like Tricyclic Antidepressants (e.g. Amitriptyline), NSAIDs, & Pregabalin*

Febrile Seizures and when to do a *Lumbar Puncture*

*Simple* febrile seizures are *generalized, last <15mins, & DO NOT RECUR within 24hrs*. *Postictal drowsiness lasts up to 10MINS*. *Clinical DX* in *children age 6mo-5-6yo*, and* do NOT require diagnostic studies or TX* *Red Flags on PE that may suggest MENINGITIS and warrant Prompt Immediate Lumbar Puncture* incl: -Signs of *INCR ICP* (e.g. morning headache, *vomiting, bulging fontanelle*) -*Meningeal Signs (e.g. nuchal rigidity)* -*Prolonged AMS (i.e. Postictal period lasting >10mins)* -*Petechial rash* -*Abnormal neurologic examination* (e.g. *somnolent, responsive only to painful stimuli*)

How does smoking relate to post-op pulmonary complications?

*Smoking Cessation at least 4wks prior to surgery DECREASES risk of postoperative pulmonary complications*

Treatment of Symptomatic Peripheral Artery Disease

*Step 1A* -Risk Factor Management • Smoking cessation • BP & Diabetes control • Antiplatelet (Aspirin) & Statin Therapy *Step 1B* -Supervised Exercise Therapy *Step 2* -Cilostazol (preferred over pentoxifylline) *Step 3* -Revascularization for Persistent SX • Angioplasty ± Stent Placement • Autogenous or Synthetic Bypass Graft

TX of SYMPTOMATIC Peripheral Artery Disease

*Step 1A:* -*Risk factor management*: *Smoking cessation; BP & diabetes control*; *Antiplatelet & Statin therapy* *Step 1B:* -*Supervised Exercise therapy* (30-45mins *walking ≥3x/wk for >3mo*) *Step 2:* -*Cilostazol* (a phosphodiesterase-3 [PDE3] inhibitor, preferred over pentoxifylline) *Step 3:* -*Revascularization for persistent symptoms*: *Angioplasty ± stent placement*; Autogenous or Synthetic *bypass graft*

Treatments for STRESS Urinary Incontinence

*Stress Incontinence p/w Leakage after increased intraabdominal pressure (cough, valsalva, sneezing, lifting, laughing),* therefore have a *Positive Bladder Stress Test (i.e. leakage of urine w/ cough on exam)* due to *outlet incompetence (urethral hypermobility/intrinsic sphincter deficiency)* TREATMENTS: • *Lifestyle modifications - weight loss, diet modifications, Kegels to strengthen pelvic floor muscles)* • *Pessary placement* • *SNRI, like Duloxetine* • *Urinary sling procedure* after failing conservative management (wt loss, dietary modification, pessary)

Which meds are considered sulfa drugs? And what AE are associated with sulfa drug allergies?

*Sulfa Drugs* incl: *Sulfonamide, Sulfasalazine, Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazide diuretics, Sulfonylureas* Pts w/ *sulfa allergies* may develop: *fever, UTI, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis* (severely low granulocytes, like neutrophils, eosinophils, & basophils), *acute interstitial nephritis, urticaria (hives), & Photosensitivity* TX of photosensitivity rash includes discontinuation of the sulfa drug, use of sunscreen, & avoidance of sun exposure

What's the next step of management for men who present with [rapidly progressive] gynecomastia and elevated beta-hCG levels, elevated estradiol levels, and normal DHEA, LH, & [low-normal] Testosterone levels?

*TESTICULAR ULTRASOUND* -*Gynecomastia* (bilateral or unilateral) is an abnormal growth of breast tissue in men, d/t *increased estrogens:androgens ratio* (estrogens cause hyperplasia of breast ductal epi and fibrosis of stromal tissues; androgens inhibit breast development) -*Combination of rapidly progressive gynecomastia, low-normal testosterone, elevated estradiol, & strikingly high beta-hCG* is likely due to *hCG-Secreting Germ Cell Tumor of the Testis* -The incr hCG secr suppresses testosterone production in Leydig cells and increases aromatase activity (converts androgens to estrogens), resulting in *incr estrogen:androgen ratio* which can *cause gynecomastia* -*Testicular U/S* needed to exclude an occult mass, even if normal physical exam

Which ABX/meds/abx categories are contraindicated during pregnancy and why?

*TETRACYCLINES* (e.g. *tetracycline, doxycycline, minocycline*) -Bc they can cross the placenta, can cause *impaired fetal bone development, & stain deciduous teeth*; also avoided in children d/t *inhibition of bone growth* -Can cause *permanent yellow or gray discoloration to bones & teeth* -NOTE: *Doxycycline* is the ONLY SAFE tetracycline to use in pregnancy & in children when there is a Rocky Mt Spotted Fever Infxn, d/t low likelihood of *FLUOROQUINOLONES* (e.g. *ciprofloxacin, levofloxacin*) -*Toxic to fetal cartilage development* -Also contraindicated during breastfeeding and in pts <18yo d/t possible damage to cartilage -May also cause harm to developing heart, kidneys, or brain *AMINOGLYCOSIDES* (e.g. *gentamicin, neomycin, amikacin, tobramycin, streptomycin, kanamycin*) -*Teratogenic *TMP-SMX during First & Third Trimesters* -First: *neural tube defects* d/t folate antagonism) -Third: *neonatal kernicterus* (jaundice in newborns) *WARFARIN* -Can cause *symmetric fetal growth restriction* (low fetal weight, low birth weight, and small head circumference) *METRONIDAZOLE* -Only Safe during second & third trimesters of pregnancy -Linked to *premature birth w/ first trimester use* -If used vaginally, can cause *congenital hydrocephalus* *CHLORAMPHENICOL* -Can cause *serious blood disorders (anemia [dose-dependent] & aplastic anemia [dose-independent]) and Gray Baby Syndrome in premature infants* *BENZODIAZEPINES* (e.g. *Clonazepam, Lorazepam*) -Can cause *[life-threatening] benzo withdrawal symptoms in newborns* (e.g. seizures, sleep disturbances, depression) -Can cross placenta and incr the incidence of *premature birth & low birth weights*

Which thyroid cancer is assoc with rapid enlargement in pts w/ a hx of Hashimoto's thyroiditis?

*THYROID LYMPHOMA* -*RAPID incr in size of thyroid goiter* (e.g. over one month or several weeks), causing *difficulty swallowing* AND a *POSITIVE Pemberton's Sign* which is *the presence of facial plethora or neck vein distension when the arms are raised overhead >60sec and confirms that the Enlarged Thyroid is the cause of the esophageal obstructive sx* -Inability to palpate the inferior edge of the thyroid is suggestive of substernal extension; palpation is *large, irregular, & non-tender swelling* -The *primary RF for development of Thyroid Lymphoma is PREEXISTING HASHIMOTO'S THYROIDITIS (elevated TSH, low T4 = hypothyroid; anti-TPO Ab present in Hashimoto) in which there is chronic lymphocytic infiltration of the thyroid* -Thyroid lymphoma should be suspected in Hashimoto pts w/ rapidly enlarging goiter and subsequent obstructive sx Note: Though papillary thyroid carcinoma is also assoc w/ Hashimoto, and also presents with a palpable nodule, it does NOT progress so rapidly.

Which medications can cause *Macrocytic Anemia*?

*TRIMETHOPRIM, METHOTREXATE, & PHENYTOIN* can interfere with *folate metabolism* and result in *folic acid deficiency macrocytic anemia* *TX: FOLINIC ACID!!!* (Leucovorin) -*Folinic acid is more POTENT than folic acid* in rescuing RBCs from the deficiency caused by chronic methotrexate use (methotrexate inhibits dihydrofolate reductase, which converts folic acid to folinic acid, for folinic acid to be utilized by cells)

Risk for which electrolyte derangement in pts with *moderate to severe megaloblastic anemia 2/2 to Vit B12 deficiency*?

*TX with vit B12* in pts with *moderate to severe megaloblastic anemia can cause HYPOKALEMIA*, which can sometimes be *severe and even life-threatening* -*HYPOKALEMIA* results following the *uptake of potassium by NEWLY-FORMING RBCs* -Therefore, *serum K levels should be monitored for the first 48hrs* -*Potassium replacement* depends on the measured serum K levels -Some physicians *transfuse PRBCs* in pts w/ *severe megaloblastic anemia BEFORE vitamin B12 supplementation to PREVENT HYPOKalemia* There is no need to monitor Hemoglobin, TSH, WBC, or PLT levels.

Who discusses organ donation with a patient's family?

*The ORGAN PROCUREMENT ORGANIZATION* NOT the Physician The physician discusses brain death/impending death & provides care until death, but the OPO discusses organ donation, assesses donor eligibility, provides support & counseling for family, and assumes patient care after death

Which classes of antihypertensives affect serum lithium levels? What antihypertensives are safe in pts requiring chronic lithium administration?

*Thiazides, ACE Inhibitors, & Angiotensin II Receptor Blockers (ARBs)* can *INCREASE SERUM LITHIUM LEVELS,* *INCREASING the RISK for Toxicity* *CALCIUM CHANNEL BLOCKERS (AMLODIPINE) are generally considered SAFE* for pts taking Lithium

When do you hear an S3?

*Third heart sound* typically caused by *blood filling a dilated ventricular cavity* in a pt with *HEART FAILURE* Signs of HEART FAILURE incl dyspnea & peripheral edema

Thyroglobulin vs. TBG (Thyroxine-Binding Globulin)

*Thyroglobulin vs. TBG (Thyroxine-Binding Globulin)* -*Thyroglobulin* is the *PRECURSOR to T4 and T3*, the thyroid hormones, and it is found within the thyroid gland -*Thyroid-/Thyroxine-binding globulin* is a *protein* that *binds thyroid hormone and carries it around the body* (think taxicab); *TBG binds most T3/T4 in blood; Bound T3/T4 = INACTIVE* ● *INCR TBG* in *pregnancy, OCP use* (*Estrogen --> INCR TBG --> Incr TOTAL T3/T4*) ● *DECR TBG* in *steroid use, nephrotic syndrome --> Decr Total T3/T4*

General Management of Gout

*_General Gout Management:_* *Acute*: *NSAIDs* (eg, *Indomethacin*), *Glucocorticoids* (e.g. *Intra-Articular Triamcinolone*), *Colchicine* *Chronic (preventive)*: *Xanthine Oxidase Inhibitors* (eg, *Allopurinol, Febuxostat*) Gout --> *NEGATIVELY Birefringent, NEEDLE-Shaped Crystals under polarizing light from arthrocentesis showing monosodium urate crystals*; Yellow under parallel light, blue under perpendicular

Rash associated with Trichophyton species

-Trichophyton causes *tinea corporis*, a dermatophyte infection common in athletes who participate in contact sports -The rash is *pruritic with central clearing and raised borders* (it is NOT tender or warm)

Tinea Versicolor Pityriasis Rosea Seborrheic Dermatitis Atopic Dermatitis Secondary Syphilis

*Tinea Versicolor (TV)* -*Non-invasive fungal infection of the skin* caused by *Malassezia spp* (Malassezia furfur, globosa, sympodialis) -Clinical findings are usu *very characteristic* and incl *Multiple, often Coalescing, Small Circular Maculae (flat) that may vary in Color (White, Pink, Brown)* -The *rash* is typically *more prominent in Spring & Summer* as the *organism inhibits pigment transfer to keratinocytes* and makes the *affected skin Paler than the unaffected tanned skin* -Lesions may *occasionally* exhibit *hyperpigmentation* compared to surrounding skin *d/t a localized mild inflam response* -Usu *ASX, or mild pruritus* -Lesions usu located on *Upper Trunk*, but *rash may also involve the Upper Arm, NECK, Abdomen* -*DX of TV Confirmed w/ KOH Prep showing Hyphae & Yeast* -*TX: TOPICAL KETOCONAZOLE* (or *topical selenium sulfide, terbinafine, clotrimazole*); *Oral Antifungals w/ extensive dz or recalcitrant infection* (ketoconazole, itraconazole, fluconazole) *Pityriasis Rosea* -Acute *inflammatory rash (presumed Post-Viral) characterized by an Initial "HERALD PATCH" on the TRUNK* that is *Followed by Smaller Pink/Tan lesions on the Trunk & Proximal Extremities* *Seborrheic Dermatitis* -*Inflammatory* disorder *characterized by erythematous patches with OILY SCALES*, predominantly involving *areas w/ many sebaceous glands* (esp the *face & scalp*) -Also assoc w/ *Malassezia spp*, but exact pathyphys unknown *Atopic Dermatitis* (*ECZEMA*) -Typically affects the *extremities* and *produces scaling & severe pruritus* *Secondary Syphilis* -Causes *Widespread MUCOCUTANEOUS Lesions* -Has a *highly variable appearance*, but *typical lesions* are *erythematous or pale pink macules* that predominantly involve the *flexor surfaces of the extremities, and the Palms & Soles* -*TX w/ IM Benzathine Penicillin G*

Tinea Facialis

*Topical Clotrimazole* is used to *TX Tinea Facialis,* which *presents as an Erythematous, Scaly, Annular Patch or Plaque that spreads without treatment* -Edges can be a little bumpy

Ichthyosis

*Topical Lactic Acid* is a *keratolytic* used to *TX Ichthyosis,* which *presents with Diffuse, Rough, DRY Skin with Fish-like Scales usu on the Extensor Extremities and Trunk* -Usu diffuse, not an isolated scaly lesion

How to tell if a lumbar puncture's high RBC count (RBC count >6,000/mm3) is d/t a traumatic LP or d/t something else, like a subarachnoid hemorrhage?

*Traumatic LP* results from *accidental damage of a blood vessel during the procedure* -- *A high RBC count WITHOUT Xanthochromia is characteristic* -WBC count may be elevated with traumatic LPs, as well as elevated protein and glucose levels *Xanthochromia* is the presence of bilirubin in the CSF and is sometimes the only sign of an acute subarachnoid hemorrhage Important findings to Differentiate Traumatic LP from SAH incl: -*Xanthochromia and Discoloration of centrifuged CSF d/t hemoglobin breakdown* -- these are characteristic of *Subarachnoid Hemorrhage* and *appear 2-4hrs after RBCs enter subarachnoid space*

Severe Malnutrition

*Types* -*Marasmus* (wasting) -*Kwashiorkor* (edematous malnutrition) -Combination of both *Management* -Rewarming for hypothermia -Antibiotics for presumed systemic infection -*Rehydration*: • /ORAL/ rehydration solution /preferred/ (if oral intake is insufficient, can use an orogastric or nasogastric tube supplying an oral rehydration solution [glucose + electrolytes]) • /Intravenous/ fluids /if in hypovolemic shock/; but give 10ml/kg (less than a normal IV bolus of 20ml/kg) over a slower period (avoid IVF if hemodynamically stable, chronically-malnourished pts d/t /risk of fluid overload & heart failure/) *Complications of Management* -Heart failure -*Refeeding syndrome*: Incr insulin leads to hypophosphatemia, hypokalemia, hypomagnesemia --> cardiac complications, rhabdomyolysis, seizures

Initial TX for Chronic Myeloid Leukemia?

*Tyrosine kinase inhibitor, IMATINIB* -t(9;22) --> bcr/abl fusion & Philadelphia chromosome --> fusion protein allows unregulated tyrosine kinase activity

How to confirm H. pylori eradication after ABX management?

*UREA BREATH TEST* or *FECAL ANTIGEN TESTING ≥4WKS After Completing ABX* can be performed to confirm eradication!! (Neither should be done <4wks [risk of false positive]) -Fecal Antigen test is more readily available, but may be less accurate than Urea Breath test -Intake of *ABX or Bismuth can result in False Negative test results for both tests* -H. pylori infection is highly associated with duodenal ulcers - >70% of pts infected! -Combination of *PPI Omeprazole, Clarithromycin, & Amoxicillin* is the commonly used *triple therapy* -Confirmation of eradication is recommended for pts w/ duodenal ulcers! -Eradication should also be confirmed in pts w/ persistent dyspepsia, MALT lymphoma, or who have had resection of early gastric cancer

What is *ulipristal*?

*Ulipristal, brand name Ella* is an *antiprogestin* and is the *most effective oral emergency contraceptive pill & may be taken up to 5 DAYS after Unprotected Intercourse* -*Emergency OCPs (levonorgestrel = Plan B; ulipristal = Ella) prevent pregnancy by DELAYING OVULATION* -The *Efficacy of ulipristal does NOT decrease with time*, *as is the case with levonorgestrel (Plan B) and combined hormonal contraceptives* Note: In *women with regular ovulatory cycles*, the *probability of pregnancy after unprotected sex* is as *HIGH AS 30% Prior to Ovulation* (e.g. *2wks after the last menstrual period*). A *NEGATIVE Pregnancy Test* in this setting *DOES NOT EXCLUDE the Possibility of Pregnancy* bc a *positive result is received only after implantation (e.g. 4wks after LMP)*

Factor VIII Deficiency aka Hemophilia A

*X-linked recessive* bleeding disorder - assoc w/ *recurrent hemarthrosis* -TX: *Recombinant factor VIII infusions* through a subQ port -HOWEVER, *INHIBITOR DEVELOPMENT* occurs in ~25% of pts with severe hemophilia A (i.e. frequent, spontaneous bleeds) as a /complication of TX/ -The immune system recognizes the /infused factor as foreign/, & *forms Ab that interfere with factor function* -Suspect an *Inhibitor* when a hemophilia A pt on factor replacement therapy *develops increased bleeding frequency* or has hemorrhage *refractory to tx* -Since *factor VIII* is part of *intrinsic* coag pathway, will see *PROLONGED PTT, but Normal PT IF factor VIII is being inhibited* -TX of an acute bleed in hemophilia A pts with inhibitor developments involves bypassing products (e.g. recombinant *activated* factor VII, *activated* prothrombin complex concentrates*) as such agents work downstream in the coagulation cascade to promote clotting without* the need for factor VIII

Does an advanced directive trump family wishes?

*YES!* Patient preference, as outlined in advanced directives, should //always// prevail in the case of any family conflict regarding the withdrawal of life support.

Uregency Incontinence

*Urgency incontinence = Involuntary Urine Leakage, occurring after a strong urge to urinate immediately* (pts unable to reach bathroom in time) -Other Presenting SX: *Incr urinary freq, nocturia, & small-volume voids* -*Diuretic use EXACERBATES sx* -Urgency incontinence is caused by *bladder detrusor muscle OVERACTIVITY,* leading to an *involuntary intense contraction* that *causes leakage* -Though detrusor overactivity is *usu idiopathic,* it can be caused by *Neurologic DZ (e.g. multiple sclerosis) or Bladder Abnormalities* -*RF* for urgency incontinence: *increasing age, Stroke, depression, Diabetes, Obesity, Caffeine intake, tobacco abuse* -NO leakage of urine with valsalva/cough! (*Negative bladder stress test*) -*Management BEGINS w/ Timed Voids & Bladder Training* -- pt determines a baseline voiding interval and gradually increases the time b/w voids, eventually voiding q3-4yrs -*Other initial measures incl Weight Loss, Smoking Cessation, & Caffeine & Alc Avoidance* -If lifestyle modifications don't help, can *add an Antimuscarinic, like Tolterodine, Solifenacin, or Oxybutynin* • Antimuscarinics *improve bladder capacity & inhibit detrusor m contraction during bladder filling by Blocking ACh release in bladder* • The *anticholinergic properties* of these meds freq result in *AE (e.g. dry mouth, constipation, drowsiness, blurry vision) that may limit their usefulness* • To *minimize AE,* antimuscarinics are *initiated at the Lowest Dose & Titrated Up as tolerated* -If STILL persistent sx despite antimuscarinics, can be considered for *botulinum toxin injections or percutaneous tibial nerve stimulation*

Teratogenic effects of Valproate anticonvulsant mood stabilizer

*Valproate is used to TX Mania & Depression in Bipolar Disorder* It should be *avoided in pregnant women* due to the *significantly INCR risk of Neural Tube Defects, Craniofacial abnormalities, Microcephaly, Growth Retardation, Cleft Lip & Palate, Limb Defects, and Genital Anomalies*

Wallenberg Syndrome (Lateral Medullary Syndrome)

*Vestibulocerebellar Symptoms*: -*Vertigo*, falling TOWARDS the side of the lesion -Difficulty sitting upright w/o support -Diplopia & *Nystagmus (horizontal & vertical)* -*Ipsilateral Limb Ataxia* (e.g. Overshoot target) *Sensory Symptoms*: -Abnormal facial sensation or pain (early sx) -*Loss of Pain & Temp in Ipsilateral face & Contralateral trunk & limbs* *Ipsilateral Bulbar Muscle Weakness* -Dysphagia & Aspiration -Dysarthria, Dysphonia, & *Hoarseness* (d/t Ipsilateral vocal cord paralysis) *Autonomic Dysfunction*: -*Ipsilateral Horner's Syndrome* (ptosis, miosis, & anhidrosis) -Intractable hiccups -Lack of automatic respiration (esp during sleep) -DX made via *MRI* -Acute TX usu involves *IV Thrombolytics* (e.g. *tissue plasminogen activator*) Note: Wallenberg Syndrome typically has *sparing of voluntary motor fxn* in face face & body

Differences in Skin Infections Caused by Vibrio vulnificus vs. Mycobacterium marinum

*Vibrio vulnificus* (Gram neg) -Found in brackish coastal water & marine environments -Infected usu thru contaminated seafood [raw oysters], but can cause Wound infxns from *contact w/ contaminated water or shellfish [recreational activities/raw seafood handling]* -E.g. Cut hand in a *saltwater* fish tank and *rapidly dev progressive cellulitis w/ hemorrhagic bullae* -Illness tends to be mild in most pts, but those with *underlying liver dz (e.g. cirrhosis, viral hepatitis)* or certain *chronic medical conditions (e.g. diabetes, rheumatoid arthritis)* are *at risk for life-threatening infxn* -V. vulnificus wound infxns are often assoc w/ *rapidly progressive (<12hrs) cellulitis w/ hemorrhagic/necrotizing bullous lesions, & Septic Shock*; Labs show *leukocytosis* w/ left shift & *renal insufficiency* -DX by *blood & wound cultures* -*TX w/ IV Doxycycline + Ceftriaxone* (empirically if suspect in chronic dz pts d/t high risk of death) *Mycobacterium marinum* -Classically, causes a *hand infxn in aquarium handlers* -Found in *salt & fresh water* and can *cause wound infxns* -Lesions are usu *papular & ulcerative (not necrotizing & bullous!) and develop over several days (not hours)*

Types of Conjunctivitis

*Viral Conjunctivitis* - Adeno - Supportive tx Distribution: Unilateral or Bilateral Duration: 1-2wks Discharge: Watery/mucoid (crusty eyes) Assoc Findings: Viral prodrome (pharyngitis, rhinorrhea, fever) *Bacterial Conjunctivitis* Distribution: Unilateral or Bilateral Duration: 1-2wks Discharge: Purulent** accumulates after wiping away Assoc Findings: Unremitting ocular discharge (no prodrome sx) *Allergic Conjunctivitis* Distribution: ALWAYS BILATERAL Duration: <30mins to perennial Discharge: Watery Assoc Findings: Ocular Pruritus*

How do you correct hyponatremia in pts w/ decompensated heart failure (DHF)?

*WATER RESTICTION* & *Adjustment of Loop Diuretic Regimen* -*Hyponatremia in pts w/ DHF parallels the severity of HF & in an independent predictor of adverse clinical outcomes* -Low cardiac output & decr perfusion pressure at the baroreceptors of renal afferent arterioles --> Release of *Renin & Norepinephrine* --> *Secretion of Antidiuretic Hormone (ADH aka Vasopressin)* -ADH binds to V2-r in collecting duct to *promote water reabsorption*; *Renin (via angiotensin II) & Norepinephrine incr proximal sodium and water reabsorption, limiting water delivery to distal tubules* -- these actions *promote water retention* --> *Dilutional Hyponatremia* -Angiotensin II and low cardiac output stimulate thirst --> Incr water intake worsens hyponatremia -*Water intake restriction* is the mainstay of *initial therapy for hyponatremia in DHF pts* -Correction of hyponatremia does not improve clinical outcomes assoc w/ HF and is indicated only in pts with *Symptomatic Hyponatremia (e.g. confusion, seizures) or Severe ASX Hyponatremia (Na <120)* -Vasopressin-2-R antagonists (e.g. Tolvaptan) may be considered in pts w/ CHF & Na<120

Duchenne Muscular Dystrophy

*X-linked Myopathy - Defective deletion of Dystrophin on X-Ch* *Clinical Presentation*: Onset *2-3yo*; *Proximal muscle weakness* (e.g. Gower sign, calf pseudohypertrophy [fatty replacement of muscle tissue]); *Dilated cardiomyopathy; Scoliosis; Developmental delays; Intellectual disability; Hyporeflexia of Achilles tendon* *Diagnosis*: *Incr serum creatinine kinase*; *Genetic testing of dystrophin deletion*; Muscle Bx with fibrosis, fat, muscle degen *TX*: *Glucocorticoids* *Prognosis*: *Wheelchair-dependent by adolescence*; *DEATH at age 20-30* from *respiratory/heart failure*

Can you recruit incarcerated individuals to participate in clinical research studies?

*YES, but REQUIRES ADDITIONAL OVERSIGHT by an INSTITUTIONAL REVIEW BOARD* *Incarcerated* individuals have the *same rights as nonincarcerated to Consent or Refuse to Participate in Research Studies* BC the *incarcerated pop is at increased risk for inducement & coercion,* the *IRB reviews research protocol to ensure* that: -The research does not pose excessive risks to the incarcerated pop, which could constitute Exploitation -The research does not provide excessive incentives for participation (nominal payment for time and effort is sometimes permissible) -The process of participant recruitment and selection is Fair and not influenced by correctional staff

Complications of Aortic Dissection

*__Ascending Dissection__* -Aortic valve regurg -Acute coronary syndrome (RCA occlusion) -Cardiac tamponade (hemopericardium) -Stroke (carotid artery occlusion) -Horner syndrome (sympathetic ganglion compression) -Vocal cord paralysis (recurrent laryngeal nerve compression) *__Descending Dissection__* -Hemothorax or hemoperitoneum -Renal injury (renal artery occlusion) -Mesenteric ischemia (e.g. SMA occlusion) -Lower extremity ischemia -Lower extremity paraplegia (spinal cord ischemia)

How many words should child aged 2.5yo be expected to be using?

*≥50-word vocabulary with use of 2-word phrases* Kids at this age with <50 words and few word combinations have *language delay*. Next stop would be *audiologic evaluation* to assess for hearing impairments. -A formal assessment should be obtained bc the child could have been exposed to additional RFs (e.g. meningitis, recurrent/persistent otitis media, ototoxic meds) that may have occurred since the newborn & hearing screening tests, and in-office evaluations may not detect subtle hearing loss

Amyotrophic Lateral Sclerosis

-*ALS is the MC form of Progressive MOTOR Neuron DZ (Neurodegenerative Disease!)* -*ALS is a Relentlessly Progressive Disorder that Involves BOTH LOWER Motor Neurons (anterior horn cells in spinal cord & brainstem neurons innervating bulbar muscles) AND UPPER Motor Neurons or CORTICOSPINAL Motor Neurons* -At its *onset, ALS may involve selective loss of fxn of ONLY upper OR lower motor neurons, but it ultimately causes Progressive loss of BOTH UMN & LMN* -The *initial sign of the DZ with LMN Involvement is an Insidiously Developing ASYMMETRIC Weakness, usu first evident Distally in one of the Limbs* -Pts may disclose a *hx of recent dev of cramping with volitional [intentional] movements that typically occur in the Early Morning Hours (e.g. while stretching in bed)* -*Weakness is assoc w/ Progressive Wasting, Muscle ATROPHY, & Spontaneous Twitching or Fasciculations of motor units* -*Involvement of the Bulbar muscles leads to difficulty w/ chewing & swallowing, and fasciculations of the face and tongue* -*ALS w/* prominent *corticospinal involvement* is *characterized by Hyperactivity of Muscle-Stretch Reflexes (TENDON JERKS) and Frequent Spastic Resistance to passive movements of the affected limbs* -*Ocular Motility, Sensory, Bowel, Bladder, and Cognitive Fxns are PRESERVED!!! Even with advanced dz!! -*TX: RILUZOLE is a Glutamate Inhibitor* that is *currently approved for management of ALS* --though it *cannot stop underlying pathologic process, it may Prolong Survival and Delay the Need for Tracheostomy* Note: Multiple Sclerosis is usu seen in younger Females with 2 or more clinically distinct episodes of CNS dysfunction. Pts typically have sensory, visual, or bladder & bowel dysfunction.

Wolff-Parkinson White ECG

-*Accessory pathway allows cardiac preexcitation* by directly connecting the atria to the ventricles and *bypassing the AV junction*; this pathway conducts faster than the AV node and *excites the ventricles prematurely*, manifesting on the ECG as a *short PR interval* with a characteristic *Delta wave and Widened QRS complex* (>0.12sec) -WPW pts can be *ASX*, but some develop *tachyarrhythmias* *WPW Syndrome* = WPW findings on ECG + symptomatic tachyarrhythmias -Paroxysmal supraventricular tachycardia is the MC arrhythmia (w/ regular, narrow complex tachy); if get *A-fib*, they can conduct down the accessory pathway commonly resulting in *syncope* -TX with *Catheter ABLATION*

Acute Acetaminophen Toxicity

-*Acetaminophen causes HEPATOTOXICITY when taking excessively* -Within the *first 24hrs*, pts are *often ASX or have only Nonspecific Features* (e.g. *N/V, fatigue*) -*Hepatotoxicity becomes evident 24-72hrs after ingestion w/ rising aminotransferases* -- the *levels peak at 72-96hrs* and may be assoc w/ *prolonged PT & PTT (d/t hepatic synthetic dysfunction), hypoglycemia, lactic acidosis, elevated bilirubin, & acute kidney injury* -Although Fulminant Liver Failure and Death may occur, *many pts recover after 4-14d* -*Acute management* of *Acetaminophen Overdose* incL *ACTIVATED CHARCOAL,* which can *bind acetaminophen in the stomach if given within 4hrs of ingestion* -Additionally, *N-ACETYLCYSTEINE (NAC)* is given to *increase intrahepatic glutathione*, which facilitates *removal of N-acetyl benzoquinone imine, the primary toxic metabolite of acetaminophen* -HOWEVER, *NAC is MOST EFFECTIVE when Given PRIOR to Onset of HEPATOTOXICITY, preferably Within 8hrs of Ingestion* -The *Rumack-Matthew line* (based on acetaminophen blood concentration & time since ingestion) can be used to determine the need for treatment -*Bc TX is Most Effective when given Promptly, DELAYED HOSPITAL PRESENTATION is assoc with the greatest risk of worse outcomes* Note: (Acute) Coingestion of ethanol with acetaminophen overdose can actually decrease the hepatotoxic effects of acetaminophen, bc ethanol is a competitive inhibitor of the enzyme that converts acetaminophen into its toxic metabolite; but Chronic alcohol ingestion enhances acetominophen's hepatotoxic effects

Acute Mitral Regurgitation (MR)

-*Acute MR can lead to ACUTE HF!* -Acute MR can occur d/t *papillary muscle rupture*, usu in the setting of *myocardial infarction (3-5d post-MI)* or d/t *rupture of the mitral chordae tendinae* -Pts w/ *mitral valve prolapse (MVP)*, esp when it is related to *underlying connective tissue disease* (e.g. *Marfan, Ehlers-Danlos*) *are at RISK for Mitral Chordae Tendinae RUPTURE*, leading to a *flail leaflet and acute MR* -Pts w/ Acute MR usu have a *dramatic presentation* (d/t lack of time for left heart adaptation) compared to those with /chronic MR/ -*Acute MR p/w SUDDEN-onset Hypotension, Pulmonary Edema, & can rapidly progress to Cardiogenic Shock w/ poor tissue perfusion and peripheral vasoconstriction* -Cardiac exam reveals a *hyperdynamic precordium* and a *decrescendo holosystolic murmur @cardiac apex* -Pts w/ acute, severe MR have *early equalization of left atrial & left ventricular pressures*, and up to 50% (esp w/ ischemic MR) may have *no audible murmur at all (silent MR)* -DX confirmed by *rapid beside Echo*

Acute Chest Syndrome

-*Acute chest syndrome (ACS)* in *sickle cell dz* is *a potentially life-threatening pulmonary complication of SCD* -*DX of SCD defined as Presence of NEW Pulmonary Infiltrate on CXR and ≥1 of the Following*: • *FEVER >38.5C (101.3 F)* • *HYPOXEMIA* • *CHEST PAIN* • *RESPIRATORY DISTRESS* (Tachypnea or Incr Work of Breathing) -*Causes of ACS* in *children* incl *infection, asthma exacerbation, & pulmonary infarction* -Infection is the MCC, so *Empiric Broad-Spectrum ABX* should be *started promptly* -*First-line therapy* is a *third-gen cephalosporin (e.g. CEFTRIAXONE, CEFOTAXIME) + a macrolide (AZITHROMYCIN)* to cover *Strep pneumo & Mycoplasma pneumoniae* -Additional management incl *Pain Control* to *prevent splinting & subsequent hypoventilation and atelectasis* -Also *Need IVF to prevent dehydration & further sickling*

How to DX lactose intolerance?

DX is clinical & is confirmed by resolution of sx on a *lactose-restricted diet* Formal testing performed by lactose breath hydrogen test, which measures excessive lactose fermentation and hydrogen production by colonic bacteria Lactose intolerant pts need to be counseled on maintaining adequate vitamin D and calcium intake

What is the *delta-pressure in Acute Compartment Syndrome diagnosis*?

-*Acute compartment syndrome* is caused by *Increased tissue pressure within a fascial compartment that IMPAIRS PERFUSION* -It is *commonly assoc w/ Traumatic injuries of the extremities (esp long bone fractures)*, but can also *occur w/ Nontraumatic conditions, such as Ischemia-Reperfusion Injury* (where cellular damage from ischemia is exacerbated by restored blood flow and oxygen, which incr prodn of radical oxygen species); leading to *interstitial edema and intracellular swelling* -*DX is usu Clinical, but Compartment Pressure Measurement can Confirm DX* -A *DELTA PRESSURE (Diastolic BP - Compartment Pressure) ≤30 mmHg indicates Acute Compartment Syndrome* -*Definitive TX w/ Emergency Fasciotomy* -If Tx delayed, can lead to *myonecrosis, nerve damage, & permanent loss of fxn*

Radiation Proctitis

-*Acute* radiation proctitis may p/w *diarrhea, mucus discharge, & TENESMUS (ineffectual/painful straining on defecation) during/within 6wks of pelvic radiation* (e.g. for cervical cancer) -*Chronic* radiation proctitis p/w similar sx occurring *>9wks to years after radiation therapy* and is more commonly assoc w/ *strictures, fistula formation, & Rectal Bleeding!* -DX made after excluding other causes of colitis (e.g. infection, IBD, ischemia, malignancy) bc sx are nonspecific -Colonoscopy may show *continuous lesions w/ pallor, friability, telangiectasias, & mucosal hemorrhage* -Acute RP is TX w/ *supportive measures* (e.g. IVF, *antidiarrheals*); Chronic RP may need *sucralfate or glucocorticoid enemas* (sucralfate binds to mucosal interruption, forming a physical barrier to allow it to heal) Note: Angiodysplasia & ischemic colitis can p/w hematochezia, but usu in pts >60yo. Ischemic colitis assoc w/ abdo pain & bloody diarrhea; Angiodysplasia w/ painLESS bleeding

Iodine-Induced Hyperthyroidism

-*Administration of iodine (e.g. Radiocontrast agents/Angiography, Amiodarone, kelp-based dietary supplements)* to pts with *chronic iodine deficiency or preexisting nodular thyroid disease* can cause a *TRANSIENT HYPERTHYROID STATE* (*LOW TSH, Negative Thyrotropin-Receptor Antibodies, Elevated Total T3 & Free T4*) -*Iodine-induced Thyrotoxicosis* is *usu Self-Limited if the source of iodine is discontinued* -In *MILD cases, β-blockers is sufficient for symptomatic management* -However, *Older pts w/ underlying heart disease (e.g. coronary artery disease)* or those with *Persistent (>4-6wks) or Severe Hyperthyroidism* should be *TX w/ Antithyroid Medications e.g. METHIMAZOLE*

Anemia in CKD pts

-*Advanced CKD or ESRD pts commonly dev a hypoproliferative, NORMOCYTIC, NORMOCHROMIC Anemia d/t EPO Underproduction by failing kidneys* -When [new] anemia is found in CKD pts, *check iron levels!* • *Correctable causes of anemia should be identified*: basic workup for New anemia should be performed - *evaluation of iron stores, folate, B12 levels, & reticulocyte count, and FOBT* • In CKD, *iron deficiency is common*, and RBC morphology may be normal early on in deficiency (normal MCV). Pts will require *iron supplementation if low transferrin saturation & ferritin levels* -*CKD-related hypoproliferative anemia is often TX w/ EPO-Stimulating Agents (ESAs)*, such as *supplemental EPO*, to *stimulate RBC prodn within bone marrow* -HOWEVER, *vigorous hematopoiesis after ESA administration can cause Rapid Depletion of Iron Stores, even if iron levels normal on initiation!* -Therefore, *if receiving supplemental EPO (often CKD pts w/ Hb<10), should have Iron Levels checked PRIOR to Initiating EPO and at scheduled intervals while on therapy*

Akathisia Definition & Management

-*Akathisia* is an *AE of antipsychotic drugs* characterized by a *subjective feeling of Inner Restlessness, urge to move, & Inability to Sit Still* -More common with First-generation antipsychotics (haloperidol, chlorpromazine, pimozide), but can also occur w/ second-generation antipsychotics (risperidone, aripiprazole, clozapine, olanzapine, quetiapine) -Akathisia is a common cause of *medication nonadherence* and shouldn't be mistaken for increasing psychotic agitation -*Initial approach* to akathisia is *cautious reduction of antipsychotic dose & monitoring for psychotic exacerbation* -When *dose reduction is not feasible* (e.g. worsening auditory hallucinations), the *addition of a beta-blocker (PROPRANOLOL!) is indicated; Benztropine & Benzodiazepines* have also been used

Alcohol Use (Abuse) Screening

-*All adult primary care pts should be screened for unhealthy alcohol use* -*Single-Item Screening* asking the *Question, 'How many times in the past year have you had 5 (4 for women, 5 for men) or more drinks in a day?'* -- *helps to efficiently identify unhealthy alcohol use* -A *response ≥1x (i.e. One or more times in the past one year) is considered POSITIVE* -Pts who are *positive on the single-item screen should subsequently be assessed further for sx of DSM-5 substance use disorder* (e.g. *evidence of withdrawal, tolerance, craving functional impairment*) -Other screening tests to identify unhealthy use in primary care incl the 10-item Alcohol Use Disorders Identification Test (AUDIT) and the 3-Item AUDIT-C, which are widely validated but more time-intensive (appropriate for settings w/ additional staff & time) -- Both the AUDIT-C and AUDIT require scoring, with specific cutoffs screening positive for unhealthy drinking sand higher scores suggestive of alcohol dependence -A *brief counseling intervention is recommended* for pts *identified as having unhealthy alcohol use* -- this consists of a *nonjudgmental, empathetic discussion about the pt's personal risks of continued alcohol use with the goal of decreasing consumption or achieving abstinence*

Ankylosing Spondylitis

-*Ankylosing Spondylitis p/w back pain with MORNING STIFFNESS that Improves with Exercise, Insidious Onset, Presence of Sx for >3mo, Reduced range of forward flexion of lumbar spine on Schober testing, and Reduced Chest Wall Expansion* -*DX of Ankylosing Spondylitis NEEDS evidence of SACROILIITIS on Plain X-ray (earliest changes seen radiographically, best next step in Dx)* -*3 Imp Clinical Criteria for DX of Ankylosing Spondylitis*: 1. *Presence of low back pain & stiffness for >3mo, that improves w/ exercise or activity* 2. *Limitation of the ROM of Lumbar Spine* 3. *Limitation of Chest Expansion relative to normal values* -*Lumbar spine X-ray (AP & lateral views), Lateral view of Cervical Spine X-ray, & Pelvic Radiograph (incl sacroiliac joints and hip)* are used to *MONITOR DZ ACTIVITY/PROGRESSION*; *measurement of ESR can also be used* -The MC and most imp *extraarticular manifestations incl Acute Anterior Uveitis, Aortic Regurgitation, Apical Pulmonary Fibrosis, IgA Nephropathy, and Restrictive Lung Disease* d/t limited costovertebral joint motion (*uveitis p/w acute unilateral eye pain, photophobia, & blurred vision*) -*Regular Aerobic exercises (incl swimming hydrotherapy) improve overall functional status* (improve joint stability, muscle strength, & help prevent bone loss d/t immobility and use of meds) *of pts w/ rheumatologic disorders and should be Encouraged* -Know that *most ankylosing spondylitis pts do Well and have NO increased overall mortality rates, no functional or employment disabilities, and NO reduction in life expectancy* Note: *HLA-B27 is frequently (>90%) present in Ankylosing Spondylitis pts and in Other Spondyloarthropathies - therefore NOT specific for Dx of Ankylosing Spondylitis*

Alzheimer Disease (AD)

-*Alzheimer disease is the MCC of [moderate to severe] Dementia in Older Adults; advanced age is the strongest RF* -AD is d/t *low acetylcholine synthesis from Basal Nucleus of Meynert (forebrain)* -*Progressive dementia with Neuropsychiatric sx* (e.g. *apathy, agitation, delusions, hallucinations*) -*Auditory hallucinations & delusions are not uncommon in advanced dementia* (though also seen w/ [acute] delirium, the *fairly stable nature of psychotic sx* (e.g. hearing singing, paranoia about cleanliness/poisoning) is *more consistent with advanced AD than delirium* -*Apraxia* is the *inability to perform learned motor activities* (e.g. *dressing, using utensils*) that *occurs in mid- to late-stage AD* -*Sundowning* is a *regularly-appearing, relatively consistent in timing, recurring pattern of behavioral fluctuation* (e.g. *agitation*) that typically *peaks in early evening*, & is *v. common w. dementia*, likely reflecting impaired circadian regulation -*Primitive reflexes* (e.g. grasp, pout) are *seen with advanced AD* and don't require urgent investigation in the absence of other focal neurological findings -*Widespread cortical atrophy, esp in Hippocampus, with Narrowing of gyri & Widening of sulci* -*Senile plaques in gray matter*: *extracellular β-amyloid core*; may cause *Amyloid Angiopathy* > *Intracranial Hemorrhage!*; Aβ (amyloid-β) synthesized by cleaving amyloid precursor protein (APP). -*Neurofibrillary tangles*: *Intracellular, hyperphosphorylated tau protein* = insoluble cytoskeletal elements; # of tangles correlates with degree of dementia. -*Hirano bodies*—*Intracellular eosinophilic proteinaceous rods in hippocampus* *No Cure* for AD, but can *TX with Anticholinesterases, Donepezil, Rivastigmine, Galantamine* which are *First-line for AD* to *incr ACh* AE: nausea, dizziness, insomnia; *contraindicated in patients with cardiac conduction abnormalities*

Amiodarone-Induced Pulmonary Toxicity

-*Amiodarone* is a commonly used *antiarrhythmic used for TX of Ventricular & Supraventricular Tachyarrhythmias* -*Prolonged TX* w/ amiodarone is assoc w/ a *variety of AE incl Photosensitivity, Skin Discoloration, Bone Marrow Suppression, Thyroid Dysfunction, Abnormal LFTs, and Pulmonary Toxicity* -Pulm toxicity is the *most serious AE* that is responsible for *most of the Deaths assoc w/ Amiodarone therapy* -Pulm Toxicity w/ amiodarone can be seen in the form of *Chronic Interstitial Pneumonitis, Organizing PNA, ARDS, &, rarely, w/ a Solitary Pulmonary Mass* -*Chronic Interstitial Pneumonitis is the MC presentation (!!), characterized by the presence of Nonproductive Cough, Fever, Pleuritic Chest Pain, Weight Loss, Dyspnea on Exertion, and a Focal/Diffuse Interstitial Opacity on the CXR* -*Chronic Interstitial Pneumonitis* is usu *seen after months to years of amiodarone therapy*, esp in pts who are on *higher maintenance doses (>400mg/day)*; it is a *CUMULATIVE Dose Effect*, and the *serum amiodarone levels are usu WNL* in these pts -*CXR may reveal presence of Diffuse or Focal Interstitial or Alveolar Opacities* -*TX: DISCONTINUATION of Amiodarone* is the *mainstay of TX of amiodarone-induced pulm toxicity* -*Corticosteroids* can be used in *severe or life-threatening pulm dz* -The *Prognosis is usu Good in most cases*, and the *majority of pts stabilize or improve after complete withdrawal of amiodarone*

What factors suggest a potential causal relationship between a risk factor and disease?

-*An association between a risk factor and a disease is more likely to be CAUSAL if its Strength Increases as the Exposure Level Increases (i.e. Dose-Response Relationship or Biological Gradient)* -Dose-response relationship assumes that the more intense the exposure, the greater the risk of disease -Although a very strong factor in favor of causality, a *dose-response relationship is NOT necessary to infer causation*

What is the Analysis of Variance (ANOVA) test?

-*Analysis of variance (ANOVA) testing compares the MEANS OF ≥3 GROUPS* -ANOVA requires: • A *CATEGORICAL Independent variable* (e.g. treatment/intervention) used to divide the study participants into ≥3 groups • *QUANTITATIVE Dependent variables* (e.g. outcome(s)) for which an *average (mean) is calculated* -An ANOVA test can *determine whether there is a statistically significant difference* in between the ≥3 groups -A large, statistically-significant difference in mean outcome values between groups indicates that the different interventions are associated with significant changes in these outcomes

How to Diagnose Anaphylaxis & Treatment

-*Anaphylaxis* is a *severe IgE-mediated type I HS rxn* that may be *DX when Acute Allergic SX* (e.g. *rash, wheezing*) *are Present in ≥2 organ systems* (e.g. *skin, respiratory*) *After Allergen Exposure* (e.g. wasp sting) • Skin/mucosa: hives, lip/tongue swelling • Respiratory: wheezing, stridor, dyspnea • Cardiovascular: hypotension, tachycardia, syncope • GI: abdominal pain, vomiting, diarrhea -Pts with *normal blood pressure can STILL experience Anaphylaxis!*; *Hypotension is NOT required to make DX, though often present* -*Even when initial sx are less severe* (i.e. *no shock or respiratory distress*), *INTRAMUSCULAR EPINEPHRINE should STILL be given ASAP after Anaphylaxis is Diagnosed, bc Sx Progression can be Unpredictable, Rapid, & Varied* -*Early administration of IM Epi is the MOST IMP step in management of Anaphylaxis d/t its immediate & broad systemic effects* (e.g. *bronchodilation, decreased systemic release of inflam mediators, vasoconstriction*) -*Failure* to administer epinephrine early on (vs after onset of hypotension) can *result in Cardiovascular Collapse* and is assoc w/ *higher incidence of fatalities* Note: *IV Diphenhydramine & PO Hydroxyzine are antihistamines* that can *relieve pruritus and urticaria*. Although they are appropriate as *first-line tx in LOCAL allergic rxns,* they do *NOT relieve airway obstruction or prevent shock in Anaphylaxis*. Therefore, they should only be used as *adjuncts* following first-line TX w/ IM Epi

Angiodysplasias in the GI Tract

-*Angiodysplasias (Vascular Ectasias or Arteriovenous Malformations)* are *vascular anomalies composed of multiple aberrant blood vessels located in the GI tract* -*Angiodysplasias are a Frequent cause* of *OCCULT GI BLEEDING*, most commonly seen in pts *>60yo* and are often *discovered incidentally on endoscopy, appearing as small, cherry red lesions* -Pathogenesis may be d/t chronic occlusions of submucosal veins --> vascular congestion & formation of dysplastic arteriovenous collaterals -*Only a small % of angiodysplasias bleed*, but *bleeding rates are HIGHER in pts w/ ESRD, Aortic Stenosis, & von Willebrand Dz* (vWD) -- *these conditions* most likely *cause a bleeding diathesis (susceptibility)* that *leads to more frequent GI bleeding from malformed vessels* -Uremia seen in ESRD causes PLT dysfunction, and both Aortic Stenosis (which leads to Acquired vWD d/t mechanical disruption during valvular flow) and Hereditary vWD cause decreased levels of vW factor, which is required for PLT aggregation *Angiodysplasias are frequent causes of GI bleeding, esp in pts w/ ESRD, vWD, & Aortic Stenosis*

Attack Rate Definition

Defined as the *proportion of ppl in whom an illness develops out of the total population at risk for the disease*

Kids w/ *Egg Protein Allergy* and *Receiving Annual Influenza Vaccination*

-*Annual flu vaccine is recommended for Children ≥6 MONTHS to Prevent acute respiratory viral illness and spread of infection to pts at risk for life-threatening outcomes (asthma, chronic illness, age <2yo)* -*Inactivated IM Flu Vaccines Recommended!!* Live-attenuated intranasal vaccines *less efficacious & NOT currently recommended* -*Influenza vaccines are manufactured w/ egg-based products* -Children w/ *only prior urticarial reactions to egg protein ingredients CAN receive the Inactivated IM Flu vaccine W/O Restriction and don't need additional observation* -Children w/ *more severe reactions to eggs, incl Anaphylaxis Angioedema, Hypotension, or Persistent Emesis, should receive their IM Flu Vaccine under the supervision of a provider that can recognize and treat severe allergic reactions* -The *only contraindication to influenza vaccination is Severe Allergic Rxn to the Vaccine ITSELF*

Anomalous Aortic Origin of a Coronary Artery (AAOCA)

-*Anomalous Aortic Origin of a Coronary Artery (AAOCA)* is a *common cause of Sudden Cardiac Death (SCD) in Young athletes* (<35yo) -SCD is usu d/t *underlying structural heart dz, w/ Ventricular Tachyarrhythmia as the MC terminal event* -*Two types of AAOCA are commonly assoc w/ SCD*: ● *Left main coronary A originating from the Right aortic sinus* ● *Right coronary A originating from the Left aortic sinus* -These defects create *sharp curvature of the anomalous A, making it less amenable to high-volume flow* and it *passes b/w the aorta & pulm A*, making it *susceptible to external compression during exercise* -Pts w/ *AAOCA may have premonitary Sx of Exertional Angina* [chest pressure while intensely exercising, needing to stop and rest], *Lightheadedness, or Syncope*; some can *experience SCD without premonitary sx* -*Resting EKG is Unremarkable* and *Transthoracic Echo often misses or inaccurately characterizes AAOCA* -*CT Coronary Angiography or Coronary MR Angiography* provide the *best visualization of coronary anatomy*, and are the *DX tests of choice in pts w/ suspected AAOCA*

Which SLE antibody is used to monitor disease activity?

-*Anti-dsDNA antibodies* are helpful to *confirm a DX of SLE*, but are also useful to *follow the course of disease!!!* i.e. Titers of anti-dsDNA Ab correlate w/ disease activity -Anti-dsDNA Ab levels have also been assoc w/ the dev of *Lupus Nephritis*—immune complexes containing these Ab are actually seen within the glomeruli of pts with Lupus Nephritis Note: *Anti-Smith Ab do NOT correlate w/ disease activity in SLE pts. However, they are highly specific for SLE* and *may remain positive in pts w/ clinically-improving SLE* when anti-dsDNA Ab have returned to the normal range

Hair Loss in Secondary Syphilis

-*Areas of hair loss in Secondary Syphilis* are *NOT smooth and discrete* -The lesions usu have a *"moth-eaten" appearance & are assoc w/ significant scarring* -*Secondary Syphilis is TX w/ a Single IM Injection of Penicillin G*

Attributable Risk Percentage (ARP)

-*Attributable risk percentage (ARP)* describes the *percentage of disease in an Exposed group that can be attributed to the exposure* -It's sometimes described as the *percentage of disease in an an exposed group that could have been prevented by eliminating the exposure (i.e. the RF)* -ARP is calculated as the *difference in risk of disease b/w an exposed group & a nonexposed group, divided by the risk of disease in the exposed group* *ARP = [Risk-e - Risk-ue / Risk-e] x100* -ARP can also be calculated using Relative Risk *ARP = [(RR-1)/RR] x100* -RR is calculated as the risk of disease in exposed group divided by risk of disease in nonexposed group *RR = *Risk-e / Risk-ue)*

Apathetic Thyrotoxicosis

-*Atypical* presentation of *HYPERthyroidism in older* pts, characterized by *lethargy, confusion, & depression* -It is /*often misdiagnosed as dementia*/, which may also concurrently be present -A high index of suspicion is required to make this diagnosis, as *elderly pts may not have classic manifestations of hyperthyroidism* -Thyroid function tests can quickly & noninvasively prove the dx

Myotonic Dystrophy

-*Autosomal Dominant* disorder caused by *trinucleotide repeat expansion (CTG) in DMPK gene*, causing un-translatable mRNA accumulation that is *toxic to skeletal, cardiac, & smooth muscle* -Usu presents in adolescents & early adulthood; dz onset & severity depend on length of CTG repeats; more severe phenotypes present in infancy/early childhood -Characterized by *MYOTONIA (/delayed muscle relaxation/ e.g. difficulty releasing hand grip), muscle Weakness, Pain, & Atrophy* of *DISTAL Muscles* (e.g. *hand atrophy, forearm, ankles*) and *FACIAL MUSCLES* (e.g. *ptosis, flat affect, difficulty making facial expressions*) -Can lead to *facial muscle atrophy w/ ptosis, temporal wasting, & emaciated extremities; delayed relaxation on contraction of thenar & hypothenar mm* (temporal bone hollowed appearance, thin cheeks) (deep tendon reflexes normal) -Other features can incl *cardiac arrhythmias (can lead to SCD), cardiomyopathy, insulin resistance (e.g. prediabetes), cataracts, & excessive daytime sleepiness, GI disturbances (Dysphagia, constipation), and Testicular Atrophy/Hypogonadism* -*Genetic testing is confirmatory* of diagnosis to confirm CTG repeat expansion -TX is *supportive* and *life expectancy is reduced* d/t *cardiovascular and respiratory disease*

How to detect *Huntington disease*?

-*Autosomal dominant* condition characterized by *progressive neurologic deterioration resulting in death* -Can be *detected via predictive genetic screening BEFORE symptom onset* -*Predictive Screening* carries *significant psychological impacts* (can affect mood and relationships) and is *relevant to the pt's future*

*Auricular Hematoma*

-*Blunt trauma to the ear* can cause an *Auricular Hematoma*, which is a *collection of blood between the perichondrium and cartilage of the outer ear* -*PE is Diagnostic - w/ a Swollen, Erythematous, Tender area of Fluctuance at the site of hematoma* -*Complications of an UNTX Auricular Hematoma* include *rapid Infection (within 2-3d) leading to an Abscess; Avascular Necrosis* of the outer ear cartilage (bc auricular cartilage doesn't have direct blood supply & receives its blood supply via diffusion from the perichondrium); and *subsequent Fibrocartilage Overgrowth leading to a Permanent Cauliflower Ear deformity* -THEREFORE, *Management is Prompt Aspiration or Incision & Drainage of the blood collection w/ application of a pressure dressing* to *prevent hematoma reaccumulation* -Pts are *ALSO TX w/ Oral ABX to cover for skin flora & Pseudomonas aeruginosa* -*DAILY F/U for 3-5 days is recommended to assess healing and evaluate for signs of infection (fever, purulent discharge) or blood reaccumulation* Note: *Aspirin & other NSAIDs (e.g. Ibuprofen) are AVOIDED to prevent rebleeding of the hematoma*

What is *awake intubation*?

-*Awake Intubation*, either *Nasotracheal or Orotracheal*, is the *PREFERRED Method of Intubation* for *Pts with DIFFICULT AIRWAYS* -- e.g. pt w/ *upper airway obstruction (swollen lips/tongue, stridor) d/t Anaphylaxis* -In *Awake Intubation*, the *Pt INDEPENDENTLY MAINTAINS UPPER AIRWAY TONE & SPONTANEOUS VENTILATION While the Airway is Visualized w/ Fiberoptic Endoscope* to *determine whether intubation is possible* -*KETAMINE*, a phencyclidine derivative, is the *preferred agent* for *Awake Intubations bc it provides DISSOCIATION, AMNESIA, & ANALGESIA (i.e. Dissociative Anesthesia)* while *ALSO MAINTAINING UPPER AIRWAY TONE, PROTECTIVE REFLEXES, & RESPIRATORY DRIVE* • *ketamine* also causes a *sympathetic surge* that *increases blood pressure & causes bronchial smooth m relaxation*--additional benefits in pts w/ *hypotension & bronchospasm* -If *hypoxic, unstable* pts who *cannot be oxygenated or ventilated d/t an upper airway obstruction, perform an EMERGENT CRICOTHYROIDOTOMY* (aka *CRICOTHYROTOMY surgical airway*, where the *cricothyroid membrane is incised, and an Endotracheal or Tracheostomy tube is inserted for Mechanical Ventilation*) (cricothyroid membrane is the membrane between the superiorly-located thyroid cartilage and the inferiorly-located cricoid cartilage) Note: In *Rapid Sequence Intubation*, the pt is *fully anesthetized and paralyzed, using Rocuronium or Succinylcholine, causing loss of ALL upper airway tone, loss of protective airway reflexes, and loss of respiratory drive*. IF intubation is *unsuccessful*, the pt can *rapidly become Hypoxic & undergo Cardiac Arrest*

Familial Hypocalciuric Hypercalcemia (FHH)

-*BENIGN, Autosomal Dominant* disorder characterized by *Mild Hyperglycemia (usu ASX), with a Normal or Mildly Elevated PTH level, and LOW Urinary Calcium Excretion* -D/t *mutations of the calcium-sensing receptor (CaSR) that leads to Decr sensitivity to calcium* -- *Need higher than usu Calcium levels to suppress PTH release* and the *Defective CaSR causes INCR Reabsorption of Calcium in renal tubules* -FHH and Primary Hyperparathyroidism (hypercalcemia, Incr PTH) cab be distinguished by *assessment of urinary calcium excretion* • *FHH is assoc w. LOW Urinary Ca2+ Excr* (usu *<100mg/24hrs*) • *Primary HyperPTH is assoc w/ HIGH Urinary Ca2+ Excr* (*>300mg/24hrs*) despite the *Increased reabsorption of calcium, d/t accelerated bone turnover* -Confirm FHH by *testing for CaSR mutations*

Benign Paroxysmal Positional Vertigo (BPPV)

-*BPPV* is thought to be *caused by calcium debris within the semicircular canals* that *alters normal fluid flow* -It causes *BRIEF (<1min), often INTENSE Episodes of Vertigo TRIGGERED by Changes in Head Position* -Pts can have *headaches*, but tinnitus & hearing loss are NOT typical

What is the presentation & first-line TX for bacterial conjunctivitis?

-*Bacterial conjunctivitis is Highly Contagious and p/w Conjunctival Erythema and Mucopurulent Discharge* -Discharge is *thick & accumulates quickly, causing eyelid matting* -Condition is usu *Unilateral* though it can be bilateral -It's usu *self-limited, but Topical ABX are prescribed to shorten Sx duration and reduce person-to-person transmission* -MCC of bacterial conjunctivitis are *Staph aureus, Strep pneumo, Moraxella catarrhalis, & H. flu* -*First-line TX* is typically *Erythromycin ointment or Polymyxin-Trimethoprim drops* -However, *topical Fluoroquinolones (e.g. Cipro, Ofloxacin)* are *preferred for contact lense wearers d/t Higher risk for Pseudomonal aeruginosa infxn*

Bariatric Surgery & Preconception Counseling

-*Bariatric surgery* is indicated to *assist w/ weight loss* for pts in *obesity class 2 (BMI ≥35) with ≥1 comorbidity (Diabetes, HTN, Sleep Apnea)* or for those in *obesity class 3 (BMI ≥40)* -*Bariatric surgery* is *recommended in Reproductive-aged women bc it DECR the risk of long-term adverse health outcomes and obstetric complications (e.g. preeclampsia, gestational DM)* -D/t *reductions in dietary intake* and *malabsorption* assoc w/ bariatric surgery, pts can have *micronutrient deficiencies in iron, folate, calcium, & vitamins B12 & D, that can adversely affect fetal outcomes (e.g. preterm delivery, stillbirth)* -Therefore, *repro-age women are recommended to DELAY Pregnancy for ≥1yr AFTER Bariatric surgery to Optimize Weight Loss and Stabilize Nutritional Status* -Recommend *nonoral form of contraception, i.e. IUD or Implant, during this time d/t decr absorption rates w/ OCPs* -After this delay and reducing BMI, the *rates of fetal anomalies & fetal demise (stillbirth) become similar to the general population* -In pts *who DO become pregnant s/p bariatric surgery, Vitamin Supplementation & Serial Fetal Growth U/S are Recommended d/t INCR risk of fetal growth restriction & low birth weight* -Note: Bariatric surgery *does NOT incr miscarriage rates & is NOT an indication for c-section*

Pityriasis Rosea

-*Benign, self-resolving rash in 6-8wks (spontaneously)* in adolescents & young adults, probably viral -P/w a *solitary herald patch on neck/chest/trunk, followed by multiple, smaller, oval lesions* clustered in a *"Christmas tree" pattern* (the herald patch increase in size and then fades centrally, which is when the smaller lesions form on the trunk) -The rash spares the face, palms, & soles; may be ASX or Pruritic; Non-transmissible -DX is Clinical; HOWEVER, *a rapid plasma reagin test* may be indicated in sexually-active pts to *r/o secondary syphilis* (which does involve palms & soles) -NO TX required; relapse uncommon

Phototherapy for Neonatal Jaundice

-*Bilirubin levels in newborns are physiologically elevated d/t liver immaturity, lack of intestinal bacterial to break down bilirubin, and high hemoglobin turnover* -*Additional RF in developing [unconjugated] hyperbilirubinemia* incl *prematurity (<37wks gestation), exclusive breastfeeding, sibling requiring phototherapy, and East Asian race* -The *danger of very high bilirubin levels (>20-25 mg/dL) is Kernicterus*, or *bilirubin encephalopathy*, which results in *severe neurologic dysfunction* (e.g. movement disorder, sensorineural hearing loss) -*Nomograms* for full-term infants help to *determine the need for phototherapy based on the bilirubin level at a given hour of life* -*Phototherapy converts bilirubin into a water-soluble form* that can be readily *excr in the urine and stool* -As bilirubin levels physiologically rise at this age of life, a *stable bilirubin level* under phototherapy is not immediately considered a failed intervention and *phototherapy should continue w/ interval bilirubin monitoring* -Additionally, although direct sunlight can lower bilirubin levels, it is NOT recommended in place of phototherapy d/t sunburn risk

Binswanger's Disease

-*Binswanger's Dz is a type of Vascular Dementia that involves WHITE MATTER INFARCTS* -Pts usu p/w *Apathy, Agitation, & B/L Corticospinal or Bulbar Signs*

Cushing's Triad of *Intracranial Hypertension*

-*Bradycardia, systemic Hypertension, & [severe] Respiratory Depression* Intracranial hypertension causes *elevated intracranial pressure* --> HA, vomiting, blurred vision, papilledema in early stages; Transtentorial herniation of brain causing altered LOC (stupor -> coma, Dilation of Ipsilateral Pupil, Third CNIII Palsy, Hemiparesis, Decerebrate Posturing (generalized body extension), and eventual Respiratory Arrest* as ICP further elevates -Intubate pt to protect & maintain airway in case of respiratory arrest -Later, IV Mannitol can be used as an osmotic diuretic to reduce brain volume by drawing water out of cells, to acutely lower elevated ICP in emergencies -Lowering PaCO2 [to 25-30 mmHg] by hyperventilating the pt causes Cerebral Vasoconstriction -> Decr cerebral blood flow -> Reduces ICP in emergent situations; but is Contraindicated in pts w/ traumatic brain injury and in acute stroke (worsened neurologic injuries by hyperventilation-induced cerebral vasoconstriction)

Broca Aphasia

-*Broca (EXPRESSIVE) Aphasia* -*Broca area* in *LEFT Inferior Frontal Gyrus of LEFT FRONTAL Lobe* -Associated with *Defective Language PRODUCTION* -Patients appear *frustrated, insight intact* -- *they KNOW they aren't saying the right things* Broca = broken boca (boca = mouth in Spanish). *Aphasia*—higher-order *language deficit (inability to understand/produce/use language appropriately)*; caused by *pathology in dominant cerebral hemisphere (usu LEFT)*

Cystic Fibrosis Lung Disease

-*CF Pulm disease is the major cause of M&M* -Characterized by *chronic bacterial colonization w/ periodic acute pulmonary exacerbations, caused primarily by Staph aureus & Pseudomonas aeruginosa* -*Hyperinflation on CXR* is a sign of *chronic obstruction* from *thickened secretions* and *prominent bronchovascular markings indicate concurrent inflam & infxn* -*EMPIRIC ABX TX incl VANCOMYCIN (for MRSA and 2-drug coverage for P. aeruginosa), CEFEPIME/CEFTAZIDIME (antipseudomonal cephalosporins), and AMIKACIN/TOBRAMYCIN (aminoglycosides effective against Pseudomonas too)* -Other effective agents incl *carbapenem [ertapenem], certain fluoroquinolones, aztreonam, & colistin* Note: *Ceftriaxone + Azithromycin* are the recommended antibiotics for *community-acquired pneumonia requiring hospitalization*--covers MCC of PNA incl Strep pneumo, Mycoplasma pneumoniae, but do NOT work against Pseudomonas aeruginosa!!

CKD & 2º-->3º Hyperparathyroidism

-*CKD* is assoc w/ *phosphate retention* (d/t decr filtered PO4), *Reduced free serum Ca2+ levels* (d/t binding of calcium by PO4) & *Decr 1,25-dihydroxyvitamin D levels* (d/t decr renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, leads to decr Ca abso) --> leads to a *compensatory RISE in PTH levels (Secondary Hyperparathyroidism, characterized by Incr PTH, Low/Low-Normal Ca2+, & Low 1,25-dihydroxyvitamin D)* -Over time, this can lead to *autonomous PTH secretion (i.e. Tertiary Hyperparathyroidism)* -*Indications for Parathyroidectomy* in *3º hyperPTH* include *persistent hypercalcemia (>10.5) or hyperphosphatemia, very high PTH (>800)levels, soft tissue calcification or calciphylaxis, and/or intractable bone pain or pruritus*

Which patients have the greatest risk for developing *postoperative pulmonary complications* after undergoing *elective thoracic or upper abdominal surgery*?

-*COPD* -*Cigarette smoking* -*Sleep Apnea* -*Heart Failure* -These conditions should be *OPTIMIZED PRIOR to undergoing elective procedures*, including: • *Smoking Cessation ideally >4wks Prior* to procedure *for better would healing and lower rates of postop pulm complications* • *TX of any Heart Failure or COPD Exacerbations that occur preoperatively*; *surgery should be delayed until pulmonary and cardiac function is optimized/returned to a stable baseline*

How do you confirm an acute pulmonary embolism?

-*CT Angiogram of the chest* is usu *preferred for diagnostic confirmation of acute PE* -HOWEVER, in pts with *impaired renal fxn, IV Contrast should be AVOIDED* -- therefore *Ventilation-Perfusion scan is most appropriate*

How do you monitor a pt taking *cardiotoxic chemotherapy*, such as *anthracycline agents, like Doxorubicin & Daunorubicin*?

-*Cardiotoxicity* is one of the primary concerns when giving *anthracycline chemotherapy agents (Doxorubicin & Daunorubicin)* due to *direct toxic effect on the myocardium [potentially causing elevated cardiac troponins]* -The *risk of cardiotoxicity* w/ these agents is *related to the CUMULATIVE DOSE,* and is *INCREASED in pts w/ Preexisting Cardiac Disease with a LOW Ejection Fraction* -In the general pop, resting echocardiography is often used to evaluate EF, but there is potential for significant variability in the results -*RADIONUCLIDE VENTRICULOGRAPHY,* AKA *MUGA (Multigated Acquisition) Scan* is typically *used to Monitor pts Receiving Cardiotoxic Chemotherapy* as it is a *highly accurate & reproducible test* for *quantitating LVEF* (*unlike Echos*) -A *radionuclide ventriculogram* is generally *performed at BASELINE BEFORE CHEMO is initiated*, and *Before EACH Subsequent Dose of Chemo* -The *therapeutic regimen is Dependent on the Baseline Cardiac Fxn* (e.g. *anthracycline chemo is contraindicated when baseline EF <30%*, and *needs modified dosing when baseline EF <50%*) -A *DECR in the EF by ≥10% MAY WARRANT DISCONTINUATION of chemotherapy agent*

Celiac disease

-*Celiac Disease (Gluten-Sensitive Enteropathy) is a common cause* of *MULTINUTRIENT MALABSORPTION DISORDER!!* (e.g. *iron deficiency anemia & vitamin D deficiencies despite consuming a nutritious diet in a young pt*) -- these deficiencies can occur d/t Celiac Dz *even in the absence of classic GI malabsorption sx such as diarrhea* -Assoc with other autoimmune disorders concurrently! e.g. vitiligo, hypothyroidism -*Screening* for celiac dz is performed by checking *ANTI-ENDOMYSIAL ANTIBODY & ANTI-TISSUE TRANSGLUTAMINASE ANTIBODY LEVELS* -*Confirm DX w/ gold standard Small Intestinal Biopsy* *Substantial # of celiac pts develop malabsorption with minimal or no GI sx*

Diabetic Neuropathy DX & Management

-*Diabetic Neuropathy* should be *suspected* in pts w/ *diabetes who have SYMMETRIC sensory changes in the feet, that consist of injury to nerve fibers controlling pain, temperature, vibratory & proprioception sensation* -The *TUNING FORK TEST* is an easy and inexpensive way to *assess for loss of vibratory sense* -*Aggressive GLYCEMIC CONTROL is the MOST IMP aspect of TX of Diabetic Neuropathy* (Goal A1c ≤7.0%) -However, for pts *w/ severe assoc burning pain, TX w/ Tricyclic Antidepressants (Amitriptyline, Imipramine), DULOXETINE (SNRI), or certain Anticonvulsant Medications (Pregabalin, Gabapentin, Lamotrigine, Carbamazepine)* can *alter neuronal transmission of pain and decr pain* -While TCAs are effective pain control agents for diabetic neuropathy, SSRIs are NOT. -*Pain Sx of diabetic neuropathy often Spontaneously Resolve within a Year, so Eventual Discontinuation of these meds is often possible*

*Cervical Insufficiency* What are the risk factors for *cervical insufficiency* in pregnant women?

-*Cervical Insufficiency* is a *structural weakness* that *predisposes to SECOND-TRIMESTER PREGNANCY LOSS* -RF: *Collagen Abnormalities (e.g. Ehlers-Danlos syndrome), Uterine Anomalies (e.g. septate or bicornuate uterus), Prior Injury/Procedure to the Cervix (e.g. Obstetric trauma), and Cervical Conization (e.g. Cold Knife Cone)* *Cervical Insufficiency* is *DX if 1 of 3 criteria is present* • *History-based*: Classic obstetric hx of *≥2 prior consecutive, second-trimester losses* -- these pts have *high risk of recurrent preterm delivery,* and therefore *NEED Cerclage Suture Placement* to reinforce the cervix (placed at 12-14wks, and removed at term, allowing for vaginal delivery) • Exam-based: *PainLESS, advanced cervical dilation on PE in second trimester* • Ultrasound-based: TVUS finding of *ASX cervical shortening to ≤2.5cm @<24wks gestation* Note: After cerclage is placed, do NOT need to do cervical length measurements. HOWEVER, *weekly cervical length measurements ARE indicated for monitoring pts w/ a Hx of Preterm Delivery d/t to causes OTHER than Cervical Insufficiency or for pts w/ no hx of preterm delivery but who are incidentally diagnosed with a short cervix (≤2.5cm on U/S)*

Chronic Prostatitis and Chronic Pelvic Pain Syndrome

-*Chronic Prostatitis* is manifested by *>3MO of Dysuria, Pain in the genitourinary region, &/or Pain during Ejaculation* -*Prostate exam is usu Normal* but may show hypertrophy, tenderness, or edema -*Bc Sx of chronic prostatitis resemble a UTI, pts are inappropriately Rx short courses of ABX* and while this may *transiently improve Sx, manifestations generally RECUR within DAYS of ABX Cessation* -*DX of Chronic Prostatitis requires Urinalysis & Urine Culture BEFORE & AFTER Prostate Massage* with *UA revealing >20 leukocytes/hpf* -*Urine Culture* results then *differentiate b/w*: ● *Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS)* - where *Urine Cx results are ASEPTIC* ● *Chronic Bacterial Prostatitis* - where *Urine Cx results show BACTERIURIA (>10-fold INCR After prostate massage) -*CP/CPPS occurs far more commonly than CBP* -The *underlying cause of CP/CPPS is UNCLEAR* - therefore *the optimal TX is UNKNOWN*, but the best evidence *supports medications used for prostate enlargement (e.g. α-blockers, terazosin & tamsulosin, which cause smooth m relaxation), ABX, Anti-inflammatories, and/or psychotherapy*

Chronic Spontaneous Urticaria (CSU)

-*Chronic Spontaneous Urticaria (CSU) is Defined as Episodic Urticaria lasting >6WKS that generally occurs W/O apparent triggers (e.g. physical stimuli)* -*CSU Lesions* are *INTENSELY PRURITIC, presenting as Round or Serpiginous, Erythematous Plaques (i.e. WHEALS)* -*Individual lesions appear & enlarge over MINS to HRS before DISAPPEARING Within 24HRS* -*Newer lesions form while Older ones resolve*, giving *each episode of urticaria* a typical *duration of Days* -CSU is *initially TX w/ second-gen, nonsedating H1-blockers (LORATADINE, CETIRIZINE) and AVOIDANCE OF Aggravating Factors like NSAIDs, Heat, Tight-fitting clothes*

Clozapine - Use & AE

-*Clozapine* is a highly effective *antipsychotic* Reserved for the *TX of REFRACTORY SCHIZOPHRENIA & Schizoaffective disorder* -It is *NOT used as first-line* tx *d/t its association w/ NEUTROPENIA / AGRANULOCYTOSIS* • It must be Rx thru a *central pt registry* that *requires MANDATORY MONITORING of the ABSOLUTE NEUTROPHIL COUNT (ANC)* -Blood tests (*CBC*) must be performed *weekly for the first 6mo of TX, every other week for the second 6mo, and q4wks thereafter* -Physicians are *guided by an algorithm* that *specifies the minimum ANC required to initiate and continue Clozapine therapy* -Pts should be *advised to immediately report infectious sx (fever,weakness, lethargy, sore throat)* -OTHER AE of CLOZAPINE: *Weight GAIN, Metabolic Syndrome, Seizures, Pulmonary Embolus, Myocarditis, excessive salivation, Constipation, & ILEUS* Note: It is UNCOMMON for clozapine to cause hepatotoxicity and thrombocytopenia - therefore, periodic monitoring of LFTS and PLTs are Unnecessary. *Valproate requires baseline and periodic monitoring of LFTs*

When to do colonoscopy from an abnormal finding on sigmoidoscopy?

-*Colon cancer screening* should be offered to *average-risk pts starting @45yo* -*Colonoscopy is the most sensitive* test, but pts don't like bowel prep, so can offer a *Flexible Sigmoidoscopy* -- which requires less bowel prep and is an acceptable alternative for *average-risk* individuals -Note that Flex sig does not visualize the proximal colon and is *less sensitive* -If Flex Sig findings are *Normal* --> *Repeat Flex Sig q5yrs (or q10yrs if combined w/ annual fecal immunochemical testing)* -If Flex Sig findings are *ABNORMAL* (e.g. adenomatous polyp) --> Pts should *undergo colonoscopy NOW* to look at the entire colon and r/o synchronous (i.e. developing concurrently in another colon segment) polyps/adenomas/advanced neoplasia in the proximal colon

Febrile Seizure

-*Common complication of high fevers* that usu develops from a *mild viral infection* (e.g. common cold) -Febrile seizures *frequently affect children age 3mo to 6yo* -Seizures are typically *nonfocal, last <15mins, & do not occur >1x/day* -Pts w/ febrile seizures have *NO prior AFEBRILE Seizure, NO evidence of metabolic disease (e.g. asterixis, depressed sensorium), and NO signs of Intracranial Infection (e.g. neck stiffness, bulging fontanelles, photophobia)* -Febrile seizures are usu *Clinically diagnosed* and *further evaluation is typically NOT indicated* -Parents should be *reassured* that these are *common and usu SELF-RESOLVE W/O acute or long-term sequelae* -*Antipyretics* are given for general fever reduction, but parents should be informed that Tylenol *does NOT prevent* future episodes of febrile seizures Note: An *EEG* would be indicated in pts w/ *Atypical* seizures (e.g. *multiple, focal*) or with *Abnormal Neurologic Examinations* (e.g. *abnormal reflexes, developmental delay*)

Pregnant Patients with Extensive Condyloma Acuminata: Management How do children w/ HPV present?

-*Condyloma acuminata* is the dermatologic manifestation of *HPV infection* mostly caused by *low oncogenic potential* (e.g. *6 & 11*) -HPV is primarily transmitted through sexual contact, and the most common areas affected in women incl vulva, vagina, cervix, perineum, & perianal region -HPV can also be *VERTICALLY TRANSMITTED* -*Children w/ vertically-transmitted HPV* typically p/w *lesions in the oropharynx, larynx, or trachea at age 2-5*; the most severe manifestation is *juvenile-onset respiratory papillomatosis (JRP)* -There is an assoc b/w JRP, childhood HPV dz, & maternal HPV disease -HOWEVER, *C-section does NOT prevent vertical transmission or decrease the risk for JRP or childhood HPV disease* -Therefore, *Expectant Management for vaginal delivery* is the best management if the the *genital warts* are small and not obstructive -*Excision of condyloma* during pregnancy is *indicated if lesions are large and obstruct the birth control*, but *excision does not decr the risk for vertical transmission* -Excision of large obstructing condyloma during pregnancy is not always feasible d/t the *risk of bleeding complications* -If excision of obstructing condyloma is not feasible, then *c-section is indicated*

Posterior Urethral Valves (PUVs)

-*Congenital obstruction of the urethra caused by residual embryologic tissue* during GU development -Found *exclusively in BOYS* (majority of PUVs are d/t *abnormal insertion of wolffian ducts* {girls lack these} *into urethra*) -*MCC of severe obstructive uropathy in children* -Generally *diagnosed prenatally* (*antenatal U/S*), showing *bilateral hydronephrosis, thickened & dilated bladder, dilated proximal urethra* -If urethral obstruction is severe, *oligohydramnios* can result and *lead to POTTER SEQUENCE* (*pulmonary hypoplasia [can be fatal], flattened facies, limb deformities*) -Other common findings incl: *bladder distension, weak urinary stream, & recurrent UTIs* -*DX Confirmed by VOIDING CYSTOURETHROGRAM (VCUG)* -Catheterize pt, inject radiopaque dye, & *obtain images while voiding*; shows *Hallmark findings of a Dilated & Elongated Proximal Posterior Urethra during the voiding phase* (other findings incl: *dilated bladder, 25-50% have some degree of vesicoureteral reflux & ureteral dilation d/t severe outflow obstruction caused by PUV*) (*VCUG is also the test of choice for diagnosing vesicoureteral reflux & posterior urethral valves!*) -Once PUV confirmed, *Management* incl: • *Stabilize* pt, *drain urinary tract by placing a FOLEY catheter to temporarily relieve obstruction* • *Correct electrolyte abnormalities* • *Tx complications* incl *respiratory distress & infection* • *Cystoscopy for direct visualization & Primary Ablation of PUV to relieve obstruction* (Curative!) or else, *vesicostomy* -All PUV pts are at *risk for developing CKD*, but pts w/ *persistently elevated Cr after PUV ablation* are at *Incr risk for ESRD* Note: Renal ultrasounds are less sensitive for distal obstructions, and cannot definitively differentiate b/w ureteropelvic junction obstruction, vesicoureteral reflux, and PUVs.

Sx and presentation of SLE pts

-*Constitutional sx like fatigue, arthralgias/myalgias, weight loss, fever* -Facial rash--*butterfly rash* is hallmark, seen in many SLE pts after sun exposure -SLE-related inflammation in the body can manifest as pleural effusion secondarily, where the pleural effusion may cause *pleuritis or chest pain*

SLE (systemic lupus erythematosus)

-*Constitutional sx* such as *fever, fatigue, arthralgias/myalgias, and wt loss* are frequently present in SLE -*Butterfly facial rash* is the hallmark, seen in many SLE pts /after sun exposure/ -Decr breath sounds at lung base is most likely a *small pleural effusion 2º to SLE-related inflammation* -The pleural effusion may cause *pleuritis or chest pain* -Pts may have a FHX of SLE or other connective tissue disorders!! -Testing for *antinuclear antibodies (ANA)* is indicated in pts who have suggestive sx and is positive in nearly all pts w/ SLE -However, ANA can also be positive in healthy pts or who have connective tissue diseases other than SLE (hence, not specific!) -*Antibodies to double-stranded DNA (dsDNA)*, a subtype of ANA, are helpful bc they are *more specific for SLE Dx*, and, w/ a sensitivity of 66-95%, are also the *most sensitive to detect SLE* -Anti-dsDNA antibodies are also useful to follow the course of disease; *Titers of anti-dsDNA Ab correlate w/ disease activity* -Anti-dsDNA Ab levels have also been assoc w/ dev of *Lupus Nephritis*—immune complexes containing these Ab are actually seen within the glomeruli of pts w/ Lupus Nephritis Note: *Anti-Smith antibodies are highly specific for SLE, but have a sensitivity of only 25%* (vs. anti-dsDNA Ab, which have a sensitivity of ≈70%) Note: *Anti-Smith antibodies do NOT correlate w/ disease activity in SLE* pts, HOWEVER, they are *highly specific for SLE* and may remain positive in pts w/ clinically-improving SLE when anti-dsDNA Ab have returned to the normal range

Conversion Disorder

-*Conversion Disorder AKA Functional Neurologic Symptom Disorder* -*Sx are Unconscious, Motivation is Unconscious* -*Unexplained LOSS of Sensory or Motor function!* (e.g. *paralysis, blindness, mutism*), *often following an acute stressor* -- e.g. Never Have I Ever, where Devi becomes paralyzed after loss of her father -Patient *may be aware of but indifferent* toward symptoms (*"la belle indifférence"*) -More common in *females, adolescents, and young adults*

Which conditions cause a rash on the palms & soles?

-*Coxsackie A infection* (hand, foot, & mouth dz) -*Rocky mountain spotted fever* (caused by Rickettsia rickettsii; tx w/ *Doxycycline*) -*Secondary Syphilis* (fever, LAD, skin rashes, condyloma lata; Tx w/ *Penicillin G*)

Lateral Epicondylitis (Tennis Elbow)

-*DEGENERATIVE (NOT inflammatory) disorder* d/t *repeated/forceful overuse of wrist & digit extensor muscles that originate at the lateral epicondyle* (repeat backhand strikes; also with use of hand tools) -Characterized by *angiofibroblastic tendinosis* (disorganized tissue and neovessels) and true inflam infiltrates are typically scant -Pain is *most severe 1cm distal to the lateral epicondyle* and is *elicited by resisted wrist extension, passive wrist hyperflexion, or making a fist* -DX Clinical w/o imaging usu; Only need X-ray imaging if you suspect a fracture (e.g. traumatic fall) but it won't visualize soft tissue (tendon) injury -Initial Management involves *activity modification & use of a Counterforce Elbow Brace* (tendinosis strap) applied distally to lateral epicondyle to decr force transmission to tendon insertion, or a compression sleeve can be used Note: Short courses (1-2wks) of acetaminophen or low-dose NSAIDs can be useful for as an adjunct, but bc its degenerative not inflammatory, NSAID benefit is uncertain; High-dose & extended courses of anti-inflammatory agents are NOT recommended d/t AE Note: Corticosteroid injections can help short-term relief, but does not provide long-term benefits or prevent recurrence, Can also lead to tendon rupture! Surgery considered for pts w/ prolonged (>6mo), severe sx (rarely done)

First Time Chickenpox

-*Diffuse, pruritic, VESICULAR rash* is consistent w/ *Chickenpox*, or *primary infection w/ VZV* -A *Viral Prodrome (fever, sore throat, malaise) usu PRECEDES onset of Rash* - *which usu begins w/ erythematous macules & papules and dev into vesicles that later crus over* -*Crops of lesions in Different Stages of Progression are Classic*; *DX Clinical* -Most *healthy* children have a *mild course* and *recover fully w/ supportive care alone (e.g. antihistamines, Tylenol)* -HOWEVER, *Complications of VZV (e.g. Skin Infection, Pneumonia, Encephalitis) can occur*, and *RF incl Adults/Adolescents & Immunosuppressed* (e.g. taking methotrexate for systemic juvenile idiopathic arthritis, recent chronic steroid use) -*Varicella Pneumonia is the MC complication of chickenpox!* • *Varicella PNA typically presents from 1 day to 1 week AFTER the onset of rash*, with *progressive Cough, Dyspnea, & Tachypnea*; *Bilateral Crackles* auscultated • *CXR is nonspecific, showing bilateral interstitial opacities and/or nodular infiltrates* -*TX w/ IV Acyclovir for Varicella PNA*

What is *diversion and misuse* in terms of medication use?

-*Diversion* involves *transferring medication from the pt to another individual* -*Misuse* consists of *taking higher doses to achieve euphoric effects alone or in combination with illicit drugs* and is more commonly seen w/ *immediate-release preparations*

Diabetic Ketoacidosis (DKA) Management

-*DKA is characterized by ELEVATED Anion Gap Metabolic Acidosis, the presence of KETONES, and [usu] HYPERGLYCEMIA* -*Initial DKA Management* incl *Aggressive IV admin of Isotonic Fluids (Normal Saline), a CONTINUOUS IV Insulin Infusion, & POTASSIUM Supplementation if <5.3 mEq/L* -If after initial management, *subsequent labs* show *Low serum bicarb & Elevated Anion Gap (N: 10-14)*, this *indicates Ongoing Ketoacidosis*; therefore, *CONTINUED Insulin Infusion is required to correct met acidosis* -HOWEVER, *with Improved Glucose levels, Continued Insulin Infusion* is *assoc w/ Risk of HYPOglycemia* -*IF Serum Glucose falls <200 mg/dL and DKA Persist, the Rate of insulin infusion should be DECR and DEXTROSE ADDED to the IVF to Prevent Hypoglycemia -- goal is Maintain Glucose >200 d/t risk for Hypoglycemia!* -DKA pts have *TOTAL body Potassium DEPLETION (d/t urinary losses from hyperglycemia-related osmotic diuresis) and Insulin Pushes Potassium INTO Cells*; as a *result, HYPOKALEMIA may dev Rapidly w/ Insulin therapy* -Therefore, *potassium should be monitored closely* and *added to IVF if Serum K falls <5.3* -IF *serum K <3.3, Insulin should be Temporarily HELD Until After Potassium is given* -*Maintenance of IVF and Insulin infusion should be continued Until Resolution of Ketoacidosis and Normalization of the Anion Gap in DKA pts* -Use *isotonic NS if serum Na <135; and Half NS of Na ≥135* -*After Resolution of ketoacidosis* (i.e. *Normalization of anion gap*) & *Restoration of the ability to Eat*, pts w/ DKA can be *Transitioned to SQ Insulin* -- A *Long-Acting, BASAL Insulin (e.g. Glargine, Detemir) should be given ASAP && a BOLUS Insulin (e.g. Regular, Aspart, Lispro) Given with the first meal* -*Correctional (i.e. sliding-scale) insulin* should also be *given w/ meals IF the Bolus Insulin is insufficient to control hyperglycemia* -*Bc there's a slight Delay in the absorption of SQ Insulin, the Insulin INFUSION should be Continued for 1-2hrs AFTER giving SQ Insulin* -This *bridging* process *ensures sufficient time for SQ insulin to take effect* and *prevent rebound ketoacidosis*

TX of ACUTE Gout Attack

-*DX confirmed by joint aspiration* showing *negatively birefringent, needle-shaped crystals* *without any bacteria on Gram stain* -*NSAIDs (e.g. Indomethacin)* are the *first-line TX for acute gout*, BUT pts with Chronic Renal Failure or Hx of GI bleed are contraindications to NSAID use!! -*Colchicine* should ALSO be avoided in Renal Failure!! -In these pts, *Intra-Articular Corticosteroids* are the best option *when only ONE joint is implicated* Note: *Oral Prednisone (systemic effect) would be the best tx if MULTIPLE joints* were involved. Note: *Allopurinol decr uric acid production & is used to prevent gout flares, but is NOT used for acute flares*

How can you *reduce the risk for Recurrent C. diff-assoc diarrhea* after initial TX?

-*DX of C. diff-assoc diarrhea requires the Presence of Characteristic SX (Watery diarrhea, i.e. ≥3 loose stools in 24hrs; lower abdo pain, low-grade fever, & leukocytosis) AND Positive Stool Testing for toxigenic C. diff (positive PCR for toxin-producing gene ([not the toxin itself])* -*TX w/ 10 days of Oral Fidaxomicin or Vancomycin* but *Recurrence occurs within 30d of stopping ABX in ~25% of pts* -*Recurrence is marked by the Reemergence of Characteristic Sx with Positive C. diff stool testing* -Can *reduce the risk for recurrence by MINIMIZING USE OF ABX & REDUCING GASTRIC ACID SUPPRESSION* -- i.e. AVOID PPIs and H2-blockers, which alter colonic microbiome and incr risk for C. diff proliferation (even if C. diff spores are acid-resistant) Note: Probiotic-rich yogurt or other Probiotics have NOT been proven for primary or secondary prevention of C. diff infection (insufficient evidence)

What is Dantrolene and what is it used for?

-*Dantrolene is a skeletal muscle relaxant* -Used in *Malignant Hyperthermia* (d/t toxicity of inhaled anesthetics and succinylcholine) and *Neuroleptic Malignant Syndrome* (d/t toxicity of antipsychotics) *NMS*: rare, life-threatening condition characterized by *mental status change, high fever, autonomic instability, & diffuse muscle rigidity* *MH*: rare, life-threatening condition where *inhaled anesthetics (e.g. halothane, desflurane) or succinylcholine induce severe muscle contractions & hyperthermia*

How to manage preterm labor?

-*Depends on gestational age!* -*Earlier gestational ages have increased perinatal M&M risk* and require more extensive intervention to achieve good neonatal outcomes -In contrast, pts in *late preterm labor @≥34wks gestation* typically have *lower risk for perinatal morbidity* (e.g. *transient tachypnea of the new born, respiratory distress syndrome*) -*At ≥34wks gestation, tocolysis (Nifedipine*, usu given 32-34wks) *and Magnesium Sulfate* (i.e. Cerebral palsy risk reduction) *are NOT indicated bc of their risks to maternal health* (e.g. Nifedipine -> hypotension; Magnesium Sulfate -> respiratory depression) (outweigh the neonatal benefits* -Therefore, pts *in preterm labor @≥34wks gestation with no contraindications to vaginal delivery (e.g. placenta previa), receive Expectant Management* -- *give Intrapartum GBS ppx w/ Penicillin if positive/unknown GBS rectovaginal culture results*

Management of *Gallstone Pancreatitis*

-*Depends on its severity* -*MILD* disease (lack organ failure & local/systemic complications)--> Pts should undergo *Cholecystectomy within 7d of clinical improvement, usu during same hospitalization* (if don't have gallbladders removed, have a *25-30% risk of recurrent acute pancreatitis, cholecystitis, or cholangitis during the next 6-18wks*) -More *SEVERE* disease (*persistent failure of ≥1 organ systems* [e.g. hypotension refractory to IVF], *heart failure, acute necrotic collection*) --> *DELAY cholecystectomy until resolution of inflam & complications* and undergo *Eval of biliary system* to ensure No Remaining Gallstones (done by *Intraoperative cholangiogram or Preop ERCP*) Note: Although a low-fat diet is recommended for pts w/ acute pancreatitis, *Cholecystectomy is the MOST IMP intervention to Decr risk of Recurrent attacks* *Ursodeoxycholic acid TX* can be considered a *second-line* tx for pts w/ *symptomatic cholelithiasis (e.g. biliary colic) who do not desire surgery, but it does NOT play a role in tx pts w/ gallstone pancreatitis*

Methods for Tattoo Removal

-*Dermabrasion*: Involves removal of the superficial layer of the epidermis, allowing the pigment (pigment-containing macrophages) to leach out of the skin -*Cryosurgery* -*Thermal Cautery* -*Surgical Resection* -*Laser Removal* (most recent!): Involves the use of lasers of different wavelengths. The laser breaks up the pigments into smaller molecules, which are taken up and cleared by macrophages in the skin. Though it's a SAFE procedure, laser removal can leave *scar marks and skin discoloration (hypo- or hyperpigmentation)* -All these techniques can remove tattoos from ANY part of the body, and it doesn't matter how long you've had the tattoo

Drug-Induced Lupus

-*Drug-induced lupus causes Multisystem Involvement*; clinical findings can incl *fever, malaise, myalgia, arthralgia/arthritis, serositis (pleuritis, pericarditis), and/or hepatosplenomegaly/splenomegaly* -*DX* made by *history of one or more offending drugs* and a *Positive Test for ANTINUCLEAR (ANAs) or Anti-Histone Antibodies* -Some common drugs assoc w/ risk of Lupus incl: *PROCAINAMIDE, HYDRALAZINE, MINOCYCLINE, & ANTI-TNF-α Therapy (Etanercept, Infliximab)* -*TX* is generally *symptomatic,* and *discontinuation of the offending drug usu leads to resolution of the sx within weeks to months*

What is Dumping Syndrome?

-*Dumping Syndrome* is a *complication of gastrectomy, where liquid and food passage through the stomach into the jejunum is /faster/ leading to *cramping abdominal pain, diarrhea, postprandial N/V*, as well as some *neurovegetative symptoms* such as *generalized sweating (diaphoresis), dizziness, and dyspnea* -Changing pt's diet usu helps -A *HIGH PROTEIN DIET* where you eat *smaller, more frequent meals* is advised, and it should be low-carbohydrate Note: Low-fiber diet may improve diarrhea, but won't help with the rest of the features. Note: *Alprazolam* can help with the neurovegetative sx, but won't help with the digestive issues

What diagnostic modality is used to *Diagnose Sclerosing Cholangitis*

-*ERCP!!* (gold standard) -*ERCP shows alternating strictures & dilations with "beading" of intra- & extrahepatic bile ducts* -ERCP is better than MRCP at detecting damaged small bile ducts -*Primary Sclerosing Cholangitis* is classically seen in *middle-aged males with ulcerative colitis* -*PSC --> Concentric "ONION SKINNING" BILE DUCT FIBROSIS* -Assoc w/ *MPO-ANCA/p-ANCA antibodies and Incr IgM* -*PSC can lead to 2º Biliary Cirrhosis* d/t *extrahepatic biliary obstruction causing increased pressure in intrahepatic ducts leading to injury/fibrosis & bile stasis*

Management of Ectopic Pregnancy

-*Ectopic pregnancy* p/w *amenorrhea, irregular vaginal spotting, Acute Pelvic Pain, & a Positive Pregnancy Test* -*RF for Ectopic*: Tobacco use, pelvic inflam disorder, previous ectopic, & prior pelvic surgery* (e.g. appendectomy) -Pts w/ *first trimester bleeding should be evaluated for ectopic pregnancy bc is a significant cause of pregnancy-related death!* -Initial eval begins with *CBC, blood type & screen, & pregnancy test (quantitative β-hCG)* -If *Hemodynamically UNSTABLE* --> *Hypotensive/Tachycardic* w/ *signs of Hemoperitoneum (abdo rigidity, rebound, guarding) & Adnexal Tenderness*. --> *RUPTURED ECTOPIC PREGNANCY DIAGNOSED* --> *IMMEDIATE EMERGENCY SURGICAL EX-LAP* -If *Hemodynamically STABLE* --> *Pelvic Ultrasound* performed, with *surgery for those WITH Hemoperitoneum* -Note: CT scan NOT indicated in hemodynamically unstable pregnant pts who require immediate surgical intervention

Eosinophilic Esophagitis (EoE)

-*EoE p/w DYSPHAGIA* and *sometimes epigastric pain, heartburn, & regurgitation* -EoE is *characterized by a Chronic Th2-mediated inflammatory response triggered* primarily by *Food Allergen Exposure* -An *ATOPIC HISTORY (e.g. Asthma, Eczema, Allergic Rhinitis, Food Allergies) is Commonly Present in EoE pts* -Cardinal Sx of EoE is DYSPHAGIA -*Characteristic Endoscopic Findings* incl *Esophageal Rings, Strictures, & Linear Furrows* -*DX Confirmed by Esophageal Biopsy showing ≥15 eos/HPF* -*Management* includes an *Elimination Diet* (dietary modification, eliminating foods positive on allergy testing or empirically eliminating 6 MC food allergens - milk, soy, wheat, eggs, peanuts/tree nuts, fish/shellfish) *to avoid exacerbating allergens*. -*Topical Glucocorticoids (sprayed & swallowed Fluticasone, to reduce local inflam) and PPIs (esp for pts w/ concomitant GERD) should also be considered*

Infantile Spasms

-*Epileptic disorder of infancy* characterized by *symmetric spasms, developmental delay, & hypsarrhythmia on EEG* -*Corticotropin (ACTH) and Vigabatrin are the Gold Standard TX for Infantile Spasms* Note: *Vigabatrin* can cause *PERMANENT VISUAL LOSS AE!* *Hypsarrhythmia* is very *chaotic and disorganized* brain electrical activity with *no recognizable pattern*, whereas a normal brain electrical activity shows clear separation between each signal and visible pattern. It is an *abnormal interictal pattern, consisting of high amplitude and irregular waves and spikes* in a *background of chaotic and disorganized activity* seen on EEG

Exercising During Pregnancy

-*Exercise during pregnancy* is assoc w/ a *DECR risk for gestational DM, preeclampsia, & C-section* -*Low-risk* pts who exercised regularly prior to pregnancy are *encouraged to maintain moderate-intensity regimens* during pregnancy -However, exercise during pregnancy can *Exacerbate Some Obstetric Conditions*, so it is *CONTRAINDICATED in certain At-Risk pt populations* *Exercise should be AVOIDED by:* -Pts *at risk for preterm delivery* • *Cervical insufficiency, requiring placement of a cerclage to prevent preterm delivery* • Preterm labor during current pregnancy • Preterm premature rupture of membranes -Pts *at risk for antepartum bleeding* • *Placenta previa* • Persistent second- or third-trimester bleeding -Pts w/ an *underlying condition that can be exacerbated by exercise* • Severe anemia • *Hypertensive disorders of pregnancy* (e.g. *preeclampsia*) • *Restrictive lung dz* • *Severe heart dz* -Pts with *active first-trimester bleeding*

Fetal Growth Restriction (FGR) Definition, Types, & Etiologies

-*FGR* is characterized by an *estimated Fetal Weight <10th percentile or Birth Weight <3rd percentile* for gestational age -Neonates who are *small for gestational age* (SGA) (i.e. *birth weight <10th percentile*) are *ALSO considered Growth Restricted if maternal RF for poor fetal growth are present (e.g. Maternal HTN, Preeclampsia)* -*SYMMETRIC FGR*: *Global* growth lag, i.e. ALL growth parameters are small. *LOW fetal weight && head circumference for gestational age* -*ASYMMETRIC FGR*: *Weight is LOW, but Head Circumference WNL* ("head-sparing") -*Symmetric FGR* is typically d/t an *insult Early in pregnancy* (e.g. *genetic condition, congenital infxn*) -*Asymmetric FGR* is MCC by *Decr blood flow & oxygen delivery to fetus* (i.e. *uteroplacental insufficiency*) in the *Second/Third trimester*; *"head-sparing"* bc nutrients preferentially redistributed to essential organs (brain, heart); uteroplacental insufficiency can be caused by *maternal chronic HTN* -Management of Newborns w/ FGR incl *prevention & TX of assoc complications* such as *hypoglycemia, polycythemia, hypothermia, & poor feeding* -*Catch-Up Growth* is usu *achieved by age 2*, *BUT long-term growth & neurodevelopmental abnormalities can occur*

What are the *major RF for Sudden Cardiac Death in pts w/ Hypertrophic Cardiomyopathy*?

-*FHX of SCD in a Close relative <50yo* -*Personal Hx of Sustained Ventricular Arrhythmia* -*Personal Hx of Syncope likely d/t Ventricular Arrhythmia* -*Massive LVH, >30mm wall thickness* -*LVEF <50%* -Pts with *any of these RF^ (≥1)* would *benefit from Primary Prevention of SCD via Placement of an Implantable Cardioverter-Defibrillator (ICD)*

Factor V Leiden Complications

-*Factor V Leiden mutation* produces a mutant Factor V that is *resistant to inhibition by activated protein C* -HEREDITARY THROMBOPHILIA -Complications include *DVT, Cerebral Vein Thrombosis, & Recurrent Pregnancy Loss!!* d/t *hypercoagulable state* Note: *Factor V Leiden HETEROZYGOSITY* is assoc w/ *INCR risk for VENOUS thrombosis* (e.g. deep, cerebral, or mesenteric venous thrombosis); However, it RARELY leads to arterial thrombosis or emboli!

Achalasia

-*Failure of LES to relax d/t degeneration of inhibitory neurons (containing NO & VIP) in the Myenteric (Auerbach) plexus of esophageal wall* -*Primary* Achalasia is *idiopathic*; *Secondary* Achalasia may arise from *Chagas disease (T. cruzi infxn)* or *Extraesophageal Malignancies (mass effect or paraneoplastic)* -P/w *progressive dysphagia to Solids && Liquids* (vs. Obstruction, which is primarily solids) -Assoc w/ *Incr risk for Esophageal Cancer* -In Achalasia, there is *Increased Lower Esophageal Sphincter (LES) tone* d/t *loss of Nitric Oxide secretion* (which would normally allow smooth m relaxation at the LES) -Manometry findings incl *uncoordinated or absent peristalsis w/ INCR LES resting pressure* -*Barium* swallow shows *dilated esophagus w/ area of distal stenosis ("birds beak")* -TX: *Surgery, endoscopic procedures (e.g. botulinum toxin injection)*

Falls in Older Adults

-*Falls* are a major *contributor to morbidity in the elderly* but are often undiagnosed -*RF* for falls: *Hx of prior fall, frailty (e.g. weight loss, decr appetite, low BMI), & decreased muscle strength (e.g. needing extended time & arm support to rise from a chair)* -The *Home Environment* can substantially influence fall risk in elderly -- Therefore, *all pts who have FALLEN should undergo a Home Safety Assessment performed by an occupational therapist* with expertise in optimizing safety & function for everyday living -Assessment is conducted in the home, can identify hazards (e.g. loose rugs, poor lighting) and corrective solutions (e.g. anti-slip surfaces, grip bars in bathroom) -Additionally, *all pts who have FALLEN should ALSO undergo Screening & Correction of Sensory Disturbances (e.g. visual acuity, postural strength, & balance) and regular medication review w/ efforts to discontinue any unnecessary meds*

What are children with *febrile seizures* at increased risk for? What is the *prognosis of febrile seizures?*

-*Febrile seizures are DX Clinically*, often as a *complication of Viral (e.g. HHV-6, Influenza) Infection* and occur in kids aged *6mo to 6yo*, often with a Positive FHX of febrile seizure -They typically have a *BENIGN course, DO NOT require therapy, and have NO LONG-TERM Impact on Development* -- i.e. pts have *Normal Development* -However, children who experience a febrile seizure have a *~30% chance of ≥1 RECURRENCE of Febrile Seizure* and are at *INCR Risk for subsequent DEVELOPMENT of EPILEPSY (afebrile seizures)*

Kawasaki Disease

-*Febrile vasculitis* of childhood of ?etiology (*asian kids <4yo*) -DX based on *fever ≥5d* with *≥4 of the following*: • *Conjunctivitis (bilateral, nonexudative) * Mucous membrane changes (e.g. erythematous lips/tongue/oral mucosa; strawberry tongue; injected/fissured lips or pharynx) • Rash (polymorphous, erythematous, blanching, maculopapular -> desquamating, /peeling/, perineal erythema, generalized rash) • Lymphadenopathy (cervical) • Extremity edema/erythema* (hand/feet edema or erythema) -Bc /sx don't always present simultaneously/, pts who have been *febrile ≥5d but who fill ≤3 diagnostic criteria* should have /supporting lab studies/ (*C-reactive protein or ESR* would be elevated) ordered, given *ibuprofen*, and should be *reexamined the /next day/* -Labs: Incr PLTs & WBCs; Decr Hb; Incr Acute-phase reactants (*Incr CRP & ESR*); Incr AST & ALT; Sterile Pyuria -Failure to TX promptly incr risk for *serous sequelae* (e.g. *coronary artery aneurysms, thrombosis, or rupture; ventricular dysfxn*) w/ substantial risk after the 10th day of illness -TX with *IVIG & ASPIRIN* to reduce systemic inflam (IVIG improves M&M and reduces risk of cardiac sequelae); No need for long-term tx or immunosuppression after receiving tx in acute phase -Note: *All kids w/ KD* should have a *baseline echocardiogram* performed (may show some coronary artery dilatation or myocardial dysfxn) -Aneurysms may later dev, even in pts who receive appropriate TX, so *f/u studies indicated @2wk & @6wks /after/ treatment*, /even if the initial echo was normal/ -Note #2: *If pt had coronary A dilatation/aneurysms or myocardial dysfxn on /baseline/ echo, /THEN/ they would be at INCR Risk for future cardiac events*, and participation in contact sports/strenuous activities would need to be restricted -Likelihood of relapse/recurrence of KD is low (<2.5% recurrence in the first 3yrs after tx)

Empiric ABX TX of UTI in Pregnant Women

-*First-line ABX for Acute Cystitis during Pregnancy is FOSFOMYCIN, with cefpodoxime & amox-clav as alternatives* -*Empiric ABX therapy* is initiated in pregnant pts who have *dysuria, urinary freq, & positive UA results consistent with Acute Cystitis (e.g. nitrites, leukocyte esterase, blood [RBCs])* -- most common pathogen of acute cystitis is *E. coli* -*Urine Culture* is performed for *ALL pregnant pts w. acute cystitis* and is *REPEATED 1wk after completion of ABX to ensure infection resolution (test of cure)* -Urine Culture is REPEATED bc *bacteriuria during pregnancy* is *assoc w/ INCR risk for Complications, like Acute Pyelonephritis & ARDS* -*E. coli* is the *MCC of acute cystitis in BOTH Pregnant & NONpregnant women*, but *some ABX used in nonpregnant are Avoided during certain points or altogether during pregnancy d/t assoc w/ Fetal Anomalies* -*First-line ABX outside of pregnancy* incl *Nitrofurantoin, TMP-SMX, & Fosfomycin* -- However, *choice of ABX is dependent on gestational age* bc both *TMP-SMX & Nitrofurantoin are AVOIDED in First Trimester & Near Term* -Alternative options during pregnancy or in pts w/ contraindications (i.e. medication allergies) incl *β-lactams (e.g. amoxicillin-clavulanate, cefpodoxime)*, but these drugs are considered *second-line* d/t *incr bacterial resistance* Note: 3rd gen cephalosporin, *Ceftriaxone*, is NOT given in pts w/ UNCOMPLICATED cystitis. Note: Cipro (fluoroquinolone) is effective in TX acute cystitis in NON-pregnant women, but is avoided during pregnancy bc can cross placenta and is toxic to developing cartilage. Gentamicin (aminoglycoside) is avoided during pregnancy bc it crosses placenta & is assoc w/ irreversible congenital deafness. Use of TMP-SMX in first-trimester is assoc w/ birth defects (e.g. neural tube defects, cardiac defects, cleft palate), and neonatal kernicterus in the third-trimester

Screening tests for diagnosing Diabetes Mellitus

-*HbA1c ≥6.5%=DM* -*Fasting (>8hr) blood glucose ≥126 mg/dL=DM* -*Oral Glucose Tolerance Test (75-g glucose load w/ testing for 2hr) ≥200 mg/dL=DM* -*Random glucose ≥200 mg/dL in symptomatic pt=DM* -*ASX pts w/ Abnormal Screening test for DM require a REPEAT. measurement with the SAME SCREENING TEST to Confirm DX of DM* -If *TWO DIFFERENT Screening Tests are available and Results are Concordant* (e.g. *fasting glucose ≥126, HbA1c ≥6.5%*), *then NO REPEAT testing is necessary* -BUT *if TWO Different Screening Tests are Discordant* --> *Additional Diagnostic Testing Required to Confirm DM DX* EXCEPTION: -If pts w/ *SYMPTOMATIC HYPERGLYCEMIA* (e.g. *polyuria, polydipsia, weight loss, nocturia*) *AND RANDOM GLUCOSE ≥200*. --> *DX DIABETES W/O CONFIRMATORY TESTING* Note: *Glucosuria* itself is *NOT a screening test for DM*

Congenital Adrenal Hyperplasia (CAH)

-*Group of disorders* characterized by a *deficiency in an enzyme involved in steroid synthesis* -Most cases are d/t *autosomal recessive* inheritance of *21-hydroxylase deficiency* -In addition to low production of mineralocorticoids & glucocorticoids, the deficiency of 21-hydroxylase results in an excess of its substrates -These excess substrates are shunted toward Androgen Synthesis, resulting in *ambiguous genitalia* in girls, and *precocious puberty* in boys -Adrenocorticotropic Hormone (ACTH) levels are also elevated and lead to hyperplasia of the adrenal glands, further contributing to the increased production of androgens -*Salt-wasting syndrome* occurs in severe deficiencies of 21-hydroxylase and presents in the first few weeks of life w/ life-threatening emesis, dehydration, and shock -Lab findings incl *hyponatremia & hyperkalemia* (from lack of aldosterone) and *hypoglycemia* (from lack of cortisol) -*Marked elevation of 17-hydroxyprogesterone*, a substrate of 21-hydroxylase, *confirms the DX* w/ 21-hydroxylase deficiency -*High testosterone* levels are responsible for *virilization* of external female genitalia -Aldosterone & cortisol levels are abnormally low TX: -The *gold standard of TX for classic CAH* includes *Chronic Glucocorticoid & Mineralocorticoid* TX to *maintain normal blood pressure, electrolytes, growth, & weight gain, and to suppress adrenal androgens* -*Hydrocortisone* is the *MC glucocorticoid* used in infants and children -*Fludrocortisone* is given for *mineralocorticoid replacement* -*Infants may require salt supplementation* until they begin eating solid foods Note: *Virilized 46,XX girls w/ CAH can undergo clitoroplasty & vaginoplasty* when pt is stable and parents are emotionally prepared.

Hypertrophic Cardiomyopathy (HCM) - Findings

-*HCM is the MCC of SCD in Young Athletes in USA* -Assoc w/ *Systolic Murmur* -60-70% of cases are *familial, autosomal dominant* (MC d/t *mutations in genes encoding sarcomeric proteins*, such as *myosin binding protein C and β-myosin heavy chain*) -Causes *syncope during exercise* and may lead to *SCD (e.g. in young athletes) d/t Ventricular Arrhythmia (1% per year risk of SCD for all HCM pts)* -Findings: *S4, SYSTOLIC murmur*; May see *mitral regurgitation* due to impaired mitral valve closure. -*TX*: *Cessation of high-intensity athletics, use of β-blocker or nondihydropyridine Ca2+ channel blockers (Verapamil). -*Implantable Cardioverter Defibrillator (ICD) if High risk* (i.e. *have risk factors for SCD* such as *positive FHX of SCD in close relative <50yo; personal hx of sustained ventricular arrhythmia; massive LV hypertrophy w/ wall thickness >30mm; LVEF <50%*) -*Avoid drugs that decrease preload (diuretics, vasodilators)* -*Systolic murmur INCR* when: *Standing* or *Valsalva strain* (decr LV volume, worsening outflow obstruction) -*Systolic murmur DECR* when: *Squatting, Supine Leg Raise*, or *Handgrip* (incr LV volume, lessening outflow obstruction) -Note: Other than syncope (occurring d/t ventricular arrhythmia), the presence of common symptomatic manifestations of HCM (e.g. angina, dyspnea, fatigue, occasional palpitations) is NOT assoc w/ incr risk of SCD.

*Hypertrophic Cardiomyopathy (HCM)*

-*HCM is the MCC of Sudden Cardiac Death in Young athletes in the USA* -60-70% of cases are *familial, autosomal dominant* (most commonly due to *mutations in genes encoding sarcomeric proteins, such as myosin binding protein C and β-myosin heavy chain*). *Causes syncope during exercise* and may lead to *SCD (e.g. in young athletes) d/t ventricular arrhythmia* -Findings: *S4, systolic murmur*; May see *mitral regurgitation* due to impaired mitral valve closure -*TX*: *cessation of high-intensity athletics, use of β-blocker or nondihydropyridine Ca2+ channel blockers (verapamil); ICD if high risk* -Avoid drugs that decrease preload (eg, diuretics, vasodilators). -*Systolic murmur INCR* if: *Standing* or *Valsalva straining* (reduces LV volume, worsening obstruction) -*Systolic murmur DECR* if: *Squatting, Supine Leg Raise*, or *Handgrip* (increases LV volume, lessens obstruction)

When would you use CORTICOSTEROIDS in an HIV pt with PCP pneumonia?

-*HIV pts who have moderate or severe Pneumocystis pneumonia* often have *RESPIRATORY DECOMPENSATION during the first 2-3d of TX d/t organism LYSIS*, which *stimulates an inflammatory response* -To *reduce risk of intubation & death, CORTICOSTEROIDS are used* in those with *Arterial Blood Gas evidence of ALVEOLAR-ARTERIAL OXYGEN GRADIENT ≥35 mmHg &/or Arterial Oxygen Tension (PaO2) <70 mmHg on Room Air* -ABG is the standard of care and helps determine whether IV ABX and hospitalization in the ICU are needed Note: *Even despite giving concomitant corticosteroids w/ TMP-SMX for TX of PCP, pts may still have respiratory decompensation following treatment -- may need to intubated d/t significant tachypnea and poor oxygenation

HIV-associated Lipodystrophy

-*HIV* pts *on antiretroviral therapy* are *at risk for HIV-assoc lipodystrophy* by developing *alterations in fat deposition w/ NO change in Lean tissue mass* -*Manifestations* incl one or both of the following: ● *LIPOATROPHY* - *loss of subQ fat from face, arms, legs, abdomen, &/or butt*, which can give pts a *skeleton-like appearance*; esp assoc w/ *NRTIs like Stavudine & Zidovudine* ● *FAT ACCUMULATION* - *Dorsocervical fat accum --> "Buffalo Hump" & Visceral Abdominal Fat accum --> Incr abdominal girth (despite minimal subQ abdo fat)*; fat accum can occur w/ any regimen -Pts *w/ HIV-assoc lipodystrophy* have *abnormal lipid & glucose metabolism*, which often leads to *Insulin Resistance, Dyslipidemia, & an INCR Risk for Cardiovascular Disease* ● *INCR Total Cholesterol, LDL, & Triglycerides* ● *DECR HDL* -*Statin Therapy* is generally required for those w/ an *estimated 10-yr cardiovascular risk of >7.5-10%* ● Most commonly used Statins in HIV pts are *rosuvastatin, atorvastatin, & pravastatin* Note: *Gemfibrozil* can be used to *TX Hypertriglyceridemia*, an *independent RF for cardiovascular dz*. HOWEVER, *reduction of TGs has NOT been shown to definitively reduce cardiovascular risk*. As such, *fibrates are RARELY used to control cardiovascular risk* and are *used instead to reduce risk of pancreatitis for pts w/ TG?886 mg/dL*

Hazard Ratios (HR)

-*HR is a measure of risk that describes the chance of events occurring in one study arm compared to another (e.g. Treatment vs. Control group)* -HRs differ from relative risks in that they can be calculated at multiple time intervals throughout a study period -HRs are *freq used in drug trials to analyze survival or time-to-event data* *HR > 1 indicates INCR RISK* *HR < 1 indicates DECR Risk* *HR = 1 indicates NO CHANGE in Risk*

Androgenetic Alopecia

-*Hair loss in Men with Androgenetic Alopecia starts in the Frontal or Temporal areas* and *progresses gradually (Male Pattern Baldness!!)*

Nonpathologic Cardiovascular Changes seen in Intense Athletes

-*Heightened vagal tone* --> *BRADYCARDIA with or without First-Degree AV Block* -*Left ventricular hypertrophy* as detected on ECG -In the absence of other findings that might suggest underlying cardiac dz (e.g. unexplained symptoms, cardiac murmurs that may raise suspicion for HOCM, etc.), these pts should be reassured w/o further cardiac testing

Measles (Rubeola)

-*Highly contagious, potentially FATAL, vaccine-preventable disease* -Measles should be considered in pts w/ *fever & a rash*, ESP in those w/ *hx of recent foreign travel or incomplete immunizations* -*Prodromal Sx incl FEVER & fatigue, Cough, Coryza (inflam of nasal mucous membranes), & Conjunctivitis* -*After 2-4d*, pts are *ill-appearing* w/ a *classic Maculopapular Rash that starts on Face and spreads cephalocaudally (head to toe)* -Rash is *initially erythematous & blanching, but later can coalesce & appear non-blanching, hemorrhagic, or dark brown* -Some pts dev *white, pinpoint lesions known as Koplik spots on the buccal mucosa* - these *lesions appear AFTER the onset of prodromal sx & often Resolve when the rash appears (i.e. Transient Kopliks)* -*TX is SUPPORTIVE (IVF, antipyretics)*, However, *Vitamin A is indicated in Severe cases to reduce complications & mortality*

Idiopathic Intracranial Hypertension

-*IIH p/w headaches, nausea, vision changes, and papilledema (i.e. blurred optic discs on on fundoscopy) with normal neuroimaging (excl space-occupying masses) and elevated opening pressure on lumbar puncture* - often in *obese women* -Pathophysiology involves *increased intracranial Venous pressure d/t impaired CSF resorption by the arachnoid granulations and CSF lymphatic drainage sites* -*TX Goals for IIH* include *Prevention of vision loss, reduction of ICP, symptomatic relief of HA* -*ACETAZOLAMIDE is first-line TX* for symptomatic IIH, and works by *inhibiting choroid plexus carbonic anhydrase, thereby DECR CSF PRODUCTION by the Choroid Plexus* -*Weight loss & sodium-restricted diet* can help reverse sx by lowering ICP -If *vision changes progress* despite medical management, *surgical intervention* (e.g. *CSF shunt, optic nerve sheath fenestration*) may be required -Sometimes, *serial lumbar punctures or lumbar drain* may be attempted as a *temporary measure prior to surgery* Note: Transependymal flow of CSF into the periventricular white matter causes interstitial cerebral edema and would worsen IIH

Seizures in Pregnancy

-*INCR the risk for obstetric and fetal complications* (e.g. *preeclampsia, preterm labor, abruptio placentae, fetal hypoxia*) -*Antiepileptic drugs (AED) use* is ALSO assoc w/ an *INCR risk for Congenital Abnormalities*, incl *neural tube defects, congenital heart abnormalities, & cleft palate* -DESPITE these risks, the *majority of women w/ epilepsy have a normal pregnancy* -*VALPROATE* carries the *HIGHEST Teratogenicity Risk of all AEDs*; therefore, *changing to an alternate regimen* (e.g. Levetiracetam) *should be tried 6MO PRIOR to attempts to conceive* -It is preferable to *switch to the lowest possible dose of a SINGLE medication to limit teratogenicity* -*In contrast, unless absolutely necessary (e.g. uncontrollable seizure activity), NO CHANGES to AED regimen should be made AFTER CONCEPTION* ● *Abrupt changes in AEDs may TRIGGER seizures* - bc of changes during pregnancy, pts whose prior AED therapy failed are at even higher risk for seizures during pregnancy ● *In early gestation, gradually changing an AED regimen by overlapping medications exposes the fetus to possible additional teratogens* ● *Once pregnancy is confirmed, there is likely little benefit to changes in medication bc the majority of organogenesis has already occurred (wks 3-8)* -THEREFORE, *management of pregnant women on AEDs* incl providing *counseling, initiating HIGH-DOSE Folic Acid supplementation, & Screening for Congenital Abnormalities (e.g. neural tube defects) w/ serum Alpha Fetoprotein & Anatomy U/S* -If major abnormalities are present, pregnancy termination may be considered Note: *AEDs are continued* in pts whose *epilepsy is unstable w/o meds*. *Seizures during pregnancy can cause fetal hypoxia or other complications of maternal trauma (e.g. spontaneous abortion, abruptio placentae)* Note: Pts w/ epilepsy are NOT at incr risk for fetal aneuploidy.

Mild vs Moderate/Severe Immune Thrombocytopenia (ITP): Managemetn

-*ITP is d/t AUTOIMMUNE PLATELET-SPECIFIC AUTOANTIBODIES* -ITP is a *DX of EXCLUSION* presenting in *children w/ a PLT count <100,000, with Sudden onset of Bleeding* -Pts freq report a *recent viral infection, but have NO evidence of systemic dz (fever, malar rash, joint stiffness) or additional lab abnormalities* -Severity of bleeding sx is graded as follows (based on likelihood of progression to uncontrolled bleeding): • *MILD*: *ASX or Cutaneous Bleeding* (petechiae, purpura) • *MODERATE/SEVERE*: *Mucosal Bleeding* (gingival bleeding, epistaxis), *Internal Hemorrhage* (hematochezia. intracranial hemorrhage) -Pts w/ *mild or no bleeding do NOT require pharmacotherapy* and can be *managed w/ Observation & Monitoring of PLT counts* -Pts w/ *INCR bleeding risk (e.g. mucosal bleeding, epistaxis, PLT <30,000) are TX w/ IVIG* -~50% of kids w/ ITP have *SPONTANEOUS REMISSION within a FEW YEARS of DX*

What is *Intention-to-treat (ITT) analysis*?

-*ITT Analysis compares intervention groups* in a randomized trial by *including all subjects as initially allocated after randomization, regardless of what happens during the study period* -The rationale is that if subjects are doing so poorly as to switch interventions or to drop out of the study, then their outcome should be attributed to that intervention -Therefore, ITT analysis is usu conducted to avoid the effects of crossover (e.g. noncompliance to assigned intervention) and attrition (e.g. loss to f/u, drop-out), which may disrupt the benefit of randomization and introduce bias in the estimation of the effect of the intervention -ITT analysis may lead to a *more conservative estimate of the intervention's effect, but a more valid estimation of the intervention effect* -ITT analysis is used to preserve the benefits of randomization in superiority trials

Prior to surgical intervention for a perforated peptic ulcer, what should be given?

-*IV Fluid resuscitation* -*Broad-spectrum IV ABX* (with esp good coverage of Gram Negative organisms) -*IV PPI* therapy

Pediatric Immunizations in Setting of Pregnant Household

-*Immunocompetent Children CAN receive ALL standard immunizations regardless of the pregnancy status of household contacts* -Although *pregnant women should not* themselves *receive live virus vaccines* d/t the theoretical risk of fetal infection, the risk of contracting an infection from a recipient of a live virus vaccine is very LOW -*Delaying vaccines until after pregnancy is not recommended* as vaccines make it less likely that a child will contract the disease and bring it home to the mother -Infection w/ wild-type varicella and rubella poses a far more significant threat to a pregnant woman

Key Indicators of *Prognosis in COPD* pts

-*Mortality in COPD is best predicted by integrative measures* such as *Global Functional Impairment (how dyspnea & fatigue impact pt's daily life), Multidimensional Risk Indices* - such as the *BODE Index* (*low BMI, very severe Obstruction [FEV1 ≤35%], disabling Dyspnea [limits daily activities], & low Exercise capacity*) which is the most widely used instrument -*Additionally, the presence of significant Nonpulmonary (mainly CARDIOVASCULAR Dz) Comorbidities* also *elevate risk of death in COPD pts independent of the BODE index and functional impairment*

Primary Nocturnal/Sleep Enuresis Management

-*Inability to achieve nighttime dryness in healthy pts age ≥5yo without additional urinary tract sx (e.g. dysuria, urinary incontinence)* -Management *begins w/ Behavior Modifications* (e.g. *limiting fluid intake 2hrs before bed, voiding before sleep*) & *Motivational Therapy* (e.g. *reward system*) -*Continued enuresis* despite these measures for *3-6mo* warrants *ENURESIS ALARM* Therapy, a First-Line TX that has the *best long-term outcome and a low risk of relapse* (with consistent use, the alarm conditions the child to wake prior to voiding); Pt adherence & motivation required as the child is responsible for responding to the alarm -*Desmopressin (ADH analog), an Antidiuretic*, is an *alternate first-line tx* for primary nocturnal enuresis with good short-term improvement BUT has *high rate of relapse after discontinuation* -*Desmopressin* is recommended for families seeking a *short-term solution* (e.g. sleep away camp) or who have *failed/refused enuresis alarm therapy* -*AE of Desmopressin are RARE but incl Hyponatremia if taken w/ excessive oral fluids*

Infertility Workup

-*Infertility* is a couple's inability to conceive *after ≥12mo* of appropriately timed intercourse w/o contraception -For women age *≥35*, evaluation occurs after *≥6mo* of infertility -*Male factor infertility* is a common cause of infertility; the MC etiologies are testicular or genetic defects (e.g. Klinefelter syndrome, varicocele) that results in changes in sperm quality and function -*Semen Analysis*, a noninvasive, low-cost test, is the *gold standard* in evaluation of the male partner and is the *first step in an infertility evaluation* -_Sperm volume, pH, concentration, motility, and morphology_ are assessed; if abnormal, infertility can be tx w/ *intrauterine insemination or in-vitro fertilization* Note: For most women, ovulation and fertility return within a month of discontinuing oral contraceptives.

Inflammatory Breast Cancer Surgical Management

-*Inflammatory Breast cancer is a HIGHLY AGGRESSIVE and ANGIOINVASIVE breast cancer* characterized by *invasion of the dermal lymphatic system that results in classic skin changes (erythema, skin thickening & dimpling [peau d'orange])* -D/t the aggressive nature and *rapid spread of IBC through the Lymphatic System, TX Necessitates Neoadjuvant Chemo, MASTECTOMY w/ Axillary LN Dissection, and Radiation Therapy* -*Even if no evidence of distant metastases*, *Breast-Conserving Therapy (lumpectomy + adjuvant radiation only) is ABSOLUTELY CONTRAINDICATED*

Informed Consent & Minors

-*Informed consent* is typically obtained prior to any significant procedure to ensure that the patient or guardian is a knowledgeable participant in the health care decision, and is aware of the nature, alternatives, risks, & benefits of the procedure -For pts who are *minors, informed consent must be provided by a legal guardian* (a *parent* in most cases) -An *exception to informed consent* includes *EMERGENCY CARE*, in which *delaying tx can lead to harm* -This exception is based on the assumption that a reasonable patient/parent would consent to the intervention if able to do so ("implied consent"), and that the physician's duty is to seek the best interest of the pt Note: For e.g., if a grandma brought grandkid to ED d/t intussusception -- the grandma is the caretaker, NOT the legal guardian. It's appropriate to explain the procedure to her, but she cannot provide informed consent bc she is not the legal guardian. Cannot wait for legal guardian (parent) to consent to Air Enema procedure.

TTP

-*Inhibition or deficiency of ADAMTS13 (vWF metalloprotease) leading to reduced degradation of vWF multimers* -Incr large vWF multimers leads to incr PLT adhesion leads to Incr PLT aggregation & thrombosis -Labs: *Schistocytes* on PBS (fragmented RBCs d/t mechanical destruction), *Incr LDH*, normal coagulation parameters, *Thrombocytopenia (<100,000)* -Low PLT count, microangiopathic hemolytic anemia (schistocytes), Incr LDH, acute renal failure, fever, neurologic sx -TX: *Plasmapheresis, Steroids* -Children: Observe if cutaneous sx only; Glucocorticoids, IVIG, or anti-D if bleeding -Adults: Observation if cutaneous sx AND PLTs ≥30,000 w/o bleeding; Glucocorticoids, IVIG, or anti-D (Anti-RhD if Rh+ non-splenectomized pts) if Bleeding or PLTs <30,000 (will respond in 1-2wks) -Rituximab for pts who've failed initial tx; Splenectomy for refractory cases

Hospice Care

-*Interdisciplinary palliative care that provides medical care & psychosocial support at the end of life to pts with life-limiting illnesses (Prognosis ≤6mo) who have chosen to cease life-prolonging/disease-modifying, curative therapies in favor of a higher quality of life* -Available *24/7* -Pts are *permitted to Leave Hospice to receive life-prolonging/curative treatments if they wish* and are *Free to Return to Hospice as long as they continue to have a ≤6mo prognosis* -Pts on hospice *can receive palliative medical therapies (chemo, radiation, tumor debulking) to improve comfort, BUT aggressive disease-modifying therapies with curative intent is not allowed* Note: It is the role of the *Oncologist, NOT the Hospice physician* to *discuss the risks & benefits of a new chemo regimen* to the pt.

Intussusception Diagnosis & Management

-*Intussusception is telescoping of a proximal portion of intestine into a distal portion*, *most commonly at ileocecal junction* -Pathogenesis most commonly involves *hyperplasia of Peyer Patches in the Ileocecal Region, following viral infection* (e.g. adenovirus) or *rotavirus vaccine* in *children age 6mo-3yo*, acting as a lead point; *Intussusception* d/t a *Pathologic Lead Point* (e.g. *MECKEL Diverticulum*) is less common but can *occur at Any Age* -Common lead points: • Children—Meckel diverticulum, small bowel wall hematoma (IgA vasculitis) • Adults—intraluminal mass/tumor. -Intussusception causes *small bowel obstruction & vascular compromise* that causes *intermittent abdo pain, vomiting, bloody mucoid stools* -*Classic Clinical Triad* incl *severe, episodic, colicky intermittent abdominal pain; palpable sausage-shaped mass in right abdomen; & bloody, "currant jelly" stools* -- need a high degree of suspicion bc only 15% p/w triad -Most pts only have *alternating pain-free periods with bouts of pain (15-20mins) accompanied by emesis, inconsolability, & drawing up of knees to chest to ease pain* -The *bloody, mucoid stools reflect sloughing of bowel lining & bowel ischemia* -In addition to *hemodynamic stabilization* (e.g. IVF), *management* of suspected intussusception is *based on the following S&S*: • *Classic* Presentation: *Nonoperative Reduction via AIR or Water-Soluble Enema* allows for *direct visualization of the intussuscepted bowel* and is therefore both *diagnostic & therapeutic* • *Atypical* Presentation (e.g. lethargy alone): *Abdo U/S* is the diagnostic imaging modality of choice, and characteristically reveals a *target sign*. An *enema* can be performed after DX confirmed (U/S preferred d/t high sensitivity & lack of assoc radiation compared to CT Abdo) -*Delaying therapeutic care could further compromise bowel perfusion, & incr risk for bowel perf & mortality* (can perform air enema procedure without informed consent if need to) -In >90% of pts, *pain resolves after air enema reduction* -But in a pt who recently underwent air enema and now has *tachycardia, severe abdo pain, & abdo distension* --> concerning for *intestinal perforation or repeat intussusception* --> *First step is Evaluation via Abdo X-Ray* to look for free air in abdomen; If no free air, then do *abdo U/S for repeat intussusception, which can be Tx w/ repeat air enema* (*intestinal perf is a potential complication of enema reduction*, bc telescoped bowel caused venous & lymphatic congestion -> *bowel edema & ischemia*, compromising bowel wall integrity) Note: *Barium Contrast Enema* is generally *AVOIDED* with suspected intussusception d/t *risk of peritonitis if perforation* occurs Note: A *technetium 99m scan/Tc-pertechnetate scan* can *identify ectopic gastric mucosa (incr uptake) within a Meckel Diverticulum*, which is often suspected as a pathologic lead point in *recurrent intussusception cases*

Juvenile Myoclonic Epilepsy (JME)

-*JME* is a *common pediatric epilepsy syndrome* that usu *presents in otherwise healthy adolescents* -In One-third of pts, *JME BEGINS with ABSENCE SEIZURES (e.g. staring spells) up to 5yrs before other seizure types* -During *adolescence*, the *classic presentation involves Myoclonic Jerks of the Arms within the first hour of waking* (i.e. *MORNING MYOCLONUS*) that can be *AGGRAVATED by Sleep Deprivation, & Alcohol* -*Generalized Tonic-Clonic (GTC) Seizures occur LATER in the disease course* in almost all pts and *may be the event leading to DX* -Up to half of pts have a *concomitant psychiatric diagnosis (e.g. anxiety)* -*EEG* classically demonstrates *Bilateral Polyspike & Slow Wave Discharges during the interictal period* -*Neuroimaging (e.g. MRI) is usu NORMAL* and *NOT NEEDED* for DX when the clinical presentation & EEG are classic for JME -TX: *VALPROIC ACID* is the *First-line Tx* for *ALL types of JME*, and pts should be *educated on sleep hygiene and avoidance of triggers* -JME are *at risk for recurrent seizures* and *require LIFELONG Tx with Valproic Acid* *Valproic Acid AE*: *Dose-related Thrombocytopenia* & potentially suppresses other cell lines; *Life-threatening Hepatotoxicity & Pancreatitis*; Known *Teratogen* linked to *neural tube defects* (use w/ caution in reproductive-age women) -*Before* starting Tx, *Baseline CBC w/ PLTs* should be obtained & then *followed periodically* -Likewise, *liver enzymes* should be *measured intermittently*, and *lipase should be measured in any pt w/ Acute Abdo Pain* Note: *Ethosuximide* is the *first-line TX* for *typical Absence Seizures, but is NOT effective for GTC seizures* Note: Initiation of *tricyclic antidepressants* (e.g. *amitriptyline, imipramine, doxepin*) *requires a Baseline EKG & monitoring d/t risk of Cardiotoxicity-induced Arrhythmia* d/t Na c channel inhibition Note: *Gingival hyperplasia* is an Imp *AE of Phenytoin*, but does not occur w/ valproate

Chronic Primary Mitral Valve Regurgitation (MVR)

-*LATE SYSTOLIC CRESCENDO W/ MIDSYSTOLIC CLICK, Best @apex, Loudest just before S2* -Primary MVR is defined as caused by an *intrinsic defect* of the mitral valve apparatus (e.g. *leaflets, chordae tendinae*) -*Myxomatous degeneration* of the mitral valve leading to *mitral valve prolapse* (causing a systolic click) is one of the most common causes of *chronic primary MVR* -Chronic MVR is classified as *severe* in the *presence of associated sx* (e.g. *DOE, HF*) or *specific echo findings* (e.g. *LA & LV enlargement, regurgitant jet prominence*) -In pts w/ severe MVR, a large portion of the LVEF flows back into the LA, therefore, the *effective LVEF is much LOWER than estimated* by echo -Pts w/ *severe chronic primary MVR & LVEF ≤60%* are considered to have *IMPAIRED LV Systolic Fxn* - and *mitral valve repair/replacement is indicated

How does large cell lung CA vs. Squamous cell CA of lung present differently via CXR?

-*Large cell carcinoma* accounts for *10-15% of all lung cancers*, and manifests on CXR as a *large peripheral mass*. SX incl cough and dyspnea; severe pain if parietal pleura or chest wall are infiltrated. -*Squamous cell carcinoma* accounts for *25-30% of all lung cancers*, and manifests on CXR as a *cavitary lesion in a bronchus*. SX incl cough, dyspnea, wheezing, & hemoptysis. Sometimes lung SCC is assoc w/ *hypercalcemia d/t parathyroid-LIKE hormone prodn*

Croup

-*Most commonly caused* by *PARAINFLUENZA VIRUS* -*Croup is an UPPER Respiratory syndrome* consisting of *Hoarseness, a BARKY cough, & INSPIRATORY STRIDOR d/t upper airway inflammation*

Vulvar Lichen Sclerosus

-*Lichen Sclerosus* is a *Chronic, Benign Inflammatory vulvar disease common in POSTMENOPAUSAL Women* -In *Early stages* of the dz, the *vulva thins,* causing *HYPOpigmented areas and Increasing skin sensitivity --> INTENSE PRURITUS w/ assoc erosions and excoriations* -*Chronic irritation and scratching* transforms the thinned skin into *Thickened skin (i.e. LICHENIFICATION)* with *eventual formation of Vulvar Plaques,* often with *Perianal Skin Thickening in a classic "figure-of-eight" pattern* -In *Severe* cases, *normal anatomic structures are Obliterated or Atrophied,* such as the *loss of labia minora & clitoral hood,* which can *irritate & obstruct the urethra --> DYSURIA, Incomplete Voiding, & Nocturia* -Although lichen sclerosus is *clinically diagnosed*, a *Vulvar Punch Biopsy is recommended* d/t the *association with VULVAR CANCER* -*Standard TX is w/ HIGH-POTENCY TOPICAL CORTICOSTEROIDS that Decr Inflammation,* thereby *resolving Sx and Reducing the risk of malignancy* -When the clinical picture is strongly suggestive of lichen sclerosus, biopsy can be deferred unless lesions are refractory to TX

Antihypertensive drugs that affect Lithium levels

-*Lithium*, used to *TX Bipolar disorder,* is *eliminated exclusively by the kidneys* -Lithium is filtered in the glomerulus, but can be reabsorbed in the proximal tubule by proteins that normally handle Na & K -Bc *lithium has a narrow therapeutic index, drugs that affect glomerular filtration or renal reabsorption* can *dramatically alter serum Lithium levels, leading to Toxicity or loss of therapeutic effect* ● *NSAIDs* (ibuprofen), *ACE-I* (lisinopril), & *ARBs* (losartan) can all *acutely Decr GFR & therefore clearance of lithium,* potentially leading to *drug toxicity* ●*Thiazide Diuretics* (Hydrochlorothiazide) *inhibits reabsorption of Na in DCT, causing a compensatory Incr in reabsorption of Na & concurrently lithium in the Proximal tubule* ● *Some potassium-sparing diuretics* (e.g. *Spironolactone*) *can also Raise Lithium levels,* whereas *others* (e.g. *Amiloride*) can *Lower Lithium levels,* likely d/t *effects on both Na transport & glomerular filtration* *CCBS (e.g. AMLODIPINE) are usu considered SAFE in pts taking Lithium bc they don't significantly affect Na levels or GFR*

Discoid Lupus Erythematosus

-*Localized Discoid Lupus Erythematosus of the Scalp* causes *hair loss, scaling, inflammation, scarring, & Hypopigmentation of the skin* -There may be *associated lesions present over the face or extremities*

*Lumbar Spinal Stenosis*

-*Lumbar spinal stenosis is a DEGENERATIVE DZ that affects the ELDERLY (age 60s)* -*Characterized by INCR PAIN on Spinal EXTENSION* -- *hyperextension of lumbar spine causes lumbar pain to radiate into gluteal region and thighs* -The *pain usu Improves when sitting down or when bending forward (e.g. when using a grocery cart), or when bending over the knees (i.e. pain decr w/ flexion)* -*DX best Confirmed w/ Spinal MRI* -- *encroaching osteophytes at the facet joints, hypertrophy of the ligamentum flavum, & protrusion of intervertebral disks results in a narrowing of the spinal canal* -*Therapy can be conservative* or can incl a *lumbar epidural block* -*Surgical decompression via Laminectomy only when other therapies Fail*

Lung Cancer Workup

-*Lung Cancer is the MCC of cancer death in the US and worldwide* -The appropriate selection of therapy, as well as pt's prognosis, depends on the *histologic type and accurate staging* of the tumor -The important components of the current *TNM staging* system incl the *extent of local tumor spread, the presence or absence of nodal involvement, and distant metastases to other body parts* greatly influences the TX approaches in pts w/ lung cancer -It is imp to *accurately stage* the pt *before initiating any specific TX* -This is done through a *detailed clinical assessment, radiographic imaging* via CT scan or PET scan, and *radionuclide bone scans* -An *initial CT scan* should be obtained in all pts w/ lung cancer (small cell or non-small cell lung cancer) to aid in the initial staging workup -It is extremely useful in *detecting any mediastinal lymph node metastases and chest wall invasion* -It also allows for *accurate measurement of the tumor size, detection of small pleural effusions, and evaluation of liver and adrenal glands for metastatic disease* -In *early accessible lesions*, it can be useful in obtaining a *CT-guided biopsy for tissue DX* of lung cancer

Acute Viral Gastroenteritis

-*MC form of gastroenteritis* and is typically characterized by *loose,watery diarrhea, & emesis* -Exam may show *hyperactive bowel sounds, but abdomen is otherwise soft & benign* -Most *children* are *mildly dehydrated* (*slightly dry lips, moist oral mucosa, normal vitals*) and *can be managed as an OUTPATIENT* -*SX usu resolve spontaneously within Days* -*Management focuses on Hydration & Early Return to Normal Feeding* -*Freq intake of a low-osmolarity oral rehydration solution containing balanced electrolytes & Minimal sugar is IMP for replacing ongoing losses from vomiting & diarrhea* -*Fruit juices* contain excessive sugar that *may worsen diarrhea* and *soup broths lack necessary electrolytes like potassium* and are *NOT recommended* -Additionally, a *liquid diet is Needlessly Restrictive* for a child who can tolerate foods -*Kids who can tolerate oral intake should Resume a NORMAL, Age-appropriate diet -- balance of complex carbs, proteins, & healthy fats* -The *previously popular BRAT diet* (bananas, rice applesauce, toast) is *NO LONGER Recommended as its unnecessarily low in calories & protein* and can actually worsen gastroenteritis sx

Patellofemoral Pain Syndrome (PFPS)

-*MCC of knee pain in young adults, F>M* -Have *poorly localized pain at the anterior knee, worsened by activities* that involve *quadricep contraction* (e.g. squatting or going up and down stairs) -Subacute to chronic course -DX clinical -Patellofemoral Compression Test (pain elicited by extending knee while compressing patella) and induction of pain when squatting is highly suggestive -X-ray & Knee MRI are usu normal, and are only done if pt doesn't improve -TX: Supportive biomechanical management - *exercises to stretch and strengthen thigh muscles* - and avoid activities that aggravate the pain. NSAIDs may not be helpful. -Resolution of symptoms takes weeks to months

Méniére Disease

-*Méniére Disease* is a *disorder of the Inner ear* characterized by *Increased volume and/or Pressure of Endolymph (Endolymphatic Hydrops)* thought to be d/t *defective resorption of endolymph* resulting in *distension* of the *endolymphatic system* that causes *damage to both the vestibular & auditory components* of the Inner ear -Clinical features incl the following *Triad:* • *EPISODIC VERTIGO* (lasting 20mins-24hrs), commonly *assoc w/ N/V* • *SENSORINEURAL HEARING LOSS*, Fluctuating & Varying in severity & usu *worsening over time* • *Low-frequency TINNITUS* in the affected ear, often accompanied by *Aural Fullness* feeling

Net Clinical Benefit (NCB)

-*NCB* or *Clinical Usefulness of a medication* is a *measure of its possible benefit minus its possible harm* and needs to be *viewed in light of the specific clinical situation*

*MEASLES (RUBEOLA) VIRUS - RASH & MANAGEMENT*

-*MEASLES* is characterized by a *prodrome* of *Fever, Malaise*, and classic *triad* of *Cough, Coryza (rhinorrhea), & Conjunctivitis, ± Koplik spots*; *2-4 Days Later* a *MORBILLIFORM (RED MACULOPAPULAR) RASH (EXANTHEM)* that *Begins on FACE and spreads Cephalocaudally & Centrifugally (across body)*; SPARES palms & soles -Rash is *NONBLANCHING* and *Eventually COALESCES & appears Darker Red & Still Nonblanching* -*Koplik Spots*, pinpoint white papules on the buccal mucosa are pathognomonic, but often *resolve before rash onset* -Incidence of measles has DECR d/t MMR live-attenuated vaccine; however, *MEASLES OUTBREAKS* have been assoc w/ *INCOMPLETE Immunization or International Travel to Undervaccinated Regions*; *AIRBORNE TRANSMISSION* -*Children <1yo are at INCR RISK bc MMR not routinely given until age 1* -*TX is Supportive (fluids, antipyretics)* -HOWEVER, *INCR M&M assoc w/ concomitant vitamin A deficiency in children, esp <5yo children* -*VITAMIN A SUPPLEMENTATION* is therefore *recommended for Children w/ Measles to Reduce M&M* -Vitamin A deficiency is assoc w/ incr morbidity d.t higher rates of prolonged illness, hospitalization, & blindness (likely related to involvement of vit A in humoral & cell-mediated immunity*

MELAS Syndrome - Mitochondrial Encephalopathy with Lactic Acidosis and Stroke-Like Episodes

-*MELAS* is one of the *MC Mitochondrial Myopathies*, typically *affecting pts age ≤40yo & p/w Stroke-Like Episodes (e.g. hemiparesis, vision abnormalities), Seizures, Muscle Weakness, Hearing Loss, & Lactic Acidosis (d/t mitochondrial dysfunction)* -*Brain lesions*, which are the *result of defective mitochondrial energy prodn*, are termed *"stroke-like as they do NOT correspond to vascular territories* -Many mitochondrial myopathies are *MATERNALLY-INHERITED*, w/ the *condition being passed from the affected mother to Male & Female offspring* (although *heteroplasmy can result in variable clinical expression*); HOWEVER, *MALE Offspring DO NOT further transmit the condition* (i.e. *only Moms can pass down mitochondrial MELAS*)

Maternal serum AFP levels Measurement and Interpretation

-*MSAFP levels are measured at 15-20wks gestation as a SCREENING test for several fetal anomalies* -An *Elevated MSAFP (>2.5 MoMs) is freq present w/ Neural Tube Defects (e.g. OPEN Spina Bifida, Anencephaly) AND Ventral Abdo Wall Defects (e.g. Omphalocele, Gastroschisis)* -The higher the MoM value, the higher the likelihood of detecting a fetal abnormality -*Factors* such as *improper pregnancy dating & multifetal gestations* can also *raise the serum AFP level* -When measure an *abnormal AFP --> REPEAT AFP test* and ensure that other factors (e.g. maternal weight, race) are correct -*Subsequently, an Obstetric U/S is performed to obtain a Detailed Anatomic Survey*, w/ *attention given to identifying fetal malformations assoc w/ elevated AFP* -A normal AFP doesn't r/o NTDs, as CLOSED spina bifida can have Normal AFP values -*If an obstetric U/S fails to find a fetal malformation, Amniocentesis can be performed* -- *Amniotic Fluid AFP & ACETYLCHOLINESTERASE is measured* -- *Elevations in Both predict a Neural Tube Defect w/ High PPV*

Management of Uncomplicated Gallstones (e.g. causing biliary colic)

-*Management of [uncomplicated] gallstones depends on pt's symptoms, imaging findings, & presence of complications* and are *treated symptomatically with Pain Management* -Pts then undergo *prophylactic Elective Cholecystectomy (usu Laparoscopic)* to *prevent recurrence and complications* (e.g. *choledocholithiasis, cholangitis, gallbladder rupture*)

*21-Hydroxylase Deficiency*

-*Marked elevation of 17-hydroxyprogesterone*, a substrate of 21-hydroxylase, *confirms the dx of 21-hydroxylase deficiency (autosomal recessive)* -*High testosterone* levels are responsible for *virilization of external female genitalia* -*Aldosterone and cortisol* levels are *abnormally low* Note: If a pt is found w/ *hypotension, hypoglycemia, & dehydration* and a *hx of 21-hydroxylase deficiency*, they are in *ADRENAL CRISIS*. Prompt therapy with *stress-dose hydrocortisone*, in addition to *volume repletion w/ isotonic fluids and dextrose to correct hypoglycemia* is essential to *prevent M&M*. *Mineralocorticoid replacement is /unnecessary/while* pts are *on stress doses of hydrocortisone* bc of the *potent mineralocorticoid action of high-dose hydrocortisone*. -Following resolution of adrenal crisis, *gold standard TX for classic CAH* is *Chronic Glucocorticoid & Mineralocorticoid TX* to *maintain normal BP, electrolytes, growth, & weight gain and to suppress adrenal androgen*. *Hydrocortisone is the MC glucocorticoid used in infants/children*. *Fludrocortisone is given for mineralocorticoid replacement*. *Infants may need salt supplementation* until they start eating solid foods.

Nelson's Syndrome

-*Mass lesion in the sellar & suprasellar region*, a Hx of *bitemporal hemianopsia* and *hyperpigmentation* *following bilateral adrenalectomy for Cushing's disease is suggestive* of *Nelson's Syndrome* -*MRI* and *plasma ACTH* levels are required for making the DX -A *pituitary microadenoma w/ suprasellar extension* on *MRI* and *extremely high plasma ACTH levels are diagnostic*. -Pituitary enlargement and hyperpigmentation following bilateral adrenalectomy for Cushing's disease is termed as *Nelson's syndrome*!!! -The *cause of pituitary enlargement is the loss of feedback by the adrenal glucocorticoids following bilateral adrenalectomy* -The tumor in Nelson's syndrome is aggressive and is *TX by surgery &/or pituitary radiation* -Following bilateral adrenalectomy, *Prophylactic pituitary radiation* sometimes *prevents the dev of Nelson's syndrome; however, this leads to an increased risk for hypopituitarism* -Previously, bilateral adrenalectomy was the preferred tx for Cushing's disease; however, w/ the advent of better localization & improved techniques of transsphenoidal surgery, *Primary Pituitary Surgery* is now the *Preferred TX for Cushing's disease*. Note: *Prolactinoma can cause bitemporal hemianopsia but will NOT lead to increased pigmentation*.

TX for Melasma

-*Melasma* is a *HYPERPIGMENTATION disorder that p/w irregular, brown macules & patches symmetrically on the face* -*TX w/ HYDROQUINONE*, a *skin-lightening agent*

Meralgia Paresthetica

-*Meralgia paresthetica* is a *mononeuropathy of the lateral femoral cutaneous N (LFCN)* -The LFCN is a *purely SENSORY nerve* that *originates in the lumbar plexus* and *continues along the lateral edge of the psoas muscle* and then *travels under the inguinal ligament before entering the subQ tissue of the thigh* -D/t LFCN *entrapment or injury* (e.g. compression d/t tight clothing, obesity, pregnancy; iatrogenic injury d/t total hip arthroplasty) -*Clinical DX* (no imaging needed): *Meralgia paresthetica SX* are usu *unilateral* and incl *pain, paresthesia, and/or numbness in the Anterolateral/Lateral Thigh* -PE: *Diminished sensation* in a discrete area of *upper lateral thigh* -*Strength & Reflexes are NORMAL* bc LFCN does NOT contain motor fibers -SX are reproducible by tapping on inguinal ligament -Management: *Avoid tight-fitting clothes, weight loss, NSAIDs* ->90% resole spontaneously or w/ conservative measures

Renal Colic in Pregnancy

-*Nephrolithiasis* in pregnancy can present with *paroxysmal (abrupt episodes), severe ABDOMINAL PAIN* (instead of flank pain) that *radiates to the labia* (abdo pain when stone is in distal ureter) (Note: Absence of costovertebral angle tenderness and/or absence of gross hematuria does not exclude renal stones; microscopic hematuria in 70%) -Acute nephrolithiasis is MC in second and third trimesters d/t incr calcium excr and progesterone-induced urinary stasis -*First-line imaging* modality is with *RENAL & PELVIC U/S* which *avoids fetal radiation exposure* and can reveal findings of *hydronephrosis & hydroureter* that support the dx Order of imaging modalities preference: Renal/Pelvic U/S --> TVUS --> MRI (MR Urogram) or Low-dose Noncontrast CT (during second & third trimesters only)

Neuropathic (CHARCOT) Arthropathy

-*Neuropathic arthropathy* involves *repetitive bone & tissue trauma caused by Impaired Sensation and Joint Proprioception that prevents the pt from adjusting weight bearing to avoid mechanically induced wear and tear* -*ACUTE Neuropathic Arthropathy* is *characterized by an exaggerated, local inflam response that is usu triggered by minor trauma (often unbeknown to the pt)* -*PE* at this *acute stage* is reflective of *inflammation* (i.e. *significant erythema, edema, & warmth*); *X-ray usu shows Only Soft Tissue Swelling W/O Bone Involvement* -*Continued weight bearing* in pts w/ acute neuropathic arthropathy *allows progression of the dz* to the *SUBACUTE stage*, which is *characterized by inflammation-induced bone resorption* (i.e. *cytokine-induced incr in osteoCLASTIC activity*) -In the *Subacute stage,* there are *PE findings of Infalm && X-ray Findings of Osseous Destruction (e.g. Phalangeal osteolysis, partial disappearance of metatarsal heads resembling "sucked-candy")* -*TX of BOTH Acute & Subacute stages of neuropathic arthropathy* is with a *Foot CAST to reduce edema & weight bearing, protecting the foot from further injury* -*UNTx Dz --> Rapidly leads to a hypertrophic repair phase* that is *characterized by resolution of inflammatory PE findings but the dev of IRREVERSIBLE and significant bone destruction on x-ray (i.e. CHRONIC neuropathic arthropathy)* -Once Chronic stage dev (i.e. *resolution of inflam*), *foot casting is UNLIKELY to be effective*; Instead *chronic dz is managed w/ Orthotic Footwear, Surgical Bone Realignment (only in select pts), & Management of Infectious Complications (cellulitis, osteomyelitis)* -Poorly controlled chronic dz often leads to *uncontrolled tissue infection & the need for amputation* Note: NSAIDs & Corticosteroids do NOT prevent continued trauma and dz progression,

Stable Coronary Artery Disease (CAD) Initial Evaluation

-*Noninvasive Stress Testing* provides both diagnostic and risk stratification info regarding CAD and is the initial evaluation of choice in pts w/ suspected clinically-significant, stable CAD -Pts w/ *positive stress test* --> Initiate pts on *medical therapy, incl Aspirin, High-intensity Stain (e.g. Atorvastatin, Rosuvastatin), and a β-blocker (e.g. Metoprolol)* as well as *optimization of cardiovascular risk factors* (e.g. smoking cessation, BP and glucose control) -Additionally, pts w/ *High-Risk Testing Features* (e.g. ST depression at minimal exertion, poor exercise capacity, exercise-induced angina at low workload, etc.) who are *likely to have atherosclerotic dz* that will *benefit from REVASCULARIZATION* should undergo *Percutaneous Coronary Angiography* to assess for stent placement or CABG -Pts without high-risk stress testing features but w/ anginal sx refractory to several months of optimal medical management should also undergo Coronary Angiography to assess for revascularization Note: *CT Coronary Angiography* allows for visualization of atherosclerotic coronary artery lesions and risk assessment, but it /does not allow for therapeutic intervention at the time of testing/ Note: *Dobutamine Stress Echocardiography* is an alternate stress testing modality for those unable to undergo exercise EKG stress testing

Ocular Melanoma - DX & Management

-*Ocular Melanoma* is a primary malignant tumor *arising from melanocytes within the uvea (iris, ciliary body, & choroid), usu from a Choroidal Pigmented Nevus* -It often *remains ASX for a long time* and is *freq incidentally DX on fundoscopy* -When *SX* occur, it usu presents as *blurry vision* or *progressive & painLESS visual field abnormalities*, sometimes have *floaters or pain* if the *tumor impinges on nerves* -*ULTRASOUND of the EYE is the Most Sensitive Imaging Modality to DX Ocular Melanoma!* -But *MRI is used to document any extrascleral extensions for Staging & TX Decisions* -*ASX pts w/ SMALL pigmented lesions (diameter <10mm, thickness <3mm)* often experience an *extended period of SLOW growth* and can be *Managed by Close Observation W/O Tx* -- *Repeat exam in 3mo, and every 6mo thereafter* (*Local resection of choroidal melanoma is assoc w/ significant risk for ocular complications & tumor recurrence for small lesions*) -*LARGE (Diameter ≥10mm, Thickness ≥3mm) Choroidal Melanomas* OR those *P/W Assoc SX (eye pain, visual disturbances)* have a *WORSE Prognosis* than small ASX lesions; these pts should be *Referred for Definitive TX w/ RADIATION THERAPY using Brachytherapy or External Beam Radiotherapy*, which has been *shown to reduce mortality caused by metastatic dz* -*Enucleation* is the preferred TX when tumors are *very large, have extrascleral extension, or severe assoc pain* -- *Compared to Radiotherapy, Enucleation has greater functional & psychologic morbidity and NO proven survival advantage* Note: *Chemotherapy* has *NOT proven effective* in TX intraocular melanoma

Chronic Heart Failure Management

-*Optical medical therapy* for *Class I & Class II NYHA Heart failure Sx* includes use of an *ACEI/ARB*, *beta blocker* (w/ EF ≤40% once euvolemic), *aldosterone antagonist* (e.g. *Spironolactone*; if EF <30% w/ stable renal fxn & potassium), and *diuretics* -Based on current guidelines, the next step would be to add *Isosorbide Dinitrate* (*along w/ Hydralazine* if African American*) to optimize medical therapy once *progressing* from *NYHA Class II to NYHA Class III/IV* -The *combination of hydralazine + nitrate therapy* provides *symptomatic & mortality benefit in African American* pts *w/ LV Systolic Dysfunction (LVEF <40%) and NYHA Class III or IV heart failure symptoms despite optimal therapy* -It is also recommended in pts w/ *HF and low LVEF who cannot tolerate ACEI or ARBs* d/t hypotension, renal failure, or hyperkalemia, *and/or have persistent sx despite optimal therapy w/ a beta blocker, ACEI, aldosterone antagonist, and diuretic*.

Post-Marketing Surveillance is used to Detect Fatal and Serious AE - Why?

-*Post-Marketing Surveillance* is the *practice of monitoring the safety of medications or devices after they have been released on the market* -The *POWER of a study* reflects its *ability to detect a difference b/w groups, if such a difference exists* -*Power depends on sample size* -*Randomized clinical trials* are efficacy trials by design, and *may not have adequate power to look at AE, esp rare AE* -There may be *too few participants (small sample size) to detect rare AE*; *f/u times are often short*; and in some populations, *comorbidities and additional drug interactions may not be adequately represented in earlier phases of clinical testing* -The *TRUE Safety Profile* of ay medication of often *understood only AFTER its been on the market for a while and used by a large number of pts*

Herpangina

-*Oropharyngeal infection* primarily cause by *COXSACKIE Group A Virus* -- usu seen during the *SUMMER in kids 3-10yo*, who p/w *fever, drooling, sore throat, decreased appetite, headache, pharyngeal erythema, & PAINFUL posterior pharyngeal VESICLES on the posterior soft palate* (NOOO cervical LAD) -The lesions can *evolve rapidly from Erythematous Macules to Vesicles on the soft palate & tonsillar pillars,* creating a *PainFUL Pharyngitis* -DX is Clinical based on pharyngeal findings -*Therapy* is directed at *Symptomatic Relief* with *saline gargles, analgesics, & antipyretics* -Cold, non-acidic fluids or popsicles can be soothing and provide hydration -Antiviral therapy is NOT indicated in this *SELF-LIMITED Illness,* which typically *resolves within a WEEK* -*Hand Washing* by children and close contacts can *prevent spread during outbreaks* NOTE: The absence of anterior cervical LAD and tonsillar exudates makes Group A Strep (S. pyogenes) pharyngitis unlikely.

Osteomalacia

-*Osteomalacia is d/t Defective Mineralization of Osteoid, most commonly d/t Vitamin D Deficiency* -*X-rays* show *osteopenia & pseudofractures* in Osteomalacia -P/w *chronic musculoskeletal (e.g. back) pain, Elevated alk phos, & Low bone density* -Osteomalacia is usu d/t *vitamin D deficiency, which impairs intestinal absorption of calcium* -The *compensatory INCR in PTH Secr (i.e. Secondary Hyperparathyroidism) Restores Calcium levels to Normal/Near Normal, BUT leads to Renal Phosphate Wasting (Low PO4) and Impaired Mineralization of Bone* -*DX Confirmed w/ LOW Serum 25-Hydroxyvitamin D level* (STORAGE form in liver), which *reflects total body stores of vit. D*: *<20 ng/mL is Diagnostic, and <10 ng/mL is common* ● Note: 1,25-dihydroxyvitamin D levels (ACTIVE form, calcitriol, formed in kidney) should NOT be used bc they are determined primarily by PTH activity and renal fxn, and may be normal/high -*X-ray* may show *cortical thinning, loss of trabeculae, & transverse radiolucencies w/ sclerotic margins (Looser zones)* -*Osteomalacia* is a *Common Complication w/ Gastric Bypass Procedures & other Malabsorptive Conditions d/t DECR Absorption of Vitamin D from Intestines!!!* -- pts *Require Higher Doses of Supplemental Vitamin D (≥2,000 IU/day) may be necessary* -*Decr vitamin D --> Decr serum Ca2+ --> Incr PTH secretion --> Decr serum PO4* -*Hyperactivity of osteoblasts --> Incr ALP*

What is Outcome Misclassification and how do you minimize it?

-*Outcome misclassification* occurs when the *outcome under investigation is not identified correctly* -It occurs in studies that evaluate /subjective outcomes/ (e.g. assessed subjectivity by researcher, self-reported by participants) -This type of outcome is difficult to assess and may incr likelihood errors in outcome classification -*Misclassification error occurring at /different rates/ in each group* (e.g. exposed & nonexposed) is known as *differential misclassification* and may introduce bias against the null (i.e. no association) hypothesis -Misclassification error occurring at /similar rates/ in each group is known as *nondifferential misclassification* and generally introduces bias towards the null (i.e. no assoc) hypothesis; meaning if a significant assoc b/w the exposure to a RF and an outcome is found, the true association might be slightly stronger than the observed one -Can *minimize outcome misclassification* by using the /most accurate measurement/ or *validated assessment instrument* available to determine outcome status

OVERFLOW INCONTINENCE

-*Overflow Incontinence* occurs d/t *INCOMPLETE BLADDER EMPTYING*, as a result of *Decreased Detrusor Muscle Contractility &/or Bladder Outlet Obstruction* -Pts experience *constant urinary dribbling (leakage), nocturia, & a weak urinary stream* d/t *bladder distension from incomplete emptying* -Typical Exam Findings incl: *Decreased Perineal Sensation (e.g. neuropathy), & a LARGE POST-Void Residual Urine Volume (>150mL)* -Overflow Incontinence is often assoc w/ *NEUROPATHY* (e.g. *poorly controlled diabetes, spinal injury, multiple sclerosis*) -Pts w/ an underlying neuropathy can develop overflow incontinence when *additional RF (e.g. Antihistamines) result in exacerbation of sx* -*TX involves Intermittent Self-Catheterization & Correction of Underlying Etiology*

Pneumocystis jiroveci Pneumonia (PCP)

-*PCP* is seen in pts w/ *defects in cell-mediated immunity* -Most commonly seen in *HIV-infected pts w/ CD4 <200*, but can also be seen in those receiving *immune modulation following organ transplantation* -PCP has an *insidious onset* and usu p/w *low-grade fever, cough, dyspnea, & tachypnea* -*HYPOXIA is prominent* and may be *out of proportion to relatively mild findings on chest auscultation* -*CXR reveals diffuse, bilateral ground-glass opacities* -*TMP-SMX is the TX of Choice for suspected or proven PCP!!!* -IV therapy initially, with oral therapy initiated once pt has signs of clinical recovery -*TMP-SMX is highly effective* when used *Prophylactically to PREVENT PCP* in *at-risk pts*, and *failure to adhere to TMP-SMX PPX* puts pts at *incr risk for PCP infection*

How do you treat cardiac arrest due to Pulseless Electrical Activity or Asystole according to ACLS guidelines?

-*PEA* is *organized cardiac rhythm that is unable to generate sufficient cardiac output to create a measurable blood pressure or palpable pulse* -*Asystole* is the *complete absence of electrical and mechanical activity* -PEA & Asystole are managed the SAME way: • *Establish IV/IO Access & Begin Immediate CPR* w/ effective chest compressions and assisted breathing should be given first • *IV/IO EPINEPHRINE, 1mg*, should be administered *ASAP and q3-5 mins* in an effort to increase organ and tissue perfusion -Shocks (Defibrillations) are not given for cardiac arrest caused by PEA or Asystole!! -CPR should continue uninterrupted while attempted to identify and treat potentially *reversible causes of PEA* (incl: *hypovolemia, hypoxia, acidosis, hypo-/hyperkalemia, hypothermia, tension pneumothorax, cardiac tamponade, toxins [narcotics/benzos], thrombosis [pulmonary or coronary], trauma*) Note: *IV Atropine* is indicated in pts w/ *symptomatic bradycardia* (e.g. hypotension, heart failure); however, sinus bradycardia occurring *in the absence of a pulse* is now considered *PEA* [rather than symptomatic bradycardia]. Atropine is NOT used in PEA cardiac arrest

Pernicious Anemia - EGD Findings

-*Pernicious Anemia is characterized by the Autoimmune Destruction of Parietal Cells, caused by anti-parietal (less specific) and anti-Intrinsic Factor (nearly 100% specificity) antibodies* -Pernicious Anemia is *assoc w/ Autoimmune Metaplastic Atrophic Gastritis (AMAG)!* -*AMAG* is *caused by Autoimmune Aggression against the gastric mucosa* -- *immune response is mainly directed against oxyntic cells & intrinsic factor* -*AMAG has 3 components*: 1. *GLANDULAR ATROPHY primarily affecting the BODY & FUNDUS* 2. *INTESTINAL METAPLASIA* 3. *INFLAMMATION* -There's usu *FEW changes observed in the gastric antrum* and *no erosions or ulcerations are usu observed* (if present, may indicate high probability of malignancy) -In *advanced stages*, the *mucosa becomes thin & atrophic* and *Endoscopy may demonstrate ABSENT GASTRIC RUGAE (!!!) in the BODY & FUNDUS* -*Intestinal metaplasia replaces normal oxyntic glands*; sometimes, the mucosa becomes *villiform* and *resembles small intestine*

Postexposure PPX in Susceptible Individuals to Chickenpox

-*PEP* is *indicated in susceptible individuals*, incl those who are *NOT fully vaccinated against chickenpox (caused by varicella-zoster virus) & those who have NO prior Hx of chickenpox infection* -PEP *Reduces Risk of Transmission* and, *if the pt develops varicella, the Severity of infection* -Management options are dependent on pt's immune system fxn ● *ImmunoCOMPETENT*: *Healthy pts ≥21yo* should *receive PEP w/ the Varicella Vaccine within 5d of Exposure*. The vaccine can be given after 5d to prevent future infection, but is unlikely to prevent current infection ● *ImmunoCOMPROMISED*: *Bc LIVE virus vaccines are Contraindicated in Immunocompromised pts, PASSIVE PROTECTION w/ Varicella-Zoster Immune Globulin (VariZIG) WITHIN 10d of Exposure is Recommended*. *VariZIG* is *also indicated Pregnant pts & Newborns*, who are similarly at high-risk for severe dz & cannot receive live vaccines Note: Chickenpox is a highly contagious infxn caused by VZV & *spread via Direct Contact w/ Vesicles or thru Respiratory Droplets*. An *infected individual* can *transmit the virus from 2 days BEFORE the Onset of Rash UNTIL there are NO new lesions and the rash has CRUSTED OVER*

Postherpetic Neuralgia (PHN)

-*PHN* is when pts w/ *herpes zoster infections (shingles) have Persistent Pain and Allodynia (pain elicited by mild stimulus like light touch) >4 MONTHS AFTER the Lesional Rash has Resolved* -*Acute herpetic pain* is assoc w. *hemorrhagic inflammation of the dermatomal sensory nerve d/t viral replication* - but as the *zoster lesion resolves, viral replication reduces, and the pain remits (partially reduces)*, and *5% of pts will have persistent pain for >4mo* -*Risk is greatest in* those w/ *advanced age, severe initial pain, or severe zoster rash* -Pain may be *constant or intermittent* but is *almost always assoc w/ allodynia*, causing impaired sleep, decr appetite, diminished libido -*PE reveals sensory deficits (anesthesia) within the affected dermatome* -*PHN pts require Chronic TX* -*Tricyclic antidepressants (Amitriptyline) are First-line*, but should be *used w/ caution in older* pts *or those w/ cognitive impairments* -*Gabapentin* or *Pregabalin* is considered the next most effective & is well-tolerated -*Opioids* are also effective, but are *NOT used for initial Tx* d/t potential for *dependence & abuse*

Bile Salt-Induced Diarrhea

-*POSTCHOLECYSTECTOMY DIARRHEA* is a form of *bile salt-induced diarrhea* that *occurs in 5-10% of pts following Cholecystectomy* -Bile salts are conjugated bile acids -Primary bile acids produced in liver cells are secreted into the intestinal lumen, where the are converted into secondary bile acids by bacteria -These *secondary bile acids* can *cause colonic stimulation if present in excess amounts* -*Gallbladder surgery alters gut dynamics* and leads to *increased bile acid flux to the colon, resulting in an Increased Proportion of Secondary Bile Acids and causing DIARRHEA* -Bile Salt-Induced Diarrhea is *also seen w/ Ileal Resection or Short Bowel Syndrome* -*CHOLESTYRAMINE* is a *bile salt-binding resin that sequesters excess bile salts, preventing intestinal reabsorption of bile acids (liver must use cholesterol to make more, therefore reducing LDL)*, and is often *effective in bile salt-induced diarrhea*

Preterm Prelabor Rupture of Membranes (PPROM)

-*PPROM is membrane rupture (leakage of clear amniotic fluid) at <37wks gestation in the ABSENCE of associated contractions* -Presenting features incl a *gush of [clear, non-malodorous] fluid, a NITRAZINE-POSITIVE pool of vaginal fluid that "FERNS" when dry on Microscopy, and Oligohydramnios (amniotic fluid index ≤ 5)* -PPROM is likely d/t a *SUBCLINICAL Intrauterine INFXN* (e.g. *NO fever, uterine tenderness, or maternal/fetal tachycardia*) -*RF* for PPROM: *Genital tract infections (e.g. bacterial vaginosis), tobacco use, first-trimester bleeding, & Hx of PPROM in Prior Pregnancy* -*Management depends on gestational age*: ● *@ ≥34wks gestation*: *Delivery IS Indicated* as the *risks of prematurity NO longer outweigh the risks of pregnancy prolongation* (e.g. *intraamniotic infection, umbilical cord prolapse, abruptio placentae*) ● *@ <34wks gestation with NO SIGNS of Clinical Infection or Fetal Compromise* (e.g. *late decelerations*), *EXPECTANT MANAGEMENT* is indicated as the *Risks of Prematurity OUTWEIGH the risks of pregnancy prolongation*; *Prophylactic Latency Antibiotics (e.g. Ampicillin + Azithromycin)* are administered to *PREVENT OVERT Intrauterine Infection* (i.e. *intraamniotic infection*), which can result from *progression of subclinical infection that caused PPROM or from ascent of vaginal bacteria through ruptured membranes*; Additionally, *Corticosteroids are given to DECR the Risk of Neonatal Resp Distress Syndrome* -By preventing overt infection, *Antibiotics INCR the latency period (time b/w membrane rupture & delivery)*, thereby *increasing gestational age at delivery & improving neonatal outcomes* -*Ampicillin covers GBS, aerobic gram-neg bacilli, and anaerobes* -*Azithromycin covers Ureaplasma* Note: *Magnesium Sulfate* is indicated in pts *<32wks gestation who are at Risk for Preterm Delivery* as it *DECR Risk of Fetal Neurologic Complications (e.g. Cerebral Palsy)*

Levodopa: MOA Carbidopa: MOA Use in Parkinson's?

-*Parkinson Disease* is caused by *degeneration of dopaminergic neurons in substantia nigra*, leading to *progressive DOPAMINE DEFICIENCY* in the brain -Direct dopamine replacement Impossible, bc dopamine can't cross BBB--so instead *Levodopa* (i.e. *L-DOPA*), the *immediate precursor of dopamine* is used -Once *Levodopa crosses BBB*, it's taken up by nigrostriatal neurons & *converted to therapeutic dopamine in the brain* -In *peripheral tissues, Levodopa is rapidly metabolized to Dopamine & 3-O-Methyldopa* via DOPA decarboxylase & catechol-O-methyltransferase, respectively, *leaving less dopamine available for the brain, and more dopamine in the peripheral tissues where it can exert AE* -*CARBIDOPA blocks DOPA decarboxylase* and, therefore, *prevents peripheral conversion of L-DOPA to Dopamine in the Liver & Peripheral Blood* -In addition to increasing the amount of dopamine available to the brain, the *use of Carbidopa also decreases many unpleasant AE that occur d/t peripheral effects of dopamine (Nausea, vomiting, Postural Hypotension, tachyarrhythmias)* -Low doses of carbidopa (e.g. 12.5 vs 25mg) *may not be enough* to prevent these peripheral AE, but increasing carbidopa dose will help

CCBs causing Peripheral Edema

-*Peripheral edema* is a common AE of CCB therapy, w/a reported incidence of *~25% after 6mo therapy* -Edema is likely related to *preferential dilation of precapillary vessels (arteriolar dilation)* which leads to increased capillary hydrostatic pressure and fluid extravasation into interstitium -*Dihydropyridine CCBs* (e.g. *Amlodipine, Nifedipine, Nicardipine, Clevidipine) are potent arteriolar dilators and cause more peripheral edema compared to non-dihydropyridines (diltiazem, verapamil) -Other major AE of dihydropyridine CCBs incl: *HA, flushing dizziness, & gingival hyperplasia* Note: Renin-angiotensin system blockers (*ACE inhibitors or ARBs*) cause *post-capillary venodilation* and can /normalize the increased capillary hydrostatic pressure/. In clinical studies, the *combination of CCBs with ACE-I was assoc w/ significantly LOWER risk of peripheral edema compared to CCB Monotherapy* Note: ACE-I (e.g. Enalapril) can bead to development of *angioedema* in *~0.1-0.7%* of pts (far lower than amount affected by CCBs). Will cause nonpitting swelling of subcutaneous or submucosal tissue and most commonly affects the *lips, tongue, face, & upper airway*. *ACE Inhibitors do NOT cause peripheral or dependent edema!!*

Somatic Symptom Disorder

-*Preoccupation w/ multiple unexplained medical sx* suggests *Somatic Symptom Disorder* -*Sx are Unconscious, Motivation is Unconscious* -*DX Requires EXCESSIVE Preoccupation w/ ≥1 somatic sx (e.g. HA, abdo pain, fatigue) for ≥6MO!! that causes Significant Social & Occupational Impairment* -Sx may represent *catastrophic interpretations of normal bodily sensations or discomfort that generally does NOT signify serious dz* -Associated with *excessive, persistent thoughts and anxiety about symptoms that interferes with work & causes stress in relationships* -May co-occur with medical illness!! -Often make *extensive use of medical services & are rarely reassured by negative findings* -Physicians must keep in mind that these pts are *truly suffering, even if their sx are not medically explained*, and that *concurrent medical illness is not mutually exclusive* -*TX*: *Regular office visits with the SAME physician in combo w/ Psychotherapy*

Presbycusis

-*Presbycusis* is a *gradual, Symmetrical, Sensorineural hearing loss* that *affects >50% of adults by age 75* and can *significantly impair quality of life* -Pts can cause pts to *withdraw from their social lives & may stop leaving home to avoid conversations (isolation in elderly)* -Social interactions deteriorate -Must listen to radio or TV at *high-volumes or very close to source* -PE usu shows No abnormalities other than the hearing loss itself -Although *Audiometry is used to Confirm the DX*, the *Whispered Voice Test - a simple procedure that can be performed w/o equipment* can be used ● In the *Whispered Voice Test, the examiner stands behind the pt & whispers letters/numbers while occluding the non-tested ear* -- *Repeating 3/6 letters/numbers Correctly is Passing* -*Progressive social withdrawal* can lead to *feelings of depression & low self-esteem* -Most pts with *presbycusis benefit from Use of Hearing Aids (TX), which should Decr social isolation*

Pseudohypoparathyroidism

-*PseudoHYPOparathyroidism, caused by End-Organ RESISTANCE to PTH,* causes *Chronic HYPOCALCEMIA, HYPERPHOSPHATEMIA, & ELEVATED PTH*; *Signs of CHRONIC HYPOcalcemia incl *seizures, muscle cramping, hyperreflexia, basal ganglia calcifications, & b/l cataracts* -*PTH maintains calcium homeostasis*, by *triggering Calcium REAbsorption & Phosphate EXCR in the kidneys* -*PTH* also *promotes Calcium Release from Bone* and *Incr Active Vitamin D (1,25-Dihydroxyvitamin D) to Stimulate Intestinal Absorption of Ca2+* -*Pseudohypoparathyroidism* is characterized by *end-organ RESISTANCE to PTH*, resulting in *Chronic Hypocalcemia, which signals Increased PTH secretion* through a feedback loop -*Elevated PTH distinguishes PSEUDOhypoparathyroidism from TRUE Hypoparathyroidism*, which *also causes hypocalcemia and hyperphosphatemia*, but is *d/t Impaired PTH prodn* -Hypocalcemia causes *neuromuscular excitability (tetany)*, which can manifest as *Seizures, muscle Cramping, Paresthesias, Hyperreflexia, or laryngospasm*; other findings incl *Cardiotoxicity (e.g. Heart failure, QT Prolongation) and Psychosis (anxiety, depression)* -*Lab Eval is Diagnostic* and *TX is Calcium & Vitamin D Supplementation* Note: *Albright Hereditary Osteodystrophy* is a *subtle type of PseudoHYPOparathyroidism* where pts have *dysmorphic features - short stature, round facies, short 4th/5th metacarpal digits, subcutaneous calcs, developmental delay*; *Labs show Incr PTH, Low Ca2+, Incr PO4*

Corticosteroid-Induced Psychiatric Symptoms

-*Psychiatric Sx are commonly seen* in pts *taking Corticosteroids (e.g. Prednisone)* and can incl *mood changes, psychosis, & anxiety* -*SX more common in HIGH doses for PROLONGED periods of time, BUT can occur at any time* ● *High doses of prednisone (≥40mg/d)* often given for allergic, inflam, or autoimmune conditions (e.g. SLE), *may cause psychiatric sx in a Dose-Dependent fashion, w/ or w/o hx of underlying psychiatric disorders* ● *Longer duration of use can INCR risk but can occur at any time* -More common women than men -Other neuropsychiatric sx seen in glucocorticoid use incl: *sleep disturbances, restlessness, & memory loss* -Whenever possible., the *First step in TX is DOSE REDUCTION (or discontinuation if appropriate) of the offending corticosteroid* -- once reduced, psychiatric sx can be TX if they persist (e.g. CBT)

Pulmonary Contusion

-*Pulmonary contusion* is a common injury resulting from *BLUNT Chest TRAUMA* • Blunt *trauma to the lungs* results in *accumulation of edema & blood in a localized area of the lung parenchyma* -Pts typically have *chest pain* and may dev *accompanying SOB & hemoptysis*, and *CXR characteristically shows an Irregular, Localized Opacification @site of injury* -The *onset of resp sx may be delayed for ~24hrs from time of injury* and *initial CXR* may show *no airspace dz* -CT Chest is more diagnostically sensitive, However, contusions seen on CT but not on CXR are often minor and may be of low clinical significance -*Depending on the size* of the contusion, *Respiratory Distress & Significant Hypoxemia may dev up to 24hrs from time of injury* -In pts in whom there is *suspicion for significant pulm contusion,* they should be *admitted to the hospital & monitored for 24-48hrs* -In those who dev *resp sx, TX involves Adequate Pain Control to AVOID Hypoventilation,* as well as *Supportive Care to incl Pulmonary Hygiene (e.g. chest physiotherapy, suctioning), & Supplemental O2 and Ventilatory Support* as needed -W/ *adequate support and monitoring*, *most* pts experience *Resolution of Sx within 3-5d*

Management of Acute Pyelonephritis in Pregnancy

-*RF for Acute Pyelo in Pregnancy*: Age <20yo, Nulliparity, Pregestational DM, Sickle cell disease/trait, Tobacco use -*Complications of Acute Pyelo in Pregnancy*: *Pulmonary edema, ARDS, & Preterm Labor, and Renal abscess, Papillary necrosis, & Renal failure* -*D/t the risk for complications*, pyelonephritis during pregnancy *requires hospitalization for IV Hydration & Empiric TX with Broad-Spec Beta-Lactam ABX (e.g. Ceftriaxone, Cefepime)* -*Once afebrile for 48hrs, pts placed on Oral ABX for 10-14 days* -*After TX completion, Daily Suppressive Therapy is initiated and maintained until 6wks Postpartum to prevent recurrence*

Pediatric Dyslipidemia

-*RF for atherosclerosis & premature cardiovascular dz in adulthood!* -*RF* for Pediatric dyslipidemia incl *obesity, T2DM, HTN, & a relevant FHX* such as a *first-degree relative w hypercholesterolemia (total cholesterol ≥240 mg/dL) or premature CVD (<55yo in Men, <65yo in Females)* *SCREENING w/ a NON-Fasting Lipid Panel* as follows: ● *Kids W/O RF*: *Universal screening b/w 9 & 11yo and 17 & 21yo* ● *Kids WITH Cardiovascular RF*: *SERIAL screening q1-3yrs (regular intervals) starting @2yo* (*or when RF is identified*) -*Abnormal NON-fasting lipid panel* results (e.g. *Total cholesterol ≥200, LDL ≥130, HDL <40*) should be *Confirmed w/ a FASTING Lipid Panel* -Management begins w/ counseling & lifestyle changes (low saturated foods, daily exercise) -*Statin* therapy is considered in pts *≥10yo w/ persistent dyslipidemia after 6mo of lifestyle changes*

Restless Leg Syndrome (RLS)

-*RLS is characterized by Unpleasant sensations in lower extremities that occur at rest & are relieved by moving the legs* -Occurs in 5-10% of the population, and is *MC in older pts* -Nearly half of Idiopathic RLS pts have a positive FHx (autosomal dominant inheritance) -*RLS is often ASSOC W/ IRON DEFICIENCY, especially in the CNS/Substantia Nigra* -*DX of RLS is based on Clinical Hx* -- HOWEVER, *an assay of iron stores with a SERUM FERRITIN LEVELS is advised i the initial assessment* -A normal CBC doesn't r/o RLS bc Iron deficiency is freq present in the absence of anemia -*Iron Supplementation often relieves sx, even in pts w/ low-normal serum ferritin levels (≤75 ng/mL)* -*Polysomnography* may be considered to r/o other contributing sleep disorders, but *is NOT diagnostic for RLS* -*NO other tests routinely indicated* -*Management of RLS* • *Nonpharmacologic* measures incl *reduction of caffeine & EtOH, regular moderate exercise, application of heat/cold to legs PRN* • *Avoid aggravating factors* (e.g. sleep deprivation) • *Iron supplementation* • *First-line Pharmacologic agents for Moderate to Severe RLS (i.e. frequent or daily sx)* includes an *α-2-δ calcium channel ligand, e.g. GABAPENTIN, PREGABALIN* • *Carbidopa-levodopa can be considered for PRN use in pts w/ intermittent sx* but *regular use has shown paradoxically Worsening of RLS sx* (augmentation) Note: Dopamine agonists (e.g. Pramipexole) also causes augmentation & should be AVOIDED in most pts Note: β-adrenergic antagonists (Propranolol) are used for TX AKATHISIA, NOT RLS. Akathisia is a strong urge to move, commonly an extrapyramidal sx of dopamine antagonists (e.g. antipsychotic drugs)

Recall Bias

-*Recall Bias* results from the *inaccurate recall of past exposure by participants in a study* -It applies mostly to *case-control* designs and leads to *Misclassification of Exposure*

ROC Curves - interpretation of sensitivity

-*Receiver-operating characteristic* curves plot *sensitivity as a fxn of (1-specificity) at various cutoffs points for a given test*; they help to *determine thresholds given acceptable false positive and false negative fractions* -There is a trade-off between sensitivity and specificity at any particular cutoff point -The *highest sensitivity is the highest point on the Y-axis* -Sensitivity refers to the proportion of pts W/ the disease who Test Positive on a given test -*Sensitivity is proportional to true positive rates, so a negative test on a highly sensitive test helps rule out a disease*

Complications of Esophageal Variceal Bleeding

-*Recent variceal bleeding* pts are at an *increased risk of developing complications during their hospitalization* -The principal complications in these pts that lead to *increased mortality* are: *infections, hepatic encephalopathy, and renal failure* -The *MC complication is the dev of an infection*, which usu occurs as a *UTI, spontaneous bacterial peritonitis, respiratory infection, aspiration PNA, or primary bacteremia* -There is a *decreased incidence of infectious complications* with the use of *prophylactic antibiotics* -The currently preferred regimen is the use of a *fluoroquinolone (ofloxacin, norfloxacin, or ciprofloxacin) agent for 7-10d*

How does *renal artery stenosis* usu present?

-*Renal A stenosis d/t ATHEROSCLEROSIS* is most often seen in *pts >65yo* and would be very unusual in young adults -*Unilateral or Bilateral Stenosis* --> *Decr renal perfusion* --> *Incr Renin* --> *Incr Angiotensin* --> *HTN* -Main causes of renal artery stenosis: • *Atherosclerotic plaques*: proximal 1/3 of renal artery, usually in *older males, smokers* • *Fibromuscular dysplasia*: distal 2/3 of renal artery or segmental branches, usu *Young or middle-aged FEMALES (~90%)* -For *Unilateral RAS, affected kidney can Atrophy* --> *Asymmetrical kidney size*; *Renal venous sampling will show INCR Renin IN Affected Kidney, and decr renin in unaffected kidney* -For *Bilateral RAS*, pts can have a *Sudden Rise in Creatinine After Starting an ACEI or ARB or Renin Inhibitor!!!!* This is *d/t the drug's interference on RAAS-mediated renal perfusion* -Can present with *severe/refractory HTN, flash pulmonary edema, epigastric/flank bruit*

*Renal Parenchymal Disease* as a *Secondary Cause of HTN*

-*Renal parenchymal disease (e.g. Glomerulonephritis, Vesicoureteral Reflux)* is a *common cause of secondary HTN in Young Adults (age <30)* -Glomerulonephritis may dev subacutely and be *assoc w/ variable degrees of proteinuria* -*Glomerulonephritis* with *either a NEPHRITIC (i.e. Hematuria w/ less prominent proteinuria) OR NEPHROTIC (Proteinuria >3.5 grams/d and edema - facial puffiness, lower extremity swelling) Presentation* can *cause Secondary HTN d/t Increased Renal Sodium Reabsorption*

Renovascular Disease Leading to Resistant Hypertension

-*Resistant HTN* is defined as persistent HTN despite the concurrent use of ≥3 antihypertensive agents of different classes, including a diuretic at maximal tolerated dose -All pts w/ resistant HTN should be evaluated for a secondary cause of HTN -*Renovascular HTN* is the MC correctable cause of 2º HTN and should be suspected in pts w/ clinical slues suggestive of *Renovascular Disease* (e.g. malignant HTN w/ end-organ damage; onset of severe HTN (>180/120) after age 55; severe HTN w/ diffuse atherosclerosis; recurrent flash pulm edema w/ severe HTN; asymmetric renal size [>1.5cm]; abdominal bruit; unexplained rise in serum creatinine (>30%) after starting ACEI/ARBs; unexplained atrophic kidney) -*Renal Artery Stenosis (RAS)* is present in ≈1% of pts w/ mild HTN, in up to 45% of Caucasians w/ severe HTN, and in ≈25-35% of pts w/ peripheral arterial disease -Such pts should have noninvasive assessment w/ *Renal Duplex Doppler U/S or CT or MR Angiography (MRA)* for the DX of RAS -*Renal Doppler U/S* is the initial preferred modality in pts w/ renal insufficiency d/t risk of contrast-induced nephropathy w/ CT angiography, and nephrogenic systemic fibrosis w/ gadolinium-enhanced MRA -Noncontrast MRA may be performed when available Note: A high plasma aldosterone/renin ratio is seen in pts w/ Primary Aldosteronism that presents w/ resistant HTN or HTN assoc. w/ unexplained HYPOkalemia. The presence of *diffuse atherosclerosis w/ abdominal bruit makes RAS & Renovascular HTN* the likely causes of resistant HTN.

How does retinal detachment present?

-*Sudden onset of photopsia (flashes of light) and floaters*; *Sudden-onset UNILATERAL Vision LOSS, that is painLESS*. -Most classic description is "curtain coming down over my eyes" -Does NOT cause a red eye appearance -*Fundoscopy* may reveal the *retina to be elevated with folds* or cause the retina to be difficult to visualize with a direct ophthalmoscope -If the detachment is extensive, may be a relative afferent pupillary defect -If retinal detachment is suspected, *urgent ophthalmologist evaluation within 24hrs*

Vesicoureteral Reflux (VUR)

-*Retrograde flow of urine* from *bladder toward upper urinary tract* -Can be *1° due to abnormal/insufficient insertion of the ureter within the vesicular wall* (*ureterovesical junction [UVJ]*) -*Primary VUR* is d/t a *congenitally shortened intravesical ureter,* so when *intravesicular (high bladder pressure) pressure overcomes compression of the shortened ureter, urine flows retrograde up into the ureters, causing ureter dilation and Bacterial ASCENT (Febrile UTI in kids <2yo)* -Or can be *2° due to abnormally high bladder pressure* resulting in *retrograde flow via the UVJ* -*INCR Risk of RECURRENT UTIs!* -All *children <2yo w/ a Febrile UTI should undergo Renal & Bladder U/S (RBUS) to evaluate for hydronephrosis and ureteral dilation, which can suggest underlying anatomic abnormality, like VUR* -RBUS can be delayed until a second febrile UTI in *children ≥2yo* d/t a lower risk for anatomic abnormalities, which usu causes complications at an earlier age -An *abnormal RBUS or Recurrent Febrile UTIs* should undergo a *Voiding Cystourethrogram* to identify potential VUR, which *often requires TX with daily PPX ABX, with TMP-SMX, TMP alone, or Nitrofurantoin*

Subarachnoid Hemorrhage (SAH) 2º to a Ruptured Saccular (Berry) Aneurysm

-*SAH is most often the result of a RUPTURED SACCULAR (BERRY) ANEURYSM* -SAH typically p/w *SUDDEN onset of a Severe HA* and sometimes accompanied by *N/V, brief LOC, focal neurologic deficits, and/or other signs of meningeal irritation* (e.g. *neck stiffness, photophobia*) -*EXERTION* (e.g. climbing stairs) can *cause aneurysm rupture* -An *abruptly worsening HA different in intensity & location from usual HA pattern* (e.g. generalized vs occipital) *is also worrisome* -SAH is often *the worst HA of their life* -*URGENT Noncontrast HEAD CT* is the *preferred initial diagnostic test for SAH*; esp sensitive in the first 6hrs for DX SAH, but as blood degrades, CT less sensitive -Therefore, *LUMBAR PUNCTURE* is *required to completely R/O SAH in pts w/ negative CT but w/ concerning SX* -*Typical SAH CSF findings* incl *XANTHOCHROMIA* (yellow or pink tint d/t Hb degradation), *Significantly elevated INTACT RBCs (1000s) in 4 CSF tubes* (vs declining RBCs in a traumatic tap), *& Elevated Opening Pressure* Note: Brain MRI has sensitivity & limitations similar to Head CT for diagnosing SAH, so MRI is not a useful study after a negative CT scan. Urgent LP is the next best choice

Small Intestinal Bacterial Overgrowth (SIBO) - Sx & TX

-*SIBO* is *characterized by the proliferation of bacteria in the small intestine* -It is a *common complication of Roux-en-Y gastric bypass surgery* -It causes *mucosal inflam & damages brush border enzymes (e.g disaccharidases), leading to Nutrient Maldigestion, decr Vit B12 (bacterial consumption), incr folate (bacteria synthesis), Water & Electrolyte Secretion* --> *Chronic Watery Diarrhea* -Bacterial fermentation of carbs --> *Excess gas (hydrogen, methane) formation - Bloating, Flatulence* -*Bacterial deconjugation of bile acids, causes impaired fatty acid absorption & direct irritation to enterocytes* -*SIBO & Sx improve w/ ABX (Rifaximin, Amoxicillin-Clavulanic Acid, fluoroquinolones, Metronidazole), BUT RECURRENCE is Common* and *repeat ABX courses may be necessary*, and *long-term prophylactic ABX can be considered for those w/ frequent recurrences*

Stress Urinary Incontinence (SUI)

-*SUI based on Urinary Leakage w/ Valsalva* and a *Positive Cough-Stress test* -SUI is typically a *sequelae of pelvic trauma (e.g. Vaginal Delivery), Age-related connective tissue loss, or Chronic Elevated Intraabdominal Pressure (e.g. high-impact exercise, like heavy weight-lifting)* -- all these can cause *inadequate urethral support* -With inadequate urethral support, the *urethra becomes hypermobile & is unable to close adequately* -SUI is a *common cause of urinary incontinence in YOUNGER women* -*Additional RF for Stress Urinary Incontinence* incl *Obesity, increased parity, tobacco use, caffeine use* -*Initial TX* for SUI incl *pelvic floor mm Kegel exercises & lifestyle modifications* such as *caffeine restriction, weight loss, & smoking cessation* -Limiting water intake to 2L (0.53 gal) daily will improve both frequency & SUI sx -If do NOT improve w/ conservative measures, *surgical management w/ mid-urethral sling procedure* Note: *Overflow Urinary Incontinence* can be caused by *bladder outlet obstruction & p/w constant urinary dribbling, weak urinary stream, & incomplete bladder emptying*--OUI usu occurs in Men w/ BPH, or in Women as a *complication of mid-urethral sling procedure* Note: *Detrusor M Overactivity* is a cause of *Urgency Urinary Incontinence (i.e. Overactive Bladder)*, which typically p/w *sudden, overwhelming urge to void followed by an involuntary loss of urine* Note: *Intrinsic sphincteric deficiency*, a *urethral sphincter weakness that prevents the urethra from closing completely* is the *result of Neuromuscular Damage* that typically occurs during *pelvic surgery or vaginal delivery*

Treatment for Toxic Shock Syndrome

-*SUPPORTIVE therapy!* -Remove any potentially-associated foreign bodies (e.g. nasal packing, tampon) -May need *EXTENSIVE FLUID REPLACEMENT*, which can reach 20L/d -Administer *IV CLINDAMYCIN (prevent TSS toxin-1 synthesis by S. aureus) ± Antistaphylococcal Antimicrobials (VANCOMYCIN, or OXACILLIN/NAFCILLIN if susceptible) to Eradicate S. aureus organism and Prevent TSS Recurrence* Note: Corticosteroids do NOT seem to affect mortality and are NOT routinely recommended TSS can cause a diffuse rash involving palms & soles

Malingering

-*SX are INTENTIONAL, Motivation is INTENTIONAL* -There is *clear evidence of External GAIN in Malingering* -Patient *Consciously FAKES, Profoundly EXAGGERATES, or Claims to have a Disorder IN ORDER to attain a Specific 2° (EXTERNAL) GAIN* (e.g. *Avoiding work, Obtaining compensation*). -*POOR Compliance w/ TX or F/U of diagnostic tests. -*Complaints CEASE AFTER GAIN* (vs Factitious Disorder,, where pts Intentionally cause Sx for Internal 1° Gain in order to assume the "sick role" to get medical attention and sympathy).

TX of Salmonellosis

-*Salmonellosis, caused by Salmonella enteritidis, generally does NOT need to be TX w/ ABX in ImmunoCOMPETENT pts age 12mo or older* -*Symptomatic* pts should be given *replacement fluid and electrolytes, as they are at risk for dehydration* -*Since the gastroenteritis is usu Self-Limited and ABX has NOT been shown to hasten Sx resolution or improve the rate of Salmonella clearance from stool, ABX is NOT recommended for Immunocompetent Adults or Children ≥1yo--only need Supportive Therapy & Observation* -*Preemptive ABX therapy is warranted in pt groups at greater risk for complications* --incl *children <12mo (esp neonates) & ImmunoCOMPROMISED adults*; can also give ABX to *adults >50yo w/ known atherosclerotic disease* (more prone to dev bacteremia & endovascular infection) -*Effective ABX for Salmonella enteritidis* incl *Ciprofloxacin, TMP-SMX, & Ceftriaxone*

Constitutional Small for Gestational Age (i.e. Constitutional Small Growth)

-*Variant of Normal growth* -Neonate is *small in length & weight d/t GENETICS (i.e. small parents)*

Scabies

-*Scabies is a highly contagious dz* caused by *mite infestation by Sarcoptes scabiei mite, which burrows into skin & spreads through direct person-to-person contact* -Scabies usu p/w an *intensely PRURITIC RASH (often worse at night) in the flexor surfaces of wrist, lateral fingers, & finger webs, palms & soles* -- rash d/t delayed type 4 HS rxn to mite feces & ova -Scabies can also involve other body parts - *elbows, axillary folds, nipples & areola, scrotum & penis*, but is UNCOMMON on head and back in adults -PE shows *excoriations w/ small, crusted, red papules scattered around with linear burrows* -Pts can dev *small vesicles, pustules, wheals, & excoriations that obscure classic burrows in skin* -*DX Confirmed by SKIN SCRAPINGS UNDER LIGHT MICROSCOPY showing Mites, Ova, & Feces* -Treatment to eradicate mites, decr pruritus d/t dermatitis, & prescribe oral ABX for any secondary bacterial skin infections -*TX: TOPICAL 5% PERMETHRIN CREAM* over the whole body (excluding head) is *preferred for eradicating mites of scabies* -*Oral Ivermectin* is an acceptable alternative, esp for outbreaks in nursing homes or other facilities -Oral Antihistamines to decr dermatitis & assoc itching, and Topical Steroids for persistent dermatitis after mite eradication -All family members & close contacts should be TX at the same time to prevent re-infestation -Bedding & clothing should be cleaned

Scoliosis

-*Scoliosis* is the *lateral curvature of the spine*, and is *most commonly Idiopathic in ASX adolescents*. -Rarely, *Scoliosis is a Complication of Spinal Pathology* and *may be Life-Threatening* -- *Further Evaluation is Required if any of these RED Flags for a Pathologic Etiology are present*: • *Back pain* (e.g. causing *nocturnal awakening*) • *Neurologic symptoms* • *Rapidly progressing spinal curvature (≥10º/year)* • *Vertebral anomalies on x-ray* -Pts who develop scoliosis before menarche are at risk for further curvature progression E.g. of Pathologic etiology includes *spinal cord tumor*, which can extend & disturb surrounding nerves, causing constant "dull" or. "gnawing" back pain; and can cause impingement of spinal cord pathways, leading to dysesthesias (abnormal sensations), weakness, & neurogenic bladder/bowel Other pathologic causes of scoliosis include *infection and trauma* -*Diagnostic Workup of Scoliosis* often *begins with x-ray of the spine*, which may show abnormalities such as *vertebral lucencies, pedicle erosion, or widened canal.* -- HOWEVER, *MRI of SPINE* is the *GOLD STANDARD* to delineate spinal anatomy. Note: The degree of spinal curvature on x-ray determines the severity of scoliosis, but does NOT correlate with idiopathic vs pathologic etiology. Note: Certain genetic disorders involving tissue formation such as *Neurofibromatosis, Marfan Syndrome, & Osteogenesis Imperfecta* can cause *syndromic scoliosis*

Interpreting DXA T-Score

-*Screening for OSTEOPOROSIS using Dual Energy X-ray Absorptiometry (DXA)* is *recommended for Women ≥65yo and for Younger Premenopausal women w/ additional RF for Osteoporosis (e.g. current smoking, FHx of hip fracture)* -Measured with a *T-score* • T-score *-1.0 or greater* = *Normal* • T-score *-1.0 to -2.5* = *Osteopenia (low bone mass)* • T-score *-2.5 or less* = *Osteoporosis* • *HX of Fragility Fracture* (fracture that results from a fall from standing height or less) = *Also Osteoporosis*

Seborrheic Dermatitis TX

-*Seborrheic Dermatitis includes DANDRUFF, is a type of eczema p/w *mild erythema w/ greasy scales* (aka Cradle Cap) -Typically seen at the *scalp, ears, & facial skinfolds* and is rare on the legs -*TX w/ SELENIUM SULFIDE*

Secondary Hyperparathyroidism

-*Secondary Parathyroid Hyperplasia d/t DECR Ca2+ Absorption &/or INCR PO4 --> Compensatory Rise in PTH d/t HYPOCALCEMIA* -- *DECR Ca2+, Incr ALP, INCR PTH* -MCC seen in pts with *CHRONIC KIDNEY DISEASE* (e.g. *diabetic nephropathy*) which causes *hypovitaminosis D & hyperphosphatemia --> Decr Ca2+ Absorption* -*CKD --> HYPOcalcemia + HYPERphosphatemia* -Long-standing secondary hyperparathyroidism can lead to *parathyroid hyperplasia & refractory/autonomous PTH secretion (tertiary hyperparathyroidism)* -- *V.INCR PTH, Hypercalcemia*

Molluscum Contagiosum (MC)

-*Self-limited, localized skin infection* caused by a *POXVIRUS* -Characterized by *small skin-colored papules w/ indented centers* that may occur anywhere EXCEPT the palms & soles -The lesions may be accompanied by *pruritus and surrounding dermatitis* -Children are most commonly affected, but adolescents, adults, & immunocompromised individuals can also dev MC -Transmission is through *skin-to-skin contact* or *contact w/ contaminated fomites* -MC is often transmitted through *sexual contact* and may be seen in assoc w/ other STDs -It is *freq seen in HIV* pts and may be *more widely disseminated and persistent* in these pts -*HIV testing* should be considered in pts w/ MC, esp for lesions that are widespread or involve the *face* -MC DX is Clinical -Typically *self-limited, but tx may be considered to prevent further spread, reduce sx, or improve cosmesis* -Removal techniques incl physical destruction via *curettage/cryotherapy* or *chemical removal w/ topical agents* (e.g. *Podophyllotoxin*)

Shigella dysenteriae Gastroenteritis & HUS Complications

-*Shigella dysenteriae Gastroenteritis* p/w *several days of bloody mucoid diarrhea (watery becomes bloody) & crampy abdominal pain* -Most pts have *self-resolved* sx within a week; but sometimes can develop *anemia, thrombocytopenia, & renal insufficiency (Incr BUN/Cr)* -- the *triad for Hemolytic Uremic Syndrome* -*Uncomplicated* Shigella gastroenteritis is typically *TX w/ ABX to reduce sx severity* (e.g. frequency of bloody diarrhea, abdo pain) *decr duration of ASX shedding after acute illness* (contrast to E.coli O157:H7 diarrhea where HUS risk is increased w/ ABX); *Tx Uncomplicated w/ Ceftriaxone* >> Ciprofloxacin -HUS is mediated by *Shiga toxin* produced by either *Shigella dysenteriae or E.coli O157:H7* -Shiga toxin travels from the *disrupted intestinal epithelium to the bloodstream*, causing *damage to vascular endothelium* -This *microvascular injury promotes dev of Microthrombi*, esp within the *glomerular endothelial cells*, leading to *Renal Insufficiency (e.g. oliguria; Incr BUN/Cr)* -Intravascular shearing of RBCs results in *Non-Immune Hemolysis* which leads to *pallor, tachycardia, anemia, & fragmented RBCs on PBS, incr bilirubin* -Similarly, *platelet destruction* (in addition to *excessive platelet activation*) leads to *Thrombocytopenia* -*CNS involvement* (e.g. *lethargy, poor arousability, seizure*) can occur rarely -Management of HUS is *supportive*, including *PRBCs &/or PLT transfusions* -CAUTIOUS fluid replacement or restriction (d/t renal insufficiency) is needed to maintain intravascular volume, and Dialysis needed for severe kidney injury -*ANTIBIOTICS ARE CONTRAINDICATED IN HUS TX* as bacterial killing can lead to *increased release of Shiga toxin*

Vestibular Neuritis

-*Vestibular Neuritis* is an *INFLAMMATORY disorder affecting the Vestibular Branch of CN VIII (Vestibulocochlear N, originating from Pons)* that classically *Follows a VIRAL Infection* -Vestibular neuritis can be assoc with *Rapid-Onset, Significant N/V, & Gait Impairment, BUT SX RESOLVE WITHIN DAYS*

Management of Shoulder Dystocia

-*Shoulder dystocia* occurs when the *anterior fetal shoulder does NOT deliver w/ usual obstetric maneuvers (e.g. gentle downward traction of fetal head)* -Shoulder dystocia usu presents with the *retraction of the fetal head against the maternal perineum, immediately after delivery ("turtle sign")* -Shoulder dystocia is an *OBSTETRIC EMERGENCY* assoc with *incr fetal risk for brachial plexus injury, clavicular or humeral fracture, hypoxic encephalopathy, & death* -*Maternal complications* of shoulder dystocia incl *pelvic injury (e.g. fourth-degree perineal laceration) & postpartum hemorrhage* -*RF* for Shoulder Dystocia: *prior shoulder dystocia, diabetes, maternal obesity, fetal macrosomia, postterm pregnancy, & operative vaginal delivery* -Shoulder dystocia is *caused by impaction of the anterior fetal shoulder behind the maternal pubic symphysis*; it is *managed* by *performing maneuvers that help disimpact the anterior shoulder* -First maneuver is the *McRoberts Maneuver -- maternal hips are HYPERFLEXED*, helps to *decr obstruction thru bony pelvis by rotating the public symphysis cephalad and flattening the sacral promontory* -The *combination of McRoberts + Suprapubic Pressure* freq *relieves shoulder dystocia w/ no additional maneuvers required* Note: Pushing the fetal head back into the pelvis and performing an emergency C-section (Zavanelli maneuver) is indicated when all other maneuvers fail

Aplastic Crisis in Sickle Cell Disease

-*Sickle cell disease (SCD)* is characterized by abnormal hemoglobin chains that result in decreased lifespan of RBCs and chronic anemia* -- pts *compensate for this by INCR Erythropoiesis & an ELEVATED RETICULOCYTE COUNT* -*Aplastic Crisis* in SCD is characterized by *Sudden Cessation of Erythropoiesis with a Very LOW RETICULOCYTE Count (less than 1%) and resultant Acute, Severe, ANEMIA* -*Parvo B19*, which preferentially attacks erythroid precursors, is the *MCC of an aplastic crisis in SCD* *Blood Transfusions are the mainstay of TX* while Erythropoiesis recovers Note: *Aplastic Crises in SCD DIFFER FROM Aplastic Anemia, which occurs in pts W/O SCD, and aplastic anemia is characterized by pancytopenia*

Fetal Postmaturity (Dysmaturity) Syndrome

-*Signs* of Fetal Postmaturity Syndrome: *Wrinkling, peeling skin; long fingernails; thin fingers; & small for gestational age*; other signs incl a *long, thin body; decr subQ fat; sparse lanugo hair; & excessive scalp hair* -Occurs in *fetuses ≥42wks gestation* -After 40wks, the *placental fxn deteriorates* and is *no longer able to supply adequate O2 and nutrition to the fetus*, leading to *fetal malnutrition & wasting* -*Placental Insufficiency* can also lead to *fetal hypoxia, oligohydramnios, & umbilical cord compression*, increasing the risk for *fetal heart rate abnormalities (e.g. Late Decelerations)* and *In Utero Meconium Passage* (i.e. *green-stained membranes*) -*Neonatal complications* of fetal postmaturity/dysmaturity syndrome incl *meconium aspiration, resp distress, hypoglycemia, & seizures*

Complications of Acute Inferior Wall Myocardial Infarction

-*Sinus BRADYCARDIA & Atrioventricular Block* are commonly seen w/ acute Inferior wall MI and are explained by *an increase in vagal tone* (May see ST-elevations in leads II, III, & avF) -In the setting of acute inferior MI, *bradyarrhythmias* are typically *transient* and *often, but not always, responsive to IV Atropine* -In pts w/ *persistent symptomatic bradyarrhythmia* (e.g. *hypotension, dizziness, HF, syncope*) that are *NOT responsive to Atropine*, use *Temporary Transcutaneous, followed by Transvenous, CARDIAC PACING* -Once cardiac pacing is initiated, the pt w/ STEMI should be taken for *urgent revascularization by percutaneous coronary intervention* Note: In contrast to pts w/ inferior wall MI, *bradyarrhythmias assoc w/ Anterior wall MI* are commonly d/t *damage to the conduction system below the AV node*; *AV Block* in this setting is *unlikely to respond to atropine* -Norepinephrine stimulates both alpha-adrenergic & beta-1 adrenergic receptors, causing vasoconstriction & incr HR and contractility - leads to marked increase in myocardial O2 demand and there therefore *avoided* in acute MI pts

MOA of SGLT-2 Inhibitors

-*Sodium-glucose cotransporter-2 inhibitors (CANAGLIFLOZIN, EMPAGLIFLOZIN) DECR Renal Reabsorption of GLucose and Sodium* --> *Leading to INCR Urinary Glucose Excretion & Lower Blood Glucose levels* -Additionally. the *decr reabsorption of Na* --> *Natriuresis & Osmotic Diuresis, which DECR Systemic Blood Pressure, Decr extracellular fluid volume, & Decr total body sodium content* -Incr tubular sodium delivery to macula densa --> *Decr activation of Renin-Angiotensin-Aldosterone system* --> *Decr Angiotensin II & Aldosterone production* --> *Decr Angiotensin II Activity Reduces Constriction in the glomerular Efferent arteriole* --> *DECR GLOMERULAR FILTRATION PRESSURE, DECR HYPERFILTRATION, & DELAYS PROGRESSION OF DIABETIC NEPHROPATHY* Note: Bc SGLT-2 inhibitors cause reduced aldosterone prodn, this leads to reduced potassium excr, and *incr plasma potassium levels*. *Clinically significant hyperkalemia* is a *possible AE, esp in those w/ baseline kidney impairment*

TX for pts with *Somatic Symptom Disorder*

-*Somatic SX Disorder* is when *pts have ≥ 1 bodily complaints (eg, abdominal pain, fatigue) for ≥6mo* and pts have *excessive, persistent thoughts and anxiety about sx* -*TX: *Psychotherapy + REGULAR OFFICE VISITS* (e.g. monthly) *WITH THE SAME PHYSICIAN*, who can *dev a trusting physician-patient relationship* -In contrast to symptom-driven visits, regular visits decrease overall health care use -Doctors should *tx the sx conservatively and focus on the pt's functioning* -*Once a trusting physician-pt relationship is dev, strategies incl Educating the pt about the interaction of psychosocial stressors and somatic sx, & prompting stress reduction and healthy behaviors - e.g. diet, exercise, return to productive activities* -The physician *must validate the pt's physical distress and provide reassurance that serious medical illness has been ruled out* -Don't want to be dismissive or refer to a psychiatrist too early in the relationship, pt will feel invalidated and rejected

Spinal Epidural Abscess (SEA)

-*Spinal epidural abscess* is *caused by hematogenous spread of bacteria from a distant source (e.g. endocarditis), contiguous tissue infxn (e.g. vertebral body osteomyelitis), or direct inoculation (e.g. Steroid Injections, epidural anesthesia)* -Other *RF* for SEA incl *IVDU & Immunocompromised states* like *DM, excessive alcohol use, & HIV* -*STAPH AUREUS* accounts for 60% of infections by pyogenic bacteria -*Classic Triad of SX* = Days to weeks of *Fever* (may not be present) + *Severe FOCAL Spinal Pain* (e.g. lumbar spine) + *Neurologic Deficits/Dysfunction* -As Sx progress, pts can dev *radiculopathy, motor & sensory deficits, bowel or bladder dysfunction (e.g. decr rectal tone or urinary incontinence), & eventual paralysis* -Initial Eval incl: *CBC, ESR & CRP, blood cx, URGENT SPINAL MRI W/ CONTRAST* (if cannot undergo MRI, can do *CT myelography*); *CT-guided aspiration & culture, and ABX* -Most pts *TX w/ IV ABX (VANCOMYCIN + CEFTRIAXONE) & Emergency Surgical Decompression (preferably within 24hrs) to Avoid Complications of Cord Compression (affects multiple adjacent spinal levels) or Cauda Equina Syndrome*

Spondyloarthropathies - Reactive Arthritis

-*Spondyloarthropathies* are a *group of disorders* characterized by *sacroiliitis, peripheral asymmetric oligoarthritis, dactylitis, & enthesitis* (entheses are the insertion sites of tendons and ligaments to the bone surface) -*Reactive Arthritis (ReA)* is a spondyloarthropathy that p/w *Peripheral Asymmetric OLIGOarthritis*, often *assoc w/:* • *Uveitis* - bilateral eye pain, irritation, blurry vision, bilateral conjunctival injection • *Urethritis* - burning urination • *Achilles enthesitis* - pain at ligament/tendon insertion • *Dactylitis* • *Keratoderma blennorrhagica* - skin lesions appearing like psoriasis (flaky, peeling skin) that appear first on palms & soles, but may eventually spread to scalp, torso, genitals • *Circinate balanitis* - serpiginous ring-shaped dermatitis of glans penis -*Reactive Arthritis* usu *occurs after a genitourinary* (e.g. *Chlamydia*) *or gastrointestinal* (e.g. *Salmonella, Shigella, Yersinia, Campylobacter*) *infection* -*Elevated WBC count (sign of inflammation) but NO PATHOGEN is ISOLATED on synovial fluid bacterial cultures from joint aspiration* -- some studies have reported *detection of Chlamydia DNA from synovial fluid by PCR* -The *risk of Reactive Arthritis after CHLAMYDIA Infection is ~4-8% in the general population* -However, the *risk is ~20% in HLA-B27 Positive pts* -- reason unclear -Conversely, only *30-50% of pts w/ Reactive arthritis are HLA-B27 positive, suggesting a complex etiology* -The incidence of ReA after Chlamydia infection or a Predisposing G(-) Rod is Higher in individuals who are HLA-B27 positive Note: *HLA-B27 is neither sensitive nor specific for Reactive Arthritis*

Causes & RF of Spontaneous Abortion

-*Spontaneous Abortion = Pregnancy Loss (Miscarriage) at <20wks gestation* -- its the *MC early pregnancy complication* -*RF*: • *Advanced Maternal Age >35yo* • HX of PRIOR Spontaneous Abortion* • Extremes in BMI • *Substance Use* Disorder -*Causes*: MCC of spontaneous abortion is a *fetal chromosome abnormality (e.g. aneuploidy, trisomy 16)* -Other common etiologies incl *Congenital Anomalies (e.g. Teratogens), Uterine Structural Anomalies (e.g. uterine Septum, uterine Leiomyoma), Infection (e.g. Toxoplasmosis), & Chronic Maternal Dz (e.g. THROMBOPHILIA, Thyroid Disorder, Diabetes Mellitus)* • *Antiphospholipid Syndrome* - 1º or 2º *autoimmune* disorder (most commonly in SLE); *DX* based on *clinical criteria* incl *Hx of thrombosis (arterial or venous), or Spontaneous Abortion* along with *Lab findings* of *Lupus Anticoagulant, Anticardiolipin, Anti-β2 glycoprotein I antibodies*; *TX w/ Systemic Anticoagulation* • *Factor V Leiden* : *Prodn of mutant factor V* that is *resistant to degradation by activated protein C*. *Complications incl DVT, cerebral vein thrombosis, recurrent pregnancy loss* -There is *NO WAY TO PREVENT Spontaneous Abortions, but some RF can be minimized*

*Stage 2 Hypertension* Definition When would you need a *2-drug Antihypertensive Regimen*?

-*Stage 2 HTN* is defined as *systolic BP ≥140 and/or diastolic BP ≥90* -In pts whose *BP is ≥20/10 mmHg above goal*, best to start TX HTN with a *2-drug antihypertensive regimen* -The initial period requires close f/u to monitor for AE (e.g. orthostatic hypotension) caused by combination antihypertensive therapy -*First-line Antihypertensives* chosen from 4 classes of medications: *Thiazides, CCBs (amlodipine dihydropyridine), ACEI, ARBs* -*ACE Inhibitors SHOULD NOT be used with ARBs d/t RISK for HYPERKALEMIA & NEPHROTOXICITY* -Combination of *ACE Inhibitor + CCB* is *particularly effective* and the ACE-I can minimize the edema assoc w/ CCBs

Statin-Induced Myopathy

-*Statin therapy is an effective TX for hypercholesterolemia* and is *recommended for secondary prevention of cardiovascular events* in *ALL pts w/ known coronary heart disease* -*Statin-induced myopathy* is the MC complication of statin use and can range from ASX elevation of serum CK levels to Rhabdomyolysis -Statins can also *potentiate muscle injury w/ elevation of CK levels* in pts w/ an episode of prolonged vigorous exercise -Pts w/ *symptomatic myopathy* from statin use should *discontinue* therapy -In *ASX* pts, a *CK level >10x the upper limit of normal* is considered an indication for *discontinuation of statin* therapy -Pts should have their serum *CK levels rechecked* to ensure that they are *normalized PRIOR to REstarting therapy w/ statins* -This will *confirm resolution of the initial injury and avoid confounding future assessment* in case the pt were to dev recurrent sx

When would you use stratified analysis?

-*Stratified analysis* refers to *analyzing pts based on the presence or absence of a certain variable* -It can be used to *control confounding factors* and *distinguish b/w confounding and effect modification*

Preventing Neonatal GBS Infection

-*Streptococcus agalactiae (group B strep)* is a *common colonizing organism in GI & genital tracts*, and is the *MCC of Neonatal Infection in the First WEEK of Life (e.g. Meningitis, PNA, Sepsis)* -*Neonatal GBS Dz Prevention involves identifying colonized moms during pregnancy and Decreasing the Rate of Vertical Transmission via Intrapartum ABX* -Pregnant pts are *Screened @36-38wks gestation for GBS colonization via Rectovaginal Culture* -*Positive Culture* --> *Require Intrapartum ABX PPX* -Additional pt populations *requiring intrapartum ABX PPX d/t a High incidence of Early-Onset GBS Disease incl*: ● *UNKNOWN GBS STATUS PLUS Any of the Following*: • *Preterm delivery, <37wks* • *Ruptured Membranes for ≥18HRS at ANY gestational age* (if less than 18hrs, don't need abx ppx) • *Intrapartum Fever* (e.g. Intraamniotic infection) ● *GBS Bacteriuria in CURRENT pregnancy* ● *PRIOR pregnancy Complicated by Early-Onset Neonatal GBS Dz* (e.g. meningitis, sepsis, PNA) -*IV PENICILLIN* is the ABX of Choice *for intrapartum GBS PPX* and is *Most Effective when Initiated ≥4hrs PRIOR to Delivery* -Membrane rupture does NOT alter the efficacy of ABX PPX for neonatal GBS disease prevention -- *ABX PPX w/ IV Penicillin is Beneficial w/ PROLONGED ROM (≥18HRS) bc it DECREASES the Risk for Vertical Transmission of GBS* Note: C-section does NOT reduce the risk for Neonatal GBS dx and is reserved for standard obstetric indications (e.g. labor arrest, fetal heart rate abnormalities, breech presentation)

Asymptomatic Subclinical Hypothyroidism

-*Subclinical Hypothyroidism* is defined as a *Mild Elevation in TSH levels (5-10)* along with *Normal Free T4 levels* -TX is warranted in the presence of: • *Antithyroid antibodies (e.g. anti-TPO)* • *Abnormal lipid profile* • *SX of hypothyroidism* • *Ovulatory & menstrual dysfunction* -When antithyroid antibodies are present w/ elevated TSH, there is a high chance for the pt to /become overtly hypothyroid/ -Pts w/ TSH>10 are also generally tx w/ levothyroxine -Downside of tx ASX pts is the risk of overtreatment, leading to increased bone loss and A-fib

Acoustic Neuromas (Vestibular Schwannomas)

-*Vestibular schwannomas/acoustic neuromas* can *cause Unilateral SENSORINEURAL Hearing LOSS*, sometimes with *imbalance & tinnitus* -However, *SX are usu PERSISTENT & PROGRESSIVE, rather than episodic*, and *true vertigo is NOT typical* bc the *slow growth* often *allows for dev of compensation*

Treatment of Syphilis

-*Syphilis infections* are *characterized by periods of Latency and periods of Active Dz* -*TX* must be *targeted to the current stage* of illness, which is typically determined by: • *SX* • *Duration of Infxn (if known)* • *CSF Evidence of Neurosyphilis* -*LATENT Syphilis* is *defined as Serologic evidence of Infection with NO clear evidence of primary, secondary, or tertiary disease* *TREATMENT:* -Pts with *Primary, Secondary, or EARLY Latent (<12mo if infection)* should *receive a SINGLE DOSE of IM Benzathine Penicillin G* -Pts with *Gummatous/Cardiovascular Syphilis, LATE Latent Syphilis (infection ≥1yr), or Syphilis for an UNKNOWN Duration* should *receive IM Benzathine Penicillin G WEEKLY for 3WKS* -Pts with *Neurosyphilis* should *receive *IV Aqueous Crystalline Penicillin G q4hrs for 10-14 days* -Pts with *Congenital Syphilis* should *receive IV Aqueous Penicillin G q8-12hrs for 10 days* -Pts with *Tertiary Syphilis (other than neurosyphilis) who have Anaphylactic Rxns to Penicillin* can be *TX with 2 WKS of CEFTRIAXONE* -Pts with *Anaphylactic Penicillin Allergies who have LATE LATENT Syphilis or LATENT Syphilis of UNKNOWN DURATION* can receive *Alternate TX with DOXYCYCLINE for 28 DAYS*

When to do an LP for syphilis?

-*Syphilis* is an *STD caused by the spirochete Treponema pallidum* -*Hematogenous dissemination* of the spirochete *occurs Early in the dz course* and freq leads to *seeding of the CSF* -*Although nervous system infection is usu ASX at first and may clear spontaneously, any pt who has NEUROLOGIC SX (e.g. HA, blurred vision) REQUIRES A LUMBAR PUNCTURE to Evaluate for NEUROSYPHILIS* -Pts with *HIV are at greatest risk for dev Neurosyphilis, ESP when CD4 counts are <350 & rapid plasma reagin (RPR - nontreponemal testing) titers are >1:128* -*DX* is usu *Confirmed when CSF analysis* reveals an *Elevated Leukocyte count (>5) & Positive VDRL or Fluorescent Treponemal Antibody Absorption (FTA-ABS) testing* -If neuro sx/signs present, must do an LP to evaluate for neurosyphilis *PRIOR to consideration for TX* -If *NO neurologic sx, then DON'T need additional LP testing, and can Proceed to TX based on the Stage of Syphilis*

Temporomandibular Joint Disorder (TMD)

-*TMJ Disorder* can p/w *spasms, jaw fatigue, & pain* - however, the *pain & muscle spasms of TMD are NOT usu so severe as to cause abnormal posturing or inability to speak*, unless it dislocates the jaw -The *facial pain* is a *dull, UNILATERAL, facial ache that is constant, but waxes & wanes in intensity* and is *aggravated by jaw motion* -*TMJ disorder pts usu have Headaches, Jaw fatigue, & exacerbation of sx w/ jaw movement* -Other common symptoms include *earache, headache (typically frontal or temporal and often radiating to the jaw)*, and *jaw &TMJ dysfunction* (eg, *decreased mandibular range of motion, clicking with jaw movement, intermittent jaw locking*). -Clinical DX, usu doesn't need imaging -Initial management with *education, self-care measures, optimal head posture, jaw exercises, proper sleep hygiene, & avoidance of triggers (e.g. oral behaviors)* -For *persistent Sx despite education*, can use *adjunctive pharmacotherapy*: • *NSAIDs are First-line*: Usu a 2wk course of long-acting NSAID (e.g. naproxen) • For *tenderness w/ mastication mm*: *NSAID + skeletal muscle relaxant* for 2wks • *For persistent TMD sx that warrant continued adjunctive pharmacotherapy* --> *TRICYCLIC ANTIDEPRESSANTS, NORTRYPTILINE* -If refractory to pharmacotherapy/noninvasive management, can try botulinum toxin injections, or surgical referral

*Varicella Vaccine Schedule* for prevention of chickenpox (primary varicella infection)

-*TWO-doses of varicella vaccine given* - *LIVE ATTENUATED VACCINE* *FIRST Dose @12-15mo of age* (minimum age 12mo) *SECOND Dose @4-6yo* (can be given earlier than 4yo, like during a varicella outbreak) -VZV vaccination is *recommended in all children ≥12yo unless* there is an *absolute contraindication to live virus vaccines* -For children <13 years, the recommended minimum interval between doses is 3 months -Children age <13 years who have received <2 doses of varicella vaccine should receive one or two doses as necessary to be "caught up" -Adolescents ≥13 years and adults who have not received varicella vaccine and have no evidence of chickenpox should receive two doses of single-antigen varicella vaccine, separated by four to eight weeks *CONTRAINDICATIONS to Live Virus Vaccines*: -*Immunocompromised* (e.g. on immunosuppressive therapy/chemotherapy, T-cell immunodeficiency) -*Pregnancy* -*Hx of Severe Allergic Rxn (anaphylaxis) to vaccine component* -A *transplant recipient on immunosuppressive therapy should NOT receive live virus vaccines, but Healthy Household Contacts of immunocompromised SHOULD be vaccinated* -*ASX VZV vaccine recipients do NOT need to be isolated from immunocompromised* -Rarely (~3%), recipients can develop a *vaccine-assoc VZV rash caused by the attenuated VZV vaccine strain*, presents *within 1-3wks of vaccination* as a *mild maculopapular/vesicular rash* -- *if VZV rash develops, recipient should Isolate d/t potential transmission to immunocompromised persons*

What is heterogeneity testing?

-*Tests for heterogeneity are useful when performing a Meta-Analysis of several trials, or comparing different trials, to provide insight about the combinability of multiple studies* -Common tests for heterogeneity incl the *Q Statistic, which results in a corresponding P value* • Remember, the null hypothesis, H0, denotes that there is NO difference b/w the groups studied • A *small significant P value (no heterogeneity if P<0.05)* --> *Suggests there IS a difference* and H0 should be rejected. • However, a *large insignificant P value (>0.05)* --> *Suggests there is NO difference b/w the groups* and so H0 is NOT rejected. -Another commonly used heterogeneity test is the *I² index* (derived from the Q statistic) -An *I² index = 0, represents NO heterogeneity* - *I² <25% represents LOW heterogeneity* (i.e. <25% of the variability seen is d/t true heterogeneity) -The cutoffs for *moderate and high heterogeneity are I² = 50% & I² = 75%, respectively*

Thionamides for Hyperthyroidism During Pregnancy

-*Thionamides* are the *TX of choice for hyperthyroidism (e.g. Graves) during pregnancy*, since *both radioiodine & thyroidectomy surgery should be AVOIDED* *Propylthiouracil (PTU) SHOULD be used in the FIRST trimester* bc of the *teratogenic effects with Methimazole* -- incl *scalp defects, tracheoesophageal fistula, & choanal atresia* -- PTU carries less risk of birth defects -For the *Second & Third Trimesters*, can *Switch BACK TO Methimazole* because *PTU carries a risk of liver failure* Note: *Surgery* can be considered for pregnant pts with *severe sx despite thionamide use*, but in general, an attempt should be made to avoid surgery during pregnancy. Note: *Radioiodine therapy is absolutely CONTRAINDICATED during pregnancy* because it can *ablate the fetal thyroid gland*

Preeclampsia

Definition: -New onset HTN (SBP >/= 140 and/or DBP >/= 90) at >/= 20wks gestation PLUS -Proteinuria and/or end-organ damage Severe features: -SBP >/= 160 or DBP >/= 110 (2x, >/= 4hrs apart) -Thrombocytopenia -Incr creatinine -Incr transaminases -Pulm edema -Visual or cerebral sx Management: -W/o severe features: Delivery at >/= 37wks -W/ severe features: Delivery at >/= 34wks -Magnesium sulfate (seizure ppx) -Antihypertensives

Thrombolysis in Acute Ischemic Stroke

-*Thrombolysis greatly DECR Poststroke Disability, but its EFFICACY is TIME-DEPENDENT (i.e. Time is Brain!)* --e.g. w/ *Alteplase, Tenecteplase* -Thrombolysis administration is urgent, so delays in tx should be minimized -*Intravenous Thrombolysis* is the *mainstay of TX for Acute Ischemic Stroke*, provided that *TX is Initiated WITHIN 4.5HRS of clearly defined symptom onset!!!!!* ● If the *exact time of stroke onset is NOT known*, it is *defined as the last time the patient was known to be normal or at neurologic baseline* -Because the *benefit of is time-dependent, it is critical to treat patients ASAP* -*Strict Blood Pressure control is CRITICAL PRIOR to and DURING the first 24hrs After Thrombolytic Therapy* -- *BP must be ≤185/110 Before Starting TX and must be Maintained ≤180/105 for 24hrs following thrombolytic TX* *Contraindications to Receiving tPA Thrombolytic Therapy* -Pt w/ *ischemic stroke or severe head trauma in last 3mo, previous intracranial hemorrhage, intracranial neoplasm, GI hemorrhage in last 3wks, intracranial/intraspinal surgery in last 3mo* -*Sx of Subarachnoid Hemorrhage, Persistently Elevated BP (systolic ≥185 or diastolic ≥110), Active internal bleeding, Infective Endocarditis presentation, Acute bleeding diathesis (e.g. von Willebrand dz, Hemophilias)* -*Current anticoagulation use w/ INR >1.7 or PT >15sec or APTT >40sec; Current use of Direct thrombin inhibitor or Direct factor Xa inhibitor w/ evidence of anticoagulant effect by lab tests* -*Head CT shows evidence of hemorrhage, or extensive regions of hypodensity consistent w/ irreversible injury*

Sequelae of *long-term Amiodarone use*

-*Thyroid dysfunction* (hypo- & hyperthyroidism) -*Hepatotoxicity* -*Cardiac Bradyarrhythmias, Heart Block, Heart Failure* -*Chronic Interstitial Pneumonitis, Pulmonary Fibrosis* -*Neurologic Symptoms* (e.g. *ataxia, peripheral neuropathy*) -*Blue-Gray Skin Discoloration*, resulting in *Photodermatitis* -*Visual Disturbances d/t Corneal Deposits*

Tinea Versicolor TX

-*Tinea versicolor, caused by Malassezia infection, p/w Discolored HYPOPIGMENTED Macules, predominantly on the Trunk* (usu not on legs) -*TX w/ SELENIUM SULFIDE*

Transverse Myelitis

-*Transverse myelitis is a neurological disorder caused by inflammation of the spinal cord; both sides of one section of the spinal cord( -Assoc with *segmental spinal cord inflam* that can result in *extremity weakness* -A *clear SENSORY LEVEL DEFICIT* (e.g. paresthesias) is often seen -Unlike in spinal epidural abscess, pts do not have focal vertebral tenderness

What lab abnormalities are caused by tumor lysis syndrome?

-*Tumor lysis syndrome (TLS)* as a *result of rapid lysis of neoplastic cells in response to chemotherapy/immunotherapy* -TLS is characterized by *several metabolic abnormalities* incl *HYPERPHOSPHATEMIA with assoc HYPOCALCEMIA d/t formation of Calcium Phosphate complexes, HYPERKALEMIA, & HYPERURICEMIA* -*RASBURICASE* (*urate oxidase analogue*, used for *increased clearance of uric acid into allantoin, that is excr in urine*) is *empirically administered w/ chemo/immunotherapy to Reduce serum Uric acid levels, THUS hyperuricemia is less common* and *helps to reduce likelihood of Acute Kidney Injury d/t renal tubular uric acid precipitation* • However, *AKI d/t calcium phosphate precipitation remains common* bc *rasburicase does NOT affect levels Ca2+ & PO4* -The *risk for calcium phosphate stone formation* can be *Reduced by PPX IVF to maximize GFR & urine output*

Type II Error

-*Type II Error represents FAILURE TO REJECT THE NULL HYPOTHESIS, WHEN THE NULL HYPOTHESIS IS FALSE* -Type II errors are *dependent on the power of a study, which in turn is dependent on sample size* *As sample size and power INCR, the likelihood of a type II error DECR*

Management of Thyroid Cancers

-*ULTRASOUND of Neck & Cervical Lymph Nodes is the Primary Modality for Initial STAGING of Thyroid Cancer* -*Management* of differentiated thyroid cancer (e.g. papillary, follicular) *depends on extent of dz, age, & comorbidities* -*Surgery is recommended* for differentiated thyroid cancer in pts who are *good surgical candidates, BUT the specific surgery & adjuvant therapies depend on the STAGE at DX* ● *Total Thyroidectomy* is *recommended for large papillary thyroid CA, Extra-Thyroidal tumor Extension, Distant Metastases, & in pts w/ Hx of Head/Neck Radiation Exposure* ● *More Extensive Neck Dissection* is *indicated* for pts w/ *Involvement of Adjacent Neck Structures or Regional LNs* ● *Papillary Ca <1cm (microcarcinoma) w/ NO LN involvement* usu have a *favorable prognosis* and may be managed w/ *simple Thyroid LOBECTOMY*

Management of Symptomatic Ureteral Stones

-*Uncomplicated (i.e. no signs of urinary infection [fever, normal UA] or AKI [normal Cr], with improvement of pain & nausea with IVF & analgesics) Ureteral Stone* can be *managed Conservatively as an OUTPATIENT with Oral Analgesics (NSAIDs) and Increased Oral Fluid Intake (>2-2.5L/d)* -The *addition of an alpha-blocker* (e.g. *Tamsulosin*) is *also recommended* d/t *stone size >5mm* -α1 adrenergic receptors are found along the length of the ureters & mediate smooth m contraction -- *Blocking these receptors can INCR ureteral smooth m RELAXATION, decreasing spasms (& reduce analgesic requirements) and Facilitate Stone Passage* -*α-blockers (TAMSULOSIN) are most effective for stones >5mm & ≤10mm* -- they do NOT provide any additional benefit for stones ≤5mm (which are likely to pass spontaneously) or stones >10mm) Note: IV (forced) hydration has not been shown to be superior to Oral hydration for pts who can tolerate oral fluids. Hospitalization until stone passage is unnecessary as time to passage may take days to weeks depending on stone size & location in ureter. Do NOT routinely need IV ABX for infection prophylaxis in nephrolithiasis. Note: *Hospital admission for surgical stone removal* is *indicated when the obstruction from stone is causing AKI or Anuria* or when there is *Concomitant Urinary Infection* Note: *Nephrolithiasis with Urinary Infection (fever, CVA tenderness, pyuria) is Urologic EMERGENCY that requires hospital admission for IV ABX & Urinary tract Decompression (e.g. Percutaneous Nephrostomy)*

Management of Vaso-Occlusive [Pain] Episode (VOE)

-*VOEs occur in sickle cell disease* -*VOEs are Acute episodes of Minor to Severe PAIN that typically affects the back, chest, abdomen, or extremities* -*Triggers* can incl *dehydration, infection, stress, weather changes, or menstruation* -*TX* often requires *hospitalization* and consists of *prompt admin of Oral or IV Pain Medication (NSAIDs, Opiates) & Gentle Rehydration* -*Outpatient* therapy usu incle *NSAIDs and Acetaminophen* for *mild pain* and *Oral Opiates (e.g. Oxycodone) for Moderate Pain* -*IV Opiates (e.g. Morphine)* are the *First-line TX in the ED* and should be given *within 30mins of arrival* -*Rehydration* is also a key component of *VOE management*, as *dehydration is known to cause sickling and worsen VOEs* -*IVF are indicated for hypovolemic or hypotensive pts as initial fluid resuscitation*

Hyperkalemia Manifestations

-*Weakness, muscle weakness/cramps, arrhythmias* (incl sinus bradycardia), & *cardiac conduction abnormalities on EKG* -Acute renal failure, NSAID use, & ACE-Inhibitor use (e.g. lisinopril) may lead to it -On EKG: • Initially manifests as *peaked T waves* • Subsequently manifests as *prolonged PR interval, widened QRS complexes, & disappearance of P waves* • Eventually a *sine wave* (fusion of wide QRS with T waves) -If see EKG manifestations , immediately TX with *IV CALCIUM GLUCONATE* which rapidly stabilizes cardiac membrane potential but its effect is short-lived -Also TX with *β-agonists (e.g. inhaled albuterol) and Glucose + INSULIN (bolus)* to reduce serum potassium by driving potassium Intracellularly

Wernicke Aphasia

-*Wernicke (RECEPTIVE) Aphasia* -*Wernicke area* in *LEFT Superior Temporal Gyrus of LEFT TEMPORAL Lobe* -Associated with *Impaired Language COMPREHENSION* -Patients *do NOT have insight* -- *they don't realize they're saying a bunch of words that don't make sense* *Wernicke* is a *word salad* and *makes no sense*

Hemophilia A Inheritance

-*X-linked Recessive inherited bleeding disorder* that is d/t *Deficiency in coagulation FACTOR VIII (8)* -Primarily *affects males*; *Heterozygous females are silent carriers* -When only the father is affected, he can transmit the affected X-Ch to ONLY his FEMALE children - therefore: ● *If the child is FEMALE, she will receive her Father's hemophilia X-Ch, and a healthy X-Ch from her mother --> therefore she will be a silent carrier of the disease* ● *If the child is MALE, he will receive his Father's Y-Ch and a healthy X-Ch from his mother --> therefore he will be Unaffected by the disease* -Thus, neither a male nor female child will likely be affected by the disease, but there are rare exceptions -- a female child can be affected if the mother was a silent carrier for hemophilia A, or if she has impaired gene expression of her normal X-Ch (e.g. 45,X Turner karyotype, or X mosaicism) -A male child can be affected if the mother was a silent carrier despite the mom having a negative FHx -Bc all these scenarios are very uncommon, but CAN still happen, this means that this family has a higher risk of Hemophilia A compared to the general population

Chronic Granulomatous Disease (CGD) & Prophylaxis

-*X-linked immunodeficiency* where p/w *recurrent infections by catalase-positive organisms (e.g. Staph aureus, Burkholderia cepacia, Serratia marcescens, Nocardia, Aspergillus) d/t Impaired Neutrophilic Intracellular Killing d/t defect in NADPH Oxidase (prevents neutrophil respiratory burst & superoxide formation)* -In CGD, *organisms are phagocytosed, but cannot be destroyed within phagolysosomes* -Although neutrophils are defective, absolute count is normal or elevated w/ infection -Infections most commonly involve the *Skin (Abscess), Lymph nodes (Adenitis), & Lungs (PNA) and are often difficult to tx, requiring prolonged courses of Antibiotics* -*PROPHYLACTIC ABX w/ TMP-SMX & Itraconazole Antifungal therapies Decr the Risk for Life-Threatening infections by the most common organisms* -In severe cases, immunomodulatory therapy with Interferon-γgamma may also be considered

ACL Injury Presentation & TX

-*Young* athletes who *pivot rapidly*, creating a *twisting force* on the knee, and experience a *popping sensation in the knee at the time of injury*, followed by development of *rapid-onset hemarthrosis & a feeling of joint instability with weight bearing* -*Positive Lachman & Anterior Drawer tests* (highly sensitive & specific for ACL injuries) -- *affected knee shows increased anterior motion laxity of the tibia relative to the femur* -DX confirmed with *MRI* -TX: *RICE* and *± Surgery* depending on age & activity levels

Damage to the Following Lobes of the Brain Causes What Manifestations? Nondominant Parietal Lobe Dominant Parietal Lobe Nondominant Temporal Lobe Dominant Parietal Lobe

--*Nondominant Parietal Lobe* -Referring to the *RIGHT parietal hemisphere* -Manifests as *Construction Apraxia* where pts have *difficulty executing coordinated movements*, for example, *marked difficulty copying simple line drawings* -Can have *Dressing Apraxia* where pts have *difficulty wearing clothes, and struggle to get into a coat or pants* -Pts also have *Confusion* with lesions of the nondominant (right) parietal lobe -*Nondominant parietal cortex ---> Hemispatial neglect syndrome—agnosia of the contralateral side of the world* -*Left lower quadrantanopia (Right parietal lesion, Right MCA) - can't see the Left lower quadrant in both eyes* *Dominant Parietal Lobe* -Referring to the *LEFT parietal hemisphere, imp for speech & language fnxs* -Damage to the dominant parietal lobe, *esp the Inferior Parietal Lobe, presents as Gerstmann Syndrome,* where pts have *Difficulty in performing simple math (Acalculia), Inability to name individual fingers (Finger Agnosia), Impaired writing (Agraphia), and Right/Left Confusion (Difficulty in Identifying or Distinguishing the Right or Left side of the body)* -*Dominant parietal cortex --> Gerstmann Syndrome—agraphia, acalculia, finger agnosia, left-right disorientation.* *Nondominant Temporal Lobe* -Referring to the *RIGHT temporal lobe* -Lesions lead to *visual disorders (Homonymous Upper Quadrantanopia* - bilateral visual field deficit in the left superior quadrant of both eyes) and causes *Impaired perception of complex sounds (Auditory Agnosia)* -*Left upper quadrantanopia (Right temporal lesion, Right MCA) - can't see the Left upper quadrant in both eyes* *Dominant Temporal Lobe* -Referring to the *LEFT temporal lobe* -In addition to having *homonymous upper quadrantanopia*, dominant (left) temporal lobe lesions *almost always involve the Language Fxns, and lead to Aphasia* -*Wernicke's Aphasia* is usu seen in pts w/ *dominant (LEFT) temporal lobe lesions*, *characterized by the Impairment in Comprehension of Spoken or Written Language* -Pts have *difficulty in expressing their thoughts [verbally or written] in a meaningful manner* -Apraxia (inability to perform purposeful actions) is NOT seen in temporal lobe lesions -*Right upper quadrantanopia - Left temporal lesion, Left MCA) - can't see the Right upper/superior quadrant in both eyes* -*Wernicke Aphasia is associated with Right Superior quadrant visual field defect d/t Left Temporal lobe involvement*

Cyclothymic Disorder

-2yrs of fluctuating periods of mild depressive sx as well as sx of hypomania that never meet full criteria for hypomanic, manic, or major depressive episodes

SLE Tx

-A *Positive anti-dsDNA antibody test confirms Dx of SLE*!! -*HYDROXYCHLOROQUINE* is an antimalarial agent which is particularly *effective at improving arthralgias, serositis, & cutaneous symptoms* -Hydroxychloroquine may also help to *prevent future damage to the kidneys and CNS* -*Low-dose Prednisone* at a dose of 5-15 mg/day may be helpful in the *short-term* to improve the pt's sx until the hydroxychloroquine takes full effect -In pts w/ significant dz involving the kidneys or CNS, *higher-dose Prednisone* may be needed -Higher dose steroids or other immunosuppressants are typically reserved for pts w/ more severe, solid-organ manifestations

Threatened Abortion

-A *THREATENED ABORTION presents at <20WKS gestation w/ VAGINAL BLEEDING!, a CLOSED Cervical Os, & a NORMAL Fetal Heartbeat on U/S* (normal fetal cardiac activity)

Paired t-test

-A *paired t-test* can *test the difference b/w 2 paired means*; *pts serve as their own controls* (e.g. mean blood pressure before and after treatment in the same subjects are compared)

CHADS2-VASc Scoring and Interpretation for Nonvalvular A-Fib

-All *A-fib* pts should undergo CHADS-VASc score assessment to *estimate thromboembolic risk* -Score of *0* --> *lowest risk* of thromboembolic complications and can be *managed without anticoagulation* -*Men with ≥2 & Women with ≥3* scores are *high risk* & should be *managed with anticoagulant therapy (e.g. warfarin, dabigatran, rivaroxaban, apixaban)* -Pts w/ *moderate risk* should have therapy assessed in a case-by-case basis

Multiple Myeloma Findings

-A *plasma cell dyscrasia* marked by *excessive production of a monoclonal immunoglobulin* (IgG [55%], IgA [25%]) -Commonly p/w *bone pain & anemia* d/t bone marrow infiltration w/ malignant cells; /subsequent bone demineralization/ can lead to *hypercalcemia* (which can cause /constipation/), & systemic sx (fatigue, wt loss) -*Fractures* & back pain can occur d/t *osteolytic lesions*, & congestion of glomeruli with immunoglobulins/Ig fragments results in *renal insufficiency* -ESR artificially incr d/t incr viscosity of plasma from paraproteinemia -Urine dipstick may show elevated protein (*Ig light chains, Bence Jones Protein*) /but is often normal/ bc the protein part of dipsticks detect urinary albumin -Evaluation of MM begins with *serum or urine protein electrophoresis*: the presence of a *monoclonal Ig spike (M-spike)* is highly suggestive of dz, but *confirmation requires ≥10% monoclonal plasma cells on BMBx* OR *soft tissue/bone plasmacytoma* -MM pts need eval of skeletal system to determine size, #, & location of bone lesions, which helps predict symptomatic progression using *cross-sectional imaging w/ Whole-Body CT/MRI/PET scan* (routine DXA scans not recommended unless for osteoporosis)

Parinaud's Syndrome

-A *tumor of the PINEAL GLAND, causing compression of the the Dorsal Midbrain,* characteristically causes *Parinaud's Syndrome*, which is *characterized by the Loss of Pupillary Rxn, Vertical Gaze Paralysis, Loss of Optokinetic Nystagmus, & Ataxia* -*Progressive HEADACHE* is a prominent feature, and is d/t *obstructive hydrocephalus* (compression of cerebral aqueduct) *Parinaud Syndrome* (compression of *dorsal midbrain*)—*TRIAD of upward gaze palsy, convergence-retraction nystagmus, and light-near dissociation.* Some pineal tumors are *germinomas, that secr HCG*

Oromandibular Dystonia & Other Focal Dystonias

-A form of *focal dystonia* -*Dystonia* is a neurological movement disorder that causes *sustained, involuntary muscle contractions*, which *force certain parts of body* into *abnormal, sometimes PAINFUL movements or postures* -*Focal Dystonias affect a Single Muscle or Group of Related Muscles*, and include *Cervical dystonia (spasmodic torticollis, abnormal movements of head & neck), Oromandibular dystonia (lower facial & jaw mm causing involuntary opening/closing/deviation of jaw, tongue may protrude), Blepharospasm (involuntary closure of b/l eyelids - excessive blinking/twitching), Brachial dystonia (i.e. writer's cramp, spasming of hands/arms, brought on by repetitive, task-specific movements), Limb dystonia (cramping/spasming of legs or feet)* -Focal dystonias are often *task-specific* -The presence of a *sensory trick*, in which sx sometimes relieved with sensory input, is common & helpful diagnostically -TX: *Injections of BOTULINUM TOXIN to WEAKEN (NOT fully paralyze) the affected muscle provides symptomatic relief* Note: -*TMJ Disorder* can p/w *spasms, jaw fatigue, & pain* - however, the *pain & muscle spasms of TMD are NOT usu so severe as to cause abnormal posturing or inability to speak*, unless it dislocates the jaw. Jaw dislocation CANNOT be resolved with a sensory trick. Additionally, *TMJ disorder pts usu have Headaches, Jaw fatigue, & exacerbation of sx w/ jaw movement*

Torsades de Pointes

-A form of *polymorphic ventricular tachycardia* that occurs in the setting of *acquired or congenital QT prolongation* and is characterized by *cyclic alteration of QRS axis and/or morphology* (shifting sinusoidal waveforms on EKG) -Can progress to ventricular fibrillation (VF) -Long QT intervals predispose to torsades -TdP in pts w/ acquired long QT syndrome is most commonly precipitated by premature ventricular beats followed by compensatory pause (*short-long RR intervals*) that initiates the cycle of VT -Caused by *drugs, low K, low Mg, congenital abnormalities* -TX: Even though TdP is usu a brief arrhythmia that terminates spontaneously, *IV MAGNESIUM SULFATE* is first-line for tx & prevention of recurrent TdP episodes, regardless of pt's baseline serum Mg levels, if conscious & hemodynamically stable. *Temporary Transvenous Pacing should be used if unresponsive to IV mag sulfate* -Drug-Induced Long QT incl: • Antiarrhythmics (class IA, III) e.g. *Quinidine, Procainamide, Disopyramide; Amiodarone, Sotalol, Ibutilide* • Antibiotics (e.g. *Macrolides [azithromycin], Fluoroquinolones, Antifungals*) • Antipsychotics (e.g. *Haloperidol*) • Antidepressants (e.g. *TCAs [clomipramine]*) • Antiemetics (e.g. *Ondansetron*) -TdP can also be provoked in pts with *BRADYARRHYTHMIAS* (*sinus brady or frequent pauses*), referred to as "pause-dependent" long QT syndrome -Other causes of acquired long QT incl electrolyte imbalances (low Mg, low K), SSRIs (citalopram), Hypothermia, & HIV

Prophylactic Measures to Take in Unresponsive Pts w/ Hematemesis (Upper GI Bleed)

-A large amount of hematemesis is consistent w/ *upper GI bleeding* (e.g. may be d/t bleeding *varices* if pt has underlying *chronic liver disease* [e.g. ascites, spider angiomata, gynecomastia] d/t alcohol abuse) -Appropriate *STABILIZATION* of the pt's condition *should* be the first step -Pt is *at risk of airway compromise* d/t to an *unresponsive state* (w/ low GCS score) and large volume of *active hematemesis*, possibly leading to *aspiration* -*ENDOTRACHEAL INTUBATION* would therefore be the *most important FIRST step* -Two large-bore IV lines should be placed to institute *aggressive fluid resuscitation* -A blood type & crossmatch should be sent if blood transfusion is deemed necessary -After the pt's condition is appropriately stabilized, an *immediate Upper Endoscopy* would be appropriate as it is potentially both diagnostic and therapeutic -*IV Octreotide* should be initiated in a pt w/ acute upper GI bleeding highly concerning for *variceal hemorrhage* and should be administered while the pt's condition is being stabilized (it is NOT a substitute for endoscopic therapy) -Esophageal varices are one of many complications of *elevated portal venous pressure d/t cirrhosis* -Octreotide is thought to decr the elevated pressure by *decreasing splanchnic blood flow*, which may lead to *spontaneous resolution* of the variceal hemorrhage

Tabes Dorsalis

-A manifestation of *LATE NEUROSYPHILIS*, which typically manifests *years after Treponema pallidum infection* and can be *characterized by TABES DORSALIS & ARGYLL ROBERTSON PUPILS* -*Tabes Dorsalis* is a *neurodegenerative condition* that involves the *posterior spinal columns & nerve roots* -*Posterior spinal column involvement* results in *impaired vibration/proprioception, Sensory Ataxia, and instability during the Romberg test* -*Nerve root involvement* can contribute to *diminished pain/temperature sensation & areflexia* -Pts might complain of *lancinating pains* (sharp/stabbing/piercing), described as *brief shooting or burning pain in the face, back, or extremities* -Tabes dorsalis can also be assoc w/ *Argyll Robertson pupils*, which are *characterized by normal pupillary constriction with accommodation but not with light (bilateral eye reaction)*

Trigeminal Neuralgia

-Can p/w *unilateral facial pain* -However, the pain is typically *recurrent, severe, & shocklike* rather than dull, heavy, waxing & waning

Clinical Course of Alzheimer Disease (AD)

-A pt with *gradually progressive sx* (e.g. *poor memory, apraxia, language difficulties, executive dysfunction*) suggests a *diagnosis of Alzheimer Disease* (Apraxia is *inability to perform learned motor activities* (e.g. *dressing, using utensils*)) -*Onset >60yo & initially affects memory and language* predominantly -*Later* in the course of illness, *behavioral symptoms become more prominent* -Pts typically become *more easily irritable, esp when frustrated/overwhelmed* -*Paranoid Delusions* are common, & usu d/t *misattribution* -*Cholinesterase inhibitors [Anticholinesterases]* can sometimes *slow the progression of AD, BUT there is NO CURE!* (Donepezil, Rivastigmine, Galantamine) -The disease is *progressive* and the pt may eventually *die from complications of an infection, dehydration, or malnutrition* DDX for Alzheimers includes other dementing illnesses (e.g. Vascular/Lewy body/Frontotemporal dementia/Prion dz/ Normal pressure hydrocephalus) & cognitive changes d/t delirium or psychiatric illness (e.g. depression) -Behavioral sx in AD are ideally managed w/ nonpharmacological interventions , w/ antipsychotics reserved for times when agitated behaviors pose a risk to self or others

Healthy Worker Effect (HWE)

-A special type of *selection bias* that usu occurs in *occupational cohort studies* when the general population is used as the reference group -The general pop consists of healthy & unhealthy individuals; those who are unhealthy are less likely to be employed, whereas the employed workforce tends to have fewer sick individuals -Consequently, *comparisons of mortality rates between an employed population and the general population are usu /biased/* (better to compare using a demographically-similar working population without exposure to the RF of interest, which'll serve as a better basis for comparison than the general population) - This would give more valid estimates of the true effect of exposure to the RF

When do you use a *tagged red blood cell scan*?

-A tagged RBC scan is a *very sensitive* study *used to detect ACUTE GI BLEEDS*; it requires a *rapid bleeding source* It would not help in pts with an occult GI bleed (negative tagged RBC scan) bc it's too slow.

Crossover Study

-A type of *experimental study* design in which *subjects are exposed to different treatments or exposures sequentially* -The *subjects cross over from one study arm to another and serve as their own controls*

Allergic Bronchopulmonary Aspergillosis (ABPA)

-ABPA is a *hypersensitivity* disorder that occurs in pts w/ *asthma or cystic fibrosis* -ABPA is assoc. w/ *noninvasive colonization* of the airways by *Aspergillus spp* -Pathophysiology of ABPA is related to an *exaggerated IgE & IgG-mediated immune response to the Aspergillus fungus* in the context of Preexisting Asthma -Typical clinical features incl: *recurrent asthma exacerbations*, fever, lethargy, *cough w/ prodn of brown mucus plugs* (which may contain eosinophils & grow Aspergillus), occasional hemoptysis, and *fleeting infiltrates on lung imaging* (e.g. transient infiltrates in different parts of the lungs on CXR) -Other diagnostic criteria incl immediate reaction to Aspergillus antigen skin testing, *elevated total IgE* (>417 IU/mL) and *elevated Aspergillus-specific IgE*, serum precipitins to Aspergillus antigen, *central bronchiectasis on high-resolution CT, and peripheral eosinophilia* -Once DX of ABPA is confirmed, *GLUCOCORTICOIDS & ITRACONAZOLE* are used to control inflammation and prevent irreversible damage

Anemia of Chronic Disease (ACD)

-ACD is a common complication of inflammatory diseases like rheumatoid arthritis, etc. (likely d/t suppression of hematopoiesis by inflammatory cytokines) -Hematologic studies show *LOW serum Iron, HIGH Ferritin, & NORMAL Transferrin Saturation* (but 25% of ACD have Low Transferring Saturation) -*MCV usu Low-Normal to Mildly Decr* -ACD is usu a mild anemia, but 20% of pts have Hb<8 -- in these severe cases, clinicians should r/o additional concurrent causes of anemia like iron deficiency anemia, myelodysplasia, & thalassemia -TX ACD is based on TX underlying inflammatory disorder e.g. In *Rheumatoid Arthritis, anti-TNF-alpha antibody (INFLIXIMAB) Infusions* have been shown to lessen the severity of anemia. If pts have low or inappropriately normal EPO levels, can give EPO or Darbepoietin injections. -Pts w/ *severe, symptomatic anemia of chronic disease* with initial measures, may need *periodic red cell transfusions*

Acute Decompensated Heart Failure (ADHF) Management

-ADHF results from a *Critical Elevation in Intracardiac Filling Pressures* that most commonly occurs d/t *LV systolic and/or diastolic dysfunction* (e.g. *coronary ischemia, hypertensive cardiomyopathy*) -Other causes include *vascular dz, & marked preload elevations* (e.g. *excessive volume resuscitation* or *marked afterload elevations* (e.g. *severe HTN*) -Once LV filling pressures gradually increase to their critical point, this will lead to ADHF and *pulmonary edema (bilateral crackles, vascular congestion on CXR, tachypnea, hypoxia)* -*JVD* is usu present, but *lower extremity edema* /may be absent/, esp in pts w/o CHF -Early therapeutic goals include *hemodynamic stabilization, improved oxygenation* (i.e. w/ supplemental O2 or positive pressure ventilation), and *optimization of volume status* -*IV DIURETICS (FUROSEMIDE)* are an *imp* part of initial therapy, as they *reduce intravascular volume, lower intracardiac filling pressures, and improve pulm edema* -*IV Vasodilators (e.g. Nitroglycerin) reduce intracardial filling pressures* & are *recommended in ADHF w/ inadequate response to initial diuretic tx* --They *can also* be used as *Initial therapy (Prior to or Instead of IV Diuretics) in pts w/ FLASH Pulm Edema d/t severe HTN (>180/120, HTN emergency)* -*Transthoracic ECHO* should be done in *all ADHF of uncertain etiology* to evaluate for *left ventricular dysfunction (i.e. hypertensive cardiomyopathy) and valvular dysfunction (e.g. mitral regurg)* -If significant LV systolic dysfunction is present --> then evaluate for ischemic cardiomyopathy with stress testing or coronary angiography Note: β-blockers (e.g. Metoprolol) are imp in the management of CHF d/t LV systolic dysfunction. Also used in some pts w/ tachyarrhythmias or STEMI*. However, *β-blockers are CONTRAINDICATED in Acute Decompensated HF d/t negative inotropy & chronotropy, causing potential worsening of pulm edema*

Scombroid Poisoning

-AKA *Histamine Fish Poisoning* -Caused by the *ingestion of improperly-stored seafood* -If seafood is stored at temps >15C (59F), histidine can decarboxylate to *histamine* -Can occur with tuna, mackerel, mahi mahi, bluefish, & marlin -*SX of Scombroid Poisoning* incl *FLUSHING, Throbbing HA, PALPITATIONS, Abdo Cramps, Diarrhea, & Oral Burning ("spicy")* and begin *10-30mins after ingesting the fish*; *SX ARE SELF-LIMITED* -Sometimes pts describe a *bitter taste* -Physical findings incl *skin erythema, wheezing, tachycardia, & hypotension* -Other sx incl rash, diarrhea, reddening/flushing of face, neck, & upper body, sweating, HA, N/V -Occurs more frequently than pufferfish poisoning!

Systemic Sclerosis Scleroderma Renal Crisis

-AKA *SCLERODERMA* - *Triad of autoimmunity, noninflammatory vasculopathy, and collagen deposition with fibrosis* -Characterized by the *abnormal deposition of collagen in multiple organ systems* • Skin: *Telangiectasia*, sclerodactyly, *digital ulcer*, *calcinosis cutis* • Extremities: *Arthralgia, myalgia*, contractures • GI Tract: *Esophageal Dysmotility, Dysphagia, GERD* • Lungs: *Dyspnea, chronic cough* • Vascular: *Raynaud Phenomenon* -Most pts have *underlying renal involvement*, but overt SX of Scleroderma Renal DZ are less common -*Thickening of the vessel wall and narrowing of the vascular lumen in the renal arterioles result in ischemia*, which *activates the RAAS --> [MALIGNANT] Hypertension* (*malignant with CNS sx & papilledema* for e.g.) - *TX Malignant HTN w/ CAPTOPRIL* (short time to onset) *and IV Nitroprusside if CNS manifestations/Papilledema present!* -Therefore, *monitoring BP of scleroderma pts important*, presence of HTN should raise suspicion for *Scleroderma Renal Crisis* -- *TX w/ ACE INHIBITORS, esp CAPTOPRIL* -*Acute Renal Failure* is also typical of *scleroderma renal crisis* and is likely *2º to combo of severe HTN superimposed on abnormal renal vasculature* -Some pts have *microangiopathic hemolytic anemia & thrombocytopenia*, reflecting underlying inflam & vasculopathy

Tension Headaches

-Can p/w pressure and muscle tenderness in head & neck, esp during times of stress -However, the headaches are *symmetric* and do NOT typically cause focal (e.g. masseter muscle) tenderness or jaw heaviness

Hidradenitis Suppurativa Management

-AKA *acne inversa*, a *chronic inflam disorder characterized by occlusion of skin follicles*, usu in *intertriginous areas* (axillae, groin, medial thigh, perineum) or anywhere that has hair follicles -RF: FHx of HS, smoking, obesity, mechanical stress on skin (friction) -Usu dev an *initial solitary & painful inflamed nodule in an intertriginous area that can last for days to months before progressing to an abscess with purulent or serosanguineous drainage* -Nodules and pain usu improve after drainage -*Multiple recurrent nodules* can *lead to Sinus Tracts, Comedones, & significant Scarring* *MILD DZ* managed w/ *Topical CLINDAMYCIN*, but some may need intralesional steroids or oral ABX for flares *MODERATE DZ* p/w *inflammatory nodules, Sinus Tracts, & Scarring* requires *biologic TNF-alpha Inhibitors (INFLIXIMAB) and wide *surgical excision ± oral retinoids*

Verification Bias

-AKA *workup bias* -*A type of measurement bias that occurs when a study uses the Gold Standard Testing SELECTIVELY in order to Confirm a Positive (or Negative) result of preliminary [screening] testing*; this can *result in overestimates (or underestimates) of sensitivity (or specificity)* -One way to *reduce verification bias* is to *perform Gold Standard testing in a RANDOM SAMPLE of participants With Negative Results* -- these results from this analysis could tell clinicians the likely # of cases that would have been found if all participants with negative screening tests were to have been fully investigated with gold standard testing -*Verification Bias occurs when a study uses gold standard testing Selectively in order to confirm a positive (or negative) result of preliminary testing. This can result in overestimates (or underestimates) of sensitivity (or specificity)* Note: *Selection Bias* results from the *manner in which study participants are selected or lost to f/u*; *Randomization in a clinical trial reduces selection bias*

Acute Dystonia - Definition & TX?

-Acute Dystonia is a *Sudden onset of muscle spasms, stiffness, torticollis, and/or oculogyric crisis (forced, sustained elevation of eyes in a fixed upward position) occurring HOURS to DAYS after medication use (typical anticonvulsants [haloperidol, carbamazepine] or metoclopramide); can lead to laryngospasm requiring intubation!* -Acute dystonia is a type of *extrapyramidal sx* that *develops within Hours to Days of starting or increasing dose of Antipsychotics* -TX: *Benztropine or Diphenhydramine* -Very distressing acute dystonic rxns are best Tx w/ *IV or IM anticholinergic medication (i.e. Benztropine or Diphenhydramine)*

Management of Acute Diverticulitis

-Acute diverticulitis presents w/ *[LLQ] abdo pain, N/V, altered bowel movements, fever, leukocytosis, possible sterile pyuria* -*DX w/ Abdo CT with Oral & IV Contrast* -Management: • *Bowel rest* • *ABX - Ciprofloxacin, Metronidazole* • *Colonoscopy 6-8wks after resolution* -Complications: *Abscess, obstruction, fistula, perforation* -*IF SX do NOT improve after 2-3d of appropriate TX (analgesic meds, liquid diet, ± oral ABX)*, pts should be *HOSPITALIZED* and given a *REPEAT ABDO/PELVIS CT SCAN* to evaluate for complications like *abscess, obstruction, or perforation*

Scaphoid fracture

-Acute pain at wrist and tenderness of anatomic snuffbox area after falling onto outstretched hand -MC carpal bone fracture, usu caused by excessive forceful dorsiflexion at the wrist -Pts have *swelling, decreased grip strength, pain & tenderness at the radial aspect of the wrist in the anatomic snuffbox, and minimally decreased ROM (unless dislocated fracture present)* -Next step would be *hand & wrist x-rays* in full pronation and ulnar deviation to better expose scaphoid (initial x-ray may be negative if fracture is compressed or minimally displaced) -If initial x-ray negative, suspected scaphoid fractures should have addl imaging (MRI or CT wrist; Repeat X-ray in 7-14d; Radioscintigraphy bone scan in 3-5d) -Nondisplaced fractures should be tx w/ *short arm thumb spica cast*, but other fractures should be referred for *ortho surgeon eval* -Scaphoid fractures not tx appropriately or timely can result in *incr risk for nonunion and avascular necrosis*

How do you treat diarrhea caused by infectious organisms?

-Acute-onset fever, abdo pain, & diarrhea are characteristic findings of *infectious gastroenteritis* -In contrast to nonbloody viral diarrhea, bloody diarrhea suggests a bacterial cause (e.g. *Salmonella, Shigella, E. coli*); usu produce sx by *direct enterocyte invasion or toxin prodn* (e.g. Shiga toxin) -*Stool culture or Multiplex PCR is diagnostic* -Diarrhea pts should be eval for *dehydration* & first-line tx is *correction of hypovolemia* d/t dehydration; these are *self-resolving usu* -*Oral electrolyte solution* (low osmolality containing glucose & 'lytes) is preferred for pts w/ Mild Dehydration (dry lips, normal vitals) -Water alone may exacerbate electrolyte disturbances (hypoNa, hypoglycemia), and the high sorbitol content of juice can worsen diarrhea -Mod-Severe Dehydration requires *IVF* d/t ongoing losses &/or inability to tolerate PO -Empiric antibiotics are usu AVOIDED in suspected bacterial gastroenteritis (bloody diarrhea) in the Absence of Severe Disease (e.g. *Hemodynamic Instability* or *Immunocompromising conditions)

Adenomatous Colon Polyps & F/U

-Adenomatous colon polyps are at *incr risk for Colorectal Adenocarcinoma* and require an *incr freq of colonoscopic surveillance* -Polyps with *villous or tubulovillous histology, high-grade dysplasia, or size ≥10mm* are *assoc w/ additional incr in risk* and generally warrant *repeat colonoscopy in 3yrs* -Hyperplastic polyps <10mm/No polyps --> f/u in 10yrs -Hyperplastic polyps ≥10mm --> f/u in 3-5yrs -1-2 tubular adenomas <10mm --> 7-10yrs -3-4 tubular adenomas <10 mm --> 3-5yrs -5-10 tubular adenomas <10mm/tubular adenoma ≥10mm/tubulovillous or villous adenomas/adenoma w/ high-grade dysplasia --> f/u in 3yrs ->10 adenomas --> f/u in 1yr -Large (>20mm) adenomas that are removed *piecemeal* --> f/u within 6mo (incr risk d/t possible incomplete polyp removal) -Polyps w/ high-risk features of invasive malignancy (e.g. LVI, positive margins) --> Colectomy

Nested Study

-Aka *Nested Case-Control Study* -A form of *retrospective observational study* in which *subsets of controls are matched to cases and analyzed for the variables of interest*

Subacute Thyroiditis

-Aka Subacute Granulomatous Thyroiditis -AKA Subacute Thyroiditis de Quervain -Self-limited disease often preceded by an upper resp infxn, and thought to be caused by a *postviral* inflammatory process -May be *hyperthyroid early* in course, followed by *hypothyroidism* -Characterized by *fever & PAINFUL, diffusely-enlarged thyroid*, neck pain, *elevated ESR*, assoc with *thyrotoxicosis* -Thyrotoxicosis is caused by *acute inflam of thyroid and release of stored thyroid hormone d/t follicular injury,* leading to *suppressed TSH and DECR radioactive iodine uptake* on thyroid scintigraphy -*TX*: Self-limited but supportive tx during the hyperthyroid phase, with *NSAIDs* to relieve pain (glucocorticoids in severe/refractory cases) and *β-blocker* (e.g. propranolol, atenolol) to minimize hyperadrenergic sx of thyrotoxicosis (e.g. sweating, palpitations)

[Localized] Herpes Zoster

-Aka *Shingles* -D/t *reactivation of VZV from the dorsal root ganglia* of a sensory nerve following the initial VZV infection with varicella (causing chickenpox) during childhood or early adulthood -*Risk of reactivation* is *greatest* in those of *advancing age* d/t *waning VZV-specific cell-mediated immunity* -Malignancy, liver or kidney dz, & immunocompromise (e.g. chronic glucocorticoids) also incr risk -*Herpes Zoster rash* quickly evolves from *erythematous papules into grouped vesicles*, usu on *thoracic & lumbar* regions, and usu involve *unilateral, dermatomal spread of a vesicular rash (fluid-filled blisters)* -*Dermatomal Pain (burning, throbbing, stabbing, pruritic)* occurs in the majority of pts and *precedes the rash by days or weeks* -DX based on presentation alone (PCR & viral culture for atypical skin lesions) -*LOCALIZED* Shingles with *lesions <72hrs* are *TX w/ Oral VALACYCLOVIR* to *reduce (transmission risk, new lesion formation, & possibly risk of postherpetic neuralgia* (give TX if >72hrs in immunocompromised -*Analgesics* also given for *acute neuritis* e.g. NSAIDS/Tylenol, Gabapentin, TCAs, glucocorticoids NOTE: Pts w/ localized zoster are not infectious before vesicles appear, and are no longer infectious when the lesions have re-epithelialized (crusted over). Active lesions should be kept covered and wash hands frequently to prevent spread.

Female Genital Cutting

-Aka *female circumcision* or *genital mutilation* -It is a *cultural practice*, predominantly performed in some parts of Africa -It involves the manipulation or removal of external genital organs and is considered an important rite of passage into womanhood in some cultures -Most (not all) of the procedures are performed by _nonmedical practitioners_ -Anesthesia & ABX are rarely administered, and *hemorrhage and infection* can result -_Potential long-term gynecological complications_ incl genital pain, scarring, infection, infertility, and difficulty with coitus and/or vaginal delivery* -A physician's response must be /culturally sensitive and nonjudgmental/ -Many women who undergo female genital cutting do not consider it mutilation -A sensitive approach includes *asking the pt if she has any concerns about the procedure, avoiding referring to it as genital mutilation, and *educating her about the medical risks* Note: Asking the pt if they feel pressured by their family may be experienced as *culturally insensitive* as in some cultures, it is common for medical decisions to incl family members. If physician is concerned the patient is being pressured, an /open-ended approach/ is preferred, asking "How do you feel about the procedure?"

Anchoring Bias

-Aka *premature closure* -Occurs when a *diagnosis is prematurely swayed by initial impressions (i.e. an anchor) and prevent careful consideration of other possibilities/DDX* (e.g. thinking substernal burning of an atypical MI presentation is GERD) -Can be *minimized by enhancing clinician awareness* (M&M review), *providing training* (e.g. simulated cases illustrating biased thinking), and *optimizing organizational and workplace factors* (e.g. limiting distractions)

Availability Bias

-Aka *recency effect* -Occurs when clinicians' *thinking is influenced by recently or frequently seen cases* (e.g. diagnosing Influenza when a pt w/ fever & dyspnea actually has a pulmonary embolism)

Ogilvie's Syndrome

-Aka Acute Colonic Pseudo-obstruction -Characterized by dilation of the cecum & right colon in the absence of a mechanical obstruction to the flow of intestinal contents -It tends to involve the right side of the colon and NOT the SI

Hirschsprung Disease

-Aka Congenital Aganglionic Megacolon -Causes *delayed meconium passage [within 48hrs of birth] & abdominal distension* due to the *lack of innervation in the RECTOSIGMOID colon* causing *Congenital Megacolon* -Lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner plexuses) in distal colon d/t failure of neural crest cell migration -Failure to pass meconium is usu pathologic and can lead to *abdo distension, poor feeding, & bilious emesis* -Initial eval w/ Abdo X-ray to r/o free intraperitoneal air and evaluate bowel gas pattern -Presence of *multiple dilated bowel loops and absence of rectal air* are concerning for *distal bowel obstruction* -*Contrast enema* is performed to delineate level of obstruction in the distal intestinal tract - classically, *Hirschsprung Dz* shows a *transition zone* b/w a *normal or narrow caliber rectosigmoid (aganglionic segment) and a normally innervated but markedly dilated descending colon* -*Confirmation* of DX: *Absence of ganglion cells on Rectal Mucosal Suction Biopsy* -TX: *Surgical Resection* of aganglionic segment followed by anastomosis of normal bowel to anus -10% of pts have Down Syndrome (incr risk)

Factorial Study Design

-Aka Fully Crossed Design -Type of experimental study design that utilizes *≥2 interventions* and *all combinations of these interventions*

Amyotrophic Lateral Sclerosis (ALS)

-Aka Lou Gehrig Dz (e.g. Stephen Hawking) -*COMBINED UMN (corticobulbar/corticospinal) && LMN (medullary and spinal cord) Degeneration* -NO sensory or bowel/bladder deficits -Can be caused by *defect in superoxide dismutase 1* -*LMN Deficits* d/t *anterior horn* cell involvement --> *Dysarthria, Dysphagia, Asymmetric Limb Weakness, Fasciculations, Atrophy* -*UMN Deficits* d/t *pseudobulbar palsy* --> *Dysarthria, Drooling, Dysphagia, Emotional Lability (involuntary emotional responses), Spastic Gait, Clonus* -*FATAL* DISEASE -TX: *RILUZOLE* -Can present with *DIAPHRAGMATIC PARALYSIS* causing difficulty breathing, especially while supine

Frontotemporal Dementia (FTD)

-Aka Pick Disease -*Rapidly progressive* dz, dx age 50s-60s; survival length 8-10yrs after onset -Presents w/ *prominent personality & behavior changes* such as: *Disinhibition* (e.g. flirting w/ strangers, public urination), *Apathy* (doesn't care about anything), *Loss of Empathy* (e.g. less affectionate/caring), *Ritualistic Behaviors*, *Hyperorality* (e.g. overeating), *Executive Dysfunction/Fxn Decline* (e.g. cognitive decline, getting lost driving home from work) -Some 20% of pts also develop a *motor neuron dz* w/ both *upper* (e.g. *hyperreflexia*) and *lower* (e.g. *fasciculations*) *motor neuron signs*, similar to those seen in ALS (amyotrophic lateral sclerosis) -DX Clinical -Neuroimaging to r/o other etiologies (e.g. masses, stroke), and *confirm frontal/temporal lobe atrophy* -TX is *palliative* using behavior management (exercise, trigger avoidance, distraction, redirection) and symptomatically-tailored pharmacotherapy with *SSRIs or atypical antipsychotics if needed* -Abnormal inclusions of hyperphosphorylated tau proteins (round Pick bodies) or ubiquitinated TDP-43 DNA-binding protein that cause related neuronal death in the frontotemporal lobes

Amniotic fluid Index - normal vs. high vs. low

-Amniotic fluid is produced by fetal lungs & kidneys, and is removed by fetal swallowing and transplacental fluid reabsorption -*NORMAL AFI: 5-23 cm* -- suggests normal placental, fetal kidneys & lung fxn -POLYHYDRAMNIOS, AFI ≥24 cm* -- Impaired amniotic fluid removal; dx by either routine U/S or U/S to evaluate fundal height (larger than expected gestational age) -*Polyhydramnios* is assoc w/ *incr risk for Maternal Complications (e.g. resp distress d/t impaired diaphragm movement), Obstetric Complications (e.g. preterm PROM, abruptio placentae, umbilical cord prolapse, postpartum hemorrhage), & Adverse Fetal Outcomes (e.g. preterm delivery, macrosomia [big head], neonatal mortality)* -*Causes of Polyhydramnios*: Idiopathic, *maternal diabetes, multiple gestation, & congenital anomalies (e.g. duodenal atresia)* -Poorly controlled/Undiagnosed DM is assoc w/ fetal hyperglycemia --> osmotic diuresis --> fetal polyuria --> *polyhydramnios* -Mom's UA shows glucose in urine and has a fundal height greater than gestation age, suggesting underlying DM -*OLIGOHYDRAMNIOS, AFI <5 cm* -- Impaired amniotic fluid production; can be caused by *preeclampsia, abruptio placentae, uteroplacental insufficiency, renal anomalies, NSAID use [decr fetal renal blood flow --> fetal oliguria & oligohydramnios]* -Placental insufficiency is chronic in preeclampsia, causing shunting of fetal blood to the fetal brain away from kidneys, decr fetal urinary output & oligo

Chronic Granulomatous Disease (CGD)

-An *X-linked Recessive immunodeficiency* that usu occurs in *BOYS* -Pts are primarily *predisposed to Recurrent Lung Infections (e.g. PNA, Empyema, Hilar LAD) and Abscesses (Skin, Liver, Lymph Node)*, and *perirectal infections* are common -Pathogenesis of CGD involves *defect of NADPH oxidase* which is responsible for the *neutrophil's respiratory burst* (where reactive oxygen species [e.g. superoxide radicals, hydrogen peroxide] are formed and activate lysosomal proteases involved in pathogen destruction) -CGD pts w/ mutated NADPH oxidase therefore have *decreased production of superoxide anions/decr reactive oxygen species* and therefore *decreased respiratory burst in PMNs* -CGD pts have *increased susceptibility to Catalase-Positive bacteria and fungi* including *Staph aureus, Burkholderia (Pseudomonas) cepacia, Nocardia, Aspergillus -CGD pts also *develop characteristic GRANULOMAS that can involve many organ systems* (e.g. *GI tract, GU tract, Lungs*) -The pathogenesis involves migration of phagocytes to infection sites, but inability to degrade inflammatory signals and invading organisms causes chronic and focal aggregations of inflam cells (granuloma formation) Note: B. cepacia pneumonia can also be seen in pts w/ *cystic fibrosis* where they have *impaired airway clearance*, BUT granuloma formation does NOT occur. Infections in CFG are limited to the sinopulmonary tract, so perirectal abscesses wouldn't be seen

Subchorionic Hematoma

-An *abnormal collection of blood between the gestational sac and the uterine wall* (e.g. a 1.8cm, crescent, hypoechoic area b/w the gestational sac and the uterus on U/S) -Caused by a *partial separation of the chorion (outer amniotic membrane) from the uterine wall* -*RF* incl: *Use of anticoagulants, Infertility Tx, Uterine Malformation (e.g. uterine septum, leiomyoma), and a Hx of Recurrent Pregnancy Loss* -Although subchorionic hematomas can p/w *vaginal bleeding*, they can also be an *incidental finding* during routine U/S -Subchorionic hematomas appear on U/S as *crescent, hypoechoic lesions adjacent to the gestational sac* -*Majority of pts have uncomplicated pregnancies*, and *MANAGEMENT IS EXPECTANT*; pts can be followed w/ serial U/S to help provide reassurance -Complications incl: Incr risk for *Spontaneous abortion & pregnancy loss (Miscarriage) at <20wks gestation* (d/t placental dysfunction); Incr risk during *third* trimester for *abruptio placentae* (premature partial/complete separation of placenta from uterine wall before delivery causing abrupt PAINFUL bleeding), *preterm premature rupture of membranes, preterm labor & delivery, preeclampsia, fetal growth restriction, & intrauterine fetal demise* -However, most pts have an uncomplicated pregnancy Note: Hospital admission for bed rest does not improve pregnancy outcomes in pts w/ subchorionic hematomas (in fact, bed rest as assoc w/ incr risk for thromboembolism!

Postpartum Thyroiditis

-An *autoimmune* disorder that is considered a *variant* of *chronic lymphocytic (Hashimoto) thyroiditis* -Moderate to severe hypothyroidism (with significant elevations in TSH) can be assoc w/ *mild hyponatremia*, possibly d/t *decr clearance of free water and increased release of ADH* -*Classic Postpartum Thyroiditis (PPT)* is characterized by *a brief thyrotoxic phase, followed by a self-limited hypothyroid phase, and eventual return to a euthyroid state* -*Mild Hypothyroidism d/t PPT does NOT require treatment*, and typically *resolves within a few months* -However, *Moderate to Severe Hypothyroidism d/t PPT*, esp in symptomatic pts, *should be TX w/ Levothyroxine* -- which will also likely *correct the hyponatremia*!

Intertrigo

-An *inflammatory skin disorder* affecting the *intertriginous areas* (inguinal, perineal, genital, intergluteal, axillary, or inframammary) -RF: Conditions that *Incr skin friction* (e.g. obesity), *Incr moisture* (e.g. tight clothing, hyperhidrosis), or *promote fungal overgrowth* (e.g. diabetes, immunosuppression) -*Candidal intertrigo* (primarily /Candida albicans/) is the MC etiology as the fungus grows well under the warm, moist environment of the skinfolds -Pts typically dev *erythematous plaques and erosions*, sometimes w/ *satellite papules and significant inflammation* -The lesions can be *pruritic or painful* if there is significant skin breakdown -DX made Clinically but can be *CONFIRMED with KOH examination* -*Topical Antifungals* (e.g. *Miconazole, Nystatin, Terbinafine*) are the *preferred first-line TX for Intertrigo* -After antifungal tx, use of /skin-drying agents/ & correction of any underlying predisposing conditions can *reduce the risk of recurrence*

Case Control Studies

-An *observational study* design -Begins with *initially identifying individuals WITH the outcome (i.e. cases) and those WITHOUT the outcome (i.e. controls)* -The *outcome status* (i.e. *disease or condition of interest*) is *what delineates who is a case and who is a control* -Then once identified, *cases and controls are assessed* for *past exposure/history of ≥1 risk factors of interest* Note: Case-control studies *do NOT identify* individuals as cases or controls *based on risk factor status*; *ONLY on OUTCOME STATUS*

What meds to give someone who had an MI?

-An MI is most often an acute thrombosis d/t rupture of coronary artery atherosclerotic plaque; incr cardiac biomarkers (CK-MB, Troponins) are diagnostic -Commonly occluded coronary AA: LAD > RCA > Circumflex *Acute Coronary Syndrome Treatments*: -*Unstable Angina/NSTEMI*: Anticoagulation (e.g. Heparin), Antiplatelet therapy (e.g. Aspirin) + ADP-receptor Inhibitors (e.g. Clopidogrel), β-blockers, ACE inhibitors, Statins; Sx control w/ Nitroglycerin & Morphine -*STEMI*: In addition to above, Reperfusion Therapy is most important (*percutaneous coronary intervention* preferred over fibrinolysis)

St. John's Wort Efficacy

-An OTC herbal supplement used for its *antidepressant, anti-inflammatory, & wound-healing* properties -*SOME evidence of efficacy* in TX *mild to moderate depression*, but there is a *Lack of Regulation of St. John's Wort in the US* with the *potential for drug interactions!* -SJW *inhibits various CYP450 enzymes* and P-glycoprotein systems -*Drug interactions with SJW* can lead to *TX FAILURES* with many meds, incl *hormonal contraceptives, anti-retrovirals, immunosuppressive agents, narcotics, anticoagulants, and antifungals* -There is *Risk for Serotonin Syndrome* when use SJW with other *serotonergic antidepressants* -There is lack of herbal product standardization, issues regarding its safety

Bullous Pemphigoid

-An autoimmune blistering disorder (type 2 HS - Ab-mediated) most commonly affecting people *>60yo* -*DX must incl SKIN BIOPSY* (histology & direct immunofluorescence) which shows *subepidermal cleavage* and *linear deposition of IgG &/or C3 along the BM (at epidermal/dermal junction)* /before starting therapy/ (need to confirm the dx) -*IgG antibodies against HEMIDESMOSOMES* (epidermal basement membrane) -Less severe than pemphigus vulgaris -TX: Topical w/ high-potent corticosteroids (e.g. clobetasol); Systemic w/ corticosteroids, doxycycline -Prodromal phase of pruritic, eczematous, or urticarial rash may proceed the development of bullae by weeks to months -Bullae are *tense*, have erythematous bases, containing eosinophils & may rupture to form erosions with assoc *pruritis* -Lesions are localized or diffuse, involve trunk or extremities; mucosal involvement /rare/ -Nikolsky sign Negative

Follow-Up After Acute HBV Infection

-As pts recover from acute HBV infection, there is normally a *steady drop in both aminotransferases & HBV DNA levels* -Aminotransferase levels typically normalize within 2-8wks -*Pts who do not clear hepatitis B surface antigen after 6mo* are *diagnosed w/ progression to chronic HBV infection* -Some pts may dev *complications* such as *acute liver failure or coagulopathy during the initial phase* of infection -Consequently, pts should be *monitored regularly* to evaluate for the dev of chronic HBV infection or hepatic decompensation -SX resolution is variable and partially depends on severity of initial presentation -Pts w/ a milder onset may recover completely within days, whereas those w/ a more severe presentation (e.g. bilirubin >10 mg/dL) may report fatigue and nausea for months following acute infection

Smoking Cessation in Adults ≥60yo

-Assoc with a small absolute decline in mortality rate than for smoking cessation <60yo -BUT *cessation at any age* has been shown to *lower the risk of all-cause mortality and cardiovascular events* and *this benefit can be seen within 5yrs after quitting* -Quitting slows the decline in lung fxn at any age and should be promoted in all pts -*Behavioral therapy and pharmacotherapy* (e.g. nicotine replacement, bupropion, varenicline) should also be offered as appropriate Note: Although an eventual improvement in chronic cough is expected w/ cessation, there is often an *initial temporary increase in cough during the first few wks after cessation*

What condition is the use of *Ephedra* associated with?

-Associated with *Myocardial Infarction*!! -*Ephedra*, supplement previously used to treat asthma/upper respiratory sx and improve weight loss/athletic performance -*Banned by US FDA!!*

What condition is the use of *Aristolochic Acid* associated with?

-Associated with *Nephrotoxicity* (e.g. fulminant tubulointerstitial renal disease) -*Aristolochic Acid* is a compound included in many Chinese herbal weight loss regimens

Indications for Prophylactic Administration of anti-D Immune Globulin for Rh(D)-Negative Patients

-At 28-32wks gestation -<72hrs after delivery of Rh(D)-positive infant -<72hrs after spontaneous abortion -Ectopic pregnancy -Threatened abortion -Hydatidiform mole -Chorionic villus sampling, Amniocentesis -Abdominal trauma -2nd- & 3rd-trimester bleeding -External cephalic version

Placenta Previa

-Attachment of placenta to lower uterine segment (or <2cm from) internal cervical os -RF: *multiparity, prior C-section* -Can present with *painLESS third-trimester vaginal bleeding* -Bleeding is primarily from /maternal/ blood loss and therefore is usu *heavy & persistent* (as opposed to vasa previa, where the vaginal bleeding is from /fetal/ blood loss and is minimal and transient) -Also associated with *maternal signs of hemorrhagic shock* (e.g. hypotension, tachycardia) prior to severe fetal compromise

Autoimmune Hepatitis

-Autoimmune disease causing *progressive parenchymal liver damage* with severe cases progressing to *cirrhosis & liver failure within 6mo* -Most commonly in *Young to Middle-Aged Women* -*Autoimmune Manifestations common* including *arthritis, erythema nodosum, thyroiditis, pleurisy, pericarditis, anemia, & sicca syndrome* -Common Lab Findings incl: *Elevated AST & ALT levels, Normal or Near-Normal ALP, & a Normal Bilirubin level* -*AUTOantibodies* common! -- Most specific tests are *ANTINUCLEAR Ab* (homogenous staining pattern) *& ANTI-SMOOTH MUSCLE ANTIBODIES* (against actin) Note: Antimitochondrial Ab are seen in Primary Biliary Cirrhosis, which has elevated ALP (not aminotransferases)

Autosomal Dominant Polycystic Kidney Disease Manifesations

-Autosomal dominant inherited disorder, prevalence is ~1 in 500 (often have FHX of ESRD) -Characterized by *multiple bilateral renal cysts* -Pts often *ASX*, but many develop *HTN* as an early manifestation -Pts also frequently dev *hematuria (UA shows dysmorphic erythrocytes), proteinuria, and flank pain* -Most ADPKD pts have *progressive renal insufficiency* as they get older; ~50% need renal replacement therapy by age 60. *Diagnosis made by Renal Ultrasound* showing *enlarged kidneys w/ multiple bilateral cysts* (only do genetic testing if unclear by ultrasound) -Management: No specific therapies to stop illness, but *Rigorous control of Blood Pressure with ACE Inhibitors* has been shown to reduce the rate of renal decline. Aggressive control of lipids with *statins* also recommended to limit risk of cardiovascular dz -*Pts ≥18yo w/ Positive FHX of ADPKD* should be *SCREENED* using *Renal Ultrasound* and *Counseling* should be performed when diagnosed. (Note: the development of HTN is not diagnostic of ADPKD in children or adults)

Ehlers Danlos Syndrome

-Autosomal dominant or recessive, causing *faulty collagen synthesis* causing *hyperextensible skin, bleeding tendency (easy bruising), & hypermobile joints* -Multiple types -May be assoc with *joint dislocation, berry & aortic aneurysms (d/t incr fragility of cerebral A walls), organ rupture*

Bacterial Keratitis

-Bacterial conjunctivitis can progress to *Bacterial Keratitis,* which most commonly occurs in pts who wear contacts improperly (e.g. overnight) or who have decr immunity (e.g. corticosteroid use) -*Keratitis* is an *inflammation of the CORNEA* (clear tissue covering the pupil & iris, and bordered by the bulbar conjunctivae) -*Infectious Keratitis* can be d/t a variety of organisms, incl *Bacteria (e.g. Pseudomonas aeruginosa), Viruses (e.g. HSV, VZV), Fungi, or Parasites (e.g. Acanthamoeba)* -P/w *PHOTOPHOBIA, Blurred/Impaired Vision, & a Foreign Body Sensation w/ difficulty opening the affected eye* -When keratitis is suspected, *urgent ophthalmologist referral is needed to confirm the DX and begin TX* -*DX of Keratitis* made by *slit-lamp exam showing Corneal Ulceration, readily seen w/ fluorescein* -*Cultures of corneal scrapings* help to guide definitive *ABX therapy*, but *EMPIRICAL Therapy should be changed to Combined Topical ABX w/ broad-spectrum activity against G(+) & G(-) organisms, incl Pseudomonas* -Keratitis can cause *scarring or ulceration of the cornea* and *subsequent Blindness* if not aggressively treated Note: Endophthalmitis is a bacterial infxn of the deep eye (vitreous) d/t either direct inoculation into the globe (e.g. surgery, trauma)or hematogenous spread; it is NOT a complication of bacterial conjunctivitis Note: Uveitis, inflam of the middle eye (e.g. choroid, vitreous, iris, ciliary body), is d/t autoimmune diseases (e.g. juvenile idiopathic arthritis, Reiter syndrome) or systemic infection; it is NOT a complication of bacterial conjunctivitis

Typhoid Fever - Brief Overview

-Bacterial illness caused by *Salmonella infection* -Manifestations *progress slowly* and *begin with a week of fever* (often with *temperature-pulse dissociation*) *followed by abdominal pain & cutaneous "rose spots"* -By week 3, *hepatosplenomegaly, intestinal bleeding, & intestinal perforation* often occur

Intention to Treat Analysis - Basic Premise

-Basic premise of *ITT analysis* is that *participants in trials should be analyzed in the groups to which they were randomized, regardless of whether they received or adhered to the allocated intervention, regardless of whether they withdrew from the TX* -*ITT analysis PRESERVES RANDOMIZATION* -ITT analyses are performed to *avoid the effects of crossover and dropout, which may break randomization and affect the outcome*-

Anticoagulation PPX for Mechanical Prosthetic Valves

-Bc of the *inherent thrombogenicity of the implanted prosthetic material & the abnormal flow conditions induced by a Mechanical Prosthetic Valve,* ALL pts require *LIFELONG ANTICOAGULATION after valve implantation to Prevent Thrombotic Valve Dysfunction (i.e. VALVE THROMBOSIS)* && *Thromboembolic Events (e.g. STROKE)* -Currently, a *Vitamin K Antagonist (WARFARIN)* is the *ONLY acceptable oral anticoagulant to Prevent Thrombotic Complications* in pts *w/ a Mechanical Prosthetic Valve* -A Mechanical Prosthetic Valve in the *MITRAL Position* carries a relatively *HIGH Thrombotic Risk* (likely d/t local hemodynamic characteristics surrounding the valve); Therefore, a *Relatively HIGH TARGET INR of 2.5-3.5 is Recommended* -A Mechanical Prosthetic Valve in the *AORTIC Position* carries a lower risk than for Mitral, Therefore, an *INR Goal of 2.0-3.0 is appropriate* as long as there's no other factors present that increase thrombotic risk (e.g. A-fib, LV systolic dysfunction, prior thromboembolism, presence of a hypercoagulable, etc.)

How to tx patient agitation?

-Begin with *verbal and nonverbal de-escalation interventions* to avoid violence (e.g. calm voice, simple language, offer options) -However, agitated pts who have *escalated to violence* (e.g. pt raising tone/volume, restlessness, damage to hospital objects, & violence against staff) *require physical restraints and fast-acting pharmacologic management (e.g. IM antipsychotic)* d/t high risk for harm to self and others while facilitating a thorough medical eval for underlying causes of behavior (e.g. primary psychiatric disorder, substance use)

Hepatic Adenoma

-Benign epithelial tumor of liver seen mostly in *young women* taking *OCPs* -Most cases ASX and discovered *incidentally* on imaging; however, some tumors may grow large enough to cause *episodic abdo pain, rupture, or hemorrhage* -PE and labs are usu *normal* -*DX confirmed when CT abdo* reveals a *well-demarcated lesion* in the right lobe of the liver that shows *peripheral enhancement with IV contrast* (early phase) -Hepatic adenomas *≤5 cm* are often *managed conservatively* as the *DISCONTINUATION OF OCPs can result in tumor REGRESSION* -Those w/ *larger or symptomatic* adenomas usu require *surgical resection* -Malignant transformation can rarely occur (~10%); serial imaging and alpha-fetoprotein levels typically required -Other complication is *rupture & hemorrhage*

Focal Nodular Hyperplasia

-Benign liver lesion d/t *hyperproliferated normal liver cells* and no intervention is necessary -Most cases arise in *young women* and are discovered *incidentally* on imaging -*CT scan with contrast* usu shows *uniform enhancement* (not only peripheral enhancement which can be seen in Hepatic Adenomas)

Analysis of Variance (ANOVA)

-Best suited for a scenario where the *mean values of a continuous variable in several [categorical variable] groups are being compared* -Useful in studying *the difference in Mean values among several groups* -The ANOVA test gives an *F statistic (based on the variation within and b/w the different groups)* that can be *used to obtain a p-value* e.g. left ventricular wall thickness (continuous variable) compared amongst 3 categorical variables - (1) Definitie Hypertrophic cardiomyopathy, (2) No HCM, and (3) Borderline HCM

Gynecomastia on Palpation

-Bilateral, rubbery, nontender disks of tissue beneath the areolas -Typically d/t an increased estrogen-to-androgen ratio and is linked to a mildly increased risk of male breast cancer (much smaller risk compared to that conferred by BRCA mutation)

Presentation Differences Between IgA Nephropathy & Acute PSGN

-Both present with *gross hematuria & incr Cr with a recent hx of upper resp infxn* (URI) -*Acute PSGN classically presents WEEKS after Grp A Strep [S. pyogenes] infxn* (e.g. Pharyngitis, Impetigo) and *Complement levels are LOW*; UA shows *proteinuria, RBCs (hematuria), RBC casts*; Serum shows *Low C3 & CH50, Low/Normal C4, incr Cr*; *Subepithelial IC deposition along GBM (humps)* -*IgA Nephropathy presents DAYS after URI* (*synpharyngitic* - meaning occurring simultaneously as pharyngitis) with *NORMAL Serum Complement levels*; UA shows *proteinuria, RBCs, RBC casts*; Serum shows *Normal C3 & C4, Incr Cr*; *IgA-based IC mesangial deposition*

When should you hospitalize a pt w/ acute hepatitis B virus infection?

Depends on the *severity of illness* (e.g. High fever, impaired hepatic synthetic function, other signs of acute liver failure [encephalopathy]), *risk of short-term complications*, those with *significant comorbid conditions*, or a lack of access to appropriate follow-up Most cases can be handled as an outpatient with close outpatient care

Erb-Duchenne Palsy (Erb Palsy)

-Brachial plexus injury involving nerves C5-C7 -Presents w/ upper extremity adduction & internal rotation, pronated forearm, & asymmetric Moro (startle) reflex -Brachial plexus injuries in newborns most commonly caused by *stretching of the plexus* (e.g. significant neck traction) *during delivery* -Infants with *difficult extraction* (e.g. shoulder dystocia, forceps- or vacuum-assistance) often experience more traction & force and are at INCR risk for Erb-Duchenne palsy -*MACROSOMIA* (birth weight >4kg [>8lb, 8oz]), often seen with *Gestational diabetes*, is a Major RF for *Shoulder Dystocia* & therefore *brachial plexus injuries* -Most cases resolve spontaneously, improving over weeks to months Note: Breech positioning does NOT incr risk for brachial plexus injuries, but is assoc w/ deformational changes incl torticollis and developmental hip dysplasia

Breast Cancer in Men

-Breast cancer is uncommon in men (≈2500 cases DX annually in US) -However, certain _underlying genetic and hormonal abnormalities_ are assoc w/ an *elevated risk of male breast cancer*, incl: • *BRCA Mutations*— autosomal dominant mutations incr the risk of male breast cancer up to *100x*; BRCA2 mutations are considered the *single greatest RF for male Breast CA!* • *Klinefelter Syndrome*— presence of an *extra X* chromosome increases the estrogen:androgen ratio & results in a *20x* incr in the risk of male breast cancer. (Note: Klinefelter syndrome is d/t a *sporadic* error in cell division and is NOT an inherited disorder. Therefore, a FHX of Klinefelter does NOT incr risk of breast cancer) • *Hepatic Dysfunction, Marijuana Use, Obesity*— these conditions also incr the estrogen-to-androgen ratio, but confer a much lower risk of male breast cancer compared to BRCA mutations or Klinefelter syndrome

How to take care of amputated fingers, toes, ears, and genitalia that are accidentally amputated?

-Bring the body part with the pt to the emergency room! -Handling of the amputated part should be *as limited as possible* while taking care to *prevent it from drying out or being soaked in liquid* -For transportation purposes, the amputated part should be *wrapped in sterile gauze, moistened with saline, and placed in a sealed, sterile plastic bag* and that bag should be placed in an *cool environment* to *maintain a goal temperature of 1-10º C (34-50º F) to reduce warm ischemia time* (i.e. temp range b/w body and ambient temp), but not below this temperature range to *avoid inducing frostbite* E.g. Place the sterile bag containing the saline-moistened wrapped body part inside a chilled container containing ice mixed with saline or sterile water (50/50 mixture) -- this is the best combination of materials to best preserve the amputated part and keep it in that ideal temperature range Note: Putting the amputated part in a bag directly on ice (normal ice or dry ice!) can severely damage it and cause frostbite

Chronic Exertional Compartment Syndrome (CECS)

-CECS p/w *recurring episodes of compartmental pain that occur at the same time, same distance, * same intensity of exercise* -CECS is characterized by *incr pressure within a confined fascial compartment that impairs tissue perfusion - most likely d/t muscular volume expansion during strenuous exercise regimen* (military trainees) -Affected compartments are usu *bilateral, may be swollen/tense, w/ muscular tenderness*; *sometimes numbness & tingling d/t intracompartmental peripheral nerve compression* -*SX Completely Resolve with REST and are NOT present with normal everyday activity* -When PE & Imaging are done of pt *at rest --> PE & imaging normal* -*Definitive DX requires measurement of compartmental pressures immediately following exercise* -*Conservative management* may *reduce sx*, but *definitive management is elective fasciotomy*

Folate Deficiency - Quick overview

-Can *p/w weight loss, anemia, & diarrhea* -RBCs are characteristically *MACROCYTIC (Elevated MCV)*

Cross-Sectional Study Design

-Can be descriptive or analytic (can infer but not prove causation) -Subjects are *assessed at a specific point in time (SNAPSHOT, DISEASE PREVALENCE) to determine whether or not they have a certain RF and a certain disease of interest*; *some will not have been exposed or have the disease*

Mobitz Type II Second-Degree AV Block

-Can cause *bradycardia* -Ischemia, electrolyte abnormalities, medications (e.g. β-blockers, nondihydropyridine CCBs), infiltrative disease (e.g. sarcoidosis), or age-related fibrosis can all lead to *impaired electrical conduction across the AV node* -Pts may be ASX or have sx of *poor cardiac output* (e.g. *dyspnea, lightheaded, syncope*) -DX of Mobitz II AV block is made on EKG showing *intermittent nonconducted P waves* (i.e. *randomly dropped QRS complexes*) and a *regular/constant PR interval* (QRS complexes are usu wide) -It differs from Mobitz I AV block, which shows /nonconducted P waves following *progressive* PR interval prolongation/ -Unlike Mobitz I AV block (usu ASX and benign), *Mobitz II AV block has a HIGH rate of progression to complete (third-degree) AV Block* and potentially devastating outcomes (e.g. sudden cardiac death) -Therefore, in the absence of a reversible cause (e.g. pharmacological AV nodal blockage, hyperkalemia, MI), Mobitz II AV block *necessitates PERMANENT PACEMAKER placement*

Fibromyalgia - Quick Overview

-Can cause pain & muscle tenderness in young or middle-aged women -Pain is *typically widespread* and PE shows *tenderness at specific trigger points* (e.g. *midtrapezius, lateral epicondyle*)

What does a *streptozyme test* evaluate for?

-Can evaluate for a *streptococcal infection*, which can cause *PSGN* d/t *immune complex deposition* -Manifestations incl *renal insufficiency, nephritis, & LOW C3 complement levels* -Most pts have Normal C4 complement levels and a *recent Hx of strep pharyngitis or skin infection (impetigo)* -Palpable purpura uncommon (usu seen in Mixed Cryoglobulinemia syndrome)

Analgesic-Induced Nephropathy

-Can p/w *florid nephrotic range proteinuria (>3.5 g/d) -Often results from *NSAID meds* which cause a *reversible decline in renal blood flow & GFR d/t inhibition of vasodilatory prostaglandin production* -NSAIDs can also produce *acute interstitial nephritis* wherein a kidney bx would show minimal changes and a typical interstitial inflammatory pattern -Acute to subacute process Note: Multiple myeloma-induced proteinuria is usu NOT detected by urinalysis (the dye-reagent strip test unable to detect Ig light chains)

Myasthenia Gravis - Quick Overview

-Can p/w *fluctuating, fatigable bulbar muscle weakness (e.g. dysarthria, dysphagia)* that is *worse at the end of the day* -However, pain and focal muscle tenderness are uncommon -Caused by *autoantibodies to POSTsynaptic ACh receptor* (Type 2 HS rxn) -Sx: Ptosis, diplopia, weakness; worsens w/ muscle use; improvement after edrophonium (tensilon) test -Assoc w/ *thymoma, thymic hyperplasia* -If *administer AChE Inhibitor (Pyridostigmine)*: *reverses sx!*

Transient Hypertrophic Cardiomyopathy [of Newborns]

-Cardiac anomaly that occurs in *infants born to mothers with [gestational] diabetes and poor glycemic control during pregnancy* -Occurs in the *late second to early third trimester* due to *Fetal HYPERINSULINEMIA* in response to *maternal & fetal hyperglycemia* -Insulin triggers glycogen synthesis, *excess glycogen & fat deposited in myocardium, esp in IVS* -A *Hypertrophic Interventricular Septum* is usu *ASX*; However, IF *LV outflow tract obstructed*, manifestations of *congestive heart failure* may occur -Can cause *respiratory distress* (tachypnea, nasal flaring, retractions), *tachycardia* (heart murmur), *hypoxia*, and *failure to thrive* -Despite *pulmonary edema presence, crackles usu not auscultated* -*Pulmonary congestion & Cardiomegaly on CXR* -*ECHO CONFIRMS DX* -Although transient tachypnea of the newborn is a common cause of tachypnea and resp distress in newborns, *auscultation of a murmur* makes *cardiogenic* pulmonary edema d/t transient HCM the most likely etiology -Poorly controlled gestational DM causes incr infant risks for: *macrosomia, hypocalcemia, hyperviscosity d/t polycythemia, & respiratory difficulties* -- Most of these can be avoided w/ *strict glycemic control* throughout pregnancy (*Ideal fasting blood glucose ≤95*) *TX* • If *ASX* --> *No TX* needed • If *HF SX* --> *Propranolol & Fluid management* indicated -*Prognosis*: *SPONTANEOUS RESOLUTION* expected within a few weeks of life; Echo findings normalize within a year Note: *Hypoplastic left ventricle (hypoplastic left heart syndrome)* is an embryologic malformation that occurs early in the *first* trimester in moms with *PREgestational diabetes*; pts p/w *cyanosis* and abnormality is seen on second trimester U/S

Mitral Valve Prolapse (MVP)

-Cardiac auscultation of MVP typically reveals a *nonejection click* d/t snapping of the mitral chordae as the valve cusps extend into the atrium during systole, followed by a *systolic murmur of mitral regurgitation* -In each pt w/ MVP, there is a *critical left ventricular size* at which *prolapse occurs during ventricular contraction*; therefore, the timing of the click and murmur during systole varies depending on LVEDV • W/ *increased venous return* (e.g. squatting, supine leg raise), *LVEDV* is relatively *high* and the critical point at which prolapse occurs is reached *late in systole* or *NOT reached at all* (disappearance of the click) • In contrast, maneuvers that *decrease venous return* (e.g. standing, Valsalva) result in relatively *low LVEDV*, *earlier reaching* of the critical prolapse point during systole, and an *earlier click & murmur* -In general, a critical point that occurs at a relatively large left ventricular size (high LVEDV) is consistent w/ more *severe MVP* Note: Like MVP, the systolic murmur of hypertrophic cardiomyopathy (HCM) becomes LESS prominent w/ INCR venous return.

Hand Foot & Mouth Dz

-Caused by *COXSACKIEVIRUS infection* usu in *young kids in summer or fall* and in *communal settings* (e.g. day care) -Virus is shed in stool and is *transmitted by fecal-oral route* (diaper changes) *or by direct contact w/ respiratory. oral, or vesicular secretions* -Clinical features include a *PAINFUL [Anterior] Oral Mucosa Enanthem (Vesicles on tongue, buccal mucosa, that rupture to form ulcers) WITH a Maculopapular or Vesicular Exanthem (Rash) on the hands & feet (palms & soles), Nonpruritic (no excoriations) but occasionally painful* -Coxsackievirus can occasionally cause *Herpangina*, a condition *differentiated from hand-foot-mouth dz by the Absence of an Exanthem and the presence of Oral Ulcers affecting the Posterior Oropharynx (not anterior)*

Rickets Disease

-Caused by *vitamin D deficiency* -Causes pathologic *genu varum* (*"bowleg"*) in children (causes osteomalacia in adults, w/ bone pain & muscle weakness) and is treated with vitamin replacement Note: Breastfed infants should receive oral vitamin D

Staging of Pressure (Decubitus) Ulcers

-Caused by constant, unrelieved pressure, leading to reduced blood flow and necrosis of skin and subQ tissues -4 stages based on depth of involvement: *Stage I*: characterized by *nonblanchable erythema* of *intact* skin *Stage II*: *superficial* ulcers causing a *partial thickness loss* of epidermis, dermis, or both *Stage III*: *deeper ulcers* causing a *full thickness loss W/ damage to subQ tissue* that may extend to (but not through) any underlying fascia *Stage IV*: *very deep ulcers* causing a *full thickness loss W/ extensive tissue destruction* that may *damage adjacent muscle, bone, or supporting structures* -Initial management of pressure ulcers includes local wound care, repositioning to reduce pressure, pain control, & nutritional support -*Shallow ulcers (stages I & II)*, which do not extend into subQ, are managed w/ *occlusive or semipermeable dressings to maintain a moist wound environment* -*Full thickness wounds (stages III & IV)* require *DEBRIDEMENT OF DEVITALIZED (I.E. NECROTIC) TISSUE* and *specialized wound dressings* may be needed

Scarlet fever

-Caused by group A β-hemolytic Streptococcus (S. pyogenes) -P/w *"sandpaper rash" (small papules), strawberry tongue, & cirumoral pallor* -Typically accompanies *streptococcal pharyngitis* (e.g. pharyngeal erythema/exudate) and does NOT cause conjunctivitis -TX with *oral Amoxicillin*

Laryngomalacia

-Causes *chronic stridor in infants*, typified by *"floppy" supraglottic structures* that *collapse on inspiration* -May be d/t laryngeal hypotonia (d/t delayed maturation or neuromuscular disorder), redundant supraglottic soft tissue, and inflam 2º to reflux -*Inspiratory stridor* begins in neonatal period and is *loudest at age 4-8mo* -- *worse when supine*, better when prone, and *exacerbated by feeding or URIs* -DX Confirmed by *visualizing larynx by Flexible Fiberoptic Laryngoscopy* -- see an omega-shaped epiglottis and collapse of supraglottic structures on inspiration -TX reflux usu improves sx -Most infants w/ laryngomalacia will feed, grow, and ventilate normally w/ *spontaneous resolution of stridor by age 18mo* -Infants w/ feeding difficulties, tachypnea, cyanosis, or failure to thrive may need *surgery*

Primary HSV type 1 Infection in Children

-Causes *gingivostomatitis in kids* -These pts tend to be *febrile, and ill-appearing with vesicles on the anterior oral mucosa, gingivae, and perioral skin*

Breast Milk Jaundice

-Common cause of *UNCONJUGATED HYPERBILIRUBINEMIA in EXCLUSIVELY-BREASTFED Infants* that *Develops within the First 3-5 DAYS of life & Peaks by 2 WEEKS OLD* and is seen in *WELL-appearing, healthy, ASX infants w/ jaundice of face, neck, & chest* who are breastfeeding successfully -D/t *High β-glucuronidase activity in breast milk* that *deconjugates intestinal bilirubin* and allows for *increased intestinal bilirubin absorption & enterohepatic circulation of bilirubin* -*TX*: Frequent f/u and monitoring of infant's hyperbilirubinemia and to *Continue Breastfeeding Exclusively* (encouraged!) as the *jaundice should resolve spontaneously by age 3MO* (Good prognosis!) Note: Breast milk jaundice very rarely causes kernicterus, so there's no benefit to stopping breastfeeding. NO anemia seen in breast milk jaundice

Thyroid effects of Amiodarone

-Causes *thyroid dysfunction* d/t its high iodine content and intrinsic effects on thyroid metabolism -Both hypo- & hyperthyroidism can occur, but hypothyroidism is more common -The *large iodine load suppresses synthesis of thyroid hormone* (Wolff-Chaikoff effect) (which causes incr TSH & decr T4) and *amiodarone also directly inhibits the conversion of T4 to T3* (causing incr T4, decr T3) -In pts w/ /normal thyroid fxn/, this can lead to a /transient subclinical hypothyroidism/ in the first few months of amiodarone use -In pts w/ /preexisting chronic lymphocytic (Hashimoto) thyroiditis/, it can cause /over & prolonged hypothyroidism/ -Conversely, it can cause *hyperthyroidism* d/t *increased thyroid hormone synthesis* in pts w/ nodular thyroid dz or latent Graves dz (*amiodarone-induced thyrotoxicosis type 1*) or due to a *destructive thyroiditis* w/ release of preformed thyroid hormone (*amiodarone-induced thyrotoxicosis type 2*) -Pts on CHRONIC Amiodarone therapy should have *periodic monitoring of TSH q3-4mo*

Tuberculous Meningitis

-Causes 2-3wks of prodromal sx (e.g. headache, low-grade fever, lethargy), followed by progressive sx of meningeal irritation (e.g. nuchal rigidity, vomiting, confusion) -Cranial nerve palsies, coma, & seizures may occur -*Choroidal tubercles* (yellow-white nodules near optic disk) are often detected using fundoscopy -Suspicion for tuberculous meningitis raised when brain imaging shows *basilar meningeal enhancement* and *CSF* shows *elevated protein* (>250), *LOW GLUCOSE* (<45), *Lymphocytic Pleocytosis*, *elevated Adenosine Deaminase* -DX requires *serial lumbar punctures* with *CSF examination for acid-fast bacilli using smear & culture* -TX: *Prolonged TX* is required w/ *2mo of 4-drug therapy (isoniazid, rifampin, pyrazinamide, & either fluoroquinolone or injectable aminoglycoside), followed by 9-12mo of continuation therapy (isoniazid + rifampin)*' -Since antitubercular tx can result in /transient worsening of CNS inflam/, tuberculous meningitis pts are typically given *6-8wks of Adjuvant Glucocorticoid therapy (dexamethasone or prednisone)* which *significantly reduces M&M* Note: INH, RIF, & pyrazinamide are all bactericidal with *good CSF penetration*, so /intrathecal/ meds not required NOTE: Tuberculous meningitis *IS assoc w/ HIGH RISK of Long-term Neurologic Sequelae*; Prompt TX /reduces this risk but many pts *have permanent neurologic damage*/

Central Brain Herniation - Presentation

-Central herniation occurs when the *diencephalon & midbrain become caudally displaced* [downward] *through the tentorium cerebelli*, causing *compression of brainstem* and rupture of branches of the basial A --> further ischemic injury -Common findings incl: • *Cushing Triad - HTN, Bradycardia, Irregular Respirations* • *Unconsciousness* • *Midsized, FIXED Pupils* • *Abnormal Limb Posturing* (*starts as decorticate [flexor] posturing, followed by decerebrate [extensor] posturing* as brainstem injury progresses caudally) -TX focused on *DECR ICP & correcting the underlying etiology* (e.g. intracranial hemorrhage evacuation) to *prevent tonsillar herniation* - which can *compress the medulla* and cause *cardiac & resp arrest*

When would you need to place a cerclage?

-Cerclage placement is indicated to *prevent preterm delivery* in pts w/ *hx of cervical insufficiency*, a structural weakness in the cervix that can lead to *spontaneous, painLESS, second-trimester pregnancy loss* RF for cervical insufficiency: Cervical trauma, cervical surgeries (e.g. conization), and congenital anomalies

Central Hypothyroidism

-Characterized by *LOW Thyroid Hormone (low T4) levels WITH LOW/LOW-NORMAL TSH levels* (TSH secr by anterior pituitary) -Central hypothyroidism should *prompt assessment of other pituitary hormones && pituitary imaging (MRI)* -Central hypothyroidism is suggested by typical clinical features including *low serum Na (decr renal water clearance), borderline low TSH, & low free T4 levels* -Normally, low thyroid hormone levels (free T3, free T4) should cause a substantial increase in TSH levels -- *but in central hypothyroidism, the low free T3 is NOT accompanied by elevated TSH, strongly suggesting hypothalamic or [anterior] pituitary disease*

Premenstrual Syndrome (PMS)

-Characterized by *affective & somatic SX during the second half of the menstrual cycle (late luteal phase)* that *consistently resolve with the onset of menses* -Typical SX incl *depression, anxiety, irritability, bloating, & breast tenderness* -*Premenstrual Dysphoric Disorder (PMDD)* is a *severe form of PMS* characterized by *predominant anger & irritability* and can cause impairment in activities of daily life -*Pharmacologic management for PMS/PMDD* should be considered, esp in those w/ *severe sx* (e.g. *impaired work performance*) -*SSRIs* are *FIRST-line therapy for PMS/PMDD* -*FLUOXETINE* has been most extensively studied and *relieves both affective & somatic SX of PMS/PMDD* -HOWEVER, *any single SSRI may not relieve SX in 1/3rd of pts*; therefore, *Trialing with a Different SSRI (e.g. Citalopram) is usu warranted* given an *overall effectiveness & favorable AE profile* -IF *SSRIs are INEFFECTIVE, switching to combined estrogen/progestin OCPs is reasonable* in those *without contraindications* (e.g. migraines w/ aura); *progestin-ONLY contraceptives are NOT effective* Note: Bupropion is effective in TX depression, and is useful in combination with SSRIs bc it can reverse many adverse sexual effects assoc w/ SSRI use, but *use of bupropion alone has limited benefit in PMS/PMDD* Note: Pts w/ *no SX relief from SSRIs or combined OCPs can try a GnRH Agonist (LEUPROLIDE)* -- However, *Leuprolide suppresses estrogen prodn & induces Sx of Menopause* (e.g. decr bone mineral density, atrophic vaginitis); therefore it is usu NOT recommended unless other therapies are ineffective

Acute HBV Infection

-Characterized by *elevated aminotransferases, positive hepatitis B surface antigen, hepatitis B IgM core antibody, hepatitis B e antigen (indicator of high infectivity), and detectable hepatitis B DNA*. -Nearly *70% of pts w/ acute HBV infxn are ASX* -The remaining 30% dev SX such as *anorexia, nausea, jaundice, & RUQ discomfort*; however, even symptomatic pts are at *very low risk of acute liver failure* or other significant complications -Most cases of acute HBV (even w/ marked elevations in aminotransferases) *resolve spontaneously* and can be managed w/ *outpatient supportive care & close f/u* -Hospitalization is reserved for those w/ severe illness, increased risk of short-term complications, or significant comorbid conditions -This generally incl pts w/ significant fever or hemodynamic instability, impaired hepatic synthetic fxn (e.g. abnormal coagulation markers), or other signs of acute liver failure (e.g. Encephalopathy) -Hospitalization can also be considered for pts age >50, have poor oral intake, or have minimal social support Note: Antiviral therapy is recommended for pts w/ immunosuppression, concurrent Hepatitis C, severe hepatitis, or fulminant hepatic failure.

Histrionic Personality Disorder

-Characterized by *excessive superficial emotionality and attention seeking* -*Using appearance* to attract attention, *dramatic but shallow and shifting emotions* regarding a romantic breakup, and continued inappropriate familiarity and seductive behavior towards a physician -Histrionic personality disorder pts exhibit *excessive emotionality* and may attempt to *manipulate the physician-patient relationship through seduction and dramatic descriptions of new sx* at each visit -*Eagerness to move on to more exciting romantic opportunities and disappointment after not receiving attention* are also characteristic -*Firm boundaries* are required to *protect the physician-patient relationship* -Histrionic personality disorder should be differentiated from borderline, dependent, and narcissistic personality disorders, but these can also co-occur Note: *Borderline personality disorder can also exhibit attention seeking, manipulative behavior, and rapidly shifting emotions. As well as self-injurious and suicidal behavior, intense anger, chronic feelings of emptiness, and identity disturbance*

Anterior Uveitis (aka Iritis)

-Characterized by *pain, redness, variable vision loss, and a constricted & irregular pupil* -To properly distinguish iritis from other causes of a red eye, it is *imp to visualize the anterior segment of the eye w/ Slit Lamp Examination* -- If *LEUKOCYTES are identified in the ANTERIOR SEGMENT of the eye*, which *contains aqueous humor found b/w the cornea and the lens*, then the *DX of Iritis is Confirmed* -A hazy "flare", which is indicative of protein accumulation 2/2 to a damaged blood-aqueous barrier, may also be seen -*TX for Iritis depends on etiology*, but typically includes *Antimicrobial therapy for Viral or Bacterial causes, and Topical Corticosteroids for Noninfectious causes*

Statin Myopathy

-Characterized by an *Elevated CK level and NORMAL ESR* (conversely to normal CK & elevated ESR in polymyalgia rheumatica)

Factitious Disorder

-Characterized by the *INTENTIONAL Falsification of SX in the ABSENCE of obvious external rewards (i.e. NO 2° external gains - e.g. avoiding work, obtaining compensation)* -*SX are Intentional, Motivation is UNCONSCIOUS* -Patient *consciously creates physical &/or psychological symptoms* in order to *assume "sick role" and to get medical attention and sympathy (1° [INTERNAL] gain).* *Factitious Disorder Imposed on SELF* (formerly *Munchausen Syndrome*) -Chronic factitious disorder with *predominantly physical signs & sx* -*Characterized by a Hx of Multiple hospital admissions & willingness to undergo invasive procedures* -More common in *females & healthcare workers* *Factitious Disorder Imposed on ANOTHER* (formerly *Munchausen Syndrome BY PROXY*) -*Illness in an individual being cared for* (most often a *child*, also seen in *disabled or older adults*) *is DIRECTLY CAUSED (e.g. Physically HARMING a child) or FABRICATED(e.g. LYING INTENTIONALLY about a child's sx) BY the CAREGIVER* -*Form of child/elder abuse!!*

Sjogren syndrome

-Chronic autoimmune condition primarily affecting the *lacrimal & salivary glands* (exocrine glands) by lymphocytic infiltration, in 40-60yo Females -Findings: • Inflammatory joint pain • Keratoconjunctivitis sicca (decr tear production & subsequent corneal damage -> gritty, burning sensation; stringy discharge) • Xerostomia (decr saliva production -> dental caries, dry mouth & tongue) • Presence of antinuclear antibodies, rheumatoid factor (can be in the absence of rheumatoid arthritis), *antiribonucleoprotein antibodies*: *SS-A (anti-Ro) and/or SS-B (anti- La)* in 50% • Bilateral parotid enlargement -Labial salivary gland bx can confirm dx -Complications: Dental caries, *mucosa-associated lymphoid tissue (MALT) lymphoma* (may present as *parotid enlargement*) -The *Schirmer test* is used to confirm *dx of keratoconjunctivitis sicca* (filter paper placed along lower eyelid measured after a bit of time; too little wetting of tissue is consistent w/ *abnormal tear production*) -Existence of a *focal submandibular mass* should raise concern for a *B-cell non-Hodgkin lymphoma* in pts w/ SS, -Sjogren dz results in *polyclonal B cell activation* and infiltration of the salivary glands -In some pts, this *lymphocyte activation* can result in dev of a *B-cell lymphoma* (lifetime risk is 5% for SS pts)

Treatment for Ichthyosis Vulgaris

-Chronic, *inherited* disorder caused by *mutations of the Filaggrin gene that result in epidermal hyperplasia & defective keratinocyte desquamation* -Skin is *rough & dry, w/ white or gray fish-like scales* most noticeable on *extensor legs* (spares flexures & face) -*TREATMENT* ● *Long Baths to remove scales* ● *Frequent Moisturizing w/ Keratolytic-Containing Products to smooth & hydrate skin; *keratolytics (e.g. UREA, Lactic Acid, Salicylic Acid) not only Soften keratin, but also Loosen & facilitate shedding of scales* Note: Topical, high-potency corticosteroids (e.g. Clobetasol cream) do NOT help w/ Ichthyosis vulgaris

Acute Otitis Media

-Classically p/w *fever, ear pain, & bulging, erythematous, immobile tympanic membrane* -Clinical DX, but DX requires: • *Fluid EFFUSION in Middle Ear* -> Limited tympanic membrane mobility on insufflation • *Tympanic Membrane INFLAMMATION* -> *Bulging* of tympanic membrane (sensitive & specific!) -Other nonspecific signs of eardrum inflam incl *otalgia, tympanic membrane erythema, & fever* -Most common *bacterial pathogens* are *Strep pneumo, NONTYPEABLE H. flu, & Moraxella catarrhalis* -*H. flu can cause Otitis-Conjunctivitis Syndrome*, in which *purulent conjunctivitis co-occurs at the same time as AOM* -*Recurrent infection within 2wks of Tx* is sometimes *caused by the same pathogen as the initial infection d/t Resistant Strains* -Recurrent *infections ≥2wks after TX completion is likely d/t different pathogens* -Initial *uncomplicated AOM TX Empirically w/ 10d course of High-Dose AMOXICILLIN* -*Repeat infection within a month of initial TX is concerning for β-lactamase-producing strains of nontypeable H. flu, Strep pneumo, or Moraxella catarrhalis* -- *AMOXICILLIN-CLAVULANIC ACID* (w/ β-lactamase inhibitor) is the preferred *TX for Recurrent AOM* if pt already received Amoxicillin within the same month Note: Viral and bacterial causes of AOM are indistinguishable on otoscopy, but *viral causes (e.g. adenovirus) tends to cause concurrent sx* such as *nonpurulent* (rather than purulent) *conjunctivitis, pharyngitis, URI, & gastroenteritis*

Transient Synovitis

-Common cause of *hip pain in kids age 3-8yo* (DX of exclusion) -Self-limited, often postinfectious conditions (usu following viral infxn [upper resp infxn, gastroenteritis]) that presents with &unilateral hip pain and limp, but still with the ability to bear weight* on the affected extremity, and no signs of infection (e.g. high fever, elevated inflam markers) -Often have pain w/ internal rotation and limited ROM -Pathogenesis involves *transient inflam of the synovium* -Pts well-appearing and afebrile (or low-grade fever -Does not cause signifiant incr WBC or inflam markers) -U/S: Small joint effusions (uni-or bilateral); effusion in the contralateral hip w/o pain may represent asx synovitis

Polymyalgia Rheumatica

-Classically, pts *>50yo w/ subacute onset of muscle pain, most prominent in the SHOULDERS & HIPS (pelvic girdle mm), and a NORMAL Creatine Kinase (CK) level -- characteristic features of polymyalgia rheumatica (PMR)* -PMR is an *inflammatory disorder of the PROXIMAL joints, bursae, & tendons* -- the *muscle itself is UNaffected*, therefore *muscle Strength & CK levels WNL* -Pain in the soft tissues is actually *referred pain from nearby joints*, and *tenderness (if present) is typically MILD* -*Active range of motion* may be *limited d/t pain or stiffness*, but *passive ROM is usu Normal* -Though NO specific tests for PMR, *acute-phase inflam markers (e.g. ESR, CRP) are VERY SENSITIVE* and, when *elevated in pt w/ classic sx*, is considered *adequate indication to initiate TX w/ Low-Dose Glucocorticoids (e.g. Prednisone 20mg daily)* (TX of Choice!) -*Rapid relief of sx is expected*; therefore, failure to improve rapidly w/ glucocorticoid therapy should question the diagnosis Note: PMR is *freq assoc w/ Giant Cell Arteritis (GCA)*, which causes *HA, jaw claudication, vision loss, & tenderness over the temporal A*. To *prevent vision loss, HIGH-dose Glucocorticoids* (e.g. *Prednisone ≥60mg daily*) should be *started immediately* in pts in whom there is a consideration for GCA. But in pts w/ *sx of UNcomplicated PMR, TX should be deferred until obtaining ESR & CRP* bc glucocorticoids can rapidly normalize these inflam marker abnormalities, and cloud the dx

Brain Death Diagnosis

-Clinical criteria suggesting *brain death* include *Clinical/Brain Imaging Evidence of a Devastating Cause (i.e. a CNS catastrophe of Known Etiology), Absence of confounding factors (e.g. major endocrine or electrolyte disturbances, drug intoxication), AND Hemodynamic STABILITY (core body temp >36C [97F], Systolic BP >100; i.e. NO HYPOTHERMIA)* -If pts meet the ^above *positive clinical criteria* --> should Undergo *Neurologic Examination* to *document absent Cortical (Cerebral) & Brainstem Functions (Reflexes)* including: • *Coma* • *Absent motor response to pain* • *Absent pupillary light reflex* (i.e. *fixed & dilated pupils*) • *Absent corneal reflex* • *Absent oculocephalic (vestibulo-ocular) reflex* (i.e. *caloric testing produces NO conjugate eye deviation*) (Remember, normally, adding cold water to left ear causes both eyes to deviate to the left and then nystagmus to the right; & normally, adding warm water to left ear causes both eyes to look right; so *in comatose brainstem-injured pts, adding cold water to left ear produces NO eye response) (also *abnormal oculocephalic doll's eye test*, where *comatose-intact brainstem pts show conjugate movement of eyes in direction opposite to head movement; BUT in unconscious-brainstem dysfunction pts, an absent or asymmetric response is seen* • *Absent gag/cough reflex* with *tracheal suctioning* -If pts have *positive clinical criteria & abnormal neurologic findings* should undergo *APNEA TESTING* to *CONFIRM BRAIN DEATH (i.e. Brainstem Failure) DIAGNOSIS* - baseline PaCO2 & PaO2 obtained -> pt pre-oxygenated & disconnected from ventilator -> *Absence of respiratory response w/ a PaCO2 >60 (or >20 from baseline) and a Final arterial pH of <7.28* are considered a *positive apnea test*

Fat Embolism

-Clinical dx; consider this in a pt w/ multiple complicated fractures -Typically manifests 24-72hrs after severe trauma -Characterized by *triad of respiratory insufficiency, neurological impairment, & petechial rash* (rash on trunk; petechiae result d/t occlusion of dermal capillaries by fat globules, leading to extravasation of erythrocytes) -Other findings may incl: fever, tachycardia, AMS -NO abnormalities of platelet function have been documented -*Early immobilization & operative fixation of fractures reduces the chance of fat embolism*!! -Supportive care is the mainstay of therapy for clinically-apparent fat embolism

Irritant Contact Dermatitis (ICD)

-Clinical findings characteristic of ICD incl *pruritus, erythema, & scaling* of the skin -As sx become chronic, *hyperkeratosis & painful fissuring* are commonly seen -Sx are often worst where the skin is thinnest, at the dorsum of the hands, fingertips, & finger webs -*ICD is the cause of 80% of all cases of occupational hand dermatitis* -It is d/t *repeated exposure to irritants* (e.g. detergents, solvents, oxidizing agents) over time and may occur after days, weeks, or months of exposure to the irritant -ICD is *esp common in pts w/ underlying atopic dermatitis* and in healthcare workers who use occlusive gloves frequently -Other causes of hand dermatitis w/ similar features incl *allergic contact dermatitis, which is immune-mediated*, and *dyshidrotic eczema*, which is characterized by vesicular lesions *involving the palms and soles* -All of these disorders are initially managed w/: • Identification & avoidance of offending agents • Washing hands w/ lukewarm water & mild cleansers • Freq use of emollients • Topical glucocorticoids

Radiation-Induced Cardiotoxicity

-Clinical manifestations: *Coronary artery disease with Myocardial Ischemia and/or Infarction, *RESTRICTIVE CARDIOMYOPATHY WITH DIASTOLIC DYSFUNCTION, Pericardial disease, Valvular abnormalities, and/or Conduction defects* -Long-term survivors of Hodgkin lymphoma are at risk of dev cardiovascular complications d/t chemo &/or radiation -Radiation causes diffuse fibrosis in myocardial interstitium, along w/ progressive fibrosis of pericardial layers, cells in conduction system, and cusps and/or leaflets of valves -Radiation also affects intimal layer, w/ arterial narrowing typically involving the ostial parts of coronary vessels Note: *Anthracyclines (e.g. doxorubicin)* cause *dose-dependent decline in ejection fraction --> Dilated Cardiomyopathy* (NOT assoc w/ valvular dz or coronary artery dz)

Time-to-event Data

-Collected when the elapsed time before an event occurs is of significant interest -Accounts not only for the total number of events to both groups, but also for the timing of the events, which can be important when assessing treatment benefit -*Commonly used in Survival Analysis* where the *event of interest is Death* -*Survival analysis is commonly used to assess mortality benefit in prospective studies and clinical trials* - it *accounts not only for the number of events in both groups, but also for the timing of the events throughout the follow-up period*

Gallstone Pancreatitis Complicated by *Acute Cholangitis*

-Combo of *acute abdo pain & elevated serum lipase* is sufficient to *DX Acute Pancreatitis*, which most commonly d/t *alcohol & gallstones* -Additional sx of *fever and jaundice* makes *concomitant Acute Cholangitis* likely -Most frequent *causes of Acute Cholangitis are Choledocholithiasis, Biliary Stenosis, & Compression from Malignancy* -*To DX Acute Cholangitis, need all 3*: • *FEVER* or other inflammatory signs (e.g. *Leukocytosis, elevated CRP*) • *JAUNDICE or Abnormal LFTs* • *BILIARY DILATION* or evidence of the etiology on imaging (abdo U/S) -If all 3 diagnostic criteria are met, the next most appropriate test is *URGENT ERCP* --*ERCP can confirm the Dx and Provide Life-Saving Biliary Drainage!!* -If pt has *contraindications to ERCP* (e.g. hemodynamic instability, neurologic compromise), or if unavailable, *biliary drainage w/ percutaneous cholecystostomy* is an acceptable alternative -Although *cholecystectomy* will *eventually* be needed, it is not needed acutely

Invasive Pulmonary Aspergillosis

-Common cause of *pulmonary dz in pts w/ severe immunocompromise (e.g. s/p hematopoietic stem cell transplant), esp those w/ Prolonged Neutropenia or on Chronic Corticosteroids (at incr risk for life-threatening infection)* -*Pulmonary Aspergillosis is the MC manifestation of Aspergillus*, and is *characterized by Classic TRIAD of [Productive] COUGH, PLEURITIC CHEST PAIN, & HEMOPTYSIS [blood-streaked sputum]* -*Chest imaging usu reveals [cavitary] Nodules/Nodular Infiltrate w/ Surrounding Ground-Glass Opacities ("Halo Sign") or Cavitations with Air-Fluid Levels ("Air Crescent Sign")* -*DX Confirmed by Serum Fungal Biomarkers (Galactomannan & β-D-glucan assay) && Sputum Sampling for Fungal Staining and Culture* -Bronchoscopy with BAL and/or Biopsy may be required if these diagnostic tests are inconclusive -*TX with IV VORICONAZOLE and a REDUCTION of Immunosuppressive Medications is the Standard of Care, BUT 1yr Mortality >80%* -*Fluconazole is sometimes given for Candida PPX, BUT it is INEFFECTIVE AGAINST ASPERGILLUS!!*

Symptomatic Carotid Artery DZ

-Common cause of *stroke and TIA* -Symptomatic carotid A dz is DX when a pt w/ carotid stenosis develops TIA or nondisabling stroke in the vascular distribution of the diseased vessel -Manifestations arise d/t *low-flow states (obstructing lesions) or embolic disease* -Pts w/ *Symptomatic HIGH-grade (70-99%) carotid lesions and a life expectancy ≥5yrs, should undergo CAROTID ENDARTERECTOMY (CEA) to reduce future risk of stroke* -Risks of CEA likely outweigh potential benefits for pts who are poor surgical candidates (multiple comorbidities) , those w/ an ipsilateral stroke w/ persistent disabling neuro deficits, and those with 100% occlusion of the internal carotid A -*Management of lower-grade (<70%) lesions may be done either Medically (aspirin, statins, antihypertensives, control of athherosclerotic RF-hyperglycemia, HTN, smoking) or Surgically, depending on degree of stenosis and sex of pt

Heart Failure w/ Preserved Ejection Fraction (HFpEF)

-Common cause of HF -Chronic HFpEF manifests w/ *mild interstitial edema* (i.e. *Kerley B lines* on CXR) *without* alveolar edema (i.e. NO crackles on PE) but can eventually progress to alveolar edema which would show alveolar opacification on CXR -Echo shows *normal LVEF and left atrial dilation*, and *diastolic dysfunction is not always detectable* -Chronic systemic HTN & obesity are most prominent contributors to HFpEF, causing *concentric LVH & myocardial interstitial fibrosis* that lead to *diastolic dysfxn* and *eventual decompensated volume overload* -ACUTE HF would show significant alveolar edema (crackles) bc pulm lymphatics wouldn't have had time to adapt to backflow) Note: BNP <100 can excl clinically significant HF, but *obesity often causes falsely LOW BNP*

Hypothyroid Myopathy presentation

-Common cause of muscle weakness and can be assoc w/ CK elevation -Also assoc with myalgias, delayed reflexes, and other symptoms of hypothyroidism -Elevated TSH, low thyroxine (T4)

Gestational Thrombocytopenia

-Common cause of thrombocytopenia in pregnancy and is a *benign, ASX* condition defined by a *platelet count of 70,000-150,000* -Develops in the *second or third trimester* in pts w/ NO prior Hx of thrombocytopenia or associated fetal thrombocytopenia, and *resolves after delivery* -Etiology is not well-understood, but may be a combination of hemodilution + accelerated platelet destruction -However, *the risk of fetal & maternal hemorrhage is NOT increased* -Management is conservative & incl serial CBCs, w/ frequency depending on severity -The pt should be evaluated again postpartum to ensure resolution

Colles Fracture (Distal Radial fracture)

-Common fracture caused by falling onto an outstretched hand -Dorsally-angulated or displaced distal radius fracture that is usu assoc w/ visible angulation proximal to the wrist joint ("dinner fork deformity") -Lateral radiographs can confirm

Traveler's Diarrhea

-Common in those who travel from resource-rich to resource-limited countries, occurring at rates as high as 50% -The vast majority of cases are *bacterial* in origin, and the leading cause is *Enterotoxigenic Escherichia coli (ETEC)* -ETEC is transmitted via *contaminated water or food* and releases *enterotoxins in the intestine* that cause *watery diarrhea & crampy abdominal pain* **1-3 days after inoculation** -Fever, N/V, and myalgias may also occur -Infections are usu *self-limited* and *resolve w/ supportive therapy in 3-4d* -*Travelers to developing countries* can reduce their risk of ETEC infection by *avoiding peeled, uncooked fruits and vegetables; unpasteurized dairy products*; food from *street vendors*; and *untreated water* (incl *ICE*)

Primary CNS Lymphoma (PCNSL)

-Common malignancy in pts w/ *advanced HIV* infections -Strongly related to *EBV* -It is usu assoc. w/ a significant degree of immunosuppression -Most PCNSL pts have a *persistently depressed CD4 count (<50)* -Institution of HAART therapy is assoc. w/ an improved prognosis, esp in pts who demonstrate an improvement in the immune status (e.g. incr in CD4 count and decr in viral load), bc the degree immunosuppression seems to be the major determinant of these pt's survival Note: *Radiation therapy, combined w/ Corticosteroids*, induces a rapid response in 20-50% of pts; however, /this does not seem to significantly prolong the overall survival/

Cyanide Poisoning

-Commonly caused by combustion of common items (e.g. plastics, polyurethane foam) containing carbon & nitrogen; seen in structure fires, occupational exposures (e.g. mining), & cyanide-containing meds (sodium nitroprusside) -Cyanide acts as a *potent toxin* causing *inhibition of mitochondrial oxidative phosphorylation* thereby *blocking ATP prodn* and forcing cells to switch to *anaerobic metabolism* and leads to *cellular hypoxia, lactic acid formation, & metabolic acidosis* -Bc tissues cannot use oxygen, venous blood remains saturated (bright red) and it makes the *skin look red (Cherry red skin)* -*Early acute toxicity* is characterized by *headache, confusion, anxiety* (which can lead to *seizures, coma*), *severe elevated anion gap metabolic acidosis with incr lactic acid, and w/ compensatory cardioresp stimulation* (e.g. *tachycardia, tachypnea*) -But as ATP is depleted, *organ dysfunction* occurs and pts develop *bradycardia & hypotension (circulatory collapse, death within mins to hours unless treated promptly)* -Management: *Decontamination, Supportive care (e.g. 100% O2, IVF, vasopressors)*, and *Empiric TX* with *hydroxocobalamin ± sodium thiosulfate*

Number Needed to Harm (NNH)

-Number needed to harm is a *measure that indicates how many pts need to be exposed to a risk factor over a specific period of time before a harmful event occurs in 1 pt* -NNH is the inverse of the attributable risk (or the absolute risk increase) i.e. *NNH = 1/AR* or *NNH = 1/ARI* -The *absolute risk increase* is the *difference in incidence rate between the exposed and non-exposed pts*!!!! -The *attributable risk* is the *difference in risk between exposed and unexposed groups*

How should a physician handle communications with a large family system that is very involved with the pt's care?

-Communicating with a large family of a pt can become complicated when numerous family members ask questions and try to direct the pt's care - can become challenging to balance respect for family's communication style and cultural values with the need to provide clear & consistent info focused on the pt's best interests -When communicating w/ a *large family system*, it often helps to *establish a Primary Point of Contact* who is able to concisely communicate the family's Q's & concerns to the care team -Having a one single contact person can *minimize conflicting or redundant information being conveyed* and *facilitate consensus* for pt who prioritize family decision-making -If the pt has the decision-making capacity, they should determine which family member is the primary communicator Note: Having daily family care conferences is most helpful when Q's & requests can be addressed at a single, designated time. But if there's family coming in & out all day, then one single daily meeting will be unlikely to address all their concerns adequately

Small Bowel Obstruction

-Complete obstruction of intestinal lumen leads to dilation of the stomach and proximal SI -This causes *abdominal distension, N/V, and intermittent abdominal pain* -*Postop adhesion formation* is the MCC of SBO in pts w/ a Hx of prior abdominal/pelvic surgery -Some less common causes incl hernia, neoplasm, volvulus, intussusception, & stricture formation in pts w/ inflammatory bowel disease.

Ehlers Danlos Syndrome (EDS)

-Connective tissue disorder caused by *COL5A1 & COL5A2 mutations (autosomal dominant)* -EDS is characterized by *joint hypermobility, recurrent joint dislocations, hyperextensible skin w/ easy bruisability, & delayed healing with atrophic scars (velvety skin)* -EDS can have *skeletal abnormalities*, incl *thoracolumbar scoliosis, pectus excavatum (sunken breastbone), & pes planus (flat feet)* -Other features incl *hernias, cervical insufficiency, & uterine prolapse* -*Mitral Valve Prolapse w/ myxomatous degeneration of valvular apparatus* is an EDS Complication and can lead to *rupture of the chordae tendinae & acute mitral valve regurg* Note: *Marfan Syndrome can also cause scoliosis and myxomatous mitral valve degeneration and chordae tendinae rupture leading to Acute Mitral Regurg. However, skin findings are much less prominent in Marfan*; velvety skin with atrophic findings --> c/w EDS!!

MOA of Combined Estrogen/Progestin Oral Contraceptive Pills

-Contraception achieved by suppression of GnRH pulses by small, constant doses of estrogen and progestin, thereby reducing FSH & LH secretion, and inhibiting ovulation -However, E&P can also affect the endometrial lining, and can cause *breakthrough bleeding* bc *progestins* create a *thin, atrophic endometrium that can shed erratically*, esp w/ OCPs w/ *low doses of estrogen* which normally acts to thicken and stabilize the endometrium -Therefore, can TX breakthrough bleeding with an OCP containing a higher dose of estrogen -Other common OCP AEs: breast tenderness, nausea, headaches, moodiness (usu in first few months of use) -Non-contraceptive benefits incl *tx of dysmenorrhea & AUB (e.g. anovulation, leiomyoma)*, *reduction of acne & hirsutism (e.g. PCOS), and DECR risk for ovarian & endometrial cancer*

Radiocontrast-Induced Acute Kidney Injury

-Contrast-assoc AKI develops *1-2days (24-48hrs) after contrast administration* -Assoc with *urinary muddy brown casts* on urinalysis -Most pts w/ CA-AKI have *nonoliguric* AKI *esp in the absence of underlying CKD)

Disseminated Intravascular Coagulation - Quick Overview

-DIC is a *consumptive coagulopathy*, leading to *both bleeding & thrombosis*, usu assoc w/ *sepsis, trauma, malignancy, or obstetric complications* -DIC usu causes an *elevated D-dimer (d/t accelerated fibrinolysis), prolonged PT & activated PTT (d/t depletion of clotting factors), often w/ low fibrinogen (d/t consumption)*

Severe DKA Treatment

-DKA is defined as metabolic acidosis (pH <7.3 or serum bicarb <15) in the setting of hyperglycemia (serum glucose >200) -Begins with *volume repletion* w/ *isotonic fluids* (e.g. Normal Saline, Ringer's lactate) given *over an hour* followed by initiation of an *insulin drip* -A small bolus [of fluids] given over an hour prior to initiating insulin therapy has been shown to minimize the risk of cerebral edema compared to starting an insulin drop immediately -*Potassium-containing IV fluids* should be administered *simultaneously w/ the Insulin Drip* for pts w/ Normal or Low K+ levels as insulin moves potassium intracellularly and causes hypokalemia -Ongoing management consists of blood work q1-2hrs & close titration of IVF to correct electrolyte derangements and acidosis -Pts should be closely monitored for signs of cerebral edema (e.g. AMS, lethargy, HA, vomiting) -A head CT should be ordered for pts in whom cerebral edema is suspected -Once the metabolic acidosis has resolved and the anion gap has closed, the pt can be transitioned to a subcutaneous insulin regimen

How many doses and at what ages is Diphtheria-tetanus-acellular pertussis (DTaP) given?

-DTaP is composed of *diphtheria toxoid, tetanus toxoid, & conjugated pertussis antigen (pertactin)* -*5 doses* are given at ages: • *2, 4, & 6 months old* • *15-18mo old* • *4-6yo* *Absolute Contraindications to TDaP* incl: -Encephalopathy after previous dose within 7 days (d/t the pertussis component -- meaning kids can't receive pertussis immunization, but CAN receive tetanus & diphtheria [Td] toxoid vaccines) -Anaphylaxis to vaccine component immediately after vaccine administration *Relative Contraindications* (given but delayed if risks perceived to outweigh benefits) -Extremely high fever (≥40.6 C [105 F]) -Seizures following previous DTaP vaccination -Ongoing evaluation for a neurologic condition

Triggers for Sickle Cell Crises

-Decongestants (bc they cause blood vessel constriction, triggering crisis) -High Altitudes -Cold weather -Swimming in Cold water -Heavy physical labor -Physical/Psychological stress -Pain -Alcohol and tobacco use -Loss of fluids (e.g. N/V) leading to Dehydration

Extrapyramidal Symptoms

-Develop within hours to days of starting or escalating antipsychotics -*Acute Dystonia*: Sudden, sustained contraction of neck, mouth tongue, & eye muscles after hours to days; Tx w/ *Benztropine, Diphenhydramine* -*Akathisia*: Subjective restlessness, inability to sit still after days to months; Tx w/ *Beta blocker (propranolol), Benzo (lorazepam), Benztropine* *Drug-Induced Parkinsonism (Bradykinesia)*: Gradual-onset tremor, rigidity & bradykinesia, masked facies after days to months; Tx w/ *Benztropine, Amantadine* *Tardive Dyskinesia (Chorea, esp orofacial)*: Gradual-onset dyskinesia of mouth, face, trunk, & extremities after prolonged therapy (>6mo to years after); Tx w/ *Valbenazine, Deutetrabenazine*; Benzodiazepines, Botulinum toxin injections also

Subclinical Thyrotoxicosis

-Defined as *LOW TSH w/ Normal Thyroid Hormone concentrations (normal Free T4 & Total T3) ± hyperthyroid symptoms* -*Transient fluctuations in thyroid markers can be seen, esp w/ acute illness*, but *persistently suppressed TSH levels warrant further eval* -*Causes of Subclinical Hyperthyroidism* Incl: ● *Exogenous thyroid hormone* ● *Graves Disease (anti-TSH receptor autoantibodies)* ● *Nodular Thyroid Disease (e.g. Thyroid Adenoma, Toxic Multinodular Goiter)* ● *Inflammatory Thyroiditis (e.g. Silent Thyroiditis, initial stages of Subacute de Quervain Granulomatous Thyroiditis)* -*TX with Antithyroid medication or Radioactive Iodine is warranted* for pts w/ *Persistently Severe TSH Suppression (<0.1 μU/mL)* (bc at a higher risk for progression to overt hyperthyroidism); *TX also warranted for those at INCR Risk for Complications d/t Age (≥65yo) or Comorbid conditions (e.g. heart disease, osteoporosis)* -Pts w/ *mildly suppressed TSH levels (0.1-0.5 μU/mL)* often experience *spontaneous remission* and can be *monitored w/ periodic thyroid fxn tests*

Chronic Spontaneous Urticaria

-Defined as *episodic urticaria lasting >6wks that occurs W/O apparent triggers* -Lesions are *intensely pruritic*, presenting as *confluent round or serpiginous erythematous plaques* (i.e. *wheals*) -Individual lesions appear and enlarge over mins to hrs before *disappearing within 24hrs* -~40% of cases accompanied by angioedema -*IDIOPATHIC 80-90%* of the time; Clinical DX -Bc of its *association w/ atopic & rheumatologic diseases, a limited lab eval* consisting of *CBC, inflam markers, LFTs, & urinalysis* is recommended, esp when other sx (e.g. arthritis, wt loss, fever) are present to look for potential underlying disorders -Standard management of CSU primarily involves second-generation H1 antihistamines, often at higher than usual doses and in combination with H2 antihistamines and leukotriene modifiers. Short courses of systemic glucocorticoids to control severe exacerbations may be needed. -*Sx are usu controllable w/o difficulty*, with >50% responding to standard therapy -It is usu *self-limited* and *resolves spontaneously within 2-5yrs*

Elder Abuse

-Defined as abuse (e.g. physical, sexual, psychological, financial) or neglect (e.g. abandonment) of individuals >65yo Indicators: *RF*: -Advanced age (>80yo) -Depression -Female -Hx of Hip Fracture or Stroke -Social isolation -Difficulty caring for self -Dementia -Poor socioeconomic status -Suspicious caretaker behavior -Indication of financial exploitation *Physical Signs*: -Skin tears, abrasions, & bruises lacking adequate explanation, esp on the trunk or other unusual locations -Fractures in sites not typical of osteoporotic fractures (e.g. long bones of arms & legs) [*spiral fractures*] -Dehydration & Malnutrition -Pressure Ulcers -Signs of Sexual Abuse (e.g. bruised breasts, anogenital trauma) -Pts should be interviewed *alone* and asked *direct questions* about living arrangements and abuse/neglect -If elder abuse is suspected, agencies such as the Adult Protective Services should be involved immediately.

Likelihood Ratio (LR) definition

-Defined as the *probability of a given test result occurring in a pt w/ a disorder compared to the probability of the same result occurring in a pt w/o the disorder* -LRs are *calculated from sensitivity & specificity* • For a *positive test result*: *Positive LR = Sensitivity/(1-Specificity)* • For a *negative test result*: *Negative LR = (1-Sensitivity)/Specificity* -*Just as sensitivity & specificity are INDEPENDENT OF DISEASE PREVALENCE, LRs do NOT change with prevalence of disease!* -LRs can be used to calculate the *post-test odds ratio (post-test odds = pre-test odds x LR)*, providing clinically relevant info for individual pts based on their pre-test odds of dz -Other *advantages of LRs* are that they *can be used w/ tests that have >2 possible test results* and they *can be used to combine the results of multiple diagnostic tests* Note: *Odds ratio is calculated in Case-Control studies to compare the exposure of participants w/ dz (cases) to the exposure of participants w/o the dz (controls)* Note: *Relative risk is calculate in Cohort studies; participants followed over time to assess RF for developing a given dz. Relative risk is the ratio of the probability of an outcome occurring in the exposed group vs probability of it occurring in non-exposed group*

Solitary Pulmonary Nodule (SPN)

-Defined by the following features: • Rounded opacity • ≤3cm in diameter (>3cm is considered a "mass") • Surrounded by pulmonary parenchyma • No associated LN enlargement -The first step in evaluating an SPN is to compare previous x-rays or CT scans; a nodule w/ stable size and appearance over 2-3rs has a low risk for malignancy and requires no further workup -If the SPN has changed in size or appearance from previous imaging or if no previous imaging is available, the next step is to obtain a *CT scan of the chest* -CT scan has *high sensitivity* and may identify other SPNs that either are too small to detect on x-ray or are located in areas obscured on x-ray (e.g. costophrenic angles) -CT scan also allows for *better characterization* of the appearance of an SPN -An SPN that is partially solid (heterogeneous) or has a spiculated (spikes radiating from the surface), rather than rounded, surface is more likely to be malignant -In contrast, an SPN w/ a ground-glass appearance is less likely to be malignant -The size of an SPN strongly correlates w/ the chances of it being malignant -Nodules <0.6cm are unlikely to be malignant and generally don't require f/u; *Nodules >0.8cm require additional management or surveillance* -In addition to size, other factors that influence the probability of an SPN being malignant incl patient age, sex, smoking hx, FHX, location of the nodule in the lung, and radiographic appearance of the nodule -Nodules >0.8cm that are intermediate or high probability for malignancy (i.e. ≥5% probability) based on these factors require tissue diagnosis w/ *biopsy or surgical excision* -For pts in whom the need for tissue diagnosis is unclear, PET scan can be helpful; Nodules demonstrating high metabolic activity on PET scan are more likely malignant than benign and warrant biopsy or surgical excision

Hawthorne Effect

-Describes the *impact on subject's behavior from awareness of being observed by researchers* -Often *occurs in studies that look at behavioral outcomes* -Alterations in behavior d/t participation (or d/t potential for participation) awareness may significantly *impact how the subjects report on the outcomes of the study* -May result in an *overestimation of an intervention's effect* being reported not only by the participants (subjects), but also among the candidates for participation -Such *overestimation of the outcome* is a *threat to internal validity* of any study -*To MINIMIZE THE HAWTHORNE EFFECT*, *subjects should be kept unaware that they are being studied* if possible

Differing normal grief from a major depressive episode

-Difficult as sx overlap b/w the two -*Grieving* individuals tend to have *intermittent* periods of sadness that *revolve around reminders of deceased* -In contrast, *Depressed* individuals are more likely to have *continuous* sadness and *pervasive anhedonia*, and they experience *greater social & occupational dysfxn* -Like any other stressor, loss of a loved one can trigger a major depressive episode that may require Treatment

Digoxin Toxicity

-Digoxin *directly inhibits the Na/K-ATPase pump which indirectly inhibits the Na/Ca2+ exchanger, leading to Incr intra-myocyte Ca2+ --> Incr Cardiac Contraction* -Used in *Heart Failure* (*INCR Contractility,* positive inotropy), *A-Fib* (*Decr Conduction at AV node & depression at SA node* by *stimulating vagus nerve*) -*Digoxin TOXICITY is characterized by N/V/D (cholinergic effects), Anorexia, Fatigue, Confusion, Visual Disturbances (yellowed vision), & Cardiac Abnormalities (Arrhythmias, AV Block)*; can also lead to *Hyperkalemia (poor prognosis)* -Digoxin Toxicity can be *precipitated by the addition of VERAPAMIL CCB,* which *inhibits the renal tubular secretion of Digoxin, resulting in ~70-100% INCREASE in SERUM Digoxin Levels* -Other Meds that can lead to *Digoxin Toxicity* incl: *QUINIDINE, AMIODARONE, & SPIRONOLACTONE* -*Antidote TX for Digoxin Toxicity = Digoxin-specific antibody fragments + Normalizing K+ levels, Mg2+, & cardiac pacer*

Primary & Secondary Causes of Dilated Cardiomyopathy

-Dilated cardiomyopathy can lead to *symptomatic LV systolic dysfunction (EF <40%)* -Most cases are *IDIOPATHIC (Primary)*, but *Coronary Artery Disease (CAD) leading to Ischemic Cardiomyopathy* is the *Most Common Secondary Etiology* -Many pts w/ *Ischemic Cardiomyopathy do NOT have typical anginal Sx* and *Initially P/W SX of Heart Failure (dyspnea, volume overload)* -Therefore, *ALL pts w/ Unexplained NEW-Onset Heart Failure should be evaluated for CAD w/ STRESS TESTING or CORONARY ANGIOGRAPHY* -Although acute MI causes irreversible myocardial death, pts w/ *chronic myocardial ischemia (like from CAD) often have viable myocardial tissue w/ Reversibly-Depressed Contractility* -In these pts, *Coronary Revascularization* can lead to *Improvement of Sx, Systolic Fxn, & long-term mortality* Note: BNP levels can be used to differentiate HF exacerbation from other causes of dyspnea, and Troponin Levels are used for the detection of myocardial necrosis & infarction. These tests are more appropriate for evaluating Acute Sx rather than Chronic Progressive Dyspnea, and are unlikely to influence management in pts w/ known dilated cardiomyopathy & LV systolic dysfunction determined by Echo.

Central pontine myelinosis

-Dreaded complication of an overly rapid correction of plasma hypotonicity (of low serum sodium=hyponatremia) of significant duration (Na≤120 for>2d) -Osmotic shock to oligodendrocytes --> rapid cell shrinkage, apoptosis, demyelination of adjacent neurons; central pontine gray matter is esp at risk bc highest density of oligodendrocytes -Classically p/w paralysis of all extremities (quadriplegia d/t demyelination of corticospinal tracts) & lower cranial nerves = altogether called *locked-in syndrome* -Cerebral function and upper cranial nerve function are typically spared; therefore, pts remain conscious and are able to communicate via blinking & vertical eye movements (horizontal eye movements through lower CN) -Typically irreversible

Management of Gestational Diabetes in Postpartum Period

-During 2nd & 3rd trimesters, the placenta increases secretion of diabetogenic hormones, which INCR Maternal Insulin Resistance to Promote Fetal Growth -However, women w/ insufficient pancreatic fxn to overcome the increased insulin resistance may develop GDM -GDM is usu dx at 24-48wks gestation using a *2-step approach* -- a *1hr glucose challenge test* & a *3hr glucose tolerance test* -Initial management incl dietary modification, but if blood glucose levels are not sufficiently controlled, then *either insulin (first-line) or an oral antihyperglycemic (e.g. metformin)* is indicated -*After placental delivery, maternal insulin resistance rapidly decreases, and glucose concentrations normalize to PRE-pregnancy levels* -Therefore, *GDM pts can DISCONTINUE Antihyperglycemic Therapy POSTPARTUM* bc their condition was placenta-mediated -However, some GDM pts may had /undiagnosed pregestational T2DM rather than simple GDM/ -For this reason, *GDM pts are screened with fasting blood glucose levels @48-72HRS Postpartum AND with a 2hr Glucose Tolerance Test @6-12WKS Postpartum* -Additional screening *q3yrs* bc *prior-GDM pts are at incr risk for T2DM*

Postdural Puncture Headache

-During placement of *neuraxial anesthesia (epidural), Unintentional Dural Puncture may occur* --> *CSF leakage, low CSF pressure* --> *Slight herniation of brain & brainstem* -Pts typically develop a *positional headache (i.e. worse when upright [sitting/standing], and improves when supine [lying down]) within 72hrs of procedure* -Other *assoc sx* incl *N/V, neck stiffness* -Most are *self-limited*, but pts with *severe sx that interfere w/ ADLs can be TX with Epidural Blood Patch*

Schizoaffective Disorder

-Dx would require a depressive or manic episode CO-OCCURRING w/ sx of Schizophrenia AND a lifetime hx of ≥2wks of psychosis sx in the absence of mood episodes

Dyspepsia Presentation & Initial Diagnostic Evaluation

-Dyspepsia are often *functional (idiopathic)*, but *nearly 25% have an organic cause* such as *peptic ulcer dz, GERD, or NSAID-induced gastritis* -Characterized by *epigastric pain*, often assoc w/ *postprandial fullness &/or nausea* -Pts *≥60yo with NEW Dyspepsia* are High-Risk & should undergo *Upper Endoscopy w/ Biopsy to r/o Malignancy* -*Upper endoscopy* is also recommended in those *<60yo w/ significant weight loss, overt GI bleeding, or >1 alarm feature (persistent vomiting, progressive dysphagia or odynophagia, palpable mass or LAD, unexplained iron deficiency anemia, FHX of GI malignancy)* -Pts with *dyspepsia age <60yo w/o alarm signs should be Tested for H. pylori infection* (e.g. *stool antigen, urea breath test*) and *treated if positive* (PPI + Clarithromycin + Amoxicillin/Metro) -Those who are negative for H. pylori or who fail to respond to therapy can be tx empirically with a PPI (pantoprazole, omeprazole)

Nonfunctioning Pituitary Adenomas

-E.g. Pt w/ amenorrhea & hypogonadism w/ suppressed LH and low-normal FSH levels but *increased alpha-subunits* -This presentation strongly suggests nonfunctioning pituitary adenoma, which usu *arises from gonadotropin-secreting cells (gonadotrophs)* in the pituitary gland -Normal gonadotrophs secr LH & FSH (dimeric hormones consisting of a common alpha-subunit and a different beta-subunit), but the *dysfunctional cells in most gonadotroph adenomas secr primarily just the common alpha-subunit* -Clinical Sx of alpha-subunit Overproduction are usu *minimal* (hence, *nonfunctioning* adenoma) -DX is not apparent until the adenoma is large enough to cause HA or visual disturbances (blurry, diplopia) d/t mass effect -*Preferred therapy for most nonfunctioning pit adenomas is Trans-Sphenoidal Surgery* which can provide *rapid relief of assoc neuro sx*; pts may regain normal gonadal fxn after resection -*Adjuvant Radiation* (field therapy or stereotactic radiation) may be used in pts w/ *incompletely resected adenomas* (but is not first-line d/t slow onset of action, risk of damage to surrounding neurologic tissues, and can lead to delayed hypopituitarism) Note: *Dopaminergic meds (e.g. Cabergoline)* are the preferred TX for *prolactin-secr adenomas (prolactin levels >200)* but don't help gonadotropin-secr adenomas. *Octreotide*, a somatostatin analogue, acts on somatostatin-r in the pituitary to *inhibit release of growth hormone* and is sometimes used in *GH-producing adenomas (Acromegaly)*

Subclinical Hypothyroidism

-Elevated TSH (repeat measurement), Normal free T4 (thyroxine), mild symptoms or ASX -MCC is *chronic lymphocytic (Hashimoto) thyroiditis* which is assoc w/ *ANTI-THYROID PEROXIDASE (ANTI-TPO) ANTIBODIES* (seen in >90%) -TX warranted for most pts w/ significant elevations in TSH, goiter, or convincing hypothyroid sx -For ASX pts w/ mild TSH elevations, an anti-TPO Ab titer increases the likelihood of progression to overt hypothyroidism & can identify pts who will benefit from tx -Subclinical hypothyroidism is assoc w/ pregnancy complications incl *recurrent miscarriages, severe preeclampsia, preterm birth, low birth wt, & placental abruption* -Anti-TPO Ab are assoc w/ incr risk for pregnancy loss, even in women who are euthyroid - so tx of these women may reduce the risk of recurrent miscarriages

Recurrent Calcium Kidney Stones - Management

-Elevated urinary calcium (i.e. hypercalciuria) greatly increases the risk for recurrent calcium (e.g. calcium oxalate, calcium phosphate) renal stone formation -Most pts w/ recurrent calcium stones can be TX with *increased fluid intake (e.g. ≥2 liters/day) and Dietary measures (incr fruits & veggies, less animal protein, incr potassium)* -However, some pts still have continued stone formation despite these measures, warranting addition of medication -*THIAZIDE DIURETICS are First-Line Pharmacotherapy for pts W/ HYPERCALCIURIA & RECURRENT CACIUM RENAL STONES* -Thiazides work by *reducing urinary calcium concentrations* by up to 50%, by creating a relative hypovolemia that *INCREASES THE REABSORPTION OF BOTH SODIUM && CALCIUM in the PCT & Loop of Henle* -So by *thiazides increases renal Ca reabsorption, this decreases [urinary Ca] and significantly reduces incidence of calcium stones* -Bc reabsorption of Na & Ca is tightly coupled, a *low-sodium diet is crucial* so that the Thiazide can work effectively

Diagnosis of Major Depressive Disorder

-Episodes characterized by *≥5 of the 9 diagnostic sx lasting ≥2wks*, one of which *must be pt-reported depressed mood or anhedonia* -SIGECAPS: Sleep disturbance; loss of Interest; excessive Guilt; low Energy; impaired Concentration; Appetite/weight changes; Psychomotor agitation/retardation; Suicidal ideation -This diagnosis requires *significant functional impairment & may be given regardless of an identifiable precipitant*

Dark urine following strenuous exercise - DDX?

-Exercise-induced hematuria -Myoglobinuria from rhabdomyolysis -March hemoglobinuria from RBC trauma (d/t repetitive trauma in feet causing red cell destruction) ALL of these cause positive blood on urinalysis -If RBC intact cells are present on microscopy--> Exercise-induced hematuria -If no intact RBCs on microscopy --> May be Myoglobinuria or Hemoglobinuria -Presence of RBC casts suggests a glomerular cause of hematuria -Do *REPEAT URINALYSIS IN 1wk* if think its exercise-induced, to ensure hematuria resolved -If rhabdomyolysis is suspected, serum creatine protein kinase (CPK) is more helpful than serum myoglobin -Only think about cystoscopy if hematuria persists beyond 1wk

Lab Findings in Hypothermia

-Extensive biochemical abnormalities! -Anion Gap Metabolic & Respiratory Acidosis (low Bicarb) -Azotemia (elevated BUN & Cr) -Hyperkalemia -Hyperglycemia (insulin stops working at temps <30ºC [86ºF]; glucose goes down with warming in nondiabetics) -Hemoconcentration (high hematocrit) -Sequestration of WBCs and PLTs (d/t splenic sequestration) -Coagulopathy (incr aPTT & PT d/t impaired coagulation [cold-induced inhibition of clotting pathways]) -Most of these lab abnormalities will resolve with appropriate warming and hydration, with improved tissue perfusion and active external warming. Want to support blood pressure and tissue perfusion with [warmed] IVF -Note: The usual increase in core temperature with external warming is *~1-2º C/hr* -Note: *Pulmonary Edema* is common in significant hypothermia, and usu improves with warming

TX of Pediatric [Functional] Constipation

-FIRST *dietary modifications* - *incr fluid and dietary fiber intake, decr dairy products* -NEXT step is *Laxative therapy* -- *OSMOTIC Laxatives (e.g. Lactulose, Polyethylene Glycol, Magnesium)* cause *retention of fluid in gut lumen & stool, causing softer bowel movements* -*Acute && LONG-term Osmotic Laxative use is SAFE for pediatric constipation* TX w/ *Stimulant Laxatives (bisacodyl, senna) or Rectal Enemas (Phosphate)* are generally *reserved for Acute relief of fecal impaction -- NOT long-term use*

Fibromyalgia (FM)

-FM presents most commonly in young to *middle-age women* with *widespread pain, fatigue, and cognitive/mood disturbances* -Pts typically have a fairly *normal PE* except for *Point Tenderness* in areas such as the *mid-trapezius, lateral epicondyle, costochondral jxn, & greater trochanter!!* -FM is a Clinical DX & has NO specific diagnostic lab findings!! -Limited lab testing is recommended to r/o common /conditions that mimic FM/, such as *anemia* (CBC) and *inflammatory arthropathy* (ESR or CRP) -Additionally, *Hypothyroidism* is prevalent in this pt population, and *Hypothyroid Myopathy* freq presents w/ findings similar to those of FM; a serum assay for *TSH* is warranted for most pts -In contrast, /serologic testing/ (e.g. Antinuclear Antibody, Rheumatoid Factor) has /low specificity and is NOT recommended/ in the absence of additional objective findings

Family Medical Leave Act (FMLA)

-FMLA is a *federally mandated benefit offered by large employers (>50 employees)* -*FMLA provides Employees with UP TO 12 WEEKS OF UNPAID LEAVE* (in *contrast to disability benefits, which provides compensated time off*) -*The employer MUST allow the employee to Return to the job, or its Equivalent, after leave is completed* -*Conditions appropriate for FMLA* Incl: • Employee has *serious illness or qualifying health condition* (incl *pregnancy*) OR, • Employee is *caring for an immediate family member (spouse/parent/child) with a serious illness (e.g. cancer)* -The Employee *MUST also have been with the Employer for ≥1year* -FMLA requires *certification from the provider caring for the person with the serious illness*

What are the most common acute drug reactions associated with *St. John's wort*?

-GI distress -Dizziness -Fatigue -Photosensitivity -Dry mouth -Longer term studies have found an increase in anorgasmia, urinary frequency, and swelling

What is the Genetic Information Nondiscrimination Act (GINA)?

-GINA *prohibits employers and health insurance companies from requesting and/or requiring predictive genetic testing to determine employment and health insurance eligibility* -As a result, *exclusion of employees at Higher risk for genetic disease* using the results of predictive genetic testing is ILLEGAL* -GINA protects employees by *preventing employers from requesting genetic info* to influence hiring, firing, compensation, promotions, or any decisions affecting terms of employment -Physicians should *educate pts about their rights* (*"It's your right to decline testing"*) *and legal protections against genetic discrimination* (*"It's illegal to request genetic testing"*) *under GINA*

Food Protein-Induced Allergic Proctocolitis (FPIAP)

-FPIAP is a *benign, self-limited condition of infancy* -A *non-IgE-mediated food allergy*, most commonly to *cow's milk or soy protein* that results in *colonic inflam & bleeding* (mucus- & blood-streaked stools) -Presentation involves a *well-appearing infant age <6mo w/ blood-streaked stools ± mucus* -Minority of pts have concomitant eczema or FHx of atopy -Clinical Dx, Confirmed by SX Resolution after *avoidance of offending food protein* -Infants taking cow's milk or soy-based formulas should be *switched to an Extensively Hydrolyzed Formula*, which is soy-free and in which highly allergenic cow's milk protein (e.g. casein) are already broken down and no longer antigenic -*Most FPIAP pts tolerate extensively hydrolyzed formula*, and *bloody stools Resolve in 1-2wks* -Rarely, an *amino acid-based ("elemental") formula* that contains *no intact proteins* may be required -It is *NOT recommended to switch from soy-based to cow's milk-based formula d/t potential cross-reactivity between the proteins* -USU not required, but *Flexible Sigmoid/Colonoscopy with Biopsy* may be considered if *refractory* after dietary changes or pts have *severe/atypical sx* (findings show mucosal inflam, eosinophilic infiltration confined to distal colon & rectum)

Definition of Failure to Thrive (FTT) - in terms of percentiles

-FTT is defined by *weight below the 5th percentile or down-trending weight percentiles crossing 2 or more major percentiles (e.g. 50th, 25th, 10th)* -Causes of FTT include: • *Inadequate calorie intake* - very often d/t *psychosocial stressors*, incl *poverty (lack food access), lack knowledge to properly feed (excessive water:formula powder ratio), poor parental/child relationship (neglect/abuse)* • Inadequate calorie absorption* - e.g. *cystic fibrosis, celiac disease* • *Increased calorie requirements* - e.g. *hyperthyroidism, congenital heart disease*

Myasthenia Gravis presentation

-Fatigability with repetitive nerve stimulation -TX w/ pyridostigmine -Can p/w *ptosis* (upper eyelid droopiness) and *proximal* muscle weakness would be expected (not distal, and no grip myotonia)

What's the first step in assessing GI bleed? And how can you tell if it's upper or lower GI Bleed?

-First step is *assessing hemodynamic stability* and *determine whether the source is upper or lower GI tract* (the ligament of Treitz separates) -*Bright red blood from the rectum (BRBPR)* is nearly always d/t a *lower GI bleed* -Hematemesis & melena are more common in upper GI bleed, but sometimes an UGIB can present w/ BRBPR if bleeding is particularly brisk -*Hemodynamic compromise, orthostasis & BUN/Cr ratio >20:1 are suggestive of UGIB*' -A nasogastric lavage with aspiration of bile and absence of blood increases the likelihood of LGIB if the bleeding source is unclear; however, it can miss a distal UGIB -Initial management incl fluids, blood type, cross & match -*Colonoscopy* has diagnostic & potentially therapeutic abilities in LGIB, and would be the next best step -If no bleeding source is found, *EGD* is performed -In pts who are *hemodynamically unstable or if UGIB suspected*, *EGD* should be considered to first excl a brisk UGIB (a non-contrast abdo CT can be helpful evaluating bleeding into peritoneum/retroperitoneum, but is NOT routinely used for evaluation of a GI hemorrhage)

Infant botulism

-Flaccid neuropathy in babies <1yo following the ingestion of *Clostridium botulinum spores* - usu found in honey, & environmental dust/soil (rural/farm areas where soil is often disturbed) -Immature GI tract of infants /lack protective enteric microbiota/, allowing spores to colonize and *produce in-situ neurotoxin* -*Botulinum neurotoxin inhibits PREsynaptic acetylcholine release into the neuromuscular junction* causing *dysfunction of the skeletal & smooth mm* and *autonomic dysfunction) (e.g. (decreased salivation, fluctuating HR/BP*) -Nonspecific early manifestations incl *CONSTIPATION & poor feeding* -Overtime, pts develop *oculobulbar weakness* resulting in *ptosis, impaired pupillary constriction, poor suck, &/or absent gag reflex* -Muscle weakness can progress to *DESCENDING PARALYSIS (FLOPPY BABY)* and *Respiratory Failure* -Neurologic exam reveals *Symmetric HYPOtonia, Diminished/Absent Deep Tendon Reflexes, & Decreased Strength* -DX Clinical; *Confirmation* by *stool C. botulinum spores or toxins* -TX: *IV Botulism Immune Globulin Antitoxin therapy* should be given *ASAP* in the illness course to *reduce the severity and duration of sx* -Give IV-BIG as soon as Dx is suspected and shouldn't be delayed awaiting confirmatory stool studies -*Close monitoring of resp fxn* usu in an ICU in case of sudden deteriorations -*Supportive care* includes *laxatives* for constipation and *nasogastric feeds* for poor suck -Infants often require *hospitalization for a few months*; However, a *Full Recovery* is expected with IV-BIG Note: Antibiotics are avoided as they can cause colonic C. botulinum to lyse, increasing toxin absorption

Plantar Warts (verrucae)

-Form of *cutaneous* warts usu d/t *HPV* -Plantar warts most often occur in *young adults* or those w/ certain occupations (e.g. meat, poultry, fish handlers) -More extensive dz in pts w/ atopic dermatitis or reduced cellular immunity (e.g. HIV, organ transplant) -Infection usu occurs via *skin-to-skin contact* and has an *incubation period of 2-6mo after exposure* -Clinical DX, w/ *visualization of single/multiple hyperkeratotic papules on the sole of foot* -*Scrapings* of hyperkeratotic debris can *Confirm DX* by showing *thrombosed capillaries* (aka *seeds*) -Shave or punch biopsy rarely needed to confirm dx in uncertain cases -*TOPICAL SALICYLIC ACID* is the preferred initial TX; Initial response seen in 2-3wks, and *pts assessed q2-3wk intervals for resolution* -Alternative TX is liquid nitrogen cryotherapy but can cause local burning and hypopigmentation Note: *TX is CONTINUED for an ADDITIONAL 1-2wks AFTER Clinical Resolution to Eradicate HPV virus and Prevent Recurrence!!* -Some pts require TX for several weeks or months

Group B Streptococcus Management of Neonates

-GBS is the MCC of early-onset (<7 days old) Neonatal Sepsis -GBS is transmitted via ascending colonization of maternal genital tract -- risk minimized w/ intrapartum ABX PPX prevents transmission -Indications for ABX PPX incl maternal GBS bacteriuria, positive maternal rectovaginal culture for GBS (obtained at 36-38wks), a Sibling with Invasive GBS dz, or an Unknown GBS status w/ certain RF (e.g. rupture of membranes >18hrs) will warrant PPX -*PPX is ADEQUATE if Ampicillin, Penicillin, Cefazolin is given ≥4HRS BEFORE DELIVERY* -Admin of vancomycin, clindamycin, or other ABX is Inadequate d/t bacterial resistance & slower distribution across placenta into amniotic fluid -*WELL-Appearing Neonates of gestational age ≥35wks born to moms with INADEQUATE (e.g. not administered ≥4hrs before delivery) but Indicated Intrapartum PPX against GBS should be OBSERVED [only] for signs of sepsis over 36-48hrs, d/t a lower risk of infxn compared to those who are ill/premature* (which is when early-onset GBS sepsis would develop) -*Blood cx and Abx are indicated for clinical signs of neonatal infxn, intrapartum maternal fever [during L&D], or preterm delivery [<35wks] prompted by potential infxn (e.g. preterm labor)*

Helicobacter Pylori infection & TX

-H. pylori is an imp RF for developing *Peptic Ulcer DZ (PUD), Gastric Cancer, and Mucosa-Assoc. Lymphoid Tissue Lymphoma (MALT)* -H. pylori accounts for *70-80% of Duodenal ulcers & ~50% of Gastric ulcers* -*Eradication* significantly *DECR Risk of PUD Recurrence!!* -Preferred initial regimens depend on local antibiotic susceptibility for H. pylori: • *Limited Clarithromycin Resistance*: Initial regimen is *TRIPLE Therapy with a PPI (omeprazole), Clarithromycin, & Amoxicillin x14d* -- Can use *Metronidazole* if penicillin-allergic • *Clarithromycin-Resistant Area ≥15% Resistance*: Initial regimen with *QUADRUPLE Therapy with PPI, Bismuth, Metronidazole, & Tetracycline x14d* (or a PPI w/ 3 antibiotics) Note: Pts w/ H. pylori infection are at INCR risk for Ulcer formation in the setting of NSAID use; pts should be encouraged to avoid NSAID use until completing tx. However, in the absence of Abx therapy, the infxn will likely PERSIST, placing the pt at continued risk for complications assoc w/ H. pylori. Pts also won't need /indefinite PPI use/ to manage PUD, usu only needed for 2wks and rarely needed >12wks

Management of Hydatidiform Mole (HM)

-HM is the result of *abnormal fertilization of an empty ovum by 2 sperm or 1 sperm those genome duplicates* -Resulting gestation contains *hypertrophic & hydropic trophoblastic villi* that cause *markedly elevated β-hCG (>100,000 IU/L)* -HM is a *premalignant* disease, that can *develop into Gestational Trophoblastic Neoplasia (GTN)* (e.g. *Choriocarcinoma*) -TX of HM involves *uterine evacuation via suction curettage/hysterectomy and surveillance for the development of GTN* -- *Serial Quantitative β-hCG levels are followed as a marker for disease progression and/or remission* -- followed *weekly until undetectable, and then monthly for an additional 6mo after undetectable* -If there is a plateau or increase in β-hCG - this leads to a DX of GTN (evaluate w/ pelvic U/S for pelvic mass & uterine enlargement, CXR for lung metastasis, and Tx w/ Methotrexate) -During this surveillance period, *CONTRACEPTION is required* as pregnancy makes it difficult to determine the significance of a rising β-hCG level -*GTN rarely develops >6mo after TX for HM* - therefore, only after the 6mo can pts try to conceive again -

What are the *neuropsychiatric sx of SLE?*

-Headache -Seizures -Polyneuropathies -Cognitive dysfunction -Anxiety -Mood changes -*New-onset psychosis* -- occurring in 5% of pts Psychosis d/t SLE can be symptomatically TX by antipsychotics, but sx usu respond well to*Oral Steroids within 2-4wks*

Who needs *postexposure PPX after exposure to Herpes Zoster (Shingles)*?

-Healthcare workers who *do NOT have immunity to VZV* (i.e. *who did NOT have varicella [chickenpox] as a child and/or absent/incomplete varicella vaccine*) typically *Receive Postexposure PPX WITH the VARICELLA VACCINE WITHIN 5-DAYS of Exposure* -- this *reduces risk of transmission by 80%* -For those who *do NOT have immunity to VZV && are ALSO Immunocompromised or Pregnant* --> *Require Varicella-Zoster IMMUNOGLOBULIN or Antiviral Therapy (if immune globulin is unavailable)* -Healthcare workers who had a *previously documented Hx of Varicella (chickenpox as a child) OR have received the 2-dose Varicella Vaccine* are *considered IMMUNE TO VZV* -- *Those who are IMMUNE do NOT require postexposure PPX after being exposed to someone w/ herpes zoster* Note: The *ZOSTER Vaccine* (different than the varicella vaccine) is *recommended for ppl >60yo to reduce the risk of Herpes Zoster*; it is NOT used for postexposure ppx.

Caffeine Intoxication presentation

-Heart palpitations, anxiety, psychomotor agitation -In severe cases --> may precipitate a seizure, cardiac arrhythmia, and/or hallucinations

Saw Palmetto

-Herbal supplement used to tx benign prostatic hyperplasia, but AE incl hepatic injury -Generally well-tolerated and typically causes only mild side effects (e.g. *GI discomfort*, HA, dizziness) -Saw palmetto should be used cautiously in pts undergoing surgery d/t a *possible increased risk of Perioperative Bleeding* (likely d/t *platelet dysfunction*) Note: Other popular herbal remedies assoc w/ increased bleeding risk include ginkgo biloba, ginseng, and garlic

Which microbial infection is a human bite most likely to transmit? (Causing cellulitis)

-Human bites can cause a polymicrobial infection associated with aerobic (α-hemolytic streptococci [Strep pneumo], Staphylococcus aureus) and anaerobic bacteria -*Eikenella corrodens* is a gram-neg anaerobe commonly found in infections d/t human bites TX: -Tx must include *anaerobic coverage*, particularly against Eikenella corrodens -*PO AMOXICILLIN/CLAVULANATE* (or IV Ampicillin-Sulbactam if IV therapy indicated) is the drug of choice as it covers all the common pathogens in human bite infections Note: Cephalexin & Clindamycin don't provide coverage against E. corrodens

Risk factors for preterm labor

-Hx of preterm delivery -Multiple gestation -Genitourinary tract infection (e.g. group B streptococcus)

Intrahepatic Cholestasis of Pregnancy (ICP)

-ICP typically occurs in the *third trimester* and is likely d/t increased estrogen & progesterone levels that cause hepatobiliary tract stasis and decreased bile excretion -Results in *Elevated Total Bile Acids (≥10 umol/L)*, which is *diagnostic for ICP* and can cause a *generalized, intractable pruritus that is worse on the palms & soles, with NO assoc. rash*; some pts have *RUQ pain and elevated AST & ALT* (Alk phos is also often elevated but isn't specific for ICP, bc the placenta produces ALP too) -ICP *does NOT incr risk of maternal complications*, BUT bc *bile acids can pass transplacentally*, this *DOES Incr risk for fetal complications (e.g. IUFD, meconium-stained amniotic fluid, neonatal RDS)* -Management allows maternal relief from pruritus and *prevents fetal complications* -- *First-line TX is URSODEOXYCHOLIC ACID* which is SAFE in pregnancy and improves pruritus and may decr obstetric complications -Additionally, pts require *regular fetal assessment (e.g. nonstress test) & Delivery @37wks gestation* -Can also add an antihistamine

How to you manage diabetic gastroparesis?

-In addition to *improving control of hyperglycemia, Dietary Modification* is generally the *first step* in management of diabetic gastroparesis -*Smaller-volume, more frequent meals* is usu helpful in limiting sx (N/V, postprandial fullness, bloating, regurg of undigested food, succussion splash auscultation) -*Foods high in fat or Insoluble Fiber can SLOW gastric emptying & should be AVOIDED* -- Encourage a low-fat diet w/ soluble fibers! -If dietary modification, glucose control in diabetic gastroparesis, FAILS to improve SX or if pts have moderate to severe sx, *promotility meds* can be helpful -- *METOCLOPRAMIDE* is a *first-line agent but may have significant AE, e.g. extrapyramidal sx (drug-induced Parkinsonism)*

Define Odds Ratio

-OR is a *measure of association between an exposure and an outcome* -*OR >1* --> Exposure is assoc w/ HIGHER odds of outcome -*OR <1* --> Exposure is assoc w/ LOWER odds of outcome

Complications of IVC Filter Placement

-IVC Filters are an option for pts w/ *acute venous thromboembolism (i.e. DVT or PE) who have ABSOLUTE CONTRAINDICATION TO ANTICOAGULATION* (e.g. intracranial hemorrhage from hemorrhagic stroke, or active bleeding not readily controllable like erosive gastric cancer) -IVC filters are placed percutaneous transvenous, just below renal veins, where they block movement of lower extremity clots to lungs -The *IVC Filters DECREASE (~halve), BUT DO NOT ELIMINATE, the Risk for Recurrent PE!!* -*HOWEVER, IVC Filters ~DOUBLE the Risk for RECURRENT DVT!!* -*Rates of recurrent DVT are Elevated even beyond the underlying thrombotic predisposition & Independent of Anticoagulation status* -IVC filters should be removed as soon as feasible and Anticoagulation should be offered at the earliest safe opportunity (e.g. after bleeding controlled), EVEN WHILE IVC Filter IN PLACE* COMPLICATIONS: -*Deep vein thrombosis at the insertion site* -*IVC thrombosis* -*Recurrent pulmonary embolism* -*Filter erosion, fracture, or migration* -Migration can be due to guidewire entrapment and inadvertent dislodgment during central line placement. If an operator experiences resistance when trying to remove a guidewire in a patient with an IVC filter, abdominal imaging should be obtained to assess the position of the wire relative to the filter

Child receives IVIG for Kawasaki Disease - How does this affect their ability to continue with normal childhood immunizations?

-IVIG is composed of *pooled antibodies* -These antibodies *interfere w/ body's /normal/ immune response to Live vaccines* -Bc of this, pts should *defer Live vaccines for 11-MONTHS* after receiving IVIG Vaccines usu given at age 4 incl Live vaccinations (second dose of MMR & varicella)

How to manage TX Disseminated Herpes Zoster?

-If Localized (unilateral) herpes zoster *progresses*, i.e. *rash becomes bilateral and spreads to adjacent dermatomes, ± increasing pain in areas of skin lesions*, then this indicates a *DISSEMINATED Herpes Zoster (Shingles) Infection* -Disseminated infections are characterized by the *appearance of lesions outside the primary or immediately adjacent dermatomes* -*Hospitalization for IV ACYCLOVIR is REQUIRED* d/t *INCR Risk for Varicella-related Complications (e.g. Ocular, Neurologic, bacterial superinfection) -Pts w/ herpes zoster may *TRANSMIT VZV through DIRECT contact (primarily) or Aerosolized/Airborne Particles (rarely)* to Healthcare personnel & others -CDC recommends the following *precautions for pts w/ herpes zoster until lesions are crusted over (i.e. no longer infectious!!): • *Localized* infection - *Standard* precautions & *lesion covering* • *Disseminated* infection - *Standard* precautions *PLUS Contact & Airborne Precautions* [while hospitalized] -Only staff with known immunity to VZV (s/p 2-dose varicella vaccine) should be allowed to interact with pts w/ active VZV infection; but bc *vaccination is not 100% effective*, *precautions above still needed*

Management of Acute Cystitis in PREGNANT pts?

-If clinically suspected, *TX Empirically w/ ABX* and use urine culture to confirm infection and modify abx regimen, should the sx not improve with empiric tx -Most common pathogen is *E.coli*, less commonly *Proteus mirabilis & Klebsiella pneumoniae* -*RF for UTI in Pregnancy*: Presence of ASX bacteriuria, nulliparity, Pregestational DM, & Tobacco use -First-line ABX in Pregnant pts incl *Beta-Lactams (e.g. Cefpodoxime, Amox-Clavulanate)* AND *Fosfomycin* d/t the safety profile of these Abx throughout the *entirety* of pregnancy -*Nitrofurantoin & TMP-SMX* can be safely used in the *second trimester*, but are /avoided in the third trimester/ -However, if no other Abx can be used (e.g. pt allergy, Tx-resistance), then nitrofurantoin & TMP-SMX can be used as *second-line* agents -*Bc there is a high risk for Persistent Bacteriuria*, a *URINECX is Repeated ONE WEEK AFTER TX Completion for Test of Cure!* Note: First-line ABX for NON-pregnant pts incl Nitrofurantoin, TMP-SMX, & Fosfomycin

Management of Refractory Anaphylaxis

-Immediate *INTRAMUSCULAR EPINEPHRINE* is first-line tx -*Additional Epinephrine administration (IM or IV)* may be required for symptom resolution in *refractory* cases (no significant change after 10 mins) -Can give up to 3 doses of IM Epi, and then do a slow IV infusion of Epi if still severe/refractory -Fluid resuscitation, bronchodilators, antihistamines (incl IV Benadryl), and glucocorticoids may be given as *adjunct* therapies, but do NOT take priority over epinephrine Note: IV Diphenhydramine can help relieve sx of pruritus and urticaria, but it does NOT tx bronchospasm or shock

Neuropsychiatric Symptoms in pts with Dementia

-In *Dementia* pts, *neuropsychiatric symptoms* (e.g. *disorientation, agitation, aggression*) *are COMMON* and may become *MORE PRONOUNCED,* particularly @night (*sundowning*), *as the dementia progresses* -TX options incl *behavioral interventions*, *antidementia drugs, & antidepressants* -Although sometimes used, esp in times of severe aggression, *Antipsychotics are assoc w/ INCR Mortality & Multiple AEs*, including *extrapyramidal symptoms (e.g. Iatrogenic Parkinsonism [bradykinesia], Akathisia [restlessness], & Dystonia [sustained, involuntary muscle contractions])* -/Secondary Parkinsonism/ results in *cogwheel Rigidity, pill-rolling Resting Tremors, Masked Facies, Shuffling Gait, & Bradykinesia* -In pts who display sx of secondary parkinsonism d/t use of antipsychotics, *the antipsychotics should be discontinued* in favor of *behavioral interventions* (e.g. sensory activities, music therapy, distraction techniques, communication skills training for caregivers) -Antipsychotics should only be used if pts are a safety concern to themselves or caretakers (i.e. aggression), but their use should be *minimized as much as possible* -Increasing the antipsychotic doses in pts showing increased agitation will likely worsen secondary parkinsonism sx and they actually have been shown to be /ineffective for managing agitation/ -*Haloperidol>> Risperidone & Olanzapine* show the *highest risks for Drug-Induced Parkinsonism*

In herpes zoster, which manifests first? The rash or the pain?

-In *herpes zoster (aka SHINGLES), d/t reactivation of VZV from dorsal root ganglia of a sensory nerve* (following initial infection w/ varicella [chickenpox] during childhood/early adulthood), often has *Dermatomal PAIN (burning, throbbing, stabbing, pruritic) PRECEDING Unilateral Dermatomal RASH (begins as erythematous papules, evolves into grouped vesicles, & crusts over within 7-10d) by Days or Weeks; Pain may be Severe!*

Illness Anxiety Disorder

-In *illness anxiety disorder*, pt has *MINIMAL or NO Actual SX, but is Preoccupied with having a Serious Undiagnosed Specific Disease* (e.g. pt fearing they have a brain tumor) -*Preoccupation with acquiring or having a serious illness, often despite medical evaluation and reassurance*; *minimal to no somatic symptoms* -*Sx are Unconscious, Motivation is Unconscious*

Heimlich Maneuver in Children <1yo vs ≥1yo with Complete Airway Obstruction

-In contrast to *partial airway obstruction,* in which the child can *still move enough air to cough & gag, Complete Airway Obstruction* is characterized by the *inability to cough, speak, or breathe with severe respiratory distress or tripod positioning, & cyanosis* -In *Conscious Children ≥1yo w/ complete airway obstruction* --> *[upward] Abdominal Thrusts* should be performed *immediately* -In *Conscious Children <1yo w/ complete airway obstruction* --> *Place child face/head down on rescuer's arm, and administer alternating back blows & chest thrusts* -If the child were *UNCONSCIOUS* --> *Immediately initiate CPR*

Mallory-Weiss Syndrome

-In contrast to Boerhaave syndrome, a Mallory-Weiss tear is a *mucosal* (i.e. *partial thickness*) *tear* of the esophagus -A Mallory-Weiss tear can also present w/ *hematemesis* following nausea & vomiting; however, perforation does NOT occur, so fever, chest pain, mediastinitis, left pleural effusion (d/t fluid leakage), and hemodynamic instability would be unlikely

Delivery Options for Twin Gestations

-In general, the *delivery of second twin is assoc w/ Incr risk for umbilical cord prolapse, abruptio placentae, malpresentation, & neonatal death* -- to minimize these risks, vaginal delivery is offered selectively *Dichorionic/Diamniotic Twins* -*Mode of delivery depends on fetal presentation* -When twins are *vertex/vertex, can attempt vaginal delivery* -IMP: *after delivery of twin A, the cervix often constricts (i.e. cervical dilation decreases) d/t lack of engagement (i.e. high station) of twin B; the cervix completely dilates again when the presenting part of twin B descends into the pelvis* -*After the delivery of twin A and BEFORE the descent of twin B, U/S is used to REConfirm the presentation of twin B* -- *If twin B is Still in Vertex presentation & has a reassuring FHR tracing (i.e. normal baseline, moderate variability, accelerations, no decelerations)*, *then twin B can be Expectantly Managed* -*Indications for C-Section delivery of twins* includes *Monoamnionicity (inner membrane), Malpresentation of Twin A, and a Nonreassuring FHR for Either Twin during Labor* -A *Forceps-Assisted Vaginal Delivery* is *indicated for a Protracted Second stage of labor (when cervix is completely dilated, ready for childbirth), FHR Tracing Abnormalities During the Second Stage of Labor, Maternal Exhaustion, or Maternal Contraindications to the Valsalva Maneuver (e.g. cardiac or neurologic disease)* -Criteria for *operative vaginal delivery incl complete cervical dilation (10cm) & Fetal head engagement, when the widest part of fetal head has passed thru the pelvic inlet [ischial spines]* Note: *Oxytocin admin* is *indicated for labor protraction d/t inadequate uterine contractions (adequate contractions occur q2-3mins)*

When to transfuse PRBCs?

-In hemodynamically stable pts with NO active bleeding or symptoms of severe anemia (chest pain, syncope), then transfuse when Hb <7 g/dL. Note: In Anemic pts, fatigue and exertional sx (dyspnea) are NOT generally considered indications for transfusion. Note: Presence of melena (indicates chronic blood loss), does NOT indicate active bleeding -Pts w/ stable coronary artery dz or those planning to undergo major surgery, should maintain a Hb ≥8 g/dL -Pts w/ acute coronary syndrome, severe thrombocytopenia, or malignancies with high risk of bleeding may require higher transfusion thresholds

Definition of an *acute asthma exacerbation* and *treatment*

-Increase in asthma sx (e.g. cough, dyspnea, & wheezing) combined with a >20% /reduction/ in peak expiratory flow rate -Most common trigger is a /viral URI/ -Emergency medical care needed for pts w/ severe sx (e.g. hypoxemia, difficulty speaking, accessory muscle use, reduction in peak expiratory flow >50% from baseline) -Mild cases can be treated as an outpatient with *systemic corticosteroids PO* • Prednisone 40-60mg PO daily for 5-10d

Lab evidence of hemolysis

-Increased Indirect/Unconjugated Bilirubin (intra & extra) -Increased LDH (intra & extra) -Increased reticulocytes (intra & extra) -Increased Urobilinogen in Urine (intra & extra) -Decreased Haptoglobin (intra) -Increased Schistocytes on blood smear (intra) -Increased Spherocytes on blood smear (extra) -Splenomegaly (extra)

Celiac Disease

-Indicated by *anti-tissue transglutaminase Ab & villous atrophy on small bowl Bx*, and *improvement of sx w/ gluten-free diet* -*Chronic malabsorptive disorder of SI* caused by *immune-mediated hypersensitivity to gluten* -SX: *Diarrhea, abdo pain, weight loss, nutritional deficiencies d/t malabsorption (e.g. iron, folate, B12)* -MCC of persistent/recurrent sx is *continued gluten intake* from inadvertent ingestion or poor compliance -- *Detailed dietary intake first!* -*Serologic studies* (e.g. *anti-tissue transglutaminase, anti-gliadin antibodies*) CORRELATE with Disease Activity* and can help to *assess compliance* -- *Antibodies should DECR by 50% in 8WKS and NORMALIZE within 12MO of a gluten-free diet* -Inappropriately elevated titers indicated continued gluten ingestion -Pts w/ persistent sx despite dietary compliance should get a *repeat upper endoscopy to evaluate for other Diagnoses or Refractory Sprue* -*UNTX Celiac leads to long-term sequelae* --> *Osteopenia, Severe Anemia, & INCR Risk for Malignancy*

Cohort Studies

-Individuals are *initially identified as EXPOSED or NONEXPOSED to a Risk Factor of interest* (e.g. treatment) and then the *incidence of an outcome (i.e. disease) is compared between the exposed and nonexposed groups* -*At the start of a cohort* study, *BOTH exposed && nonexposed groups must NOT have the outcome*

Macrocephaly

-Infant w/ *macrocephaly (head circumference >97th percentile for age) who have OPEN Anterior Fontanelle and RAPIDLY Expanding head circumferences should have a HEAD ULTRASOUND to evaluate for pathologic intracranial processes* (head u/s is best in infants w/ an open anterior fontanelle - fast, no radiation, no sedation) *Neuroimaging* is Required for *Pathologic Intracranial Process* in the following circumstances: -*Rapidly expanding head circumference (>2cm/month in infants <6mo)* -*Neurologic abnormalities* (e.g. Seizure) -*Developmental delay* -If head ultrasound is normal, then reassurance and observation are appropriate

Risk factors for cervical cancer

-Infection w/ high-risk HPV strains (e.g. 16, 18) -Hx of STIs -Early onset of sexual activity -Multiple or high-risk sexual partners -Immunosuppression -Oral contraceptive use -Low socioeconomic status -Tobacco use

Central Retinal Vein Occlusion

-Like central retinal artery occlusion, can also p/w *PainLESS, acute, or subacute monocular vision loss* -Central retinal vein occlusion is usu d/t *NON-embolic causes* (unlike its counterpart) -Exam shows *tortuous & dilated veins, diffuse hemorrhages, disk swelling, & cotton wool spots*

What is the timeframe to treat seasonal influenza and with what?

-Influenza can be *TX w/ Antiviral medication, OSELTAMIVIR or ZANAMIVIR* to *reduce sx duration* and potentially, the *risk of developing influenza-related complications* (e.g. Secondary Pneumonia) -However, antiviral therapy efficacy precipitously declines when initiated >48hrs after sx onset -Therefore, the CDC recommends that *healthy individuals with >48hrs of Sx receive SYMPTOMATIC care ALONE (e.g. acetaminophen)*; BUT IF *<<48HRS OF INFLUENZA SX, CAN RECEIVE OSELTAMIVIR* -In pts who require hospitalization, or have *severe/progressive* illness, or are at *high-risk* (e.g. *>65yo, immunocompromised*) of *influenza-related complications* should be *TX with Antivirals REGARDLESS of Sx Duration*!! -Although influenza vaccination is an imp preventive modality, vaccination does not guarantee immunity to active influenza strains, and full preventative effects (humoral Ab response) may take >2wks to develop

Antithrombin Deficiency

-Inherited deficiency of antithrombin III -Has NO direct effect on the PT, PTT, or thrombin time, but *diminishes the increase in PTT following heparin administration* -Hereditary, but can also be *acquired* in renal failure/nephrotic syndrome --> antithrombin loss in urine leads to *decr inhibition of factors IIa and Xa*

Annual Deductibles and Maximum Out-of-Pocket Spending

-Insurance plans generally require that pts *spend a Minimum amount out-of-pocket*, known as the *DEDUCTIBLE, before insurance covers expenses* -*AFTER meeting the plan deductible,* pts *may STILL incur additional cost-sharing (i.e. additional out-of-pocket spending on covered health care services) for in-network services* ● E.g. of pt *cost-sharing* incl *copayments* (i.e. copays, a fixed amount per service, such as an office visit) and *coinsurance* (i.e. a fixed percentage of the cost of a health care service, such as a hospital stay) Sample Case: -Pt met annual deductible of $3000 (i.e. she paid $3000 this year to other providers for covered healthcare services). She went to urgent care and received a bill for $1000 for services rendered. Her responsibility for the $1000 urgent care bill *depends on her plan's Out-of-Pocket Maximum, that describes the pt's Annual Cost-Sharing LIMIT:* ● *IF* her *deductible equals her out-of-pocket maximum* (i.e. both are $3000), *then* the pt has *already reached her maximum cost-sharing limit by meeting the deductible, so her insurance plan would be required to pay 100% of this bill* ● *IF* her *deductible is LESS than her out-of-pocket maximum* (i.e. her deductible is $3000, but her out-of-pocket maximum is $5000), *then* the pt has *NOT reached the plan's maximum cost-sharing limit yet*, and she would likely have to *pay for at least part of the bill* (e.g. pay co-insurance, a percentage [such as 20%] of the urgent care bill) Note: Some insurance plans incentivize pts to seek care at in-network facilities by offering lower copayment or coinsurance rates. However, even w/ in-network status, the out-of-pocket maximum and cost-sharing responsibilities above the deductible may still apply.

Urinary Incontinence Management

-Involuntary leakage of urine -RF incl: Increased age, hx of multiple vaginal deliveries, obesity, vaginal atrophy, tobacco use, & caffeine intake -INITIAL Eval involves: *Thorough Hx, Physical, & Urinalysis* -*Reversible* underlying causes incl: Excessive fluid intake, stool impaction, medications, delirium -*Urinary leakage, frequency, pattern, volume, & aggravating/relieving factors* reviewed -PE looks for *vulvovaginal atrophy, pelvic masses, pelvic organ prolapse, & urethral hypermobility* -A *Bladder Stress Test* (i.e. *leakage of urine w/ cough/Valsalva*) is performed for evaluation of *stress urinary incontinence* -*Urinalysis* evaluates for *underlying pathology, infection/malignancy* -For the majority of pts, the *initial eval is sufficient to classify the type of Uncomplicated urinary incontinence* (e.g. *stress, urgency, overflow*) and *NO FURTHER EVAL is Indicated* -Only do *Further Evaluations IF* the *Hx, Physical, or Urinalysis suggest Complicated Incontinence* (e.g. *Mixed [stress+urgency]* or *Underlying Pathology*

Paranoid Personality Disorder

-Involves a *pervasive, lifelong pattern of suspiciousness and mistrust of others* (e.g. pts can be aggressively confront their spouse about it) -These individuals are usu *hypervigilant & hostile, and interpret others' motives as malevolent* -They are *controlling in relationships* and may be *pathologically jealous* -It is differentiated from psychotic disorders by the absence of persistent psychotic sx (delusions, hallucinations) and the nonspecific nature of the distrust (generalized mistrust to every interpersonal interaction*

Calcium Homeostasis

-Involves blood transport as: • *Albumin-bound Ca2+ (45%)* • *Ionized Ca2+ (40%)* (Physiologically Active form!!) • *Ca2+ bound to inorganic & organic anions (15%)* -*Hypoalbuminemia* causes *DECR Total Plasma Ca2*, BUT the *Ionized, physiologically active Ca2+ is Stable (bc hormonally-driven)* -Therefore, low albumin pts can be ASX, as the total plasma Ca2+ does not correlate with physiologically active form -*[Serum Ca2+] DECR by 0.8 mg/dL for every 1 g/dL decrease of [serum albumin] *Corrected Ca2+ (mg/dL) = (measured total plasma Ca2+) + [0.8(4.0 mg/dL - measured serum albumin)]* -If the *corrected* calcium level is WNL, no further interventions needed (if it were lower than normal, tx w/ oral calcium citrate or calcium carbonate) -*Direct measurement of Ionized Ca2+* is more accurate in pts w/ *Acid-Base disorders* (*acidosis INCR iCa2+; alkalosis DECR iCA2+*), *primary hyperparathyroidism, CKD, & MM* (elevated proteins can incr corrected calcium)

Adjustment Disorder

-Involves emotional sx causing *marked distress & functional impairment* that *develop within 3mo in response to a stressor* -Adjustment disorder requires that *sx cause a clear impairment in social & occupational functioning* -It's imp to identify adjustment disorders that occur in response to a medical dx (common w/ new cancer dx) as *counseling/psychotherapy* can improve sx and promote return to functioning

Brain Death

-Irreversible absence of all cerebral & brainstem reflexes (incl pupillary, oculocephalic, oculovestibular (caloric), corneal, gag, sucking, swallowing, & extensor posturing) -There are no spontaneous breaths, regardless of hypercarbia or hypoxemia -Brain Death DX requires a CNS catastrophe of known etiology w/ an absence of confounding factors (e.g. endocrine or electrolyte disturbances, drug intoxication) and hypothermia -A *positive apnea test* can confirm brain death by documenting an *absent respiratory response off the ventilator for 8-10mins w/ a PaCO2 >60mmHg (or >20mmHg from baseline) and a final arterial pH <7.28* Note: Brain death pts can have spontaneous movements, but these originate from the peripheral nerves or spinal cord. (e.g. finger flexion, truncal mvmts, flexion at the hip, knee, and ankles w/ foot stimulation, plantar reflex, limb mvmt to painful stimuli, alternating flexion/extension of toes)

How does long-term glucocorticoid use cause increase the risk for osteoporosis?

-It *promotes bone loss by inhibiting proliferation and differentiation of osteoblast precursor cells, promoting osteoclast differentiation and activity, and suppressing intestinal calcium absorption and renal calcium reabsorption* - this *INCR Risk for Osteoporosis warrants enhanced protective measures* *Strategies to Prevent Corticosteroid-Induced Osteoporosis* Incl: • Regular weight-bearing exercise • *INCR dietary calcium intake (1200 mg/day ± supplementation)* • *SUPPLEMENTAL VITAMIN D* -If the pts are *HIGH-RISK* (i.e. those taking *medium- to high-dose glucocorticoids* - e.g. *≥7.5mg/d of prednisone* - or those who have an *estimated 10yr risk for osteoporotic fracture ≥20%*) should *additionally take a Bisphosphonate*

What is a Kaplan-Meier curve?

-It is a commonly used graphical representation of the probabilities that subjects survive in a study without an event -- i.e. depicts the probability of survival at various time points during the study -Probability is calculated based on the proportion of subjects who are alive (or "at risk" for an event of interest) at a given time -X-axis denotes time, y-axis denotes cumulative event-free survival starting from 1.0 (i.e. 100% of pts alive without having experienced any event) at the beginning of the study -As the study progresses, events occur and the proportion of subjects who are still alive/"at risk" for an event of interest decreases -- as demonstrated by vertical downward dips in the curve -The event-free survival rates of ≥2 curves can be displayed simultaneously and compared -P-value <0.05 is considered significant (i.e. there is a <5% probability that the event-free survivals are different due to chance)

What is Interpersonal Psychotherapy and what is it used for?

-It is an evidence-based treatment for *DEPRESSION* -It focuses on 4 problem areas: *grief over loss, interpersonal disputes, role transitions, & interpersonal skill deficits*

Kava kavar major AE

-Kava kava is a supplement *used for anxiety and insomnia, and menopause* -HOWEVER, *HEPATOTOXICITY & LIVER FAILURE* is a potentially serious AE that may occur *several weeks to 2yrs after intake*

*LICHEN PLANUS*

-LP is an *immunologically-mediated [non-infectious] skin disorder, affecting mostly middle-aged adults* -Typically *involves the skin, nails, mucous membranes of mouth, & external genitalia (vulva & penis), & often WRISTS* -Classic *skin lesions* are *shiny, discrete, intensely pruritic, polygonal-shaped violaceous plaques and papules* that are most *frequent on the flexural surfaces of the extremities* -A characteristic *whitish, lacy pattern* called *Wickham Striae*, *is often seen on the lesion surface* -*Mucosal lesions* appear as *papular, atrophic, erosive lesions or may present only as lacelike, reticular Wickham striae, esp on the tongue & buccal mucosa* -*Genital LP* presents w/ *intensely pruritic violaceous papules* on the *glans penis or vulva* -*DIAGNOSIS mainly CLINICAL*, based on classic skin lesions in a characteristic distribution -If needed, can *confirm DX with Punch Biopsy/Deep Shave* (KOH prep and microscopy of skin scrapings not enough) -*TX w/ CORTICOSTEROIDS - topical -> intralesional -> systemic -> oral retinoids* -*LICHEN PLANUS is often ASSOC W/ ADVANCED LIVER DISEASE 2º to HEPATITIS C VIRUS Infection* --> *Screen for anti-hepatitis-C antibodies* when Dx LP, esp those w/ additional RF, IVDU Hx

Likelihood ratio

-LR is an expression of sensitivity and specificity that can be used to assess the value of a diagnostic test -*Positive LR* (LR+) represents the value of a positive test result -*Negative LR* (LR-) represents the value of a negative test result *LR+ = sensitivity / (1 - specificity)* ^probability of a pt with the disease testing positive divided by the probability of a pt without the disease testing positive. LR+ = true positive rate/false positive rate (LR- = (1-sensitivity) / specificity* ^probability of a pt with the disease testing negative divided by the probability of a pt without the disease testing negative. LR- = false negative rate/true negative fate -Test results with *LR>1 suggest disease presence* (the *higher the LR, the more likely the disease presence*) -*LR<1 argues against the disease* (the *lower the LR, the less likely the dz presence*)

Dynamic Left Ventricular Outflow Tract Obstruction in Hypertrophic Cardiomyopathy

-LVOT obstruction in HCM is caused by an *enlarged interventricular septum combined w/ systolic anterior motion of mitral valve* -LVOT obstruction *worsens w/ LOW LV blood volume*; therefore, symptomatic management aims to /maintain relatively high blood volume throughout the cardiac cycle/ -*Beta blockers* (e.g. metoprolol) are first-line for HCM complicated by LVOT obstruction - bc they incr LV blood volume to reduce obstruction in 2 ways: (1) *Negative Chronotropy* (reduce rate of contraction) incr diastolic filling time to incr LVEDV (2) *Negative Inotropy* decr contractility to cause blood ejection to complete at a *higher LVESV* -If can't use beta-blockers (e.g. pt w/ asthma/COPD, bradycardia, impotence), then use *nondihydropyridine calcium channel blockers (e.g. Verapamil, Diltiazem)* as a suitable alternative Note: Dihydropyridine CCBs (e.g. Amlodipine, Nifedipine) & other balanced vasodilators (e.g. ACE Inhibitors) are contraindicated in HCM bc they reduce LV blood volume (by casing venous dilation, reducing LV preload arterial dilation reduces afterload) and can worsen LVOT obstruction & HCM sx. Diuretics (e.g. furosemide) are avoided in HCM bc they reduce LV preload & can worsen obstruction.

Common reasons for medication nonadherence:

-Lack of understanding of illness or how medication works -Side effects -Costs -Complicated treatment regimens -Denial of illness -Stigma related to mental illness Physicians should explore pts' perspectives in an empathetic, open-ended way

Effect of Levothyroxine on Heart? Which patients should you be concerned about?

-Levothyroxine can *increase myocardial oxygen demand* resulting in *myocardial infarction, angina, or cardiac dysrhythmias* and is of concern in pts with *Coronary Artery Disease* -Cardiac disease pts with hypothyroidism (elevated TSH, low TOTAL T4) need to SLOWLY be started on Levothyroxine and gradually increased Note: Hypothyroidism (in the absence of myxedema coma or other severe symptoms) usu only MILDLY increase perioperative risk/outcomes, but treating a newly-diagnosed-with-Hypothyroidism cardiac pt with levo prior to surgery would greatly increase their risk for poorer outcomes

Drug Interactions of Levothyroxine

-Levothyroxine has a narrow therapeutic index, bioavailability is sensitive to a number of dietary factors: *DECR Levothyroxine Absorption* -Bile acid-binding agents (e.g. cholestyramine) -*Iron, calcium, aluminum hydroxide* -*PPIs*, Sucralfate *INCR TBG Concentration* -Estrogen replacement, oral contraceptives -Tamoxifen *DECR TBG Concentration* -Androgens, Glucocorticoids -Anabolic steroids *INCR Thyroid Hormone Metabolism* -Rifampin -Phenytoin -Carbamazepine

Lithium Toxicity

-Lithium (used as a mood stabilizer for bipolar disorder and tx acute manic episodes and prevents relapse) has a *narrow therapeutic index*, and levels *≥1.5 mEq/L confirm toxicity*, and levels *≥2.5 mEq/L require emergency management!* -*Lithium AE*: *Tremor, hypothyroidism, polyuria (causes nephrogenic diabetes insipidus), teratogenesis, Ebstein anomaly in newborns if taken by pregnant mom, neurologic sx like slurred speech, confusion, tremors, & ataxia* -*Narrow therapeutic window* requires close monitoring of serum levels -Almost exclusively *excreted by kidneys*; most is reabsorbed at PCT with sodium -*Thiazides* (e.g. chlorthalidone, hydrochlorothiazide, metolazone) and other *nephrotoxic* agents are implicated in lithium toxicity -*Lithium toxicity risks include low GFR (elderly, renal failure), volume depletion, & drug interactions* -Thiazides incr sodium excretion in the distal tubule, causing slight volume depletion; the resulting increased PCT reabsorption of Na also promotes lithium reabsorption --> toxicity -- *Thiazides causes INCR Lithium reabsorption!* -*ACE inhibitors* and *NSAIDS* also INCR lithium levels TX: *Discontinue* Lithium, *hydrate* aggressively with *isotonic sodium chloride*, consider *urgent hemodialysis for extreme toxicity* (defined as ≥4 mEq/L or ≥2.5 mEq/L w/ severe neuro sx or acute kidney injury)

Hepatic Sarcoidosis (Systemic Granulomatous Disease)

-Liver involvement occurs in 50-65% of sarcoidosis pts; most pts ASX or have nonspecific sx (e.g. weight loss); more severe dz can lead to jaundice, abdo pain, cirrhosis, & manifestations of portal hypertension -Isolated elevation of alkaline phosphatase and GGT (suggesting liver origin rather than bone origin of ALP elevation) with normal AST and ALT (this pattern can be seen in *infiltrative* liver diseases (e.g. granulomatous disease, infection, certain mediations) -Additionally, along with Hypercalcemia, and CXR showing signs of hilar adenopathy (bilateral hilar fullness w/o parenchymal opacities), and hepatomegaly == all findings combined suggest Hepatic Sarcoidosis -Liver infiltrated by noncaseating granulomas, visible on CT & MRI, but *Liver Biopsy* recommended to r/o other causes of granulomatous dz (e.g. TB) and metastatic malignancy -Initial TX of symptomatic hepatic sarcoid is w/ *systemic glucocorticoids e.g. prednisone*

Multifocal Atrial Tachycardia (MAT)

-MAT EKG: Narrow QRS complexes w/ distinct P waves of different morphologies and variable PR segments and R-R intervals -MAT may result from *atrial conduction abnormalities* triggered by disturbances such as *RA enlargement, catecholamine surge (e.g. sepsis), or electrolyte imbalance* -MAT is most commonly seen in *elderly pts >70yo* w/ an *acute exacerbation of underlying pulmonary dz* (e.g. COPD) -Pts usu p/w sx of underlying resp illness (cough, wheezing, SOB) and the *tachycardia* itself is usu ASX (maybe palpitations) -*Electrolyte disturbances* (e.g. *hypokalemia, hypomagnesemia*) are also common causes of MAT; *repletion of lytes* will often lead to conversion to sinus rhythm -Cardiac exam of MAT reveals an *irregular rhythm w/ rapid rate* -DX confirmed by EKG: *Distinct P waves of at least 3 different morphologies, irregular R-R intervals, Atrial rate 100bpm*; the elevated atrial rate differentiates MAT from a dx of wandering atrial pacemaker. -Best TX is *appropriate management of inciting illness*; admin of bronchodilators, systemic corticosteroids, & non-invasive ventilation Note: *IV nondihydropyridine CCBs (e.g. verapamil, diltiazem) and Beta-blockers (e.g. esmolol)* can be used to control the *rapid ventricular rate* (RATE CONTROL by slowing conduction of AV node) in MAT pts, but they don't address the underlying cause of MAT; You CAN use these for Rate Control in *persistent MAT* despite correction of potential underlying causes

Infantile [strawberry] Hemangioma

-MC pediatric vascular lesion! -Hemangiomas appear as a *patch of telangiectasias at birth*; they *quickly progress into a bright red, NONTENDER, NONBLANCHING nodule, and continue to PROLIFERATE during the first year of life* -*After age 1*, most hemangiomas undergo *gradual, spontaneous involution through age 9, and require NO intervention* -*Complications* incl *ulceration, bleeding, & scarring* -Lesions near anterior neck may obstruct airway during proliferative stage and those on eyelid may obscure vision -- such lesions may require *β blocker therapy (e.g. propranolol) or, rarely, surgery*

Biliary Atresia

-MC reason for *pediatric liver transplant* -*Progressive Fibro-obliterative destruction of bile ducts --> Obstruction of Extrahepatic Biliary Tree --> Cholestasis* -Often *presents as Newborn with Persistent Jaundice after 2WKS of life, in the first 2MO of life, with CONJUGATED HYPERBILIRUBINEMIA* (Incr Direct Bilirubin >20% of t.bili), *Darkening Urine, Acholic Stools, & Hepatomegaly*

Familial Tremor or Benign Essential Tremor (ET)

-MCC of *postural tremor; incidence increases with age* -The *familial cases usu have an Autosomal Dominant Inheritance Pattern, and presents at a relatively Younger age* -The *tremor in pts w/ Familial Dz is usu present in the Distal Upper Extremities (fingers) and becomes much more pronounced with outstretching of arm*; also *increases at the end of an activity or movement* (i.e. it can cause *difficulty with performing fine motor tasks*) -ALL pts w/ ET *typically DON'T have any other neuro signs* -The *Absence of a resting tremor (which worsens at rest but improves with voluntary activity), Absence of rigidity (incr resistance to passive movements), Absence of Bradykinesia (slowing of voluntary movements), and Absence of Gait Difficulty differentiates Essential Tremor from an early-onset Parkinson's Dz* -The presence of a *positive FHX & a head tremor is also more suggestive of benign ET* -*Benign ET or Family Tremors USU DON'T cause any significant disability*, and the pt can *Expect to have a NORMAL Life Expectancy* -There are *NO assoc neurological sx in pts w/ benign ETs* -TX is not necessary in all pts and should be delayed as long as possible d/t the need for *indefinite* TX -Pts w/ *Significant Disability d/t the Tremor that is affecting ability to perform fine motor tasks with hands can be TX w/ β-BLOCKERS (MC First-line Agent in TX Benign ET)* -Several studies have shown *efficacy of PROPRANOLOL in reducing tremors and the assoc disabilities*

Marfan Syndrome (MFS)

-MFS is an *autosomal dominant* disorder caused by *mutations in the FBN1 gene* encoding the protein *fibrillin-1* -Characteristic findings of MFS incl *tall stature, increased arm span to height ratio, & myopia/ectopia lentis* -DX is based on the presence of multiple clinical features -The main cause of M&M in MFS pts is *Aortic Root Disease*, manifesting as *aneurysmal dilation, aortic regurgitation, and/or dissection* -Pts w/ suspected MFS require an *ECHOcardiogram* prior to sports participation (d/t *risk of SCD*) -If aortic root disease and/or FHx of aortic dissection or sudden cardiac death is present, pts are *counseled* to *avoid strenuous physical activity*, with intense/contact sports (e.g. track, basketball, football) generally restricted

Medullary Thyroid Cancer (MTC)

-MTC is a *NEUROENDOCRINE TUMOR* that *Arises from the Calcitonin-Secreting PARAFOLLICULAR (C) Cells of the thyroid* -Typically *presents as a Solitary thyroid Nodule, although Metastasis is often Present at the time of DX* -*Serum CALCITONIN is usu ELEVATED, BUT Serum Calcium is freq NORMAL d/t counterrregulatory effects of PTH* -Most cases of MTC are *Sporadic*, but a substantial minority present as a component of *Multiple Endocrine Neoplasia Type 2 (MEN2)*, an *autosomal dominant* disorder caused by *germline mutations* involving the *RET protooncogene on Ch.10* -THEREFORE, *germline RET testing is indicated in initial evaluation of MTC pts* -*MEN2 is also assoc w/ PHEOCHROMOCYTOMA in ~40% of cases*, which can lead to *life-threatening hemodynamic complications during [thyroid] surgery* -Bc overt symptoms (e.g. hypertensive episodes, flushing) may NOT always be present in pheochromocytoma pts, *ALL MTC pts should be Screened for Pheochromocytoma w/ a Plasma Free Metanephrines Assay PRIOR to thyroidectomy surgery*

What is the best treatment for binge eating disorder?

-Mainstay of TX is *PSYCHOTHERAPY* -*Cognitive-behavioral therapy* has the most evidence of benefit for *binge eating disorder* -Meds can be considered, and include *SSRIs (e.g. Sertraline), Stimulant Lisdexamfetamine (Vyvanse)*, and the *antiepileptic, Topiramate*; these are all First-Line Pharmacotherapy for BED Note: The antiobesity agent, *Orlistat*, has NOT shown benefit in decreasing binge episodes and is NOT recommended for use in BED

General management of A-fib pts

-Managed with *anticoagulation* (e.g. rivaroxaban) and *rate control* with *atrioventricular nodal blocking agents* (e.g. β blockers), or *rhythm control* with *antiarrhythmic* agents -Each strategy has similar rates of thromboembolism and long-term survival -D/t somewhat limited efficacy and the incr risk of AE of antiarrhythmic drugs, /most AFib pts are managed w/ conservative rate-control strategy/ -Need rhythm control when: • Inability to maintain adequate heart rate control using rate-control agents (like beta-blockers) • Persistence of symptomatic episodes (e.g. heart failure exacerbation) on rate-control agents

Management of Acute Gout Attack in Renal Transplant Pts

-Management of acute gout is *challenging* pts w/ *Renal Failure* or who've undergone *Renal Transplant, as NSAIDs (e.g. Indomethacin) ~ which are usu first-line TX ~ are relatively CONTRAINDICATED* -*Low-Dose Colchicine (dose renally adjusted) is usu Effective*; HOWEVER, *Concurrent use of CYCLOSPORINE* (*immunosuppressant used in renal & solid organ transplants, which decreases uric acid excretion*) *can cause Delayed Clearance of Colchicine, leading to Colchicine Toxicity* (e.g. *MYONEUROPATHY, Myelosuppression/Agranulocytosis, Nephrotoxicity*) -Additional options for management of acute gout incl *Systemic and Intra-Articular Glucocorticoids* -Bc many pts receive glucocorticoids as part of their anti-rejection regimen, a *temporary increase in the dose* is a convenient way to *terminate an acute gout flare* and is *esp helpful in Polyarticular Gout* -HOWEVER, Systemic Glucocorticoids are assoc w/ significant AE, and *Intra-Articular Glucocorticoids (e.g. TRIAMCINOLONE)* are *better tolerated* for those w/ *monoarticular sx* -For *gouty arthritis following renal transplant*, consider TX w/ *Urate-lowering therapy w/ Xanthine Oxidase Inhibitors (Allopurinol, Febuxostat)* or a *Uricosuric (promotes uric acid excr) agent* (e.g. *Probenecid*) -- but only *Initiate AFTER Acute attack is fully TX* Note: If pt taking *Azathioprine* (sometimes used following organ transplant), *Xanthine Oxidase Inhibitors (Allopurinol, Febuxostat) can impair metabolism of azathioprine*

Delayed Gastric Emptying

-May be d/t *mechanical obstruction (intrinsic or extrinsic) or impaired motility (e.g. gastroparesis)* ● *Intrinsic* Obstruction - e.g. *peptic ulcer stricture, gastric malignancy, bezoar/foreign body, gastric volvulus, small bowel mass* ● *Extrinsic* Obstruction - e.g. *malignancy, superior mesenteric artery syndrome* ● *Impaired Motility* - e.g. *meds (anticholinergics), autonomic neuropathy (diabetes), nerve injury (post-surgical), idiopathic (postviral)* -The *FIRST STEP in evaluating delayed gastric emptying* is to *EXCLUDE Mechanical Obstruction via EGD*, especially in those at risk for peptic ulcer dz (e.g. NSAID use) -Sometimes *CT/MR enterography* is needed *if small bowel pathology is of concern* -ONCE Excluded, NEXT STEP is to *Confirm Impaired Motility w/ a Scintigraphic Gastric Emptying Study to confirm DX of Gastroparesis* Note: *Gastroduodenal Manometry* can be used to *distinguish b/w myopathic (e.g. amyloidosis) and neuropathic (e.g. multiple sclerosis) etiologies*

Recurrent Pneumonia in Elderly Smokers

-May be the *first manifestation of bronchogenic carcinoma!* -E.g. Pt w/ multiple/recurrent episodes of bacterial pneumonia in the same lung lobe, responding to ABX, but left with a persistent scar on CXR after treatment -This is most likely d/t a *partial obstruction of the bronchus or a branch of the bronchus supplying that lobe -Most likely cause of an *endobronchial obstruction in elderly males w/ extensive smoking hx* is *BRONCHOGENIC CARCINOMA* -A *carcinoid tumor* can be anther cause of endobronchial obstructions, esp in *younger & non-smoking pts* -Endobronchial lesions compress the airway lumen and prevent adequate clearance of secretions, causing secretion stasis, and recurrent PNAs, even after successful tx of previous episodes. Next step would be High-Res CT scan to diagnose interstitial lung dz -Best Diagnostic Test for endobronchial obstructive lesions is *Flexible Bronchoscopy to Confirm the DX (Definitive DX)* -Other causes of nonresolving PNA or Pulm infiltrates are Bronchoalveolar Cell CA, Lymphoma, Eosinophilic PNA, Bronchiolitis Obliterans Organizing PNA (BOOP), Systemic Vasculitis, Pulmonary Alveolar Proteinosis, & Drugs (Amiodarone) causing Pulmonary Fibrosis

Acute Cyanide Toxicity

-May occur in the setting of *renal failure* and *nitroprusside use* -*Nitroprusside* is a potent vasodilator that works both on *arterial & venous* circulation and is used for *hypertensive emergency management*—It has rapid onset and offset of action!! -MOA: Metabolism of nitroprusside releases _nitric oxide_ (responsible for vasodilation) & _cyanide ions_. Cyanide eventually converted to *thiocyanate*, which is excreted _renally_. However, *prolonged infusion* (e.g. >24hrs), esp in a pt with *renal insufficiency*, can lead to cyanide toxicity -The most important AE of Nitroprusside is *cyanide accumulation and toxicity* -Pts w/ chronic renal failure or those receiving a high-dose or prolonged infusion of sodium nitroprusside are at increased risk for cyanide toxicity -Cyanide causes toxicity by *inhibiting mitochondrial oxidative phosphorylation*, forcing cells to switch to anaerobic metabolism -Widespread cellular hypoxia -> *Metabolic ACIDosis* & *organ system dysfunction* -Neuro sx: *Confusion, seizures* -Other sx: GI (vomiting), cardiovascular & respiratory instability (e.g. bradycardia, bradypnea) -As a result, LOW infusion rates (<2 microgram/kg/min), short-term usage, and close monitoring are recommended -TX involves *cessation of nitroprusside & administration of Sodium Thiosulfate*

Assessing Adrenal Reserve

-Measurement of *baseline ACTH levels* & performing an *ACTH Stimulation test* (w/ *cosyntropin, synthetic ACTH*) would be the most practical way to assess adrenal reserve *Primary Adrenal Insufficiency* -Decr gland fxn --> *Decr Cortisol, Decr Aldosterone* --> *Hypotension, Hyponatremia, Hyperkalemia, Metabolic Acidosis, Skin/Mucosal Hyperpigmentation* -*Subnormal increase in Cortisol after ACTH Stimulation* i.e. High serum ACTH levels, Low Cortisol levels after stimulation *Central Adrenal Insufficiency* -Also *Subnormal increase in Cortisol after ACTH Stimulation* d/t *adrenal atrophy* from chronic ACTH deficiency -After ACTH Stimulation, pts have *Low serum ACTH levels, Low Cortisol levels* (Diagnostic!) -If there's still concern for central adrenal insufficiency after a Normal ACTH stimulation test (where you give ACTH Stimulation -> Incr Cortisol levels), then you can further assess the HPA Axis with a *metyrapone test* or *insulin-induced hypoglycemia test*

Primary Prevention & Secondary Prevention Tactics in Reducing Risk of Rebleeding of Esophageal Varices

-Medical TX can reduce risk of rebleeding in pts w/ esophageal varices d/t portal HTN -This TX is considered *Primary Prevention* if the pt has NOT previously had a bleeding episode, but has known esophageal varices; Whereas TX for those w/ MULTIPLE bleeding episodes would be classified as *Secondary Prevention* -First-line preventive agents are *nonselective Beta Blockers* (e.g. *propranolol, nadolol*), which help reduce pressure in the portal venous system -The combination of *beta blockers + repeat surveillance endoscopy w/ band ligation PRN* results in an even Lower Mortality Rate than either TX alone -The addition of an *oral nitrate* to beta blocker therapy may further reduce rebleeding.

Medication-Related Hair Loss -- via *Telogen or Anagen Effluvium*

-Medication-related hair loss *typically manifests as DIFFUSE Non-Scarring THINNING, rather than as discrete bald patches (as in alopecia areata)* *Telogen Effluvium* -Usu begins *~3mo after some precipitating event, such as an illness, stressor, or new medication* -*β-blockers, anticoagulants, systemic retinoids, anticonvulsants, & antithyroid medications* are *freq implicated Causes of Telogen Effluvium* *Anagen Effluvium* -*Chemotherapeutics (e.g. Antimetabolites, Alkylating agents, Mitotic Inhibitors)* can cause *Anagen Effluvium, which usu begins within 1-2wks of Chemo initiation* Telogen hairs are resting/shedding hairs Anagen hairs are actively growing hairs Catagen hairs are resting hairs

What are the most common *causes of mental status change in elderly* pts?

-Medications -Infections (e.g. UTI, PNA) -Metabolic abnormalities Note: Thyroid dysfunction, both HYPOthyroid and Thyrotoxicosis, can also frequently cause mental status change in the elderly, but it may present with *nonspecific or atypical sx*. Thyroid disorders are most likely in pts with a *subacute or chronic decline in mental function*

Number Needed to Treat (NNT)

-NNT represents *the # of pts who need to be TX to prevent ONE additional bad/negative outcome/event* in a period of time (assuming the tx is beneficial) -*NNT is the INVERSE of the Absolute Risk Reduction (ARR)* or *NNT = 1/ARR* -ARR is calculated by Subtracting the Experimental Event Rate (EER) from the Control Event Rate (CER) or *ARR = CER - EER* -The CER refers to the standard (already-used) control intervention -NNT is a useful measure to evaluate the efficacy of a given therapy -NNT values for the same treatment will vary depending on what the outcome is, the period of observation, and the comparison group used

What co-infections are tested for in pts with newly-diagnosed HIV?

-Need lab testing to stage the dz, determine appropriate antiretroviral therapy, & identify coinfections & comorbidities -*Prior to initiating antiretroviral therapy, testing for Hepatitis B Virus is required*, some treatment regimens can *target both infections* Pts are also usu screened for *tuberculosis, hepatitis C virus, & STIs (Treponema pallidum, Neisseria gonorrhoeae)* *Emtricitabine (FTC), lamivudine (3TC), tenofovir disoproxil fumarate (TDF), and tenofovir alafenamide (TAF)* are ARVs (NRTIs) *approved to treat HIV that are also active against HBV.*

What organisms are the most common causes of pediatric sepsis and what should you empirically treat them with?

-Neonates at high risk for serious *bacterial* infxns incl *Bacteremia, UTI, & Meningitis* If ≤28 days old: -*Strep agalactiae (GBS), E. coli, Listeria monocytogenes (Listeria if <7 days) -TX with combo *Ampicillin + Gentamicin* if bacteremia or UTI, but *if suspect meningitis, give Ampicillin + Cefotaxime/Ceftazidime* (better CSF penetration) If >28 days old: -*Strep pneumoniae & Neisseria meningitidis* -TX with *Ceftriaxone ± Vancomycin (if suspect meningitis, or if MRSA is suspected)* e.g. would suspect MRSA if pt also has a concomitant skin infection Note: Ceftriaxone is NOT given in the first mont of life bc it can displace albumin bound w/ bilirubin into the CSF (crosses BBB), and increases risk of Kernicterus

Malignant Pleural Mesothelioma

-Neoplasm tightly linked to *occupational asbestos exposure* (e.g. those who worked with cement, tile, automobile brake pad, or *shipbuilding* industries prior to asbestos control initiatives; also roofing, & plumbing) -Tumors primarily form on the pleura, but other mesothelial surfaces can be affected - peritoneum, tunica vaginalis, & pericardium -Malignant pleural mesotheliomas tend to present after *weeks or months of nonspecific sx* incl cough, dyspnea, wt loss, night sweats, fatigue -*Pleural Effusion* is almost always present and is noted on physical exam (dullness to percussion, decr breath sounds) and CXR -Pleural fluid analysis often shows an *EXUDATIVE Effusion* with *L (acidic) pH, Low Glucose levels* and high or low protein levels; *Cytology can be negative for malignant cells* -CXR also shows *irregular pleural thickening, calcifications and/or a mass* -DX typically made by* thoracocentesis with cytology (~35% sensitivity)*, but most cases need *VATs procedure w/ biopsy or open thoracotomy* -TX: *Surgery, systemic chemo, and/or radiation* is often *PALLIATIVE*, cure is Uncommon. Median survival 9-13mo

Febrile Neutropenia

-Neutropenia is defined as Absolute Neutrophil Count <1500 neutrophils/mm3 (severe ANC <500) -Pts w/ *ANC <1000 are at higher risk for overwhelming bacterial infection d/t an absent or blunted neutrophil-mediated inflammatory response* -FN is a *medical emergency* and starting *empiric ABX therapy* can avoid progression of infection to severe sepsis & life-threatening complications -These pts should be started on *empiric, IV broad-spectrum antibiotics ASAP after blood/urine cultures obtained* -Monotherapy with an *antipseudomonal β-lactam agent (e.g. cefepime, meropenem, piperacillin-tazobactam)* provides both *gram neg & gram pos coverage* and is recommended initially Note: Vancomycin has no gram neg activity

What is Technetium-99m bone scanning used for?

It detects areas of *bone remodeling due to /integration of radiolabeled phosphate analogues/* -It is primarily used to evaluate for *BLASTIC bone lesions* like *Paget disease of bones aka Osteitis Deformans*

What does Odds Ratio measure?

-OR is a measure of *association b/w risk factor/exposure and disease/outcome* -*Classically used in case-control studies*, but can also be used in cross-sectional studies • *OR >1* - odds of a RF in pts w/ Dz are HIGHER than in those w/o Dz • *OR <1* - odds of a RF in pts w/ Dz are LOWER than in those w/o Dz • *OR =1* - RF has NO effect on the odds of a Dz occurring -ORs can be *Unadjusted* (i.e. *not accounting for confounders*; e.g. univariate analysis) or *Adjusted* (i.e. *accounting for confounders; e.g. multivariate analysis, multiple regression*) -*Confounders* are *additional independent variables* that *may also be assoc w/ the exposure and with the outcome*, and may *mask the real association b/w exposure and outcome if not adjusted* -Factors statistically associated with the outcome in univariate analysis may not be significant in the multivariable analysis once all other factors have been adjusted for in the model

Chronic Silicosis

-Occupational disease affecting the lungs assoc w/ sandblasters, foundry workers, miners, and masons -CXR shows *upper lobe nodules & lower lobe emphysema* (usu won't see pleural thickening; but maybe see "eggshell" calcifications of hilar lymph nodes) -Macrophages respond to silica dust leading to fibrosis -Incr risk of cancer, cor pulmonale, and Caplan syndrome (rheumatoid arthritis, pneumoconiosis [coal dust exposure] with intrapulmonary nodules)

What is nonresponse bias?

-Occurs *when a proportion of study participants become nonrespondent* -Nonresponse affects studies that use *questionnaires or surveys to collect data* from participants -*Nonresponse increases the risk for bias* -It *introduces a bias in estimates when nonrespondents differ from respondents in the outcome of interest*, and it *contributes to a decr in statistical power* given that the *sample size has been reduced*, and an *increase probability of a type II error (i.e. probability of failing to reject a false null hypothesis [false negative])* -Nonresponse may *potentially bias a study* if the nonrespondents are *systematically different from respondents in important characteristics* (e.g. exposure, disease status) that the study is designed to identify

Pufferfish Poisoning

-Occurs LESS frequently than scombroid poisoning! -Poison found in pufferfish, blowfish, balloon fish, etc. -Characterized by the prominence of *NEUROLOGICAL SX* (e.g. *perioral tingling, incoordination/ataxia, weakness, paralysis, etc.*) that develop *10-45 mins after ingestion* -Begin with numbness & tingling around mouth, salivation, N/V and then progresses to paralysis, LOC, resp failure, and can lead to death

Organophosphate Poisoning

-Occurs after exposure to/ingestion of agricultural *pesticides* or *sarin* (biochemical warfare); *sudden onset of sx* -Mech: *Inhibition of Acetylcholinesterase --> Cholinergic Toxicity!* by allowing ACh accumulation within synapses within neuromuscular jxns -Presents with *muscarinic effects of DUMBELS* • Defecation • Urination • Miosis (pinpoint pupils) • Bronchospasm/bradycardia (decr SpO2, incr RR, wheezing, coarse breath sounds, incr sputum prodn) • Emesis • Lacrimation • Salivation -*Nicotinic effects*: Muscle weakness, paralysis, fasciculations -CNS: *Hypoxemic Respiratory failure, seizure, coma* -Management: • *Emergent resuscitation* (e.g. Oxygen, IVF, Intubation) • *Atropine & Pralidoxime* (atropine is a competitive inhibitor of acetylcholine; pralidoxime is a cholinesterase-reactivating agent) for reversal • Activated charcoal (if within 1hr of exposure)

Breastfeeding FAILURE Jaundice

-Occurs during the *First WEEK of Life* and is caused by *lactation failure from inadequate milk supply, poor latching, or infrequent feeding* with *mild unconjugated hyperbilirubinemia* -This *decr in oral intake* results in *decreased bilirubin elimination in stool & increased intestinal absorption of bilirubin*, thereby *increasing serum bilirubin d/t increased enterohepatic circulation*

Serum Sickness

-Occurs in *Type 3 Hypersensitivity* which is driven by *immune complexes* composed of antigen-antibody complexes (mostly IgG) that activate complement, attract neutrophils, and PMNs release lysosomal enzymes -Typically p/w a *Rash and Renal Failure 1-2wks after Antigenic exposure* --> *Antibodies to foreign proteins formed* --> *Ab-Ag complexes form and deposit in tissues* --> *Complement activation* --> *Inflammation & tissue damage* -Can also present with *associated polyarthralgias*

Physiologic Jaundice

-Occurs in almost every newborn *d/t increased RBC count w/ a shorter RBC lifespan, decreased hepatic bilirubin clearance, & increased enterohepatic circulation of bilirubin* No anemia though

Rh(D) Alloimmunization

-Occurs when an Rh(D)-negative mother develops antibodies against Rh(D) antigen -Alloimmunization can lead to *hemolytic disease of an Rh(D)-positive newborn and/or fetus*; maternal IgG anti-D antibodies cross the placenta and destroy fetal RBCs -When severe anemia develops in the fetus, it can lead to heart failure and subsequent *hydrops fetalis* (e.g. pleural or pericardial effusion, ascites) -Therefore, antibody screening is performed in all pregnant women at the first prenatal visit and at 28wks gestation to identify Ab that incr the risk of hemolytic disease (typically anti-D) -Positive antibody screening indicates that alloimmunization has already occurred, and anti-D immune globulin is NOT administered -*Negative anti-D antibody screening* confirms a lack of antigen exposure and is an indication to proceed with *anti-D immune globulin prophylaxis at 28wks gestation* -This prophylactic anti-D immune globulin neutralizes any occur Rh(D) antigen exposure that may occur b/w the third trimester and delivery -The *Postpartum dose of anti-D immune globulin*, administered <72hrs after delivery, reduces the risk of alloimmunization from fetomaternal hemorrhage assoc w/ delivery -The postpartum dose, w/ the addition of the antenatal dose at 28wks gestation, reduces the risk of alloimmunization to <1%.

Obesity Hypoventilation Syndrome

-Often p/w dyspnea and may lead to RIGHT-sided heart failure, resulting in JVD, lower extremity edema, & hepatomegaly, and a compensatory incr in serum HCO3 (it would NOT cause paroxysmal nocturnal dyspnea [dry cough worse when lying down at night] and pulmonary interstitial edema)

Macular Degeneration Presentation

-P/w *progressive distortion & vision loss, primarily from the CENTER of the visual field -- i.e. Central Scotomas* -The *"DRY" Macular Degeneration* form can have *cellular debris (drusen) accumulate b/w the retina & choroid*, which can sometimes lead to *retinal detachment* -The *"WET" Macular Degeneration* form is *more severe, with blood vessels growing up from the choroid behind the retina, which can also cause retinal detachment*

Biliary Colic

-Often secondary to *gallstones* -*Biliary colic is d/t contraction of the gallbladder, which forces gallstones or sludge into the cystic duct* --> *Incr pressure within gallbladder causes PAIN* --> *Pain usu decreases when gallbladder relaxes and stone moves back away from the cystic duct* -Pts dev *Epigastric or RUQ discomfort with Radiation to the Back & Right Shoulder!!* -Assoc Sx incl *N/V, diaphoresis* -An *entire single episode* of biliary colic usu lasts *<6hrs* -Although *fatty meals can trigger the pain*, many pts develop *nocturnal symptoms or pain INDEPENDENT of meals* -*PE of pts w/ uncomplicated gallstones* is usu *benign W/O peritoneal signs or guarding* -*Transabdominal U/S* is *initially preferred for diagnosing gallstones* as it is reliable, noninvasive, & readily available w/o need for contrast or radiation -- *preferably, ideally, performed AFTER an 8HR FAST and can show Gallstones (echogenic foci w/ shadow) or Sludge (echogenic foci w/o shadow)* -Obesity can make visualization more difficult, but is NOT a contraindication for U/S Note: *Pancreatitis can p/w midepigastric pain radiating to back & elevated serum lipase*. However, *pancreatitis* typically causes *Severe Pain w/ Inability to Tolerate Oral Intake* and *PE reveals Significant Tenderness in Epigastric region*. *Radiation to the shoulder would be UNEXPECTED*

Sydenham Chorea

-One of the major criteria of Acute Rheumatic Fever (JONES criteria) (need 2 major/1 major + 2 minor criteria) -*Sydenham chorea, aka Saint Vitus dance*, is the *most common acquired chorea in children* - *Involuntary, irregular movements of limbs & face* - and develops *1-8mo AFTER the initial Strep (GAS) infection* (Carditis and arthritis develop within 3wks) -*Emotional lability*, and *decline in school performance* are the earliest neurologic manifestations, followed by *distal hand movements* that *progress to facial grimacing & feet jerking* -Usu *irregular & rapid jerking movements of face, hands, & feet* -Pts also have *decreased muscle strength throughout (decr muscle tone)*, and the *relaxation phase of the patellar reflex is usu delayed* -*Positive Pronator Drift* (involuntary hyperpronation of extended arms) is present -DX of Sydenham Chorea is made based on clinical presentation -TX: Pts w/ Sydenham Chorea should be started on *ORAL PENCILLIN ASAP to eliminate carriage of Grp A Streptococcus*; *Intramuscular Penicillin [long-acting] should be CONTINUED until ADULTHOOD with the goal of preventing Recurrent Rheumatic Fever & worsening rheumatic heart dz [secondary prevention] even if no active pharyngitis* -Oral penicillin is the best method of primary prevention against acute rheumatic fever!! -Note: *TX of Sydenham Chorea itself is primarily supportive* with *complete resolution occurring within months* in most; *Corticosteroids* can reduce sx duration, but are usu reserved for *severe cases*

Comparing Confidence Intervals - How to tell if one or multiple are statistically significant?

-Overlapping CIs may or may not imply a statistically significant difference -*Nonoverlapping* areas imply a statistically significant difference -*If both values (difference from placebo) are negative and neither CI includes the null value (i.e. 0), then both treatment groups showed a statistically significant decrease compared to placebo* -*When CIs of means or proportions for ≥2 groups DO NOT OVERLAP, it is always correct to establish a statistically significant difference b/w the groups* -However, *when CIs DO OVERLAP, there may or may not be a significant difference* between the groups

How do *Tension HA* present and managed?

-P/w *Bilateral, steady, "band-like," pain* with *NO* photo- or phonophobia & NO aura -*Acutely TX* w/ *Analgesics, NSAIDs, Acetaminophen, and Caffeine* -*PPX w/ TCAs (amitriptyline)*, behavioral therapy

Neuroblastoma in Kids

-P/w *abdominal mass, weight loss, signs of Excess Catecholamine Secretion* is concerning for *NEUROBLASTOMA*, the *most common extracranial solid tumor of childhood, usu <2yo* -*Neuroblastoma, of neural crest origin, involves a painLESS mass originating in the adrenal medulla or along the sympathetic chain* -If large, can compress bowel (constipation), bladder (urinary incontinence), or renal artery (RAAS activation & HTN) -Neuroblastomas are derived from cells of primitive sympathetic ganglia and *secr catecholamines (e.g. epi, norepi)*, which *contribute to elevated BP and can cause Flushing & Sweating* -*Elevated Urine/Serum Catecholamine Metabolites aid DX; Biopsy is Confirmatory* -Assoc w/ *N-myc amplification* NOTE: Wilms tumor, is the MC *renal malignancy in children*, typically *presents @5yo w/ a Unilateral, painFUL, abdo mass, with HTN & hematuria*. NO FLUSHING/SWEATING IN WILMS

Euglycemic Diabetic Ketoacidosis in the Setting of SGLT2 Inhibitor Use

-P/w *acute anion gap Metabolic Acidosis* assoc w/ *abdo pain, N/V* with a *positive urinalysis for ketones* -*Euglycemic DKA is a known & recognized complication of SGLT2 inhibitor (e.g. canagliflozin) therapy* -SGLT2 inhibitors lower blood glucose by *reducing reabsorption of glucose in the kidney (UA positive for glucose)*, which leads to a *low insulin-to-glucagon ratio* because *high blood glucose levels are the primary stimulus for insulin release* -Euglycemic DKA pts taking SGLT2 inhibitors can be *triggered by prolonged FASTING, major illness, intense exercise, excessive alcohol intake, or an abrupt reduction in concurrent insulin dose* -- these conditions *further lower the insulin:glucagon ratio and exacerbate relative insulin deficiency* to the point of *stimulating ketogenesis* -In contrast to typical DKA, which as assoc w/ v. high glucose levels, *blood glucose in euDKA is usu <250 mg/dL* due to the *increase excretion of glucose in the urine* -Management includes *aggressive hydration, discontinuation of the drug, and control of blood glucose with insulin*

Hypertriglyceridemia-Induced Acute Pancreatitis

-P/w *acute pancreatitis* with characteristic *abdo pain [tender to palpation w/o rebound/guarding], serum lipase ≥3x normal, & pancreatic edema on U/S* -*Severe hypertriglyceridemia*, often assoc w/ a *genetic predisposition* (e.g. *hereditary dyslipidemia*) or *uncontrolled DM* -*Hypertriglyceridemia-Associated Pancreatitis (HTAP)* most commonly occurs in pts w/ *Triglyceride levels >1000mg/dL* (but can have *normal LDL*) -*INSULIN* can be used to *TX HTAP Acutely by activating lipoprotein lipase* and increasing the movement of triglycerides out of plasma into tissue, which prevents further pancreatic damage* -*Apheresis*, which *directly filters TGs from blood* may also be used in *severe* cases -HTAP pts require *chronic lipid-lowering therapy to prevent future recurrence* -*FIBRATES* (e.g. *FENOFIBRATE, GEMFIBROZIL*) are the *most effective* meds available for *lowering TG levels and preventing HTAP recurrence* -*Incr exercise, low-fat diet, & alcohol abstinence* are also recommended Note: Statins are potent cholesterol-lowering drugs to prevent CVD in high-risk populations (LDL ≥190mg/dL, age ≥40 w/ T2DM). Although Statins weakly lower triglycerides, fibrates are more effective and are preferred for preventing HTAP recurrence

Central Retinal Artery Occlusion Presentation & Management

-P/w *acute, painLESS, monocular vision loss* in pts *>6oyo w/ underlying cardiovascular risk factors* -Most commonly d/t *carotid atherosclerosis*; less commonly caused by *cardiac embolism, small vessel dz (e.g. HTN, DM), & vasculitis (e.g. giant cell arteritis)* -Fundoscopy shows *diffuse ischemic retinal pallor & a cherry red macula spot* (d/t preserved circulation via the posterior ciliary arteries) -Evaluation: Labs to exclude giant cell arteritis (ESR, CRP), Carotid artery imaging, & Cardiac evaluation if suspect a cardioembolic source -Can cause *irreversible retinal damage within 90-100mins* - so *Need URGENT OPHTHALMOLOGY CONSULT & Interventions to lower intraocular pressure* (e.g. ocular massage, anterior chamber paracentesis, *IV Acetazolamide/Mannitol*); Possible *intra-arterial thrombolytics* -Long-term management w/ atherosclerotic RF modification (lipid-reducing & antiplatelet agents) for prevention of recurrent vascular events -*Prognosis poor for those w/ severe vision loss at time of presentation*

How to diagnose acute pancreatitis?

-P/w *acute, severe epigastric pain radiating to back and assoc w/ N/V; worse when eating, lean forward to relieve pain* -*Diagnosis requires 2 of 3 criteria* • *Acute onset of Persistent, Severe Epigastric Pain* • *Elevation of Serum Lipase or Amylase ≥3x upper limit of normal* (LIPASE MORE SPECIFIC, ≥3x normal) • *Characteristic findings o pancreatitis on Abdo Imaging* (*contrast-enhanced CT, MRI*) -In pts w/ *typical abdo pain, LAB ANALYSIS (i.e. SERUM LIPASE) is SUFFICIENT to Confirm Dx of Acute Pancreatitis* -- i.e. Start with serum blood tests only to look for markers (faster, cheaper, no added exposure to ionizing radiation), and then add abdo imaging if unclear. Also, CT scan has low sensitivity in the first 72hrs of presentation -Once diagnosed, need to *determine etiology* Causes: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hypertriglyceridemia (> 1000 mg/dL), ERCP, Drugs (eg, sulfa drugs, NRTIs, protease inhibitors, *furosemide, didanosine*), Infections (HIV, Ascaris) -*Gallstones & Ethanol* account for >65% of cases -*Hypertriglyceridemia* causes up to 14% of cases, usu when *Triglyceride levels >1000* -- need a Lipid panel! Note: *IV ABX* are NOT indicated in routine management of acute pancreatitis, but ARE indicated in pts w/ *Extrapancreatic Infections* (e.g. pneumonia) and in those who dev *infected pancreatic necrosis (persistent abdo pain, or improvement followed by deterioration [leukocytosis, fever] detect w/ CT Abdo w/ contrast showing gas within pancreatic necrosis)*

Postpartum Endometritis

-P/w *fever >24hrs postpartum & uterine fundal tenderness* -Postpartum endometritis is the MCC of postpartum fever, caused by inoculation and *infxn of the endometrial cavity by vaginal flora during labor or delivery* -RF: Hx of *Bacterial vaginosis, GBS colonization, prolonged ROM, protracted labor, operative vaginal delivery, C-section* - these RF are assoc w/ *incr vaginal bacterial load or facilitate bacterial ascent into uterus* -Other presenting features incl: *purulent vaginal discharge, BOGGY uterus, & incr vaginal bleeding* -It's a *polymicrobial infxn* of the *uterine decidua* caused by *ascending vaginal flora during labor, delivery, or the immediate postpartum period* -Therefore, infxn is common in pts w/ *prelabor rupture of membranes (i.e. membrane rupture prior to contractions @≥37wks gestation) or with Protracted labor* - both will incr exposure of the uterine cavity to ascending bacteria -*C-section* is the MOST significant RF for postpartum endometritis, esp when performed after labor starts or membranes rupture -Postop course after c-section delivery is assoc w/ /necrosis of myometrium along the hysterotomy repair, the presence of foreign bodies (sutures), & the potential for incisional hematomas/seromas. all of which amplify infection risk/ -Need to TX using a *broad-spectrum antibiotic regimen* that includes *penicillin-resistant ~anaerobic~ coverage* -Most appropriate therapy is *Clindamycin + Gentamicin* • Clindamycin covers aerobic G+ cocci and penicillin-resistant anaerobes (e.g. Bacteroides fragilis) • Gentamicin covers G- (e.g. E. coli) and some G+ (e.g. Staph) bacteria -*TX continued until Afebrile for 24hrs* -*Ampicillin-Sulbactam + Gentamicin* would be another acceptable combination that covers G+, pencillin-resistant anaerobes, and G-

Pelvic Inflammatory Disorder (PID) - Presentation & Management

-P/w *fever, abdo pain, cervical motion tenderness, & mucopurulent cervical discharge ± dysuria* -*RF*: Multiple sex partners, prior PID, inconsistent barrier use, Age 15-25 -*Complications*: *Tubo-ovarian Abscess, Infertility, Ectopic pregnancy, Perihepatitis* -- risk for all these are reduced w/ prompt ABX -PID is a *polymicrobial infection,* and *ABX should cover Chlamydia, Neisseria, & vaginal flora (e.g. E. coli, Mycoplasma)* that can *contaminate upper genital tract* -*TX w/ Broad-Spectrum ABX (e.g. CEFOXITIN + DOXYCYCLINE)* -*Cefoxitin covers G(-) bacilli (e.g. E.coli); Doxy covers G(+) (e.g. Streptococcus), G(-) (e.g. Neisseria), & Atypical organisms (e.g. Chlamydia, Mycoplasma)*

Statin Myopathy presentation

-P/w *mild muscular pain*, although pts may occasionally severe myopathy w/ elevated creatine kinase levels -However, statin myopathy is /not classically associated with joint pain/ and usually occurs in the *first few months*; it is unlikely on chronic therapy

Non-Classic GERD

-P/w *periodic retrosternal chest main* that can *mimic angina* -*Resulting erosive esophagitis --> *Transitory Dysphagia* --> *Result in a Peptic Esophageal Stricture if UNTX* -*Peptic stricture formation* is a well-known *complication of GERD* that can *cause obstructive dysphagia* (difficulty swallowing solid food, prolonged & careful chewing, swallowing smaller portions, incr water intake w/ food) Note: Barrett's esophagus (pre-malignant complication of GERD) does NOT cause dysphagia.

Clubfoot (Talipes Equinovarus) Presentation & Management

-P/w *plantar-flexed, ADducted, & inverted feet* due to a *developmental deformity*of the *talus* bone -In congenital clubfoot, the tissues around the talus are underdeveloped and the muscles are shortened & contracted, causing an *internally-rotated* foot and the foot is *fixed* (cannot be manipulated back to midline) and *resists ROM testing* -The *ipsilateral calf* may be *less muscular* and, in unilateral cases, /shortened leg length/ is apparent on the affected side -If *UNTX*, the child will attempt to *bear weight on the lateral aspect of the inverted foot* and the ability to stand & walk will be affected -*First-line TX* is *nonsurgical* and involves *stretching and serial casting* -After nonsurgical tx is complete (i.e. normal foot position attained), an *Achilles tendon release procedure* is often performed to *incr ROM* -If response is inadequate or if clubfoot recurs, then *reconstructive surgery* can be considered

Polymyositis (Inflammatory Myopathy)

-P/w *progressive, painLESS Proximal Muscle Weakness* with *elevated muscle enzymes (creatine kinase, transaminases) & inflam markers (CRP)* -Polymyositis is an *inflammatory myopathy* triggered by Unknown, possibly viral, antigens -Peak incidence occurs at age 40-50 -Proximal m weakness manifests as: difficulty climbing stairs, getting into/out of low chairs or cars, working w/ arms overhead (e.g. combing hair) -*Joint pain/swelling* may be present -Can also involve the upper esophageal musculature, leading to *dysphagia w/ regurg & aspiration* -*DERMATOMYOSITIS* is a similar disorder but w/ characteristic skin sx: Malar rash, Gottron papules over knuckles, Heliotrope (erythematous periorbital) rash, "shawl & face" rash -Most Polymyositis pts have detectable *autoantibodies (e.g. antinuclear antibody+ [ANA], anti-Jo-1+, anti-SRP+, anti-Mi-2 Ab) -Definitive diagnosis w/ *muscle biopsy* -Polymyositis & dermatomyositis may occur as paraneoplastic syndromes, so pts should undergo careful examination & age-appropriate screening tests -Polymyositis is *tx w/ systemic glucocorticoids*, often WITH *corticosteroid-sparing agents (e.g. methotrexate, azathioprine)*; a good response shows improved muscle strength and normalization of muscle enzymes and inflammatory markers* -*Pulmonary Complications*: *interstitial lung disease (ILD)*, infection, (d/t immunosuppressive therapy), drug-induced pneumonitis (e.g. methotrexate pneumonitis), and respiratory muscle weakness -ILD is esp common in pts w/ *positive anti-Jo-1 Ab* and can be identified on *high-resolution CT imaging* as ground-glass opacities, reticular changes, honeycombing, or patchy consolidation -*Pulmonary fxn tests* should be done to distinguish ILD from resp m weakness and will show decr vital capacity, total lung capacity, & diffusing capacity -ILD may progress despite steroids & MTX tx, even if myopathic features improve

Neonatal sepsis & meningitis presentation

-P/w *subtle & nonspecific sx* incl *temperature instability (fever or hypothermia), irritability, lethargic, poor feeding, and/or hypotonic (weak suck, decr muscle tone), often w/ FULL fontanelle* -*Difficult to console, poor feeding causing fewer wet diapers, somnolent* -*Jaundice* (d/t *sepsis-assoc cholestasis*), *respiratory distress, & seizure* may also occur -Neonates w/ meningitis don't get nuchal rigidity or positive Kernig or Brudzinski signs!!! -Neonates w/ *suspected infection but hemodynamically stable* urgently require *full eval* with *CBC w/ differential, Urinalysis, CSF analysis, & cultures of all 3 fluids* /followed by/ *empiric admin of antibiotics (ampicillin & gentamicin)*

Retinal Detachment Presentation

-P/w *vision loss (peripheral --> central) and Photopsia w/ showers of floaters* -Usu assoc w/ *trauma, previous eye surgery, aging, & severe myopia* Nearsightedness (myopia) is a common vision condition in which near objects appear clear, but objects farther away look blurry.

Acute Angle-Closure Glaucoma Presentation

-P/w *vision loss, SEVERE EYE PAIN, headache, N/V* usu unilaterally -Pts may report *seeing light halos* -Exam shows *conjunctival redness and a dilated, poorly-reactive pupil*

Diffuse/Distal Esophageal Spasm (DES)

-P/w dysphagia and retrosternal chest pain within seconds of eating -Pts frequently experience [intermittently] *sensation of both solids and liquids getting stuck* in their throat; may be triggered by hot or cold foods -*DES is assoc w/ GERD* -May be d/t impairment of the inhibitory neurons innervating the esophagus, causing *disordered & premature simultaneous contractions of the distal esophagus on Esophageal Manometry (Gold Standard for Diagnosis, showing premature contractions w/ normal distal esophageal sphincter relaxation)* -Barium esophagogram can be normal or show a *corkscrew* appearance of the esophagus - but this isn't sensitive or specific for DES diagnosis -Current first-line *TX is CCBs (e.g. Diltiazem)*; Tricyclic antidepressants are also suggested for pts w/ primarily chest pain; alternatively nitrates

Peripheral Artery Disease (PAD) Management

-PAD is the result of atherosclerotic narrowing that most commonly occurs toward the proximal end of large peripheral arteries (e.g. iliac, popliteal) -Typical cardiovascular RF (e.g. advancing age, diabetes, smoking, HTN) incr the risk of developing PAD -Depending on the severity of PAD, pts can have pain w/ exertion (*claudication*), rest pain, tissue ulceration, or gangrene. -*PAD signifies Systemic Cardiovascular Disease* and marks an INCR risk of Myocardial Infarction & Stroke -The initiation of *ASPIRIN* has demonstrated decreased incidence of stroke in pts w/ PAD and is recommended at the time of DX!!! -In addition, pts age ≤75yo should be initiated on *HIGH INTENSITY STATIN THERAPY* (e.g. *Atorvastatin* 40-80mg daily, *Rosuvastatin* 20-40mg daily), *regardless of baseline cholesterol levels*; this lowers the risk of cardiovascular events and may, in some cases, improve claudication sx -In addition to RF management, a *supervised exercise program* is the best initial management for *claudication d/t PAD* -Pts should participate in 30-45mins of supervised walking ≥3x/wk for >3mo -Pts may experience *moderate increases in symptom-free walking distance* -*For pts w/ persistent sx despite smoking cessation, antiplatelet (aspirin) and statin therapy, and supervised exercise therapy, the addition of twice-daily Cilostazol may lead to improvement in sx.* Note: *Cilostazol* is a phosphodiesterase-3 inhibitor that provides symptomatic improvement in some pts w/ claudication d/t PAD; however, initiation of Cilostazol is not recommended until lifestyle modifications (e.g. smoking cessation, exercise) have failed.

TX of Peripheral Artery Disease (PAD) (asymptomatic)

-PAD results from *atherosclerotic narrowing of peripheral arteries and represents established atherosclerotic cardiovascular disease (ASCVD)* -PAD pts should be *initiated on antiplatelet (e.g. aspirin) and high-intensity statin therapy for secondary prevention of cardiovascular events* - so should pts who have had *stroke or TIA!* *High-intensity Statins*: • Atorvastatin 40-80mg • Rosuvastatin 20-40mg *Moderate-intensity Statins*: •Atorvastatin 10-20mg, Rosuvastatin 5-10mg, Simvastatin 20-40mg, Pravastatin 40-80mg, & Lovastatin 40mg

IgA Neprhopathy

-Presents several days after URI or spontaneously, and is MC in young adults -Production of *pathogenic IgA* is triggered by *mucosal infection (Respiratory or GI)*, or less commonly, it occurs *spontaneously* -*IgA is deposited in the mesangium* (*IgA-based IC deposits in mesangium; EM w/ mesangial IC deposition*), leading to a spectrum of dz ranging from *ASX to Microscopic Hematuria to Gross Hematuria w/ Nephritic Syndrome* (e.g. *HTN, Elevated Cr*) -*Flank Pain* (CVA tenderness) common - d/t stretching of the renal capsule -*Urinalysis* shows *proteinuria, hematuria, & RBC casts* -Serum *complement levels are WNL* bc of weak complement-fixing activity of IgA -DX clinical, but can be confirmed w/ kidney Bx -*Recurrent episodes of hematuria are common*, but IgA nephropathy is a *benign* dz with *NO Chronic kidney injury* -Clinical predictors of progressive dz incl /HTN, elevated Cr, & persistent proteinuria/

Paget's disease of bone (PDB)

-PDB is a common condition in *older adults* that is d/t *increased bone turnover* -*Head CT* characteristically shows a *thickened calvarium w/ an inhomogeneous bone density or "cotton wool" appearance* that is typical -Most PDB pts are *ASX* and *DX made incidentally on radiographic or abnormal lab studies* -- *Elevated serum & bone-specific ALP, normal Ca2+ & PO4 (but can be elevated if bone fracture/immobilization); plain radiographs show osteoLYTIC or Mixed Lytic/Sclerotic lesions* -Next step in management is to obtain *calcium and alkaline phosphatase levels*; PDB pts have an *elevated ALP & normal Ca2+ level* -If needed, can differentiate the elevated ALP of PDB from the elevated ALP of hepatobiliary dz by measuring the *bone-specific fraction* -PDB pts should ALSO have a *Radionuclide Bone Scan to identify other involved sites* (better than x-ray!) -*BISPHOSPHONATES* are the *mainstay of TX of PDB* as they *reduce bone turnover* -Most pts, incl those w/ bone pain or involvement of high-risk locations (e.g. skull involvement) should be considered for TX -*HEARING LOSS* is a *common complication of PDB* -- possibly d/t compression of the auditory nerve by bony overgrowth or involvement of the cochlea &/or cochlea capsule itself -*TX of PDB w/ CALCITONIN or BISPHOPHONATE therapy may SLOW the Progression of Hearing Loss, but does NOT appear to reverse the loss that's already happened*

Primary Dysmenorrhea

-Painful lower abdo cramping assoc w/ menses and no identifiable pathologic cause -Common in adolescents and is d/t *excessive prostaglandin production* which stimulates uterine contraction causing lower abdo pain that radiates to back and legs -In pts w/ severe sx that limit daily functioning, a *pelvic physical examination* is performed to *excl secondary causes* (e.g. Infection, Endometriosis, Mullerian abnormalities) -*First-line management in Non-Sexually Active* pts is *NSAIDs (e.g. Naproxen)* - which reduce prostaglandin synthesis and are most effective at or before the onset of sx -If NSAIDs are *ineffective/intolerable*, THEN *combined OCPs serve as second-line therapy* (*OCPs would be First-line in Sexually-Active* pts) Note: A *Pelvic ultrasound* is only indicated if a secondary cause of dysmenorrhea is suspected on pelvic exam (e.g. endometrioma, leiomyoma) OR if BOTH NSAIDs & OCPs (hormonal contraception) have failed

Patient AUTONOMY

-Physician respects the *patient's decision to withhold or withdraw life-sustaining treatment.* -*Competent* adult may *formulate and provide valid consent to withhold or withdraw life-supporting treatment* in the event that any injury or illness renders them incapable of decision making using an *Advance Directive* -*An Advanced Directive //overrides// the wishes of all family members!!!*

Ethical Principles in Heathcare

-Physicians have an *ethical responsibility to report impaired, incompetent, or unethical colleagues* to appropriate authorities -D/t the position of trust and disparity of power in the physician-patient relationship, a *pt cannot provide meaningful consent for sexual contact* in this setting -*Any kind of sexual contact or innuendo is inappropriate, unethical, & potentially harmful to the pt* -*Suspected misconduct should be reported to the appropriate state regulatory body* for further investigation; this is typically a division of the *state medical board* (*Office of Professional Medical Conduct*) -A *physician crossing professional boundaries* by having *sexual relations with his/her pts MUST be reported to the state medical board for further investigation* -If a physician is found *guilty of unethical conduct*, a likely result will be *license suspension or termination* Note: Advising termination of the physician-patient relationship or ceasing to perform breast exams is insufficient. With reason to suspect *sexual misconduct*, the offending physician should be investigated by the state medical board

What is Pioglitazone and what are its AE?

-Pioglitazone is an oral drug used for tx of type 2 DM as monotherapy or combined with another agent (glitazone/thiazolidinedione family); often used in pts w/ NASH and/or in those wanting to avoid insulin & minimize cost -Works by *increasing Insulin sensitivity in peripheral tissues* (e.g. liver, muscle, adipose tissue) by *binding to & stimulating PPAR-gamma* nuclear transcription regulator receptors on collecting tubules --> *Increased renal sodium reabsorption & fluid retention* leading to *symptomatic heart failure* in ~5% of pts, esp those w/ *underlying heart dz* (e.g. prior MI) -- for this reason, pioglitazone is *contraindicated in CHF pts* -AE: *Weight gain, edema, HF (fluid retention), Incr risk of fracture*

Abruptio Placentae

-Placental detachment from the uterus before fetal delivery, and can occur *after severe abdominal trauma* -Risk factors: trauma (eg, motor vehicle accident), smoking, hypertension, preeclampsia, cocaine abuse. -Presentation: *Abrupt, PAINFUL bleeding* (concealed or apparent) in *third trimester*; possible *DIC, maternal shock, fetal distress. Life threatening for mother and fetus.* -In *concealed abruptions* (blood trapped b/w placenta and uterine wall), there may not be any vaginal bleeding -Additional clinical manifestations: *abdo pain, high-frequency, low-amplitude contractions, & uterine tenderness* -If abruption is small, FHT tracing may be normal, w/o evidence of compromise -Large abruptions are assoc w/ DIC & fetal demise -Clinical DX! May see large clots on U/S -*Fetomaternal hemorrhage in Rh(D)-Negative mothers* is another serious complication of placental abruption, as it can result in *alloimmunization* -A *Kleihauer-Betke test* is indicated to *detect & quantify amount of fetomaternal hemorrhage* by calculating percentage of fetal RBCs in maternal circulation - this helps determine *amount of Rho(D) immunoglobulin* to be administered to *decr the risk of alloimmunization*

Symptomatic Congenital Hypothyroidism Presentation

-Poor feeding, hypothermia, jaundice, hoarse cry, somnolence/lethargy, constipated, puffy (myxedematous) facies, macroglossia, umbilical hernia, large fontanelles, hypotonic, dry skin, hypothermia, prolonged jaundice -Presents w/ *chronic sx* (not acutely) -Test T4 and TSH levels

What is the postexposure prophylaxis routine for rabies?

-Postexposure PPX includes *wound cleaning* PLUS *immunization w/ Killed vaccine && Rabies Immunoglobulin* -Example of *passive-active immunity*

ACUTE CORONARY SYNDROME (ACS)

-Pt clinical presentation w/ *substernal chest discomfort, relief w/ nitroglycerine, & ECG findings of ST-segment depression in leads II, aVF, & V3-V6* -- *is consistent w/ ACS - Unstable Angina/Non-ST-Elevation MI (NSTEMI)* -*ALL* such pts should be *managed w/:* 1. *DUAL ANTIPLATELET THERAPY*, with *Aspirin + Clopidogrel*/Prasugrel/Ticagrelor (*Platelet P2Y12-receptor blocker*) 2. *NITRATES* 3. *β-BLOCKERS* 4. *STATINS* 5. *ANTICOAGULANT THERAPY*, with *Unfractionated Heparin, LMWH, Bivalirudin, or Fondaparinux* -In multiple randomized trials, *TX w/ DAPT & ANTICOAGULANT Therapy* has been shown to *Significantly Reduce the Risk of Nonfatal MI and Cardiovascular Death in ACS pts* Note: *Emergency cardiac catheterization & revascularization WITHIN 90MINS from the First Medical Contact is the GOAL of TX in STEMI (NOT NSTEMI)!!!*

Vesicovaginal Fistul

-Potential complication of pelvic surgery that p/w *painLESS, continuous leakage of urine (clear, malodorous fluid) into the vagina* that presents *days to weeks of surgery* -Typically caused by *unidentified intraop injury to bladder or vaginal tissue*, which *becomes devascularized & necrotic, leading to a Tissue defect and aberrant connection* -*RF* incl *scarring from prior pelvic surgery (e.g. c-sections) & poor tissue healing (e.g. diabetes, smoking)* -Discharge has an *elevated pH (basic) compared to the highly acidic vaginal secretions (pH 4.0-4.5)* -Bc some urine is lost thru vagina, pts also have *small volume voids & erythematous, pruritic vulvar skin from constant contact w/ urine* and a *need for freq pad changes* -*Small vesicovaginal fistulas may be subtle on speculum exam*, appearing as *subtle areas of red granulation tissue with fluid pooling* -Clinical suspicion for small fistula *requires eval w/ a Bladder Dye Test*, which done by *instilling dyed fluid (methylene blue) into bladder (thru urethra) and staining of tampon in vagina blue is diagnostic* -*Minor fistulas sometimes heal on their own with continuous bladder drainage, otherwise, repair is Surgical TX*

Pemphigus Vulgaris

-Potentially fatal autoimmune skin disorder with *IgG antibody against Desmoglein* (component of desmosomes, which connect keratinocytes in the stratum spinosum); Type 2 HS rxn -*Flaccid Intraepidermal bullae* caused by /acantholysis/ (separation of keratinocytes, resembling a "row of tombstones") -*Oral Mucosa ALSO involved!* -Immunofluorescence reveals antibodies around epidermal cells in a *reticular (net-like) pattern* -Nikolsky sign Positive

Neuraxial Analgesia (aka Epidural Analgesia for Labor & Delivery)

-Pregnant women in *active labor* receive the *most effective pain relief from neuraxial analgesia*, w/ a *low risk of AE* to mother & fetus -*Contraindications* to neuraxial analgesia in thrombocytopenic pts incl *SEVERE Thrombocytopenia (plts <70,000)* or *Rapidly Decreasing Platelet Count* (often assoc. w/ preeclampsia w/ severe features) -In these pts, there is an *increased risk of Spinal Epidural Hematoma* Note: *IV labor analgesia* is an option for those who have contraindications to neuraxial analgesia or those who prefer a less invasive intervention Note: Indications for platelet transfusion incl a platelet count <10,000, active bleeding w/ a platelet count <50,000, or planned major surgery w/ a platelet count <50,000

Vascular Dementia (VaD)

-Presents *following stroke* and pts will p/w *sudden or stepwise decline in executive fxn (i.e. impaired ability to plan, solve problems, & think abstractly) that interferes with activities of daily living* -Pts often have *focal neurologic findings* on examination (e.g. *hemiparesis, pronator drift, positive Romberg sign*) due to *prior [possibly unrecognized] strokes* -VaD is the second MC form of dementia after Alzheimer's -Major RF incl *hx of stroke, HTN, HLD, DM, smoking hx, coronary A dz, & A-fib* -VaD can *result from large artery cerebral infarctions (cortical or subcortical), small artery infarctions in subcortical areas (lacunar infarcts), or chronic subcortical ischemia* -Pts who *develop dementia* following a *recently diagnosed stroke* usu have *sudden or stepwise decline in cognitive fxn* -Other pts W/O a hx of recent stroke may either have progressive or stepwise decline* and *clinically unrecognized cerebrovascular dz* detected only on imaging

Plaque Psoriasis

-Presents as *erythematous plaques with silvery scales* -Lesions are *PRURITIC, multifocal, & most commonly present on EXTENSOR SURFACES (e.g. Knee)* -Patients with *chronic plaque-type psoriasis* usually present with *symmetrically distributed, cutaneous plaques* -The *scalp, extensor elbows, knees, and gluteal cleft* are common sites for involvement; *palms and soles* can be affected and cause *painful fissures* -Plaques may be asymptomatic, but pruritus is common -The extent of involvement can range from *limited, localized disease to involvement of the majority of the body surface area* -Psoriasis plaques are erythematous with sharply defined margins -In patients with highly pigmented skin, *postinflammatory hyperpigmentation* may be prominent and *may obscure erythema*. The plaques can range from less than 1 to more than 10 cm in diameter. A *thick, silvery scale is usually present*, although bathing may remove the scale, and applications of emollients may make the scale temporarily invisible.

Granuloma Annulare

-Presents as an *ASX, firm, smooth, annular plaque with raised borders* -- Ulceration is usu NOT present -Cause unknown. -Seen in assoc with DM, Dyslipidemia, Drug Exposure (allopurinol, amlodipine, diclofenac, gold, levetiracetam), and Malignancy -Granuloma annulare (GA) is an often *self-limited disorder (resolve spontaneously within a few years)* that can affect both *children and adults*. -*Localized GA*, which classically presents as an *erythematous or skin-colored, annular plaque without scale*, is the most common form of GA -The *generalized form of GA*, which accounts for approximately 15% of cases, typically presents with *numerous papules and plaques on the trunk and extremities*

How does meckel's diverticulum present?

-Presents in a *child ≤2yo w/ painLESS rectal bleeding (hematochezia, BRBPR, or melena) ± Iron Deficiency Anemia* (can also occur at any age) -MC congenital anomaly of GI tract -Can also p/w *Acute Abdominal Pain* due to *complications*: • *Intussusception* (recurrent, atypical) • *Diverticulitis* (mimics appendicitis) • *Bowel obstruction, perforation* (peritoneal signs) -A *TECHNETIUM-99 NUCLEAR SCAN IS HIGHLY SPECIFIC FOR MECKEL'S DIVERTICULUM*

Clostridium difficile infection (CDI) presentation and initial management

-Presents in pts w/ *abdominal pain/cramps, watery [nonbloody] diarrhea, leukocytosis, and recent antibiotic use* -Stool test for C. diff toxin antigen (of toxin A &/or B) or Dx by PCR -Risk factors incl *recent hospitalization, advanced age, & recent ABX use* (most commonly, *fluoroquinolones >>, cephalosporins, & clindamycin, ampicillin*; also assoc w/ PPIs) -*Oral Fidaxomicin (macrolide)* is appropriate TX for primary CDI in most pts, incl those w/ severe or non-severe dz (distinction based on degree of leukocytosis [severe >15,000] or serum creatinine elevation [severe >1.5]) -In addition to starting fidaxomicin, *the inciting antibiotic* (e.g. ciprofloxacin) *should be discontinued ASAP* bc its continued use is assoc w/ prolonged diarrhea and incr likelihood of tx failure -Can also be treated with *oral vancomycin* -If Abx still needed to treat the primary infection, then the inciting medication should be *switched to a lower-risk ABX* Note: Oral metronidazole is NO LONGER a first-line agent for tx of C.diff infxns bc it's less effective than other agents like Fidaxomicin for achieving symptomatic cure

Acute fatty liver of pregnancy

-Presents in the *third trimester* with *N/V, epigastric pain, malaise, & elevated transaminases*

Neonatal Gonococcal Conjunctivitis

-Presents w/ copious purulent eye drainage and eyelid swelling typically at age 2-5d -Infants acquire *gonococcal conjunctivitis* through *contact w/ infected maternal genital secretions* -*Gonococcal conjunctivitis has an earlier and more severe presentation compared w/ chlamydial conjunctivitis* -Infection usu begins at *2-5d* w/ severe eyelid swelling, *mucopurulent discharge*, and chemosis (conjunctival injection) -DX: Gram stain w/ G(-) intracellular diplococci; Positive culture on modified Thayer-Martin media -TX: Infected infants should receive a *single IM dose of a third generation cephalosporin (e.g. Cefotaxime or Ceftriaxone)* for TX -W/o prompt tx, gonococcal conjunctivitis leads to *corneal ulcerating, scarring, and blindness* -Can be prevented in neonates by screening pregnant women & tx their infections -Most infants w/ gonococcal conjunctivitis are born to moms who did not receive screening or had negative screening early in pregnancy & were subsequently infected -Therefore, *ALL infants should receive //Topical Erythromycin PPX// within an hour of birth!!*; this tx is highly effective in the *prevention* of gonococcal dz

Bacterial Vaginosis (BV)

-Presents with a *THIN* (not thick purulent), *gray vaginal discharge W/O assoc cervical inflammation!!* -*Clue cells* are observed on *wet mount microscopy* -Treated with *METRONIDAZOLE*

Trichomoniasis

-Presents with a *friable, punctate cervix (strawberry cervix!) and green, frothy, vaginal discharge* -*Protozoa* are seen on *wet mount microscopy* -Treated with *METRONIDAZOLE*

Lewy Body Dementia

-Presents with dementia and ≥2 of the following: • Fluctuating cognition (e.g. alertness, attention) • Visual hallucinations • Parkinsonism • Rapid eye movement sleep behavior disorder (i.e. loss of normal REM sleep atonia) -Usu presents around age 75 and is 4x more common in Men -Survival time after initial dx is 8yrs -Second leading cause of dementia behind Alzheimer's -TX: *Cholinesterase inhibitors* (donepezil, galantamine, rivastigmine) for cognitive impairment, *Carbidopa-levodopa* for parkinsonism, and *Melatonin* for REM sleep behavior disorder -*Antipsychotics* may be used to tx functionally-impairing visual hallucinations or delusions in DLB, however, note that *DLB pts are extremely sensitive to antipsychotics* and may be assoc w/ *significant worsening of confusion, parkinsonism, or autonomic dysfunction*

Abusive Head Trauma (AHT)

-Previously known as *"shaken baby syndrome"* -*AHT* refers to *injury from shaking &/or blunt force to the head* -Injuries usu result from *repeated acceleration-deceleration forces* as the infant's brain collides against the inside of the cranium -*Young children <1yo, are at greatest risk* esp if they are *"fussy" w/ frequent crying/colic*; an *unstable home env (single-parent home, parental drug/alcohol abuse)* is also a RF -*Delayed presentation to medical care* following the alleged injury & a *vague and inconsistent history of events* is *suspicious for AHT* -*Irritability & vomiting are signs of Increased Intracranial Pressure from AHT* that can be overlooked, and medical attention is not sought until the child is *apneic, seizing, or comatose* -PE may show *suspicious bruising patterns*, such as *bruises on butt*, but *oftentimes there is no external sign of injury* -In the majority of AHT cases, *Fundoscopy shows RETINAL HEMORRHAGES*, which are often *multilayered & bilateral*, and are a result of *shearing forces on retinal vessels* -*Abnormal neurologic findings are concerning for Intracranial Bleeds & Diffuse Brain Injury* -*AHT --> Retinal Hemorrhages, Intracranial Bleeds, & Diffuse Brain Injury* characteristically -In a *symptomatic pt*, after primary survey & stabilizing (e.g. airway secured), next step is *EMERGENT HEAD CT SCAN*,the *preferred method for evaluating AHT in a symptomatic pt (e.g. lethargic, vomiting)*, bc is fast, widely available, & cost effective; needed to *determine whether neurosurgical intervention is required* -CT scan detects *intracranial bleeding, cerebral edema, & hypoxic-ischemic changes*; *Subdural Hematomas* (caused by shearing of bridging veins) are the MC bleed seen in this setting, and *appear on Head CT as crescents overlying the brain, typically w/ a mixed-density pattern d/t varying stages of injury* (compared to homogenous hyperdense pattern seen in accidental head trauma) -In *asymptomatic pts*, less time-sensitive, *HEAD MRI* can provide *more detail regarding the extent & timing of the injury* while avoiding radiation exposure Note: *Head Ultrasound is used primarily to grade intraventricular hemorrhage in preterm infants*. It is NOT as sensitive as Head CT and is *NOT* the preferred imaging modality for assessing AHT

Priapism Management

-Priapism is a persistent, painful erection (>4hrs) that can lead to *irreversible ischemic injury if not corrected promptly* -Characterized by impaired OUTflow from the corpora cavernosa, leading to *acidosis, anoxia, & tissue ischemia* (Medical Emergency!) -RF for ischemic (low-flow) priapism: *PDE-5 Inhibitors (e.g. Sildenafil), Intracavernosal injections (e.g. Alprostadil), certain meds (e.g. Trazodone), & Sickle Cell DZ* -DX of ischemic priapism confirmed by *blood gas analysis of corporeal aspirate* (can do doppler U/S if unclear dx) -At the onset of Sx, priapism may be terminated w/ simple interventions (e.g. *urination, cold compresses*), but *SX >4hrs require invasive TX* -*Aspiration of corpora cavernosa* (followed by irrigation w/ cold saline) is advised, with *Intracavernosal injection of an Alpha Agonist (e.g. PHENYLEPHRINE)* if aspiration does not help Note: *Angiographic Embolization* is the TX of choice for *NONischemic (high-flow) Priapism*, which is much less common than ischemic, and is often *d/t a traumatic fistula from the cavernosal artery*

CLuster Headaches

-Primarily in *MEN* -Characterized by *episodic headaches* occurring *1-8x/day* over a period of *weeks* lasting 15mins-3hrs -The pain is typically *orbital, supraorbital, or temporal, and usu Unilateral & severe* -Pts usu also experience*restless agitation* (unable to sit still) and *ipsilateral autonomic symptoms of the ipsilateral trigeminal branch* such as *lacrimation, conjunctival injection, ptosis, miosis, rhinorrhea, & nasal congestion* -TX: *Acutely*, tx with *SUMATRIPTAN & 100% O2 for >15mins by nonrebreather mask* (O2 provides relief in >70% of pts) NOTE: *First try 100% O2, and pts who experience partial/no response are THEN given Intranasal Sumatriptan /contralateral/ to the side of headache* -Use *Verapamil 240mg or more, for prophylaxis*, esp at the onset of a cluster period

When are *preoperative pulmonary functions tests (PFTs) recommended*?

-Prior to lung resection to estimate postoperative lung volumes -To optimize preoperative COPD control if baseline clinical status cannot be determined -To evaluate the cause of dyspnea or exercise intolerance (e.g. cardiac dz vs. deconditioning)

Definition of Negative Predictive Value

-Probability of *NOT having a disease* given a *NEGATIVE test result* NPV = TN/(FN+TN) = d/(c+d)

Prolactinomas

-Prolactinomas are a relatively common cause of *amenorrhea, infertility, & galactorrhea* in women -Elevated prolactin levels suppress GNRH, LH, and estradiol, leading to sx of hypogonadism including *hot flashes, vaginal dryness*, and potentially *osteoporosis* if left untreated -Male pts can dev sx of *hypogonadism and gynecomastia* -Large adenomas may also cause HA and compression of the optic chiasm, leading to visual field defects (bitemporal hemianopsia) -The *DX of prolactinoma is strongly suggested by prolactin levels >200 ng/mL* (normal 5-20 ng/mL) -Mild elevations (20-200 ng/mL) may also be d/t a prolactinoma, but other causes such as *medications (e.g. certain antipsychotics), nipple stimulation, pregnancy, hypothyroidism, and stress should also be considered* -If prolactinoma is suspected, *MRI of the pituitary can confirm the DX* -In most cases, *hyperprolactinemia will respond to tx w/ dopamine agonists* (e.g. *Cabergoline, Bromocriptine*), which *decrease both the size and prolactin secretion of the adenoma* -*Surgical intervention* can be considered in *pts who fail to improve w/ dopamine agonist therapy*, esp if they have *significant neurologic sx*

What is Dialectical Behavior Therapy (DBT)? And which psychological condition is it used for?

-Psychotherapy is first-line tx for pts w/ borderline personality disorder, esp with DBT!! -DBT is a structured treatment *developed for borderline personality disorder* that consists of *weekly individual psychotherapy and group skills training for ~1yr* -DBT techniques incl *skills training to target self-injurious behavior and impulsivity* and *mindfulness training to target emotional dysregulation* Note: Other types of psychotherapy developed to treat BPD incl *schema-focused therapy, mentalization-based therapy, & transference-focused therapy* Also Note: Medications (e.g. mood stabilizers, antipsychotics, antidepressants) do not treat the core of BPD pathology, but can be used adjunctively to target specific sx clusters assoc w/ the disorder (e.g. mood instability, impulsivity, aggression) or to treat comorbid conditions (e.g. major depression)

Acute Arterial Occlusions d/t Cardiac Left Atrial Myxoma

-Pt p/w *acute onset lower extremity pain, diminished pulses, paleness, & coolness of left foot* for e.g., consistent with *acute arterial occlusion* -This can occur d/t an *EMBOLUS* from a *Proximal source, Acute Thrombosis of an Atherosclerotic Plaque, or Direct Trauma to the involved artery* -Sudden onset of sx in a young, healthy, previously asx pt is most consistent with *embolus* -*Most emboli originate from a Cardiac Source*, and may occur d/t *A-fib, Severe Ventricular Dysfxn, Endocarditis, Valvular DZ, Atrial Myxoma, or a Prosthetic Valve* -In a pt w/ a *regular heart rhythm* and an *apical diastolic murmur*, this makes *left atrial myxoma* the most likely cause of the embolus -*Atrial Myxomas are MC primary cardiac tumors*, most occurring in the *left atrium* -Tumors are usu *pedunculated* with a stalk coming from the *atrial septum*, & can be *extremely friable* -- leading to the *release of tumor emboli into systemic circulation* sometimes -Some large tumors can p/w signs & sx of *mitral valve obstruction* (causing a *diastolic murmur & "tumor plop"*), *rapidly worsening HF, & new-onset A-fib* -DX Confirmed by *Echo* (TEE > TTE), and *prompt surgical resection indicated*

Boerhaave Syndrome

-Pt presents w/ *retrosternal chest pain* after *repeated episodes of vomiting* is classic for spontaneous esophageal perforation (*Boerhaave Syndrome*) complicated by acute mediastinitis -Other assoc. sx are: dyspnea, odynophagia, epigastric pain, & shoulder pain -Boerhaave syndrome is characterized by a *full-thickness (TRANSMURAL) tear of the esophagus* d/t sudden elevation in esophageal pressure (e.g. vomiting), allowing gastric contents to enter previously sterile sites (e.g. into the mediastinum, causing *mediastinitis*) -Most tears occur in the *distal third* of the esophagus, and the negative intrathoracic pressure within the chest results in an influx of esophageal contents into the pleural cavity, causing inflammation and *pleural effusion* (typically on the *left*) -The effusion can be accompanied by *pneumomediastinum, pneumothorax, or both* -*Fever* d/t mediastinitis often takes >4hrs to dev, which can delay DX -Urgent management is needed as mediastinitis carries a high mortality rate that doubles if it is not properly TX within 24hrs of DX -The best initial *diagnostic test* for *esophageal perforation* is an *Esophagogram w/ Water-Soluble Contrast* (e.g. diatrizoate) — provides a definitive DX in 90% of cases -If the test is negative but clinical suspicion is high, Barium Contrast can be used -Water-soluble contrast is preferred as barium can produce further mediastinal irritation and injury in Boerhaave syndrome pts Note: Chest CT can be of value if the DX is unclear after esophagogram or if pt cannot tolerate the procedure. However, it is NOT the test of choice as it may fail to detect small tears.

Small Intestinal Bacterial Overgrowth (SIBO)

-Pt w/ *chronic watery diarrhea w/ assoc bloating & excessive flatulence* -Initial testing, incl multiplex PCR testing for infectious pathogens, negative -SIBO is caused by *proliferation of colonic bacteria in the small bowel, leading to excessive fermentation, inflam, & malabsorption* -*SIBO is a common complication of underlying SCLERODERMA*, which can *alter intestinal motility d/t smooth muscle atrophy & fibrosis* -SIBO can be DX by *jejunal aspiration*, which *directly measures the bacterial load in the small bowel* -- but this is INVASIVE and avoided in uncomplicated cases -*SIBO can be Confirmed w/ a CARBOHYDRATE BREAT TEST*, in which a *dose of fermentable carbs (lactulose, glucose) is taken orally; the breath is sampled for hydrogen & methane (produced by gut bacteria) at regular intervals (q30mins)* -In Normal Pts --> Colonic bacteria ferment any nonabsorbed substrate after 2-3hrs -But *a rise in breath hydrogen <90mins suggests fermentation in small bowel --> Indicating SIBO* -Management: *Correction of underlying abnormality, dietary modification, & oral ABX* (e.g. *RIFAMPIN*, Ciprofloxacin) -A satisfactory response to TX further confirms DX. *Recurrences are common* Note: Diarrhea from small intestinal condition is usu LARGE volume, whereas Colon pathologies are SMALL volume but Frequent

Pulmonary Hypertension - Presentation & General Supportive Measures

-Pt w/ *progressive exertional dyspnea, elevated pulmonary artery systolic pressure, & poorly-functioning, hypertrophic right ventricle* has *Pulm HTN* -*Management of Idiopathic Pulmonary Arterial HTN (Group 1 PAH)* (note, *all forms of PH require general supportive measures to maintain physiologic homeostasis - normoxia, euvolemia, sinus rhythm*) ● *AVOID PREGNANCY*: *Maternal & Fetal mortality remain unacceptably high (25-50%), even w/ optimal pharmacotherapy.* Guidelines *strongly recommend AVOIDING pregnancy, & Advise Non-Estrogen-based CONTRACEPTION (lower risk for venous thrombosis) for women of childbearing age* ● *Regular AEROBIC Exercise*: Supervised cardiac/pulm rehab program, done as tolerated is safe & effective for restoring functional status - but strenuous weightlifting & Valsalva maneuvers inhibiting venous return should be avoided ● *Nutritional Support*: A dietary plan to regulate salt & fluid intake and achieve weight loss/gain (e.g. pulmonary cachexia), targeting a healthy BMI -*Pulm HTN* pts should be *referred to an Accredited PH Program* d/t superior outcomes w/ psychosocial outcomes, family planning assistance

Osteomyelitis in Sickle Cell Disease Patients

-Pt w/ SCD with *fever, focal bone pain, elevated inflammatory markers (CRP>8), after MILD trauma* should be *suspected for OSTEOMYELITIS* - a bone infection most commonly spread *hematogenously* in children -Initial diagnostic testing should incl: *CBC, CRP, ESR, blood culture* -*X-rays* should be obtained to evaluate alternate causes of pain; the late finding of *periosteal reaction/elevation seen in osteomyelitis* -*MRI* has excellent sensitivity if dx unclear -Most common etiology is the *gram-positive cocci Staph aureus, INCLuding MRSA*; However, with *SCD pts*, there's *incr risk of osteomyelitis d/t gram-negative organisms, incl Salmonella* -SCD pts have *functional asplenia* d/t repeated splenic microinfarctions, rendering *vulnerability to encapsulated organisms* (e.g. *Salmonella, Strep pneumoniae*) -*EMPIRIC ABX* should incl *gram-pos coverage w/ Nafcillin, Oxacillin, or Cefazolin if rates of MRSA are low, or Clindamycin or Vancomycin if MRSA is suspected*; Additionally, *SCD pts require gram-neg coverage with a third-generation cephalosporins (e.g. Ceftriaxone, Cefotaxime)* -ABX therapy should begin promptly after initial lab studies are drawn to reduce further M&M Note: Bc of functional asplenia, *prophylactic penicillin* is recommended for children age 2mo-5yo to prevent infection from encapsulated organisms; however, penicillin has a narrow spectrum of activity and would NOT provide coverage for Staph aureus

What does it mean if a screening test has a *low sensitivity and low PPV, but a High Specificity and High NPV*?

It means that this screening test *will be highly accurate in identifying individuals WITHOUT the disease* High specificity --> High probability of a negative test in those W/O the dz High NPV --> High probability of NO disease in those with who test Negative on the screening test

Corneal Laceration

-Pt w/ eye pain, tearing, conjunctival erythema after scratch to the eye raises concern for *corneal injury* (e.g. abrasion or laceration) -Can cause an *open globe injury* (e.g. *perforation*) if extends through the full thickness of the cornea -A *positive Seidel sign (i.e. concentrated fluorescein uptake [indicates corneal epithelial defect] w/ subsequent clearing in a waterfall pattern [indicating washout of fluorescein by draining aqueous humor] on slit-lamp exam) indicates Full-Thickness Corneal Laceration* - an Ophthalmologic *EMERGENCY* that requires immediate consultation - many will need urgent operative repair Note: Saline irrigation is contraindicated in full-thickness corneal lacerations for risk of introducing env pathogens from surface of eye into globe, incr risk of infxn -In contrast to corneal abrasion, laceration is a *deeper* & more serious injury -Abrasions will have concentrated fluorescein uptake AT the site of corneal epithelial defect WITHOUT subsequent waterfall-pattern washout (negative Seidel sign) -Abrasions are tx w/ topical antibiotics and outpt ophthalmology f/u

Immune Thrombocytopenia (Idiopathic Thrombocytopenic Purpura)

-Pt w/ lower extremity *petechiae & isolated thrombocytopenia* suggest *immune thrombocytopenic purpura (ITP)* -Presumptive dx of ITP made when hx, PE, CBC, differential count, & Peripheral blood smear (PBS) show *isolated thrombocytopenia* WITHOUT any obvious causes -*ITP is d/t platelet destruction by Antiplatelet Autoantibodies*, which are most often directed *against membrane proteins* (e.g. GPIIbIIIa) -Circulating platelets are rapidly removed by autoantiboides, limiting the role of platelet transfusions; *splenic macrophage consumption of platelet-antibody complex* -May be primary (idiopathic) or secondary to autoimmune disorder, viral illness, malignancy, or drug rxn -Labs show *incr megakaryocytes on BMBx* -TX: *Steroids, IVIG; Rituximab or Splenectomy for refractory ITP* -Platelet count decreased, causing increased bleeding time, but normal PT & PTT, no incr in plasma D-dimer

Psychogenic Nonepileptic Seizures (PNES)

-Pt w/ seizure behavior assoc w/ forceful eye closure and absence of self-injury, incontinence, or postictal confusion -PNES is considered a *type of Conversion Disorder*, as the clinical findings are inconsistent w/ seizures or other known neurological conditions -*Suggestive features of Psychogenic Nonepileptic Seizures* incl *forceful eye closure, side-to-side head or body movements, rapid alerting and reorienting, and memory ability to recall the event* -PNES events usu occur in front of witnesses, and these pts may model their behavior after a friend or relative w/ epilepsy -Unlike real seizures, *PNES is NOT assoc w/ abnormal cortical activity during the episode* -*Video-EEG Monitoring* is considered the *gold standard* for DX, as it is more likely to capture an event and demonstrate the *lack of assoc epileptiform activity* -A *PSYCHIATRIC ASSESSMENT* is CRUCIAL as many pts w/ PNES often also have *comorbid psychiatric disorders and/or a hx of trauma*

Orthostatic Proteinuria

-Pt with *Isolated Proteinuria on Urinalysis is consistent w/ Orthostatic Proteinuria* - when a *higher than normal protein excr during the day (when standing upright) occurs, but normal protein excretion at night (when lying supine)* -Orthostatic proteinuria is the *MCC of proteinuria (non-nephrotic range, <3.5g/d) in ADOLESCENTS* and *rarely occurs >30yo* -*Degree of proteinuria is MILD* and *other significant renal abnormalities (hematuria, AKI, HTN) are ABSENT* -*DX Confirmed by comparing the urine protein:creatinine ratio in urine samples collected in both the Standing & Supine positions*; Can *Also Confirm w/ a SPLIT 24-HR URINE COLLECTION to compare protein excr divided between Daytime (after morning void until bed time) and Nighttime periods* -- *confirmed when significantly Elevated Daytime protein excretion, but Normal Nighttime excretion rate* -It is a *benign condition in adolescents, usu resolving spontaneously, causing NO significant effect on renal fxn and NO dev of significant glomerular pathology in the future* -- THEREFORE *NO further diagnostic (e.g. invasive kidney biopsy) Workup or TX (e.g. ACEI, oral steroids) is required* -Pts should be *reassured and will resolve with age; monitor periodically*; *Reconfirm orthostatic proteinuria if persistent proteinuria*

Pneumocystis jirovecii Pneumonia (PCP) in HIV pts

-Pt with *advanced HIV (maybe not on antiretrovirals) with INDOLENT pulmonary sx, significant HYPOXIA, and CXR evidence of B/L Interstitial Infiltrates, raises strong suspicion for PCP* -P. jirovecii is an *atypical FUNGUS* that causes *OPPORTUNISTIC Pulmonary Infections in those w/ Significant IMMUNOCOMPROMISE* -Pts w/ *HIV w/ CD4 <200 are at GREATEST RISK* and *usu p/w INDOLENT FEVER, NONPRODUCTIVE Cough, Dyspnea, & Weight Loss* -*PROFOUND HYPOXIA & Tachypnea* are common and *CXR usu reveals Bilateral Interstitial or Alveolar Infiltrates (e.g. diffuse interstitial ground glass opacities bilaterally)* -Pts with *high pretest probability for PCP often receive EMPIRIC TX (TMP-SMX, Dapsone, Pentamidine), but DEFINITIVE DX Requires Isolation of Organisms in Respiratory Secretions (Induced Sputum Analysis, Bronchoalveolar Lavage, Lung Biopsy)* Note: Often Empiric TX for BOTH PCP (w/ TMP-SMX ± Prednisone) AND Community-Acquired Pneumonia (Ceftriaxone, Azithromycin) are given -*Induced sputum* is the *least invasive* way to obtain resp samples, *BUT diagnostic sensitivity is only 50-90% (Low Sensitivity) --THEREFORE, *if induced sputum analysis is negative for Pneumocystis*, these *negative results necessitate FURTHER testing if PCP is still highly suspected* -In pts w/ *suspected PCP w/ negative induced sputum testing, the Next Diagnostic Test of Choice is a Fiberscopic Bronchoscopy w/ Bronchoalveolar Lavage* -- this test is *Highly Sensitive, 90-100%! for DX of PCP* -Disc-shaped yeast seen on methenamine silver stain of lung tissue or with fluorescent antibody. Note: Strep pneumo is the MCC of community-acquired PNA and usu manifests ACUTELY (not indolently like PCP) with Fever, chills, Productive cough, dyspnea, and LOBAR (not interstitial) Infiltrates Note: Staph aureus PNA typically causes severe, rapidly progressive, necrotizing PNA w/ high fever, septic shock, & multilobar cavitary infiltrates.

*ANABOLIC-ANDROGENIC STEROID ABUSE*

-Pt with *changes in mood, worsened acne, & hirsutism (virilization)* suggest likely *anabolic-androgenic steroid abuse* -*Anabolic Steroids* (e.g. *testosterone, trenbolone, boldenone, stanozolol, nandrolone*) are popular among young ppl and *athletes* looking to *improve physical appearance and performance* -In *women,* they may also be *assoc w/ eating disorder Sx*; additionally, women may exhibit *clitoromegaly, bilateral temporal hair loss, & an Irreversible voice deepening* -*Mood SX* can occur in *men & women* -*INCR aggressive behavior* can also be seen (but *more notably in men*) -Other *AE of Anabolic Steroids* incl: *Impaired endogenous testicular fxn, Decr testicular size and sperm count, Gynecomastia in men, & Ovarian Dysfunction in women* -*Hepatic dysfunction* may occur, *HDL levels Decr*, and *High doses of anabolic steroids can cause Cardiac Dysfunction* -Additionally, pts can *develop Erythrocytosis d/t Androgen-Stimulated Erythropoiesis*; erythropoietin used to enhance athletic performance can also increase erythropoiesis but does NOT cause androgenic hormonal changes

Viral Gastroenteritis

-Pt with *emesis, Watery Diarrhea, abdo tenderness, & Hyperactive bowel sounds* -*SX EXACERBATED BY FRUIT JUICE* -- *High in Fructose or Sorbitol --> Increases Osmotic Load --> Fructose Malabsorption in the Small Intestine!!* -A mild, *transient lactase deficiency* with dairy intake can *result from gastroenteritis* d/t inflam & damage to intestinal epithelium -*FLUID REPLETION* is the *First-line TX* for *Viral Gastroenteritis* -Signs of mild dehydration incl: moist mucosa but dry lips, normal vitals, brisk capillary refills -*Oral rehydration w/ Hypo-Osmolar solution containing electrolytes & small amount of glucose is the best*; *IV hydration if severely dehydrated* -Hydration with water alone can cause dangerous hypoglycemia or hyponatremia

Constitutional Delay of Growth & Puberty

-Puberty is considered *delayed if no secondary sexual characteristics* (typically testicular enlargement [≥4 mL] or breast development) *are present by age 14 in boys or age 12 in girls* -A pt w/ *short stature* but *normal growth velocity* (4-6 cm/yr) most likely has *constitutional delay of puberty* -A FHX of *"late bloomers"* would support this DX; however, this Hx is not always present -In contrast to Familial Short Stature, in which short stature and normal growth velocity are accompanied by a normal bone age, *constitutional delay is assoc w/ a delayed bone age* on x-ray of the wrist -Height and pubertal development typically correlate more closely with bone age than with chronological age -On f/u, pts w/ constitutional delay of puberty often demonstrate an onset of puberty similar to that of family members, and reaching the midparental adult height is expected following the pubertal growth spurt.

Why would a patient take methadone? Is methadone safe during pregnancy and/or breastfeeding?

-Pts (incl pregnant women) w/ *opioid use disorder* are often TX with an *opioid agonist* such as *Methadone, which prevents withdrawal sx without inducing euphoria, and reduces cravings for recreational opioids (heroin)*, which have greater risk for M&M -Methadone is *SAFE during pregnancy* and can be transitioned to during *any trimester*, although *early & sustained adherence to a methadone program decreases rates of relapse, drug overdose, & neonatal morbidity* (e.g. *preterm delivery, growth restriction, neonatal opioid withdrawal syndrome*) -Pregnant pts w/ an *active substance use disorder (e.g. opioids, marijuana) are advised AGAINST breastfeeding* bc recreational drugs are unpredictable (laced with other substances, inconsistent dosing) -In contrast, pregnant pts on a *stable Methadone regimen are ENCOURAGED to breastfeed w/o needing to decr/discontinue methadone tx* -*Methadone concentrations in breastmilk are LOW, are unrelated to maternal dose, & rarely cause AE* (e.g. neonatal resp depression) -*Candidates for breastfeeding while on methadone tx* must be willing to *continue with a methadone program postpartum & demonstrate adherence to therapy* -- including having *negative toxicology screens* (i.e. positive for prescribed meds [incl methadone] only) and *attending regular prenatal visits*

When should colon cancer screening begin?

-Pts at *average risk* for colon cancer should *start colon cancer screening at AGE 45* -For those w/ *first-degree relative with colon cancer OR those w/ High-Risk Adenomatous Polyp (≥10mm, high-grade dysplasia, villous elements)*, *Screening Colonoscopy* is *Recommended Beginning at AGE 40 OR 10YRS Before the Relative's Age @DX, whichever comes first*

In addition to routine prenatal labs, what additional testing should you do for pts at high risk for preeclampsia?

-Pts at high risk for preeclampsia include pts with *sickle cell disease* or *existing hypertension* also diabetes, SLE -These pts should receive a *24hr urine collection for total protein at the initial prenatal visit* to *establish baseline renal fxn & dictate pt management* (i.e. early delivery) in case of worsening hypertension • Pts w/ worsening chronic HTN have BP elevations w/ NO significant changes in proteinuria - these pts managed as outpts and delivered at term (37-39wks gestation) • Pts w/ *superimposed preeclampsia* have worsening HTN & progressive proteinuria &/or signs of end-organ damage - these pts require inpatient care and preterm delivery (34-37wks gestation) -In high-risk pts, *aspirin therapy beginning at ≥12wks gestation (ideally before 16wks) decr the risk for preeclampsia* -24hr urine collection identifies pts w/ nephrotic-range proteinuria (>3.5g/d) who are at risk for thromboembolism and require anticoagulation during pregnancy and postpartum -Oral antihypertensives safe in pregnancy incl *labetalol & nifedipine* and are used to *maintain BP <140/90*

Diaphragmatic Paralysis

-Pts typically p/w *SOB worse while supine* (therefore easily confused with congestive heart failure) -Ventilatory function is worsened by lying down, i.e. decreased forced vital capacity worsened while supine than upright -Supine SOB --> *Poor sleep, Daytime fatigue, & Morning Headaches* -Pulm auscultation nonspecific, maybe atelectasis in lower lobes -One PE clue suggestive of Diaphragmatic Paralysis is *PARADOXICAL Abdominal RETRACTION During INSPIRATION* while Supine -- occurs bc diaphragm is not contracting -A *sniff test using fluoroscopy* can be helpful to confirm the diagnosis -The *MCC of Bilateral Diaphragmatic Paralysis* are *NEUROLOGIC Diseases* such as *ALS* -- therefore, in pts with this presumed dx, presence of neuro signs & sx should be sought out elsewhere in body Note: Pts presenting with *additional neurologic sx* (e.g. lower extremity atrophy and tongue fasciculations, both representing lower motor neuron signs are suggestive of a neurologic dz like Amyotrophic Lateral Sclerosis) Note: The dyspnea associated with interstitial lung disease does not usu worsen while lying supine.

Tricyclic Antidepressant Overdose

-Pts w/ TCA overdose can develop *CNS findings* incl *mental status changes (e.g. drowsiness, delirium, coma), seizures, & resp depression* -*Anticholinergic* effects incl *dry mouth, dilated pupils, flushing, hyperthermia, & urinary retention* -*CardioTOXIC Effects* (e.g. *sinus tachycardia, hypotension, & arrhythmias)* cause most of the *mortality* in TCA overdose pts -EKG can show *prolonged [widened] QRS interval (>100msec)* and evidence of arrhythmias (e.g. *ventricular tachycardia, ventricular fibrillation*) -TCAs can also reduce calcium influx into myocardium, *increasing peripheral vasodilation --> Hypotension* -TCA overdose can cause *ACEDEMIA*, which can *mildly increase serum potassium* -*IV SODIUM BICARBONATE* is the most effective agent for managing TCA-induced cardiotoxic effects (QRS widening or ventricular arrhythmias) -- NaHCO3 *increases serum pH (more alkalosis) and increases extracellular sodium* -Pts who are *refractory to sodium bicarb may respond to Adjuvant Magnesium or Lidocaine (class IB)*

Resuming Sex after an MI

-Pts w/ cardiac dz are often anxious about ability to engage in sex, esp after an MI -*Sexual activity is assoc w/ an Incr in HR & BP, and a small but measurable Absolute INCR in RISK of MI* -In general, *based on cardiovascular dz (CVD) status, pts classified into 3 categories in regards to sexual activity*: ● *LOW-Risk pts*: Can perform *light-intensity exercise w/o sx & should be able to initiate/resume sex*. E.g. Those w/ *Few CVD RF, controlled HTN, ASX LV dysfunction, or Successful revascularization of clinically significant lesions (>50-60%)* ● *HIGH-Risk pts*: Should be *referred for a detailed assessment Prior To Advising on activity*. E.g. Those w/ *Refractory Angina, NYHA Class IV HR, Significant Arrhythmias, or Severe Valvular Dz* ● *Indeterminate/Intermediate-Risk pts*: *Stress Testing is Recommended* to *Reclassify them as low- or high-risk* and to *help guide decisions* -In the *period immediately following an Acute MI, the myocardium may be vulnerable to increases in O2 demand* -Nonetheless, *MI pts who've undergone Successful Revascularization or who have NO Evidence of Ischemia on Exercise Stress Testing* can be *considered LOW-RISK* and may *Safely Resume Sex soon after MI, Within 3-4WKS*

Pyelonephritis in Children

-Pyelonephritis usu p/w *fever, N/V, & flank pain, costovertebral tenderness, & pyuria* (leukocyte esterase positive on dipstick urinalysis or ≥5 WBC/hpf on microscopy) -RF: Female sex, hx of bladder or bowel dysfunction (e.g. chronic constipation) -TX presumptively if clinically suspicious after PE findings and urinalysis w/ *empiric ABX like Ceftriaxone (3rd gen cephalosporin) to prevent renal scarring* -ORAL ABX preferred in most kids w/ UTIs (incl Pyelo), but need *INPATIENT IV ANTIBIOTICS* WHEN: •*Hemodynamically instability* (BP & HR) •*Inability to tolerate PO* (e.g. persistent vomiting) • Failure to improve on PO ABX • *Infants <2months old* d/t *incr risk of sepsis* Note: High fever does not influence whether to give IV Abx or not. If hemodynamically stable with high fever, can tx with PO. However, if after PO tx, pt still has persistent fevers, then can consider IV Abx

Vit B12 Deficiency in Pernicious Anemia

-Pts w/ primary hypothyroidism are predisposed for other autoimmune diseases, like Pernicious Anemia -*Vit B12 deficiency in pernicious anemia is d/t a deficiency of Intrinsic Factor secreted by the stomach due to Atrophic Gastritis* (dietary B12 binds to IF secreted by the parietal cells in gastric mucosa; this IF-B12 complex is carried to the terminal ileum for receptor-mediated absorption) -*Pernicious Anemia* results from the *autoimmune destruction of Parietal cells*, leading to *Achlorhydria & Decreased prodn of Intrinsic Factor* -- this *lack of IF leads to vit B12 deficiency* -RBCs are *Macrocytic* d/t *ineffective erythropoiesis d/t defective nucleic acid synthesis* -*Neurologic involvement in Vit B12 Deficiency* is characterized by *involvement of Posterior (loss of proprioception) & Lateral (brisk reflexes) Columns in the spinal cord (i.e. SUBACUTE COMBINED DEGENERATION) and leads to Ataxia, Loss of Proprioception, Loss of Vibratory sensations, & Peripheral Neuropathy* -*Severe spasticity, weakness, & peripheral nerve (e.g. loss of ankle jerk) involvement* can occur -*SX and Signs are more prominent in the LOWER > upper Extremities* -*TX w/ Supplemental Vit B12*

What is the Jarisch-Herxheimer reaction?

-Pts who *dev an Acute Febrile Syndrome within 24hrs of Initial TX for a Spirochetal Infection (e.g. Syphilis, Leptospirosis, Tick-borne Spirochetes)* usu have the *Jarisch-Herxheimer RXN* -This rxn is thought to be *d/t the Rapid Lysis of Spirochetes, releasing bacterial proteins into the bloodstream, & triggers an Innate Immunologic Response* -*Manifestations* commonly incl *fever, malaise, chills, HA, & myalgias* -Although there is *NO Effective Prevention for the Jarisch-Herxheimer rxn,* *symptoms are generally Self-Limited & Resolve within 48hrs* -Most pts require NO TX, but those w/ *severe* manifestations can be *TX w/ an antipyretic (e.g. acetaminophen)* Note: Since the Jarisch-Herxheimer rxn is NOT mediated by mast cells or basophils, *Antihistamine therapy is INEFFECTIVE*. And Corticosteroids have NOT been shown to prevent or improve Sx.

TX for Varicella Herpes Zoster (Shingles)

-Pts who *present <72hrs AFTER Rash Onset* --> *TX w/ ORAL VALACYCLOVIR 3x/d for 7 DAYS + Analgesia (NSAIDs, Ibuprofen)* to *reduce risk of transmission, new lesion formation, & (possibly) risk of postherpetic neuralgia* -Pts who *present >72hrs AFTER Rash Onset* --> *TX w/ Analgesia (NSAIDs, Ibuprofen) & Topical Rash Care (e.g. Zinc Oxide Cream)* (no antivirals given after 72hrs!!) -*PO* Valacyclovir x7d preferred in *uncomplicated* cases (i.e. localized herpes zoster, to 1 dermatome or 1 dermatome & immediately-adjacent dermatomes)* -*IV* Valacyclovir x7d is given when pts are *Immunocompromised (e.g. HIV)* or *zoster lesions are widely Disseminated* Note: Oral acyclovir requires dosing 5x/d, so PO Valacyclovir is preferred as it is taken 3x/d. Note: *Steroids (e.g. Prednisone) are generally CONTRAINDICATED in Uncomplicated Zoster d/t INCR Risk of Secondary Bacterial Infections & little proven benefit* Note: Pts w/ *herpes zoster may transmit VZV to others from the Onset of the lesion Until it is Completely Crusted Over (Dry)*. Most *transmissions are via direct contact*, but *aerosolized virus from active lesions* occasionally cause infection. Pts who are *TX as an Outpatient* should be *advised to keep "wet" lesions covered until completely crusted over* to *prevent transmission to others*

Workup of *Hypercalcemia*

-Pts with *mild hypercalcemia* are often *ASX*, but *common initial manifestations may incl Constipation, Fatigue, Nausea, & Nephrolithiasis* -First step in Evaluation of Hypercalcemia is to *Repeat Serum Calcium w/ concurrent measurement of Serum PTH* to *distinguish PTH-Dependent* (e.g. *Primary Hyperparathyroidism*) *from NON-PTH-Dependent causes* -*Hypercalcemia + Elevated/High-Normal PTH suggests Excessive Secretion of PTH* -*Hypercalcemia + LOW PTH (<20pg/mL) suggests NON-PTH-Dependent etiology* -*Urinary calcium* should be *measured in pts w/ PTH-Dependent Hypercalcemia* to then differentiate *Familial HYPOcalciuric Hypercalcemia* (rare disorder d/t mutations in the calcium-sensing receptor, leading to *LOW urinary calcium excretion*) *from Primary Hyperparathyroidism (in which urinary calcium excretion is Normal/Elevated), but only after confirming PTH-Dependent Hypercalcemia Note: Even when *malignancy is suspected*, *PTH is STILL the first step in evaluating Hypercalcemia* as the *incidence of primary hyperparathyroidism is higher in cancer pts* than in the general population.

Suspected Acute Coronary Syndrome (ACS) - Management

-Pts with *suspected ACS but unremarkable EKG and serum troponins should be Observed with Serial EKGs and Serial Troponins to Confirm or R/O the DX* e.g. Pt with several *cardiovascular RF* (e.g. *HTN, HLD, FHX*) *dev typical anginal pain during exertion* -*STABLE Anginal Pain* usu *RESOLVES within a few MINS of Rest or Sublingual Nitroglycerin admin*; *Anginal pain that lasts >20 MINS is Suggestive of ACUTE CORONARY SYNDROME* -*Initial EKG may be Non-DX or Normal* in >50% of pts p/w *Myocardial Infarction* and *Serum Troponins can remain Undetectable for 6-12hrs following the onset of MI Sx* -For pts in whom the *initial EKG & troponins are unremarkable, but there is reasonable suspicion for ACS, the most appropriate approach is Further Observation with Serial EKGs and Troponin Levels (3 troponins 6hrs apart & several EKGs 30mins apart)* -*Subsequent elevation in serum troponins with or without EKG findings of ischemia* (e.g. *ST depression, T-wave inversions with prominent R waves*) will *Confirm Non-ST-Elevation MI* -Alternatively, *Reoccurrence of Typical Anginal Pain in the ABSENCE of troponin elevations may Confirm UNSTABLE Angina*

When should you be concerned about the lack of menses in a teenager?

-Puberty in girls typically *begins with breast development (THELARCHE, in girls ages 8-12) and pubic hair growth (PUBARCHE)*, and is later *followed by onset of menses (MENARCHE) about 2-2.5yrs later* -Timing of menarche varies, but is *normal if menses occur by age 15 in girls WITH secondary sexual characteristics* -A *lack of menses by age <15 is NORMAL if secondary sexual characteristics are present, then Reassurance and Observation are indicated* Note: Growth spurts typically occur shortly BEFORE the onset of menses Note: *Constitutional Delay of Puberty* characterized by a *Delayed Bone Age*, may be considered in *girls age >12 w/ Short Stature and NO breast development (which is the first sign of puberty)*

Pruritic Folliculitis of Pregnancy

-Rare subset of *Atopic Eruption of pregnancy* -Characterized by *pustules assoc with hair follicles* -The *rash typically begins on the abdomen, but can become more generalized* -The *assoc pruritus is MILD*

Appropriate diagnostic testing in pts suspected to have *clinically significant, STABLE coronary artery disease (CAD)*?

Need to do some form of *stress testing* if suspect *clinically significant (e.g. Stable Angina) CAD* as the best initial diagnostic intervention *Exercise ECG stress testing is preferred* when possible; however, in pts who are *unable to perform adequate exertional walking* (e.g. *severe osteoarthritis*), these pts require *Pharmacologic Stress Testing (e.g. Adenosine Myocardial Perfusion Imaging, Dobutamine Echocardiography)*

Acute lung transplant rejection (ALTR)

-Recipient Pt p/w *dyspnea, nonproductive cough, low-grade fever, hypoxemia, & CXR showing perihilar opacities w/ interstitial edema and small pleural effusions* is consistent with *acute lung transplant rejection* -ALTR is a *cell-mediated response (Type 4 HS)* that most commonly occurs *within 6mo of lung transplant* -ALTR is usu effectively *TX with High-Dose Glucocorticoids (e.g. pulse dose prednisone)*; HOWEVER, such tx can /markedly worsen an acute infection and should not be initiated until infection is ruled out/ -Lung transplant recipients are at *incr risk for both Opportunistic (e.g. CMV, invasive aspergillosis, pneumocystis PNA) and Nonopportunisitc (e.g. Influenza, Adenovirus) infections* that *can have similar clinical presentations* to ALTR -Therefore, *Diagnostic Workup of ALTR* should include *Bronchoalveolar Lavage & Lung Biopsy* -- these results help to evaluate for infection and confirm acute rejection with biopsy findings of submucosal lymphocytic infiltrate, perivascular inflam Note: Pulmonary embolism would also cause SOB & effusions, but won't explain progressive symptoms >2wks and interstitial edema on CXR

HIV Postexposure PPX (PEP) for High-Risk Occupational Exposures

-Recommended following occupational exposure to *blood or potentially infectious body fluids* from an *HIV-POSITIVE* source patient via *Percutaneous exposure* or *exposure to Mucous Membranes or Nonintact Skin)* -If the HIV status of the source pt is unknown but they have RF for HIV, then *PEP should be initiated while awaiting HIV test results* -Although the *risk of transmission during sex* with an individual with an *undetectable viral load is LOW* and likely negligible, the *risk from occupational needlestick injury in these pts hasn't been established* -- therefore, *PEP is indicated, REGARDLESS of viral load in source pt* -*Standard PEP* consists of *triple-drug therapy*; *tenofovir-emtricitabine w/ raltegravir is preferred* d/t a low AE profile and few drug-to-drug interactions -PEP should be started *immediately*, preferably in the *first few hours* following exposure, and *continued for 4wks* -*Exposed* healthcare workers should *undergo HIV testing immediately* to *establish baseline serologic status*; testing should be *repeated @6wks & @4mo* afterwards

What is the Standard PEP for HIV exposure?

-Recommended for Occupational-related healthcare workers and infants (i.e. perinatal transmission) and for HIGH-RISK Contact in Non-occupational pts (e.g. exposure to Vagina, Rectrum, eye, mucous membranes, non-intact skin [or percutaneous exposure], exposure to Blood, Semen, rectal or vaginal secretions, breast milk, or any body fluid with visible blood) - *Give ASAP, initiate within 72hrs and Continue for 28 days* Regimen: *2 nucleotide/nucleoside reverse transcriptase inhibitors + Integrase Inhibitor* *TENOFOVIR, EMTRICITABINE + RALTEGRAVIR*

Recurrent C. diff infection (CDI)

-Recurrence of CDI is common, affecting 15-30% of pts whose infection initially responds to antimicrobial therapy (with *FIDAXOMICIN or Macrolide*) -*Risk is esp incr* in pts taking *prolonged antibiotics for other concurrent infections* -When CDI recurs, it is *usu d/t persistent spores from initial infxn, rather than from drug resistance or infxn w/ new strain* -Spores (Abx resistant) that survive initial course of ABX can germinate into fully functional bacilli in the colon and proliferate -*To reduce risk of recurrence, tx for CDI is often extended throughout the course of other ABX therapies* -Can also *repeat prior regimen or consider fecal microbiota transplant*

Vertebrobasilar Insufficiency

-Refers to *reduced blood blow in the base of the brain, typically secondary to emboli, thrombi, or arterial dissection* -*Labyrinth & brainstem commonly affected* and symptoms can incl *vertigo, dizziness, dysarthria, diplopia, & numbness in lips & digits* -Vertigo is NOT positional and usu spontaneously resolves -*RF for Vertebrobasilar Insufficiency*: *Diabetes, HTN, Hypercholesterolemia, Arrhythmia, Coronary A Dz, circulatory problems, & Cigarette smoking hx*

Diagnosis of Cervical Insufficiency

-Refers to a *structural weakness of the cervix that predisposes to PAINLESS (i.e. NO uterine contractions) Cervical Dilation & Second-trimester pregnancy Loss* -Pts can experience *pelvic pressure* when gestation distends the vagina, with an *incr in vaginal discharge d/t loss of mucus plug* or with *light vaginal bleeding (blood show)* from cervical dilation -*Bulging or Prolapsing amniotic membranes can be present* (*poor prognosis*) -*DX of cervical insufficiency* can be *Retrospective by HX (≥2 prior painLESS, Spontaneous Second-trimester Losses)* OR, *in a Current Pregnancy at <24wks by U/S (Cervical Length ≤25mm)* OR based on *Physical Examination (painLESS advanced cervical dilation* - e.g. 3cm dilated w/ 100% effacement on digital exam) -*Risk Factors for Cervical Insufficiency* (which are not always apparent) include *Collagen Abnormalities (e.g. Ehlers-Danlos Syndrome), Uterine Anomalies (e.g. septate, bicornuate, or unicornuate uterus), Obstetric Trauma, & Surgical Trauma (e.g. s/p Cold knife Cone Biopsy, LEEP)* -*Management includes CERCLAGE PLACEMENT*, where a suture is placed to reinforce the cervix, has been shown to prevent second-trimester loss and preterm delivery in cervical insufficient pts ● In pts w/ *hx-based Dx, Prophylactic Cerclage is placed at 12-14wks*, prior to cervix shortening or dilating ● In contrast, pts w/ *U/S-based or PE-based Cervical Insufficiency DX (i.e. painLESS cervical dilation) in a Current pregnancy, Emergency/Rescue Cerclage Placement* can be *performed at time of Dx* -HOWEVER, *Prolapsing Amniotic Membranes are a predictor for Imminent (i.e. within the next several DAYS) Delivery & Indicate a POOR PROGNOSIS* • Prolapse of membranes into vagina causes prolonged exposure to vaginal flora a *high risk for intraamniotic infection (chorioamnionitis), preterm membrane rupture, abruptio placentae, previable or preterm delivery, & maternal mortality* • *Prolapsed membranes Incr the likelihood of complications to Cerclage Placement d/t High Risk of Iatrogenic Membrane Rupture* Note: Previable PROM refers to ROM before 20wks gestation and Periviable PROM refers to ROM from 20-25 6/7 wks of gestation.

Secondary (functional) Mitral Valve Regurgitation

-Refers to mitral regurg occurring *d/t a disease process involving the left ventricle* (e.g. *myocardial ischemia, dilated cardiomyopathy*) -Mitral valve is usu intrinsically normal, and so the management of secondary MVR mainly involves *optimizing LV function* (e.g. *medication, cardiac resynchronization therapy*) rather than mitral valve surgery -Other secondary causes incl: connective tissue diseases like Marfan or Ehlers-Danlos Syndrome; Rheumatic fever; Chordae rupture

Case Fatality Rate Definition

-Refers to the *proportion of ppl w/ a particular condition who end up dying from the condition* -It differs from *mortality rate*, which describes the *general population's likelihood of dying from the disease*

How does GILBERT SYNDROME present?

-Relatively common, *benign condition* d/t *Mildly Decreased UDP-glucuronosyltransferase Conjugation* -Typically manifests in *Adolescence as periodic ASX/Mild Jaundice* usu with *stress, illness, or fasting* due to *Elevated UNCONJUGATED Hyperbilirubinemia* -It *RARELY presents before puberty (i.e. ADOLESCENCE)* and is less common in girls

What is normal fasting blood sugar levels? What is hypoglycemic?

Normal FASTING Range is *70 to 100 mg/dL* *Suspected Hypoglycemia* is a blood sugar level *<60 mg/dL*

Flail Chest

-Result of *double rib fractures in more than one site*, leading to *paradoxical movement of the flail segment during inspiration* -Often accompanied by *muscular spasm & pain, and pulmonary contusions* --> *HYPOXEMIA & incr work of breathing* -Paradoxical or segmental chest wall movement makes the dx of flail chest obvious, but many cases can be occult, where gross findings are absent d/t muscle splinting, shallow breathing, or mechanical ventilation -*Uncomplicated* cases managed *nonoperatively* w/ *supplemental O2, noninvasive positive-pressure ventilation, & meds for pain control* -*Severe* cases may need *mechanical ventilation and surgical stabilization*

Mitral Stenosis in Pregnancy

-Rheumatic heart dz & age-related calcification, radiation-induced are all causes of MS in adults -MS pts present with exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, hemoptysis, can present with pulmonary edema ± right heart failure (e.g. lower extremity edema); atrial fibrillation, incr risk for systemic embolization -DX of Mitral Stenosis: Opening snap w/ mid-diastolic rumble at apex; Echo shows incr transmitral flow velocity -TX of MS: Percutaneous valvotomy or surgical repair/replacement -Severe MS if mitral valve area is ≤1.5cm2 -MS can remain ASX for years and experience gradual onset of sx (usu dyspnea, then cough & hemoptysis [d/t pulm edema], then right-sided HF) -*Increased cardiovascular demand* can hasten symptom development in mitral stenosis pts -Normal *physiologic changes of pregnancy* include *incr plasma volume, heart rate, & cardiac output*, which all *incr flow gradient across the mitral valve*, leading to *worsening sx* in previously stable mitral stenosis pts

Schizoaffective Disorder, Bipolar Type

-SX that meet criteria for a *manic episode* and criteria for *schizophrenia* (≥2 of the following: Delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, negative sx) -Manic Sx incl: Grandiosity, pressured speech, & decr need for sleep -Psychotic Sx incl: Delusions and auditory hallucinations -Pt w/ hx of *persistent* auditory hallucinations even while stable mood indicates *psychotic sx lasting ≥2wks in the Absence of a major depressive or manic episode*, thereby meeting the criteria for Schizoaffective Disorder Note: In Major Depressive w/ Psychotic Features, or Bipolar Disorder w/ Psychotic Features, the psychotic sx occur exclusively *during mood episodes*

Pragmatic Study

-Seeks to *determine whether an intervention works in real-life conditions* (*real-life conditions will contain confounders*, with no way to control these confounders)

Explanatory Study

-Seeks to address *whether an intervention works in optimal conditions and how/why it does or does not work* Note: *Randomized controlled trials are considered explanator*, as randomization and other methods to control for confounders are not performed in the real world (unlike in pragmatic studies)

Antiglomerular Basement Membrane Antibodies

-Seen in *Goodpasture disease*, which is assoc w/ *acute glomerulonephritis(\* -Pts often have *pulmonary sx (e.g. alveolar hemorrhage, hemoptysis)*; *systemic sx RARE*

Cardiac Syncope

-Several causes incl: • *Aortic stenosis or Hypertrophic Cardiomyopathy* • *Ventricular Tachycardia* • Sick sinus syndrome • *Advanced AV block* • *Torsades* de pointes -Cardiac syncope d/t *ventricular tachycardia* (VT) occurs *abruptly* & usu has *no warning sx* (maybe palpitations) -The arrhythmia *spontaneously terminates* within a few mins, resulting in *cardiac output restoration* and rapid pt recovery w/ *no residual sx* -Recognition of cardiac syncope is CRUCIAL d/t *High Risk of Sudden Cardiac Death* -*Absence of autonomic prodromal sx* (e.g. nausea, diaphoresis, warmth feeling), which are usu present prior to benign syncopal event, *suggests cardiac syncope* -Presence of *underlying structural heart dz* (e.g. Q waves suggesting ischemic scarring from prior MI, cardiomyopathy w/ low EF) *specifically suggests cardiac syncope d/t VT* -These pts should be *admitted for telemetry monitoring* (to attempt to detect arrhythmia) and *echo* (to eval LV fxn, wall motion abnormality) and depending on the findings, TX w/ some *combo of Medication (e.g. Amiodarone), Catheter Ablation, or Placement of Implantable Cardiac Defibrillator* may be indicated

Diabetic Ketoacidosis (DKA)

-Severe DKA (pH <7.1, bicarb <5 mEq/L, AMS) should be *admitted to an ICU* for close monitoring bc at greatest risk for complications (e.g. cerebral edema!) -Tx begins w/ volume repletion w/ *isotonic fluids* (e.g. normal saline, Ringers lactate) given over an hour followed by initiation of an *insulin drip* -*Potassium*-containing IV fluids should be given *simultaneously w/ the insulin drip* for pts w/ normal or low K levels as insulin moves K intracellularly and causes //hypokalemia// -Ongoing management consists of blood work q1-2hrs and close titration of IVF to correct electrolyte derangements and acidosis -Pt should be monitored for signs of //cerebral edema// such as AMS, lethargy, HA, V -Head CT should be ordered if cerebral edema is suspected -Once met acidosis has resolved & anion gap closed, pt can be transitioned to a subQ insulin regimen.

SX of *Cauda Equina Syndrome*

-Severe lower back pain -Urinary or Bowel incontinence -Motor weakness or Sensory loss in legs Bilaterally -Saddles anesthesia

Causes of tongue enlargement: DDX

-Severe, longstanding hypothyroidism -Amyloidosis -Acromegaly -Mucopolysaccharidosis -MEN2B: Mucosal neuromas, marfanoid habitus, medullary thyroid CA, pheochromocytomas

Sexual activity after a Myocardial Infarction

-Sexual activity can incr the risk of MI d/t the assoc tachycardia and acute rise in BP -Most pts w/ *uncomplicated* MI (i.e. *no recurrent angina, no arrhythmias, normal ventricular function*) and *successful revascularization* are at LOW risk of cardiac complications and may *resume normal sexual activity ~2wks after initial cardiac event* -*Erectile dysfunction* is common in pts w/ cardiovascular dz d/t decreased penile blood flow, endothelial dysfunction, and vasoactive medications -Apprehension regarding sexual activity after MI, sudden onset of ED, and *normal nonsexual nocturnal erections* suggest a likely *psychogenic* etiology - initial management incl more detailed psychological assessment and counseling -*Phosphodiesterase-5 Inhibitors* (e.g. *Sildenafil*) are the First-Line TX for most pts w/ ED, including those W/ Cardiovascular disease. HOWEVER, *PDE-5 Inhibitors are CONTRAINDICATED in pts Taking NITRATES (e.g. isosorbide mononitrate) as concomitant use can cause a precipitous DROP in BP --> Syncope* Note: β-Blockers (e.g. carvedilol) is assoc w/ incr risk of ED, but are strongly recommended in pts w/ symptomatic atherosclerotic dz and should NOT be discontinued soon after an MI

Features & Treatment of Trichomonas vaginalis infection

-Sexually transmitted protozoan parasite infection demonstrating *motile, flagellated organisms* on Pap smear or wet mount -Clinical Features in Women: *ASX* or *Dysuria, urinary frequency, dyspareunia, vaginal pruritus, & a green, frothy, malodorous discharge* -Sometimes vaginal and cervical punctate hemorrhages ("strawberry cervix") seen -If ASX, usu identified incidentally on routine cervical cytology -Irritation and exposed bleeding areas in vagina, as well as presence of Trichomonas, can *incr rates of HIV transmission* - therefore, screening recommended in HIV-positive pts & women w/ multiple STIs -*Regardless of sx, BOTH PARTNERS are TX w/ Oral METRONIDAZOLE* to *reduce the risk of REinfection and HIV transmission* -Sexual partners should undergo clinical eval and STI testing too, after expedited partner therapy

Chronic Mesenteric Ischemia

-Should be considered in pts with *dull, crampy epigastric abdominal pain that WORSENS with meals/after eating*, who has had a *negative initial workup* (*U/S, CT, Endoscopy*) -- should especially consider in pts w/ *multiple atherosclerotic RFs, a Hx of coronary artery disease, smoking hx, T2DM, HLD, peripheral vascular dz* -Sometimes this dz is called *Intestinal Angina* since it *presents as abdo pain when there is increased O2 demand in the bowel after eating* -The pain can be so bad that pts avoid food, causing *weight loss* -D/t the large number of collateral vessels supplying the bowel, *multiple high-grade stenoses are usu needed in the mesenteric vasculature before pts become Symptomatic* -*CT Angiogram, MR Angiogram, or Duplex U/S* can all be used to DX, but *ANGIOGRAPHY Remains the Gold Standard for Diagnosis, & intervention w/ Angioplasty and/or Stenting can be done in the same setting* -Noninvasive tests are helpful to *localize the obstruction* and identify the best route that the obstruction can be reached with angiography

Managing Asthma Exacerbation During Pregnancy

-Similar to non-pregnant pts *Supplemental O2* -Maintain *SaO2 ≥95% if pregnant* (vs ≥90% in non-pregnant) *Bronchodilators* -Nebulized or Inhaled *Albuterol* -Inhaled *Ipratropium* *Systemic Corticosteroids* -If incomplete response to bronchodilators, or have high-risk asthma features (e.g. prior intubation)m or a breakthrough acute exacerbation despite taking controller medications -Oral preferred (e.g. *Prednisone*) *Additional Therapy* -*IV Magnesium Sulfate* (MgSO4) or *Terbutaline* (β2-agonist to reduce uterine contractions) if *severe or refractory bronchoconstriction* -Epinephrine is CONTRAINDICATED -Intubate for respiratory failure -The minor risks of short-term systemic corticosteroids are greatly outweighed by their beneficial impact in reducing maternal-fetal mortality & morbidity

Infantile Hypertrophic Pyloric Stenosis

-Smooth m hypertrophy of pylorus causing gastric outlet obstruction, resulting in classic *nonbilious, projectile emesis* most commonly seen in *firstborn Boys age 3-6wks*, usu right after oral intake -Palpate olive-shaped abdo mass in epigastrium sometimes -*Visually prominent peristaltic waves* can be seen and represent exaggerated gastric contractions -*Dehydration* is common (decr urine output, sunken fontanelle, dry mucous membranes, drop in weight percentiles) -*DX Confirmed by Abdo U/S - Thickened, Elongated Pylorus Muscle* -Electrolyte abnormalities w/ protracted vomiting: *Hypokalemic, hypochloremic metabolic alkalosis* d/t gastric losses and activation of renin-angiotensin-aldosterone system; *hyponatremia* also occurs and is caused by *free water retention* in response to hypovolemia and Aldosterone (Low Na, Low K, Low Cl, High HCO3, High pH) -TX: Correct electrolyte derangements and dehydration first (*IVF*) to *rehydrate & stabilize* the pt prior to surgical *Pyloromyotomy* and reduce risk for postop apnea

Adverse effects of SGLT-2 inhibitors?

-Sodium-glucose cotransporter 2 reduces glucose and sodium reabsorption at the proximal renal tubule e.g. Canagliflozin, dapagliflozin, empagliflozin -*SGLT-2 inhibitors* therefore *reduce hyperglycemia by promoting glucosuria* by blocking glucose reabsorption at PCT -AE: Incr risk of *genital candidiasis and UTIs, hyperkalemia, dehydration (orthostatic dehydration), polyuria caused by osmotic diuresis, and weight loss*

Early Localized Lyme Disease

-Spirochetal illness caused by *Borrelia burgdorferi* and *transmitted by deer tick Ixodes scapularis during blood feeding* -*SX* of *early localized Lyme dz* typically occur *within 1-2wks of tick bite transmission*, and is characterized by *ERYTHEMA MIGRANS (slow-spreading erythematous rash, starting as a confluent macule & progresses over days into a bulls-eye shape [central clearing]; enlarging, macular rash) & VIRAL-LIKE SX (malaise, fatigue, arthralgias, myalgias, neck stiffness, &/or HA) ± Facial Palsy* -*DX* of *Early* localized Lyme dz is *made CLINICALLY bc B. burgdorferi serology* is often *Falsely Negative* and is *not recommended* -*EMPIRIC TX with PO DOXYCYCLINE* is usu curative Note: In contrast to early localized dz, pts w/ *Early Disseminated* (*multiple erythema migrans lesions, carditis, neuritis*) and *Late dz* (*arthritis, peripheral neuropathy*) *Lyme dz* should *always undergo serologic testing PRIOR to TX* bc the *humoral response against the organism is fully developed* - B. burgdorferi enzyme-linked immunosorbent assay followed by Western blot is used DX Note: *IV Ceftriaxone* is the *preferred therapy* for *severe manifestations of Lyme (e.g. carditis w/ advanced AV block, radiculopathy, meningitis)*

Strychnine Poisoning Presentation

-Strychnine is an ingredient in rodenticides and some illicit drugs -It *blocks inhibitory glycine neurotransmission* within the spinal cord, resulting in *powerful, uncontrollable muscle contractions* -Classically causes *episodic contractions* that look like *tonic-clonic activity* BUT in a *FULLY AWAKE* pt (aka *Awake Seizure*)

Conditions that cause decreased radioactive iodine uptake on thyroid scintigraphy

-Subacute (de Quervain, subacute granulomatous) thyroiditis (painful) -Silent (painless) thyroiditis (Riedel thyroiditis) -Postpartum thyroiditis -Surreptitious thyroid hormone abuse -Iodine-induced thyroiditis

Romantic Relations b/w Physicians & Patients

-The formal position of the American Medical Association is that *any romantic relationship or sexual interaction b/w a physician and patient* constitutes *PROFESSIONAL MISCONDUCT* -It is expected that if a physician decides to enter a romantic or sexual relationship w/ a pt, he or she will at least *terminate the physician-patient relationship beforehand* -However, many ethicists argue that it is never appropriate to date a patient (even years after the physician-patient relationship has ended) Note: (DON'T DO THIS!) Telling the patient that asking for a date in inappropriate is critical of the pt and may be humiliating to them. (DO THIS INSTEAD) It is *better to explain that romantic relationships b/w physicians and patients are unethical*

Alcoholic Ketoacidosis

-Suggested by a pt with impaired mental fxn with ketonuria and mildly elevated plasma glucose levels -Plasma glucose levels can be low, high. or normal -High plasma glucose levels are speculated to be due to impaired insulin secretion combined with increased insulin resistance -Biochemically, pts with alcoholic ketoacidosis will have increased anion and osmolal gap -Most pts with alcoholic ketoacidosis respond to an administration of *dextrose normal saline* (Insulin is generally NOT required) -Dextrose leads to an increase in insulin secretion, which leads to the metabolism of ketone bodies to bicarbonate -Almost all alcoholics are likely thiamine-deficient unless proven otherwise. Note: DKA pts tend to have blood glucose levels generally higher than 250 mg/dL Note: Do NOT discharge the pt after initial TX as these pts are likely to develop alcohol withdrawal, electrolyte imbalance, and aspiration pneumonia. Furthermore, glucose administration can increase the utilization of thiamine, thus aggravating thiamine deficiency and leading to Wernicke's Encephalopathy

Venous Air Embolism (VAE)

-Suggested by sudden-onset resp distress following removal of a central venous catheter -Pts w/ suspected VAE should immediately be placed in *left lateral decubitus* position to trap air on the lateral right ventricular wall and help prevent right ventricular outflow tract obstruction and embolization of air into the pulmonary circulation -*High-flow O2* is also important to encourage *absorption of the air embolus* (in severe cases, can use hyperbaric O2)

When should you do *surgical resection* for Lung Cancer treatment?

-Surgical resection is the TX of choice for pts w/ *stage I* and *some stage II non-small cell lung cancers*; however, it is *NOT as effective in pts w/ stage III disease*, and most pts require *adjuvant radiation* and chemotherapy as well

Ethylene Glycol Ingestion - Manifestations & Management

-Sweet-tasting substance in antifreeze, engine coolant, & brake fluids -Can cause *Encephalopathy (AMS), emesis, Tachypnea (compensatory for metabolic acidosis), and Seizures (generalized tonic-clonic d/t Hypocalcemia)* -Clinical Course: • Intoxicating effects and GI irritation (similar to ethanol) • Metabolized into *oxalic acids & glycolic acids* that cause *metabolic acidosis* w/ *compensatory hyperventilation* • *Oxalic acid metabolites bind to calcium* and form *calcium oxalate* and causes *HYPOCalcemia*, which can lead to *Seizures, Tetany, and/or Arrhythmias* (typically ~4-12hrs after ingestion) • *Calcium oxalate crystals* can precipitate in *urine* and cause *tubular obstruction*; also with *Glycolic acid-Induced Direct Nephrotoxicity* leading to *AKI* (LATE Finding though!) -Lab findings: *Elevated serum osmolality* (incr osmolal gap), *Anion gap Metabolic Acidosis w/ low bicarb*, and*Hypocalcemia* -*ANTIDOTE TX* with *FOMEPIZOLE* which *inhibits Alcohol Dehydrogenase* (which usu converts ethylene glycol into its toxic metabolites); could also use *ETHANOL* alternatively -Fomepizole preferred to ethanol bc more potent inhibitor -Bc definitive testing (ethylene glycol serum levels) takes too long, if suspect then empirically tx with Fomepizole to reduce M&M -Other things to additionally give incl IV sodium bicarb* to reduce tissue penetration of organic acids, and in severe cases (i.e. renal failure), *hemodialysis* to remove EG & toxic byproducts

Tumor Lysis Syndrome - Lab Abnormalities and Consequences

-TLS is caused by rapid destruction of malignant cells (e.g. after initiating chemotherapy), which *releases intracellular potassium, purine nucleic acids (metabolized to uric acid), and phosphate into bloodstream* -This leads to: • *HYPERKALEMIA* - monitor carefully for risk of arrhythmias (limit potassium intake, appropriate IVF, K-lowering therapies [patiromer, hemodialysis]) • *HYPERURICEMIA* - *Rasburicase* (recombinant uricase that catalyzes metabolism of uric acid to allantoin) is *given Empirically* to *reduce serum uric acid levels* to help *prevent renal tubular precipitation of uric acid* • *HYPERPHOSPHATEMIA w/ assoc HYPOCALCEMIA* -Incr serum phosphate binds w/ free calcium, causing hypocalcemia and the *formation of calcium phosphate complexes* --which can *precipitate in renal tubules & cause renal stones* -Therefore, even after receiving uric acid-reducing therapy, pts receiving chemotherapy *may still develop AKI d/t Renal Tubular Obstruction & direct cellular injury (i.e. Acute Nephrocalcinosis)* (Urinalysis shows no casts or cells) -The risk for calcium phosphate stone formation is reduced by *maximizing the GFR & urine output w/ prophylactic IVF* Note: Acute tubular necrosis causes muddy brown casts, and acute interstitial nephritis causes pyuria on urinalysis

Temporomandibular Joint Disorder

-TMJ disorder can p/w *headaches, muscle spasms, jaw fatigue, & facial pain* -PE reveals *tenderness of the muscles of mastication (masseter, temporalis) & TMJ*, as well as *pain, crepitus, &/or audible clicks from the joint* -SX exacerbated by jaw motion -Initial Management: Education, soft diet, warm compresses, & avoidance of triggers -*NSAIDs* are the first-line of medication -Muscle relaxants (e.g. cyclobenzaprine) can be added for pts w. assoc muscle spasm

Management of Varicose Veins

-TX aimed at relieving symptoms (leg cramping, heaviness, fatigue, swelling), but can be cosmetic -*Initial management* should begin with *conservative measures such as leg elevation, compression stockings, & weight reduction* which all helps to decr venous pressures in lower extremities Note: *Compression stockings should NOT be used in pts w/ underlying Arterial Insufficiency* -*Injection Sclerotherapy* ± anesthetics is used in pts w/ *symptomatic, small varicose veins who've Failed ≥3-6mo of conservative therapy* (injecting sclerosing agent into vein -> endothelial damage & sclerosis -> prevents further vein filling) -*Surgical Ligation & Stripping* is used in pts w/ *large, symptomatic varicose veins with ulcers, bleeding, or recurrent thrombophlebitis of the veins* Note: External Laser TX is NOT used to tx varicose veins!

Cardiovascular effects of Cocaine Intoxication

-The initial management of *myocardial ischemia d/t cocaine intoxication* focuses on *reduction of myocardial oxygen demand & improvement in myocardial oxygen supply* -Bc ß-blockers are contraindicated in the setting of acute cocaine ingestion, *IV BENZOS* are given PRN to reduce sympathetic outflow and to alleviate HTN, tachycardia, & coronary vasoconstriction -*Nitroglycerin* is also given to reduce BP and LV wall stress -Bc cocaine stimulates platelet activity & encourages thrombus formation, *thrombotic occlusion* of coronary arteries can occur (even in young pts!) -Therefore, *Aspirin should be given early!!* -In pts w/ persistent ST elevation despite initial medial therapy, *Coronary Angiography w/ Percutaneous Coronary Intervention (PCI)* should be *performed w/o delay!!* -Prompt recognition and restoration of myocardial blood flow is critical to minimize myocardial necrosis and to reduce cardiac M&M Note: PCI has been shown to improve survival in pts w/ STEMI and has a lower rate of recurrent infarction and intracranial hemorrhage compared to IV fibrinolysis (e.g. alteplase). Fibrinolytic therapy is recommended only in pts w/ STEMI for whom PCI canNOT be performed within 2hrs of first medical contact

Toxic Megacolon TX

-TX of toxic megacolon is aimed at *reducing colonic inflammation, restoring normal colonic motility, and decreasing the likelihood of perforation* -*Initial therapy is supportive (repleted with blood products, intravenous fluids, and electrolytes [eg, potassium]) and medical (initially admitted to ICU, placed at complete bowel rest, and NG tube decompression may be required; enteral feeds later on to hasten mucosal healing and stimulates normal motility when clinically improved)*, which is successful in preventing surgery in up to 50%, but the rest need surgery -Patients should be given *broad-spectrum antibiotics to treat sepsis* and, /in case of colonic perforation/, *histamine-2 blockers or proton pump inhibitors for ulcer prophylaxis and venous thromboembolism prophylaxis*. -*All medications that can impede colonic motility (eg, opiates, anticholinergics) should be stopped!!!* -In *IBD-assoc Toxic Megacolon, IV GLUCOCORTICOIDS is FIRST-LINE* - it does NOT incr risk for perforation! (Note: Do not give glucocorticoids to C.diff- or other infectious megacolon) -Patients with IBD-related toxic megacolon who *do not respond to intravenous glucocorticoids within three days* should be considered for a *trial of infliximab or cyclosporine as second-line therapy* -*5-ASA, Sulfasalazine should be restarted for IBD after tx w/ glucocorticoids*

Difference b/w tetanus immune globulin and tetanus toxoid? When to give each?

-Tetanus immune globulin (TIG) provides *passive and immediate /but temporary/ immunity* -Tetanus toxoid-containing vaccines provide *active and prolonged /but delayed/ immunity* -These vaccines are recommended q10yrs & can be given as tetanus/diphtheria toxoids adsorbed (Td), tetanus toxoid/reduced diphtheria toxoid/acellular pertussis (Tdap), tetanus toxoid (TT), or diphtheria/tetanus toxoids adsorbed (DT) -If *clean/minor* wound, & have had ≥3 tetanus vaccinations *and* a booster within the past 10yrs - do not need add'l booster -A tetanus toxoid vaccine recommended for pts who last received tetanus vaccine >10yrs ago or who are unimmunized/unsure/incomplete vaccine status (<3 doses) -Pts with *dirty* (dirt/feces/saliva) or *severe wounds* (punctures/crush injury/ burns/ frostbite) have incr risk of /*Clostridium tetani*/ d/t favorable anaerobic growth env. These pts need *tetanus booster alone (tetanus toxoid)* (NO TIG) if their vaccine hx is up to date but their last vaccination was ≥5yrs ago -Pts w/ severe/dirty wounds who are immunocompromised (HIV) or have unimmunized, uncertain, or incomplete tetanus vaccination should receive *TIG && tetanus vaccine booster (tetanus toxoid)* -Bc the early doses of tetanus toxoid only prime the immune system but do not confer immunity, while TIG provides immediate, temporary immunity in these pts

How does the Power of a study relate to sample size, which relates to Confidence Interval?

-The *Power* of a study is the *ability to detect the difference between 2 groups (e.g. treated vs nontreated, exposed vs unexposed)* -*Increasing the Sample Size will Increase the Power of a study*, and as a result, the *Confidence Interval of the point estimate (e.g. Odds Ratio) becomes Narrower* -A *widened confidence interval is likely d/t a smaller sample size, leading to insufficient Power to detect the difference between exposed & unexposed subjects, resulting in a Lack of statistical significance, p >0.05 (CI contains the null value [0 for odds ratio])*

Interpreting *Receiver Operating Characteristic (ROC) Curves*

-The *area under the curve (AUC)* of a receiver-operating characteristic curve is the *measure of the ability of a diagnostic test to discriminate b/w two patient states (e.g. Positive & Negative)* -The *greater the AUC, the closer the AUC value is to 1.0, and the better the diagnostic performance is of the test*

How do you tx the hyponatremia with SIADH?

-The *normovolemic hyponatremia in SIADH* is *secondary to the combo of water retention and the loss of Na & K* (e.g. can be caused by small cell lung CA) -In chronic SIADH, the loss of sodium is more significant than the amount of water retained!! (urine is concentrated [salty]m but the pt is not volume depleted) -*Unless there are neurologic sx arising from the hyponatremia*, *Mild to Moderate SIADH-Hyponatremia* should be *corrected Slowly with Water Restriction* (neuro sx, seizures, & coma can occur when Na <120 mEq/L) -Once water restriction is initiated, the plasma sodium concentration will slowly begin to normalize - an ideal rate of increase is 0.5 mEq/hr. -Pts should be monitored for volume depletion, as a sodium deficit may become apparent, requiring concomitant admin of salt Note: *Demeclocycline and Lithium* work to *blunt the response of the collecting ducts to ADH, ultimately increasing the excretion of water* -- but these are indicated in pts w/ *persistent, severe hyponatremia* that has failed to resolve with *water restriction, salt intake, or loop diuretics (furosemide/torsemide)* Note: *Furosemide lowers the urine osmolality & blunts renal response to ADH*, thereby *increasing water excretion*. Since loop diuretics decrease NaCl reabsorption in the loop of Henle (i.e. allow more NaCl to be excr in urine), they should be administered concomitantly with hypertonic saline or salt tablets

Which are the preferred medications for the treatment of Acne in Women who May Become Pregnant?

-The *preferred* meds include *Topical Erythromycin, Topical Clindamycin (Inflammatory Acne), or Azelaic Acid (Comedonal Acne)*; these are designated *FDA pregnancy risk Category B* and are *generally considered SAFE* -The risk of teratogenicity with topical retinoids is considered LOW and most (e.g. tretinoin, adapalene) are designated Category C (use if only potential benefit outweighs risk) - i.e. *topical tretinoin & benzoyl peroxide should be AVOIDED in pregnancy (Category C)* -*Tazarotene and Isotretinoin are Potent Teratogens that are absolutely CONTRAINDICATED in Pregnancy (Category X)*

Risk of Progression from Acute to Chronic HBV Infection

-The *risk of developing SX in acute HBV infection progressively increases w/ age* d/t *enhanced immune response to the virus (more mature immune system)* -As a consequence, the *risk of progression* from *acute to chronic HBV infection DECREASES with age* -The *progression rate for perinatally-acquired infection is 90%* d/t increased *immune tolerance* -Pts infected at age 1-5 have a 20-50% progression rate to chronic HBV infection, but for *adults* the progression rate is under 5%

Standardized Incidence Ratio (SIR)

-The *standardized incidence ratio (SIR) is a Measure used to determine if the Occurrence of Cancer in a Small Population is Higher or Lower Relative to an Expected Value that is derived from a Larger Comparison Population* -*SIR is calculated by dividing Observed Cases (Oc) by Expected Cases (Ec):* *SIR = Oc / Ec* -Expected Cases (Ec) is calculated based on age/sex-adjusted incidence rates of dz in a Control Population that is usu much larger *SIR = 1* --> Implies that the *Observed incidence of cancer is Equal To the Expected value* *SIR > 1* --> Implies that a *Higher Observed incidence of cancer was seen compared to the Expected value* (e.g. *SIR = 1.5 means a 50% HIGHER observed incidence*)

Type 1 (alpha) Error

-The probability of *rejecting a null hypothesis when the null hypothesis is TRUE* -Conducting *multiple independent hypothesis tests* w/o proper adjustment to the alpha level, increases the rate of type 1 error == i.e. *When evaluating multiple secondary endpoints* (e.g. fasting glucose, changes in renal parameters), there is a *higher probability of erroneously finding a statistically significant result w/ one of these endpoints* (e.g. higher likelihood of type 1 error) *d/t chance alone* -This phenomenon is known as the *multiplicity*, or *multiple testing, problem* -The rate of type 1 error will increase depending on the alpha level for individual tests and the number of independent tests.

Stooling in Breast-Fed [Only] Infants

-The very first bowel movement of a newborn is the *meconium* (thick, black, tarry stool) occurring within the first 48hrs of life, or during childbirth (meconium-stained amniotic fluid) -After this, the typical freq of stool passage in *exclusively breastfed* newborns is 6-10x daily, or ~1 soft, yellow-green stool per episode of breastfeeding -After the first MONTH, the *stooling frequency often decreases to 1 episode q1-2 days or less*, with some having only 1 or 2 bowel movements/week Contrast to *formula-fed infants*, who tend to have *relatively solid stool* consistency, and generally have a frequency of *1-2 bm's per day* Note: Adding supplemental water to the diet or diluting infant formula (esp before 6mo of age) is not recommended bc can cause dangerous Hyponatremia or other electrolyte imbalances

What medications should pts with *Coronary Artery Disease (CAD) and Prior Myocardial Infarction* be started on? And why?

-They should be started on appropriate therapy for *secondary prevention of cardiovascular events* -*β-BLOCKER, HIGH-INTENSITY STATIN, ANTIPLATELET THERAPY, && ACE INHIBITOR OR ANGIOTENSIN-RECEPTOR BLOCKER* -In pts w/ a *recent MI, β-blockers reduce short-term morbidity (recurrent symptoms, reinfarction, size of infarct) as well as short- & long-term mortality (if continued)* -*β-blockers also improve survival in CAD pts & pts w/ LV systolic dysfunction* -Though use of β-blockers may *mask sx of hypoglycemia in diabetics*, their *use after an MI is assoc w/ Improved Survival Rates, so diabetes is NOT considered a contraindication* -In addition to pharmacologic therapy, the pt should also undergo *further eval and risk stratification (transthoracic echo, myocardial perfusion stress test, possibly coronary angiography)*

How do you handle an *Early Pregnancy of Undetermined Location*?

-This refers to when a *pregnancy CANNOT BE VISUALIZED on U/S* usu because the *β-hCG is below the discriminatory zone (i.e. β-hCG ≤3,500 IU/L)* --These pregnancies can be *either intrauterine or ectopic!* -In *Stable* pts, the *β-hCG level must be Repeated q48hrs* to *determine whether the INCR is consistent with a Normal Pregnancy (≥35% rise q48hrs)* -*Pelvic U/S is Repeated until β-hCG is >3,500 IU/L and an Intrauterine pregnancy is visualized

Hypothyroidism in Pregnancy

-Thyroid physiology changes during pregnancy to meet increased metabolic demands -During the *first trimester, ß-hCG binds TSH receptors on thyroid follicular cells and stimulates thyroid hormone production* -The *resulting elevations in [free] T3 and T4 suppress TSH secr* -*Concurrently, elevated estrogen levels cause an incr in serum thyroxine-binding globulin (TBG)*, which leads to *higher total T3 and T4 levels* -*Thyroid hormone requirements incr by about 25-50% over the prepregnancy state* -Pts w/ normal thyroid fxn can incr thyroid hormone prodn to saturate the elevated # of thyroid hormone binding sites on TBG, but pts w/ primary hypothyroidism are unable to incr thyroid hormone prodn -Therefore, current guidelines advise that the *dose of levothyroxine be empirically increased by ≈30%* (e.g. 2 additional levothyroxine doses weekly) at the time the pregnancy is first detected -Subsequently, *TSH should be measured q4wks and the dose adjusted to maintain TSH* within *trimester-specific norms*

What is FFP used for?

-To *correct coagulopathies d/t vitamin K deficiency* and is typically *administered when the INR is ≥2* -To *reverse anti-coagulation from warfarin, coagulopathies, microvascular bleeding, increased PT/PTT*

How many hours need to have passed by before an *Ixodes scapularis tick* is able to transmit *Borrelia burgdorferi* into human host to cause *Lyme Disease*

-Transmission occurs when Borrelia burgdorferi moves from the tick gut to tick salivary glands during Ixodes scapularis blood feeding -- This migration takes 36-48hrs -*Ticks attached <36hrs are unlikely to transmit Lyme Disease* -If duration of attachment is unclear, *tick engorgement* is often used as a rough guide; *transmission risk is Low if a tick is NOT engorged* -A *rash* can develop at the site of tick attachment several hours after tick bite d/t *cutaneous irritation from tick saliva* -- BUT this does NOT indicate Lyme Dz transmission!! *No intervention/Tx necessary* Note: *Erythema Migrans (bulls eye rash) develops >3d (and more commonly 7-14d) after inoculation* (Stage 1 Lyme Dz)

Rocky Mountain Spotted Fever (RMSF)

-Transmitted by *Rickettsia rickettsii*, *vector is TICK* -Despite its name(!), disease occurs primarily in the *South Atlantic states, especially North Carolina* -*Macular, erythematous Rash* typically *STARTS at wrists and ankles and THEN spreads to trunk, palms, and soles* -Classic Triad: *Headache, Fever, Rash (vasculitis)* -TX: *DOXYCYCLINE* is preferred in *ALL pts*, *INCL Children and Pregnant women* (low likelihood of pregnant-mom-hepatotoxicity, AE of fetal bone and teeth [permanent discoloration, incorporation into fetal long bones transiently inhibiting growth]) -Early nonspecific sx (fever, nausea, myalgias, arthralgias) are followed by dev of *erythematous macules* on the *wrists & ankles* around days 3-5 of illness -Rash may *spread to trunk, palms, & soles*, and macules often *evolve into petechiae* -Although initial leukocyte count is usu normal, *thrombocytopenia*, hyponatremia, & transaminitis are characteristic -*Empiric Antibiotics* initiated ASAP w/o waiting for confirmatory test results (Rickettsia serology, skin biopsy), as delay in tx can lead to *serious complications* (e.g. *encephalitis, pulm edema, arrhythmia*) and incr mortality

Trastuzumab-Associated Cardiotoxicity

-Trastuzumab is a monoclonal Ab that targets human epidermal growth factor receptor 2 (HER2) -It is *used in addition to adjuvant chemotherapy* for the *TX of pts w/ HER2-positive tumors* -Trastuzumab may cause a *decline in LVEF*, which is usually ASX but may occasionally lead to overt clinical *heart failure* -The *incidence of cardiotoxicity is ≈5% w/ Trastuzumab monotherapy*, but it is *25% w/ Trastuzumab combined with Anthracycline (e.g. Doxorubicin) and Cyclophosphamide* -In most pts, *Trastuzumab-associated Cardiotoxicity is REVERSIBLE*; there is *complete recovery of cardiac function after TX discontinuation* -In contrast, *chronic anthracycline-associated cardiotoxicity* (i.e. *Doxorubicin-associated Cardiotoxicity*) *may NOT be reversible after TX discontinuation d/t myocyte necrosis, destruction, and replacement by fibrous tissue*

Neuroblastoma - Quick Overview

-Tumor that can arise *anywhere in the sympathetic nervous system* but *typically involves the adrenal glands* and presents as an *abdominal mass* -It usu affects *children <2yo* and does NOT cause hematuria -Most common tumor of *adrenal medulla* in kids <4yom originating from *neural rest cells*, occurring anywhere along sympathetic chain -MC presentation: *Abdo distension & firm, irregular mass crossing the midline* -Can also p/w opsoclonus-myoclonus syndrome ("dancing eyes, dancing feet") and sometimes HTN -Labs: *INCR Urinary HVA & VMA* (catecholamine metabolites) -*Homer-Wright rosettes* characteristic of neuroblastoma & medulloblastma -Bombesin & NSE+ -Assoc w/ *overexpression of N-myc oncogene*

Alopecia Areata

-Type of *NON-SCARRING Hair LOss that can affect ANY Hair-Bearing Area* -- *Non-contagious!* -Thought to be *autoimmune* that targets genetically-predisposed -*Classical Clinical Presentation is of a WELL-DEMARCATED, often Round, Discrete, Smooth, Circular, Non-Scarred Patch of COMPLETE Hair Loss over the Scalp* typically with *NO assoc scaling or inflammation present in the area of hair loss* (unlike in Tinea Capitis) -*Presence of "Exclamation Point Hairs" (hairs that taper near the insertion into scalp) especially at the Periphery of an Alopecic Plaque is considered pathognomonic, BUT NOT necessary, for DX of Alopecia Areata* -Affected areas of skin are usu *ASX*, but the dz can be *emotionally traumatic & socially stigmatizing* -Alopecia areata is *often SELF-LIMITED, but may be Relapsing & Remitting or Chronic & Progressive* -Hair loss usu dev over a few weeks and has a recurring pattern -*Most pts will have REGROWTH of Hair in Involved Areas over Time* -Pts w/ AA are at *incr risk for other autoimmune conditions* incl *autoimmune thyroid dz, vitiligo, & pernicious anemia* -*TX: Topical or Intralesional Corticosteroids are the TX of Choice in Alopecia Areata* as well as pt *education* • Advise pt that *the dz is usu Benign* • They can have *multiple relapses in spite of TX* • *Most have normal hair growth within the next 1-2yrs even w/o Tx* • *TX w/ Steroids, either intralesional or topical, can Restore normal hair growth, but does NOT cure the dz* -After steroid injection, new hair growth is seen in the next 4-6wks -Some *factors assoc w/ Higher Chance of Relapse* incl a *longer duration of the dz, a more extensive dz, involvement of peripheral areas, & onset prior to puberty* -Drug TX can promote hair growth, but does NOT cure the dz; *can still have recurrence of dz after successful drug TX*

Erysipelas

-Typically caused by *Group A Streptococcus!!* -*Erysipelas is a specific form of cellulitis* -Most common sites of involvement are the *lower extremities, but the FACE is Involved in 5-20%* of pts -The *Facial Lesion is usu Characteristic -- it is Red, PAINFUL, Edematous, & Elevated*, and usu has a *Sharp Demarcation from the uninvolved skin* -A *butterfly pattern involving the cheeks and bridge of nose* may be seen -Other characteristic features of Erysipelas are *an ABRUPT ONSET and the presence of Systemic SX (Fever, Chills, Malaise, etc.)* Note: Staph aureus is a very. very rare cause of erysipelas.

Myasthenia Gravis presentation

-Typically causes *fatiguability* (i.e. *normal initial muscle strength that fades w/ repeated use*), rather than weakness -Though Proximal muscle symptoms may resemble polymyositis, most pts have facial/oculobulbar sx, and muscle enzyme levels are normal*

Acute Cholangitis

-Typically d/t *ascension of enteric bacteria into the biliary tract in the setting of impaired biliary drainage* (e.g. *gallstone obstruction, bile duct stenosis, cholangiocarcinoma*) or *incompetence of sphincter of Oddi* (e.g. d/t previous sphincterotomy) causing infection -Pts classically have the *Charcot triad* of *RUQ pain, fever, & jaundice* (up to 75% of cases), and some pts can be *severely ill* with *additional findings of hypotension and altered mental status* (*Reynolds pentad*) -Can also p/w *sepsis* -Labs: *Leukocytosis, Cholestatic-pattern of LFTs* with *marked elevation of bilirubin (total & direct) and alk phos, and milder elevations of aminotransferases* -RUQ U/S or Abdo CT shows *biliary duct dilation* -*Aggressive IV volume resuscitation* should be given and *blood cultures* collected, *followed immediately by empiric ABX therapy offering broad coverage of enteric organisms* (e.g. *pip/tazo, cipro w/ metronidazole*) -*Definitive TX* requires *Biliary Drainage* (e.g. *gallstone removal, stent placement*), which is best done by *ERCP within 24-48hrs* or *more urgently in severe cases* Note: Cholecystectomy is NOT the priority at this time because it does not address the acute infection (acute cholangitis likely d/t gallstone dz) in the biliary tract; may need it later on though

HELLP Syndrome in Pregnancy

-Typically presents in the *third trimester* with *Hemolytic Anemia, Thrombocytopenia, & elevated transaminases*

Complications of *Staph aureus Bacteremia*

-Up to 40% of pts w/ *Staph aureus Bacteremia develop METASTATIC INFECTION* -Risk is highest in those w/ community-acquired infxns, tx delays, and persistent bacteremia or fevers -The *heart valves, lungs, and osteoarticular structures are most commonly affected* -E.g. Pt w/ persistent fever, continued leukocytosis, & worsening lower back pain raises suspicion for metastatic infxn of the spine (e.g. *vertebral osteomyelitis, epidural abscess*)--manifests as progressively worsening back or neck pain that localizes to the affected disc space; may or may not have fever and/or leukocytosis, blood cx only positive in 50% Pts w/ suspected vertebral osteomyelitis usu have *normal plain x-rays within first 2wks of infxn, so SPINAL MRI can detect osteomyelitis within days of infxn* -Confirmation w/ an open or CT-guided Biopsy

How does Infectious Mononucleosis present?

-Usu d/t *EBV* -*Systemic viral infection*, usu in *adolescents & young adults*, and typically *presents with fever, extreme fatigue, exudative pharyngitis or tonsillitis, lymphadenopathy (incl posterior cervical nodes, also may be diffusely spread in body), and hepatosplenomegaly; sometimes myalgias, anorexia leading to weight loss, N/V* -*Reactive ATYPICAL Lymphocytes* in peripheral blood smear -- *predominant cytoplasm with irregular nucleus* -- but this is *not specific to mono & can be seen in other systemic viral/inflammatory conditions*

Active and Storage Forms of Vitamin D

1,25-(OH)2 D3 -- 1,25-Dihydroxyvitamin D aka Calcitriol (ACTIVE form of vitamin D) 25-OH D3 -- 25-Hydroxyvitamin D aka Calcidiol (STORAGE form of vitamin D) When the body's serum phosphate & calcium are low, Parathyroid hormone release is stimulated, which stimulates 1-alpha hydroxylase in the kidneys (proximal convoluted tubule) to promote conversion of 25-OH D3 (storage form) into 1,25-(OH)2 D3 (active form) -*Active form, aka Calcitriol*, has the following effects to overall *Incr Serum Calcium & Phosphate Levels*: ● *BONE*: *Incr Ca2+ & Incr PO4 Released from bone* ● *INTESTINES*: *Incr Absorption of Ca2+ & PO4* ● *KIDNEYS*: Acts on Renal tubular cells to *Promote Reabsorption of Ca2+ & PO4, and Decr Urinary Excr of Ca2+ & PO4*

Hepatic Hydrothorax

-Usu presents as a *right-sided transudative pleural effusion* in pts w/ *decompensated cirrhosis and ascites* -Decompensated cirrhosis is evidenced by prolonged INR, lower extremity edema, and abdominal distension w/ shifting dullness in the setting of chronic alcohol abuse -The pleural effusion develops d/t *passage of peritoneal ascites* through the diaphragm -Usu occurs on the *right* bc the right hemidiaphragm is thinner & more likely to have porous defects than the left. -Effusion is typically *transudative*, w/ fluid to serum total protein ratio ≤0.5, fluid to serum LDH ratio ≤0.6, and fluid LDH ≤2/3 the upper limit of normal for serum LDK -Thoracentesis can drain hepatic hydrothorax, but the effusion usu recurs -Initial tx is similar to the tx of ascites and involves *Sodium Restriction* in combination with *Loop (e.g. Furosemide) & K+-Sparing (e.g. Spironolactone) Diuretics* -Presence of hepatic hydrothorax signals advanced liver dz and should prompt consideration for liver transplant

Which antibodies are seen with SLE?

-Virtually all SLE pts screen positive for *antinuclear antibody (ANA)* --BUT this is *NONSPECIFIC* and *can also be positive in healthy populations* and in *pts w/ connective tissue diseases* -BOTH the *anti-dsDNA & anti-Smith antibodies* are associated with SLE, although *anti-dsDNA are more SENSITIVE* at 66-95% while anti-Smith is only 25% sensitive, but are highly SPECIFIC for SLE -*Anti-dsDNA antibody titers* are useful to *follow the course of SLE disease activity* and have even been assoc with the dev of Lupus Nephritis Note: *Anti-Smith antibodies do not correlate w/ dz activity in SLE pts* and *may still be positive in a pt w/ clinically-improving SLE even while their anti-dsDNA ab have returned to the normal* range

When to evaluate for *secondary causes of HTN*?

-When pts have *Resistant HTN (i.e. persistent HTN despite an appropriate 3-drug regimen* -When pts have an *Abrupt onset of HTN* -When pts *Develop HTN at an unusual age (<30yo)* -When pts with have *specific abnormal findings on initial eval* such as *hypokalemia, hematuria, or abdominal bruit* *Secondary causes of HTN* incl: Renal parenchymal disease, Renovascular disease, Primary Hyperaldosteronism, Obstructive sleep apnea, Pheochromocytoma, Cushing Syndrome, Thyroid disease, Primary Hyperparathyroidism, Coarctation of aorta

Actinic Keratosis (AK)

-White pt w/ *rough, ASX facial lesions* -*Actinic keratosis (AK) is a PRECURSOR to SCC* -AK presents as *chronic, scaly papules or plaques* and is *MC in FAIR-Skinned pts* -Lesions are located *primarily in Sun-Damaged Areas (e.g. face, dorsal hands)* -Although papules are *typically erythematous, nonerythematous lesions are easily distinguished from dry skin by the characteristic Sandpaper-Like Texture* -Other clinical variants of AK incl: ● *Hypertrophic AK* -- presents with *thick scales on a red base* ● *Atrophic AK* -- presents with *soft, red macules that lack scales* ● *AK assoc w/ Cutaneous Horn* -- presents as a *cone of keratin (straight or curved), typically w/ AK or SCC at its base* -*AK Diagnosis is Clinical based on PE*; HOWEVER, *Hypertrophic AK & Cutaneous Horns usu require BIOPSY to R/O SCC* -*TREATMENT:* ● *Isolated AKs* -- TX effectively with *Liquid Nitrogen Cryotherapy* ● *Numerous or Diffuse AKs* -- TX with *Topical Therapy (e.g. 5-FU, Tirbanibulin) to cover a large area* -*TX should NOT be delayed* d/t *risk of progression to SCC*

Carbon Monoxide Poisoning

-carbon monoxide binds with hemoglobin with high affinity and reduces oxygen delivery to tissues -S/S include: nausea, vomiting, headache, weakness, and unconsciousness -death may occur with prolonged exposure -In pts with *high levels of carboxyhemoglobin (e.g. >25%), cellular hypoxia and severe metabolic acidosis with elevated lactic acid* can occur -prevention by ensuring proper ventilation when using fuel-burning devices -gas-burning devices should be inspected annually -flues and chimneys should be unobstructed -carbon monoxide detectors should be installed and inspected regularly

Exogenous Thyrotoxicosis

-e.g. Pt w/ *hyperthyroidism w/ tachycardia, tremor, Elevated Free T4, and NO goiter or extrathyroidal manifestations (e.g. proptosis) of Graves dz and NO palpable nodules to suggest toxic nodular dz* -*Exogenous thyrotoxicosis* can result from the *intake of OTC thyroid supplements (bovine/porcine, dessicated thyroid extracts) or excessive dosing of Rx Thyroid Meds* -*Thyroid gland activity will be SUPPRESSED, with DECREASED Radioactive iodine uptake (RAIU) and DECR Thyroglobulin levels* -2 tests helpful for evaluating exogenous thyrotoxicosis ● *24hr RAIU* is *LOW*: thyroid extracts suppress thyroid follicular activity (Other causes of hyperthyroidism w/ a LOW RAIU incl Inflammatory Thyroiditis, and the Rare Ectopic Thyroxine Production (e.g. struma ovarii)) ● IF RAIU LOW --> Check *Thyroglobulin Levels*: W/ exogenous thyrotoxicosis, *[thyroglobulin levels] are LOW (released in small amounts by normal thyroid follicles)* d/t the *suppressed follicular activity* (Elevated thyroglobulin levels seen in pts w/ increased follicular activity [e.g. Graves dz] or follicular injury [thyroiditis]) Note: • Graves Dz: Elevated RAIU w/ DIFFUSE Uptake + Elevated Thyroglobulin • Postpartum Thyroiditis/Subacute Granulomatous (de Quervain) Thyroiditis: Low RAIU + Elevated Thyroglobulin • Chronic Lymphocytic (Hashimoto) Thyroiditis: RAIU variable (may be normal) + Elevated Thyroglobulin d/t inflammation of thyroid follicles • Toxic Nodular DZ: Elevated RAIU w/ FOCAL Uptake, or Normal RAIU + Low/Normal Thyroglobulin as increased release form the toxic nodules may be offset by decreased release from the remainder of the thyroid

Complicated Ureteral Stone

-i.e. A *ureteral stone* resulting in *Obstruction (e.g. hydronephrosis, hydroureter), Superimposed Infection (e.g. fever, CVA tenderness), & Hemodynamic Instability* --> *LIFE-THREATENING CONDITION REQUIRING IMMEDIATE INTERVENTION* -Needs *broad-spectrum antibiotics & IVF resuscitation, and Urgent Drainage of the urinary tract* (decompression) in order to *control the infection* and *prevent further clinical decompensation* -Drainage typically performed via *PERCUTANEOUS NEPHROSTOMY* or *Placement of a RETROGRADE URETERAL STENT* --both methods show similar clinical outcomes -*Definitive stone management is Delayed until the infection is treated & pt's condition stable* Note: *[Emergency] Shock-wave Lithotripsy* is used in the management of *Uncomplicated ureteral stones*; However it may NOT lead to the Immediate Relief of ureteral obstruction Note: *Emergency Open surgical stone extraction* is associated with *significant operative risk* and is usu reserved for pts whose condition *fails to improve* with less invasive interventions or whose cases are *complex* (e.g. abnormal urinary tract anatomy)

2 Categories of Syncope

1. *CARDIOVASCULAR* causes: -Arrhythmia -Blood flow obstruction (i.e. *aortic stenosis*) 2. *NONCARDIOVASCULAR* causes: -Vasovagal -Carotid sinus hypersensitivity -Orthostasis -Seizures -TIA, etc. -25% of pts have no known etiology of their syncopal events -Most imp part of a syncope workup is the *history* -*Thorough history taking, physical exam* (incl *orthostatics*), & *EKG* will reveal the cause of syncope in ≈50% of pts -*Vasovagal syncope* is often assoc w/ a *prodrome* of tunnel vision, diaphoresis, nausea, & pallor

Uses and Risks of the following Common Herbal Medications: 1. Ginkgo biloba 2. Ginseng 3. Saw palmetto 4. Black cohosh 5. St. John's wort 6. Kava 7. Licorice 8. Echinacea 9. Ephedra

1. *Ginkgo biloba*- used for *memory enhancement*; AE, *incr. bleeding risk* 2. *Ginseng*- used for *improved mental performance*; AE, *incr. bleeding risk* 3. *Saw palmetto*- used for *BPH*; AE, *mild stomach/GI discomfort* 4. *Black cohosh*- used for *menopausal sx* (hot flashes, vaginal dryness); AE, *hepatic injury* 5. *St. John's Wort*- used for *depression, insomnia*; AE, *Hypertensive crisis and drug interactions w/: antidepressants (serotonin syndrome), OCPs, anticoagulants (decr. INR), digoxin* 6. *Kava*- used for *anxiety, insomnia*; AE, *severe liver toxicity* 7. *Licorice*- used for *stomach ulcers, bronchitis/viral infxns*; AE, *HTN, Hypokalemia* 8. *Echinacea*- used for *Tx & prevention of cold/flu*; AE, *allergic rxns (anaphylaxis), dyspepsia* 9. *Ephedra*- used for *Cold/Flu TX, weight loss & improved athletic performance*; AE, *HTN, arrhythmia/MI/sudden death, stroke, seizure*

What are the *3 criteria for Acute Liver Failure*?

1. Evidence of *hepatic injury* (e.g. elevated aminotransferases) 2. *Encephalopathy* 3. *INR ≥1.5*

Best imaging modality for picking up: 1. Primarily *OSTEOLYTIC Metastases* 2. Primarily *OSTEOBLASTIC Metastases* 3. *MIXED LYTIC/BLASTIC Metastases*

1. Primarily *OSTEOLYTIC Metastases* -(e.g. *multiple myeloma*) Poorly visible on Radioisotope (Technetium-99 MDP) bone scans (as labeled technetium is preferentially taken up in areas of NEW bone formation). *Plain X-RAYS & PET-CT* are *more effective* 2. Primarily *OSTEOBLASTIC Metastases* -(e.g. *prostate cancer*) *Easily seen on Radioisotope (Technetium-99 MDP) Bone Scans* 3. *MIXED LYTIC/BLASTIC Metastases* -(e.g. *breast cancer*) Usu seen on *Radioisotope bone scans*, but *PET CT* may be helpful in some cases

How are *inoperable Head & Neck cancers* managed?

>50,000 NEW cases of head & neck cancer DX per year in USA ~60% are *locally advanced (regionally advanced, stages III & IV) At the time of DX and are deemed Inoperable* -*COMBINED CHEMORADIOTHERAPY* promises *superior results over chemo or radiotherapy alone*, *not only increasing 5yr survival rate, but also rendering some inoperable cases operable after Tx*

Case-Control Study Case Series Study Prospective vs Retrospective Cohort Study Randomized Clinical Trial

A *Case-Control Study* categorizes patients *with and without a specific disease* and *compares the RF frequency* between the two groups A *Case Series* is a *group of case reports* regarding *individual pts who had similar clinical manifestations or received similar treatment*. Each individual case is usu described in detail. *Case reports* are sometimes used in *rare diseases* or *novel treatments* A *Prospective Cohort Study* would *follow individuals who do NOT have the disease/outcome of interest and who may or may not have a certain RF over time;* the study would then *assess for disease development [in the future] -- Looking for Disease INCIDENCE* A *Retrospective Cohort Study* would *review past medical records & histories to identify individual who do NOT have the disease/outcome of interest, and those who do and do not have a certain RF;* then would *assess for disease development -- Looking for Disease INCIDENCE* A *Randomized Clinical Trial* would follow *individuals who have been randomized to either a TX arm(s) or a Control arm,* and *compare the effect of the intervention*

Tinea Capitis

A fungal infection of the scalp characterized by red papules, or spots, at the opening of the hair follicles. *multiple foci of patchy hair loss over scalp with associated scaling and inflammation of the scalp in the areas of hair loss*

What does a *positive HCV antibody test* tell you? (e.g. Positive anti-hepatitis C virus antibody)

A positive test indicates one of the following: ● *ACTIVE, Ongoing infection (Chronic or Acute)* ● *PAST infection that has now Resolved* ● *False-Positive result* -*HCV antibody testing is used for SCREENING*, as it identified those who were exposed to the virus -HOWEVER, to *determine those w/ ongoing, Active disease, FURTHER TESTING is required* to *document HCV RNA in blood* -- this is done by *HCV Nucleic Acid Testing (NAT)* -If pts have a *Positive HCV NAT,* they would be considered *Candidates for Antiviral Therapy* -Chronic HCV infection is usu ASX, and ~1/3rd of pts have normal LFTs -- Therefore, symptomology and basic lab assessment alone is insufficient to identify those who have currently have chronic HCV infection and those who have cleared the infection -Pts with a *positive HCV NAT should undergo further eval with to identify the HCV genotype and the extent of liver fibrosis with a liver biopsy*; aminotransferases are NOT adequate for disease progression monitoring

How do you manage a pt with persistent symptoms of peptic ulcer disease despite completing appropriate tx to eradicate H. pylori?

A pt w/ *persistent PUD symptoms* (e.g. intermittent recurrence of abdominal pain, occasional nausea; intermittent burning epigastric pain) is CONCERNING for *TREATMENT FAILURE* -Given increasing ABX resistance, *H. pylori eradication should be confirmed in pts with:* • *Persistent Sx* • *H. pylori-associated ulcer* on Upper GI Endoscopy • *Evidence of an H. pylori-assoc Malignancy* (e.g. Gastric cancer, MALT) -Common methods to determine bacterial eradication incl *Urea breath testing & Fecal /Stool H. pylori Antigen testing* -Testing should *occur ≥4wks after completion of therapy* -If testing confirms eradication, but Sx remain, then other etiologies should also be considered -If testing shows that *H. pylori infection persists* after first-line therapy, then *second-line options* such as *QUADRUPLE Therapy or SEQUENTIAL Therapy* involving distinct ABX should be used Note: Repeating the upper endoscopy can help establish whether or not H. pylori has been eradication, but better to first try less invasive options (breath test, stool antigen) and reserve repeat endoscopy for pts w/ indeterminate indirect testing or those w/ other additional indications for scope

What is Ogilvie's Syndrome?

AKA *acute colonic pseudo-obstruction* -Characterized by *dilation of cecum and right colon in the ABSENCE of a mechanical obstruction to the flow of intestinal contents*. -Tends to involve the *right colon and NOT the small intestine*

Giant Cell Arteritis

AKA Temporal Arteritis -Usu in *elderly females, >50yo* -P/w *unilateral headache (temporal A) & jaw claudication when chewing* -May lead to *irreversible blindness* d/t ophthalmic A occlusion -Assoc w/ *polymyalgia rheumatica* -Most commonly affects branches of carotid A -Focal granulomatous inflam, *Incr ESR* -TX: *High-dose corticosteroids /prior/ to temporal A biopsy* to *prevent blindness*

Neuroleptic Malignant Syndrome - Quick Overview

Acute, potentially fatal, idiosyncratic rxn to antipsychotic medications and is characterized by *Fever, extreme generalized rigidity, autonomic instability, & altered mental status*

Which population is at high risk for influenza complications?

Adults who are: • Age ≥65yo • Pregnant women and up to 2wks postpartum • Underlying chronic medical illness (e.g. COPD, cardiovascular, renal, hepatic) • Immunosuppressed (e.g. HIV, immunosuppressants, transplant) • Morbidly obese • Residents of nursing homes or long-term care facilities

Wallenberg Syndrome

Aka *Lateral medullary syndrome* *Spinal trigeminal nucleus*: Ipsilateral facial loss of pain & temp *Vestibular nucleus*: Vertigo, diplopia, nystagmus, vomiting *Inferior cerebellar peduncle*: Ataxia *Nucleus ambiguus*: Diminished gag reflex *Spinothalamic tract*: Contralateral loss of trunk & extremity pain & temp

Lateral Medullary Syndrome

Aka *Wallenberg Syndrome*. Caused by *lateral medullary infarct affecting the lower cranial nerves* -Leads to *vertigo/nystagmus* (vestibular nucleus), (loss of pain/temp sensation in the IPSILATERAL face* (trigeminal) *but CONTRALATERAL body* (spinothalamic), *bulbar weakness* (lower cranial nerves), and *IPSILATERAL Horner Syndrome (descending sympathetic; ptosis & miosis)*

Wilms Tumor

Aka NEPHROBLASTOMA -MC renal malignancy in children aged 2-5yo and affects ONE kidney -Usu presents as an *ASX abdominal mass* (smooth, unilateral, doesn't cross midline), but can present with *hematuria* in 25% of cases -Other Sx incl abdo pain, HTN, fever -*Lungs* are the MC site of metastatic spread, but rarely have pulmonary sx -*Abdo U/S* is the first step, subsequently *contrast Abdo CT or MRI* needed to evaluate extent of mass -CT Chest also recommended to look for pulm mets -TX: *Surgery & Chemo* ± Radiation for late-stage dz -Survival rates excellent (90%)

What is the albumin/creatinine ratio for microalbuminuria?

Albumin/creatinine ratio of 30-300 mg/g

What is Upper Airway Cough Syndrome?

Also called, *POSTNASAL DRIP* Pts present with *chronic cough*, but also have *rhinorrhea and oropharyngeal cobblestoning* on physical exam

Initial Evaluation for Secondary Amenorrhea?

Amenorrhea is No menses for >3mo in pts w/ previously irregular menses Pregnancy test TSH levels Prolactin levels FSH levels -*Elevated FSH is consistent w/ loss of ovarian fxn (i.e. HYPERgonadotropic HYPOestrogenism = elevated FSH, low estrogen)* -- when this happens in pts *<40yo*, called *PRIMARY OVARIAN INSUFFICIENCY* (POI) -POI also includes *infertility*, hot flashes, night sweats, *vaginal atrophy* alllll d/t *LOW ESTROGEN LEVELS* -Pelvic U/S shows *thin endometrium & small (atrophic) ovaries* -After DX of POI, need to eval further to determine *underlying etiology* -*Common Causes of Primary Ovarian Insufficiency* Incl: • *Chemoradiation* • *Autoimmune Dz* (e.g. Adrenal insufficiency, hypothyroidism) • *Genetic Anomalies* (e.g. *Fragile X Syndrome, TURNER Syndrome*) -All pts should undergo *testing for adrenal antibodies, TSH, AND KARYOTYPE ANALYSIS* -Management is w/ *initiation of estrogen replacement (usu balanced by progesterone supplementation) to preserve sexual health and minimize risk of osteoporosis and cardiovascular dz*

What is the *first-line therapy for pts w/ ASX Left Ventricular Systolic Dysfunction?* (LVSD)

An *ANGIOTENSIN SYSTEM INHIBITOR (E.G. ACE INHIBITOR)* as these drugs have been shown to *Delay the onset of Symptomatic HF and Improve Long-Term Cardiac M&M* -A *ΒETA BLOCKER (E.G. METOPROLOL)* should be added d/t evidence of similar benefits in these pts *ASX LV Systolic Dysfunction (ejection fraction ≤40%) is typically diagnosed when Echo is done for an abnormal EKG or Physical exam finding (eg. cardiac murmur d/t aortic stenosis)* - consistent with NYHA *Class I Heart Failure* Note: Mineralocorticoid receptor Antagonists (e.g. *Spironolactone*) have been shown to *improve mortality in pts w/ LVSD, esp those w/ persistent symptoms despite TX w/ an ACE-Inhibitor and β-blocker* -- But Spironolactone is NOT indicated in ASX LVSD

Cushing Syndrome 2/2 Glucocorticoid Excess - Quick Overview

Cushing's Syndrome involves *Glucocorticoid EXCESS* and typically p/w *Obesity, Skin changes incl Atrophy & [Purple] Striae, Glucose Intolerance, & HTN* *Cushing Syndrome* can be caused by: ● Iatrogenic (from Glucocorticoid therapy) ● Adrenocortical Adenoma (secretes Excess Cortisol) ● ACTH-secreting pituitary adenoma (Cushing DISEASE) ● Paraneoplastic (due to ACTH-secretion by Tumors e.g. small cell lung CA)

How to choose antibiotics in a pt with foot osteomyelitis?

Bc diabetic foot infections are often *polymicrobial*, a diverse group of organisms can contribute to infection -*Gram-positive cocci, e.g. Staph aureus*, are most commonly isolated, but *Pseudomonas aeruginosa and Anaerobic bacteria (e.g. Clostridium)* are also frequently involved, esp when wounds are deep and chronic -Bc diabetic wound colonization rates are high, *superficial wound cultures have little predictive value in identifying the underlying pathologic organisms* and *should NOT be used to guide therapy* -*Positive blood cultures* are far more predictive, esp in the setting of radiographic evidence of osteomyelitis -HOWEVER, *BONE BIOPSY W/ CULTURE* is considered the Gold Standard *for identifying pathologic organisms* and is usu needed to *determine appropriate antimicrobial therapy* -Diabetic foot infections with Osteomyelitis are typically *TX with a combo of *glucose control, surgical debridement, weight Off-loading, revascularization (if needed), and Antibiotic therapy for >6wks* -*Serial inflam markers* (e.g. ESR) can help *confirm TX response*

AE of Bisphosphonates

Bisphosphonates (e.g. Alendronate, Ibandronate, Risedronate, Zoledronate) can cause *medication-induced Esophagitis (i.e. Pill Esophagitis)* d/t *prolonged medication exposure on the esophageal mucosa* -This condition is characterized by *punched out ulcers w/ an inflammatory infiltrate* on biopsy -Pts recommended to take PO Alendronate w/ water and remain upright for >30mins -Other AE: Osteonecrosis of jaw, atypical stress fractures

What is BLEPHAROSPASM?

Blepharospasm is a form of *focal dystonia*, where there is *recurrent episodes of sustained contraction of the orbicularis oculi muscles*, resulting in *involuntary, forceful eye closure triggered by increased sensory input* (e.g. bright light) -Blepharospasm can *start as unilateral, but often progresses to bilateral* involvement with *excessive blinking* -*Dystonia* is a sustained, involuntary muscle contraction, which force certain parts of the body into abnormal, sometimes painful movements of postures -*Focal* dystonias affect a single muscle or group of related muscles - the MC of which incl cervical dystonia, blepharospasm, & task-specific dystonias (e.g. writer's cramp) -Most cases *idiopathic* -TX: *BOTULINUM TOXIN INJECTIONS* to the affected muscles is *first-line& (dose is carefully adjusted to *weaken /without fully paralyzing/* the muscle) -Resultant Decr in strength alleviates discomfort -*AE of Botulinum Toxin Injections*: Like *Ptosis*; AE are generally rare and transient -TX can continue safely for many years

What type of goiter can cause palpable thyroid enlargement in adolescent girls with normal thyroid function tests and negative antithyroid peroxidase (TPO) antibodies?

COLLOID GOITER

Retropharyngeal abscess presentation

Can occur in *toddlers* and present with *fever, dysphagia, neck pain, & stridor* -Lateral neck x-ray shows *thickening of the prevertebral space (anterior to vertebra)* -CT neck better defines the extension of the abscess to nearby structures

Most common fungal cause of balanitis?

Candida albicans! Causes *thick, white discharge present around the glans penis*; can also have *satellite lesions*, and *typical erythema, swelling, & tenderness* DX confirmed by presence of *budding yeast on potassium hydroxide (KOH) microscopy* TX w/ *topical antifungal (nystatin)* -Check *blood glucose levels* in *prepubertal children w/ no RF for C. albicans* (e.g. diaper dermatitis, recent antibiotic use) bc balanitis can be the first presenting sx of *Diabetes!)* Balanitis: inflammation around glans penis -common in young, *uncircumcised* boys d/t irritation from poor genital hygiene

Tricyclic Antidepressant Toxicity

Cause: -*TCA overdose* (e.g. Manifestation: -*Respiratory Depression* -*Hyperpyrexia (FEBRILE)* -*Prolonged QT* on EKG -*TriC*yclic: *C*onvulsions, *C*oma, *C*ardiotoxicity (*arrhythmia* d/t Na+ channel inhibition) Treatment: -*Supportive* Tx -*Monitor EKG* -*Sodium Bicarbonate, NaHCO3* to *prevent arrhythmia* -*Activated charcoal*

TX of Strep Pharyngitis

Caused by *Group A Strep - Strep pyogenes* TX with *Penicillin or Amoxicillin* If penicillin-allergic, tx with *cephalosporin* (mild rxn); *azithromycin or clindamycin* (if anaphylaxis with penicillin)

What organism causes *erysipelas* and what is the treatment?

Caused by *group A strep, Streptococcus pyogenes* occurs with rapid onset and involves only upper dermis and superficial lymphatics Appearance: *bright red, well-demarcated, and raised area that is tender and tense* with *localized LAD (tender)* and *systemic sx* (e.g. fever, chills) TX with *Penicillin (e.g. Ampicillin, Amoxicillin)*

Cellulitis caused by which bug?

Caused by /*Staphylococcus aureus/* Presents w/ *acute-onset* erythema, edema, & warmth

Hereditary Angioedema

Caused by C1 esterase inhibitor deficiency -*C1 esterase inhibitor levels are decreased*, allowing *unregulated activation of kallikrein* which leads to *INCR Bradykinin levels* -Sx: Angioedema of the throat, tongue, or lips without urticaria; can also have abdo pain d/t angioedema of the intestinal mucosa -*ACE Inhibitors CONTRAINDICATED* (lisinopril, captopril, enalapril, ramipril)

Trigeminal neuralgia

Caused by compression of the trigeminal nerve (CN V) root as it enters the pons, usu by an abnormal vessel loop (can also be caused by neoplastic growth or multiple sclerosis plaque). This leads to atrophy and demyelination of the nerve and causes short paroxysms of neuropathic pain (with no associated facial rashes). Presents as unilateral, intermittent sharp pain (around the cheek and lower jaw) that lasts several seconds and is triggered by minor stimuli (e.g. brushing teeth, drinking cold H2O)

Serotonin Syndrome - Quick Overview

Caused by use of multiple serotonergic agents (MAO inhibitors, SSRIs, SNRIs, TCAs) causing neuromuscular hyperactivity and autonomic stimulation including *Myoclonus, hyperreflexia, hyperthermia, hypertonia, tremor, seizures, diaphoresis, diarrhea, confusion*

Schizoaffective disorder

DSM-5 Criteria: -Major depressive or manic episode concurrent with symptoms of schizophrenia -Lifetime hx of *delusions or hallucinations for >/= 2wks in the absence of major depressive or manic episode* -Mood episodes are prominent & recur throughout illness -Not due to substances or other medical conditions DDX: -*Major depressive or bipolar disorder w/ psychotic features*: psychotic sx occur exclusively during mood episodes -*Schizophrenia*: Mood sx may be present for relatively brief periods

Polymyalgia Rheumatica (PMR)

Characteristic Features: -*AGE >50YO* -*Subacute to Chronic (>1mo) PAIN* in the *Shoulder & Hip Girdles* -*Morning Stiffness >1hr* -Constitutional Sx - general malaise, possible weight loss -*Elevated ESR! >40mm/h* -No other apparent explanation for sx Physical Exam: *Unremarkable! NO focal tenderness or pain w/ active or passive ROM* and *NO signs of joint inflam* (e.g. no overt synovitis at joints) -When asked to identify location of pain, pts *indicate soft tissues, NOT the joints* Treatment: -*LOW-Dose GLUCOCORTICOIDS (e.g. Prednisone 10-20mg daily)* is the *TX of Choice in PMR* -- expected to produce *rapid relief of sx*, so *failure to improve rapidly* should question the diagnosis -*PMR is freq assoc w/ Giant Cell Arteritis (GCA), aka Temporal Arteritis* -*SX of GCA*: *HA, jaw claudication, vision loss, & tenderness over temporal artery* -IF GCA is suspected, consider an *expedited temporal artery biopsy* and *give HIGH-Dose Glucocorticoids (e.g. Prednisone 40-60mg or Higher daily)* Note: Antinuclear-Ab and Rheumatoid Factor level screening tests are for SLE & Rheumatoid Arthritis, respectively, and are freq positive in a number of other inflammatory and autoimmune conditions. These tests have Poor Specificity in the absence of characteristic sx (e.g. malar rash, MCP synovitis).

Porcelain Gallbladder

Characterized by dev of *punctate or curvilinear calcifications within the gallbladder wall d/t chronic cholelithiasis* -Most pts *ASX* -*DX when GB calcs incidentally found* ● GB calcs thought to be d/t chronic inflam, NOT hypercalcemia ● Hypercalcemia incr risk for nephrolithiasis, but not gallstones -Pts w/ porcelain GB are at *INCR risk for Gallbladder Cancer & often Require PROPHYLACTIC CHOLECYSTECTOMY* if they *sx of GB disease (e.g. biliary colic) or if PUNCTATE Calcs present* Note: *Curvilinear* GB calcs *minimally incr cancer risk* and generally *do NOT require intervention*

Clinical Fibromyalgia Diagnosis

Clinical DX only, No lab findings -Based on widespread MSK pain, fatigue, disordered sleep, impaired cognition -Extensive lab testing is unnecessary, but a limited eval (e.g. CBC, ESR, TSH) for common mimicking conditions w/ similar sx can be considered (e.g. anemia, inflammatory arthropathy, hypothyroid myopathy)

Acute Aortic Dissection

Clinical Presentation: -Hx of HTN, genetic disorder (e.g. Marfan syndrome) -Severe, sharp, tearing chest or back pain ->20 mmHg difference in systolic BP b/w arms Diagnosis: -EKG: Normal or Nonspecific ST- & T-wave changes -CXR: Mediastinal widening -*CT Angiography or TEE for definitive DX* Treatment: -Pain control (e.g. Morphine) -IV Beta Blockers (e.g. Esmolol) -± Sodium Nitroprusside (if SBP >120mmHg) -Emergent surgical repair for ascending dissection -The goals of initial therapy for both *ascending and descending aortic dissection* incl providing adequate pain control, *lowering systolic BP to 100-120 mmHg* and *decreasing left ventricular contractility* to reduce aortic wall stress -*IV beta blockers* such as *labetalol, propranolol, or esmolol* are preferred for *slowing the HR <60/min, lowering BP, and reducing LV contractility* -ESMOLOL is preferred in acute settings d/t its short half-life (~9mins), which allows for rapid titration for optimal heart rate & BP control -In addition to medication therapy, *Emergency Surgical Repair* is needed for *Ascending* dissection -Aortic dissection involving the ascending aorta has a mortality rate of 1-2% per hour after the onset of symptoms

Predictors of 30-day mortality in Pulmonary Embolism

Clinically: -Hypotension (SBP <90 mmHg) -Tachycardia (HR >110/min) -Tachypnea (RR >30/min) -Hypothermia (T <30 C/<86 F) -Hypoxemia (SpO2 <90%) -Altered mental status -Hx of Cancer -Age >80yo Radiologically: -Right ventricular dysfunction Labs: -Elevated troponin -Elevated BNP

Triad of Normal-Pressure Hydrocephalus

Cognitive Impairment Urinary Incontinence Abnormal Gait (magnetic gait)

Cyanide Poisoning

Common Etiologies: -Structure fires (e.g. combustion of plastics) -Occupational exposure (mining) -Cyanide-containing meds (e.g. *sodium nitroprusside*, esp in renal failure pts) Pathophysiology: -Inhibits oxidative phosphorylation & forces anaerobic metabolism -Rapidly lethal if untx *Clinical Features:* -HTN, tachycardia, tachypnea --> Circulatory collapse, death -HA, confusion, anxiety --> Seizures, coma -Cherry-red skin -Elevated anion gap metabolic acidosis w. Incr Lactic acid (d/t anaerobic cellular metabolism) Management: -Decontamination -Supportive care (e.g. 100% O2, IVF, vasopressors) -Empiric Tx w/ *HYDROXOCOBALAMIN +/- SODIUM THIOSULFATE*

Sexual dysfunction in postmenopausal women - What to ask about

Comprehensive eval of sexual dysfunction requires assessing *physiological, psychological, and relationship factors.* *Postmenopausal women* should specifically be assessed for *vaginal dryness and dyspareunia* Evidence that SSRIs and SNRIs (e.g. venlafaxine) relieve vasomotor sx, but low-dose vaginal estrogen therapy may be needed to tx vaginal atrophy

When to transfuse platelets in an otherwise healthy pt?

Consider PLT Transfusion in pts w/ life-threatening bleeding and PLTs <50,000 or in those taking Antiplatelet agents

Which rashes involve the palms and soles?

Coxsackievirus [A] causing Hand-foot-mouth dz - painful oral enanthem & maculopapular/vesicular exanthem Secondary Syphilis - assoc w/ hepatomegaly & lymphadenopathy Scabies - intensely pruritic papular rash involving interdigital spaces and NO oral involvement Rocky Mountain Spotted Fever - caused by Rickettsia rickettsii, vector is a tick; p/w headache, fever, and rash (vasculitis) beginning at wrists and ankles and spreading to trunk, palms, soles; Tx w/ Doxycycline

When would you do surgery for cryptorchidism?

Cryptorchidism = Undescended testis; empty, hypoplastic poorly rugated hemiscrotum -D/t disruption of physiologic, in utero testicular descent from abdomen to inguinal canal to base of scrotum -Premature or small for gestation age infants are at incr risk -DX made based on PE (imaging not routinely needed [U/S not sensitive in detecting nonpalpable testes], rather do exploratory surgery) -In *Infants <6mo, provide reassurance and monitor for descent* -Most testes *spontaneously descend in first few mo of life*, after that, it rarely occurs and /spermatogonia degeneration begins/ -*In all children ≥6mo (corrected for gestational age), TX of Cryptorchidism is Orchiopexy (surgical fixation)* of testis to scrotal wall -Doing orchiopexy <1yo *optimizes fertility potential & testicular growth, & reduces risk for testicular torsion* -There is *an assoc of undescended testes w/ an incr risk for testicular cancer, which is decr but not eliminated after orchiopexy, therefore need regular testicular exams*

Fecal Impaction & Overflow Incontinence

E.g. Elderly woman w/ fecal incontinence, hard stool within the rectum, & decreased anal sphincter tone -*Fecal impaction*, often DX by *digital rectal exam*, is the presence of large amounts of stool within the rectum that the pt is unable to pass -It is freq assoc w/ *constipation* and age-related changes, incl slowing of fecal transit, decreased sensation of stool in the vault, and a reduction in anal sphincter tone -*In elderly pts, fecal impaction is the MCC of fecal incontinence* d/t liquid stool overflowing around impacted stool within the rectum -In the setting of stool impaction, the most appropriate initial TX is to perform *manual disimpaction*, followed by *enema or suppository* to empty the colon -The pt should then be TX w/ an aggressive oral bowel regimen to prevent recurrence Note: Increasing dietary fiber and using stool softeners should be recommended to this type of pt w/ constipation, but these methods alone may be insufficiency for removing the obstruction caused by impacted stool. Both should be initiated after successful manual disimpaction.

Hepatic Encephalopathy (HE)

E.g. Pt w/ *cirrhosis* having AMS, elevated ammonia, and asterixis is suggestive of *HE* -HE is a spectrum of neurocognitive and motor abnormalities that primarily occurs in pts w/ hepatic disease -Although multifactorial in origin, most cases are d/t *elevated ammonia levels from a precipitating event* -Precipitating factors incl: • Drugs (e.g. sedatives, narcotics, diuretics) • Hypovolemia (e.g. diarrhea, p/w dry mucous membranes, high BUN; //one of MC precipitants of HE!//) • Electrolyte changes (e.g. hypokalemia--which helps convert ammonium to ammonia) • Incr Nitrogen load (e.g. GI bleeding) • Infection (e.g. pneumonia, UTI, SBP) • Portosystemic shunting (e.g. TIPS) E.g. HE precipitated by the use of diuretics for volume overload (ascites) which results in: • *Hypovolemia* (one of MC precipitants of HE! caused by excessive diuresis or diarrhea which reduces intravascular volume and results in *hypokalemia* and *met alkalosis*): dry mucous membranes, high urea nitrogen • *Hypokalemia*: facilitates conversion of ammonium to ammonia • *Metabolic Alkalosis*: decreases urinary loss of ammonia -Clinical Presentation: Sleep pattern changes, AMS, ataxia, asterixis -TX: Correcting precipitating causes (e.g. fluids for *volume & electrolyte repletion*, antibiotics, temporary cessation of diuretic use); Decreasing blood ammonia concentrations (e.g. Lactulose, Rifaximin)

Perforated Peptic Ulcer

E.g. Pt w/ acute abdominal pain w/ significant tenderness and guarding is suggestive of viscus perforation w/ peritonitis -A perforated peptic ulcer is the MC etiology, and is esp likely in a pt who has a Hx of "burning" abdominal sensations -In contrast to pts w/ Renal Colic, who tend to writhe in pain, pts w/ *Peritonitis* tend to *lie flat & motionless* to limit peritoneum irritation -Rupture of a hollow organ allows air into the abdomen (pneumoperitoneum) and can often be detected by an *upright CXR* -If the findings on CXR are unclear, an abdominal CT may be useful -Peptic ulcer perforation is a potentially fatal complication of peptic ulcer disease -If left untx, pt can have rapid clinical deterioration leading to death within 12-24hrs -Early DX and TX generally lead to excellent prognosis and most pts recover fully -*Emergency surgery* (open or laparoscopic) is indicated in all pts w/ perforated peptic ulcer -In preparation for surgery, pts w/ a *perforated viscus should receive fluid resuscitation & broad-spectrum IV ABX* w/ good coverage for *G(-) organisms* -*IV PPI* therapy is also suggested Note: Barium Esophagram is indicated for the evaluation of dysphagia (e.g. pts w/ suspected hiatal hernia, achalasia, esophageal webs). It is *contraindicated* in pts w/ suspected perforation.

Hypertrophic Cardiomyopathy (HCM)

E.g. Pt w/ fatigue, exertional dyspnea, systolic murmur that accentuates w/ Valsalva, asymmetric septal hypertrophy, systolic anterior motion (SAM) of mitral leaflets, and increased LVOT gradient — consistent w/ HCM -HCM is an autosomal dominant genetic disorder of the cardiac sarcomere -It has a heterogeneous and variable clinical presentation depending on the degree of hypertrophy and LVOT obstruction -Pts w/ HCM may have no sx or have severe sx of fatigue, dyspnea, chest pain, palpitations, presyncope, or syncope -Pts w/ sx of Heart Failure and increased LVOT gradient should be TX w/ *negative inotropic agents* (*beta blockers, verapamil, or disopyramide*) as the initial medical therapy -*Beta blockers* are the most commonly used agents for initial monotherapy; *Verapamil or Disopyramide* can be added to beta blocker therapy in pts w/ persistent sx

Cryptococcal Meningoencephalitis

E.g. Pt w/ hx of IVDU presenting w/ indolent manifestations of elevated ICP incl HA, blurred vision, papilledema; Head CT shows no intracranial mass; CSF analysis does not readily discern a bacterial or viral infection -Cryptococcus neoformans is a yeast that commonly causes *opportunistic CNS infections in AIDS pts (CD4 <100)* -Manifestations typically dev over 1-2wks and incl fever, HA, & lethargy -CSF studies usu reveal the following: • *Markedly Elevated Opening Pressure*, often >250-300 mmH2O • *Low Leukocyte Count* (<50) w/ a *Lymphocytic* predominance • Elevated Protein & Low Glucose • Positive India Ink Preparation or Cryptococcal Antigen test -Pts w/ HIV who have cryptococcal meningoencephalitis require *≥2wks* of fungicidal induction TX w/ *Amphotericin B & Flucytosine* -Tx in 3 stages: 1. *Induction*—//Amphotericin B & Flucytosine// for ≥2wks (until sx abate & CSF is sterilized) 2. *Consolidation*—High-dose *Oral Fluconazole* for 8wks 3. *Maintenance*—Lower-dose of Oral Fluconazole for ≥1yr to prevent recurrence Note: AIDS pts with cryptococcal meningoencephalitis often have dramatic CSF fungal burdens (>1,000,000 yeast/mm3). The yeast and capsular polysaccharide can //clog arachnoid villi//, which prevents CSF outflow and *increases ICP*. Pressure elevations can be dramatic (>250) resulting in //HA, vomiting, visual changes, papilledema, & CN palsies. If untx, brain herniation and death// may occur. Therefore, Cryptococcal Meningitis pts who dev recurrent sx of elevated ICP require *Serial Lumbar Punctures!!* until sx abate. Occasionally, recalcitrant cases require more permanent tx such as ventriculoperitoneal shunt Note: Dexamethasone is often added to the tx of Bacterial Meningitis (e.g. Meningococcal Meningitis) to reduce inflammation, morbidity, & risk of death). It is NOT recommended in tx of cryptococcal meningitis

Cat-Scratch Disease (CSD)

E.g. Pt w/ localized papule and regional LAD following cat exposure are consistent w/ CSD -CSD is caused by /*Bartonella henselae*/, a fastidious G(-) bacillus carried by the majority of cats, esp kittens -/B. henselae/ can be transmitted by a scratch or bite, or (rarely) by a flea -Pts typically have a *skin lesion* that can be erythematous, papular, or nodular -Fever is present in <50% of cases -*Regional Lymphadenopathy* follows within 1-2wks; it is the _hallmark_ of CSD and can be the presenting sign if the skin lesion goes unnoticed! -Affected LN are* tender and erythematous*; suppuration is less common -Cat exposure and sx consistent w/ CSD are usu sufficient to make a clinical dx -Mild cases in healthy pts often self-resolve within 1-4mo; however, *Azithromycin* is effective against /B. henselae/ and has been shown to decr the length and severity of sx -In unclear cases, antistaphylococcal and streptococcal coverage (e.g. Clindamycin) may be added to empirically tx the most common org causing lymphadenitis

Sudden Sensorineural Hearing Loss (SSNHL)

E.g. Sudden hearing loss with No HX of trauma or pain, normal ear physical exam, and an otherwise normal neurologic exam -- first determine if conductive or sensorineural -Tuning fork exam shows hearing loss is sensorineural rather than conductive (i.e. *In SENSORINEURAL hearing loss, the Rinne test shows air>bone conduction in both ears [normal response], and Weber test lateralizes to the UNaffected ear, AWAY from the Affected ear*) -Etiology of SSNHL is often not determined -Most cases likely from *viral infxn, microvascular events, or autoimmune processes*; sometimes a *tumor (e.g. Schwannoma)* or other cause is identified -SSNHL *can lead to PERMANENT hearing loss, so once it's identified, an URGENT OTOLARYNGOLOGY Exam is needed!* -*High-dose corticosteroids PO, and/or corticosteroids injected into the middle ear* are recommended soon after onset of SSNHL (ideally within 24hrs) MAY improve hearing outcomes; Efficacy decreases over time, w/ no effect after 6wks

How do subdural hematomas present?

Elderly pts at higher risk for subdural hematomas (d/t rupture of bridging veins from head trauma causing slow bleed into subdural space) -*Chronic* subdural hematomas present *Insidiously WEEKS AFTER initial injury* with *headache, somnolence, confusion, & focal neurologic deficits (e.g. contralateral hemiparesis) d/t compression of underlying cerebral cortex* -*Non-contrast head CT* shows a *crescent-shaped hypodensity that CROSSES suture lines* Contrast to *Acute* subdural hematomas, which produce sx *1-2 d after incident*

Raynaud Phenomenon

Exaggerated vascular response to cold temps or emotional stress causing numbness in fingers or toes due to intermittent constriction of arterioles in the skin -Assoc with connective tissue diseases (limited scleroderma), Systemic Lupus Erythematosus, vascular lesions (Buerger dz aka Thromboangiitis Obliterans of medium-vessel vasculitis), medications, Waldenstrom Macroglobulinemia, etc. -TX: Calcium Antagonists are first-line, but not all are equally effective. -Most *dihydropyridine CCBs* (e.g. *Nifedipine, Amlodipine*), as well as *Diltiazem* are proven to work in these pts. But Verapamil is LESS effective in Raynaud's!

Hypoparathyroidism Signs/Sx & Management

Findings: *Tetany, hypocalcemia, hyperphosphatemia, low PTH levels usu* -Cvosteksign: tapping facial N causes contraction of facial mm -Trousseau sign: occlusion of brachial A w/ BP cuff causes carpal spasm -Hypoparathyroidism pts tx with *vitamin D (calciferol) or its active form, 1.25-dihydroxyvitamin D (calcitriol)* -Chronic pts are usu managed with *high doses of vit D and calcium* (calciferol preferred over calcitriol, usu 25,000 to 100,000 units/d) -HIGH doses of vit D are required bc of the *defective conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (active form) in the kidneys due to the low PTH levels -Dose of vit D and calcium is adjusted to keep calcium levels b/w 8.5 & 9.0 mg/dL -After starting tx w/ vit D & calcium, pts usu have an *incr in urinary calcium excretion d/t low PTH levels* (PTH increases renal calcium absorption!!) -In pts w/ *borderline low serum calcium and high urinary calcium excretion*, the *addition of a THIAZIDE DIURETIC will not only decr urinary calcium, but also increase serum calcium levels* Note: Increasing calcium supplementation (dose) in these pts will only cause increased urinary calcium excretion despite the increase in serum calcium; incr urine Ca2+ predisposes to nephrocalcinosis, renal stones, & renal impairment

*HFrEF* management

Focuses on *SX Control* (e.g. diuresis), *preservation of myocardial function*, and *reducing mortality* *Sodium-glucose cotransporter-2 (SGLT-2) inhibitors* (e.g. *Dapagliflozin*) have been shown to *reduce mortality in pts w/ HFrEF both with type 2 DM and without*. Therefore, *SGLT-2 inhibitors are recommended in pts w/ HFrEF and persistent sx* despite otherwise optimized medical therapy

Treatment of Chronic Spontaneous Urticaria

For *Acute Urticaria <6wks*: -Mild: 2nd gen H1 blocker (loratidine, cetirizine) -Mod-Severe: H1+H2 blocker -Severe: Add oral steroids For *Chronic Urticaria >6wks* -2nd gen H1 blocker (loratidine, cetirizine) -If no improvement after 2wks, consider 1 of the following: • Incr dose of H1 blocker (2-4x) • Add 1st gen H1 blocker at bedtime (hydroxyzine) • Add H2 blocker (cimetidine) • Add leukotriene receptor antagonist (montelukast) • Brief course of PO steroids (glucocorticoids) -If /still/ no improvement, consider 1 of the following: • Try a different option from above step • Second line-therapies for immune-modulating effects (e.g. hydroxychloroquine [myopathy], tacrolimus [nephrotoxic], omalizumab [targets IgE])

What is Metoclopramide used for?

For *GASTRIC PARESIS* -Metoclopramide *stimulates contraction of lower esophageal sphincter & increases gastric emptying*

In addition to receiving vaccines recommended for the general population, pts with HIV infection should also receive which vaccines?

General Population Vaccines: -As w/ all adults, HIV pts should receive an *inactivated (IM) influenza vaccine annually*, as well as the *tetanus-diphtheria toxoids booster (Td) q10yrs WITH a ONE-Time Substitution of the Tetanus-Reduced Diphtheria-Acellular Pertussis (Tdap) Vaccine* -*HPV vaccine* can be given up to age 26yo, and can be considered for older HIV pts ADDITIONAL Vaccines for HIV: -*Pneumococcal conjugate vaccine* (against *Strep pneumo*), *Hepatitis A & B vaccines* (unless pt has documented immunity to these viruses), and periodic *meningococcus vaccine* -HIV incr the risk of complications from Live vaccines d/t immunosuppression, therefore the live (intranasal) flu vaccine should NOT be administered; and most other *Live vaccines* (e.g. *MMR*) are *CONTRAINDICATED* when *CD4 T-cell count <200*

Heparin-Induced Thrombocytopenia (HIT) (Type 2)

Heparin: -Activates antithrombin, which DECR action primarily of factors IIa (thrombin) and Xa. Short half-life. -Immediate anticoagulation for pulmonary embolism (PE), acute coronary syndrome, MI, deep venous thrombosis (DVT). -Used during pregnancy (does not cross placenta). -Monitor PTT. Type 2 HIT: -e.g. pt w/ sudden-onset right leg pain assoc w/ diminished pulses, coolness to touch, and normal capillary refill, suggesting viable acute leg ischemia* -- new-onset thrombocytopenia in the s/o heparin admin, most likely arterial thrombus d/t type 2HIT -*Life-threatening condition* that occurs in ~approx 5% of individuals who receive heparin -Risk is greatest w/ *unfractionated heparin* -An *immune-mediated condition d/t the formation of Autoantibodies against Heparin-Platelet Factor 4 Complexes*, which leads to *Thrombocytopenia (d/t PLT removal by reticuloendothelial system) and Arterial/Venous Thrombosis (d/t PLT activation)* -*4 T Score* (2pts each) • Thrombocytopenia - plts decline >30-50% • Timing - onset 5-10 days after heparin initiation or ≤1 day w/ prior recent heparin exposure • Thrombosis - New/Progressive thrombosis, skin necrosis • No other sources for thrombocytopenia likely -If suspect type 2 HIT, *immediately stop all heparin-containing products* and the instead *initiate an alternate non-heparin anticoagulant - first-line incl Direct Thrombin Inhibitors (Argatroban, Bivalirudin) and Fondaparinux* -*DX Confirmed by HIT Antibody Testing*, but results take days, so should *Empirically TX when suspicion is high or 4 T score is intermediate or high* -Even though *HIT antibodies* are *generally short-lived (2-3mo) and usu don't demonstrate an anamnestic response during heparin rechallenge*, bc the condition is *Life-threatening, pts who dev type 2 HIT are advised to AVOID ALL FORMS OF HEPARIN FOR LIFE* to limit the risk of new antibody formation and recurrence

Bipolar I vs II

I= mania II= hypomania + major depressive episodes (not mania)

What does appendiceal perforation increase the risk for in pregnant women?

INCREASES the Risk for Spontaneous Abortion, Preterm Labor, & Preterm Delivery

TX of pregnant woman for Tuberculosis

If *Latent TB*: Positive PPD but no sx of TB & neg CXR. Tx with *Isoniazid (INH) monotherapy with Pyridoxine (vit B6)* but only *AFTER DELIVERY* If *Active TB*: Positive PPD & symptomatic (e.g. lung cavitary infiltrate, AFB in sputum). Active TB infxn in pregnancy rarely causes placental infection, but /may result in a low birth wt infant./ TX with *3-drug therapy* with *Isoniazid (INH), Rifampin (RIF), & Ethambutol for 2mo followed by INH & RIF for 7 additional months*. Also *supplement w/ Vit B6, Pyridoxine!* to prevent INH-induced neurotoxicity -All 3 meds CAN cross the placenta, but are NOT assoc with significant fetal toxicity Note: Pyrazinamide, part of the 4-drug TB treatment given to /nonpregnant/ individuals, is generally NOT administered in pregnancy d/t uncertain teratogenic properties

Treatment of SUPRAVENTRICULAR TACHYCARDIA (HR>150/min)

If *stable*, *rate control with carotid massage or other vagal stimulation*; if unsuccessful, consider *ADENOSINE* if *regular, narrow QRS complex* -If *hemodynamically stable + Wide (>0.12 sec) Complex Tachycardia* --> Consider *Adenosine* if regular & monomorphic If *hemodynamically unstable*, perform *Synchronized Cardioversion* and IF have a *regular narrow complex, consider Adenosine*

TX of complete patellar tendon rupture?

Immediate management incl *immobilization of knee in extension, non-weight bearing status for the affected eg, & referral to an orthopedic specialist for Surgical Repair* -Surgical repair with *primary tendon repair* is the *TX of choice* and should be *performed promptly (e.g. within 10d) to optimize recovery of knee fxn & decr likelihood of long-term disability* (e.g. limited knee ROM, quadriceps muscle atrophy) -*PT* involves *incremental progression of weight bearing & ROM*, initiated after surgical repair is complete *TX of PARTIAL Patellar Tendon Rupture* (Extensor mechanism remains INTACT, unlike in complete tears) -Management typically *nonoperative*, with a period of *knee immobilization (e.g. 6wks) followed by PT* -While the knee is immobilized in extension, pts may be allowed to bear weight as tolerated, often with assistance of crutches

How does hypoxemia occur in COPD?

In COPD, hypoxemia is primarily d/t *ventilation-perfusion (V/Q) mismatch* causing a high A-a gradient -An adaptive response to hypoxemia consists of *hypoxic pulmonary vasoconstriction* which limits perfusion (decr Q) to hypoxic alveoli, raising the overall V/Q ratio and improving oxygenation -*Supplemental oxygen improves hypoxemia* primarily by delivering a *higher FiO2 to alveoli with low V/Q ratios* which results in much higher PAO2 to compensate the paradoxical incr in V/Q mismatch and results in overall improved arterial oxygenation -Supplemental O2 also *increases the A-a gradient* by leading to *reversal of hypoxic pulm vasoconstriction* which increases perfusion to low V/Q alveoli and consequently lowers the V/Q ratio which increases (i.e. /worsens/) V/Q mismatch and further increases (i.e. worsens) the A-a gradient

What happens if you give prune juice to an infant?

In infancy, prune juice acts as an *osmotic laxative* and *treats constipation* (hard stools), which can p/w bloody stools d/t anal fissuring Note: It is normal for infants to appear to strain while having a BM as long as stool consistency is soft

What should you do next if you see a young pt with oral infection by Candida when they have NOT had a recent history of antibiotics, inhaled corticosteroids, or systemic chemotherapy?

In the absence of these medications, or if risk factors for HIV are present, *oropharyngeal thrush* should *prompt investigation for HIV infection using a fourth-generation HIV test (p24 antigen and HIV-1/HIV-2 antibody)* and a *potassium hydroxide preparation (or Gram stain) of the mucosal scraping to confirm Candida*

What is the empiric ABX regimen given to [tunneled catheter] hemodialysis pts suspicious for catheter-related bloodstream infection?

Infxns usu caused by *coagulase-negative Staphylococci* or *Staph aureus*, but infxns with *gram-neg bacilli* also common -Initial workup: 2 sets of blood cultures, one from peripheral site, one from central tunneled catheter -*Empiric ABC therapy w/ VANCOMYCIN + CEFEPIME/GENTAMICIN* -Only remove catheter if: • Severe sepsis • Hemodynamic instability • Evidence of metastatic infection (e.g. endocarditis) • Pus at catheter exit site • Continued sx after 72hrs of empiric ABX Add *Capsofungin* to Empiric ABX regimen IF: On TPN, prolonged use of broad-spec ABX, hematologic malignancy, solid organ transplant, femoral catheterization, or Candida colonization at multiple sites

B12 deficiency leads to what complications?

Leads to *dementia and subacute combined degeneration (SCD)* that are /reversible/ with *vitamin supplementation* -SCD incl signs of dorsal spinal column dysfxn (e.g. impaired vibration, positive Romberg sign [fall over w/ eyes closed]) & lateral corticospinal tract abnormalities (e.g. spastic paresis, hyperreflexia)* -Causes *macrocytic, megaloblastic anemia* with *hypersegmented PMNs* due to *ineffective erythropoiesis* bc of *defective DNA synthesis with megaloblastic transformation of bone marrow and Intramedullary Hemolysis* -Intense erythroid hyperplasia w/o maturity, causing erythroid cell death in bone marrow -Markers of hemolytic anemia (e.g. *incr LDH, decr haptoglobin, incr indirect hyperbilirubinemia*) may become evident, but *reticulocyte response is absent* -Deficiency caused by malabsorption (eg, sprue, enteritis, Diphyllobothrium latum), lack of intrinsic factor (pernicious anemia, gastric bypass surgery), absence of terminal ileum (surgical resection, eg, for Crohn disease), or insufficient intake (eg, veganism). -Anti-intrinsic factor antibodies diagnostic for pernicious anemia.

Gynecomastia in men with small balls - Cause?

Likely *Klinefelter Syndrome (47, XXY)* -Commonly causes *gynecomastia in men&, and pts usu have *primary hypogonadism with small, firm, testes; LOW serum Testosterone, & ELEVATED LH levels* -Confirm DX with *Karyotype Analysis*

Which dairy products are lower in lactose and are usu less problematic compared to other high-lactose foods?

Low lactose: Cheese, live-culture yogurt High lactose: Milk, ice cream

Which MEN syndromes involve a Medullary Thyroid Cancer and Pheochromocytoma?

MEN 2A & 2B!

AE of Chronic Amiodarone Use

Make sure to check PFTs, LFTs, & TFTs when using amiodarone!! -Pulmonary fibrosis -Hepatotoxicity -Hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight) -Acts as a hapten (causing corneal deposits, blue/gray skin deposits resulting in photodermatitis) -Neurologic effects -Constipation -Cardiovascular effects: *Bradycardia, heart block, heart failure*

TX for minimal change disease?

Management is with *empiric immunosuppressive therapy w/ CORTICOSTEROIDS* to *counter T-cell dysregulation and cytokine mediated-damage* (e.g. *prednisone for 2-3mo*) *Minimal Change Disease*: Clinical DX, with *hypoalbuminemia, hyperlipidemia (incr total cholesterol), & proteinuria* causing *nephrotic syndrome* usu in children -Occurs *spontaneously or by infection* -D/t *cytokine-mediated podocyte foot process injury (effacement & fusion), leading to decr glomerular permeability (selective albuminuria)*, causing loss of protein incl albumin (*proteinuria w/ hypoalbuminemia*), leads to *decr capillary oncotic pressure & gravity-dependent edema* (e.g. periorbital, pretibial) -*Hyperlipidemia* d/t incr hepatic lipoprotein production in response to low oncotic pressure -*Blood pressure, complement levels, & creatinine usu normal* -Prognosis: *Over 90% achieve REMISSION WITH PHARMACOTHERAPY (corticosteroids), defined as /resolution of proteinuria/, where as only 5% of pts achieve spontaneous resolution w/o therapy* -Note that *despite treatment, the majority of pts will have ONE OR MORE RELAPSES OF DZ* so *frequent screening for urinary protein is required* -Children <5yo at highest risk for relapse, infxn is common trigger -*Relapses* usu /remain *steroid-responsive*/ -Renal *outcome is excellent* with maintenance of *normal renal fxn into adulthood*

How do you reduce the risk of rebleeding in pts with esophageal varices d/t portal HTN?

Medical treatment with *nonselective beta-blockers* (e.g. *propranolol, nadolol*) are *first-line*, bc they help *reduce pressure in the portal venous system* -The combination of beta-blockers and repeat surveillance endoscopy with band ligation as necessary, results in an even lower mortality rate than either tx alone

Why get an endometrial biopsy in a female pt with menopausal transition sx?

Menopausal transition is characterized by anovulatory bleeding, hot flashes, & sleeping difficulties prior to the cessation of menses. -Anovulatory bleeding (e.g. heavy, irregular bleeding) occurs d/t oocyte depletion and decr progesterone secretion - however, endometrium may continue to proliferate d/t unopposed estrogen secretion!! -Endometrial biopsy is indicated in *women ≥45yo with anovulatory bleeding* to evaluate for *endometrial hyperplasia or cancer*

What is a meta-analysis?

Meta-analysis is conducted by *pooling the data from several studies to perform an analysis and to increase statistical power* (i.e. *incr its ability to detect difference in outcome of interest b/w groups, if such a difference exists*) -If an outcome is rare or if the difference in outcomes b/w groups is small, then it's difficult for a single study - even a relatively large-scale one - to detect that difference, making it /unlikely that the results will reach statistical significance/ -This is where *meta-analysis* can be used to *incr the sample size, thereby increasing the power* of the analysis -*Major DISADVANTAGE of Meta-Analysis* includes *concomitant "pooling" of the biases and limitations of individual studies into one analysis*

What kind of ulcers would you use Misoprostol to treat?

Misoprostol is a prostaglandin that *inhibits gastric acid secretion & improves mucosal defenses* -It is used to *prevent ulcers assoc. w/ NSAID use* -It is *NOT routinely used to tx peptic ulcer dz assoc w/ H. pylori!!* *MISOPROSTOL TX NSAID-ULCERS*

How is viral conjunctivitis spread?

Most often present in school-aged children Viral shedding spread through EYE DRAINAGE -Pts highly contagious d/t large amount of virus in eye drainage, which is spread through contact with the drainage or through contaminated surfaces (touching/rubbing eyes) -Recommend: *Pts stay home (even if afebrile) until eye drainage resolves*. Other sx, morning crusty eyes or eye redness may persist longer than drainage, but do NOT contribute to infectivity

Number Needed to Treat Formula

NNT represents the Number of pts who need to be treated to prevent ONE bad outcome, assuming the TX is beneficial -NNT is the inverse of the absolute risk reduction *NNT = 1 / Absolute Risk Reduction (ARR)* *ARR = Control event rate - Experimental event rate*

Plantar Reflex in Adults

NORMAL --> Big toe points DOWN & digit flexion ABNORMAL (i.e. Positive Babinski Sign) --> Big toe points UP with FANNING of other toes

Statins are recommended for primary prevention of atherosclerotic cardiovascular disease in which population of pts?

Pts with *LDL ≥190 mg/dL* and in those *≥40yo with DM*

What factors are assoc w/ poor prognosis and increased risk of long-term disability in pts w/ acute low back pain?

Only a small number of pts (<20%) w/ acute back pain go on to develop chronic pain and long-term disability -*High-risk features* (so called yellow flags) *for prolonged disability* include *maladaptive coping behaviors, psychosocial comorbidities (lack social support), & high level of functional impairment* -Maladaptive coping behaviors incl *catastrophizing* (i.e. assuming the worst possible outcome) and *expectation poor recovery*

What do overlapping standard error of measurement bars suggest?

Overlapping SEM bars means a *non-statistically significant difference* between the two things being compared

How does *digoxin toxicity* present?

P/w *anorexia, fatigue, nausea, blurred vision, disturbed color perception, & cardiac arrhythmias* *Antidote* is *Digoxin-specific antibody (Fab)*

Guillain Barre Syndrome

P/w GI illness and then severe symmetric muscle weakness and absent deep tendon reflexes -Usu after *GI (e.g. Campylobacter)* or Respiratory infection, generating cross-reacting Ab to peripheral nerve components - resulting in *immune-mediated polyneuropathy* that leads to: *Symmetric ascending muscle weakness*; Paresthesias; *Dysautonomia* (e.g. tachycardia, urine retention) that can be life-threatening; *Decr or absent deep tendon reflexes* -GBS pts are at high risk for *rapid-onset respiratory failure* d/t resp m weakness -Frequent *measurement of vital capacity (tidal volume) & negative inspiratory force is required* to monitor resp status (not measuring peak expiratory flow rate, used in obstructive lung dzs); 30% of pts need mechanical ventilation! -TX: Plasma exchange (TPE) or IVIG -- give these if pt is non-ambulatory or if within 4wks of sx-onset -2wks progressive motor weakness that can lead to paralysis -2-4wks of plateaued sx -*Slow, spontaneous recovery over months* -*Time to recovery shortened using TPE or IVIG* by ~50%; but pts without intervention usu recover

β-blocker overdose

P/w bradycardia, atrioventricular block, hypotension, & diffuse wheezing -Intoxication w/ *CCBs, digoxin, & cholinergic agents* can ALSO cause similar sx, but /*wheezing*/ is /more specific for *β-blocker toxicity*/ -Most common presentation is *bradycardia & hypotension leading to cardiogenic shock* (e.g. cold, clammy extremities) -Other effects incl *hypoglycemia, bronchospasm/wheezing (β2-blockade), & neurologic dysfunction (e.g. delirium, seizures)* -First step in management is to *secure the airway & give isotonic fluid boluses* and *IV ATROPINE* for initial tx of hypotension & bradycardia -In /refractory or profound hypotension/, next step is to give *IV GLUCAGON* which increases the intracellular levels of cAMP and is *effective in treating both β-blocker AND CCB-toxicity* -Other therapies that can be used simultaneously or in succession incl *IV calcium, high doses of catecholamine vasopressors (epi or norepi [but this can cause arrhythmia]), high-dose insulin & glucose, and IV lipid emulsion therapy* (used to manage poisoning in lipophilic meds like β-blockers) Note: Cannot use Dobutamine in β-blocker overdose bc, even though it's an inotropic catecholamine w/ β-agonist effects, it can cause significant vasodilation w/ resulting worsening hypotension

Parvovirus B19 Presentation

P/w nonspecific flu-like sx (fever, myalgias) followed by variable sx depending on the age. Kids can get slapped cheek appearance (erythema infectiosum) and rarely arthralgias. Teens and adults can get *acute onset symmetric joint pain, swelling, & stiffness* in PIP and MCP joints a week after flu-like sx. May see a faint, erythematous, reticular rash, but most adults/teens don't get a rash. DX clinical but can confirm with serum serology Parvo B19 IgM antibodies TX supportive (NSAIDS); SELF-LIMITED. NO LONG-TERM SEQUELAE

Which cancers *commonly metastasize to the spinal column*?

PROSTATE BREAST LUNG NON-HODGKIN LYMPHOMA RENAL CELL CARCINOMA

Stages of Avascular Necrosis

Precollapse: ●Stage I - Normal radiograph, abnormal MRI findings ●*Stage II (TX with Core Decompression)* - No crescent sign, radiographic evidence of sclerosis, osteolysis or focal osteoporosis; *positive radiographs without femoral head collapse* Collapse: ●Stage III - Subchondral fracture, fracture in the necrotic portion and/or flattening of the femoral head on radiograph or on radiograph or CT •IIIA - Femoral head depression ≤ 2 mm •IIIB - Femoral head depression > 2 mm ●*Stage IV (TX with Joint Replacement)*- Evidence of osteoarthritis, *joint space narrowing*, degenerative acetabular change, *flattening of femoral head*

Cough-Variant Asthma

Presents w/ *chronic nonproductive cough typically worse at night* (often accompanied by *chest tightness*) and *triggered by exercise, forced expiration, and allergen exposure* (e.g. dust mites, mold). -These pts usu *lack classic asthma sx* (e.g. wheezing, rhonchi SOB). -*Physical exam is largely unremarkable*, even during periods of active sx *TX same as classic asthma*: *Bronchodilators, inhaled corticosteroids* -^If refractory to these, try *leukotriene-receptor antagonists (e.g. montelukast)*

Pustular Psoriasis of Pregnancy

Previously called *Impetigo herpetiformis* -Typically *presents as erythematous plaques surrounded by sterile pustules* -Lesions *Begin on the Skin Folds (e.g. axilla, inframammary) and spread OUTWARD to the Trunk and Extremities* -It is a *RARE DX* that typically causes *additional constitutional sx* (e.g. fever, malaise, tachycardia)

TSH, free T3, and T4 levels in Primary Hypothyroidism vs Hyperthyroidism

Primary Hypothyroidism -Elevated TSH -Decreased free T3 and T4 -Also Hypercholesterolemia d/t decr LDL-receptor expression Primary Hyperthyroidism -Low TSH -Increased free or total T3 and T4 -Also Hypocholesterolemia d/t incr LDL-receptor expression

Type 1 error (α)

Probability of rejecting a null hypothesis when the null hypothesis is TRUE

Should you give iron supplementation to sickle cell disease pts who are pregnant?

Pts with SCD typically have *excess iron* from *frequent hemolysis & transfusions* -Therefore, supplementation can result in *iron overload* and is recommended only if evaluation shows iron deficiency

Primary Biliary Cholangitis (PBC)

Progressive autoimmune dz characterized by *fibrosis & obliteration of intrahepatic bile ducts* potentially leading to *cirrhosis* most common in *women* of Northern European heritage, typical onset age 30-65 *Symptoms/Signs* -Fatigue & pruritus (most common) -Inflammatory arthritis (40-70%) -Hyperpigmented skin (25-50%) -RUQ Discomfort (10%) -Xanthelasmata (10%) & Xanthomata (5%) *Diagnosis* -*Elevated Alkaline Phosphatase* -*Positive ANTIMITOCHONDRIAL Antibody (AMA+)* (highly sensitive [95%] and specific for PBC!!) -Liver biopsy if AMA negative *TX* -*Ursodeoxycholic acid* (/helps to slow the progression of dz/ & improve transplant-free survival) -Liver transplant in advanced cirrhosis (curative for PBC, but can *recur* after transplant but at much slower progression) *Complications of PBC* -*OSTEOPENIA & OSTEOPOROSIS* metabolic bone diseases are frequent complications -Unknown reason though -Vitamin D levels usu normal, except those w/ very advanced dz; screen using bone densitometry -Calcium & vit D supplements recommended, and Bisphosphonates (alendronate) for those w/ osteoporosis

Neonatal displaced clavicular fracture

Pt Signs: *Pain with upper extremity movement, crepitus w/ edema over clavicle*; Crying every time baby picked up, fussy; palmar grasp reflex present & symmetric. -The *clavicle* is the *MC fractured bone in newborns* -*RF*: *Macrosomia, shoulder dystocia, & device-assisted delivery (e.g. forceps, vacuum)* ---BUT, many newborns *do NOT have RF* -Exam: *Pain with passive movement of ipsilateral upper extremity & crepitus & swelling over the clavicle* -The Moro reflex may be asymmetric d/t clavicular fracture or a concomitant brachial plexus injury -Brachial plexus palsy is DX clinically by the presence of arm weakness in a given cervical nerve distribution -A *plain radiograph Confirms the DX* of a fracture -Management: *Gentle Handling & Parental Reassurance*; to prevent painful movement, the affected arm can be flexed to 90° at the elbow and pinned to shirt -The fracture *heals spontaneously over several weeks W/O sequelae* (surgery, physical therapy, & casting are NOT indicated) *Moro reflex*: Normal reflex for an infant when he or she is startled or feels like they are falling; he will extend his arms and legs and neck and then rapidly bring his arms together.

TTP Mechanism

Pt p/w *fatigue & bruising, with MAHA, severe thrombocytopenia, & normal coagulation studies --> TTP* -TTP is an *ACQUIRED SYNDROME d/t FORMATION of AUTOANTIBODIES AGAINST ADAMTS13, a Plasma Metalloprotease* -- *responsible for cleaving ultralarge strings of von Willebrand factor (vWF) off the vascular endothelial wall* -When levels of *ADAMTS13 are severely deficient, uncleaved strings of vWF TRAP& ACTIVATE PLATELETS, resulting in DiffuseMicrovascular Thrombi* causing: • Platelet CONSUMPTION--> *SEVERE THROMBOCYTOPENIA* • Intravascular RBC Shearing --> *Signs of MAHA - schistocytes, Incr Indirect Bilirubin, Incr LDH, Incr Aminotransferases* • *Organ Ischemia* --> *Neurologic & Renal dysfunction* -Pts who have clinical & lab data that support the DX of TTP *require urgent TX w/ PLASMA EXCHANGE* --which *removes the AUTOANTIBODY against ADAMTS13 & REPLENISHES the enzyme with ADAMTS13 form donor serum* Note: *Antibodies against platelet antigens* are responsible for *Immune Thrombocytopenia (ITP, recent viral infection) *, NOT TTP, and may also cause *thrombocytopenia (PLT<100,000), bruising, petechiae*, but *NO MAHA! and no systemic disease (fever, malar rash, joint stiffness)*

Legionnaire's Disease (Pneumonia)

Pt w/ bilateral lung infiltrates, confusion, diarrhea, and hyponatremia following travel -Travel-assoc Legionnaire's dz d/t contaminated water supplies is often linked to cruise ships and hotels -SX that help distinguish an Atypical PNA d/t Legionella pneumophila from other causes of community-acquired PNA (CAP) include: *High-grade fever (>38.3C [101.8F]), GI sx (e.g. diarrhea), & Neurologic Sx (e.g. confusion, ataxia)* - HIGH FEVER, N/V/D, & AMS -Lung exam shows *rales* and CXR often reveals *patchy unilobar or interstitial infiltrates* -*HYPONATREMIA* and *Hepatic Dysfunction* are common -Legionella pneumophila is a *Gram-Negative Rod*that stains poorly bc it is mostly *intracellular*; therefore, *sputum Gram stain showing many neutrophils but no organisms* is also characteristic -Definitive DX made by *culture combined with urinary antigen testing* -Legionnaire's Dz is TX with antibiotics that can reach intracellularly - Newer *Macrolides (e.g. Azithromycin) or Fluoroquinolones (e.g. Levofloxacin)* - Fluoroquinolones like /Levo are favored when illness is severe enough to warrant admission/

Serotonin Syndrome (SS)

Pt: Anxiety, confusion, tremor, diaphoretic, & hyperreflexia -Likely d/t a *drug interaction* b/w a *MAOI* (e.g. Phenelzine) and an *SSRI* (e.g. Fluoxetine) -The recommended washout period for most antidepressants prior to starting tx w/ MAOI is *14d* -However, d/t fluoxetine's long half-life, it is recommended that *≥5wks elapse b/w stopping fluoxetine & starting MAOI tx* Sx of SS: -Classic triad of *mental status changes* (e.g. anxiety, delirium, confusion, restlessness), *autonomic dysregulation* (e.g. diaphoresis, tachycardia, HTN, hyperthermia, diarrhea, hyperactive bowel sounds, mydriasis), and *neuromuscular hyperactivity* (e.g. *hyperreflexia*, tremor, rigidity, *myoclonus* ocular clous) -SS diagnosed clinically, and lab tests are used to r/o other etiologies -SS usu occurs d/t inadvertent interactions b/w drugs, therapeutic use of multiple serotonergic agents, or serotonergic medication overdose.

Aortic Coarctation - Pediatric Presentation

Pts may p/w *right upper extremity hypertension*, *lower extremity claudication & hypotension*, & a *continuous* heart *murmur best heard over the left interscapular area* -Congenital narrowing of the aorta, located distal to the left subclavian artery branch -Though often *assoc w/ Turner Syndrome*, it *most commonly occurs sporadically* and affects *male* pts -Findings are caused by *impaired perfusion distal to the coarctation* with the degree of narrowing determining sx severity -Neonates w/ *severe coarctation* are at risk for *life-threatening heart failure & shock after patent ductus arteriosus closure*; while *milder narrowing* is often *ASx* diagnosed later in childhood -Inadequate lower extremity perfusion causes leg pain during exercise (*claudication*) -*Upper extremity HYPERtension with Lower extremity HYPOtension w/ weak/delayed distal pulses* (brachiofemoral delay) -Types of Murmurs Auscultated: • *Continuous murmur* due to *blood flow through collateral circulation* at left interscapular region • *Systolic murmur* at the *left sternal border* d/t *turbulent flow across coarction* • *NO murmur* if no other cardiac defects (e.g. bicuspid aortic valve) present -*CXR* reveals characteristic *rib notching* from *collateral vessels* and a figure "3" sign at the site of aortic narrowing -*ECHO Confirms DX*

What is the presentation and TX for acute symptomatic hypocalcemia?

Pts p/w *oral paresthesias, carpopedal spasm, tetany, cramping, seizures* TX with *IV CALCIUM GLUCONATE*

HIV and risk for cardiovascular disease?

Pts w/ HIV are at *increased risk for cardiovascular disease* and require *screening for HTN, HLD, DM, & tobacco use* (No need for screening echo, however)

Standardized Mortality Ratio (SMR)

Quantifies mortality in a specific group compared to the general pop. -*SMR* is the *ratio of observed to expected number of deaths* in a specific group of the general pop under the assumption that mortality rates for the group are the same as for the gen pop -*Expected # of deaths* is calculated based on *age-specific mortality rates in a standard reference population* --this value is then contrasted to the # of observed deaths in the specific group -SMR is used in *occupational studies* to determine whether the observed # of deaths in a group exposed to a certain RF exceeds what would be expected in a similar gen pop w/o RF exposure *SMR <1* indicates # of observed deaths in study group is *lower* than what is expected *SMR=1* indicates # of observed deaths in study group *equals* what's expected *SMR >1* indicates # of observed deaths in study group is *greater* than what is expected A confidence interval that does not include the null value (1.0 for SMRs) indicates a /statistically significant difference/ between the observed and expected # of deaths

Person with high-risk exposure to HIV - when to screen?

Recommended *screening test for HIV combines detection of HIV antigen (p24) and HIV-1/HIV-2 antibodies* --though excellent sensitivity and specificity, the antigen & antibody titers *are too low to detect in the first 1-4wks of infection (window period)* *Screening tests* are almost always *negative shortly after infection* as *titers are too low to be detected* *False-Negative results may occur during first 4wks of infection due to low titers of antigen and antibody (window period)*, so *REPEAT HIV SCREENING TEST >4WKS FROM EXPOSURE*

Which labs should you order for the initial workup of suspected cognitive impairment/dementia?

Routine: *CBC, Vit B12, TSH, CMP* Selective (specific RF): *Folate, Syphilis, Vit D level* Atypical (early onset): CSF -Dementia should be suspected in pts w/ evidence of *progressive cognitive decline leading to functional impairment in ADLs* -All should undergo *routine cognitive testing* (*Montreal Cognitive Assessment*) to establish an objective measure of cognitive deficit, as well as *routine labs* to r/o reversible causes of dementia -Mini-mental state examination (MMSE) score of <24/30 is suggestive of mild cognitive impairment -Montreal cognitive assessment score of <26/30 and Mini-Cog abnormal 3-word recall &/or clock-drawing test) is also suggestive -Most clinicians also routinely order an MRI Brain or CT (EEG ordered in atypical cases)

What does adenosine do to heart rate?

SLOWS IT DOWN IV Adenosine is used in hemodynamically stable pts with narrow QRS tachycardia consistent with Paroxysmal Supraventricular Tachycardia Synchronized Cardioversion is used in pts with persistent tachyarrhythmia (narrow or wide complex) causing hemodynamic instability

How to TX *Trichomoniasis* in *breastfeeding moms*?

STI! *First-line ABX regimen* is *SINGLE-DOSE ORAL METRONIDAZOLE, 2 GRAMS* -*Metronidazole CAN pass into breast milk!!* And can cause *loose stools & candidiasis* in exposed infants -*To avoid infant exposure*, *breast milk should be expressed and discarded for 24hrs after dose administration* -Trichomoniasis is characterized by vulvovaginal pruritus (edema) & erythema; a thin, frothy, yellow-green, malodorous discharge, and punctate hemorrhages in the vagina or on cervix (strawberry cervix)

TX of Latent TB

Several rifamycin-based regimens taken for 3-4mo e.g. -Daily rifampin x4mo -Daily isoniazid && rifampin x3mo

What organisms most frequently cause Infectious Urethritis in young male pts? How to diagnose and empirically treat?

Sexually transmitted: -Neisseria gonorrhoeae -Chlamydia trachomatis -Mycoplasma genitalium DX w/ NAAT testing, but urethral fluid Gram stain can quickly differentiate gonococcal (leukocytes with intracellular gram-negative diplococci) from nongonococcal (aseptic, leukocytes with no visible organisms) urethritis *Nongonococcal urethritis* is empirically TX w/ *Azithromycin or Doxycycline Monotherapy* *Gonococcal urethritis* is empirically TX w/ *Ceftriaxone Monotherapy* Note: If have continued urethritis sx after initial tx, can be d/t reinfection, med noncompliance, or resistant organism. Do a *repeat urethral fluid Gram stain* and *NAAT if positive* for gonorrhea, chlamydia, mycoplasma genitalium, & trichomonas -Most cases of nongonococcal urethritis not effectively tx w/ Azithromycin are d/t *C. trachomatis resistance, or M. genitalium, or T. vaginalis infection* -*Persistent C. trachomatis TX with Doxycycline, M. genitalium with Moxifloxacin, & T. vaginalis w/ Metronidazole

Adverse Effects of Prolonged Glucocorticoid Therapy

Skin: Atrophy, easy bruising d/t decr collagen & fibroblast formation Endocrine/Metabolic: Adrenal insufficiency; Hyperglycemia, wt gain w/ fat redistribution (central obesity, buffalo hump); Linear growth impairment in kids; Osteoporosis d/t HPA axis suppression, adrenal suppression, insulin resistance, decr pulsatile growth hormone release, Incr resorption & decr bone formation Ophthalmologic: Cataracts (screen w/ ophthalmologic exams) d/t changes in lens epithelial gene transcription Neurologic: Behavior & sleep disturbances d/t glucocorticoid-receptor dysfunction Immune: Neutrophilia; Immunosuppression (incr infection risk) d/t PMN demargination & T-cell apoptosis GI: Gastritis, ulcers, GI bleeding d/t prostaglandin inhibition Cardio: Hypertension d/t sodium retention

Stages of Lyme Disease

Stage 1—early localized: erythema migrans (typical "bulls-eye" configuration is pathognomonic but not always present), flulike symptoms. Stage 2—early disseminated: secondary lesions, carditis, AV block, facial nerve (Bell) palsy, migratory myalgias/transient arthritis. Stage 3—late disseminated: encephalopathy, chronic arthritis, peripheral neuropathy. TX: *Doxycycline (1st line); Amoxicillin (pregnant patients, children <8yo); Ceftriaxone if IV* therapy required

What is the standard caloric intake recommended for enteral feeding (i.e. by G-tube) in pts with an /intact/ functional gastrointestinal system?

Standard composition is *30 kcal/kg/day and 1 g/kg/day of protein* is satisfactory for most pts with adequate baseline nutrition Use a slightly *lower amount* for pts w/ preexisting *severe malnutrition* in order to *prevent refeeding syndrome* (e.g. 15 kcal/kg/day with 1 g/kg/day of protein)

Necrotizing Fasciitis

Sx: *fever, hypotension, swelling, & erythema* of affected area, with *incr tenderness (painful) to palpation* than is expected after visual inspection -Nec fasc is a *fulminant infxn of subQ tissue that spreads rapidly along the fascial planes & leads to extensive tissue necrosis and shock* -TWO types of nec fasc: *Type I*: Less common, and usu seen in pts w/ *underlying Diabetes or Peripheral Vascular DZ*. Usu it's a *polymicrobial infxn* - often isolate Staph aureus, Bacteroides fragilis, E. coli, Group A Strep (Strep pyogenes), and Prevotella spp. *Type II*: More common form! Usu in pts w/ NO concurrent comorbidities. Pts report *hx of laceration, blunt trauma, or surgical procedure* as their predisposing factor. Often caused by *Group A Strep (Strep pyogenes)* -*Crepitus* is more common if *anaerobic* organisms like *Clostridium perfringens or Bacteroides fragilis* are involved d/t gas production -Need to do *URGENT, aggressive Surgical Exploration & Debridement* of the involved tissue to reduce M&M if you suspect nec fasc -- this also helps provide tissue samples for diagnostic purposes -Additionally, provide appropriate *ABX & Hemodynamic Support* -When don't know what organism is involved, *give broad-spec ABX* incl, *Pip-tazo or a Carbapenem (imipenem, meropenem)* to cover Grp A Strep and anaerobes, give *Vancomycin* to cover S. aureus & MRSA, and give *Clindamycin* to inhibit toxin formation by strep/staph spp -Once *culture* isolates organism, can *narrow ABX therapy* Note: Pseudomonas can produce nec fasc in /immunocompromised/ pts, not in otherwise healthy adults Note: CT might help detect gas in subQ tissue, but surgery shouldn't be delayed to get imaging in pts who are critically unstable

TX of Schizophrenics When to stop antipsychotics?

TX with *antipsychotic medications, adjunctive psychosocial interventions* (e.g. social skills training, CBT, family interventions) *Antipsychotic [atypical type] medication should be maintained INDEFINITELY in pts w/ schizophrenia - including those experiencing their first psychotic episode* (Tx with *RISPERIDONE*) -Many pts initially show rapid improvement w/ antipsychotics, with even further symptomatic & functional improvement on maintenance antipsychotic therapy over those next several months -Those who discontinue meds have higher rates of relapse --> rehospitalization, overall poor outcome

What is the Hawthorne effect?

The *HAWTHORNE EFFECT* is when *participants MODIFY THEIR BEHAVIOR d/t Awareness that they are being studied*

When should you *add* an *Aldosterone Antagonist* (*Spironolactone, Eplerenone*) to *initial optimized medical therapy* for pts with *heart failure with reduced ejection fraction (HFrEF)*?

The *INITIAL optimized medical therapy for HFrEF, LVEF ≤40% incl:* ● *Angiotensin System Neprilysin Inhibitor* (e.g. *Sacubitril-Valsartan*); *ACEI or ARBs are alternatives* ● *β blocker* (e.g. *Metoprolol Succinate*) ● *Loop Diuretic* (e.g. *Furosemide*) --given when *symptomatic volume overload* -You should *add an Aldosterone Antagonist (Spironolactone, Eplerenone)* when pt has *Persistent Sx despite 3-drug initial regimen and when LVEF ≤35% on recent echocardiogram* -*Aldosterone antagonistas IMPROVE MORTALITY & Reduce HF-related Hospitalization* and are therefore *indicated in the following populations:* ● *NYHA Class II-IV HF (essentially ANY Sx) & LVEF ≤35%* ● *STEMI complicated by LVEF ≤40% & Either HF Sx or Comorbid Diabetes* -D/t *risk of Hyperkalemia, aldosterone antagonists should be Avoided in pts w/ underlying Hyperkalemia (Serum K >5) or Advanced Renal Failure (Cr clearance <30mL/min)* -Note: Spironolactone (but not eplerenone) is assoc w/ endocrine AE (gynecomastia, decr libido), sometimes use-limiting

How does *severe Aortic Stenosis* sound on auscultation?

The following findings are consistent with *Severe AS*: -A *soft/low-intensity, single second heart sound (S2) heard during Inspiration* (MOST SPECIFIC SIGN) d/t simultaneous closure of the aortic and pulmonic valves during S2 during inspiration -A *delayed & diminished carotid pulse* (*Parvus et Tardus*) -*LOUD and LATE-Peaking SYSTOLIC murmur* -An *Early-peaking of an AS murmur* is suggestive of *Mild to Moderate AS* bc less LV pressure (attained in early ventricular systole) is needed to overcome the valvular stenosis

How to definitively diagnose cause of aspiration pneumonia?

Though a *bedside swallowing assessment* may be helpful, *definitive diagnosis is made w/ Videofluoroscopic Swallowing Study* -Undetected dysphagia (p/w oropharyngeal sx like dysarthria & drooling) can lead to weight loss and frequent aspiration pneumonia -- often a freq complication of Parkinson's dz -A multidisciplinary intervention (dietary service, nursing, speech therapy) is required to address nutrition & reduce the risk for recurrent aspiration PNA -- e.g. switching to thickened liquids & a modified swallowing technique

What is CURB-65? How is it used?

To *determine the appropriate clinical setting for TX of Community Acquired PNA* 1 point for each of the following: -*C*onfusion -*U*rea >20 mg/dL -*R*espirations ≥30/min -*B*lood pressure (systolic <90 or diastolic <60) -*A*ge ≥65yo 0 pts: Low mortality —> Outpatient TX 1-2 pts: Intermediate mortality —> Likely inpatient TX 3-4 pts: High mortality —> Urgent inpatient admission; possibly ICU is score >4pts

What is the purpose of case-control studies?

To identify potential risk factors for uncommon (rare) diseases

Why should *antidepressants be AVOIDED in bipolar disorders?*

Use of antidepressants can *destabilize mood, and INDUCE MANIA*

When to do heterophile antibody testing?

Used to diagnose *EBV-causing infectious mononucleosis* -Pts would present with *fever, pharyngitis, [diffuse] lymphadenopathy, and fatigue*

How do iron-deficient infants present?

Usu with * ASX microcytic anemia!*. If *SX, p/w lethargy, irritability, conjunctival pallor, & a precordial systolic flow murmur. Severe anemia --> Cardiomegaly & Tachypnea* -D/t *inadequate dietary iron*, often seen in *infants >6mo who don't eat enough iron-rich foods or in infants who drink cow's milk before age 1* -*Premature* infants also *at risk d/t inadequate iron stores* -*LOW MCV <11 g/dL; Elevated RBC distribution width (INCR RDW), & LOW RBC [total] count* -*Mentzer Index (MCV/RBC) >13* --> *Suggests Iron Deficiency, rather than α & β thalassemias (which have a Mentzer Index <13)* -Although *breastfeeding is recommended for at least the First Year of Life, IRON SUPPLEMENTATION* (e.g. Iron-fortified cereals, pureed meat, Vitamin C-rich foods [to enhance iron absorption]) *should be introduced ~@6mo* (≥3 servings) -TX: Those already iron deficient, will need *ORAL IRON SUPPLEMENTATION* to replenish iron stores.

Classic triad of Wernicke Encephalopathy and its cause

Wernicke Encephalopathy is caused by *THIAMINE DEFICIENCY (VITAMIN B1, water-soluble)* and causes a triad of *AMS, GAIT ATAXIA, OPTHALMOPLEGIA* (e.g. paralysis or weakness of eye mm; nystagmus, etc.)

When should pregnant women receive their Tdap shots?

Women should receive the *tetanus toxoid, diphtheria toxoid, and acellular pertussis (Tdap) vaccine BETWEEN 27-36WKS GESTATION* -- NOT at the time of conception -- *REGARDLESS of their vaccination status* -Maternal immune response produces antibodies (IgG) that maximally cross the placenta in the third trimester, conferring protection to the infant

Cold Caloric Stimulation to test the Oculovestibular Reflex

Works by irrigating auditory canal with cold water and observing the reflexive eye movement A NORMAL response is characterized by a *transient, conjugate, slow deviation of gaze TO the side of stimulus (brainstem-mediated), followed by saccadic correction to the midline (cortical correction)* i.e. Water inserted in right ear causes both eyes to deviate to the right before slowly correcting back to the midline. A caloric response cannot be voluntarily suppressed; therefore, the normal oculovestibular rxn strongly suggests psychogenic coma (unconscious, unresponsive) The cold caloric response is also present in conscious people, producing not only deviation of the eyes towards the simulated ear, but also nystagmus )with the fast phase away from the irrigated side), severe vertigo, N/V. If nystagmus occurs, the pt is awake and not truly in a coma - can be a useful confirmatory test for psychogenic unresponsivelness

Do uncircumcised boys have an increased risk for UTI during infancy compared to circumcised boys?

YES!

Which are the standard pediatric immunizations in the US?

_*Inactivated (killed)*_ -Polio -Hepatitis A -Influenza (injection) _*Toxoid (inactivated toxin)*_ -Diphtheria, tetanus _*Live Attenuated*_ -Rotavirus -Measles, Mumps, Rubella -Varicella _*Subunit/Conjugate*_ -Hepatitis B -Pertussis -H. flu type B -Pneumococcal -Meningococcal -HPV

Empiric TX of Community Acquired Pneumonia (CAP)

_*Outpatient*_ -Macrolide or Doxycycline (healthy) -Fluoroquinolone* or Beta-lactam + Macrolide (comorbidities) _*Inpatient (non-ICU)*_ -Fluoroquinolone* (IV) -Beta-lactam + Macrolide (IV) _*Inpatient (ICU)*_ -Beta-lactam + Macrolide (IV) -Beta-lactam + Fluoroquinolone* (IV) *Respiratory Fluoroquinolones (e.g. Levo, Moxi) -Anti-pneumococcal beta-lactam (e.g. Ceftriaxone) -Macrolide (e.g. Azithromycin)

Thrombotic Thrombocytopenic Purpura

_Pathophysiology_ -TTP is d/t *decr ADAMTS13 activity* --> *decr degradation of vWF multimers* --> *incr large vWF multimers* --> *incr PLT adhesion & aggregation* --> *disseminated microvascular thrombosis* (ADAMTS13 is a vWF-cleaving protease) -*Acquired* (autoantibody) or *Hereditary* -*PREGNANCY* is assoc w/ an ADAMTS13 deficiency that becomes *more pronounced with incr gestational age and persists into postpartum period and can cause TTP!* _Clinical Features_ -Kidney failure -Neurologic manifestations (e.g. coma, confusion, AMS, seizure) -Fever -Abdominal pain/Nausea (GI sx) -Petechial rash (microangiopathic thrombotic clots) _Lab Abnormalities_ -*Hemolytic anemia* (*Incr LDH, Decr Haptoglobin, Schistocytes on PBS*) --> can cause hyperbilirubinemia & scleral icterus! -*Thrombocytopenia* -*Elevated T. bili* _Management_ -*Emergent Plasma Exchange (Plasmapheresis)* bc TTP is life-threatening! -Steroids

Diabetic Ketoacidosis in Children

__*Clinical features*__: -Polyuria/nocturia -Polydipsia/polyphagia -Vomiting, abdo pain -Wt loss, fatigue -Kussmaul respirations (deep rapid breathing) -Dehydration __*Lab findings*__: -Glucose >200 mg/dL -Bicarb <15 mEq/L -pH <7.3 -Anion gap >14 -Serum/urine ketones __*Management*__: -10 mL/kg isotonic fluid bolus over 1hr -Insulin infusion + isotonic fluids with potassium __*Complications*__: -Cerebral edema

Food Protein-Induced Allergic Proctocolitis - General

e.g. *Blood-streaked stools in a Well-appearing infant age <6mo is most commonly d/t Anal Fissures or Food Protein-Induced Allergic Proctocolitis (FPIAP)* -- Absence of a fissure and *presence of mucus in stool makes FPIAP likely* -FPIAP is a *Benign, SELF-LIMITED NON-IgE-Mediated Rxn MCC by COW'S MILK PROTEINS (casein, whey)*, which are *typically found in Standard Formulas && in Breastmilk (D/T MATERNAL DAIRY INTAKE)* -*SX dev weeks to months AFTER initial exposure to the offending food protein* -MC presentation is at *Age 1-4WKS w/ painLESS, Blood-Streaked Stools that may be Loose & Contain Mucus; Hemoccult Test Positive* -FPIAP is a *Clinical DX* -*TX involves Removal of the Offending Food Protein from the Infant's diet* -*Breastfeeding can CONTINUE if desired Following MATERNAL ELIMINATION OF DAIRY from her diet* -Sequential maternal elimination of other potential allergens (e.g. eggs, soy) is reserved for infants w/ persistent sx to avoid a significantly-restrictive maternal diet -*Alternatively, Infants can be SWITCHED to an EXTENSIVELY HYDROLYZED FORMULA containing Predigested Proteins*, BUT a *soy-based formula is NOT Recommended* d/t *potential cross-reactivity b/w cow's milk & soy proteins* -FPIAP is a *benign* condition of infancy *with NO long-term sequelae* and are *NOT at incr risk of dev chronic GI conditions such as IBD* -*Blood-streaked stool SX Resolution within 2wks of dietary elimination of the food allergen, and repeat hemoccult testing for microscopic blood is NOT usu req* -*Almost all pts can Tolerate the offending protein (e.g. milk, yogurt, soy) by Age 1yo, when gradual reintroduction of such foods is recommended* -*Dev of an IgE-mediated food allergy is Extremely RARE* and *Anaphylaxis would NOT be expected* upon re-exposure to cow's milk

Hookworm Infections

e.g. *Child p/w abdo sx (discomfort, diarrhea, tenderness, distention, hyperactive bowel sounds), poor growth (reduced height and weight percentiles), eosinophilia, & [microcytic] anemia* -Hookworms are *intestinal nematodes* (e.g. *Ancyclostoma duodenale, Necator americanus*) *prevalent in Developing Tropical or Subtropical nations* -Eggs shed into ground, hatch when moist, larvae invade human hosts thru bare feet or ingestion, and migrate thru the lungs (often causing a transient nonproductive cough) to the pharynx, where larvae are swallowed and complete their maturation in the gut; adult worms attach to epithelial cells in the small intestine, and feed on capillary blood -Hookworm infection is *often ASX*; with *increasing worm burden, pts have Nonspecific GI SX (diarrhea, abdo pain, distension) OR, rarely, Obstruction* -After several *months,* *IRON DEFICIENCY ANEMIA develops* -*EOSINIPHILIA* is commonly part of the body's immunologic response to organisms - helpful to distinguish hookworm infxn from other causes of chronic diarrhea -*Stool OVA & PARASITE Testing* is *very sensitive* for *hookworm infxn d/t HIGH worm & egg burden in symptomatic hosts* -*Antiparasitic TX (ALBENDAZOLE, NITAZOXANIDE) is CURATIVE,* although *reinfection is common in endemic areas*

*Pregnancy-induced pruritus/skin changes*

e.g. *Intense abdominal pruritus with no primary underlying skin lesion* -Common, *benign* condition that typically p/w during the *third trimester d/t dry skin*; *w/ localized, focal pruritus over the abdomen without an underlying primary skin lesion* -Scratching can cause *secondary, linear excoriations* -Common pruritic locations are the *scalp, anus, vulva, & abdomen* -*TX* options incl *oatmeal baths, UV light exposure, & antihistamines* -Pregnancy-related pruritus does NOT incr risk for pregnancy complications -Sx managed expectantly -Other *normal skin changes in pregnancy* incl *abdo striae, hyperpigmentation (e.g. linea nigra, melasma), & incr nail & hair growth* Note: *Intrahepatic Cholestasis of Pregnancy* has *generalized pruritus in the absence of a rash, most intense on palms & soles, with elevated serum bile acid levels*; *Incr risk for IUFD, management incl Delivery @37wks*; *definitive TX for intrahepatic cholestasis of pregnancy IS Delivery, however, Ursodeoxycholic acid alleviates assoc pruritus by decr both cholesterol reabsorption from small intestine & hepatic excretion of cholesterol*; these changes cause a decr in the [cholesterol] in bile & an increase in the flow of bile

Narcolepsy

e.g. *Young* pt with *fragmented sleep, hypnagogic hallucinations, & sudden onset of sleep during the day* -*Narcolepsy: Recurrent lapses into sleep or napping multiple times within the same day, occurring at least 3x weekly for 3mo and ≥1 of the following: Cataplexy; Hypocretin-1 Deficiency by CSF analysis; REM sleep latency ≤15mins* (DSM-5) -*Typical age of onset* for narcolepsy is *late teens to early 20s* and can cause *excessive daytime sleepiness* -*POLYSOMNOGRAPHY (SLEEP STUDY) can DX Narcolepsy*--characteristic findings incl*multiple spontaneous awakenings and reduced sleep efficiency* (total sleep time/total recording time) *and reduced latency of rapid eye movement (REM) sleep* -Polysomnography can also excl other causes of excessive daytime sleepiness, like sleep apnea -*TX* is focused on *reducing daytime sleepiness* • Older stimulant medications (Methylphenidate, Amphetamines) are Effective BUT can be Highly Addictive and have severe AE • *MODAFINIL* is a *novel stimulant w/ better AE profile and lower abuse potential* and is *First-line Med for Narcolepsy* • *Nonpharm Interventions* incl *scheduled naps during day and good sleep hygiene -*Cataplexy* is the *sudden onset of muscle weakness, often triggered by Intense Emotional Episodes (e.g. anger, laughing, surprise)* and is a *common sx of Narcolepsy (70% of pts)* -Although stimulants and behavioral interventions are imp initial steps in TX of sleepiness assoc w/ Narcolepsy, they may be Insufficient for Management of Cataplexy -*Cataplexy can be TX w/ a SNRI (Venlafaxine) or SSRI, and/or TCA; Sodium Oxybate* can improve nocturnal sleep, relieve excessive daytime sleepiness, and has anti-cataplectic properties but is rarely used d/t abuse potential and regulations Note: *Hypnagogic Hallucinations* (e.g. feelings of people walking around, hearing one's name called when just falling asleep) are *NOT evidence of a psychiatric dz, but are Characteristic for Narcolepsy*; likely to result from a *combo of REM sleep dreaming & wakefulness*

Acute HIV Infection - Manifestations

e.g. *Young* pt with a *wide range of nonspecific Sx* and has had *significant weight loss* -*Acute HIV* is marked by *dramatic viremia 2-4wks after HIV viral acquisition PRIOR to the onset of HIV-specific humoral immunity* -Pts may have *few or no Sx or may dev a Mononucleosis-Like Illness* that incl *fever, lymphadenopathy, weight loss, sore throat, myalgias, diarrhea, and HA* -Although these *manifestations are Nonspecific*, *PROLONGED SYMPTOMS* or the *presence of Mucocutaneous Ulcers or Generalized Rash should ALWAYS Raise the Suspicion for HIV* -The pt should give a *detailed sexual history* including *# of partners, condom use, sex for money, MSM, & STDs* -A *prior/current Hx of IVDU* should also be noted -*DX of Acute HIV* is typically made with a *combination of Fourth-Generation HIV Test & HIV Viral Load* -Although less common in Acute HIV, *Seborrheic Dermatitis (dandruff, scaly facial rash) occurs frequently in HIV pts* Note: Poor nutrition may result in vitamin deficiency &/or weight loss, but is unlikely to cause such prominent acute symptoms (e.g. intermittent fevers)

Preeclampsia with Severe Features

e.g. 37wks gestation, BP ≥160/110, proteinuria, & signs of end-organ damage (e.g. HA, visual sx) -Severe elevations in BP incr risk of seizure, stroke, hepatorenal failure, & abruptio placentae -Preeclampsia also causes placental infarction & ischemia, which can result in fetal growth restriction and demise -RF for Preeclampsia incl nulliparity and advanced maternal age (>35yo) -Initial management of Preeclampsia w/ Severe Features is *maternal stabilization* -Short-acting *antihypertensives* (e.g. *labetalol, hydralazine*) are administered for BP control -*IV Magnesium Sulfate* is used for *seizure ppx* -Once pt's condition is stabilized, *delivery planning* is initiated (w/o severe features, delivery at ≥37wks; W/ severe features, delivery at ≥34wks)

*Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency*

e.g. 3d/o African American baby w/ *anemia & rapidly worsening unconjugated hyperbilirubinemia* is concerning for G6PD deficiency -*G6PD Deficiency* is an *X-linked RBC enzymatic defect, most commonly found in pts of African, Middle Eastern, & Southeast Asian descent* -This defect *increases susceptibility of RBCs to HEMOLYZE*, which typically occurs on *exposure to oxidative stress* (e.g. *sulfa drugs, fava beans*) -*G6PD deficiency* can also *result in Severe Unconjugated Hyperbilirubinemia & Anemia on the 2nd & 3rd days of life, causing Jaundice* -The *timing of jaundice development* helps to *differentiate G6PD deficiency from Hemolytic Dz of the Newborn d/t ABO incompatibility*, which *presents within the first 24hrs of life and w/ a Positive Coombs test, typically in infants w/ blood type A or B born to moms with blood type O* -Newborns w/ anemia & unconjugated hyperbilirubinemia should be tested for G6PD deficiency by *directly measuring G6PD activity* -Neonatal *jaundice from G6PD-D should be TX w/ Supportive Care* (e.g. adequate hydration) *in Mild cases,* and with *Phototherapy &/or Exchange Transfusion in Severe cases*

Chronic Bacterial Prostatitis (CBP)

e.g. 3mo hx of *urinary Sx & pelvic pain w/ evidence of urine leukocytes and bacteriuria* --suggesting *chronic bacterial prostatitis* -CBP is common in *young & middle-aged men* primarily d/t *intraprostatic reflux of urine w/ microbial seeding of the prostate* -Pathogens are similar to those that cause cystitis and incl *E. COLI (75-80%), Klebsiella, Enterococcus, Proteus, & Pseudomonas* -*INCR Risk* in those w/ *DM, smoking, & Urinary tract hardware or manipulation* -*SX Manifestations last >3mo* and usu incl *recurrent UTI (dysuria, frequency, peritoneal discomfort), pain in the GU region, and/or pain w/ ejaculation* -Prostate Exam is often NORMAL, but may show Hypertrophy, Tenderness, or Edema -*DX requires URINALYSIS BEFORE & AFTER Prostatic Massage (OR Examination of Expressed Prostate Fluid)* -HOWEVER, pts w/ *chronic/recurrent urogenital sx & bacteriuria* are often *treated presumptively* -*FIRST-LINE TX is 6WKS of a FLUOROQUINOLONE (CIPROFLOXACIN) or TMP-SMX for 6WKS*; pts may have *recurrent sx if treated for shorter duration*

Patellar Tendon Rupture

e.g. Acute knee pain and difficulty walking after jumping from ladder -*Patellar tendon rupture* may be caused by *sudden, forceful contraction of the quadriceps* (e.g. *landing after jumping*) -The *risk for rupture is greater* in pts w/ *tendinous fragility* (e.g. *chronic kidney dz*) -*Patellar tendon rupture* typically occurs *just distal to the patella's inferior pole* -Classic exam findings incl: • *Knee Effusion & Anterior Knee Tenderness, esp over the Inferior Patellar Pole* • *Palpable defect* (i.e. *gap in tendon*) *Inferior to the Patella* • *Inability to Actively Extend the Knee Against Gravity or Maintain a Straight Leg while Flexing at the Hip* d/t *disruption of the knee's extensor mechanism* -*DX* usu made on *PE & plain x-ray*, which commonly reveals a *high-riding patella (i.e. patella alta) d/t unopposed contraction of the quadriceps* -Management requires *early surgical intervention (<10d)

Acute Coronary Syndrome (ACS)

e.g. Although of young age, a pt w/ RF for coronary artery disease (e.g. active smoking, possible FHX), typical chest pain in terms of location (substernal), and inferior lead T-wave abnormalities of EKG raise reasonable suspicion for ACS -Pts w/ suspected ACS should be given *aspirin 325 mg* and can be given *sublingual nitroglycerin* if experiencing *active* chest pain -Further evaluation should consist of *troponin I levels* and, in the setting of ongoing chest pain, *serial EKGs* approximately every 30 mins. -The general recommendation is the collection of *at least 2 troponin levels 3 hrs apart*, keeping in mind that levels may require up to 6-12hrs from the onset of sx to become detectable -Patients w/ *significantly elevated troponin levels* are diagnoses w/ *non-ST elevation myocardial infarction*, and those w/ *negative troponin levels but ongoing chest pain &/or evolving ischemic EKG changes* may be diagnosed with *unstable angina* -Pts w/ negative troponin levels and no other clinical suggestion of ACS can be d/c'd with a diagnosis of noncardiac chest pain, or undergo stress testing for further evaluation Note: A *treadmill exercise test is appropriate for further DX and risk stratification in pts w/ negative troponin levels but with moderate probability of clinically significant CAD*. However, *stress testing should not be performed until ACS has been ruled out!!*.

Metastatic Lung Cancer

e.g. Heavy smoker w/ a large lung mass with liver lesions and a brain lesion -Lung cancer is the 2nd MC cancer in men and is the leading cause of cancer-related death -Most cases present late in the disease course with pulmonary sx (e.g. cough, hemoptysis, dyspnea, chest pain) or manifestations related to distant metastases (e.g. seizures) or paraneoplastic syndromes (e.g. hypercalcemia) -The diagnostic evaluation of suspected lung cancer begins w/ staging, which uses physical exam & radiographic imaging (e.g. CT scan of chest & abdomen) to establish the extent of disease -A *biopsy* is then needed to confirm malignancy and determine the histopathologic type of the tumor -Pts w/ disease limited to the lung/mediastinal LN should undergo sampling of one these areas -Those w/ evidence of advanced dz (e.g. supraclavicular LN involvement, metastases) should generally have a biopsy of the distant site of spread -Enlarged scalene or *supraclavicular LNs* are the easiest target for initial biopsy d/t their superficial location, which makes sampling low risk and minimally invasive -If these LN are not involved, biopsy of a distant metastatic site (e.g. liver, adrenal gland, bone) should generally be attempted -However, brain biopsy is rarely performed d/t the highly invasive and high-risk nature of this procedure

What are low BMI females at risk for?

e.g. Low BMI d/t regular sport/activity (ballet dancers, gymnasts, runners) -May become *HYPOESTROGENIC* and present with *exercise-induced amenorrhea* -At special risk of developing *OSTEOPENIA* and even *OSTEOPOROSIS* -/Spontaneous fractures/ have been reported, with osteoporosis/osteopenia confirmed though *bone densitometry* -TX: *improving caloric intake*; if not possible, then start on *hormonal replacements* with *OCPs* and supplementation w/ calcium & vit. D Note: *Exercise-induced Amenorrhea is a DX of exclusion*. *Thyroid Hormone and Prolactin levels are needed to rule out other underlying causes of amenorrhea*. -Exercise-induced amenorrhea is d/t a *decr. in the pulsatile secretion of LH*, which leads to a *decline in estrogen prodn* --> *Osteopenia, Osteoporosis, Breast & Vaginal Atrophy, mild Hypercholesterolemia, & Infertility*

Pseudotumor Cerebri

e.g. Male pt w/ freq headaches, rhythmic pulsating sound in ears when bending over, vision dims when straightens; ophthalmologic exam shows peripapillary flame hemorrhages, venous engorgement, & hard exudates; some constriction of visual field in inferior nasal quadrant, but normal visual acuity. Pt taking ACNE medications -AKA *Idiopathic Intracranial HTN* -Arises from *chronically elevated intracranial pressure* with *no obvious findings on imaging*; assoc w/ dural venous sinus stenosis -Findings: *HA, tinnitus, diplopia (usu from CN VI palsy), No change in mental status* -*PAPILLEDEMA* seen on exam, and may lead to *progressive optic atrophy & blindness* (occurs d/t impaired optic nerve axoplasmic flow) -Visual field testing shows *enlarged blind spot & peripheral constriction* -*LP shows INCR opening pressure*, which *provides temporary HA relief* -Most commonly seen in *Obese PREmenopausal Women, but can occur in MEN too!* -*Thought to occur 2º to Endocrine Disorders* (e.g. hypoparathyroidism, hypothyroidism, adrenal insufficiency, Cushing dz) *and 2º the usage of some meds* (e.g. *ISOTRETINOIN, All-trans-Retinoic Acid, Excess Vit A Minocycline, Tetracycline, Cimetidine, Corticosteroids, Danazol, Tamoxifen, Levothyroxine, Lithium, Nitrofurantoin)* -*TX*: *Weight loss, Acetazolamide*; *Invasive procedures for Refractory* cases (e.g. *CSF shunt placement, optic nerve sheath fenestration for visual loss*)

Ongoing Epistaxis Management

e.g. May occur d/t a hot, dry climate and possible minor nasal trauma (e.g. nose-picking) -The *anterior nasal septal mucosa* is vulnerable to bleeding as it is where the sphenopalatine, greater palatine, anterior ethmoid, & superior labial arteries anastomose (*Kiesselbach Plexus*) -*Nostril Pinching* directly compresses the Kiesselbach plexus and usu readily controls bleeding after 5-10mins -If anterior epistaxis does not cease, *topical vasoconstriction* is indicated -*Oxymetazoline* is the preferred agent in kids and should be applied w/ a //squirt bottle or cotton pledget// then apply direct pressure again -Pts should be advised to moisturize the nasal mucosa w/ saline sprays or a humidifier to prevent epistaxis d/t dry weather; and avoidance of nose-picking or rubbing Note: Although beneficial in the acute setting, *topical vasoconstrictors should NOT be used for >3d d/t the risk of //rebound congestion//* Note: *Chemical (silver nitrate)* or *electrical cautery* is indicated //if direct compression & topical vasoconstriction are unsuccessful//. Simultaneous *bilateral cauterization should be avoided d/t the risk of septal ulceration and perforation*

Transient Tachypnea of the Newborn (TTN)

e.g. Newborn with respiratory distress (tachypnea, grunting, nasal flaring, and subcostal & intercostal retractions) and CXR showing a flattened diaphragm, mild cardiomegaly, and a prominent horizontal fissure on the right side. -TTN is a condition caused by *retained fetal lung fluid* after delivery -Pts born *prematurely* or by *cesarean section* are at *increased risk*, as typical resorptive mechanisms are activated at term and during labor -TTN also occurs *more frequently in infants born to moms w/ diabetes*; this is d/t *impaired fluid clearance in the diabetic fetal lung* -TTN *presents shortly after birth* w/ *tachypnea*, increased work of breathing (e.g. retractions, nasal flaring), and often *cyanosis* -However, *breath sounds are usu clear on exam* -*Hyperinflation* (i.e. flattened diaphragm), *mild cardiomegaly*, prominent vascular markings, *fluid in the interlobar fissures*, and pleural effusions may be seen on CXR -TX for TTN is *supportive* and includes *supplemental O2 PRN* -SX generally *resolve spontaneously* within 72hrs w/ *NO long-term complications*

Anticholinergic Toxicity

e.g. Overdose of Paroxetine (antidepressant with anticholinergic activity) or *Excess Atropine* (competitive inhibitor of acetylcholine at muscarinic-R)_ -Characterized by *dry mucous membranes, flushing, mydriasis (pupil dilation), urinary retention, & decr bowel motility*

Constrictive Pericarditis s/p CABG

e.g. P/w *peripheral edema & elevated JVP with clear lung fields, suggestive of RHF, most likely d/t Constrictive Pericarditis* -*Pericarditis is a common complication of CABG surgery,* and some degree of *postop pericardial effusion develops* in 85% of pts -*Most pts are ASX* from the small effusions -However, *continued pericardial inflammation occurring over months may lead to dev of a Thickened, Fibrous Pericardium, and CONSTRICTIVE PERICARDITIS* -*Constrictive Pericarditis* is an *imp cause of Right Heart Failure* - pts usu have *peripheral edema, ascites, & hepatic congestion w/ hepatomegaly*, which can *progress to cirrhosis (cardiac cirrhosis)* -Other findings may incl *elevated HVP w/ prominent "y" descent and hepatojugular reflux, Kussmaul's sign (incr, or lack of decr, in JVP on inspiration), and pericardial knock (mid-diastolic murmur)* -*EKG* in Constrictive Pericarditis may be *nonspecific* (e.g. *tachycardia*) *or can show low-voltage QRS complexes* -*CXR often reveals Calcified Cardiac Borders* -*Echo* may show *increased pericardial thickening or calcification, atrial enlargement, & abnormal septal motion*; However, *these findings are neither sensitive nor specific* for the DX -*TX* involves *supportive care (e.g. anti-inflammatory agents) or pericardiectomy for refractory cases*

Neuropsychiatric Sx in Alzheimer Disease

e.g. Pt w/ moderate to severe dementia from AD, with new mental status changes (e.g. *inattention, altered consciousness, daytime somnolence*) is concerning for *DELIRUM* -Ability to *detect delirium in the setting of AD* becomes *increasingly difficult as dementia progresses* bc *neuropsychiatric sx* (e.g. *apathy, agitation, delusions, hallucinations*) can be *seen with BOTH* -HOWEVER, *Sudden changes (hours to days) & Rapid Fluctuations in Consciousness* (e.g. somnolent to agitated within minutes) are *NOT expected with Progressive Dementia of AD, and should raise concern for DELIRIUM*, which *indicates an unstable underlying medical condition* that must be *urgently identified & treated* -- this distinction is important bc *delirium may be the only sign of acute illness in dementia pts!* (DELIURIUM IS A MEDICAL EMERGENCY) -In addition to under-recognition d/t shared features with advanced dementia, *delirium is often misdiagnosed Depression in Elderly pts* who most commonly p/w a *hypoactive, withdrawn state* -- However, *depression* tends to follow a *more gradual course w/ less fluctuation*

Management of a PARTIAL Small Bowel Obstruction in an Adult

e.g. P/w [abrupt onset] N/V, crampy lower abdo pain & distension for couple days; no recent BM; unable to eat d/t repeat emesis. PE: Dry mucous membranes; distended abdo w/ incr bowel sounds, tympanic note throughout, & tenderness on deep palpation of lower abdomen. Labs show marked electrolyte abnormalities. GI Obstruction Series in ED reveals multiple air fluid levels in small intestine (c/w DX of SBO), and some air in distal colon -Intestinal dilation proximal to blockage and intestinal decompression distal to blockage -*Compromised blood flow* due to* excessive dilation or strangulation* may lead to *ischemia, necrosis, or perforation* -Most commonly caused by *intraperitoneal adhesions (fibrous band of scar tissue), tumors, and hernias* -*SBO Management: gastrointestinal decompression (e.g. NG tube), volume resuscitation, bowel rest* -The *presence of air in distal colon* makes the *DX of Complete obstruction LESS likely* -*Partial SBO* should *initially be managed w/ Observation (hospital admission) & Supportive TX* -If pt *fails to improve in next 12-24hrs* --> *Early Surgical Intervention is Recommended* -If a pt had signs of *impending strangulation (incarcerated hernias) or mesenteric ischemia*, should undergo *urgent surgical intervention to prevent further clinical deterioration* Note: Insertion of a Rectal Tube is NOT indicated in pts w/ SBO

Addison's Disease - Chronic 1º Adrenal Insufficiency

e.g. Pt p/w *weight loss, abdominal pain, asthenia (general weakness w/o effort), amenorrhea, fatigue, weakness, & poor appetite* *Decr gland fxn --> Decr cortisol, Decr aldosterone --> Hyponatremic Hypotension, Hyperkalemia, Metabolic Acidosis, Skin/Mucosal Hyperpigmentation* -*Addison Disease*— *Chronic 1° adrenal insufficiency*; caused by *adrenal atrophy or destruction* ;Most commonly due to *autoimmune adrenalitis* (*resource-rich* countries) or *TB* (*resource-limited* countries). -PE shows *muscle tenderness, decreased axillary & pubic hair (d/t decr adrenal androgen prodn), and Increased pigmentation (d/t co-secretion of ACTH and melanocyte-stimulating hormone)* -More *specific* findings are *Electrolyte Abnormalities*: *HYPONATREMIA* (85-90%), *HYPERKALEMIA* (60-65%), & an *assoc MILD HYPERCHLOREMIC METABOLIC ACIDOSIS* -*HYPOGLYCEMIA* can also be seen in chronic adrenal insufficiency -*Next Step in Eval* --> *Measurement of Morning Plasma Cortisol with Concurrent ACTH* -- *LOW Cortisol w/ HIGH ACTH is DX for Primary Adrenal Insufficiency* -If *results equivocal* --> *ACTH Stimulation Test* NOTE: *Hypoaldosteronism* usu *presents as ASX Hyperkalemia w/ Mild Metabolic Acidosis*; *Hyponatremia is generally NOT seen* unless there is *concurrent cortisol insufficiency*. Also *NO hyperpigmentation*

Brain Herniation

e.g. Pt p/w hypertension, bradycardia, & irregular respirations (Cushing triad), fixed pupils, & extensor posturing of the extremities -- this combo is most c/f *brain herniation* -Brain herniation occurs when a *rapid incr in ICP (e.g. d/t intracranial hemorrhage) leads to protrusion of the brain through openings in dural folds or the foramen magnum*

Anaphylaxis presentation in a Surgical Patient

e.g. Pt w/ *Hypotension, elevated peak pressures <40mmHg (e.g. Bronchospasm), & Decreased End-Tidal CO2 (e.g. decreased cardiac output and CO2 delivery to the lungs) shortly after Anesthetic Induction* is *concerning for Anaphylaxis* (pt also with *tachycardia, bilateral wheezing*) -*Anaphylaxis* is classically *caused by an Acute IgE-mediated Release of Inflammatory Mediators (e.g. Histamine) in Response to an Allergen* -In the *perioperative setting*, the *MC allergens are Neuromuscular-Blocking Agents (Rocuronium), antibiotics, skin antisepsis products (e.g. povidone-iodine, chlorhexidine), and blood products* -Bc anaphylaxis is a *Clinical DX* that depends on *Hx & PE*, the *DX can be challenging in surgical pts* bc: • Pt *inability to communicate sx* • Ongoing physiologic stress, volume shifts, & medication effects, initially attributed to shock • *Concealment of skin findings under surgical drapes* -If there is *concern for anaphylaxis, FIRST do a THOROUGH PHYSICAL EXAMINATION*, especially *inspection under surgical drapes* for *cutaneous signs* (e.g. *rash, flushing*), which are present in most anaphylactic pts -Once diagnose anaphylaxis, *Promptly Administer EPINEPHRINE* NOTE: *Malpositioning of the endotracheal tube into a (R/L) mainstem bronchus can cause increased peak pressures* (i.e. the smaller radius of the bronchus [compared to trachea] increases resistance) *and hypoxemia* (e.g. from contralateral lung atelectasis). This results in *ventilation of a single lung, and collapse of the contralateral lung or a lobe of the intubated lung, manifesting as unilaterally absent breath sounds* (e.g. ETT in right main bronchus cause atelectatic collapse of left lung - white out atelectasis on CXR).

Tick Paralysis

e.g. Pt w/ *ataxia, weakness, & absent deep tendon reflexes after a camping trip to Washington state* -Tick paralysis is a *rare, potentially life-threatening disorder seen primarily in Australia Western North America* -Most cases in USA are d/t Dermacentor andersoni (Rocky Mountain wood tick) and Dermacentor variabilis (American dog tick) -*NEUROTOXINS* in the *tick saliva* are *transmitted to the host over 4-7d of tick attachment* and can result in: • *Brief Prodrome of fatigue & paresthesias* • *Gait Ataxia & ASCENDING Paralysis* that *develops over HOURS* • *ABSENT Deep Tendon Reflexes* -*Fever is usu Absent and Sensation/Sensory is rarely affected* -Labs & imaging usu normal -If suspect tick paralysis, Need to do a *Meticulous Skin Exam to find the tick!* -*Tick REMOVAL eliminates the precipitating neurotoxin* and usu results in *Significant Clinical Improvement within a few hours* -Most pts *recover completely without further intervention or meds*

Benzodiazepine Withdrawal

e.g. Pt w/ *confusion, restlessness, tremors, psychosis, & autonomic instability (e.g. tachycardic, HTN, incr Temp) several days after abrupt discontinuation of lorazepam* -*Withdrawal Sx (seizures, sleep disturbances, depression)* from *Intermediate-* (12-24hrs) to long-acting* (>24hrs) benzos typically *peak after several days*; while withdrawal sx from *short-acting* (<12hrs) benzos *occur within 24hrs* -Prompt recognition is crucial as *benzo withdrawal can be LIFE-THREATENING* -*TX of Choice is a BENZODIAZEPINE (e.g. Diazepam)*, which should be *given intravenously in severe cases* of withdrawal (e.g. *markedly abnormal vital signs, delirium, seizures, psychosis*) -Once withdrawal sx are controlled, *benzos should be tapered gradually* Note: Though Haloperidol is commonly used to tx agitation & delirium, it is not the TX of Choice for benzo withdrawal. Psychosis sx should resolve with benzo tx for withdrawal Short-acting (<12hrs) (Midazolam) Intermediate-acting (12-24hrs) (Alprazolam, Lorazepam) Long-acting (>24hrs) (Diazepam, Clonazepam)

When is *Coronary Revascularization* Indicated?

e.g. Pt w/ *crescendo angina pectoris, severe multivessel coronary artery disease (CAD) W/ Involvement of Proximal LAD, & LV systolic dysfunction* -*Goals of TX in CAD pts* are to *improve sx, reduce cardiovascular morbidity, & improve overall survival* -- done using a comprehensive approach w/ *aggressive lifestyle modifications, optimal medical therapy, & coronary revascularization in appropriately-selected pts* -*Coronary Revascularization* is indicated primarily for *2 groups of pts w/ Stable Angina*: ● Pts w/ *Refractory Angina despite maximal medical therapy* (e.g. nitrates, CCBs) ● Pts in whom *revascularization will improve long-term survival* -- *includes those w/ Left Main Coronary Stenosis & those w/ Multivessel CAD (ESP when involves the proximal LAD) along w/ LV Systolic Dysfunction* Note: In pts with *DIABETES + MULTIVESSEL CAD*, Coronary Artery Bypass Graft surgery is SUPERIOR to Percutaneous Coronary Intervention w/ drug-eluting stents d/t a LOWER rate of All-Cause Mortality & Myocardial Infarction w/ CABG* Note: *PCI w/ bare metal or drug-eluting stents is an excellent revascularization option* for pts w/ *refractory angina d/t severe Single- or Two-vessel CAD that does NOT involve the proximal LAD*. However, *CABG >> PCI in pts w/ Multivessel CAD (esp involving proximal LAD) & LV dysfunction*, w/ *lower rates of repeat vascularization & improved clinical outcomes*

Pt with caustic ingestion and evidence of respiratory distress - what's the next step?

e.g. Pt w/ *evidence of severe Oropharyngeal Damage (hoarseness, odynophagia, inability to control salivary secretions, edematous & erythematous oropharynx, necrosis w/ grayish exudate formation)* AND *respiratory distress (tachypnea, hypoxemia on room air) following* a *Caustic Ingestion* -*LARYNGOSCOPY would be the next best step!* Should be *performed FIRST* to *assess the likelihood of Impending Airway Compromise* -Once laryngoscopy is done, pts should *undergo Upper Endoscopy Within 24HRS to Determine Severity of GI Injury* • *Minimal Damage* --> *Discharge* • More *Severe Injuries* --> *Require ≥7 days of Monitoring* for Possible *Perforation & Complications* -In the event of *perforation, mediastinitis, or peritonitis* --> *Emergency Surgery* Note: Although *activated charcoal is helpful in acute poisoning, it does NOT have a role in managing caustic ingestions*

Pelvic Inflammatory Disorder

e.g. Pt w/ *fever*, abdominal pain, *purulent cervical discharge*, and *cervical motion tenderness* -*Gonococcal Cervicitis* predisposes the upper reproductive tract (e.g. uterus, fallopian tube) to the polymicrobial infection of PID -Acute complications of PID incl *tubo-ovarian abscess, pyosalpinx, & perihepatitis* (e.g. *Fitz-Hugh-Curtis syndrome*) -Long-term complications include *infertility & incr risk of ectopic pregnancy* d/t fallopian tube damage -*RF for PID* incl *multiple sexual partners, age 15-25, previous episodes of PID, inconsistent use of barrier contraception, & a partner w/ an STI* -Studies show that among all PID RF, having *MULTIPLE SEXUAL PARTNERS* is associated with the *HIGHEST INCR (4.6-20x) in risk for PID occurrence!*

Stress Hyperglycemia

e.g. Pt w/ *hyperglycemia & ketoacidosis* in the s/o *sepsis w/ fever, hypotension, dehydration, & tachycardia, but Normal HbA1c* most likely has *stress hyperglycemia* -*Stress Hyperglycemia* is a *potential complication of severe illness (e.g. Sepsis)*, defined as *transiently Elevated Blood Glucose levels in the context of severe illness in pts W/O known diabetes* -During illness & stress, *Hyperglycemia can result from the release of HIGH levels of Stress Hormones* (e.g. *cortisol, catecholamines, pro-inflam cytokines*) -*RF* for stress hyperglycemia incl *severe illness, Temp >39C (102.2 F), Sepsis, Meningitis, & ICU admission* -Assoc w/ incr morbidity in critically ill pts -In *hyperglycemic critically ill Adult pts, glucose-containing IVF are Minimized and INSULIN is administered* to achieve a *blood glucose target of 140-180 mg/dL* -For *hyperglycemic critically ill Children,* the *optimal blood glucose target & data on insulin therapy are INCONCLUSIVE* ● NO relationship b/w stress hyperglycemia & persistent abnormal glucose metabolism or subsequent DX of DM has been demonstrated -Pts w/ a *NORMAL HBA1C RULES OUT CHRONIC Hyperglycemia*. Additionally, no prior hx of wt loss, polyuria, polydipsia, or polyphagia means pt does NOT meet the diagnostic criteria for DM. In the absence of classic DM sx or elevated HbA1c, pt's hyperglycemia is best explained by stress d/t illness

Management of Choledocholithiais

e.g. Pt w/ *prolonged abdo pain & jaundice w/ LFT abnormalities and a dilated common bile duct (CBD)* likely has *Choledocholithiasis (CBD Stones)* -Pts commonly have *typical Biliary Colic SX (RUQ pain, N/V)*; HOWEVER, *unlike cholelithiasis, CBD stones cause Accompanying BILIARY OUTFLOW OBSTRUCTION, leading to Cholestatic Liver FXN Abnormalities (Elevated Bilirubin, Elevated ALP out of proportion to Aminotransferases)*,and more *prolonged pain* -*Pancreatic enzymes, WBC, & Vitals are usu normal* -Choledocholithiasis is *DX by Visualization of a stone within the CBD*; However, *Ultrasound is INSENSITIVE for detecting DISTALLY-Located Stones!* -Therefore, *ERCP* allows for *both DX & TX (stone removal)* and is the best next step in management of pts with: • *Visualized choledocholithiasis* • *High-risk features* (e.g. *Dilated CBD* on imaging, *Elevated serum Bilirubin*) • *Evidence of Acute Cholangitis* (*fever, RUQ pain, jaundice, hypotension, confusion*) --> These pts also require *IV ABX & TX of Sepsis* -In pts in whom choledocholithiasis is *suspected but don't have any of the above criteria*, a less invasive *MRCP* should be considered instead -*After ERCP, [nonemergent] Laparoscopic Cholecystectomy* is performed on a *nonemergent* basis to *prevent future complications* -Although intraoperative (during cholecystectomy) CBD stone removal is occasionally performed, it is technically challenging and rarely performed since the ERCP -*Immediate cholecystectomy* is usu reserved for pts w/ *emergent indications* (e.g. *hemodynamic shock, gallbladder perf*) *who are at LOW risk for surgery*

DIPHTHERIA

e.g. Young pt who *did not receive age-appropriate vaccinations* with *fever/chills/malaise, sore throat (hoarseness, dry cough), & pharyngeal erythema & grey patches/exudate coalescing into a PSEUDOmembrane* suggests *Diphtheria infection* -Diphtheria is caused by *toxigenic strains of CORYNEBACTERIUM DIPHTERIAE, a gram-positive bacillus transmitted via Respiratory Secretions* that largely affects *children <15yo* and causes *oropharynx colonization, affecting throat/tonsils* -*Exotoxin* released by bacteria is *absorbed systemically* an can result in *dose-dependent damage to the Heart (arrhythmias, myocarditis), Nervous System (neuropathies), & Kidneys(AKI/renal failure)* -*MYOCARDITIS* occurs in up to 2/3s of pts; severe cases are assoc w/ *complete heart block or heart failure* -Vaccination with *Diphtheria TOXOID Vaccine* significantly reduces likelihood of infection w/ toxigenic strains of diphtheria; reducing risk of active infection & limits ASX carriage of toxigenic strains (causing population-wide declines in prevalence) After exposure to *Diphtheria Toxin*, *UNVACCINATED pts should be given Preformed Antibodies (passive immunization with Diphtheria Antitoxin) and ABX w/ Erythromycin* (Clarithromycin, Azithromycin, Clindamycin, Rifampin, Quinolones, Tetracyclines, TMP-SMX, Vancomycin, & Daptomycin also work)

Anterior Shoulder Dislocation

e.g. Pt w/ *shoulder pain after falling on an outstretched arm w/ shoulder deformity and an x-ray demonstrating humeral head that is Anterior, Medial, and Inferior to the Glenoid Fossa* -- *c/w Anterior Shoulder Dislocation* -P/w *painful and slightly ABDUCTED and EXTERNALLY Rotated Shoulder*; some may have *Numbness over the [Lateral] Shoulder d/t Axillary Nerve Compression* -Additional findings incl *protrusion of the acromion, flattening of the deltoid prominence, & anterior axillary fullness d/t the humeral head's displacement* -*DX Confirmed w/ Plain Radiograph* -*TX is CLOSED REDUCTION (e.g. Traction-Countertraction, Scapular Manipulation)*, which is commonly performed using Procedural Sedation* to minimize pt's discomfort and increase the likelihood of procedural success -*Successful Reduction is accomplished by hearing &/or feeling a clunk during the procedure and seeing return of the normal shoulder contour* -*POSTREDUCTION X-RAY should be Performed to Confirm Successful Reduction and R/O Complications that can occur during reduction (e.g. glenoid fracture)* -In addition to improving pain, *reduction also usu improves Axillary Neuropraxia* -Should be done w/o delay to control pain and prevent ligamentous or neurologic damage -Note: Emergent Orthopedic Surgical Repair is Indicated when closed reduction is Unsuccessful or when the dislocation is assoc w/ major fracture (e.g. humeral neck fracture) or neurovascular compromise (absent peripheral pulses)*

Tumor Lysis Syndrome (TLS) s/p Initiating Chemotherapy - AE on PT

e.g. Pt w/ DLBCL developing *cardiac arrest* the day *after administration of chemotherapy/immunotherapy* meds. -*Chemotherapy/Immunotherapy meds LYSE TUMOR CELLS, releasing intracellular Potassium, Phosphate, & Nucleic Acids (metabolized to Uric Acid) into the circulation* -- when *large amounts of these substances are released at a rate that exceeds their renal elimination* ==> *TUMOR LYSIS SYNDROME* -*TLS* is a *complication of chemo/immunotherapy* that typically develops in pts who have *tumors w/ High Cell Burden (e.g. widespread, bulky LAD) or Rapid Turnover, or those Receiving Combination Therapy* -*Early TLS SX are Nonspecific* (nausea), and can *mimic sx caused by chemotherapy* -*Severe Manifestations of TLS* incl: • *AKI* d/t *renal precipitation of uric acid (rhomboid/rosettes) & calcium-phosphate renal crystals (wedge-shaped prism)* • SEIZURES* d/t *neuronal hyperexcitability* caused by *hypocalcemia* (i.e. *calcium-phosphate formation*) • *CARDIAC ARRHYTHMIAS* d/t *Hyperkalemia & myocardial calcium-phosphate deposition* -*Severe Hyperkalemia on EKG* shows a *widened QRS complex (sine wave pattern)* which can *precipitate cardiac arrest* (i.e. *progression to ventricular asystole & loss of pulse*) -*Although PRE-TX w/ IVF & Uric Acid Level Reduction (e.g. ALLOPURINOL) LOWERS the Risk of Developing TLS, it MAY STILL OCCUR Despite these measures*

Acute HCV Infection

e.g. Pt w/ RUQ pain, elevated bilirubin, & markedly elevated aminotransferase levels suggest acute hepatitis. A Hx of IV drug use causes increased risk for Hepatitis B or C -*Acute HCV infection* can dev 2-26wks after viral exposure -Most pts w/ acute HCV are ASX -Symptomatic pts typically dev malaise, nausea, jaundice, & RUQ pain that can last for 2-12wks -Lab studies usu show elevated aminotransferase levels that can be 10-20x the upper limit -Most pts dev *anti-HCV antibodies 2-6mo after exposure* -HCV RNA can generally first be detected within days to 8wks following viral exposure -If a pt has negative anti-HCV antibodies, but may not have formed anti-HCV antibodies yet, do testing HCV RNA by *PCR* to document acute HCV infection

Sporotrichosis

e.g. Pt w/ abrasion to cheek, subsequently dev a nodular, ulcerative lesion at site of injury and similar lesions along proximal lymphatic chain, indicating *Nodular Lymphangitis* -Nodular lymphangitis (w/ nodules along the LNs) can be caused by uncommon pathogens (e.g. *Mycobacterium marinum, Nocardia, Leishmania, Sporothrix schenckii*) -Sporotrichosis is a *fungal infection* caused by *direct inoculation of dimorphic Sporothrix (found in soul & decaying plant matter) into the skin (cutaneous) or subcutaneous tissue* -Most cases arise during *outdoor* recreational or vocational activities (e.g. *hiking, gardening, landscaping*) -Manifestations are *subacute or chronic*: • Initially manifests as a *painLESS papule @inoculation site* • Eventually *ulcerates & drains a nonpurulent, odorless fluid* • Over *days, similar lesions dev along the proximal draining lymphatic chain* -*Systemic Sx RARE* -H&P sufficient for DX, but *culture of aspirated lesional fluid* is often ordered for *confirmation* -*TX w/ ITRACONAZOLE 3-6MO is usu Curative*

Cardiogenic Shock

e.g. Pt w/ chest discomfort, tachycardia, hypotension after complicated percutaneous coronary procedure, most likely d/t an abrupt coronary occlusion leading to impaired contractility of the involved pericardium -Hemodynamic parameters from pulmonary artery catheterization in cardiogenic shock show *low cardiac index (CI)* d/t impaired cardiac contractility, *elevated pulmonary capillary wedge pressure (PCWP)* d/t volume overload, with a compensatory *elevation in systemic vascular resistance (SVR)* to maintain adequate tissue perfusion pressure

Streptococcal Tonsillopharyngitis

e.g. Pt w/ fever & sore throat w/o upper respiratory sx and PE findings of tonsillar exudates and cervical LAD -*Group A Strep (GAS) pharyngitis* is most common in children 5-15yo, and occurs in the late fall, winter, and early spring -Signs & Sx: Abrupt onset of sore throat, fever, absence of cough & viral sx, abdominal pain/vomiting -*Tonsillar erythema & exudates and tender anterior cervical LNs* are often seen on PE -DX confirmed w/ *throat culture* or *rapid antigen testing* PRIOR to initiation of ABX -The rapid streptococcal antigens test (RSAT) is highly specific, and *ABX can be initiated after positive RSAT* -However, d/t the test's poor sensitivity, *throat cultures must be obtained after all negative RSATs in children* -Throat cultures are not necessary if the RSAT is positive!! -*Penicillin & Amoxicillin* are the first-line TX options for pts w/ Streptococcal Pharyngitis -The goals of TX are to reduce SX severity & duration, decr spread to close contacts, and *prevent acute rheumatic fever*

Mixed Cryoglobulinemia Syndrome

e.g. Pt w/ renal insufficiency w/ PALPABLE Purpura, elevated rheumatoid factor, and Hypocomplementemia* -Mixed cryoglobulinemia syndrome is a *vasculitis d/t the deposition of immune complexes (polyclonal IgG & IgM rheumatoid factor) within the vascular wall of small- and medium-sized vessels* -Most cases *arise in those w/ CHRONIC HEPATITIS C VIRUS* (e.g. pt w/ hx of IVDU), *but pts w/ lymphoproliferative disorders, autoimmune dz, and other infections are also at risk* -*TRIAD of Manifestations*: • *PALPABLE PURPURA* • *WEAKNESS* • *ARTHRALGIAS* -Other *nonspecific sx (e.g. nausea) & peripheral neuropathy* also freq occur -*Labs usu reval Elevated Rheumatoid Factor & Hypocomplementemia (Low C3, C4, CH50)* -*~20% of pts dev GLOMERULONEPHRITIS (red cells [blood], RBC casts, proteinuria) W/ or W/O Renal Insufficiency* -*TX* divided into *2 stages:* 1. *Initial immunosuppressive therapy* - *stabilizes end-organ damage (e.g. glomerulonephritis) using Rituximab. + Prednisone* 2. *TX of Underlying DZ* - *targeted therapy against the condition that triggered the cryoglobulinemia* -Pts who receive immunosuppressive TX with Rituximab. + Prednisone *require PPX against opportunistic infections* such as *Pneumocystis pneumonia* -- HOWEVER, *immunosuppression is typically tapered over 1-3mo; ABX PPX would NOT be necessary in the long-term management of mixed cryoglobulinemia*

Arthropathy in Hereditary Hemochromatosis

e.g. Pt with *Polyarticular arthropathy, assoc w/ hepatomegaly (palpable liver below right costal margin), and positive FHX for diabetes* -- should make you think of *Hereditary hemochromatosis* -HH is an *autosomal recessive* disorder *characterized by IRON DEPOSITION* in a *variety of tissues* -*Clinical manifestations* usu begin in the *fourth to sixth decades*, with *women presenting later d/t menstrual iron loss* -The *Initial Eval of HH* incl *Serum IRON Studies, which show INCR levels of Iron, Ferritin, & Transferrin Saturation* -*DX Confirmed w/ Genetic Testing for hemochromatosis-assoc mutations (e.g. HFE)* -*Arthropathy of HH* shows *significant variability* -The *2nd & 3rd metacarpophalangeal joints are commonly affected*; also *freq affects the KNEES, Ankles & Shoulders* -*X-ray* shows *Subchondral Cysts, Sclerosis, Osteopenia, & Hook-like Osteophytes* -*Joint aspiration* can identify *CALCIUM PYROPHOSPHATE DIHYDRATE (CPPD) CRYSTALS in ~50% - Rhomboid-Shaped, & POSITIVE-Birefringence under Polarized light*; can also find *incr leukocyte count of predominantly PMNs, and Gram stain shows No organisms* -*CPPD Deposition* in HH can cause a *chronic arthropathy or an Acute Inflammatory Arthropathy resembling gout (i.e. PSEUDOGOUT)* -*TX of HH* involves *Serial Phlebotomy* to *reduce excess iron stores* -- BUT *know that joint sx usu DON'T improve w/ phlebotomy* -D/t the *assoc chronic liver dz*, *HH pts have an INCR (~20x) RISK for HEPATOCELLULAR CARCINOMA*, accounting for ~30-45% of deaths in HH pts -*TX of HH w/ phlebotomy can lead to Improved hepatocellular fxn, w/ reduced progression to cirrhosis and an assoc reduction in the risk of HCC* -*Phlebotomy also Alleviates Fatigue, Reduces Skin Pigmentation, & Lowers the Risk of Heart Failure, and MAY improve glycemic control*

Candida Endophthalmitis

e.g. Pt with *UNIlateral vision LOSS, eye PAIN, & Fundoscopic evidence of Vitreous Haze & Off-White Chorioretinal Lesions* -*Candida endophthalmitis is an infection of the structures & fluid chambers (usu) of the eye* -*RISK* is *Greatest in Hospitalized pts w/ Indwelling Central Catheters*, which provides a portal of entry from the skin -Additional RF: *GI surgery/perforation* (another entry portal), *Immunocompromise (e.g. neutropenia), & Total Parenteral Nutrition* -Candida usu *seeds the highly vascular choroid layer via the bloodstream* during *transient/persistent fungemia* -*Candida replicates in the choroid* and *spreads to the retina*, leading the dev of *fluffy, yellow-white chorioretinal lesions w/ indistinct borders* -*Spread to the vitreous chamber* is marked by a *vitreous haze or floating white fungal balls* -Manifestations *begin w/ floaters & a progressive loss of visual acuity* -*Eye PAIN* occurs *late in dz* -Fever & other systemic sx may be present in the setting of fungemia or the seeding of other organs -*Blood cultures required, but often negative; DX Confirmed w/ Vitreous Fluid Sampling* -*TX: Systemic Antifungal therapy w/ FLUCONAZOLE or VORICONAZOLE* -Those w/ *Vitreous Infection*, typically undergo *intravitreal injection w/ Amphotericin B or Voriconazole and VITRECTOMY*, which eliminates fungal microabscesses that may be resistant to systemic antifungal therapy

Actinic Keratosis (AK)

e.g. Scaly hyperkeratotic lesion on the helix of the ear -AK is a premalignant condition caused by excessive sunlight (UV light) exposure, most commonly occurring in *sun-exposed areas* such as the face, scalp, ears, upper chest, and dorsal hands & forearms -Characterized by small, rough, erythematous, and keratotic papules that are often easier to feel than they are to see -These lesions occur on skin that often shows signs of *chronic photodamage* such as dyspigmentation, wrinkling, thinning, & telangiectasia -AKs can spontaneously regress and recur in a particular location but some may resolve spontaneously -However, they are considered premalignant lesions as 1-20% of AKs will evolve into *invasive squamous cell CA (SCC)* if left untreated (the majority of SCC of the skin arises in pre-existing AK) -For this reason, AKs should be treated early w/ destructive (*liquid nitrogen cryosurgery* or *surgical excision & curettage*)or pharmacologic (*5-fluorouracil [5-FU] cream, topical diclofenac, imiquimod*) measures to prevent degeneration into invasive SCC -The most commonly employed destructive TX for AKs is *cryodestruction w/ liquid nitrogen* (best for a few lesions) -Field therapy w/ 5-FU cream, topical diclofenac, imiquimod is recommended when numerous small lesions are present -*Biopsy* is indicated for AK • DX is unclear • Lesions >1cm in diameter • Lesions are indurated • Ulceration is present • Presence of tenderness • Lesions are growing rapidly • Lesions fail to respond to appropriate therapy -Biopsy-proven SCCs should be TX w/ Mohs micrographic surgery or by Excision w/ 4mm margins

Extrapulmonary Sarcoidosis Manifestations

e.g. Young patient w/ unilateral facial nerve palsy, hepatomegaly, and lymphadenopathy -Sarcoidosis is a multisystem granulomatous disease of unknown origin that primarily affects *young adults*, w/ African Americans being at particular risk -Most cases involve the lungs, but extrapulmonary manifestations frequently occur and are often (≈30%) the presenting feature *Skin*: Papular, nodular, or plaque-like lesions; Erythema nodosum *Eye*: Anterior Uveitis (iridocyclitis or iritis); Posterior Uveitis; Keratoconjunctivitis Sicca *Muscle & Joint*: Acute Polyarthritis (esp ankles); Chronic Arthritis *Nervous System*: *Facial Nerve Palsy* *Reticuloendothelial System*: *Hepatomegaly* (≈20%) and Peripheral LAD* (≈40%); Splenomegaly *Cardiovascular*: Atrioventricular Block; Dilated/Restrictive Cardiomyopathy *Endocrine*: Central Diabetes Insipidus; *Hypercalcemia* *Löfgren Syndrome*: Erythema Nodosum; Hilar Adenopathy; Migratory Polyarthralgia; Fever -Extrapulmonary Sarcoidosis is almost always accompanied by *significant fatigue* -Screening for suspected cases usu begins w/ a *CXR* as >90% of pts have *bilateral hilar or mediastinal adenopathy*, and may show *interstitial infiltrates on CXR* -Additional testing is then required for confirmation. -Sarcoidosis pts commonly have elevated calcium, ESR, and alkaline phosphatase [if the liver is involved]. -Angiotensin-converting enzyme levels are also increased in 75% of cases, but this test has poor diagnostic sensitivity/specificity and cannot be used for confirmation -Suspected sarcoidosis cases are typically confirmed when: • Diseases that cause similar SX are excluded (e.g. TB) • *Biopsy* reveals *noncaseating granulomas* -Biopsy should be done on the involved location that's easiest to assess, usu a palpable lymph node or skin lesion (*excisional LN biopsy*) for confirmation. -If no superficial lesion is present or the DX remains uncertain after initial BX, then bronchoscopy w/ transbronchial BX is often performed

Reasons Necessitating Unilateral Termination of the Physician-Patient Relationship by the Physician

● A *Nontherapeutic Relationship* (e.g. *recurring missed appointments, pt noncompliance*) ● *Inappropriate Pt Behaviors* (e.g. *verbal abuse, physical threats*) ● *Nonpayment of Outstanding Bills* or the *Pt Declining to Follow a Payment Plan* -Regardless of the reason, the *termination process must NOT constitute patient abandonment (i.e. withdrawal of treatment W/O notice)* -Generally, a *physician can safely terminate a relationship W/O constituting pt abandonment once the pt has NO IMMEDIATE Medical Need AND has had Reasonable Time to find an Alternative Provider* -The *duration of time depends on multiple factors* (e.g. pt diagnosis, alternate provider availability), *but 30 DAYS is typically ADEQUATE Notice* -When a physician is terminating the patient-physician relationship, they *MUST notify the pt of the termination in WRITING, give a CLEAR END DATE, and Provide Medical Records to the next physician* Note: Nondiscrimination laws protect pts from being turned away based on race, religion, sexual orientation, disability, or medical diagnosis (e.g. HIV/AIDS). Pts CAN be turned away on the basis of Finances, but the physician has a duty to Provide Emergent Medical Care until the pt can find another doctor