Medicine

ABCD criteria of suspicious skin lesions

A: Asymmetry B: Borders-bad if rugged or blurred C: Color- bad if 2 or more colors D: Diameter-bad if >6 mm E: Elevation (raised surface) and Evolving

CHF m

ACE inhibit

what drug do you use for diabetic patient with hypertension?

ACE inhibitor cuz it will protect kidney also

Diabetes acute manifestations and chronic manifestations

ACUTE: insulin deficiency and glucagon excess due to unopposed glucagaon -decreased glucose uptake -increased proetolysis -increasd lipolysis All these contribute to dehydration, acidosis. Which can then lead to coma, death. CHRONIC -Nonenzymatic glycosylation ---Small vessel disease: retinopathy, glaucoma, nehphropathy ---Large vessel disease: Atheroscelrosis, CAD, peripheral vascular occlusve disease, gangrene. MI most common cause of death. -Osmotic damage ---Neuropathy (motor, sensory, AND autonomic degeneration so bladder and/or bowel incontinence can be seen, also impotence) ---Cataracts *Diabetic gastroparesis (delayed gastric emptying, rom autonomic neuropathy of Gi tract) presents with anorexia, nausea, vomiting, early satiety, postprandial fulness, and impiared glycemic control. Prokinetic agents (metoclopramide, erythromycin, cisapride) are useful in the management of symptoms. **Diabetic retinopahty: 3 main categories: 1. simple retinopathy: microaneurysms, hemorrhages, exudeates, retinale edema 2. pre-prolieferative: cotton wool spots 3. prolieferative or malignant retinoapthy: consists of newly formed vessels. -patients are normally asymptoamtic at first despite early signs of retinopathy (microaneurysms). Visual impairment occurs with developmend of macular edema. Argon laser photocoagulati ois the suggested treatemnt.

AD?

AD: males and females equally affected, vertical inheritance AR: horizontal inheritance would be more present with multiple children being affected from unaffected parents X-linked recessive: mroe males than females affected X-linked dominant: more females than males affected

Admission Orders stuff

ADA-Vitamin L A: Admit to: (name of admitting doctor and unit) D: Diagnosis A: Allergies : Allergies V: Vital Signs I : Ins (diet (clears, general, npo, etc) , ivf) T: Telemetry or other monitoring A: Activity M: Meds **Good Med mnemonic to know: BP SAD E. Bowels, Pain, Sleep, Abx, Dvt prohy, emesis I: Is and Os N: Nursing : Nursing L: Labs *Vital Signs- Vital signs q one hour (in ICU) "VS" typically includes temperature, blood pressure, heart rate and respiratory rate. If you want any additional vital signs they should be want any additional vital signs, they should be ordered specifically Example: Monitor CVP q one hour Monitor pulse ox q 4 hours All IVF orders need the type of fluid, any additives, p and the rate. Examples: D5.45NS with 20 KCl at 100cc per hour LR at 85 ccper hour .9NS at TKO (to keep open rate) Heplock IV (this means the IV is capped off and no fluids) Maintenance IVF: 4-to-1 thing A: Activity Examples: As tolerated bed rest no weight bearing to right foot ambulate with assist only Consider how frequently you want UO checked: • UO q one hour (typical for ICU pt with foley) • UO q shift NURSING Can include many things. Examples: Call HO for BP>170/90 <90/60 HR>120<60 RR>30<12 T>38 Call HO for BP>170/90, <90/60, HR>120<60, RR>30<12, T>38, UO<30cc/hour or 200/shift, Glucose >200<70 Dressing changes: wet to dry to right leg wound tid Keep leg elevated Call HO for any change in mental status Check and record pedal dopplers q 4 hours JP to bulb suction Foley to gravity Incentive spirometer q one hour while awake Teds and boots at all times unless ambulating

Indications for emergent hemodialysis

AEIOU Acidodi Elctrolyte disturbances Ingestions Overload (volume) Uremia

Absolute indications for emergent dialysis

AEIOU Acidosis: refractory to medical therapy Electrolyte abnormlaities: bad hyperkalemia toxic Ingestion: methanol, ethylene glycol, salicylates, lithium, valproate, etc. fluid Overload: volume overload refractory to diuretics. Uremia: percarditis, bleeding, encephalophty

What is kind of unique in how neuromuscular respirator failure might present

ALS or myasthenia gravis An increased residual voume/TLC ratio is commonly seen in obstructive diosrders but it may also be caused by a nerumuscular restrictive disorder. IN such cases, the normal FEV1/FVC ratio and low maximum respiratory pressures indicate neuromuscular weakness rather than an obstructive lung disease. So these patients have increased RV/TLC ratio, normal FEV1/FVC ratio, low maximum respiratory pressures, and normal Dlco.

BNP vs ANP

ANP released from atria BNP is released from ventricles. Measurement of serum BNP can help distinguish between CHF and other causes of dyspnea.

DDx of otalgia

AOM: Middle ear effuson PLUS acute eardrum inflammation ( bulgin eardrum, fever) Otitis media with effusion: Middle ear effusion without acute inflammation Bullous myringitis: Serous liquid-filled blisters on tympanic membrane Cerumen impaction: Liquid or hard wax in auditory canal obstructing eardrum visualization Hemotympanum: Purple or red eardrum +/- bulging. Its bleeding in middle ear going on, possibly from trauma. Otitis externa: Pain with tragal traction, erythematous and swollen external auditory canal. Drainage can happen.

Murmurs

AORTIC REGURG -Early diastolic decresendo mumru that is high pitched, blowing in quality, and best heard along left sternal border at 3rd and 4th intercostal spaces. The wide pulse pressure (systolic - diastolic), example would be a BP of 150/45. Pulmonary congestion. Water hammrer pulse-"bounding pulse i think" Best heard in some patinets only by applying firm pressure with diaphragem wiel the patient is sitting up, learning forward, and holding the breath in full expxpiration. The most comon cause of isolated AR in young ppl in developed countried is congenital bicuspid aortic valve. The mostt common cause in undeveloped is rheumatic heart disease. AORTIC STENOSIS: 3 most common causes of AS in general population : -Senile calcific aortic stenosis. People OVER age 70. -Bicuspid aortic avalve. -Rheumatic Heart disease. symptoms are syncope, anginal pain, dyspnea -radiates to carotids -remember that murmur of hypertrophic cardiomyopathy can easilty be confused ith that of aortic stenosis. Both cause a systolic crescendo-decrescendo murmur and an S4. Howver, the murmur of hypertrophic cardiomyopathy is usually best appreciated in the lower left sternal border and it does typically rdiate to the carotids. -Severe AS: soft, single S2 (as opposed to a normal split S2), delayed and diminisehd carotid pulse "parvus and tardus", loud and late-peaking sytolic murmur. Tx of choice is aortic valve replacement. balloon valvulotomy is not as good, only considered in certain clinical settings (patients with HD instability or significant comobidities) MITRAL STENOSIS -opening snap and low pitched mid-diastolic murmur ar the apex; pulmonary edema. heard best when patient lying on left side. MITRAL REGURG -holystlic murmur radiation to axilla MVP -causes mid-to-late systolic click that may be followed by a late systolic murmur. sytolic murmur of MVP starts longer (and is longer and softer) with standing, valsava, and inhalation of amyll nitrate. Its delayed in onset and shorter in duration with squatting, leg elevation, and handgrip. *most common valvular abnormality among the residents of industrialized nations, typically caused by redundant valve tissue at the valve ring (Barlow's syndrome) and may be associated with mild mitral regurg. fyi: aortic valve stenosis is most common congenital heart defect Tricuspde valve stenosis -mid-diastolic rumble best heard along left sternal border VSD -harsh holosystolic murmur at 4th left intercostal space -palpable THRILL -small restrictve ones have LOUDEST murmur, large nonrestrictive ones have a softer murmur -most common congenital heart defect, spontaneous closure in 40-60% of ppl during early childhood ASD and large left-to-right shunts -wide and fixed splitting of 2nd heart sound -may have mid-systolic ejection murmus resulting from increased flow across pulmonic valve -mid-diastolic rumble resulting from increased flow across tricuspid valve

Heart Sounds with Dr. Schaefe

AS vs MR-How to differentiate cuz both very common and sometimes hard to know which one you're hearing Location: ASL sash (you hear it everywhere) MR: hear it at apex Duration: AS: mid/late MRH holo after pause: AS: increases MR: no change Midsystolic murmurs grade 2/6 or less are considerd innocent murmurs, espcially when they are short in duration. Severe AS: late peaking (cuz it takes so long for valve to open). Delayed and Diminished upstroke pulse (carotid). No S2. Radiate to carotid. General stuff. -You hear S2 sounds more on Aortic and Pulmonic valve. -Another way to know if its systolic or diastolic is feel the carotid upstroke. Carotid upstroke is during systolic. If murmur happens during upstroke then you can know its systolic. -An innocent murmur you can hear on upper left sternal border, its soft, its systolic, and you get normal S1 and S2. If it's holosystolic it's not going to be innocent. -YUou can hear it on "Sash" area=arortic -Sometimes you can confuse splitting with S3. Good clinical thing to know that you're prob not going to hear an S3 during a normal exam with person laying down and you;'re using the diaphragm. If you hear something during that then its most likely a splitting sound. Most of time you really have to hunt for the S3, like have person lay on left side and listen with bell on mitral region. S3-you gotta look for it most of time, have person lay on left side and listen with bell. indicates some kind of volume overload. Like if healthy young person has slow heart rate, that means more blood builds up in LV so you get S3. S4-always pathologic, a lot of blood hitting stiffened LV

What lab values charactreize alcoholic hepatitis?

AST>ALT over 2, elevated GGT ( an enzyme found in liver cells and oother cells) and elevated ferritin (an acute phase reactant). The absolute values of AST and ALt almost always <500 in alcohohlic liver disease.

DDx of chronic cough

ASTHMA *Cough induced by forced expiration is characteristic of airway hyperreactivity, and is usually suggestive of asthma; howver, this presentation has also been described in some patiehts with COPD who can sometimes have overlapping asthma. *GERD is present in up to 75% of sthma patients and is in fact the primary trigger of asthma in many patients. Halfo of patient suffereing from GERD-induced asthma do not report classic heartburn symptoms. Asthmat that presents in adulthood and is worst after measls, exercise, or laying down (nocturnal asthma) should raise suspicion for underlying GERD. Also hoarseness. So if you suspect GERD, trial of PPI can be both diagnostic and therapeutic for the asthma symptoms. GERD POSTNASAL DRIP ---for patients with suspected postnasal drip initial empiric Tx include oral 1st generation antihistamine ( chlorpheniramine) OR combined antihistamine-decongestant (brompherniramine and pseudoephedrine). Dr. Castillo likes to start with Claritin, then goes to Allegra, then Montelukast, then Zyrtec if going from non-drowsy to drowsy. Benadryl is the most drowsy. also--always consider ACE-inhib use as cause of dry cough. the mechanism by which they cause cough is INCREASED kinins and possiblty the activation of the arachidonic pathway. **Uworld ALGORITHM for chronic cough -stop ACEinh, put on 1st generation antihistamine if suspect post nasal drip, do PFTs if suspect asthma, do empiric PPI if suspect GERD. If it ain't working then do a chest x-ray, if you suspect other things first off like parenchymal disease, or purulunet sputum then just go straight to chest x-ray. *for treatment of postnasala drip, patient who do not respond after 2-3 WEEKS may require further investigation (sinu imagin, PFTs, CT scan) or empiric sequential therapy for GERD, cough-variant asthma, chronic sinusitis, and non-asthmatic eosinophili bronchitis.

AKI has pre-reanl, post renal, and intrinsic. What are the intrinsic causes?

ATN due to ischemia, toxins like medications, myoglobin from rhabdo, IV contrast, crystal induced (common etilogies are acyclovir, sulfonamides, MTX, etyhlene glycol, protease inhibitors). AIN Vascular disorders and atheromatous emboli Nephrotic and nephritic syndromes AIN STUFF TO KNOW Inflammation of interstial part of kidney. ATN is damage to actua tubule part. Causes: Systemic: sarcoidosis, Sjogens, lymphoma Systemic infections like Legionella, Strept. Medications: Beta-lactams, diuretics, NSAIDS, PPIs, allopurinal -usually associated with exposure to medications such as beta lactams and proton pumop inhibitors. However, AIN usually occurs 3-5 days after drug exposure. Patients can develop findings that include skin rash, eosinophilia, esoinophiluria, and pyuria. You see: -rash, fever ( other signs of systemic hypersentivitiy) -eosinophilia -eosinophils in urein -WBC casts! (pyelo causes WBC casts as well). -also RBC casts i think. Tx; stop durg, give steroids if severe ***Analgesis nephropathy Most common form of drug-induced chronic renal failure. PAPILLARY NECROSIS and chronic tubuloINTERSTITIAL nephritis are the most common pathologies seen. -Occurs with heavy long-term use of analgesics such as aspirin, acetaminophen, or other NSAIDs. Nephropathy is usually chronic but may present acutely with hematuria, pyuria, proteinuria, and renal colic. Sloughing of the papilla may cause hematuria and present acutely as renal colic. Urine studies show hematuria, proteinuria, and pyuria with SBC casts, but the urine culture is usually sterile. Discontuination of the analgesis will cause stabilization or even improvement of renal function.

how do you diagnose diverticulitis?

Abdominal CT. You wanna avoid sigmoidoscopy cuz might cause perforation, but can be done if clincialy indicated after resoulation of the diverticulitis.

AAA Dx and Tx

Abdominal or pack pain, pulsatile mass in abdomen, hypotension Gold standard for Dx: Angiogram. US, MRi, CT w/ contrast are really good as well. Strognest predictor of AAA expanision and rupture? large diameter, rapid rate of expanision, and cigarrette smoking

Why do you see abnromal bleeding in chronic renal failure?

Abnromal bleeding is a common manifestation in patients with chronic renal failure. Abnromal bleeding and bruising are characterisitic of uremic coagulopathy. Nowadays, ecchymoses and epistaxis are the only major bleeding mainfestionats seen due to the advent of dialysis; however, GI bleeding, hemopericardium, subdural hematoma, and bleeding from surgical or invasive sites can still occur due to uremic coagulopathy. The pathogeneis iss multifactorial, but the major defect involves platelt-vessel wall and plateley-platelet interaction. PT, PTT are normal. BT is prolonged. DDAVP is treatment of choice. Platelet transfusion is not indicated because the transfused platelets quickly become inactive. *extremely high yield question for USMLE

Raynaud phenonemonn

Abnromal vasoconstricition of digital arteries in response to cold or emotional stress. PRIMARY -no underlying cause -usually women age <30 -no further evaluation -Ca channel blockers for persistent symptoms SECONDARY -secondary to systemic disease, espeically autoimmune -workup should include CBC, CMP, UA, ANA, RF, ESR, Complement

Primary care: peds stuff

Accidents and injuries are leading cause of death in children over 1 year: -A child should sit in rear-facing car seat until the child is both 1 year old and wieghs at least 20 lb. Leading cause of death of infancts younger than 1 year of age is SIDS. -make sure infants sleep on back on firm mattress with nothing else in the crib: this includes pillows, positining devices, and toys.

Hydrocele

Accumulation of fluid around the testis and spermatic cord and between the parietal and visceral layers of the tunica vaginalis. Communicationg hydroceles usually present in infancy and are frequently reducible but may also increase in sixxze with the Valsavla maneuver. Noncommunication hydroceles do not usuallychange in size with positional changes. IN addition, they transilluminate.

CYP450 inhibitors, increased bleeding if on Warfarin

Acetaminiophen, NSAIDS Antiobiotics/antifungals (metronidazole) Amiodarone Cimetidine Cranberry juice Omeprazole Thyroid hormone SSRIS

Osteoarthritis

Acetaminophen should be the initial treatment for patients with mild to moderate pain from osteoarthritis. Also, if a particular joint is too bad, intra-articular corticosteroid injections may provide relief for varying amounts of time, but should only be done very 4 to 6 months so as to avoid cartilage destruction. Surger, such as joint replacement, is usually reserved for people with severe disease that affects their daily functions. 6 criteria used to diagnose: age >50 crepitus bonly enlargement bony tenderness lack of warmth/significant morning stiffness if three or more criteria are met, the specificity for OA is 69%. Bouchard's nodes: at PIP joints. Present in OA and RA. Heberden's nodes: at DIP joint. Present in OA. REMEMBER there can be morning stiffness similar to RA but with OA the morning stiffness goes away after 30-60 minutes. Hip osteoarthritis you have limited internal and external rotation. Classicaly, internal rotatoin WORSENS the pain.

Achalasia vs Diffuse esophageal spasm

Achalasia -weight loss, cough, diffuse chest pain -LES can't relax on swalloing -looks like birds beak on barium swallow -relieved by nitroglycerin DES -dysphagia, diffuse chest pain -swallowing induced large wave -looks like corkscrew on barium swallow -releived by nitroglycerin

HIV skin stuff

Acute HIV: present generalized rash appearing as small and well-circumscribed red macules or papules Chronic HIV: associated with variety of skin lesions including molluscum, Kaposi sarcoma, and recurrent herpes zoster *also seborrheic dermatitis is common in HIV infection and can be a presenting feature.

Mono type disease and how to differentiate

Acute HIv infection : smptoms within first 6 omonths of infection -can present as mononucleosis type syndrome with FEVER, night sweats, arthralgias, LYMPHADENOPATHY, 2-4 weeks aftr infection. The presence of PAINFUL MUCOCUTANEOUS ULCERATIONS (a chracteristic manifestation), SKIN RASH (50%) and PROLONGED DIARRHEA (30%) may help differenate acute HIV infection from other conditions such as mono. **The painful oral uclrers, arthralgisa, and rash can make acute HIV infection loook a whole lot like SLE. HOwver, you will rarely see DIARRHEA in SLE, which you see often in acute hiv.

Acute Liver Injury and Failure. Intern Boot Camp

Acute Liver Injury and Failure Acute Liver Injury: liver injury +synthetic dysfunction + hepatic encephalopathy. In someone without prior liver history. -main goal is to make sure person does not go into acute liver failure. Acute Liver Failure: Causes: Lab Tests: -get tylenol level: tx is nAC Viral Hepatitis: Hep B, Hep C, reactivation of Hep B, Hep D, Hep E. HSV: fever comes with it Shock liver Autoimmune hepatits: ANA, Anti-Smooth, quantitative IgG. If those are positive, definitive diagnosis is liver biopsy. Tx: steroids. Wilsons: dont wanna miss. mortality rate of 98% without transplant. Get ceruloplasmin, 24 hour copper. Hepatic vein clot. Budd Chiari. Also: Check Factor 5, only one that is not Vitamin K dependent. If its lower, you have liver problem. Labs: every 6 hours, get CBC, CMP, coags, ammonia. Imaging: Get abdominal US for clot Manifestations/Treatment by Organ System: Brain: Encephalopathy. bad encephalopathy can lead to increased ICP, that is the danger. Ammonia >150 increased risk for high ICP. Ammonia important in acute liver problem, in chronic liver patient, ammonia level not that useful. Tx: lactulose. Neuro checks every hour. wanna get neuro involved. Don't give them narcotics for any reason, it will throw off the euro exam. Liver: Bleeding problems, clotting problems. Important that we do q1hour fingersticks, these patients get really hypoglycemic cuz gluconeogenesis is impaired. Heart: will get a low EF, it will look like sepsis. Lungs: Develop ARDS pretty quickly. Adrenal: adrenal insuffiency so they will be hypotensive, so will require pressers if that happens. Kidney: renal insufficiency. Other: prone to infection, so wanna get CXray, blood cultures, urine cultures. Do all this every 48 hours.

Digoxin toxicity?

Acute digoxin toxicity typically presents with GI symptoms (anoreia, nausea, vomiting, abdominal pain). Chroinc digoxin toxicity presents with less pronounced GI symptoms but more significant neuologic and visual symptoms (changes in color vision, sctoomas, blindness). Amidoarone can increase the serum levels of digozin and cause toxicity in a patient on a stable digoxin regimen. Also verapamil and quinidine do this as well, so can cause digoxin toxicity. Patients chronically taking digoxin should have close and ROUTINE monitering of their digoxin levels. Digoxin-specific antibody (Fab) is antidodote for digoxin toxitycty.

What is acute acalculous cholecytitis?

Acute inflammation of the gallbladder in the absence of gallstones, most commonly seen in hospitalized and severely ill patients in the following conditions....extensive burns, sever trauma, prolonged TPN, prolonged fasting, mechanical ventilation.

Gastritis

Acute of chronic inflammation of the stomach Etiology: -Incrased acid: by smoking, alchohol, stress -Decreased mucosal barrier: NSAIDs, steroids, H pylori -Direct irritant: pancreatic and biliary reflux, infection -Autoimmune Signs: pain worsened by food, relieved by antacids Dx; endoscopy Tx: similar to PUD-no NSAIDs, + Triple therapy to destory H. pylor if present, no alchohol and cigarretes, H2 blockers, antacids Coplications of chronic gastritis: gastric atrophy, metaplasia, carinoma, lymphoma. Pernicious anemia due to decreased production of intrinsic factor from parietal cells

Lumbar disk herniation

Acute onset of back pain with or without radation down one leg. Patients usually recall an inciting even. As with lumbar spinal stenosis, the pain may be radiating and be associated with neurologic symptoms. However, in disc herniation, lumbar flexion and sitting will make the pain worse.

Treatment of sinusistis.

Acute sinusti: Antibiotic tx is NOT indicated. Can go with antihistamines and antiinflammatory medications. If severe symptmos persist go with antibiotics Persistent chronic sinusitis: may require subspecialist

Acute mesenteric ischemia vs Chronic mesenteric ischemia vs acute colonic ischemia

Acute: Sudden onset of abdominal pain due to actue occlusion of mesenteric vessel by emboli or thrombosis; emergency. Usually the SMA involved. Lab data may show elevated Hb and Hc% secondary to hemoconcentration and leukocytosis. Chronic: Episodic postprandial dull pain, due to slow narrowing of vessels, due to atherosclerosis; weight loss associated, not emergency Gold standard Dx: angiogram acute colonic ischemia: usually due to transient reduction in blood flow to colon due to hypovolemic states or transient ischemia to the bowel. It affects primarily the watershed areas (splenic flexure, rectosigmoid). Patients have lateralized abdominal pain followed by BLOODy diarrhea. Pain is mild to moderate and no as severe as acute mesenteric ischemia.

Acyclovir toxicity?

Acyclovir nephrotoxicity. It causes crystalline neprhopathy if adquate hydration is not also provided.

You are working up something else and a CT scan reveals an adrenal mass, or "incidentaloma." What do you do

Adrenal massess are common. Even if patient has no ssymptoms to suggest adrenal pathology, all adrenal masses require workup for hormone hypersecretion or malignancy. In any patient with an adrenall mass, essential lab studies are.. 1. serum electrolyes 2. dexamethasone suppression testing 3. 24 hour urine catecholamine, metanephrine, vanillylmendelic acid and 17-ketosteroid measurement Surgical excision is required for fall functional tumors, massses with evidence of malignancy, and all tumors greater than 4cm. Otherwise you do serial abdominal imagin and remove if they increase with size.

Patient with adrenal insufficiency and calcifications in adrenal glands?

Adrenal tuberculosis. Most common cause of primary adrenal insuficency in developing countries. In developed countries, it is autoimune adrenalitis that is the most common cause of primary adrenal insufficiency.

Know Lead anemia

Adult lead toxicity is usually due to occupational expsoure. Patients may present with nonspeicif symptoms (fatigue, irritability, insomina), myalsias, hypertension, nephropathy, neurocognitive deficits, and peripheral neuropathy. Diagnosis is made via blood lead levels, complete blood count with blood smear, and x-ray fluorescence to measure bone lead concentration. Treatment of lead poisoning is via chelation therapy.

INflammatory chronic prostatisis

Afebrile and have irritative voiding symptoms. US normal, cultere negative from prostatic secretions. Lukeocytes count greater than 10 on prostatic secretions.

Noninflammatory chronic prostatitis?

Afebrile and hvae irritative voiding symptoms. Expressed prostatic secretions show a normal number of leukocytes and culture of these secreetions is negative for bacteria. Iq

Which withdrawals are life threatening, which are not?

Alchohol and benzodiazepine withdrawals are life threatening Opioid and cocaine withdrawal are NOT

Alcoholic cirrhosis

Alcoholic fatty iver is reversible form of liver injury, often precedes cirrhosis AST/ALT ration > 2 GGT is most sensitive serum marker for alcohol bingeing *AST is also released from other tissues, such as heart and skeletal muscle. THerefore , elevations of ALT, which is minimally produced in nonhepatic tissues, are more specific for diagnosing liver disease.

Cyclophosphamide?

Alkylating agent ferquently used as an immunosuppressant in SLE, vasculitis, and certain cancers. It has serious side effects, like acute hemorrhageic cystitis, bladder carcinoma, sterility, and myelosuppression.

Vaccines for adults

All adults should have tetanus and diphtheria boosters (Td) at least every 10 years, with a one-time dose of Tdap to all adults age > 19 as immunity from previous vaccination tends to wane at that time. -Tetanus immune globulin: is indicated for patients who have not completed the primary service (3 doses) of tetanus immunizations or in patients who have an unclear immunization history. When looking at an injury. -Also with injuries: Tetanus booster vaccination can be omitted in patients who received a tetanus booster within the past 5 years and in patients with clean minor wounds who have received vaccination within the past 10 years. All adults require yearly influenza. -contraindicaations: standard contras, history of severe anaphylaxis to eggs Pap smear at age 21 with pap smear every 3 years. For woman age 30-65, screening is recommended with Pap smear every 3 years or with a combination of Pap smear and HPV testing every 5 years if both initial tests are negative. -Normal person >65: gets PCV 13 folowed by PPSV23 6-12 months later -Very High Risk person <65 (immunocompromssed, CKD, sickel cell): get PCV13 followed by PPSV23 -Person who is current smoker or has chronic liver, diabetes, or heart disease: PPSV23 is given ALONE when <65. When they reach 65, they then get the normal sequential PCV13 followed by PPSV23. Be sure to wait at least one year between the ALONE PPSV23 and the PCV13. -PPSV13 (4 doses) all infants and children should get. Zoster vaccine: -indicated in immunocompetent patients older than 60 years for the prevention of herpes zoster (shingles). Its a live vaccine and is contraindicated in people with active, untreated TB, immunocompromosed patients, patients receiveing chemo, radiation or large doses of corticosteroids. Immunization should be avoided if an immunocompromised person is living in the househould. Hep B: 3 doses Hep A: Given in 2 doses, minimum time interval between first and second dose is 6 months. *Hep A and B vaccines are indicated in adults with chronic liver disease, homosexual men, injection drug users, househoud contacts with Hep A or Hep B. Meningococcal vaccine is indcated for adults with asplenia, military recruits, all college students in dorms, terminal complement deficiency, travelers to Mecca. --So at age 11-12 person should get primary menigococcal vaccination. In addition, all patients who were vaccinated before age 16 should get a BOOSTER vaccination at ages 16-21. Misconceptions about containdications to vaccination: Following are NOT contraindications: mild illness ( common cold, low grade fever, mild diarrhea), recent exposure to communicable disease, breastfeeding, current antibiotic therapy, history of nonspecific reaction to penicilin HIV people: everything goes with normal adult with some exceptions... -if CD4 count is < 200 then no live vaccines -if CD4 count >200 then can get MMR and VZV but no other live vaccines -Should get the Pneumococcal conjugate vaccine (13 valent) if not previously reveived -SHould get pneumococcal polysaccharide vacicine (23 valent) every 5 years *explanations of the pneumoncoccal vaccines. 2 types are given in the US. 1. Pneumococal polysaccharride vaccines (PPSV23): contains capsular material from 23 serotypes that have historically been responsible for the majority of pneumoccoal infections. Because polysaccharids alone cannot be presented to T cells, the vaccine induces a relatively T-cell-independent B-cell response that is less effective in young children and elderly. 2. Pneumoccocal conjugate vaccine: consists of capsular plysaccharids from 13 of most common serotypes that have been covalently attached to inactivated diptheria toxin protein. This polysaccharide-protein conjuage induces a T-cell dependend B cell response, resulting in improved immunogenicity due to formation of higher -affinity antibodies and memory cells.

Platelet disorders

All of the increse bleeding time (how long you bleed) and decrease plaetelet count (excepto glanxman thromboasthenia, Uremia, VWD). Bernard soulier syndrome: defect in platelt plug fomration. Increased bleeding time and low plateltes. Glanzmann thrombasthenia: defect in platelt plug fromation by another mnechanism. Periph smear shows no plaetles clumpgin. Normal bleeding time and normal plateltes. ITP (immune thrombocytopenia): make anti Gp2b antibodies so spleen macrophages start to eat the platelt/antibody complexes. Trigggers by viral illness commonly. Lab: increased megakaryocytes on bone marrow biopsy. ONLY PTT INCREASED, low platelets, and increased bleeding time. Tx: steroids, IVIG. If still a problem then splenectomy. **all ITP patients should be tested for HIV and Hep C. TTP: FAT RN Fever Anemia Thrombocytopenia Renal dysfunction Neurologic abnormality you don't have the vWF metalloprotease ADAMTS 13 so you can't degrade the vWF multimers--> platelets aggregation and thrombosis. Labs: schicstocytes and increased LDH TX: exhange transfusion (cuz you wanna get rid of the antibodes against ADAMT13 in the plasma and steroid). platelet transfusion contrindicated. PT and PTT are NORMAL in TTP, unlike in DIC. Low plateltes and increasd bleeding time. ALSO.. Uremia: qualitative plaelet disorder can be result of uremia. Metabolic by products inhibit plaetletes. NORMAL platelet count. -PT, PTT are normal. BT is prolonged. DDAVP is treatment of choice. Platelet transfusion is not indicated because the transfused platelets quickly become inactive. VWF deficiency= high PTT and increased bleeding time. NORMAL platelet count. Tx: DDAVP DIC: you have prolonged aPTT (due to depletion of clotting factors), PT, and LOW PLATELETS. low fibrinogen (due to consumption), elevated D-dimer (due to accelerated fibrinolysis). *Tx: Reverse underlying cause, RBC transfusion, platelet transfusion, and shock management. VIT K deficiency (not really platelte disorder but wanted to include): due to inadequate diet, malabsorption, or liver disease. An acutely ill person with liver disease can become Vit K deficient in 7-10 days. You see HIGH PT and HIGH PTT. Normal platelets. Antiphospholipid syndrome: low platelets, prlonged PTT, false positive VDRL. prophy w/low dose heparin. Hemophilia (not really platelet disorder but wanted to include): XR so almost only in males. normal plateltes, normal bleeding time, normal PT. High PTT. Decreased or absent factor 8 or 9. you see hemarthrosis, hemophilic arhtropathy, intramsuscular hematomas, GI bleeding. Tx: Give factor 8 or 9.

How do you treat newly diagnosed HCV infection?

All patients should be evaluate for antiviral treatment. LIVER BIOPSY should be done first because if offers the best clinical predictor of disease progression and helps assess likely response to treatment. It can also determine the stage of disease, rule out other concomitant liver disease (hemochromatosis) and guide treatment decisions (duration, suveillance).

Management of acute COPD exacerbation?

All patients should receive.. -oxygen -bronchodilators -systemic glucocorticoids: 40mg prednisone for 5 days. if needs longer then need to taper afterwards. **prolonged prednisone usage may require Bactrim prophylaxis -in addition: antibiotics are indicated for patients with the following: 2 of 3 cardinal symptoms of acute COPD exacerbation (dyspnea, cough, sputum production), moderate to severe COPD exacerbation or mechanical ventilation, -if still not cutting it, then you go to NPPV (non-invasive positive pressure ventilation). You want to try at least a 2 hour trial of this before you go to mechanical ventilation with endotracheal intubation. TRIGGERS: 70% of exacerbations are due to viral or bacterial infection (URI). The other 30% is environmental pollution, PE, and unknown etiology. Medical history — By definition, patients present with the acute onset or worsening of respiratory symptoms, such as dyspnea, cough, and/or sputum production, over several hours to days. These symptoms should be characterized further in terms of the following features: ●Time course of the symptoms ●Comparison to baseline level of symptoms ●Severity of respiratory compromise (eg, dyspnea at rest, dyspnea climbing stairs) ●Delineation of sputum characteristics (eg, amount, purulence, blood) Associated features that would suggest an alternate diagnosis or comorbidity include: ●Constitutional symptoms (eg, fever, chills, night sweats) ●Chest pain, chest pressure, or peripheral edema ●Risk factors for thromboembolic disease or coronary disease ●Upper respiratory symptoms that might suggest a viral respiratory infection The past history of exacerbations should be ascertained: number of prior exacerbations, courses of systemic glucocorticoids, and exacerbations requiring hospitalization or ventilatory support.

Use of Chest X ray and sputum culture in diagnosing pneumonia?

All patients with suspected pneuonia shold get a chest X-ray. Sputum culture is optional in outpatient setting due to low yield of culture results and high success rate of empiric antibiotics. Exceptions may apply if there is concern for certain specific organisms or for epidemiologic reasons ( MRSA, Legionella, M tuberculosis, endemic fungal infection)

Gilberts vs Crigler-Naijjar Type 1 vs Crigler Najjar Type 2 vs Rotor vs Dubin Johsnon

All unconjugated hyperbilirubinemia Gilberts-tend to see symptoms by triggers like fasting, fever, stress, fatigue, etc. Crigler Type 1-Severe jaundice and kernicterus. Phototherapy or plasmapheresis are typically helpful in short term, though liver transplat is only curative option. Crigler Type 2-Mild. No kernictuers going on. IV phenobarbital can reduce serum bilirubin. Treatment often unnecessary in midler cases. Rotor-benign condition in which there is a defect of hepatic storage of conjugated bilirubin, resulting in its leakage into plasma. Chronic and mild hyuperbilirubinemia of both unconjugated and conjugated forms develops. Tx is unnecessary. Dubine Johsnon-results in conjugated hyperbilirubinemia. A dark granluar pigment is present in the hepatocytes of patients with Dubin-Johnson.

Osteoporosis screening?

All women age >orequal 65, or postmenopusal women w/ one or more risk factors for fracture, or men with risk factors for fracture.... should get the DEXA scan of spine and hips. Ealier screening can be considered for women with additional risk factors. Protocols for repeat screening are not well established. Osteoporiss is defined as bone density >2.4 standrad deviations below the mean for a yong adult (Tscore <-2.5) . Osteopenia is Tscore -1 to -2.5 Risk factors: poor calcium/vit d intake, smoking, steroids use, lack of weight bearing exercise, low BMI, heavy alcohol use *Also it is recommended that all women over age 50 should get at least 1200 mg of calcium and 400-800IU Vit D per day. If dietary intake not sufficienty, supplements can be used. *About half of all women will have an osteoporosis related fracture *Asian and Caucasian women are at higher risk for osteoporosis than African American women

Explain the asthma categories and Txs

Allergens that may be responsible for asthma include house dust mite allergens, cat allergens, dog allergens, and cockroach allergens. Of these, house dust mites have the strongest association with asthma; thse may be responsible for 60-90% cases of asthma. there are 4 categories: intermittent, mild persistent, moderate persisitent, and severe persistent. INTERMITTENT Daytime symptoms <orequal 2x/week, nightitime awakenings lessorequal 2x/month, beta agonists lessorequal 2x/week, normal baseline FEV1 and FEV1/FVC and no limitations on daily activities. Tx: short acting beta 2 agonist (albuterol) PERSISTENT -Mild: symptoms >2 days/week but not daily, nighttime awakenings 3-4x/month, minor limitation on activities, and normal PFTs Tx: PRN albuterol inhaler and inhaled corticosteroids (low dose) -Moderate: symptoms daily, weekly nighttime awakenings, moderate limitation on activitie and FEV1 60-80% of predicted Tx: PRN albuterol inhaleer, inhlaed corticosteroids, long acting beta2 agonist -SEvere: symptoms throughouth the day, frequent nighttime awakenings, extremely limited activity, and FEV1<60% predicted Tx: PRN albuterol inhaler, long acting beta 2 agonist, high-dose inhaled corticosteroids. Oral prednisone can also be used in cases of severe persistent asthma. ***after the long acting beta agonist it kind of gets personalized. This is the step wise pattern that dr. basil follows...albuterol prn..then low dose inhaled steroids...then long acting beta agonist...then increase to medium dose corticosteroid...then anticholinergic...then montelukast. This is just outpatient mainetnance medications, inpatient asthma treatment would not follow this. ASTHMA ASsOCIATIONS -Allergic rhinitis, asthma, atopic dermatitis -Nasal polyps, aspirin, asthma -ABPA allergic reaction to aspergillus antigen. Doesn't mean infection. characterized by fleeting infiltrates, recurrent asthma exacerbations, and central bronchiectasis. -Churg Strauss SOME COMMON MEDICATIONS -Duoneb: albuterol and ipratropium -Advair: steroid and long acting beta agonist -Symbicort: this one used in COPD. Steroid + long acting beta agonist. -Singulair: Montelukast

Primary Care: Allergic rhinitis

Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses and pharynx. Inlfammation of the mucous membranes is ultimatley triggered by an IgE mediated response to an extrinsiv protein. In susceptible people, exposure to certain foreign proteins leads to allergic sensititization which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When the specific allergen is inhaled into the nose, it can bind to the IgE in the mast cells, leading to the delayed release of a number of mediators. CAUSES: depends on whether its - perennial rhinitis (symptoms occur at consistent level throughout the year), seasonal rhinitis (only at specific seasons), a combinatin of the two, or in relation to workplace (occupational rhinitis). -perennial rhinitis typically caused by allergens within the home (dust mites, pets), but can also be caused by outdoor allergens that are present year-round -some patients are senstiive to multiple allergens can have perennial allergic rhinitis with seasonal exacerbations. although food allergy can cause rhinitis, particularly in children, its rarely a cause of allergic rhinitis in absence of GI or skin symptoms. Seasonal alelrgic rhinitis is commonly caused by allergy to seasonal pollens and outdoor molds. SYMPTOMS sneezing, itching of eyes, nose or ears, rhinorrhea, postnasal drimp, congestion, anosmia, headace, earache, tearing, red eyes, drowsiness. PHYSICAL EXAM FINDINGS: -"allergic shiners": dark circles around eyes related to vasodilation or nasal congestions -"nasal crease" can be seen in some cases: Its a horizaontal crease across the lower half of the bridge of the nose caused by repeated upward rubbing of the tip of the nose by the palm of the hand "allergic salute". -mucosa of nasal turbinates may be swollen (boggy) and have a pale, bluish-gray color. -thin and water secretions frequently associated with allergic rhinitis whereas thick and purulent secretions are usually sinusitis. -otoscopy should be performed to look for tympanic memrane retraction, air fluid levels, or bubbles. -Dennie-Morgan lines (prominent creases below the inferior eyelid) are associated with allergic rhinitis. -"cobblestoning" of the posterior pharnyx is often observed. this is caused by streaks of lymphoid tissue on the posterior pharynx. TREATMENT: 4 major categories: patient eduction, allergen avoidance, pharmacologic, immunotherapy PHARMACOLOGIC -1st generation antihistamines: diphenhydramine (Benadryl), chlorpheniramine, hydroxyzine --watch out for anti-cholinergic effects -2nd generation antihistmaines: loratadine (Claritin, desloratadine, fexofenadine (Allegra), cetirizine (Zyrtec) -Decongestants:oral or intranasally. used to provide symptomatic relief of nasal confestion. These agents constrict blood vessels in the nasla mucosa and reduce the overall volume of the mucosa. most common one is pseudoephedrine (SudaFed a big one) -Corticosteroid nasal sprays: are the most effective treatment and 1st LINE THERAPY for long term management of mild to moderate persistent symptoms of allergic rhinitis. Reduces inflammatory response in nose. Systemic absorption is low. Side effects include nosebleeds, pharyngitis, and URIs. Maximal effectiveness after 2-4 weeks of use. -Leukotriene inhibitors (montelukast and others): are indicated for both allergic rhintis and persistent asthma. Are useful, but not proven to be superior to steroid nasal sprays alone. -Oral corticosteroids: effective but many side effects, only for severe cases. -Desensitization therapy: if frequenlty attempted i patients who remain symptomatice despite maximal medical therapy. The first step is to test for specific antigens to whith the person is allergic. Second step is to inject the patient with higly diluted concentrations of this antigen. The concentration of the antigen in the injection is gradually increased, in an effort to reduce the patient's inflammatory response to the antigen. Injections are typically iven weekly or biweekly. Expensive, time consuming, and requires numerous injections. Patients and physicians mut be prepared to address severe, even anaphylactic, reactions that may occur.

What should be done iniitalluy in case of acute abdominal pain?

Although an abdominal CT scan is usually necessary for definitie diagnoses of acute abdominal pain, initial screening with supine and upright abdominal X-rays should be done first to look for air-fluid levels, suggestive of a bowel obstruction, and free peritoneal air, suggestive of a perforated viscus.

Sucralfate?

Aluminum sucrose sulfate, topical therapy for PUD and GERD. Sucralfate adheres to the mucosal surface and promotes healing by unknown mechanism.

Management of hyperglycemmia and diabetes mellitus in the hospital setting

American Diabetes Association suggests the following glycemic goals in the hopsital setting: -premeal 100-140 -post-meal/random <180 -patients with insulin infusion 140-180 Insulin is the mainstay therapy for treating diabetes in the hospital setting and has 3 basic components: 1. Basal (intermediate or long-acting) insulin for controlling glucose levels between meals (necessary for all patients with type 1 diabetes and most with type 2 diabetes) 2. Nutritional boluses (short-acting) of insulin to control blood glucose increase following a meal (not required if patients are not eating) 3. Correctional boluses (short-acting) of insulin to decrease high glucose levels (commonly referred to as "sliding scale")

Drugs/supplements that affect warfarin

Amiodarone therapy: this is used as a type of rhythm control for A-fib so there can be times where you're using this and patient is on Warfarin for A-fib as well. Amiodarone slows warfarin metabolism in liver by inhibiting cytochrome enzyme system. It is recommended that the warfarin dose be reduced by 25-50% to compensate for the increase in serum concentration of warfarin after initiating amiodarone therapy.

Apple-green birefrignece under polarized light after staining with Congo red on renal boipsy?

Amyloidosis which causes nephrotic syndrome

Explain a blood pressure of 165/75 in old person

An example of isolated systolic hypertension, an important cause of hypertension in elderly patients. It is caused by decreased elasticity of the arterial wall. ISH should always be treated due to its association with an increased risk fo cardio events. Initial treatment involves monotherapy with a low dose thiazide, an ACE inhibitor, or a long-acting calcium channel blocker.

What is an anal fissure? tx?

Anal fissure are slit-like tears of the anal canal. Initial treatment of both acute and bhronic anal fissures includes dietary modification (high-feber diet and large amounts of fluids), a stool softener, and a local anesthetic. If chronic fissure is refractory to Tx then go with lateral sphincerotomy, provides wider aperture for stooll to pass

Hair loss

Androgenetic alopecia (male pattern baldness): starts in the frontal or temporal areas and progresses gradually Alopecia areata: smooth and discrete areas of complete hair loss. There is no associated scaling, scarring, or inflammation. -exact etiology unknown. can commonly recur in patients even after successful treatment and normal hair growth -Tx: topical or intralesional steriods are the preferred first line treament in patients with alopecia areata. Tinea capitas: have associated scaling and inflammation of the scalp in areas of hair loss. Discoid lupus erythematous: causes hair loss, scaling, inflammation, scarring, and hypopigmentation of the skin. there may be assoicated lestions present over the face or extremeties.

Evaluation of anemia in end stage renal disease

Anemia in patients with ESRD is usually due to decreased renal eryhtropoietin, but other causes like iron deficiency should be ruled out before starting eryhtropoietin-stinulating agents (ESAs). ESA is recommended for ESRD patients with... -hemoglobin <10 with a target of 10-11.5 over 4-6 weeks. *irone deficiency can develop due to blood bloss from frequent blood testing, GI blood loss (common in those with ESRD) or dialysis itself. *Absolute iron defieincy is defined as transferin <20% or ferritin <100ng/mL. However, the underlying inflammation associated with ESRD and dialysis can significantly increase serum ferritin and nake it less accurate measure of iron defieincy. Other things like serum iron, transferrin satrutation, TIBC can help clarify. ***ESRD patients with transferrin saturation <orequal 30% and ferritin <orequal 500 ng/mL requires iron supplementation, preferably with IV iron instead of oral iron. If ferritin >500 thise usually reflects good iron stores and will respond to ESA most likely. If not, usually means the ESRD has a "functional iron deficiency" (normal iron stores with inability to mobilize it in response to erythropoietin), defined as transferrin saturation <20% with ferritin 100-800. Because ESAs increase iron demand, these patients should have iron studies prior to starting ESAs. Testing should continue periodically, espeically in those without appropriate response to ESAs.

Basophilic stippling what causes?

Anemia of chronic disease Alchohl abuse Lead poisoning Thalasesemas

What is angiodysplasia and what are the associations?

Angiodysplasias are a common cause of recurrent or occult PAINLESS lower Gi bleed in ELDERLY patinets. They have been reporte dto cause lower Gi bleed in patients with AORTIC STENOSIS (Heyde's syndrome) and end-stage RENAL diseae (due to uremic dysfunction f platelets). They are dilated, ectatic, thin-walled vessels that are lined by endotherlium and prone to recurrent and chronic painless bleeding.

Treatment for fibromusclar dysplasia

Angioplasty with stent in the renal artery stensosi

Shoulder pain

Anterior shoulder pain: seen in patients with acromioclavicular or glenohumeral joint osteoarthritis. OR biceps tendonitis. Posterior shoulder pain: least common. Usually refered pain from the cervical spine. Common causes are nerve impingement due to disc herniation and spinal stenosis at the cervical spine level. Lateral shoulder or deltoid pain: classic pattern of pain seen in patients with rotator cuff tendonitis or tear, impingement syndrome, and frozen shoulder. *Rotator cuff tendonitis and tears are two most common causes of chronic choulder pain in middle aged to older patients. Its accompanied by weakness/pain when you do ABDUCTION AND EXTERNAL ROTATION. *Frozen shoulder refers to a stiffened glenohumeral joint, most commonly caused by rotator cuff tendonintis. Suspected when lateral pain is accompanied by stiffness and decreased ROM in abduction and external rotaiton.

Linear immunoglobulins found on immunofluorescence microscopy from renal biopsy?

Anti-glmoerular basement disease (Goodpastures)

Recurrent UTIs are a common problem in otherwise healthy young women. What can be done in a woman who has had more than two UTIs in 6 months or more than 3 UTIs in a year?

Antibiotic prophylaxis can be considered in these women. Can be either continuous or solely postcoital. Can be flouroquinolaneds, sulfamethoxazole-trimethoprim, and nitrofurantoin are commonly used. Postcoital voiding and increased intake of cranberry juice may help to decrease the risk of UTIs in some women. Further diagnostic evaluation in these patients is typically unrevealing unless there is clnical evidence to suggest the presence of nephrolithiasis or obstruction.

Management of H.pyolori in patietns with gastric mucosa-associated lymphoid tissue (MALT) lymphoma w/o metastases.

Antibiotic therapy and lymphoma might regress afterwards.

C. Diptheria treatemetn

Antibiotics are NOT a substitute for antitoxin Give antitoxin and antibiotics

Warfarin therapy

Anticoagulation therapy. Target INR is less than 1.5, fresh-frozen plasma reverses the action of warfarin immediately. So use it for emergent situation. Vit K reverses the action of warfarin but takes 8-12 hours to be effective. All patients with INR>5 and no serious bleeding should recieve oral vitamin K in addition to holding warfarin. ORAL vit K (as opposed to IV or subcutaneous) is preferred route at any supratherapeutic INR unless there is serious bleeding. *** Supratherapuetic INR= >3.0 Therapeutic INR= 2-3 (except in case of valve replacement then its 2.5-3.5 Subtherapeutic INR= <2.0

Antithrombotic therapy in patients with mechanical heart valves

Antithrombotic therapy with aspirin and warfarin is recommended for ALL patients with mechanical aortic or mitral valve replacement to reduce rates of systemic thromboembolism.

Flu treatment?

Antiviral therapy must be started within 48 hours to significantly decrase the disease duration and severity. Oseltamivir (Tamiflu) Zanamivir (Relenza)

Status Epilepticus

Any seizure or recurrent seizures without return to baseline lasting 20 min Prolonged firing may result in neuronal death Tx: ABC, vitals, IV access, rapid bedside glucose, Labs, Lorazepam if that fails then phenytoin

What is the use of IV pyelography?

Anytime you wanna visualize the ureters and kidneys. Like supsicion of infection , tumor, renal damage Contrast is injected into a peripheral vein, followed by radiographs, allowing visualization of renal parenchyma

Well-knonw complication of giant cell or temporal arteritis. what is giant cell?

Aortic aneurysisms due to involvement of branches of aorta. giant cell arteritis (temporal arteritis) should be suspected in patinets with temporal headaches, jaw claudication, and vision loss (anterior ischemic neuropathy) Patients with the visual symptoms should be started IMMEDIATELY (before diagnostic testing is performed) on high-dose systemic steroids to reduce the progression of visual complications. polymyalgia rheumatica is associated with GCA. Low dose steroids are recommended for patients with polymyalgia rheumatica without evidence of GCA. Temporal artery biopsy should be done to confirm the diagnosis of GCA. But start the steroids BEFORE that.

Findings for ascending aortic dissection vs pneumothorax vs PE vs pleural effusion vs aortic anuerysm

Aortic dissection-false lumen is created between media and adventitia of aorta. Seere chest pain that radiates to back. Hypertension main risk factor. Chest x-ray reveals a widened mediastinum. Pneumothorax-Classic x-ray finding is radiolucency at apex of lung. A severe pneumothrax can cause esophageal and mediastinal deviation. Pleural effusion-cause blunting of costophrenix angles. PE-dyspnea, tachypnea, pleuritic chest pain, and tachycardia. In most cases the xray is normal. Most common ECG finding is sinus tachycardia. Chest x-ray sugesting thoracic aortic aneurysm shows widened mediastinal silhouette, increased aortic knob, and tracheal devation. Ascending AAs usually due to cystic medial necrosis or connective tissue disorders. Descending usually due to atheroscelrosis.

Chronic diarrhea types and tests

Apart from history and routine lab tests, a stool analysis i part of initial workup. Some of the specific things to look for in the stool sample include microscopic examination for leukocytes and parasites and ova, occult blood, special staining for fat, pH and electrolytes for calculating osmotic gap. OSMOTIC diarrhea -infests nonabsorbale solutes--> osmotic water loss in stool. -examples are Mg containing antacids, lactose intolerance, -Test: Fecal electroleyes and caclulation of osmotic gap: If Osmotic gap = 290-2(Na+K)>50 m0sm thi suggests the presence of unmeasured solute indicating osmotic component to diarrhea ---Lactose Intolerance: insuficcient amounts of lactase enzyme in brush border of duodenum, therby resulting in inability to break down ingested lactose into glucose and galactose. Levels of this enzyme decline naturally with aging and as much as 75-90% of Asian, African and South American populations are lactose intolerant. Lab tests results for lactose intolerance? - Positive hydrogen breath test. preferred method. **free lactose is fermented by colonic bacteria to form fatty acids and hydrogen gas. Test involves measuring the amount of hydrogen gas exhaled in the few hours after consuming a lactose-containing beverage. In preparation for the test, patients should fast for eight hours. -Positive stool test for reducing substances -Low stool PH -Increased stool osmotic gap *Yogurt is a good alternative source of calcium for patients with lactose intolerance, as studies have shown that the fermented milk and live cultures in yogurst contain beta-galactosidase, which is well tolerated in these patients. SECRETORY Diarrhea-oversecretion of water by small and large bowel which can be caused by bacteria, neuroendocrine tumors (carcinoid, VIPoma), IBS, INFLAMMATORYDiarrhea-IBD MALABSORPTION Diarrhea - a problem of either digestion (lack of digestive enzymes or bile acids) or transport (prblem with bowel mucosa). Digestive problems-chronic pancreatitis, bile acid malabsoprtion. transport problems-celiacs, tropical sprue, wwhipples -Tests: -- D-xylose test: distinguishes digestion vs transport problem. xylose requires transport but not digestive enzymes to be absorbed. so if you see adequate amounts in blood then absorption not a problem. ---Small bowel biopsly (whippels, celiac sprues) ---72 hour fecal fat: steatorrhea may bee seen in malabsoprtion due to panreatic insufficnecy. fat malabsorption you commonly see voluminous and difficult to flush stool, don't really see that with carbohydrate malabsorption (lactose intolerance), that is more flatulence and watery diarrhea. **Also dont forget endocrine conditions like hyperthyroidism, Addison's, or DM2

What is aplastic crisis? Aplastic anemia?

Aplastic crisis: transient arrest of erythropoeises that results in a severe drop in hemoglobin and virtual absence of reticulocytes on peripheral smear (reticulocytes < 1%). You see in sickle cell and Parvovirus B19. Aplastic anemia: pancytopenia, low retieculocytes and hypoplastic bone marrow.

Signs and symptoms of PE

Are nonspeicific and highly variable. It is a diagnosis that should be suspected in any patient who presents with some combination of sudden-onset shortness of breath, pleuritic chest pain, low-grade fever, and hemoptysis. Tachypnea, tachycardia, and hypoxemia are common exam findings. Calf swelling and Virchow's triad (stasis, endothelial injury, and hypercoagulable state) are not always present in PE.

Cocaine and/or speed intoxication

Are sympathomimetics: syndroem of catecholamine excess.. Tx: Benzos for excess sympathetic, cooling measure for hyperthermai, nitroglycerine and heparin to control chest pain. IV fluids should be given in case of possible rhabdo and ECG should be obtained to look for MI

Direct Thrombin inhibitors

Argatroban Bivalirudin Derivatives of hirudin, the anticoagulant used b leeches. Used instead of heparin for anticoagulating patients with HIT. No inhibitor.

Post-infarction complications

Arrhythmias (within 48 hours) Ruptures (within 4-5 days) Dresslers syndrome ( 1 or 2 weeks after cardiac injury), you get fever, pericarditis. LIkely hypersenstivity process.

Explain frostbite

As the body reduces cutaneous blood flow in freezing temperatures to maintain the core body temperature, capillary blood becomes more vicous, and ice crystal sform in the extracellular space. This causes direct tissue injury and osmotic pressure that cause intracellular dehydration.

Abnormal uterine bleeding, how do you treat?

Assess degree of ilness. Hgb >12--- give iron supplement, OCPs if sex active Hgb 9-12---> Iron supplement HgB <9 --->stabilize, give IV conjugaed estrogens with high-dose OCPs. Next step is dilatation and curettage.

What uremic syndrome?

Associated with chronic renal failure that affects multiple organ systems Systemic effects: write down what Uworld says

Azathioprine

Associated with pancreatitis, liver toxicity, and dose depenedent bone marrow suppression.

Prophylaxis agasint Mycobacterium avium complex in HIV patients with <50 CD4 count?

Azithromycin.

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Cortisol Mnemonic

BIG FIB Blood pressure increase: upregulates alpha 1 receptros, most glucocorticoids have some degree of mineralcorticoid action so increased Na/H20. Insuin resistance Gluconeogenesis, lipoolysis, proetolysis (corsitol breakds down musckle for AAs, for gluconeogenesis. so you get muscle loss ) Fibroblast activity decrease (so you get striae) Inflammatory and immune response decrease Bone formation decrease Normal people Morning: highest cortisol level Night: when cortisol levels drop

Gallstone disease

BILIARY COLIC: waxing and waning, poorly localized postprandial upper abdominal pain radiating to the back. Caused by CCK stimulated gallbladder contractions following food ingestion. Condition is generally produced by gallstone obstruction at the gallbladder neck or gall bladder dysfunction (if its gall bladder dysfunction causing the trouble, then its called BILIARY DYSKINESIA). Things to differentiate it from acute cholecystisis are...no elevated leukocyte count, normal LFTs, afebrile, no abdominal tenderness (negative Mursphys) and RUA Pain < 6 hours. -no wall thickening or CBD dilation on ultrasound Tx: elective cholecystectomy *Biliary dyskinesia diagnosis: confrmied by CCK-HIDA scan. HIDA injected IV, after it fills the gallbladder, CCK is injected IV to stimulate gallbladder contraction. A gallbladder ejection fraction of less than 35% at 20 minutes is dagnostic of biliary dykinesia. ACUTE CHOLECYSTITIS Cholecystitis. Usually form obstructing stone. -May be febrile or not febrile, tachycardia, RUQ pain, gaurding, Murphy's sign -elevated leukocyte count -RUQ pain lastin >8 hrs Dx: Abdominal US first. IF unclear after that, seems like you do a HIDA. HIDA-study of choice. Technetium 99m labeled is injected IV and teaken up by hepatocytes. Normally, the gallbladder is outlined within 1 hour, absence of visible gallbladder on HIDA=cholecystitis. -you also see eleveated PMNs, alk phosph, total bili Tx: Cholecystectomy, Antibiotics *ERCP uses a fiberoptic camera and fluoroscopy to visualize the biliary and pancreatic ducts for diagnostic and theraputic purposes. It would be reasonable to perform ERCP if the patient had choledocholithiasis or a gallstone in the COMMON BILIARY DUCT (CBD) causing CBD dilatation. In such cases, sphincterotomy can help facilitate passage of stones. Also it is useful for CHOLANGITIS. *The HIDA scan is a nuclar medicine study used to diagnose gallbladder obstruciton Whit this technique, a nuclear tracer is injected into the blood and is excreted from the liver into the bile. Typically, the radiotracer can be seen pooling in a normal gallbladder. Failure to visualize tracer in the gallbladder is suggestive of obstruction. Ultrasonography demonstrates cholecystitis in this patient, so the scan would not add to the diagnosis. A HIDA scan can be used in patients WHERE ULTRASOUND CANNOT make a clear diagnosis of acute cholecystitis. ACALCULOUS CHOLECYSTITIS -What is it? Acute inflammation of the gallbladder in the absence of gallstones,caused by biliary stasis, most commonly seen in hospitalized and severely ill patients in the following conditions....extensive burns, sever trauma, prolonged TPN, prolonged fasting, mechanical ventilation. Imagin studies show gallbladder wall thickening and distention and pericholecystic fluid. The emergemcy treatment of choice is antibiotics and percutaneous cholecystoostomy, followed by cholecystectomy when the medical condition stabilitizes. CHRONIC CHOECYSTITIS -repeated bouts of biliary colic and/or acute cholecystitis leading to gallbladder wall inflammation and fibrosis CHOLEDOCHOLITHIASIS -may or may not be jaudiced, RUQ abdominal tenderness -ultrasound shows gallstones in gallbladder, CBD usually dilated -elevated LFT VALUES -CDB diameter >5mm *Gallstone pancreatitis should be considered if amylase and lipase are high -Tx: hospital observation for development of cholangitis, ERCP clearance of CBD stones, in addition to cholecystectomy. CHOLANGITIS-infection of biliary tract -Charcot's triad: Jaundice (so you see elevaetd LFTs in cholangitis or choledokolithiasis), Fever, RUQ pain. most commnly caused by obstruction of bile ducts by gallstones or strictures. May lead to sepsis and ogan failure. -air in the biliary tree is consistent -Tx: antibiotics and supportive care. If really severe , do ERCP or surgery to decompress bile duct SEPTIC CHOLANGITIS -Reynold's pentad: Charcot's triad + Hypotension + Altered mental status. A worse cholangitis. I think you do ERCP or surgery here. EMPHYSEMATOUS CHOLECYSTITIS -common form of acute cholecystitis in elderly diabetic males. It arises due to infection of the gallbladder wall with gas-forming bacteria. Dx confirmed with aabdomnial x-ra y showing air fluid levels in gallbladder or an ultrasound showing cuvilinear gas shadowing in the gallbladder.

Diet for diarhhea?

BRAT Bananas, Rice, Applesauce, Toast

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Hypothyroidism during pregnancy

Because a fetus depends on meaternal thyroid hormone for the first 10 to 12 weeks of gestation, the thyroid levels of pregnant women with hypothyroidism should be carefuly montired. Because of estrogen eleveation during pregnancy, TBG levels increase. Levothyroxine requirements may increase 30% to 50% during first trimester

Acute A-fib tx in hemodynamicall stable pt?

Beta blockers prefrredd. Calcium channel blocers are an alternative. If LV systolic dysfunction present, oconsider digozin or amiodarone (useful for rhtym control). Candidates for cardioversion include: hemodynamically unstable, those with worsening symptoms, and those who hare having their first every case of Afib

Where is McBurney's point?

Between belly button and Right anterior iliac spine. This of a line between the two, divide it into thirds. McBurney's point would be 1 third distance from iliac spin to belly button, also is two/third distance away from belly button. Typically the area of greatest discomfort in acute appendicitis.

Presentation of venous insufficiency

Bilateral lower extremity pitting edema, varicose veins, ulcers So think about this if you see extremity edema without signs of heart failure, (like normal JVP, crackels on exam, etc). Its functional or anatomic venous abnormalities that lead to venous reflux or dilated lower-extremity veins Tx is leg elevation, exercise, and compression stockings VARICOSE VEINS-refers to visible, palpable, and tortuous superficial veins of legs, usually on calf or medial thigh. most patients are asymptomatic. some patiens may complain of leg cramping, heaviness, fatigue, swelling. symptoms are generally worse in eveining with prolonged standing and improve with leg elevation. Tx: leg elevation, compression stockings, sclerotherapy, surgical ligation. **compression stockings should not be used in patients with an underlying arterial insufficiency Injection sclerotherapy is used in patients with symptomatic,small, varicose veins who have failed at least 3 TO 6 MONTHS of conservative treatemnt. it involves injection of a sclerosing agent into affected vein cauing endothelial damage and sclerosis of vein, thus preventing further vein filling. Surgical ligation and stripping is used in patients with large symptomatic vaircose veins with ulcers, bleeding , or recurrent thrombophlebitis of the veins.

UA-bilirubin? UA-hemoglobin?

Bilirubin-extravascular hemolysis Hemoglobin-intravascular hemolysis

Hematuria in adult >35?

Bladder tumors are the most common malignancy associated with painless hematuria in adults. Patients age >35 with gross hematuria should b eevaluated for urological neoplasms with diagnostic imaging (CT urogram) and cystoscopy.

What are complications of peptu ucler disease?

Bleeding is most common. Therei s also perforation, penetration, and gastric outle obstruction.

Describe the types of hematuria and what they mean?

Blood at beginning of urination (inital hematuria) typically indicates a lesion in the urethra such as urethritis. Hematuria t the end of voiding, called terminal hematuria, often suggests a prostatic or bladder cause. Hematuria during the entire urinary cycle (total hematuria) may indicate disease within the ureters or kidneys. A renal cause of hematuria will not show clots. *Another way to think about hematuria is whether it is non-glomerular (more common) or glomerular. With glomerular, you're gonna see blood AND protein, RBC casts, dysmorphic RBCs. With non-glomerular, you're gonna hve blood but NO protein and normal looking RBCs. --some common glomerular causes of hematuria are glomerularnephritis', basement membrane disorder (alpot syndrome). IgA nephropathy is most common GN in adults. so that can definitely give you hematuria after an URI.

Urinalysis values to know

Blood: On a dipstick and range is from 0 to 4+ RBC: units are hpf. Range is 0-3/hpf WBC: units are hpf. Range is 0-3/hpf

Radiation proctitis presentation?

Bloody diarrhea, mucous discharge, and tenesmus (ineffectual/painful straining on defecation) during or months after the completion of pelvic radiation therapy. Dx is usually made after excluding other causes of colitis (infection, IBD, ischemia, malignancy).

What are you gonna see with Plerual effusions on x-ray?

Blunting of costophrenic angles.

Primary hyperparathyroidism and familial hypcalciuric hypercalcemia

Both can hypercalcemia secondary to an elveated or high "normal" PTH level. FHH: urinary calcium creatinine clearnace ration is <0.01 PHP: urinary creatinine clearance ratio is >0.02 FHH is AD benign disorder caused by abnormal calcium sensing recptors in parathyroid glands and renal tubules. The abnormality hinders PTH suppression in setting of hyecalcemia. So patients are hypercalcemia and "high-normal" or "borderline eleveated" PTH levels.

How do you know if stone is obstructing cystic duct or common bile duct?

Both will have high bili, alkphosph, high ALT and AST. But you're gonna see SEVERE icterus and VERY high allk phosph with common bile duct obstruction.

Hyperosmolar hyperglycemic state vs DKA

Both you can see total body potassium deficit due to excessive urinary loss caused by glucoruia-induced osmotic diuresis. Both you also have total phosphate depltion due osmotic diuresis. DKA -DM 1 usually -Glucose 250-500 -bicarb <18 -elevated anion gap -positive ketones -less pronounced altered mentation compared to HHS HHS-characterized by very high glucose, mental status changes, and no ketoacidosis. most common causes are infections, dehydration, major ilnesses and drugs. Tx: Initial managment is high flow IV fluids, continuous IV insulin infustion, and careful potassium replacement. Patients with HHS intially require very high doses of IV insulin due to insulin resistance induced by stress, infection, corticosteroids, and hyperglycemia. Are frequently hyperkalemic but have a total body potassium deficit, so aggressive reduction of serum potassium should be avoided, overall potassium deficiency will become unmaksed with fluids and insulin. -DM 2 usually -Glucose >600 -bicarb>18 -normal anion gap -negative or small keontes -serum osmolality>320 -frequently develop NEUROLOGIC symptoms (lethary, blurry vision, obtundatino) due to severe hyperlgycemia and elevaetd serum osmolality

Asbestos exposure put you at risk for what?

Bronchogenic carcinoma-MOST COMMON cancer it can cause. Smoking acts synergistically to further increase the risk. You see bibasilar, end-inspiratory crackles and fingernail clubbing as the disease progresses. PLEURAL PLAQUES helps differentiate asbestosis from other causes of pulmonary fibrosis. Asbestosis causes fulmonary fibrosis in lung and pleura (plaques) and potentially cancer in lung and pleura. Plueral mesothelioma: Typically unilateral pleural abnormality with large pleural effusion on CXR. Also, bronchogenic carcinoma is more common in patients with asbestosis exposure, especially smokers.

Tx of cystitis and pyelonephritis

Bugs that cause UTI mnemonic? SEEKS PP S. saprophyticus E. coli (about 80-85% of causes) Enterobacter Kliebsiella Serratia Proteus Pseudomona (especially with GU instrumentaiton) Dx of UTI : -Urine dipstick tha tmeasures leukocyte esterase and nitrites. -UA that you can vicualize pyuria -Urine culture is definite test. A + is >10,000 colony forming units. UNCOMPLICATED CYSTITIS: patients can be treated without a urine culture. Culture done if patient fails initial therapy. -Tx: Nitrofurantoin for 5 days or TMP/SMX for 3 days or Fosfomycin single dose or Flouroquinoles if above options cannot be used COMPLICATED CYSTITiS: refers to infections associated with factors that increase the risk of antibiotic resitance or treatment failure. Factors like diabetes, CKD, pregnancy, immunocompromosed, indwelling catheter, infection, etc. These patietns should have urine culture PRIOR to thearpy -Tx: FLOUROQUINOLONES 5-14 days. PYELONEPHRITIS: get urine culture prior to therapy. -Outpatient: Fluoroquinolones -Inpatient: IV antibiotics (fluoroquinolens, ceftriaxone) **diabetic patients: diabeitc patients with acute pyelonephritis are gnerally treated with IV for 48-72 hours. Once the patient has a clear response, treatment can be switched to oral antibiotics for a total course of 10-14 days. Fluoroquinolones and TMP are good options for oral therapy, wich the choice of antibiotics usually individualized based on culture and sensitivity results. **When should you image pyelonephritis? If patient has persistent clinical symptoms despite 48-72 hours of therapy, history of nephrolithiasis, complicated pyelonephritis, or unusual urinary findings (gross hematuria, suspicion for urinary obstruction). COMPLICATED PYELO: progression of initial pyelonephriis to renal corticomdullary abscess, perinephric abscess, emphysematous pyelonephritis, or papillary necrosis. Patients can develop sepsis with multiogran failure, shock, renal failure. Complicated pyelonephritis occurs more commonly in patients with conditions such as DIABETES, kidney stones, IMMUNOSUPRRESION, or other anatomic abnormalities of urinary tract. **INTERSTITIAL CYSTITIS: also known as painful bladder syndrome, is a chronic, painful bladder condition of uncertain etiology. The pelvic pain in intersittial ystitis is a slassically EXACErBATED by BLADDER FILLING and relieved by VOIDING. other symptoms are urinary urgency and frequency, chronic pelvic pain. Dx is clinical. tx is not curative, focus on quality of life, amitrypityline. .

Stuff from sub-internship

Bumex: diuretic used for HF when furosemide not working Pneumonia antigen tests: strep Ag, legionella Ag Anemia: give ferrous sulfate BID -If azithro not working for COPD then go with Levo -if etiology of Pulmonary HTN is unknown, you want to do a right heart cath to get an idea of type. 5 types of pulmonary HTN. 1. PAH: mean pulm artery pressure >25mmHg at rest 2. PH cuz left heart disease 3. PH due to chronic lung disease w/hypoxemia 4. chronic thomboembolic pulm HTN 5. PH due to unclear multifactorial stuff bowel regimen: Miralax BID, Docusate-Senna BID asthma; >12.5% increase in FEV1 after bronchodilator challenge COPD managemnt points -Venturi masks can give precise Fi)2 -NC can give flow rate up to 6L w/Fi02 40% -when higher Fi02 is needed, simple facemask. nonrebreathers generally not needed . COPD stage 1 <80% COPD stage 2 50-80% COPD stage 3 <50% COPD stage 4 <30% ESRD can mess up BNP values -if you have concern for infection, BP can be low with infection. So you might wanna stop some anti-HTNs like amlodipine. -asthmatics shouldn't have low 02 if that happeneing then maybe no air movement is going on so now you're worried and maybe should intubate. -with bridging warfarin, do it at least 5 days. you also want INR therapeutic for at least 1 day after bridging before you stop warfarin and leave heparin. You don't normally bridge when treating A-fib. w/ DVT tx you do. -BNP increseased in fluid overlaoded state. -hemolysis workup: smear, haptoglobin, LDS and T bili. -can't do D-dimer in COPD case, it messes it up. PE can cause COPD exacerbation. -with giving fluid and seeing a dcrease in Hgb. common misconception says the Hgb is "diluted" w/fluid bolus. that not true according to Dr. morgan stanley but i just don't remember the reason why. -mucous plugging on CXR, pneumonia can cause. but a mass can cause it as well. so wanna f/u on that. -Volume down OR volume overload can cause AKI. -you can get increased lactate from albuterol use. -if on Lasix at home, FeNa gonna be not very accurate. So you can use Fe urea to see if pre-renal. -pericarditis ST elevation looks different from MI St elevation, its very steep increase and sharp peak. As opposed to the plateu looking peak of MI ST elevation. -diuretic conversion is 2:1 IV to PO. if you give someone diuretic IV to get euvolemic and the person does just that, don't stop the diuretic. send him home on PO doase to continue to be euvolemic. PO is also better absorbed. -when you start diuresing someone, you prob wanna put on tle in case electrolytes get all screwed up. -with Warfarin INR jump from 1-->11.8 in a day, that is too fast. You generally want like 1-->1.4---> 2.0. warfarine takes 48 hours to reflect on INR. -contrast induced nephropathy shows up 24-48 hours after. can take 48hours to 5 days to resolve. -with bicarb, you only start getting worred after 35. you can still diurese above 35 just use acetazolamide. Dont use aacetazolimde if has AKI. HCAP Tx is 7 days. CAP tx is 5 days. -2 cases in which you TREAT asymptomacit bacteruria: pregnancy and upcoming GU procedure "early CAD" -ACS <55 yrs -ACS <45 yrs Goal HR of someone w/F-fib w/RVR: 110. studies have shown no different in mortality between 110 and lower HRs.

NSAIDS usually do not cause AIN, but how they bad for kidneys?

By inihibiting prostaglandin synthesis they decrease the GFR, which can precipitate renal failure in a patietn wtih underlying renal problems.

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Thyroid cancers.

CARCINOMA (4) -Papillary: most common, good prognosis, propensity for lymphatic spread; lymphadenopathy. Radiation and family history. Tx: of high-risk ones are near-total or total thyroidectomy. If lymph node metastases in the lateral neck, concomitant modified radical neck dissection should be performed with total thyroidectomy. Papillary carcinoma of thyroid frequently metastasizes to cervical lymph nodes, but distant metastasis is uncommon. -Follicular: good prognosis, hematogenous spread Tx: surgery followed by radiodine ablation *<4cm in size can do thryoid lobectomy cuz most are adenomas <4cm or confirmed carcinoma then total thyroidectomy should be done. follicular carcinomas cannot be diagnosed by FNA; capsular or vascular invasion on histology confirms diagnosnsos of malignancy. -Anaplastic: older patients invades local structure, very ppor prognosis -Medullary: from parafollicular C cells; produces calcitonin LYMPHOMA -assoicated with Hashimotos thyroiditis. good prognosis. Tx: surgery followed by radioidine ablation Genral clinical presentation is painless enlargement of thyroid, more advanced signs of local invacion are hoarseness, dhysphagia, cough. *Age is a very important prognositc factor in papillary and follicular tumors

Primary care: Common disorder of cervical spine

CERVICAL RADICULOPATHY -compression of a spinal nerve leads to arm pain, numbness, tinglinig, or weakness. Most common ocmplaint is unilateral neck pain radiating to the arm in a dermatomal pattern. -most common cause is cervical osteoarthritis and disc herniation. -DDx includes shoulder patholog (rotator cuff problem), peripheral nerve entrapment (carpal tunes or cubital tunnels syndrome), thoracic outlet syndrome, zoster, and pancoast tumor (can preesnt with brachial plexus symptomts) Dx: best way to diagnose is MRI of cervical spine Tx: most patients can be treated with NSAIDS, time, PT, epidural injections). Surgery for more severe cases. CERVICAL MYELOPATHY -Neuroloic dysfunction secondary to spinal cord compressino (cervical stenosis) in the cervical spine. Dx made by MRI of cervical spine. -earliest symptom is gait disturbance. pain not a common finding. patients often strat relying on a can or walker and if untreated can lose ability to walk. Tx: surgery to decompress the spinal cord when dx made.

how does CHF exacerbation cause tachypnea?

CHF exacerbation can cause tachypnea as LV dysfunction allows fluid to pool in the lungs, causing a plerual effusion and hypoxemia due to reduced ventilation. Tachypnea causes hypocapnea and respiratory alklkosis.

How can CHF cause a respiratory alkalosis?

CHF exacerbation can cause tachypnea as left ventricular dysfunciotn allows fluid to pool in th elungs, causing a pleural effusion and hypoxemia due to reduced ventialtion . Tachypnea causes hypocapnia and respiratory alkalosis. Exam typically shows signs of fluid overload, S3 and S4 gallops, cardiomegaly, and bibasilar crackles in the lungs.

Most common causes of hyperkalemia?

CKD, medications, or disorders impairing renin-angiotensin axis. Common offending medications include: beta blockers, potassium sparing diuretics,ACE inhib, ARBs, NSAIDS

Bone marrow recipient gets pneumoninits and diarrhea?

CMV penumontiis. xray faindings show multifocal diffuse pathcy infiltrates. Bronchoalvealor lavage is diangositsc.

CMV vs EBV

CMV: atypical lymphocytes on smer and negative monospot. Sore throat and lymphadenopathy are not common. EBV: sore throat and lymphadenopahty, positive monospot. Also atypical lymphocytes. Also splenomegaly, fever, and mild hepatitis. **Heterophiel antiodie are very sensitive and speciic, but may be negative early in illness. Repeating the test may be helpful. For this reason, a negative antibody test does not exculde the diagnosis of infectious mono. **Atypical lypmhocytes: sually found in EBV infection, but can also be seen in CMV, lympoblastic leukemia, and toxoplasmosis.

What should you consider in someone who has pinkish-red skin hue, polyycythemia, nausea, dizziness, and headaces?

CO poisoning

Explain COPD Only therapies proven to prolong life in COPD patients. What is the mainstay therapy for impvroving quality of life?

COPD is marked by progressive decrease in expiratory flow rate which gives you FEV1/FVC of less than .7. As airflow limitation increases, more air is trapped during expiration and FRC and total lung volume increases. VC decreases as well. THERAPIeS Smoking cessation, oxygen, and lung reduction in certain patients. The mainstays of treatment are inhaled bronchidilators, especially ANTI MUSCARINICS like ipratropium and tiotropium. You can add short acting beta agonists to this for greater symptom relief. If you have more severe COPD, after the anti muscarinics and short acting beta agonists...then you go to inhaled corticosteroids and long acting beta agonists.

What do you have to remember about COPD patients and oxygen?

COPD patients have baseline chronic hypoxia dn chronic hypercapnia. This shift the repsiratory drive from a hypercapneix to a hypoxic drive. Hypoxia caues pulmonary vasoconstriction, directing blood to better ventilated or perfused areas. Deoxyhemoglobin has a HIGHER C02 affinity, which increases CO2 excretion as it is carried by the hemoglobin back to the lungs to be exhaled. So if you give TOO MUCH supplemental oxygen in COPD patients, you're gonna have an increase in oxygenated hemoglobin which has a LOWER C02 affinity and C02 will be released in the surrounding areas, as opposed to only the lungs I guess. So you're going to WORSEN the hypercapnia and give C02 narcosis (start having seizures) THe goal oxyhemoglobin saturation in these patients is 90 to 94% (not >95%). There is also this per Doc Morgan...for COPD exacerbation. Imagine 7.38 psh with C02 of 70 (COPD patients are hypercapneic) and Bicarb of 34 (cuz its trying to compensate). High C02 people will come in somnolent, with decreased RR. You prob gonna have to ventilate but you wanna do it carefully, why? You slowly decrease the c02 because HC03 needs days to compensate. If you let the person blow off too much C02 too fast he will become alkalotic because his bicarb is still 34 cuz it takes days to adjust. So if this happens and if you take person off the ventilator, patient will try and retain all the C02 he can cuz of so high bicarb and RR will go down a lot-->no respiratory drive.

Criteria for long term home oxygen therapy for COPD patients?

COPD patients with Pa02<55 or Sa)2<88% are candidates for long-term home oxygen treatment. Patient with signs of pulmonary hypertension or hematocrit >55% should be started on home oxygen when the Pa02 <60 mmHg.

Serum markers for MI

CPK: elevates within 4-8 hours, peak at 24 hours. A subgroup of CPK is CK MB which is specific for myocardial tissue damage. Troponin T or I: very sensitive and specific. Elevated within 3 hours and can last a week. Myoglobin: nonspecific. elevates and goes down in 24 hours.

Types of stones and treatment

Calcium oxolate: strongly radiopauge, treat with thiazides to decrease calciuria. 75% Struvite 15% -moderately radiopaque. Common in Proteus UTIS due to high urinary ph. Proeus makes urease which cleaves urianary urea giving two molecules of ammonia, the conjugate base of ammonium ion. Tx: by lowering urine Ph. uric acid -are needle-shaped. -radiolucent (not seen on x-ray but could be seen on US or CT), increased in myeloproliferative disorder and gout due to increase purine turnover -treat by raising urine ph (use potassium citrate). Cystine -hexagonal crystals, moderatley radiopaque. Seen in congenital cystiuria, NOT homocystinuria. -Treat by raising urine Ph

Lower GI bleeds causes

Can U Cure Aunt Di's Hemorrhoids? Cancer or polyps UGI bleed Colitis (infections, IBD, ischemic, etc) Angiodysplasia Diverticulosis Hemorrhoids Signs: hematochezia, melena (tarry stool, usually associated with Upper GI bleed but can occur w/ascending colon bleed)), tachy, hypotension Dx:NG tube aspiration. If no blood, positive bile on NG tube aspirae... -then do colonoscopy to find source. If you can't find the source and the patient stops bleeding then do small bowel studies (capsule endoscopy). But if you can't' find source and th patient does not stop bleeding do a Technetium-99 labeled ertyrhoctye scintigraphy. It localized source of blood loss so that region can be further evaulated by coloscopy or angiography. If blood found, and plus/minus bile on NG tube aspirate.. -then do upper endoscopy. Tx: IV fluids, blodo, embolization or surgery

How do go about learning the cause of a peritoneal fluid buildup?

Can accumulate due to a number of different causes including -portal hypertension a. presinusooida: splenic or portal vein thrombosis b. sinusoidal: cirrhosis c, postsinusoidal:right heart failure, constrictive pericarditis, Budd-Chiari syndrome -non-porta hypertensive a. malignancy, pancreatitis, nephrotic syndrome, TB Portal hypertension cause (cirrhosis) is INCREASED hydrosttic pressure within hepatic capillay beds. To distinguish among these, you gotta know if the fluid is transudative or exudative. This is done using the serum ascites albumin gradient (SAAG). SAAG is calculated by SUBTRACTING the ascites albumin concentration from the serum albumin. Difference of 1.1 or greater means its transudative consistent with portal hypertension. If its less that is not consistent with portal hypertension at that means the fluid is from another mechanism, like infection, inflammation, low serum oncotic pressure like nephrotic syndrome, malignancy, or TB. In addition to cirhosis, other cuases of portal hypertension, such as constrictive pericarditis, right-sided heart failure and Budd Chiari syndrome (thrombosis of hepatic veins and/or suprahepatic inferior vena cava).

Chronic Hep C manifestations

Can by asymptomatic or present with fatigue and nonspecific symptoms (arthralgias, myalgias). Patients usually have waxing and waning elevations in transaminsase levels. Extrahepatic sequelae can include HEME: essential mixed cryoglobulinemia (iimmune complexes depositing) SKIN:porphyria cutanea tarda (fragile skin, photosentivie, vesicles and erosions) RENAL: membranous glomerulonephritis.

explain theophyline toxicity

Can manifest as CNS stimulation (headache, insomnina, seizures), GI disturbances (nausea, vomiting), and cardiac toxicity (arrhythmia). Inhibition of the cytochromie oxidage system by other medications, diet, or underlying disease can alter its narrow therapeutic window.

What do you look for to diagnose lung abscess? sympotmos?

Can occur from infection behind a blocked bronchus. Usually due to anaerobes and may be associated with alcohol abuse or aspiration. You will probably see an AIR FLUID LEVEL on CXR. CLinical features include foul smelling sputum, indolent symptoms, concurrent periondotal disease.

Explain exercise-induced bronchoconstriction

Can occur in asthmatics or in people without pre-existing asthma. Bronchial smooth muscle constriction may be triggered by exertion or passage of large volumes of dry cold air causing mast cell degranulation. May otherwise by asymptomatic. Clinical symptoms are not sufficient to make a diagnosis of EIB and bronchoprovocation testing with exercise or inhalation of dry,cold air is recommended. A fall in FEV1 of >15% is diagnostic, >10% is positive. Tx: includes pre-exercise warm-up for infrequent EIB, short-acting Beta2 agonists for persistent symptoms, and daily inhaled corticosteroids for those requiring daily Beta2 agonist therapy.

Calcium gluconate used for ?

Cardiotoxicity due to hyperkalemia. EEG of hyperkalemia shows peaked T waves.

Most common cause of death in dialysis patients?

Cardiovascular disease is the most common cause of death in dialysis patients. It accounts for approximately 50% of all deaths in this population. Cardiovascular disease is also the most common cause of death in renal transplant patients.

Hypothyroid patient has wrist pain?

Carpal tunnes syndrome occurs in approximatley 30% of patients with hypothyroidism. Deposition of mucopolysaccharide protein complexes within the perineurium and endoneurium of the median nerve is though to be primarily responsible for its pathogenesis.

What is hepatic hydrothorax

Cause of transudative pleural effusion in patient with cirrhosis who have no underlying cardiac or pulmoary disease to account for development of such an effusion. hepatic hydrothorax usually results in a right-sided pleural effusion. Initial treatment is usually with salt restriction and diuretics. TIPS placement is considered in patients with refractory hepatic hydrothorax. . Hepatic hydrothorax signals adavanced liver disease and should prompt consideration for liver transplant.

What do you need to remember with molluscum contagiosum

Caused by POXVIRUS. SMALL SKIN COLORED PAPULES with INDENTURED CENTERS occur anywhere except palms and soles. Spread through SKIN TO SKIN CONTACT. can be asymptomatic or prurritic ad can be ossacsionally be accompanied by surrounding dermaititis. Children are most commonnly affected but adolescentsa, adults and immunocomprmoised can get it too. MC often transmitted through sexual contact. HIV TESTING should be considered in patients with MC, especially if they have lesions involiving the face. Tx: its self limited.

Herpes zoster opthalmicus

Caused by VZV. Characterized by dendriform corneal ulcers and a vesicular rah in trigeminal distribution. You have fever, malaise, burning, itching in periorbital region

Scombroid poisoning

Caused by eating of improperly stored seafood. Seafood that is stored it too warm place, histidine turns into histamine. Symptoms are flushing, headache, palpitations, cramps, diarrhea. Symtpoms begine 10-30 minutes after ingesting teh fish, and are self limited.

Stevens-Johnson Syndrome

Caused by: druggs; sulfonamides and anticonvulsants -oral cavity almost always involved - +Nikolsky sign: separation of normal epidermis at basal layer caused by sliding finger pressure Diagnosis: Clnical criteria: Curtaneous lesion plus at least two mucousal surfaces involved

Primary care: Cough

Causes -URI: prob most common cause of acute cough -pulmonary disease: COPD, cF, asthma, etc -CHF w/pulmonary edema -smoking -postnasal drip: can be caused by URIs, rhinitis (allergic or nonallergic), chronic sinusitis, -GERD -asthma -ACE inhibitors Tx: 1. treat underlying cause 2. smoking cessation, if smoking is the cause 3. postnasal drip a. treat with 1st generation antihistamine/decongestant b. is sinusitis: consider antibiotics c. allergic rhinitis: consider a nonsedating long acting oral antihistamine 4. nonspecific treatment a. codeine b. dextromethorphan c. benzonatate (tessalon perles) capsules d. guaifenesin and water improves effectiveness of antitussive medication

Weight Loss Differential Diagnosis

Causes to be Considered in the first 12 hours Common causes Cancer Depression Poor home situation Substance abuse Other causes Tuberculosis HIV Hyperthyroid Addisons Malabsorption

Abdominal Pain Differential Diagnosis

Causes to be Considered in the first 12 hours Bowel perforation Ectopic pregnancy Abdominal aortic aneurysm Myocardial infarction Appendicitis Mesenteric infarction Ovarian torsion Common causes Irritable Bowel Constipation Reflux Somatoform disorder Other causes Gallstones Peptic ulcer Pancreatitis Diverticulitis Bowel obstruction Crohn's Disease Kidney stones Pelvic inflammatory disease Ovarian cyst Dysmennorhea Mesenteric angina Mittelschmerz

Altered Mental Status Differential Diagnosis

Causes to be Considered in the first 12 hours Drugs and medications Hypoxia Hypoglycemia Sepsis Meningitis Stroke/CNS bleed Tumor Common causes Sundowning (in the elderly) Depression Psychosis Systemic infection Multiple medical problems Other causes Electrolyte abnormalities Encephalopathy Toxic Severe HTN Adrenal insufficiency B12 deficiency Hypothyroid

Fever, Including FUO (Fever of Unknown Origin) Differential Diagnosis

Causes to be Considered in the first 12 hours Endocarditis Abdominal abscess Meningitis Venous thromboembolism Common causes Viral Pyelonephritis Line infection Pneumonia Drug fever Sinusitis Invasive gastroenteritis Other causes Tuberculosis Lymphoma Multiple myeloma Sarcoidosis Autoimmune Crohn's disease Renal cell carcinoma

Chest Pain Differential Diagnosis

Causes to be Considered in the first 12 hours Myocardial infarction/Angina-pressure, radiates to left arm shoulder or jaw, DIAPHORESIS is a key symptom also Aortic dissection-severe pain that radiates to back, unequal pulses or unequal blood pressure in right and left arma Pulmonary embolism-often pleuritic, associated with tachypnea and tachycardia Common causes Gastroesophageal reflux Musculoskeletal pain Costochondritis-sharp pain , REPRODUCIbLE TENDERNESS (touch chest wall and feel the pain) Somatoform disorder Other causes Pneumonia Pneumothorax Lung cancer or mets Pericarditis-chest pain radiating to shoulder, neck, or back, worse with deep breathing or coupgh, relieved by sitting up and leaning forward Zoster Esophageal spasm Esophagitis

GI Bleeding Differential Diagnosis

Causes to be Considered in the first 12 hours Peptic ulcer Varices Common causes Diverticulosis Angiodysplasia Hemorrhoids Gastritis Other causes Colon cancer Ischemic colitis Inflammatory Bowel disease Invasive gastroenteritis Mallory-Weiss tear Esophagitis

Dyspnea Differential Diagnosis

Causes to be Considered in the first 12 hours Pulmonary embolism Congestive heart failure Angina Severe anemia Common causes Anxiety COPD Asthma Pneumonia Obesity Deconditioning Other causes Interstitial lung disease Pneumothorax Pleural effusion Neuromuscular disease Lung cancer

Diarrhea Differential Diagnosis

Causes to be considered in the first 12 hours Clostridium difficile Common causes Viral Irritable Bowel Lactose intolerance Antibiotics Other causes Bacterial Parasites Medicines Inflammatory bowel Malabsorption

Why might a biopsy proven celiacs patient have negative results of IgA anti-tissue transglutaminase and IgA anti-endomysial antibodies?

Celiac ppl commonluy have selective IgA deficiency.

Goals of fluid resuscitation?

Central venous pressure 8-12 mm Hg Mean arterial pressure greater than 65 mmHg Urine outpu greater than 0.5 mL/kg/h Central venous oxygen saturation greater than 70%

Microscopic colitis?

Characterized by chronic watery diarrhea witout bleeding, there are 2 types: collagenous colitis and lymphocytic colitis. Diagnosis is made by histologic examination of colonoscopic biopsy specimens. Cause is unkown.

Paget's disease?

Characterized by increased bone remodeling and abnormal osteiod formation. Patients may be asymptomatic or present with headaches, deafness, neuropathy, or bone/back pain. Lab data shows elevaetd Alk Phosph but normal calcium, phosphorous and other liver enzymes. Tx: asymptomatic: no tx required. Symptomatic: oral or IV aminobiphosphonates

What do you see in hypopituitarism

Characterized by.. 1. glucocorticoid defieincy: hypoglycemia, hyponatremia, eosinophilia (cuz glucocorticoids normally decrease eosinophils). 2. tesosterone defieicny 3. hypothryoidism this is a cause of seondary adnreal insufficiency so rememver you DON"T see hypoaldsteronism in this. cuz aldosterone secretion from the adrenal glands is ACTH-independent, an primarily regulated by the RAAS axis, so potassium is gonna benormal.

Lightning strikes someone.

Chest compressions while giving vasopressos (epinephrine or vasopressin) and identiftying and treating reversible causes of cardiac arrest.

Metabolic alkalosis divided how?

Chloride responsive: urine chloride <20 due to hypovolemia and hypochloremia. Saline responsive because normal saline administration restores arterial volume, vorrects hypochloremia, and increases urinary bicarb excretion. -vomiting or prolonged NG tube drainage -diuretics (prior use and also current use) -laxative abuse -pyloric stenosis Chloride unresponsive: urine chloride >20. Saline resistant. Excess mineralcorticoid causing hydrogen an dpotassium loss and increased sodium retention leading to increased EC volume. Kidneys respond by excreting both sodium and chloride to result in high urine chloride. -Mg or K deficiency seevere -increased mineralcorticoids -licorice -Bartter, Gitelman syndromes (pt will be hypovlemic/euvolemic here, as opposed to being hypervolemic in case of increased minearlcorticoids). *one instance where Chlroide>20, hypovolemic/euvolemic pt. can actually be a saline response case and that is in the case of Current diuretic use.

Gallbladder inflammatio, ischemia, or infection

Cholecystitis. Usually form obstructing stone. -Fever, tachycardia, RUQ pain, gaurding, Murphy's sign Dx: HIDA-study of choice. Technetium 99m labeled is injected IV and teaken up by hepatocytes. Normally, the gallbladder is outlined within 1 hour, absence of visible gallbladder on HIDA=cholecystitis. -you also see eleveated PMNs, alk phosph, total bili Tx: Cholecystectomy, Antibiotics

Gallbladder stones name?

Cholelithiasis Dx: RUQ ultrasound to detect gallstones -AST/ALT to look for hepatitis -ALk phosh and bilirubin to look for common duct stones -amylase/lipase to look for concomitant pancreatitis if asymptomatic, do nothing as only 20% developsyptoms. Gallstones: 70% cholesterol, 20% are pigment, 10% are mixed

Patients on TPN (total parenteral nutrition) for 2-3 weeks may devellop what?

Cholestasi. This can progress into fibrosis if TPN is continued.

What is atheroembolism?

Cholesterol embolism. A common complication of cardiac catheterization and other vacular procedures. You see cutanoues findings ("blue toe syndrome", livedo reticularis (reticular, lacy skin discoloration/erythema that blanches on pressure), cerebral or itestinal ischemia, acute kidney injury, and Hollenhorst plaques (bright, yellow, refractile plaques in retinal artery). Tx: is supportvie and includes statin thearpy for risk factor reduction and prevention of cholesterol embolism.

Chronic MR vs chronic AR

Chronic MR lead to volume overload which leads leads to increased stroke volume and increased LV EF and can mask LV systolic dysfunction in the early compensated stage. Chronic AR leads to to increased stroke volume and CO, but have normal LV function and tend to maintain a normal LVEF.

Pyruvate kinase deficiency signs?

Chronic hemolysis Hepatosplenomegaly Skin ulcers Pigmented gallstones

Workup when there are symptoms&/or signs of adrenal insufficiency.

Chronic primary adrenal insufficiency (addisons) -due to disease, automimmune, TB, metastasis. Defieicny of aldosterone and cortisosl, causing hypotension, hyperkalemia, hyponatremia hyperchloremic acidosis, and skin and mucosal hyperpigmentation. Involves all 3 cortical divisions. Secondary insufficiency is different (commonly get from abruptly stopping steroids after long use or not tapering well enough) -decreased pituiatry ACTH so you get no skin hyperpigmentation. Diefiency of mineralcorticoid usually does not occur (cuz it relies more on RAAS system) so you do not develop hyperkalmiea or metabolic acidosis.. You see eosinopihlia in BOTH cuz both have decreased glucocortidcoids. *Also remember about Acute adrenal insufficiency (waterhouse frideriechens syndrome) that can be due to Neisseria meningitis, septicemia, DIC and endotoxic shock * Also the best screening tests for patients with suspected adrenal insufficiency are early-morning cortisol, ACTH, and cosyntropin (ACTH analogue) stimulation. An increase in serum cortisol >20 30-60 minutes after giving 250 cosyntropin virtually RULES OUT primary adrenal insuffinecy (Addisons) ------------ Signs of adrenal failure, or Addison's disease? Most have nausea, vomiting, abdominal pain, etc. Hyponatremia is most common, cuz of mineralcorticoid deficiency Hyperkalemia is also common due to dcreased activation of aldsoterone receptors. You get hyperkalemic, hyperchloremic, acidosis. Weight loss, hyperpigmentation, low blood pressure and vitilitgo as well ---------- Common cause of primary adrenal insufficency (Addison's disease) in endemic areas? Common cause of secondary adrenal insufficency (most common cause of adrenal insufficency that is seen in hospital according to Dr. basil?) --TB is a common cause globally. Causes aldosterone deficiency and presents with Non AG, hyperkalemic, hyponatremic metabolic acidosis. Common cause of secondary adrenal insufficency: not tapering sufficient when taking someone off steroids, if someone has been using steroids for longer than 2 weeks and if you just abruptly stop you will be left with an adrenal gland being insufficient, so that is why you taper when you take someone off steroids --Another thing to remember about adrenal isufficiency, if the person has increased physilogical stress they should receive a stress dosage of IV hydrocortisone. People with adrenal insufficiency are eductaed to increase their corticosteroid dosage during stressful event, such as infection or surgery.

How does primary sclerosing cholangitis present?

Chronic progressive disorder of unkown etiology with inflammation, fibrosis and stricutring of medium and large sized intrahepatic and extrahepatic bile ducts. Continued bile duct destruction leads to end-stage liver disease and portal hypertension. Frequently associated with UC. Labs usually show unexplained elevated LFTs in a cholestatic pattern. (elevated ALT and AST, severely elevated Alk phosph and bilirubin. Dx: Not US. Cholangiogram shows multifocal narrowing and duct dilataion "beading". Also "onion" skin fibrosis. Tx: Only cure is liver tranplant

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Tx: of hairly cell leukemia?

Cladribine. Hairy cell leukemia characterized by lymphocytes with hair like projections and a TRAP stain. Bone marroy become fibrotic, thus leading to dry taps.

What is laxative abuse and how does it look?

Classic description of factitious diarrhea. Characterized by very frequent, watery, nocturnal diarrhea. The diagnoses can be confirmed with the characteristic biopsy finding of dark brown discoloration of the colon with lymph follicles shining through as pale patches (melanosis coli).

Primary care: Ankle Sprains:

Classification based on severity: -Grade 1: partial rupture of ATFL (anterior talofibular ligament) -Grade 2: complete rupture of ATFL and partial rupture of CFL (calcaneofibular ligament) -Grade 3: complete rupture of both ATFL and CFL Dx: Ankle radiographs are not necessary if the following conditions are met (Ottawa rules): -patient is able to walk four steps at the time of injury and at the time of evaluation -there no bony tenderness over distal 6 cm of either malleolus *Ottawa ankle rules only apply to nonpregnant adults w/normal mental status who don't have other painful injuries and who are seen within 10 days of injury. Tx: RICE (rest, ice, compression, elevation) in acute period, then controlles free range of motion exercises with gradual return to weight bearing. Surgery is rarely necssary acutely, even for grade 3 sprains. Chronic ankle instability (recurrent ankle sprains) needs furter evaluation by an orthopedic surgeon.

Clinda good for what?

Clindamycin good for Gram +s and anareboes. Not good for Gram negatives.

Type 2 RTA

Cna't reabsorb bicarb properly. Fanconi syndrome setting usually. You get low urine ph. Low to normal potassium.

Chest pain, dilated pupils, blood crusted nose?

Cocaine abuse--> drug induced vasospasm. Can cause ST segment elevations.

Sinusitis picture.

Common cause of PNDS and cough. Acute sinustis is bacterial infection that usually involves an obstructed maxillary sinus. Chronic sinutisi i spersistent of sinus inflammation for >3 months. SIGNS: purulent nasal discharge, sinus pain worse on bending forward, fever, tenderness to precussion over sinuses. DIAGNOSIS: CT scan is very senstive not not specific. CT scan should be reserved for hospitalized patients, or for the diagnosis of chronic sinusitis.

Prolactinoma

Common cause of amenorrhea and infertitily in women.

Lumbar spinal stenosis

Common cause of back pain in patients over 60. Spinal canal narrows can compresses the lumbar nerve roots. Characterized by back pain radiating to the buttocks and thigns that interferes with walking and lumbar extension. This is the "NEUROGENIC claudication". Pain with walking. But unlike the vascular claudication associated with PVD, this pain remaines when standing still. These people dipslay the "shopping cart sign", pain is relieved with while leaning forward.

What is dumping syndrome?

Common complication of gastrectomy. Treatment is aimed at decreseing the speed of the passage of fluids and food into the small gut. A high-protein and low-carbohydrate diet is advised, as well as smaller but more frequent meals throughout the day.

Drug induced lupus?

Common drugs that cause are hydralazine, anti-TNF drugs, minocycline, procainamide. A big cause are TNF alpha inhibitors like infliximab. Many patients who use TNF alpha inhibitors develop autoantibodies, including ANA, anti DsDNA, anti-SMmith..rarely, these patients will develop drug-induced lupus. Causes MULTISYSTEM INVOLVEMENT, clinical findings unclude fver, lasaisem, myalgia, arthritis/arthralgia, serositis (pleuritis, pericarditis) and or hepatomgealy/splenomgealy. Diagnoisei is made by typical sysmptoms, histroy of taking an offending drug, and a positive test for ANTINUCLEAR AND ANTI-HISTONE ANTIBODIES>

What is hyposthenuria?

Common in patient with SICKLE CELL ANEMIA and sickle cell trait. Its kidney's impairment in concnetrating urine, whic results in NOCTURIA.

PVCs are common in who? what they look like?

Common in patients post-MI and can be recognized by wide QRS, bizarre morphology and comopensatory pause. Even though they may indicate a worse prognsosi, treatment is not indicated unless the patient is symptomatic.

Describe seborrheic dermatitis?

Common inflammatory disease that affects areas with sebacious glands, like scapl (dandruff), face, chest, body folds, umbilicius. Plaques are fine, loose, yellow, greasy looking, pruritic, erythematous. increased associations with Parkinsons or HIV. Just so you aware this is different from seborrheic keratoses which are common, benign neoplasms that present as brown to black, well-demarcated, "stuck-on" appearing papules with waxy surfaces.

Clavicle fracture tx

Common injury. Criteria for rteurn to sport ractivieies are always controversial and essnetially equate to a judgement cally be physician. For contact athletes: patient needs long time. normal process of bone remodeling takes approximately 10 to 12 months, but most atheletes can't be inactive for such a long period of time. For non contact athletes: gradual return to usual activities may be alllowed 4 to 6 weeks after injury. Cuz by then the patient normally has.. 1. painless, full, active ROM 2. near normal strenght 4. evidence of bridging callus.

Hemochromatosis

Commonly associated with calcium pyrophosphate dihydrate deposition in joints, leading to chondrocalcinosis and associated symptoms including pseudogout and chronic arthropathy. Other manifestaions include diabetes, hyperpigmentation, dilated cardiomyopathy and liver disease with hepatomegaly and fibrosis. Diagnosis is suggested by iron overolad on serum iron studeis, and can be confirmed by ggenetic tests or liver biopsy. Primary treatment is phlebotomy.

Obstructive uropathy symtpoms?

Commonly due to renal calculi. -Flank pain -Poor urine output, can have intermittent episodes f high volume urination, which can occur when oan abstruction is overcome by a large volume of retained urine. -UA can shows some RBCs and WBCs but no casts. Renal dysfunction only happens when there bilateral renal dysfunction.

Transposition of great arteries seen in who?

Commonly in infants of diabete mothers and in males. Physical Exam findings are cyanosis, single loud second heart sound, no murmur.

Atrrial Flutter cause origin?

Commonly involved a reentrant circuit arount the tricupsid annulus

When and describe how you see Legionella?

Commonly spread by cooling towers and water supplies. Travel-associated infection is well documented. Symptoms that help distinguish Legionella from other CAPs include high grade fever (39.0), GI symptoms, and neurologi deficits. X-ray most often reveals focal lobar consolidation. Stains poorly because primarily intracellular, so sputum gram stain showing many neutrophils but no organisms is also characteristic. For Dx you gotta culture the bacteria on charcoal agar and/or urinary antigen testing. Treat with macrolides or fluoroquinolones.

What is like the one thing kidney donors are at increased risk for after procedure?

Complications with future pregnancies.

Concentric vs Eccentric hypertrophy?

Concentric hypertrohy of the heart is seen following chronic pressure overload, as with valvular aortic stenosis or untreated hypertension. Eccentric hypertrohpy of the heart develops following chronic volume overload, as seen in valvular regurgitation.

ARDS etiology? Dx? Tx?

Condition that results from increased permeability of alveolar capillaires causing fluid to fill avleoli. Etiology: Shock, sepsis (most common cause), aspiration, severe pancreatitis, blood transfusion Diagnosis -Bilateral FLUFFY infiltrates on X-ray -----cuz of alveloar collapse owing to leakage of protein0rich fluid in intersitium and alveoli -Pa02/Fi02 <200 -Pulmonary wedge pressures of less than 18 mm HG (low filling pressure exclude diagnosis of pulmonary edema). You see 3 majors physiology alterations 1. Hypoxemia unresponsive to supplemental O2 2. Decreased pulmonary compliance, as the lungs become proressively stiffer and harder to ventilate 3. Decreased FRC Tx:02 treatment does not help the hypoxia in ARDS. Tx is hemodynamic support and treatemtn of underlying disease. in ARDS, mechanical ventilation with low tidal volumes and PEEP (positive and expiratory pressure) can improve oxygenation. PEEP improvess oxygenation by preventing alveolar collapse ath the end of expiration, which increases the functional residual capacity and decreases the work of breathing. Potential complications of PEEP include barotrauma and tension pneumothorax, alvelaor damage, and hypotension.

What is supplemental oxygen not going to work for?

Conditions when the V/Q =0 (shunt). LIke ARDS, or intracardiac shunt. Conditiions when there is just a V/Q mismatch, supplmental oxygen will work. Examples are obstructive lung disesae, atelectasis, pulmonary edema, pneumonia.

Acute "mechanical" back pain wthout neuroogical deficit, management?

Conservative approach is preferred for a period of 4-6 weeks. This includes early mobilization, muscle relaxants, and NSAIDs. Bed rest and physical therapy has not been shows to be helpful.

Treatment for Hyperkalemia mnemonic

Controlling K Immediately Diverts Bad arrhythmias Calcium gluconate (usually for K+ over 7.0 or rapidly rising K+ due to tissue breakdown). Insulin and glucose (also usualy for K+ over 7.0 or rapidly rising K+ due to tissue breakdown) Kayexalate, Diuretics Dialysis Bicarbonate Albuterol REmember you see PEAKED T WAVES initially, then PR interval and QRS complex prolongation, disappearnce of P waves, and eventually a sine wave. Immediate treatment: only until definitive therapy is initated -IV clcium gluconate: GOAL is immediate cardiac membrane stabilization! acts in minutes -Insulin, albuerol, and bicarb all shift K into cell. acts in minutes Definitive therapy -Kayexalate, diuretics, and dialysis remove K+ from body Algorithm for hyperkalmiea causes evaluation... First you gotta to ECG to look for abnormalities Second decide if needs acut e therapy...acute therapy (calcium gluconate, insulin with glucose) is typically reerved for patients with ECG ghanges, potassium>oor equal 7, or rapidly rising potassium due to tissue breakdonw. Dialysis should be reserved for patients with renal failure and those with severe life-thretening hyperkalmie unresponsive to insitial therapy. Third step is exclude acute treateable secondary causes (uncontrolled hyperglycemia, tumor lysis syndrome). Fourth: have a revew of recent/current medications as these afre frequenty the cause. Common ones are -nonselective beta blockers, - potassium sparing diuretics (triamterene, amiloride), -ACE inihibitors, ARBs, and NSAIDs -Digitalis -Cyclosporin -Succinylcholine -Trimetoprim -Heparin.

Crackes (rales), Wheezes/rhonci, pleural rub

Crackles- by excessive airway secretion. causes are bronchitis, pneumonia, pulmonary edema, atelctasis, fibrosis. Wheezes- caused by rapid airlfow through obstructed airway. Asthma, pulmonary edema, bronchitis. Rhoncus-transient airway pluggin. Causes: Bronchitis. Pleural rub-inflammation of the pleura. Causes pneumonia, pulmonary infarction.

Rhabdomyolysis

Crush injury a cause. Also high temp. Also immobilization. ALso cocaine use. -A body temperature of 105.8, may cause rhabdomyolysis and organ system damage. Large blood on dipstick with no RBCs by microscopy on urinalysis suggests rhabdomyolysis, the result of muscle breakdown. -prolonged immobilization causes direct muscle dmage and release of creatine phosphokinase (CPK) -cocaine is potent vasoconstrictor that causes hischemia and direct toxic effect on myocytes. Initially develop hypocalcemia due to precipiattion of calcium with the phosphorous released from the dmaged muscles. Muscles also release potassium and CPK. -So lab values you could see are hypocalcemia, hyperkalemia, increased CPK, increaesd creatinien, dipstick that is positive for blood BUT NO RBCs seen on microscopy because its the myoglobin causing the positive dipstick Main danger associated with CPK levels greater than 20,000 is acute renal tubular necrosis due to myoglobinuria. So it rhabdomyolysis leading to myoglobinuria leading to acute renal failure. Tx: Immediate IV fluids, followed by alkalinzation of urine.

Well known side efect of indinavir (protease inhibitor)

Crystal induced nephropathy

PML (progressive multifocal leukoencephlopathy)

Cuased by JC virus. Its a late manifestaion of AIDS and happens in abou 4% of the population. Characterized by neuro deficits. No treatment for it but regression for well over two years have been seen with highly active antiretroviral therapy.

Rotator cuff tendonitis

Cuased by impingement, most common in people who perfrom reptitive arm movements above the head. Presents with pain when lifting the arm. May be differentiated from rotator cuff tear and frozen shoulder by injection of the joint with lidocaine. In the case of isolated rotator cuff tendonitis, any pain and limitation of motion is resolved by an injection.

Primary Care: Carpel Tunnel

Cuased by median nerve compression within the tight confines of the carpal tunnel, causing numbness and pain in median nerve distribution. If long-standing and severe, atophy of thenar muscles may be seen. Usually worrse at night. SOmtimes patient pain/numbness can go as far back as the shoulder. Associated conditions: hypothyroidism, diabetes, repetitive use of hands in certain activities, pregnancy, recentr trauma Dx -Tinel's sign: tap over median nerve at wrist crease, causes paresthesias in median nerve distribution -Phalen's test: palmar flexion of the wrist for 1 minute; causes paresthesias in median nerve distribution -EMG and nerve conduction velocity study for definitive diagnosis *compression of median nerve results in loss of normal myelination. Axonal loss may also occur if the compression is particularly severe. Nerve conduction studies will therefore demonstrate slowed conduction along the median nerve at the level of the carpal tunnel, with a normal conduction velocity proximally. If axonal loss present then you will see reduced amplitudes. **EMG if frequently combined with nerve conduction studes and may be helpful in demostrating that other nerves are not involved by detecting denervation in muscles typically innervated by median nerve with relative sparing of those that are not. Tx: 1. Nighttime Wrist splint should be worn at night during sleep. Thepruprse is to prevent wrist flexion during sleep (which compresses the nerve). This should be done in patients with symptoms for less than 10 months. 2. Local corticosteroid injection or oral steroids should be attempted if nightitme splinting alone doesn't help. 3. Surgical release is very effective, this should be used in patients who have failed other measures and have had moderate to severe symptoms for at least 6 months. **NSAIDs have shown no benefit for carpal tunnel patients when compared to placebo and therefore are not generally recommended.

What should you give someone who is getting splenectomy?

Current recommendations state that patients should recieve anti-pneumococcal, Hameophilus, and meningococcal vaccines severeal weeks before the operation, and daily oral penicillin prophylaxis for three to five years following splenectomy.

MEchanism of Niacin side effects?

Cutaneous flushing and puruitis, explained by prostaglandin-induced peripheral vasodilatation. Can be reduced by low-dose aspirin.

Cyanide toxicity

Cyanide toxicity comes from too much nitroprusside being used (probably in setting of trying to manage bad hypertension). Nitroprusside metabolizes to cyanide. Also a lot of smoke inhalation can cause cyanide accumulation. cyanide blocks oxidative phosphorylation and promotes anaerobic metabolish, causing lactic acidosis. with cyanide toxicity, you treat with HYDROXyOCOBALAMIN or SODIUM THIOSULFATe, which directly bind s cyanide milecules. An alternate treatment is induction of methemoglobinemia with nitries to increase Fe3+ in hemoglobin. Cyanide binds avidly to Fe3+ and so methemoglobinemia provides an laternate binding site.

Malaria findings

Cyclical fever accompanied by nonspecific constitutional and gastrointestinal manifestations, with anemia and thrombocytopenia commonly noted on laboratory analysis. Blood smear are gold standard for diagnoses. The cyclical fever coincides with RBC lysis by the parasites. Typical cycle consists of a cold phase characterized by chills and shivering, followed by a hot phase with high-grade fever, followed by a sweating stage with diaphoresis and resolution of fever.

normal fever?

Cytokine activation during inflammation is underlying patho. Temps usually < 104. Fever results from the thermoregulatory center's temporary upregulatio of body temperature (regulate at hypothalamus), not from failure to dissipate heat.

Peripheral neuropathy mnemonic

DANG THE RAPIST Diabetes / drugs Amyloid Neoplasm / nutritional a. thiamine: painful sensory neuropathy. b. b12, b6 , E Guillain-Barre Trauma Heredity Endocrine / electrolytes / entrapment Renal/radiation a. chronic renal failure gives you symmetric, distal, mixed sensorimotor neuropathy. Tx: to reverse the neuroapthy of chronic renal failure is renal tranplantation. There are presumed to be neurotoxins in the blood of patients with uremia that are not removed by routine dialysis. Alcohol/AIDS Porphyria / paraneoplastic syndrome Infectious (lyme, HIV, leprosy, diptheria, ) / immunlogic / ischemic Sarcoid Toxins a. NO: nitric oxide induced neuropathy also you get megaloblastic anemia b. lead, arsenic, other metals How to confirm peripheral neuropathy? Nerve conduction studes confirms peripheral neuropathy-that is a disturbance of sensory and motor nerve funciton in limbs. With severe neuropathy of the hands or feet, ulcerations and pressure sores will develop over the skin that is innervated by the damaged nerves. The most severe sensory deficit affects the most terminal elements of the limbs. Metabolic or nutritional problems are the usual cause of glove-and-stocking pattern of sensory disturbance. Diabetes mellitus, thiamine deficiency, and neurotoxin damage (caused by some insecticides_ are the commonest causes of these sensory disturbances. Affected persons usually report the sensatino of pins and needles in the hands and feet, but with some neruopathies, severe pain may develop along with the loss of sensory acuity.

Describe Kussmal respirations

DEEP, RAPID breathing.

Schistocyte, helmet cell. Same thing.

DIC, TTP/HUS, tramuatic hemolysis (mechanical valve)

DKA

DKA presents as how? Presents with metabolic acidosis, polyuria, dehydration, decreased levels of consciousness, and diffuse abdominal pain, and is often PRECIPITATED by acute infection. DKA is characterized by an osmotic diuresis that reduces total body K+ stores even though the serum K+ level may be elevated. Its the extracellular shift that causes paradoxical hyperkalemia (high potassium in blood although total stores are low). Dx? -Diagnosis of DKA is based on a blood glucose level less than 250 mg/dL, AG metabolic acidosis, serum Co2 less than 15 meq/L, and positive serum or urine ketone concentrations Results fron insuline deficiency, so lipid oxidation and metabolism happens rather than glucose metabolishm. Lab data: glucose 400-800 usually, metabolis acidosis, and hyperketonemia. Cerebral edema is a potentially life-threatening complication in DKA Tx presenting as headache, personality change, vomiting, and decreased reflexes. Episodes of DKA can be precipitatied by bacterial infection Tx: Fluids and insulin. The improvement in acidosis levels often are associated with a fall in serum potassium levels, so addition of POTASSIUM to the IV fluids is usually indicated to prevent serious hypkalemia. ****Early potassium supplementation is very important in the reatemnt of patients with DKA. Treatment with insulin and IV fluids leads to a decrease in serum possium levels even if they are initially elveated. All hyperkalemic patients whouls start receiving potassium once serum potassium level goes below 4.5. IN patient s with normal or low potassium levels, potassium replacement should be started with initiation of IV fluid therapy. What is the most reliable indicator of metaolic recovery when you're treating for DKA? -Arterial ph or anion gap. Serum ketones level correct later than arterial ph or anion gap. So arterial ph or anion gap should guide therapy.

DKA

DKA presents as how? Presents with metabolic acidosis, polyuria, dehydration, decreased levels of consciousness, and diffuse abdominal pain, and is often PRECIPITATED by acute infection. DKA is characterized by an osmotic diuresis that reduces total body K+ stores even though the serum K+ level may be elevated. Its the extracellular shift that causes paradoxical hyperkalemia (high potassium in blood although total stores are low). Dx? -Diagnosis of DKA is based on a blood glucose level less than 250 mg/dL, AG metabolic acidosis, serum Co2 less than 15 meq/L, and positive serum or urine ketone concentrations Results fron insuline deficiency, so lipid oxidation and metabolism happens rather than glucose metabolishm. Lab data: glucose 400-800 usually, metabolis acidosis, and hyperketonemia. Cerebral edema is a potentially life-threatening complication in DKA Tx presenting as headache, personality change, vomiting, and decreased reflexes. Episodes of DKA can be precipitatied by bacterial infection Tx: Fluids and insulin. The improvement in acidosis levels often are associated with a fall in serum potassium levels, so addition of POTASSIUM to the IV fluids is usually indicated to prevent serious hypkalemia. ****Early potassium supplementation is very important in the reatemnt of patients with DKA. Treatment with insulin and IV fluids leads to a decrease in serum possium levels even if they are initially elveated. All hyperkalemic patients whouls start receiving potassium once serum potassium level goes below 4.5. IN patient s with normal or low potassium levels, potassium replacement should be started with initiation of IV fluid therapy. What is the most reliable indicator of metaolic recovery when you're treating for DKA? -Arterial ph or anion gap. Serum ketones level correct later than arterial ph or anion gap. So arterial ph or anion gap should guide therapy. -If serum glucose falls to <200 mg/dLbut the patient still has an elevated anion gap, the rate of insulin infusion should be halved and the patient should recieve IV fluids with 5% dextrose to prevent hypoglycemia.

UA-ketones?

DKA, alcohohol ketoacidosis (will have increased osmolol gap), starvation ketosis

Diseases of the venous system

DVT Chronic venous insufficiency Superficial thrombophlebitis

DVT stuff to remember, when and when maybe not do anticoagulation

DVT PRophylaxis -LMWH -LOW dose unfracitonated heparin -Complression boots *DVT stuff to remember, when and when maybe not do anticoagulation DVT below the knee (distal). Calf vein clot. -You can choose whether to anticoagulate or just wait. Many of these just dissolve be themselves within 14 days. So just send serial duplexes to make sure it's not moving. DVT above the knee (proximal). Uworld says iliofemoral vein clot. -If DVT moves above the knee then you have to anticoagulate. Tx is unfractionated heparin or LMW heparin cuz of the rapid anticoagulation effect to decrease propogation of clot. Warfarin is started after the patient is adequatly anticoagulated on heparin and then continued for 3-6 months in the case of a first DVT. **in patient who got DVT due to time-limited risk factor (surgery, pregnancy, OCP use, trauma), warfarin anticoagulation should be used for a minimum of 3 months. If patient got idiopathic DVT, then 6 months minimum treatment should be done, then re-evaliuate. *Patinet may be interested in rivoaroxaban (Xarelto) if they don't hwant daily heprin injections or they don't wat the dietar restrictions or frequent INR monioring with warfarin. It doesn't require lab monitoring or daily injections, but there is no antidote in the vent of major hemorrhage. Initial evaluation of possible DVT? Ultrasound for initial in ppl with moderate to high risk. If patient has low probablit, a D-dimer can further assess risk, with an ultrasound peforemd only in patients with a positive D-dimer. Posivie D-dimer is over >500 ng/ml.

A decrease in LES tone? An increase?

Decrease-scleroderma (also has absence of peristaltic waves which GERD doesn't have), GERD. Increase- achalasia

Type 4 RTA

Decreased aldosterone. Ph is low. HYPERKALEMIA is hallmark.

Main reason for orthostatic hypotension in elderly?

Decreased baroreceptor responsiveness.

Sideroblastic anemia

Defect in heme synthesis Causes: myelodyspoalit syndromes, alchohl, lead, vit b5 defieincy, copper deiciency and INH You see rigned sideroblasts with irone laded mitochondria in bone marrow Tx: pyridoxine (Vit B6)

What is HIV virologic failure?

Defined as failure to achieve a viral load (VL) <200 copies/mL within 24 weeks (6 months) of antiretroviral (ART) and may be due to drug resistance or noncompliance. Following ART initiation, VL should be measured approximately every 3-6 months. In treatment-naive HIV-positive patients, antiretroviral therapy should decrease the viral load to <50 copies/mL within 6 months.

Definition of fever of unkown origin (FUO)

Defined as fever greater than 38.3C on multiple occasions over a course of at least three weeks in the settinf of a negative basic evaluation. In 50% of cases, the unerlying cause is never identified. Of the cases with an identifiable cause, connetive tissue disorders,infection, and neoplasms, in that order, are most common. Basic eval with history, phycisal exam, CBC, blood chemistries, blood cultures, UA, chest X-ray and hepatitis erologies should be done before the patient is calssified as having FUO. About 50% of patients with FUO will never be diagnosed with an underlying condition.

What is peripartum cardiomyopathy?

Defined as heart failure with a left ventricular ejectino fraction less than 45% that is diagnosed between 3 months before and 6 months after delivery in the absence of an identifiable cause. Patients with a history of peripartum cardiomyopathy who have severe or persistent LV dysfunction have a high risk for further LV function decline, recurrent heart failure, and death with a subsequent pregnancy. These patients should be advised to avoid pregnancy

what is Fulminant hepatic failure?

Defined as hepatic encephlaopthy that develops within eight weeks of the onset of liver failure. Only way of treating is liver tranpslant, regardless of etiology.

Define anaphylaxis and Tx

Defined as severe allergic rxn characterized by sudden collapse or symptoms involving > 1 organ system after expousre to an offending antigen. So can involve oropharynx, skin, GI tract (nasuea, diarrhea, vomiting, cramps) , lungs (wheezing), and Cardio (hypotension) system. You got a question wrong cuz person had wheezing but not yet in respiratory distress. "however, given that the skin finding are generalized and ccompanied by wheezing on auscultation, this partient is experiencing anaphylaxis and more aggressive treatment is warranted." IM epinephrine is Tx. Why? -B2 agonist effect: Bronchodilataion and decreases release of inflammatory mediators -Alpha1 effect: Vasoconstriction which raises BP and decreses upper-airway edema. IM epinephrine is most important and should be given first. Some supplemental therapies for anaphylaxis are bronchodilators, antihistamies, methlpredisolone.

What is obesity hypoventilation syndrome. Compare it so sleep apnea

Definedy by -obesity BMI >30), -daytime hypercapnia (PaCO2 > 45) and -alveolar hypoventilation. Arterial blod gas will show hypercapnia, hypoxemia, and respiratory acidosis as a result of altered lung mechanics due to obseity and nocturnal hypoventilation. Tx: Wieght loss and Noninvasice positive pressure ventilation are first-line therapyeied for OHS. Patients with sleep apnea alone hypoventilate at night which causes transient hypoxia and hypercarbia that resolved during wakefulness. Patietns with obesity hypoventilation syndrome, however, do not have respiratory mechanics that allow them to resume normal ventilation during wakefulness and hence develop chronic respiratory failure.

Management of delirium in hospitlilized patient?

Delirium: (waxing and waning of consciousness). Most likely due to toxci-metabolites or infection. If the elderly patient is agitated, use typical (haloperidol} or atypical antipsychotics ( risperidone, quetiapine). Benzos are not recommended in this setting. Benzos may be used to treat agitation in young patients, but in older patients they are contraindicated cuz they are at increasd risk for adverse events, may experience worsening agitatino (paradoxic effect), and tend to metabolize benzodiazepines slowsly, making their effects very long lasting.

Dengue Fever

Dengue hemorrhagic fever (DHF) is the most serious dengue viral infection and is due to increased capillary permeability leading hemoconcentration, pleural effusion, and ascites. CIRCULATORY FAILURE can develop with significant plasma leakage and is sometimes referred to as dengue shock syndrome. Patients typically have marked thrombocytopenia (<100,000) and prolonged fever.

Algorithm to evaluate hemoptysis Person has massive hemoptysis, what do you do?

Depends if its mild/moderate or massive (>600ml/24hr). If mild/moderate---> cxr, cbc, coags, renal function, UA--->CT scan plus/minus brochoscopy----> treat cause; peristent bleeding treated via bronchospic intervntions, embolization, or resection. If massive---> secure airwaya and breathing. If bleeding stops---> pick up where "cxr" starts in "mild/moderate" paragrapsh. I bleeding doesn't stop, go straight to treat cause; persistent bleeding treated via bronchospic interventions, emboilization, or resection. The greatest danger in masive hemoptyis is not exsanguination but asphyxiation due to airway flood with blood. INitial managemetn involves establishing ADEQUATE PATENT AIRWAY, maintaining ventilation and gas exchange, and ensuring hemodynamic stabilityu. Patients shoudl be placed with the bleeding lung in the dependent position (lateral position). Bronchoscopy is the proceudre of choice to identify the site and attempts early theraputic inervation. If this faily then go to pulmonary arteriography which can precisley identify the bleeding vessels and do therapetuci embolization. IF this fails then do thoracotomy.

Signs of Opiod overuse

Depressed mental status Respiratory depression Pupillary constriction

COPD refers to what

Describes the chronic bronchitis and emphysema Chronic bronchitis-chronic productve cought on most days for >3 months in each of 2 successive years

What are Baker cysts?

Develop as a result of excessive fluid production by an INFLAMED SYNOVIUM, as OCCURS IN CASES OF Rheumatoid arthritis, osteoarthritis, and cartilage tears. The excess flui accumulates in the popliteal bursa which expands, creating a tender mass in the popliteal foss. Baker cysts occasionally burst and release their contents into the calf, resulting in an appearance similar to a DVT.

Statins

Diabetic patients age 40-75 should receive statin therapy regardless of baseline lipid levels. Dose intenstiy can be selected based on overall 10-year risk of cardiac events. Those w/ 10year risk of atheroscleroti cardio disease <7.5 should get moderate statins Those with 10 year risk >7.5 should get high intensity. ALso know these Statins recommendations: -Person with clinically sign. atherossclerotic disease gets high intesity stain if under 75 yrs and moderate statin if over 75 -Person has LDL>190: gets high intestity statin -Person has estimated 10year risk>7.5: moderate to high intesity * the 10 year risk stuff is estimated by the ASCVD risk calculator **Remember: statin therapy can induce myopathy which can range from asymptomatic elevation of serum CK to rhabdo. Statins can also potentiate muscle injury w/CK elevation after prolonged vigorous exercise. ***In ASYMPTOMATIC patients, a CK level >10 upper limit normal indicates you should STOP statin therapy. restart it once CK levels have normalized. i think if symptomatic, stop statin until CK levels reach normall.

Who gets osteo from contigous spread and who gets from hematogenous spread?

Diabetic patients: pathogenic mechanism of osteomyelitis adjacent to a foot ulcer is contiguous spread of infection. Direct incoluation can be a way too. Hematogenous spread is most likely way in hematogenous osteomyelitis, which is typically observed in children.

What arrythmia is specific for digitalis toxicity?

Digitalis can increase ectopy in the atria or ventricles which cn lead to atrial tachycardia. Digitalis toxicity causes increased ecotpy and increased vagal tone. Atrial tachycardia with AV block occurs from the combination of these two digitalis effects, and is relatively specific for digitalis toxicity.

Know diastolic and systolic hear failures pg 291 first aid step 1, and cardiomyopathies

Dilated cardiomyopathy mnemonic: ABCCCD, Tx is basically same for CHF

Main mechanism of nitrates

Dilation of veins (capacitance vessels). So preload decreases and as a result less blood in the heart so you have decreased oxygen requirement of the heart.

What are some first generation anithistamines? what are side effects?

Diphenhydramine, chlorpheniramine, doxepin, hydroxyzine. Have significant anticholinergic effects in addition to their antihistamine effects. Common side effects are dry eyes, oral mucosa and repsiratory passages, urinary retention and dysuria, highly sedating. Use of the drug must be d/c before driving, machine work, diving or flying planes.

Explain TIBC

Direct measure of amount of iron that can be bound by transferrin and is indirect measure of transferrine levels. In iron deficiency anemia, transferrin production is upregulated and serum iron is low, resulting in increased rather than decreased TIBC.

Needs for glucocorticoid taper

Discontinuation of corticosteroid therapy has 3 primary risks: 1. unmasking latent symptoms of the condition being treated 2. steroid withdrawal syndrome (nonspecific symptoms such as fever, fatigue, and headache associated with normal cortisol levels) 3. adrenal insufficiency due to suppression of HPA axis One published reginmen for tapering steroids after long term use involves a weekly decrease in prednisone dose by 2.5-5mg until a daily dose of 7.5mg is reached. Once the patient reaches this dose, it is converted to 10mg of hydrocortisone daily. Hydrocortisone is discontinued once the morning (pre-dose) plasma level of cortisol is >10micrograms/dL. Just an example, no evidence that this is better than other regimens.

Type 1 RTA, acidosis refers to metabolic acidosis

Distal tubule problem in hydrogen secretion. So can't acidify urine properly. So high urine ph. Also hypokalemia.

Meds for chronic constipation treatment

Docusate sodium is a surfactant stool softener that increases stool hydration and is most effective when there is a need to avoid straining (postoperative patients). Docusate is less effective than laxatives for chronic constipation and is not useful for long-term therapy.

HIV patient with eye problems?

Don;t always think CMV cuz VZV and HSV can cause severe intraocular inflammation. HSV, VZV retinits: can cause severe, acute retinal necrosis with PAIN, KERATITIS, uvieitis, and pale lesions and central retinal necroris on fundoscopic exam. CMV retinits: PAINLESS,, not associated with keraitits or conjunctivitis. You see hemorrhages and fluffy or granular lesions around retinal vessels. *Ocular problems occur in about 1/2 of advanced HIV patients.

Treatment for paeople with prolactinomas?

Dopamine-agonists such as bromocriptine or cabergoline

Healthcare worker may have stuck himself with needle from HIV patient?

Draw his blood for baseline HIV serology and right away give HIV postexposure prophylaxis with 2 NRTI and maybe 1 protease inhibitor. Repeate testing looking at serologic status at 6 weeks, 3 months, and 6 months.

Other causes of folic acid defieicny besides poor diet and/or alcoholism

Drugs: drugs that can impar absoprtio of folic acid (phenytoin) or antagonize its physiolgic effects (methotrexate, trimethoprim). Extremely high yield quesiton for USMLE

What is "flail chest"?

Due to crush injury usually, cuasing muliptle rib fractures. Leads to an unstable chest wall segment that moves in paraosicical motion with respiration. The flail segmentt tends to retract inward during inspiration (instead of normally bulging outwrd) and bulges out during expiratino (instead of normally intracting inward). Normally these patiets have respiratory distress and tachypnea with shallow breaths. Classic x-cray findings show multiple rib fractures overlying a lung contusion.

why is Anemia common in Chronic kidney disase patients? what are common side effects of the tx?

Due to erythropoeitin deficiency and is treated to a target HgB of 11 with eryhtropoeisese stimulating agnets. Know: that the most common side effects of erythropoeitin therapy are.. 1. Worsening of hypertension. Not well understood why. 2. Headaches 3. Flue like symptoms **also know that when you give supplemental erythropoietin, now you have all these new RBCs using iron. So if you don't give enough iron with it, you're gonna get iron defieicny anemia. *Extermely high yield USMLE question

Heat exhaustion

Due to inadequate fluid and salt replacement. Altered mental status NOT present. Cause is inadquate sodium and water replacement dring pysical activity because of body's inability to maintain adquate cardiac output.

HIV tests

During acute symptomatic phase: HIV RNA viral load is most appropriate -Antibodies to HIV do not commonly occur until about 6 weeks after infection and may therefore be negative during the acute symptomatic phase. Tests for HIV-specific antigens, such as p24, can also detect the presence of virus in acute setting but be careful for the reason above. Patients diagnosed with HIV infection on the basis of an HIV viral load measurement should have confirmatory serologic antibody testing performed at a subsequent point in time.

Cirrhosis dx and signs

Dx: CT scan help, definite Dx by liver biopsy Physical exam: -loss of appetite, nausea, vomiting -jaundice and pruritis -signs of portal hypertension: (varices, spider telangiectasia, ascites, edema, caput madusae -bleeding (from decreased clotting factors in liver) -encephalopathy-due to incrased NH3 -Dupuytren's contractures: contractures of palmar fascia resulting in flexion of fourth digit -Gynecomastia, hypogonadism (so erectile dysfunction seen commonly), spider angiomatas, palmary erythema. why? Liver can't metabolize estrogen like it should cuz its damaged. causes all this. -hypothyroidism-Liver responsible for making TBG which is needed in making T3 and T4. A abad liver aing gonna do it. Early in cirrhosis, LFTs are high and there is hepatomegaly; as cirrhosis advances, LFTs begin to normalize (liver is burned out) and liver liver atrophies (nonpalpable) Tx:- cease alchohol, - avoid hepatotoxins (like acetaminohpin, isoniazid), -spironolactone (potassium sparing diuretic) for ascites, HE TREATMENT -lactulose for hepatic encephalopathy (broken down by colonic bacteria and causes NH3 to convert to NH4, which cannot cross the blood brain barrier), -mannitol for advanced HE -Rifaximin (antibiotic) can deccrease the number of ammonial producing bacteria in the colon, they are usually added to lactulose if the patient does not improve within 48 hours. - Laxatives may also be beneficial. ASCITES TX Stepwise approach of treatment for ascites 1. Na and water resriction 2. SPironolactone 3. Loop diuretic (not more than 1L/day of diuresis for risk of hepato-renal syndrome) 4. Frequent abdominal paracentesis (2-4L/day, as long as renal function is okay) Shunts are generally indicated for symptomatic varices (after first bleeding) Hepatology lecture notes: -Cirrhosis associated with HE ascites and spontaneous bacterial peritonitis esophageal varices (and bleeding) hydrothorax HCC hepatorenal syndrome: you see rise in creatinine, give fluids portopulmonary hypertension: you see excessive pressures in pulmonary circuit. pt is short of breath. dont know why it happens. hepatopulmonary syndrome: vasodilatory components go to lungs and create shunts-->dysoxia. Dx: echo and bubble study. bubble study is bubbles should not pass through lungs to left heart. However, if you do see them passing through that means the pulmonary vessells are really dilated and thats why they passed through.

Organophosphate toxicity

Dx: RBC cholinesterase activity can be used to confirm the diagnosis of organophosphate toxicity and assess degree of severity Tx: atropine, pralidoxime

According to uworld what is the preferred screening test for HIV?

ELISA then confirmed with western blod. ELISA sensitivity if greater than 99.9%. Western blot has specificity greater than 99.99%. BUT NMH lecturer said that the HIV antigen/antibody test is the new best test.

Epinephrine, norpine

EPINEPHRINE -Low infustion rates: Beta 1 effects predominate causing increased heart rate, stroke volume, and contractility. -Higher infusion rates: alpha affects predominate, increasing BP and SVR.

Elderly person looks like being abused in nursing home, what do you do?

Each state has nursing home ombudsmen who can investigate.

Neurosyphillis

Early neurosypphillis may prfesent with symptoamtic menigitis, ocular syphillis, and otosyphilis. Patietns with syphilitic menignitis are usually not as sick as those with acterial menigitis and frequently have a prodorome several days preceding presentation of meningitic smptoms. Cranial neuropathies, especially of the optic, facial, or audiotry nerves, can occur.

AFi

Ectop

Know Multiple Myeloma vs Waldenstrom macroglobulinemia vs MGUS (monoclonal gammopathy of undetermined significance) vs amyloidosis

Eleavted total serum protein with normal albumin suggests disorders like MM, amyloidosis, Waldentrom macroglobulinemia, and MGUS. M protein: monoclonal immunoglboulines secreted by excess plasma cell clones. Waldenstrom is basically excessive IgM antibody in the blood which causes hyperviscosity. So look for IgM skpike and hyperviscosity (findings for hyperviscosity are blurry vision, nasal bleeding, headach). you can do a serium viscosity study. Common signs: 1. Increased size of spleen, liver, and lymph nodes 2. Tiredness due to anemia 3. Bruises and bleeds easily 4. Night sweats, 5. Headaches and dizziness 6. Visual problems 7. Pain and numbness in extremeities MM-similar symptoms wo Waldenstrom but involved immunoglobulins are IgG or IgA - Also, rarely have hyperviscosity syndromes. -CRAB (hypercalcemia, renal insuffiency, anemia, bone lytic lesions). -SO YOU WANNA ORDER SERUM AND URINE PROTEINELCTROPHORESIS: >orequal 3 g/dl M protein on SPEP (serum protein electrophoresis) w/>orequal 10% plasma cells in bone marrow -increased risk of infection due to both a total decrease in functinal antibodies and leukopenia that develops as the bone marrow is filled malignant cells -..Elderly person with bone pain, renal failure, and hypercalcemia? ...has multiple myelopma until proven otherwise. About 50% of multiple myeloma patients develop some degree of renal insufcciency; this is most likely due to obstruction of the distal and collecting tubules by large laminated cases containing paraproteins (mainly Bence Jones protein). -Dx confirmed by bone marrow biopsy showin sheets and clusters of plasma cells. *complete x-ray skeletal sries should be performed once patient is diagnosed with MM. Other imaging reserved for patietns with bone pain and negative initial x-ray skeletal surverys. On x=ray, you're looking for lytic lesions, diffuse osteopenia, or fractures in nearly 80% of patients. MGUS -M protein < 3g/dl, < 10% of plasma cells on bone marrow -a metastatic skeletal bone survery ir recommended in MGUS patients to exclude lytic lesions suggesting MM. Amyloidosis -Patients with primary (light chain) amyldoidosis may present with elevated monoclonal protein but usually have other findings (nephrotic syndrome, heart failure, hepatomegaly). A abdominal fat pad biopsy would be considered is there was strong concern for amyloidosis.

Viral encephalitis CSF findings?

Elevated WBC Lymphocytic predominance Normal glucose Elevated protein concnetraion Early empiric thearpy with IV acyclovir should b einitated as soon as possible for suspected herpes simplex virus encephalitis.

Lab tests in hemolytic anemia?

Elevated reticulocyte count and LDH Decreased haptoglobin and hemoglobin/hematocrit.

elevateed CPK means what ?

Elevted creatine phosphokinase points toward muscle injury.

Goodpastures treatment?

Emergency plsmapheresis cuz you want to remove the anti-glomerular basement membrane antibodies.

Meningitis treatment?

Empiric antiobitics: Vanc plus ampicillin plus cefepime if immunocompromsed. Age2-50: Vanc plus 3rd generation cephalosporin Age>50: Vanc + ampicillin + 3rd generation cephalosporin *remember, if you suspect bacterial meningitis you gotta hve steroids at the saeme time you give empiric antibiotics. This will help treat Strept pneumoniae and you only discontinue the steroids when culters come back and you know that its anything besides Strept pneumonia.

Pneumonia in HIV patient? what is likely cause?

Encapsulated bacteria, especially Pneumococcus, are the most common cause of pneumonia in HIV patients.

Parenteral vs enteral nutrition?

Enteral nutrition is provided through a feeding tube *Enteral feeding is preferred to pareneteral feedings for people who have a functionaing GI system. A gastrostomy tube can either be placed surgically or percutaneously by endoscopy or IR. THe standard caloric intake reommended for enteral feeding is 30kcal/kg/day and 1g/kg/day of protein. Lower amount used if severe preexisting malnutrtion to prevent refeeding syndrome. *preferred way of providing nutrition in patients with severe acute pancreatitis cuz of lower complication rates Parenteral nutrition is provided through a large peripheral or central IV line.

Erythema nodosum.

Erythema nodosum is a condiction of painful, subcutaenous, pretibial nodules. It can be a symptoms of more serious disease processes including sarcoidosis, TB, histoplasmosis, recent streptococcal infection and inflammatory bowel disease. The association of EN with sarcoidosis is particularly strong in young, black women. Cough, arthritis, uveitis, and hilar adenopathy on chest x-ray are also associated with sarcoidosis.

Pericardial tamponade:

Etiology: pericarditis, trauma, rupture due to post Mi, aortic dissection Signs: -Becks triad: hypotension, muffled heart sounds, JVD -Also maximal apical impulse hard to palpate -Pulsus paradoxus: systoloci BP decreases by >10 mm Hg with inspiration -Narrow pulse pressure: only small difference between systolic and diastolic blodo pressures What causes the pulsus paradoxus is due to reduces stroke volume during inspiration. Which is due to more of the blood entering RV during inspiration bulging leftward into LV due to incresed pressure around RV. So you get reduced LV volume and output, causing BP to fall with inspiration. Tx is pericardiocentesis with pericardial effusion and tamponade in patients with hemodnamic INSTABILITY or cardiogenic shock. I fthe patient is hemodynamically stable, urgent pericardiocentesis is not needed. TEE is typaicallly performed in ther ED for rapid diagnosis and early treatment. **Pulsus paradoxus can also occur in asthma, COPD, constricitve pericarditis, OSA, obesity, PE and severe pectus excavatum. **Low voltage QRS complexes on ECG are seen in patients with moderate or large pericardial effusion. A large pericardial effusion that develops slowly over time does not cause cardiac tamponade and therefore does not need pericardiocentesis. Low-voltage QRS on ECG is also present in patients with obesity, severe hypothyroidism, amyloidosis, and anasarca.

Cutaneous cryptococcous

Extermelty important questions for USMLE step-3 Cutaneous cryptococcosis can occer as an early manifestation of disseminated cryptococcosis in patienths with HIV disease. It manifests as multiple, discrete, REDDISH COLORED PAPULES with central umbilication. HIstopathologic examinaion of thebiopsy specimen from th eskin lesions is necessary to confirm the diagnosis of cutaneous cryptococcosis.

Esophaeal motor disorders

Extermely high yield for USMLE, know all of this. Esophaeal motor disorders ACHALASIA -weight loss, cough, diffuse chest pain -LES CAN'T RELAX on swalloing -looks like birds beak on barium swallow. --Esophageal motility study usually required to confrim diagnoses because of how other disorders can mimic achalasia. You find SMALL-AMPLITUDE contractions in esophagus, incomplete relaxation of LES, and higher-than-normal pressure in body of esophagus. -relieved by nitroglycerin -Tx: Safest and most effective treatemnt for this condition is surgical treatment with an esophagomyotomy. Also botulinum toxin injection. --histopathology reveals absent or declining neurons in myenteric plexus. manometry reveals absent peristalsis. DES (diffuse esophageal spasm): etioloy unclear but common in young females and associated with emotional factors and functional GI disorders. -dysphagia, diffuse chest pain, often precipiated by ingestion of hot or cold liquids -swallowing induced large wave. will have HIGH-amplitude peristaltic contractions in body of esophagus. This is diagnsotic. -lower esophageal sphincter has normal relaxation, unlike in achlasia -looks like corkscrew on barium swallow -releived by nitroglycerin Tx: antispasmodics, dietary modulation, psychiatric counseling. If surgery needed, long myotomy guided by manometric evidence. Really effective if performed correctly. -also known as nutracker esophagus *Dysphagia to solids AND liquids often indicated a motility problem (like achalasia, DES). Dysphagia to ONLY solids indicated mechanical obstruction ZENKER's DIVERTICULUM -elderly -dyshpagia and regrurgitation -halitosis -at risk for aspiration pneumonia -occurs due to posterior herniation between fibers of the cricopharyngeal muascle Dx: A contrast (barium) esophgram Tx: surgical: most common procedures is a cervical pharyngocricoesophageal myotomy (incising the cricopharyngeus). *When Zenker's causes Zymptoms it requires Zurgery. Asymptomatic Zenker's is treated only if it >2cm in size. SCLERODERMA -fibrosis and atrohy of the esophogeal smooth muscle, lower esophageal sphincter become incompetent (low tone) and with time leads to reflux esophagitis and strictures. A decrease in LES tone? An increase? Decrease-scleroderma (also has absence of peristaltic waves which GERD doesn't have), GERD. Increase- achalasia EVALUTATION OF DYSPHEGIA 1. History of difficulty initiating, swallowing with cough , choking, or nasal regurgitation. ------Yes--->likely oropharyngeal dysphagia--->Videofluoroscopic modified barium swllow or nasopharyngeal laryngoscopy or EGD** ------No--->Likely esophageal dysphagia. So Go to step 2. **structural leasions that lead to dysphagia in the pharynx and upper esophagus may be visualized w/nasopharngeal laryngoscopy. **esophagogastroduodensocpy (EGD) is most helpful when patient has LOWER esophageal symptoms. Not recommended as initial eval for patients with upper esophageal lesions as upper esophas often not visualized well during scope insertion and perforatino possible. **videofluroscopic barium swallow if a functional test providing visualization of pharynx and upper esophagus as patient swallows. The test assesses neuromuscular disorders but is less useful for identifiygin structural lesions than the direct visualization that laryngoscopy offfers. 2. Dysphagia with SOLIDS AND LIQUIDS? -YES. So likely motility disorder (achalasia, DES, scleroderm)-----> So do barium swallow followed by possible manometry. (Barium swallow more effective than manometry at evaluating motility disorder). -------------If motility disorder probably by barium swallow, do an esophgeal motility study (manometry) to confirm diagnosis. -NO. the dysphagia is primarily solids (although might be progressing to liquids). So likely mechanical obstruction. Go to step 3. 3. HIstory of prior radiation, caustic injury, strictures, or esophageal surgery? -Yes.---->Barium swallow followed by possible endoscopy. These patients have risk of perforation with endoscopy and should get barium swallow first. --No.--->Upper endoscopy. **if you have mechanical obstruction: -Favors cancer: progressive dysphagia, barium swallow shows Asymmetric narrowing of esophagus. Also ppl with GERD normally get cancer only after 20 years. --Favors stricture: non progressive dysphagia favors esophageal rigns. You tend to see SYmmetric narrowing on barium swallw. **if you have motility disorder: --intermittent dysphagia suggests a primary esophageal motility disorder -progressive dysphagia indicates secondary causes such as achalsia or scleroderma

Fer

F

Hereditarary hypercoagulatbility syndromes

FACTOR V LEIDEN -production of mutant factor V that is resistatn to degradation by activated protein C. Most common cause of inherited hypercoagability in whites. PROTHROMBIN GENE MUTATION -incread production of prothrombin--> plasma levels and venous clots ANTITHROMBIN DEFICIENCY -deficiency of antithrombin, dimishes heparin affect PROTEIN C or S deficiency -can't inactiveate factor V and VIII. Think this if you see skin and tissue necrosis after warfarin administration. OTHER.. OCPs: increases hypercoagulability cuz estrogen induces increased production of coagulation factors Homocystinemia: hypercoagulable state

Fondaparinux? Rivaroxaban?

FACTOR Xa INHIBITOR -Oral-Rivaroxaban (Xarelto). Used for prophylaxis, Tx of VTE. Also for nonvalvlar A-fib. -Oral- Apixaban. Also can be used for prophylaxi, Tx of VTE and for nonvalvular A-fib. -Injection-Fondaparinex DIRECT THROMBIN INHIBITOR -Oral: Dagagtroban (Pridaxa). Approved for DVT, PE, nonvalvular A-fib. NOT used for prophylaxis for VTE. -IV: Argotobran: continuous IV drip. Usually used in case if patient has HIT -IV: Bivalirudin: sometimes used in ACS cases but not often LMWH Enoxaparin (Lovenox) Unfortunatley, if patient has kidney problems you probably wanna stay away. these are cleared renally. LMWH vs Coumadin -cancer patietns w/VTE. LMWH is better than Coumadin. -no data comparing LMWH and oral 10as. -for valvular A-fib, the only anticoag approved is Coumadin.

TTP Mnemonic

FAT RN Fever Anemia Thrombocytopenia Renal dysfunction Neurologic abnormality

Fresh frozen plasma vs Cryoprecipitate

FFp: increases coagulation factor levels. Uses: DiC, cirrhosis, warfarin overdose *Vit K takes 12-24 hours to take effect. (Promotes clotting factor synthesis in liver). *Prothrombin-complex concentrate (PCC), (has Vit K dependent clotting factors 2, 7, 9, 10). is actually better that FFP for warfarnin overdose duz it takes quicker to prepare/administer and requires less volume infusion Cryoprecipitate: containes fibrinogen, factor 8, 13, vWF, and fibronectin. Use: Treat coagulation factor deficiences involving fibrinogen and factor 8 and Vwf disease.

Hereditar colon cancer syndromes

Familiar polyposis coli (FAP) -get bunches of polys by age 25 -APC gene -adenomatous polyps are the type of polyp -Screening upper GI endoscopy should be performed after a diagnosis of FAP is made -Tx;: prophlylactic total colectomy HNPCC (or Lynch syndrome) -Auto Dominant. -3 or more relative of patient devleop colon caner -there is Lynch 1 (hereditary site specific colon cancer) and Lynch 2 (cancer family syndrome). Remember that Lynch II is distinctly associated with a high risk of extracolonic tumors, the most common being endometrial carcinoma, which deveops in up to 43% of females in affected families. *The Amsterdam critera are used to clinically daignose HNPCC and consist of... 1. at least 3 relatives with histologically confimred colorectal cancer, one of whom is first-degree realtive of other 2. involvment of at least 2 sucessive generations 3. diagnoses of at least one of cancers before age 50 *screening for patients with HNPCC should start at 20 or 25 or 10 years earlier than the youngest family member with colorectal cancer. Gardner's syndrome -AD -Polyposis coli, supernuemerary teeth, osteomas, fibrous dysplasia Peutz-Jeghers syndrome -multpile polyposis of fmall intestine with multiple pigmented melanin macules in oral mucosa -hamartomas are the type of polyp *BRCA1 (usually receptor negative) is the one that is associating with colon cancer * BRCA2 (usually hormone receptor positive) *when to screeen for BRCA? patients with a history of ovarian cancer in 1st or 2nd degree relatives at age <50 or in multiple generations.

Why would a CF patient have bleeding problems?

Fat malabsorption is common in CF patients cuz pancrease messed up so fat-soluble vitamin absorption is messed up. Vit K is one of these and important for factors "1972" and protein C and S.

SLE (Lupus)

Fatigue, fever, weight loss, non-deforming ARTHRITIS, ORAL ULCERS, serositis, hematologic abnormalities, proteinuria, BUTTERFLY RASH. Greater than 90% of patients have arthritis, most commonly affecting the MCP and PIP joints of the hands. -the arthritis is a MIGRATORY arthritis. Lab findings: -hemolytic anemia, thrombocytopneia, and leukopenia -low serum complement -Anti ANA, anti DsDNA, anti Smith antibiodies *patients with a high pretest probability of SLE and ANAs (titer >1:160) should get more testing like complement levels and more specific autoantibody testing like anti DsDNA -proteinuria and elevated serum creatinine (renal involvement) *the anti DsDNA are more senstivie for lupus, the anti Smith antibodies are more specific for lupus. antiDsDNA correlates with disease ACTIVITY. anti ANA can be positive in many patients who are healthy or who have connective tissue diseases other than SLE. Renal biopsy is REQUIRED in all patients with new onset lupus nephritis. This is because you can have different classes and Tx depends on class. Immunosuppressive therapy may be given once the lupus nephritis is classified. Tx: -Hydroxychloroquine is an anti-malarial agent that is particularly effective at imporiving arthralgias, serositis, and cutaneous symptoms in SLE. -Low dose, short term prednisone may be used in patients with acute mild manifestations of SLE, whereas higher dose steroids or other immunosuppressants are typically reserved for patients with more severe, sold-orgran manifestations. **SLE is a SIGNIFICANT risk factor for the development of PREMATURE CORONARY ATHEROSCLEROSIS and coronary artery disease in young women. Due to a combination of traditional (hypertension, hyperlipidemia) and disease-related risk factors (chronic inflammation, steroid use).Cardiovascular events are the leading cause of mortailty in SLE patients.

Acute bacterial prostatitis?

Febrile with suprapubic or perineal pain. Irritative voiding symptoms may be present, Tender prostate is noted on rectal examination and UA shows bacterirua and pypyuria. Obtaining a mid-stream urine sample would be the most appropriate next step to help direct antibioitc therapy. Treat with TMP-SMX or fluoquinolones. **Important: UTIs in men usually represent prostatitis as opposed to cystitis, particularly if there are symptoms of urinary obstruction. Prostatic massage and Foley catheter should be avoided in obstructed prostatitis patient 2/2 bacteremia risk. Put in a suprapubic catheter.

Vertebral osteomyelitis workup

Fever (may or may not be present), back pain, and FOCAL spinal tenderness---> Blood Cx, ESR/CRP, Plain spinal x-rays---> Increased ESR/CRP but normal X-ray---> MRI followed by CT guided bone biopsy for confirmation Vertebral osteomyelitis most likely due to hematogenous spread of recent UTI.

Classic triad of brain abscess? Important predisopsing factors?

Fever, severe headaches (nocturnal or monring) and focal neurologic changes. Predisposing factors: Congential heart disease and recurrent sinusitis and otitis media/mastoiditis and dental infection. OM/Mastoiditis: Direct spread into temporal lobe Frontal or ethmoid sinusitis: Direct spread into frontal lobe Dental infection: Direct spread into frontal lobe Congental heart disease: Increaeses risk of hematogenous spread to brain because if the pulmonary circulation is bypasssed the bacteria in blood misses an important area where blood is filtered and removed by phagocytes. With hematogenous spread you generally see multiple abscesses along distributeion of middle cerebral artery (gray-white matter junction). KNOW: - If brain abcess is due to untrated sinusitis the cause is Viridan strept or anaerobic bacteria. - If the brain abscess comes aftery neurosurery, penetrating trauma or distal staphyl infection (endocarditis, osteomyelitis) causes hematogenous dissemination...the cause is Staph. aureus.

Differentiate fibromyalgia vs polymyositis vs polymyalgia rheumatica

Fibromyalgia: young women, widespread pain (characterized by diffuse pain on both sides of body and above and below the waist as well as axial skeletal pain), cognitive difficultures, many have fatigue and sleep disturbances. No lab values. Dx made with pain index and symptom. Tx: exercise is the foundation of managements, with medications (duloxetine, tCAs) reserved for patients who fail inital therapies. Polymyositis: symmetrical proximal MUSCLE WEAKNESS, ELEVATED MUSCLE ENZYMES (creatine, aldolase, LDH). Biopsy is way to diagnose. Polymyalgia rheumatica: Age > 50. Aching and morning pain. SIGNIFCIATLY ELEVATED ESR. -common way to treat is steroids and methotrexate

TYpes of hyponatrmia

First calculate serum osmolarity to determine classification of hyponatermia. If low then you're hypotonic, to know if you're hypervolemic, euvolemic, or hypovolemic you gotta clinically assess volume status. Explained on page 246-247 on First Aid Medicine HYPOTONIC HYPONATREMIA: Hypervolemic: CHF, cirrhosis, nephortic: -if you measure UNa, if its >10 then AKI or CKD. If <10 then CHF, cirrhosis, or nephrotic. Tx: Na and Water restriciton. Euvolemic: -------UNa>20, Uosm<300. Psychogenic polydipsia, beer potomanis, -------UNa>20, Uosm>300.(can think of it like urine osmolality > than serum osmolality). SIADH (COMMON) -------------Tx: depends on symptoms for SIADH, look at next card. **i thnk hypothyroidism, secondary adrenal insufficency is here as well but not sure if should be where psychchogenic polydipsia and beer potomoanias is either. What i knoew for sure is that psychogenic polydipsia and beer potomoanis have urine osmolality < 100. Hypovolemic: Lose water and salt, but more salt than water. -------Renal causes: UNa+ >10. diuretics, UT obstruction, primary adrenal insufficiency, bicarbaturia (RTA, metabolic alklsosis) ------ Nonrenal causes: UNa+ <10. GI losses (diarrhea, vomiting, NG suction) skin lossess (burns)etc. Tx: normal Saline. ISOTONIC hyponatremia "pseudohyponatremia" HYPERTONIC Hyponatremia: you have alot of glucose or mannitol added to serum and thus water from ICF comes into serum and make you look hyponatremic although the Na in serum really hasn't changed. Still have symptoms of hyponatremia though. There is a corrected Na equation, sees what Na+ concentraion would be if you "corrected" for hyperglycemia. Its Na=((glucose-100)/100) x1.6 *quick way, for every 100 over 150 glucose, that should decrease sodium by 1.6. So increase your Na by 1.6 for every 100 glucose over 150 and that should be your corrected sodium. This came from a medstudent. *Chronic hyponatremia (>72hours) should be corrected slowly to prevent central pontine myelinolysis.

Primary care: Pregnancy stuff

First day of LMP i sused to dtermine estimate delivery date: from the first day of LMP subtract 3 months and add 7 days. -if unreliable info, a 1st trimester US is pretty accurate -Low-risk normal women: 400-800micrograms of folic acid is sufficient -Women w/ diabetes or on anti-convulsant drugs: 1mg of folic acid daily -Women w/previous history of child with neural tube defect): 4 mg folic acid daily Advanced maternal age: over 35 at time of birth For women who are Rh negative, the next step is to assess the antibody screen or indirect Coombs test. If antibody screen is negative, there is no isoimmunization and RhoGAM is given at 28 weeks' gestation and again at delivery is baby is confirmed as Rh positive. The RhoGAM is given to prevent isoimmunication.

Treatment of acute asthma exacerbation (hospital admission). What tests do you order?

First give supplemental oxygen..then 1. inhalsd Beta agonist: via nebulizer or MDI+spacer. Assess patient response to bronchidilators (clinically and with peak flows) 2. Corticosteroids: can be PO or IV. Oral is 40-60mg, IV is 60-80. Taper them when clinical improvement is seen. Initiate inhaled corticosteroids at beginning of tapering schedule. 3. Thirs line agen is IV magnesiusm, helps with bronchospasm but only used i patient has not responded to albuterol, steroids, or oxygen. *it also acts as a bronchidilator, its use in asthma is restricted to life thretening exacerbations. **antibiotics if severe exacerbation or suspicion of infection **intubation for patients in respiratory failure or impending respiratory failure **MD+ spacer = nebulizer in terms of effectivenss. **although asthma can be diagnosed with pFTs and spirometry, ain acute setting when patient is SOB, peak flow measuremtn is quickest method of diagnosses *IV theophyline not used in management of acute asthma exacerbatino cuz not as good as broncho dilator as beta-2 agonist and combining IV thophyline w/inhaled beta 2 agonist may give toxicity. What tests to order in acute asthma exacerbation: 1. PEF-to see how decreased/how changed from baseline 2. AGB-you gonna see increased A-a gradient 3. Chest Xray-rule out pneumonia, pneumothorax

Evaluation of gross hematuria

First step is getting UA and urine culture. A UA confirms presence of hematuria and can differentiate between infectious, glomerualar, and extraglomerular causes. Evaluate for glomerual causes: possible renal US, 24-hour urine studies, serological studiens, eventual renal biosy.

After blood transfustion ordered, what cmopatibility testing done?

First the patient's ABO and Rh types are determined. After this, the patient's serum is screened for unecpected antibodies, a procedure called pretransfusion antibody screening. This is intended to detect any of all clinically significant RBC antibodies. If negative the patient can safely be transfused. If positive, further investigation has to be done to evaluate identity of the antibody. *The major difficulties in finding cross-matched blood in patients with a history of multiple transfusions is alloantibodies (e.g. patients with sickle cell anemia or myelodysplasia). Most commonly implicated RBC antigens in that case are E, L, and K.

Pain medication approach with Dr. basil

First you wanna ask, is it nociceptive or neuropathic? Neuropathic: examples are shingles, trigeminal neuralgica, diabetic neuropathy (can also use NSAIDS but wanna watch out for dat kidney function) etc. Use stuff like pregablin or gaba pentin. Nociceptive: you have NSAIDS, Opiates, Acetominophen. within opiates you have short acting and long acting. Long acting: long acting oxycodone,?? - a Uworld question of cancer patient said that you wanna use morphine first cuz its strong and quick, figure out the dose, then use the equivalent in long acting narcotic. If you were to just start off with long acting then the patient is going to go hours without pain relief.

Algorithm for evaluation of a thyroid nodule

First: clinical evaluation, TSH level, and US ---if cancer risk factors or suspicious US findings---> then do Fine Needle Aspiration ---if no cancer risk facotrs or suspicious findings--> then look at the TSH you measured..then... ..if TSH is normal or high do Fine Needle Aspiration ..if TSH is low then do radionuclide scan (iodine 123 scintigraphy). -----if "hot" nodule that meas its hyperfunctioning (increased isotope uptake in the nodule with decreased surrounding uptake)--->low cancer risk, treat hyperthyroidism -----if "cold" nodule means its hypofunctioning (decreased isotope uptake compared to surrounding tissue )--->higer cancer risk so you should do a Fine Needle Aspiration

Smoking cessation

Five As -Ask, Advice, Assess, Assist, and Arrange follow up. PHARMACOLOGIC 1. Varenicline: partial agonist at a subunit of nicotinic acetylcholine receptor. Considered first line therapy. 2. Nicotine patch: Patch should be worn for 16 hours per day (but not during sleep at night cuz it can cause headaches). Patient should NOT continue to smoke while using the patch, there have been case reports of MIs in these patients. 3. Nicotine chewing gum: less expensive than patch and have similar quit rates. Many who don't have success with that just don't use enough of it. -aslo you're not supposed to just chew it continuously. Patient should chew the piece of gum until the patient feels a peppeary taste in mouth then should "park" the gum in a cheek until the sensation goes away and then chew the gum again until peppery sensation returns. its a common pitfall. 4. Bupropion (Zyban). Can take this combines with nicotine replacement therapy. *Pregnant smokers: should be encouraged to quit without use of any pharm agents. But if its needed, varenicline and buproprion are both category C and relatively safe in pregnancy.

How do you treat Salmonella?

Fluid and electrolyte balance correction. NOT antibioitcs because it will not shorten the GI course and may incresae the risk of HUS.

Non-ketotic hyperglycemic coma treatemtn

Fluid replacement is most important first step. When hypovoleima present Normal saline should be starte initially then replced with .45% saline. 5% dextrose is given once blood glucose levels has been lowered to 350, it prevents development of cerebral edema. Insulin should be given too. Potassium should be given once to potassium reaches level.

What is ventricular remodeling at how do you treat it?

Following a MI, ventricular remodleing occurs and gradually cause dilatation of the LV with thinning of the ventricular walls. This can result in CHF. ACE-inhibitors have been shown to limit ventricular remodeling. ACE inhibitors should be initated within 24 hours of myocardial infarction in all patients without a contrainidication.

Foscarnet uses

For CMV or acyclovir-resistant herpes simplex virus

What is Rome criteria?

For irritable bowel syndrome Recurrent abdominal pain/discomfort >orequal 3 days/month for past 3 month AND >orueqal 2 of the following -symptoms improvement with BM -change in frequency of stool -change in form of stool Tx: usually on specific treatemtn is necessary, just manage like below -high-fiber diet helps -diarrhea: diphenoylate, loperamide -constipation: colace, psyllium, cisapride -may help to avoid dairy and excessive caffeine -Tegaserod maleate (Zelnorm) is a serotonin agonist recently introduced for the treatment of IBS. In a short-term study, it improved abdominal pain, bloating, and constipation in women

Goals of treatment with hypercholesterolemia

For patient with 0-1 risk factors, keep LDL<160 For patient with 1-2 risk factors, keep LDL<130 For patient with knonw atherosclerotic disease, keep LDL<70

Orthostatic hypotension?

Frequent cause of syncope and presyncope. It is defined as systolic BP decrease of at least 20 mmHG or diastolic BP decrease of at least 10 mm Hg within 3 minutes of standing.

Drugs that can cause esophagitis

Frequent cause: Potassium chloride Tetracyclines Aspirin and many NSAIDS Alendronate (bisphophonate) Quinidine Iron Dx: made clnically (sudden onset pain with swallowing and restrosternal pain) but is confirmed with endoscopy

The causes of pulsus paradoxus?

Frequent finding in cardiac tamponade but can alos occur in other conditions like asthma or COPD.

M

G

Heinze bodies

G6PD deficiency

Bite cell

G6PD defieicny

what condition is present in many asthmatics and may be the primary trigger in many of them?

GERD. So if you have adult with asthma symptmos that are worse after meals, exercise, or laying down they are likley to have GERD-induced disease. Where GERD is suspcted, a trial of PPIs can be both diagnostic and therapeutic.

Side effects of methotrexate?

GI symptoms Oral uclers or stomatitis rash alopecia hepatoxicity pulmonary toxicity bone marrow suppression Give FOLD ACID supplementation to reduce the incidence of adverse effect s of MTX therapy without loss of efficaacy.

Etiologies of gastritis Mnemonic

GNASHING Gastric reflux Nicotine Alchohol Stress H. Pylori Ischemia NSAIDs Glucocorticoids (long term use)

What happens in Gi lossess due to voimiting?

Gastric contents are rich in hydrogen, chloride, and potassium. Therefore vomiting causes hypochloremic metabolic alkalosis and hypokalemia. Bicarb levels rise as a result of hydrogen loss and activation of the renin-angiotensin system. The administration of isotonic sodium chloride and potassium is used to reverse these electrolyte abnomalities.

Peptic Ulcer Disease

Gastric ulcer pain made worse by food Duodenal ulcer pain is better by food -commonly associated with acid hypersecrtion. Acid-reductino therapy results in a high rate of ulcer reductino but eradication of H.pylori helps mainatin a long-term ulcer cure. Most common causes are H. pylori infection or ingestion of NSAIDs. Management algorthim: after H&P and Lab studies...do endoscopy and test for H.pylori (serology, urea breath test, urease assy, cultures). - If H pylori found then treat that with tripple therapy w/ Omprazole, Amoxicilin (1 gram BID), Clarithromycin (500 mg BID for 2 weeks). Metronidazole 500mg BID can be substituted for amoxicillin in penicillin allergic. If this fails than go to quadruple therapy using a PPI and bismuth-based triple therapy ( bismuth, tetracylcine, and metronidazole). - If H.pylori is negative, then probably NSAID use is culprit. Stop the NSAID use can use prostaglandin analogue. *remember though people with NSAID induced ulcers can also have H.pylori involvement Complications: MOST COMMON: Hemorrhage. OTHERS: 1. perforation (important to get UPRIGHT chest x-ray if concerned about this so air within peritoneal cavity can be visualized beneath diaphragm.), Tx: emergency surgery, but remember in preparation for the surgery you need tove give IV fluids to resuscitate, broad spectrum IV antibiotics, and IV PPI therapy. 2.penetration 3. obstructions Surgical therapy: surery indicated for both kinds of ulcers (duodenal and gastric) if complications arise like GI hemorrhage, perforation, intracrtable pain, obstruction. Ulcer disease is intractable if t persists for more than 3 months despite active drug therapy or th eulcer recurs within 1 year after healing or if ulcer disease is characterized by cycles of prolonged activity with brief remission. *Gastric ulcers should undergo biopsy eraly in evaluation process cuz of risk of carcinoma. *Gastrectomy, vagotomoy (more popular now i think) are some surgeries done. -Only ulcers associated with acid hypersecretion require a vagotomy (type 2-body of stomach, with concomitant duodenal ulcer) or (type 3-prepyloric). So Type 1 (in the body and lesser curvature) and type 4 (near gastroesophageal junction) ulcers do not require vagotomy. How do you confirm its been treated? Either urea breath or fecal antigen testing can be used 4 weeks to confirm H.pylori eradication. H. pylori serology should NOT be used since it may remain positive a year or more after eradication. *duodenal ulcers have low risk of malignancy but gastrick ulcers have HIGH risk, so surveillance endoscopy is generally indicated as well to confirm healing of gastric ulcers. but endoscopy does not confirm H.pylori eradication.

When is bronchoscopy used?

Generally indicated if there is conern for obstructing mass that may be causing rescurrent pneumonias in the same anatomical location. Even then, CT scan of chest is the preferred initial study, so bronchoscopy used when CT has given unclear results. 2nd thing its used for is recurrent epidosed of hemoptysis. ALSO, brochoalveolar lavage can be done with bronchoscopy. You basically do BAL for two reasons, evaulation of suspected malignancy and opportunistic infection.

Erythema Multiforme

Gneral name used to describe an immune complex-mediated hypersentitivity reaction to different causative agents Drugs, Viruses (HSV a big one), bacteria, fungi, idiopathic Clinically three groups: Erythema multiforme "minor": "Target lesions" Erythema multifrome "major"" : Rash + mucuosal involvement + constitutional symptomms Maximal variant erythema multiforme: Stevens Johnson syndrome Palms and soles are often affected, targetoiod lesions.

Why generally when ferritin decreases, the TIBC increases?

Gneral principle, whenever the ferritis is down the liver will start to pump out more transferrins to go and find more irion

Causes of Pulm HTN, way to think about it

Go from heart back. So first is left sided heart failure. Now go to lungs: COPD, chronic PE, OSA, KNOW 5 classes of Pulm HTN. Need to diagnose with Right Heart Cath. 1. PAH-mean pulmonary >25mmHg and other stuff ruled out. 2. PH due to left heart diseas: mean pulmonary pressure >25mmHg, pulm wedge pressure >15mmHg, normal or reduced CO 3. PH due to chronic lung disease and/or hypoxemia 4. Chronic thromboembolic pulmonary HTN 5. PH due to unclear multifactorial KNOW: pulmonary artery HTN often presents with sympotoms similar to CHF as patients typically have dyspnea or chest pain on exertion due to an inability to increase CO w/exercise. A LOUD S2, ENLARGED PULM ARTERIes on imagin, and signs of RIGHT HEART STRAIN on EKG (right axis deviation) should all suggest pulm htn. Echocardiography is test of choice cuz it evaluates for RV hypertrophy, right atrial size, findings of right ventricular failure, and valvular incompetence. Tx: direct towrad underlying cause. If the pulm HTN is idiopathic, a vasoreactivity test (pulm arterial pressure response to vasdilator is measured with right hieart cath) can predict which patients will be responsive to calcium channel blocker. IN patients with a negative vasoreactivity test, treatment is generally started with a prostanoid, endothelin receptor antagonist, or phosphodiesterase-5 inhibitor.

Management of sprain

Goal is to decreases edema and residual stiffness RICE therapy-rest, ice, compression, elevation Early use of joint and appropriate rehabilitation is key toh healing process

Diagnosis of UTI

Gold standard: URINE CULTURE.

Constrictive pericarditis

Granulation and scarring of pericardium secondary to acute pericarditis. one of the signs is Kusmaul's sign: paradoxic rise in JVD during inspiration. pericardial "knock" may be heard In US common causes: viruses, cardiac surgery, chest radiation, idiopathic In developing countries most common cause: TB

Radioidine therapy is more likely to cause permanet hypothryoidism in what kind of hyperthryoidism?

Graves cuz since the whole thryoid gland is hyperfunctional, all of it will take up the radioiodine and get ablated. Toxic adeonma and multinodular goiter usually remaine fine after radioidinte therapy cuz only the autonomous areas of the thyroid are destroyed cuz other parts of the gland is spared because function is suprpressed due to the hyperthyroid state.

CYP450 Inducers, decreased effect of Warfarin

Green vegetables Carbamazepine Ginseng OCPs Phenobarbital Rifampin St. John's wort

INdications for cystoscopy

Gross hematuria with no evidence of glomerular disease or infection Mmicroscopic hematuria with no evidenc of glomerualr disease or infection but increased risk for malignancy reurrent UTIs obstructive symptoms Irritave symptoms wtihout urinatry infection abnormal bladder imaging or urine cytology

Acute Hep B? Chronic Hep B? Acute Hep A?

HEPATITIS B -Acute Hep B infection: early phase: +HbsAg, +HbeAg, +IgM anti core, ++++HBV dna window phase: +IgM anticore, +HBV dna recovery phase: +IgG anticore, +anti Hbs, +anti Hbe. -Chronic HBV carrier: +HBsAg, +IgG anti-core. -Acute flare of chronic HBV: +HgsAg, +IgG anticore, +HbeAg (likely), + IgM anticore, +HBV DNA -Vaccinated for HBV: +anti-HBs -Immune due to natural HBV infection: + anti-Hbs, +IgG anti-core -Greatest risk for exposure for Hep B are multiple sexual partners and injection drug users. More than 90% of adulte with acute hep B nifection will reover completely. A minority will proceed to develop chronic Hep B infection, and about 0.5% will develop fulminant hpepatic failure. Fulminant hepatic failure is defined as hepatic encephalopathy that develops within eithgt weeks of onset of acute liver ailure. Only tx is liver transplant. Note: when you're vaccinated, you are vacinated with HbsAg, NOT the core antigen. So you form anti-Hbs antiboides and get ammunity. BUT you don't form any antibodies to the core, so your'e gonna be anti-HBc. Chronic Hep B: +Hep B surface antigen, + IgG antibody to Hep B core antigen, IgM antibody to Hep B core is NEGATIVE. Defined as +Hep B surface antigen foro > 6 months. **With what do you treat acute Hep B? Interferon and lamivudine are used in the treatment of acute Hep B infection but have no role in treatment of FHF. ***When and with what doyou treat Chronic Hep B? With acute liver failure or clinical cirrhosis and HIGH serum hep B virus DNA Treatment aslo recomended for patients without cirrhosis but with positive HBeAg, Hep B DNA>20,000, and serum alanine transaminases >2x upper limit of normal. ----ENTECAVIR and TENOFOVIR have become preferred therapies due to lower drug resistance and ability to be used in decompensated cirrhosis. Acute Hep A: a. +IgM antibody to Hep A (IgM anti-HAV) which appears at onset of acute phase of illness and becomes undetectable in 3 to 6 months. b. IgG anti-HAV also becomes positive during the acute phase but persists for decades and is a marker of immunity to to further infection. c. a person with + IgG anti-HAV titer but a negative tier for IgM anti-HAV has had Hep A in the past or has received the vaccine -Hep A does not cause chronic liver disease. Acute Hep C: are usually asymptomatic and therefore rarely present clinically, but 60-85% of persons who acquire acute hepatitis C develop chronic infection. Gold standard is presence of HCV RNA in serum. -the anti-HCV antibody test is the screening test for at-risk persons; a positive test in a person with one of the risk factors confirms exposure to the virus. -the HCV RNA test is required to determine active infeciton rather than just exposure to the virus. Chronic Hep C: -Can by asymptomatic or present with fatigue and nonspecific symptoms (arthralgias, myalgias). -Patients usually have waxing and waning elevations in transaminsase levels. -Extrahepatic sequelae can include essential mixed cryoglobulinemia, porphyria cutanea tarda (fragile skin, photosentivie, vesicles and erosions) and membranous glomerulonephritis. Candidates for Chronic Hep C treatment: -age >18, detectable HCV RNA in serum, liver biopsy showing bridging fibrosis, compensateed liver disease (INR<1.5, no ascites), stable other labs like creatinine,. Contrainidications to treatment: ongoing alchohol or drug abuse, major uncontrolled ddepression. Med:peginterfron plus ribvirin. If HCV genotype 1 then add an addditional protease inhibitor.

Patients with PID should be screened for??

HIV, syphilis, hepaitits B, cervical cancer(pap smear), and hepatitis C if they have history of IV drug use

All the liver cysts and stuff

HYDATID CYST-cysts in liver due to infection with Echinococcus granulsos. Seen with dog contact and sheep contact. you see "eggshell" calcifications on CT exam Echinococcus liver cyst management? -Total pericystectomy. Definitive treatment requires surgical resection, enucleation, or evacuation of cysts. At time of surgery, inject silver nitrate or hypertonic saline into cyst. SIMPLE HEPATIC CYST-belived to be congenital in origin. If cause symptoms usually report dull RUQ pain, abdominal bloating, or early satiety. PYOGENIC LIVER ABSCESS Pyogenic liver abscess shoudl be considered in DDx but its usually secondary o surgery, GI infection, or appendicits. Also presentation mroe severe than with amebic liver abscess. These you initially treat with perutaneous catheter drainage and antibiotics against gram-negative and anaerobic organisms. HEPATIC ADENOMA Hepatic adenoma-benign tumor msot often seen in you or middle aged women taking OCPs. Severe intra-tumor hemorrhage and malignant transformation are the most dreaded complications. Common Physical exam findings are palpable abdominal mass, hepatomegaly, or jaundice. Alk phosph and GGT are most commonluy elevaetd with those patients with intratumoral bleeding or multiple adenomas. HEMANGIOMA Most common benign liver tumor. Frequently asymptomatic. Spontaenous rupture is rare. Biopsy is contraindicated cuz can result in life-threatening hemorrhage. FOCAL NODULAR HYPERPLASIA Second most common benign liver tumor, occuring mostly in reproductive age women. Most FNHs are asymptomatmic, if symptomatic then excise. * "central" scare pattern on CT scan, CT can be used to differentiate from hepatic adenoma. Biopsy may be needed if tumor can't be differnetiated from hepatic adenoma. PRIMARY LIVER TUMOR -Turmor originating in levers. Most common are hepatocellular carcinoma and cholagniocarcinoma. Hepatic angiosarcoma is one thats kinda rare but more common in older men who have been exposed to toxins such as vinyl chloride gas, inorganic arsenic compounds, and thorium dioxide. SECONDARY LIVER TUMOR: tumor in liver that came from other spot

Ventricular aneurysm findigs?

Hallmark ECG findings of -persistent ST-segment elevatin after recent MI -deep Q wanves in the same leads

What are you looking for on x-ray for pulmonary infarction?

Hampton's hump: a wedge-shaped opacity in the infarcted segment also pleural effusion on affected side as well a

N-acetylcysteine has what uses?

Has 3 primary uses: dissolution of mucus, protection aginst induced renal failure, and therapy for acetaminophen overdose.

Whipples vs Tropical Sprue

Have similar symptoms. Whipples is far more severe and has more constitutional symtoms, particulary with CNS involvement. Tropical sprue you see flattened villi in jejunum, Dx by small bowel biopsy. Tropical sprue can be similar to celiac in syomtoms and findings but tropical spure often has megaloblastic anemia due to B12 deficiency. Tx: is B12, folate, and tetracycline.

CAGE

Have you ever felt that you should cut down on your drinking? Have you ever felt annoyd by people criticizing your drinking? Have you ever felt bad or guildy about your ruiking? Have you ever had an "eye opener"

Signs of Respiratory Distress

Head bobbing: bobbing up and down of the patient's head due to accessory muscle use Nasal flaring: enlargement of both nares during inspiration to try to increase air entry Grunting: closure of the glottis with expiration, thought to help infants generate the positive pressure necessary to stent airways open Retractions: inspiratory depression of soft tissues in relation to the cartilaginous and bony thorax, or Paradoxical breathing: asynchrony of chest and abdominal wall motion during respiration (chest wall draws in during inspiration instead of moving outward with the same motion as the abdominal wall)

Screening for hyperlipidemia

Healthy adults over 20: measure a nonfasting total cholesterol and HDL every 5 years -if normal, repeat screening after 5 years -if high and risk factors, go get a complete lipoprotein profile (TG and LDL calculation) Adult already with CAD: go straight for lipoprotein profile

Diagnosis of PE

Helical CT: most common, fast. Downside: IV contrast can damage kidneys PUlmonaryangiogram: The gold standard for detection of PE. Very sensitive. Downside: Invasive. V/Q: Looks for perfusion at site of PE.

Hematochezia vs Melena

Hematochezia: blood in stool that is red or maroon-colored Melena: black tarry stools; color is produced when heme is oxidized by intestinal flora

High serum albumin can indicate what?

Hemoconcentration, as occurs in dehydration.

Treatment of

Heparin

How is heparin given

Heparin -Therapeutic: IV bolus of 70-80, then continuous IV infusion 15-20/hr. Now monitored using antifactor 10a levels. So anytime you see continuos drip you know its therapeutic. -Prophylactic: Low dose heparin that is given by injection, every 12 hours. LMWH -Therapuetic: given as a weight adjusted dose. 1mg/kg BID. -Prophylactic dose: once a day.

PE

Heparin does not dissolve already existing clots, rather it prevents futuer ones from forming. Signs and symptoms of PE -Are nonspeicific and highly variable. It is a diagnosis that should be suspected in any patient who presents with some combination of sudden-onset shortness of breath, pleuritic chest pain, low-grade fever, and hemoptysis. Tachypnea, tachycardia, and hypoxemia are common exam findings. Calf swelling and Virchow's triad (stasis, endothelial injury, and hypercoagulable state) are not always present in PE. *about 10% of thse ppl will have occlusion of a peripheral pulmonary artery by thrombus, causing pulmonary infarction. These small periheral thrombi are more likely to cause pleuritic chest pain and hemoptysis. How do you determine if PE likely or unlikely? modified Wells Criteria, score above 4 is PE likely. -When a PE likley what do you do? First start anticoagulation (LMWH or unfractionalted heparin) BEFORE you do a CT angio because although it won't do anything for existing clot it will help stop any more from happening. THen do the CT angio for diagnoses. **Patients with clinical evidence of PE should be tarted on anticoagulant therapy while undergoind diagnostic evaluation. However, those with features of DVT should only have the daignosis confirmed before starting canticoagulation. -When a PE unlikely what do you do? D-dimer is useful to EXCLUDE PE from patients where its UNLIKELY they have PE. Below 500 would be excluded. DIAGNOSIS OF PE Helical CT: most common, fast. Downside: IV contrast can damage kidneys PUlmonaryangiogram: The gold standard for detection of PE. Very sensitive. Downside: Invasive. V/Q: Looks for perfusion at site of PE. --the classic thingg to look for is an mismatched defect", an area of perfusion defect without ventilation defect. -can use if patient doesn't tolerate contrast for CT -REMEMBER THO: a low probablity VQ scan still does NOT rule out PE if clinical suspicion is high TREATMENT OF PE: Heparin or LMW heparin-usually only therapy in STABLE patients *LMWH, fondaparinux (injectable factor Xa inhibitor) and rivoraxaban (oral factor Xa inhibito) are other ways to treat acute pe in stable patient. BUT they are all renally excreted so if pt has KIDNEY PROBLEMS DON"T USE THEM. *Once the heparin produces therapeutic anticoagulation (goal PTT 1.5-2 times normal), warfarin is initiated. Current guidelinens recommend EARLY INITIATION of warfarin (same day as parenteral therapy is started) over dealyed initiation and continuatino of parenteral anticoagulation for a minimum of 5 days and until the INR is >2.0 for at least 24 hours. Thrombolysis (tPA) or pulmonary embolectomy if hemodynamically UNSTABLE TREATMENT OF CHRONIC PE: Prolonged: Orally anticoagulated with warfarin for 6 months Patients with multiple thromboembolic episodes and patients with an ongoing risk factor may need anticoagulation for indefinite period The Wells score:[20] clinically suspected DVT — 3.0 points alternative diagnosis is less likely than PE — 3.0 points tachycardia (heart rate > 100) — 1.5 points immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points history of DVT or PE — 1.5 points hemoptysis — 1.0 points malignancy (with treatment within six months) or palliative — 1.0 points **remember, Troponins CAN be elevated in the setting of large pulmonary emboli (presumably due to acute right heart overload) , would not indicate acute cardiac ischemia. ***PE ppl with elevated Trops levels are asociated with a HIGHER risk of death. in PE, elevated trops generally resolve within 2 days, in contrast to the more prolonged elveations seen in MI patients. **Massive PE causes pulmonary hypertension, which can lead to acute RV dysfunction, tricuspid dilation which leads to tricuspid regurgitation. Echocardiography is useful in diagnosing the typical findings of RV strain; like increased RV size, tricuspid regurg, decreased RV function, and presence of RV thrombus.

Total cholesterol levels

High is >240 Normal is < 200

Solitary Pulmonary Nodule in lung algorithm

High malignancy risk---> straight to surgery excisiton Intermediate risk a. if smaller than .8 cm---> serial CT scans b. if larger than .8cm-->FDG-PET* ( 18-flurodeeoxyglucose positron emission tomography scan)----> if suspicious for malignancy then surgicaly excise, if not suspicious for malignancy then do serial ct scans *it looks like FDG-PET is the preferred study here if available, but flexible bronchoscopy or percutaneous needle biospy of pulmonary nodule seems like can be done in place of or with this test. BUT remember that fiberoptic bronchoscopy is more useful in assessing large CENTRAL nodules or massess. Not really useful for evaluating peripherally located massess. Low malignancy risk: serial CT scans CLINICAL and X-ray features: can be useful in differentiating benign from malignant nodules to help avoid unnecessary invasive biopsies or procedures. Suggestive of benign patterns of calcification: popcorn, concentric or laminated, central, and diffuse homogenous calcifications. Suggestive of malignancy: eccentric calcification (area of asymmetric calcification), reticular or punctate.

What is gluten?

High molecular weight proteins found in wheat, rye, and barley Celac Dx made by small bowel biopsy. Other test can be presence of anti-gliadin IgG/IgA, anti-endomysial antibody treatment is avoidance of all grains except rice and corn

Esophageal variceal bleeding

High pressure bleed and and emergency Tx: 1. aggressive hydration 2. IV Octreotride (somatostatin). It inhibits visceral blood flow and that's why it works for upper GI and variceal bleeds. Also inhibits GI motility and that's why it can be used for refractory diarrhea 3. Prophylactic antibiotics After these three things then you go to urgent endoscopic therapy (scleotherapy, band ligation). AFter that, you course of ation depends on what the bleeding status is.. -No further bleeding: give secondary prophy (beta blocker) and endoscopic band ligation 1-2 weeks later -Continued bleeding: balloon tamponade (temporary) then you do TIPS or shunt surgery -Early rebleeding: repeat endoscopic therapy then if still bleeding do TIPS or shunt surgery

History, exam, and management approach to diarrhea

History: -quantity: Large-volume (usually small bowel cause) vs small volume (usually large bowel cause) -quality: color, fould odoer, blood, mucus, fatty -length: acute (< 2 weeks), persistent (> 2 weeks), chronic (> 4 weeks) -associated symptoms: fever, chills abdominal pain, nausea, vomiting, weight loss, -other questions: food intake prior to onset, travel history, predisposing conditions, medications, recent antibiotic use or hospitlization, lactose intolerace, sick contacts Exam -Genearl appearance: does patient look acutely ill -Vitals: fever, tachy, hypo, orthostatic hypo -Abdominal exam: tenderness, distention, hepatomegal, ascites -Skins : turgor, rash -Rectale exam: tenderness , mass, stool apearance, occult blood less that 2 weeks diarrhea: usually infections. --workup: fecal leukoctyes, stool cultre, stool test for C dificile toxins, stoos examination for ova and parasites -Shigella Salmonella E.coli C. dif Campylo bact. Yersinia "SSECCY" (sexy) Tx of infectious diarrhea: Empiric treatment with Ciprofloxacin or TMP-SMX plus metronidazole for anaeraobic covervage

Syndromes associated with lung cancer

Horner's syndrome Pancoast syndrome/Superior sulcus syndrome-causes shoulder pain radiation to arm **Pancoast syndrome consists of shoulder pain (50%-90%), Horner's syndrome (15%-50%), and hand muscle atrophy and weakness (10-20%). However, asymmetric lower-extremity DTRs in setting of back pain suggests that tumor has spread to spinal cord and needs URGENT intervention. Superior vena cava sndrome-obstructs vena cava and venous returne. ONe with facial swelling and other stuff SIADH Eaton-lambert Trousseau's syndrome-venous thrombosis associated with metastat cancer PTH-like hormone-results in high calcium, low phospohate, seen in squamos cell lung cancer

How and why do you need to differentiate between COPD and asthma?

How: Spirometry before and after administartion of a bronchodilator (usually albuterol). Reversal of airway obstruction by the bronchodilator suggests asthma. Patients with COPD may have a partial bronchodilator response, but normal airflow after bronchodilator administration rules COPD out. Differentiating between the 2 is therapuetically relevant as INHALED CORTICOSTEROIDS are the PRIMARY long-term intervention for asthma and long acting ANTICHOLINERGIC INHALER is the PRIMARILY preferred for COPD.

Primary hyperparathryoidism

Hyeprcalcemia "stones, bones, groans, an dpsychiatri overtoens" A chloride-to-phosphorous ratio of greater than 33:1 is consistent with a diagnosis of primary hyperparathyroidism. Most commone metabolic complications: stones *Hyperparathryoidism is associated with high secretion of calcium in urine, low serum phosphate, high serum chloride, and low seru mbicarb.

Tumor Lysis syndroem

Hyper..phophatemia, kalemia, uricemia Hypo...calcemia (cuz released phosphate binds to calcium) Allopurinol may greatly reduce the possibility of acute urate nephropathy.

What are the ways malignancy causes hypercalcmia?

Hypercalcemia of malignancy is most commonly (80%) due to parathyroid hormone-related peptide (PTHrP) production. Other mechanisms include excess vitamin D production, bone metastasis with local cytokine release to induce bone resorption, and ectopic PTH production. But most common by far is producing PTHrp, either systemically or locally by bone mestastses. Systemic PTHrP levels are not incrased.

Virschow's triad?

Hyperocagulable, sedentary, vascular injury

Allergic bronchopulmonary aspergillosis test

Hypersensitivity reaction to Aspergillus antigens is seen in some patients with underlying asthma. WHen the airways of such patients become colonized with Aspergillus, the intense igE and IgG mediated immune response leads to the characteristic recurrent episodes of fever, malaise, cough with brownish mucoud expectoration, wheezing and symptoms of bronchial obstruction. A SKIN PRICK test for Aspergillus should be initialy performed in all asthmatic patients who are suspected of having ABPA. If the skin prick test is posisitve, serum total IgE levels and preciipiating serum antibodies to Aspergillus fumigatus should be measured. Tx: corticosteriod is effective in controlling episodes of acute inflammation and preventing progressive lung fibrosis.

Causes of aortic dissection

Hypertension Connective tissue disease like MARFANS and Ehler Danlos Pregnancy Cocaine Traumau

Which is more of a risk factor for stroke, hypertension or smoking?

Hypertension is more

What do you see with hypokalemia, hyperkalemia, hyponatremia, hypocalcemia, hypermagnesemia.

Hypocalcemia: remember it can occur during or immediately after surgery in patients requireing blood transfusions. Hyperactive DTRs Hypermagnesemia: Decreased DTRs.

Insulins

Hypoglycemic episods during exercise in type 1 diabetes can be managed by decreasing the insulin dose, eating before exercising, and voiding 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 one inject of glargine insulin at bedtime. Important to understand that normal ppl have basal insulin production even without food intake, most type 1 diabetics do not.

Common side effects of Beta 2 agonists

Hypokalemia (K+ driven into cell)--> may present with muscle weakness, arrhtythmias, and EKG abnormalities Other common side effects are tremor, papliations and headache Keep thsee in mind when treating asthma exacerbations for instance with high doses of beta-2 agonists.

Elevated serum creatine kinase and myopathy, what should you consider?

Hypothyroidism should always be considered. There are also polymyositis/dermatomysosis, inclusion body myositis, vasculitis, mixed connectice tissue disease.

Causes of hypernatremia

Hypovolemic (most common). Renal loss, diarreha, sweating, burns, iatrogenic, diabetes insipidus as well. Tx: mild (no symptoms): 5% dextrose in .45% saline. Severe (symptomatic): treat with normal saline first to restore volume deficit. then switch to .45% saline in order to better replace free water deficit. Isovolemic: Diabeteis insipidus (central or nephrogenic) -Tx: Hypotonic fluid (5% dextrose preferred over .45% saline). Vasopressin for DI. Hypervolemic: Mineralcorticoid excess ( Conn's tumor, Cushings) -Tx: half normal saline to correct hypertonicity. Diuretics to increase Na excretion. *correction of chronic hypernatremia should be done GRADUALLY OVER 48-72 hours to prevent neruo damage due to cerebral edema

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Treatment of colon cancer

I think... Do hemicolectomy in order to remove draining lymph node basin as well. If lymph node involvment has been confirmed then you wanna do adjuvant chemotherapy. Liver is most common site of metastases from colon cancer. You can do hepatic resection if liver is the only site of metastsis and lesion is able to be resected with clear margins.

Acromegaly algorithm for testing for it

IGF-1 level testing first, this is constantly elevated wheras GH levels fluctuates during the day. After IGF1-1 if its high then measure GL levels following oral glucose load. If GH inadequaltey suppressed then go for MRI or brain. *most common cause of death in acromeglay patients is cardiovascular.

Causes of peripheral edema

INCREASED CAPILLARY HYRDROSTATIC PRESSURE -heart filailure -primary renal sodiumretention (nrenal disease and drugs0 -venous obsrcution (cirrhosis and venous insufficiency) DECREASED ONCOTOC PRESSURE (hypoalbiuminemia) -proetin loss (neprhotic synrome and protein-llosing enteroptahy) -decreased albumin sythensis (cirrhosis and malnurtrition ) INCREASED CAPILLARY PERMEABILITY -burns, trauma, sespsis -allergic reactions -ARDS -malignant ascited LYMPHATIC OBSTRUCTION /INCREASED INTERSITTIAL ONCOTOC PRESSURE -malignant ascited -hypothyroidism -lymph nodedissection **Dont forget peripheral edema is common side effect of CCBs. It is most common with dihydropyridine CCBs (amlodipine, nifedipine). The combination of CCBs with ACE inhibitors is associated with a significant reduction in CCB-associated peripheral edema.

Chronic glucocorticoid therapy side effects and what to do

INCREASED RISK OF OSTEOPOROSIS -for this reason its important to provide the lowest dose of steroids for shortest duration, and add vitamin D as well as calcium supplemetation to the patient's thera[y. -Also, if treatment w/steroids gonna be more than three months (or six months if low doses , <10mg/day), then bone densitometry is indicated for every year.

Explain the difference bweteen intravascular hemolysis and extravascular hemolysis

INTRAVASCULAR -due to significant RBC structural damage resulting in RBC destruction withink the intravascular space. ---microangiopathic, dic, transfusion rxcs, infections, PNH, IV Rho D infusuion EXTRAVASCULAR -RBCs are destroyed by phagocytes in the reticuloendothelial system (lymph nodes, spleen). As a result, there is less HbG release than in intravascular hemolysis. So you don't see as low as hapto, as high LDH, or as hjigh indirect bili as you do with intravascular. ---causes are antibody mediated (AIHA), intrinsic RBC enzyme (G6PD defieincy), or membrane (hereditary spherocytosis ) defects, hemoglobinapthies (sicle cell, thalassemia). infections too.

NDICATIONS FOR SPECIALIZED RBC treatment

IRRADIATED -Bone Marrow transplant recpiients -Acquired or congenital ceullular immunodeficiency -Blood components donated by first or 2nd degree relatives LEUKOREDUCED: involves reducing the number of transfused leukocytes through filtering or other methods such as saline washing, freezing, and deglycerolizing or buffy coat removal. It also reduces the risk of HLA allimmunization. -Chronically transfused patients -CMV at risk -Potential transplant recipietns -Previous febrile nonhemoltyic tranfustion reaction WASHED -IgA deficiency ---Residualt plasma in red cell concentrates contains proteins, including IgA. IgA defieicnt patients develop antibodies against IgA. These antibodies can react with IgA-containing donor products and induce an anaphylactic reaction that can progress rapidly to loss of consciousness, shock and respiratory failure. To reduce this risk, red cells should be washed to remove as much of the plasma as possible for patients with IgA deficiency or prior allergic transfusion reaction. -Complement dependent autoimmune hemolytic anemia -Contiued allergic reactions with red cess transfusion despite antihistamine treatment

Immune thrombocytopenia

ITP (immune thrombocytopenia): make anti Gp2b antibodies so spleen macrophages start to eat the platelt/antibody complexes. Trigggers by viral illness commonly. Lab: increased megakaryocytes on bone marrow biopsy. ONLY PTT INCREASED, low platelets, and increased bleeding time. Tx: steroids, IVIG. If still a problem then splenectomy. **all ITP patients should be tested for HIV and Hep C. It patient has platelets >30,000 without bleeding can generally be observed without treatment. Steroids therapy if 1st LIne treatment option for ITP in adults patients with paltelets <30,000 or with bleeding.

Alcoholic ketoacidosis treatment:

IV dextrose containing saline and thiamine. Insulin generally not required. Dextrose leads to an increase in insulin secretion, which leads to the metabolism of ketone bodies to bicarbonate. Almost all alcohohlics are likely to be thiamine-deficient unless proven otherwise.

How do you know when to use oral vs IV antibiotics in pyelonephritis?

IV: systemic manifestations. Vomiting, hypotensive for example. Oral: no systemic signs of toxicity and mild disease

Explain ITP

Idiopathic thrombocytopenia purpura is usually diagnosed after excluding other possible causes of thrombocytopenia. These patients should be tested for HEPATITIS C AND HIV as thrombocytopenia may be the initial presentation of HIV infection (up to 5%-10% of patients). Treatment of the underlying infection can affect the platelet count. Also, treatment usually involves systemic glucocorticoids for patents with severe thrombocytopenia (<30,000) or significant bleeding

CF patient has pulmonary infection, what is probably cause?

If influenz present and/or under age 20: Staph Aureus. You treat with IV vancomycin. Over age 20: Psueudomonas

Person swallows a battery?

If lodged in esophagus it should be removed immediatly under direct endoscopic visualization. If it has made it into stomach, can usually pass without complications and outpatient management is indicated.

HIV person has syphillis or late latent syphillis, what do you do?

If neurologic symptoms are presents you need to do a LP to examine the CSF for neurosyphillis, which must be excluded before starting antibiotic therapy. Cuz choice of antibiotics differ depending.

IgA nephropaty vs postinfectious glomerulonephritis

If patient presents with hematuria immediately after an infection, think IgA nephropathy. If a patient presents 2 weeks after infection, think postinfectious glomerulonephritis. Also, IgA nephropathy has normal serum complement levels. Postinfectious glomerulonephritis you get low C3 complement. IgA nephrotphay usually follows an acute URI. Post streptococcal usually follows 10 days after throat/skin infection.

Approach to arrhythmias

If the QRS complex is narrow (<.12 sec) then that means the conductin pathway is taking the fastest route, i.e. AV node-->bundle of His-->Purkinjie fibers. THat means the origin of the arrhythmia is probably before that, so supraventricular. Know the 5 major supraventricular arrythmias... -paroxysmal supraventricular tachycardia (PSVT) sometimes called AV nodal reentrant tachycardia. is its >150, narrow complex regular, unidentifiable P waves..gonna be SVT. a.adenosine commonly used for this and carotid massage commonly used -atrial flutter -atrial fibrillation -multifocal atrial tachycardia a. characteristicallly occurs in setting of chronic lung disease and is manifested by three or more P-wave configurations on the ECG w/associated tachycardia -paroxysmal atrial tachycardia If the QRS complex is Wide (>.12 seconds), that means not the fastest route being taken for ventricular depolarization. SO the origin of the arrhythmia is probably Ventricular. Know the 5 major ventricular arrhythmias -PVC a. often not associated with symptoms, although they can cause palpiattions or a sensation that the heart has stopped, owing to the post-PVC compensatory pause. If symptoms can be clearly correlated with PVC, treatment may be appropriate although many patients respond well to simple reassurance. 1st line therapy is almost always a Beta Blocker or Ca channel blocker. -ventricular tachycardia a.wide QRS and ventricular rate > 100 -ventricular fibrillation -torsades de pointes -accelerated idioventricular rhythm a. wide QRS complex and heart rate between 60/min and 100/min. no clinical features.

Celiac labs?

IgA endomyseial antibodies and IgA tissue transglutaminase antibodies Biopsy most reliable test though

COPD exacerbation inpatient thing to remember, per Doc Morgan

Imagine 7.38 psh with C02 of 70 (COPD patients are hypercapneic) and Bicarb of 34 (cuz its trying to compensate). High C02 people will come in somnolent, with decreased RR. You prob gonna have to ventilate but you wanna do it carefully, why? You slowly decrease the c02 because HC03 needs days to compensate. If you let the person blow off too much C02 too fast he will become alkalotic because his bicarb is still 34 cuz it takes days to adjust. So if this happens and if you take person off the ventilator, patient will try and retain all the C02 he can cuz of so high bicarb and RR will go down a lot-->no respiratory drive.

What is cor pulmonale?

Impaired function of the RV caused by PULMONARY HYPertenSION that occurs due to COPD, interstiia diseases, pulmonary vasculature problems (idiopathis pulmonary arteiral hypertension) or OSA By convention, RV dysfunction due to left heart disease or congenital heart disease is NOT considered cor pulmonale. Gold stnadard for diagnosis: Right heart cath because it can show ELEVATED PULMOANRY ARTERY SYSTOLIC PRESSURE (>25 mm Hg).

Impetigo is more superficial than Cellulitis.

Impetigo-only epidermis Celluluitis=acute deeep infection of dermis and subcutaneous tissue *when cellulitis is showing systemic signs, tx is IV nafcillin or cefazolin. Vanc is you suspect MRSA. *H/o of diabetes is likely predisposing ppl. Cellulitis is infection of deep dermis and superficial fat, in comparison to erysipelas which involves the superficial dermis and lymphatics. Locan anesthetis would not be effective in reducing pain cuz acidic environemnt of the infectino neutralizes the medication rendering it ineffective. Also, remmber that chronic foot infection can serve as a nidus for bacterial cellulitis and should be eradicated in patients with recurrent cellulitis.

Golden yellow crusts from rupture vesiculopustules? what is Tx?

Impetigo. Tx is topical mupirocin or oral erythromycin. Impetigo you get PAINFUL NON-ITCHY pustules and HONEY crusted lesions. caused from either S. aureas or Strept. pyogen Penicillin is no longer used for tx as S. aureaus is almost universally resistant to penicillin.

Explain Reticulocyte index

Important initial test in evaluating anemia because indicates whether effective erythropieses is happneing in bone marrow. A riculocyte index>2% implies excessive RBC destruction or blood loss. The bone marrow is responding to increased RBC requirements. So you look for blood loss or hemolytic anemia. Seek out other indicators of hemolysis, like increased indirect bili, increased LDH, decreased haptoglobin, splenomegaly). <2% implies inadquate RBC production by bone marrow. this is the one with MCVs anemia you look at.

Explain the pathophys of why pain shifts in appendicitis?

In acute appendicitis, the initial peri-umbilical pain is referred pain and visceral in nature.. (what happpens is afferent visceral pain fibers from the appendix accompany the sympathetic nerves and enter the spinal cord at the level of the 10th thoracic segment, thereby leading to periumbilical pain.) ....however,, as the disease ensues, inflmmation of the parietal pertineum and skeletal muscles causes somatic pain, which is well localized (RLQ) and more severe in intensity.

Relationship of bilirubin levels and anemia/

In hemolytic anemias you will see incread indirect bilirubin. Non hemolytic, like iron deficiency anemia, you will have normal bilirubin levels.

When can a patient have sex after MI?

In most cases they are low risk can resume soon after MI, within 3-4 weeks (Princeton guidelines ) and possibly as early as 1 week (AHA). If high risk (refractoy angina, class 4 CHF, significant arrhythmias, etc) then refer for answer to qeustions.

HTN screening?

In person of average risk: BP measurement every 2 years after 18.

Anti-nausea medications

In setting of recent chemo: Seratonin antagonists like Ondansetron (Zofran). Can be used as managagment or prophylaxis. General nausea and vomiting. Antidopamine agents such as metoclopramide (reglan) and prochlorperazine **Overusing high doses of metoclopraimde can cause metoclopraimde induced acute dystonia. Diphenhydramine IV is tx. Motion sickness vomiting: Scopolamine. Nausea secondary to gastroparesis. Motilin receptor agonist, these promote GI motility Erythromycins primary use is antibiotic but it does also function as a motilin receptor agonst and can help treat nausea secondary to gastroparesis. Promethazine is a nonselective antihistamine used in treament of nausea or vomiting.

Rash includes palms and soles? doesn't include?

Includes palms and soles: -syphillis -Rocky Mountina -erythema multiforme Doesn't include palms and soles -varicella

What maneuvers increase venous return? decrease venous retunr? SVR? right sided murmurs? left sided murmus

Increase: Inspiration, squating (after prolonged time sqautting the afterload will increase) Decrease venous return: valsalva, standing Increase SVR? Hand grip, squatting Insipiration increases right sided murmurs, exhalation increases left sided murmus *good thing to know is that hypertrophic cardiomyopathy murmur increases when less blood is going through it, so anything that decreases preload. whereas AS murumr will increase with more preload. also, hypertrophic cardiomyopathy like the only murmur that decreases with increased SVR (hand grip). *MVP also l0uder with less preload and softer with more preload. Has click.

What lab value do you expect to increase if you give someone/change to higher dose steroids?

Increased WBCs. Leukocytosis. So remember to not get freaked out if you see high WBCs after giving steroids. You still wanna make sure though other values aren't pointing towards another cause like infection. Specifically, its NEUTROPHILIA by increasing the bone marrow release and mobilizing the marginated neutrophil pool.EOSINOPHILS and LYMPHOCYTES are DECREASED.

Portal hypertension

Increased portal vascular resistance caused by cirrhosis, protal vein obstruction, or hepatic vein thrombosis. Complications: esophageal varices, splenomegaly, ascites hemorrhoids, caput meduseae Tx: Shunts to decrese pressure. -TIPS (transjugular intrahepatic portocaval shunt) between hepatic and portal veins -liver transplant In addition to cirhosis, other cuases of portal hypertension, such as constrictive pericarditis, right-sided heart failure and Budd Chiari syndrome.

Incrased tactile fremitus =? Decreased?

Increased tactile fremitus= increased density of lung parenchyma (consolidation) Decreased tactile fremitus=excess subcutaneous tissue on the chest, air, or fluid in pleural activity (pneumothorax, pleural effusion) or overexpansion of lung

Increases ESR? Decrases ESR

Increases ESR: infections, autoimmune diseases, malignant neoplasma, GI dsease (UC), pregnancy Decreases ESR: polycythemia, sickle cell, CHF, microcytosis, hypofibrinogenemia

If UA is red or brown

Indicates presence of hemoglobin, myoglobin (as with rhabdomyolysis) or red food (beets).

Explain what you see in severe asthma attack? What is tx?

Indicators in severe asthma attack include normal to increased Pc02 values, speech difficulty, diaphoresis, altered sensorium, cyanosis, and 'silent lungs". During asthma exacerbation you see hyperventilation (tachypnea), P02 usually depressed. PC02 usually decreased as well due to hyperventilation. If PC02 is normal to incrased that means C02 retention and thus severe airway obstruction and/or respiratory muscle fatigue. other signs of poor repiraroy drive are decreased breath sounds, no wheezing, decreased mental status, marked hypoxia ith cyanosis. Lung hyperinflation and tachycardia are typical findings during asthma attack are not indicators of severity. Tx for severe attack showing signs (normal or increased PaC02) of incoming respirtatory failure the treatment is endotracheal intubation and mechanical ventilation , inhaled short acting beta 2 agonist, inhaled ipratropium, and systemic corticosteroids. Also, a one time IV magnesium sulfate infustion ir also recoommeneded for dever asthma exacerbation without improvement after 1 hour of therapy or for life threatening asthma with imending repiratory failrue.

ECG diagnosis of MI?

Infarct location Leads with Q waves Anterior wall (LAD) V1-V4 Anteroseptal (LAD) V1-V2 Anterolateral (LAD or LCX) V4-V6 Lateral wall (LCX) 1, avL InFerior wall (RCA) 2, 3, avF All coronary ateries supply a specific region of the ventricle. -Lateral wall of left, posterolateral parts: Left circumflex artery -Anterior wall of left, anteriolateral wall of left: LAD -Right ventricle and inferoposterio walls of left: right coronary arter

Conjunctivitis, Differentiaion of.

Infectino of conjunctiva. Most common eye disesae seen in community medicine. Most cases caused by bacterial or viral. Other causes are allergy and chemical irritants. BACTERIAL: Staph, Strept, Heamophilus, Moraxella, Psudomaona. No blurring of vision and only mild discomfort. Disease usually self limitied, lasting 10-14 days if untreated. A sulfonamide instilled locally three times daily will usually clear the infection in 2 to 3 days. **watch out for N. gonorrhaea conunctivitis whic is an emergency cuz an lead to blindness. **also watch out for C. trachomaticA-C. causes recurrent epithelial keratitis. Leading cause of preventable blinness worldwide. VIRAL: "pink eye" "epidemic keratoconjunctivitis". Highly contagoious and spread by person to person. Most common cause is adenovirus. -Usually assoaciated with pharyngitis, fever, malasie, and lymphadenopahyt. Red conjunctiva w/ discharge and exudates. Local sulfonamide therapy might prevent secondary bacterial infection. Hot compresses reduce discomfort of lod edema. Weak topical steroids may be necessary to treat the corneal infiltrates. Disease usually lasts at leas 2 weeks. -usually has VIRAL PRODROME ALLERGIC or chemical irritants cause of conjucntivitis -ITCHING, tearing, redness, stringy discharge, sometimes photophobia -Tx: oral antihistamines or topical antihistamine or anti-inflammatory eye drops. But usually subsides in 24 HOURS even WITHOUT treatment. *eye "stuck shut" in morning: all of them. *water scant string mucus: viral and allergic. bacterial has purulent, white, yellor or green in color. thick in consistency.

Esophagitis etiologies

Infections: -viral: --- HSV, VZV have vesicles. CMV has intranuclear inclusions. Candida will have white plaques. ---Bacterial: -radiation -corrisives -medication: "pill esophagitis" (direct effects of a medication on esophageal mucosa). Common ones are potassium chloride, tetracyclines, bisphophonates, and NSAIDS. **Infectious isophagitis is common in patients withs advacned HIV. Most common cause in HIV patients is Candica, BUT REMEMBER, in patients whose predominant symptoms is pain with swallowing WITHOUT dysphagia (DIFFICULTY Swallowing) or thrush, VIRAL ESOPHAGITIS is more likely than candicaal esophagitis. Drugs that can cause esophagitis Frequent cause: Potassium chloride Tetracyclines Aspirin and many NSAIDS Alendronate (bisphophonate) Quinidine Iron Dx: made clnically (sudden onset pain with swallowing and restrosternal pain) but is confirmed with endoscopy Tx: PPI is treatment of choice for erosive or severe esophagitis. THere is also nonerosive esophagitis which im not sure what the best therapy is for. So esophagitis generally occurs in immunocomproised ppl (AIDS, malignancy, diabetes) and may present with dysphagia, oral thrush, or odynophagia. Endoscopy w/washings, culture and biopsy may reveal the cause.

IVC filter indications? Complications?

Inferior vena cavae filters may be used in aptients with lower extremity DVT when - anticoagulation is contraindicated (hemorrhagic stroke, active bleeding). - Anticoagulation failure (recurrent or extending thromboembolish while fully anticoagulated) is another indciation for IVC filter placement IVC filters are usually placed in the IVC just below the renal veins to decrease risk of thromboembolism from all likely venous pathways. They can be permanent or temporary. Long terms complciations of IVC filter placement include recurrent DVTS and IVC thrombosis. IVC filters to not appear to affect overally mortality significanctly.

Peri

Inflammation of eyelids and periorobital tis

Enteritis definition?

Inflammation of the small intestine, usually resulting in diarrhea, may be a result of infection, immune repsonse, or other causes.

Explain ARDS

Inflammatoiry condition due to infections (sepsi, pneumonia), trauma, or other causes (massive transfusions, pancreatitis). Lung gets injured--->this causes release of proteins, inflammatory cytokines and neutrophils in alveolar space---> leads to bloody and proteinaceous fluid into alveoli--->alveolar collapse due to loss of surfactant and alveolar damage----> end result is BAD GAS EXCHANGE, DECREASED LUNG COMPLIANCE (stiff), and PULMONARY HYPERTENSION Findings include respiratory distress, diffuse crackles on phpysical exam, severe hypoxemia, and bilateral alveolar infiltrates on chest imagin. PaO2/Fi02 is DECREASED and indicated the degree of ARDS severity.

Influenza

Influenza A and B-epidemic disease: cause most infections - H1N1 (a type of influenza A) Influenza C: causes minor illness incubation 1-3 days Duration is 2-4 days If diahrrhea and vomiting occur (H1N1) VACCINE IM -For all children over 6 months -Best given mid-September to mid-November since peak of flu season is late December to early March -Killed virus Intranasal -Live vaccine for children over 5 years old -Not for reactive airway disease kids or immunosuppressed H1N1 vaccine -there is also IM and intranasal, its two doses apart fom each other here

Sickle Cell stuff

Inhereited disorder that results from presence of Hemoglobin S. Most severe and common form is sickle cell anemia, in which only Hemoglobin S (HbSS) is present. CLnical manifestations rarely presents prior to 6 months of age, when fetal hemoglobin levels decline and fnctional asplenia typically develops. BEST diagnostic test is hemoglobin electrophoresis because it precisely determines which form of sickle cell disease is present. Peripheral blood smear can give you findings suggestive of sickle cell with the unusually shaped RBCs but does NOT provide a definitive diagnosis. Vaso-occlusive episodes are the most common clinical manifestation of sickel cell desisease and may be precipitated by dehyrdation, illness, weather changes or stress. Tx consits of IV opiates followed by gentle rehydration with .25 or .5 normal saline to treat dehydration and prevent further sickling. cuz patients with SCD have decreased abilituy to renally excrete sodium Patients with SCD are at increased risk for bacteremia secondary to encapsulate organissm due to the funcational asplenia. so all patients with SCD presenting with fever should have blood cultures and started on IV abx. A common bone complication of sickle cell disease? Aseptic necrosis of femoral head. Involves oclusion of end arteries supplying the femoral head, bone necrosis and eventual collapse of periarticular bone and cartilage. What two types of cell do you see on peripheral smear in sickle cell patient? - Spindle shaped cells (sickle cells) and target cells Common head complication of sickel cell patients and what to do about it? - Stroke is a common complication of sickle cell disease secondary to sludging and occlusion in the cerebral vasculature. Exchange transfusion is the recommended treatment acutely since in helps to decrease the percentage of sickle cells and prevent a second infarct from occurring. What is dactylitis? Earliest manifestion of vaso-occlusive disease in sickle cell anemia. Acute onset of pain and symmetric swelling of hands and feet. What is acute chest syndrome? Criteria is new pulmonary infilitrate on chest x-ray PLUS >orequal 1 of the following: -increased work of breathing, cough, tachypnea, wheezing -fever -hypoxemia -chest pain Tx: 3rd generation cephalosporin and a macrolide, pain control, and IV fluids. What is hyposthenuria? Common in patient with SICKLE CELL ANEMIA and sickle cell trait. Its kidney's impairment in concnetrating urine, whic results in NOCTURIA. another pulmonary problem in sickle cell patients that is a common cause of morbidity and mortality is pulmonary hypertension Folate deficiency can happen in Sickle cell due to increased red blood cel turnover and increasd consumption of folate in the bone marrow. So daily folic acid supplemenation is recommended in all SCD patients to correct the underlying folate deficiency. What is aplastic crisis? Aplastic anemia? Aplastic crisis: transient arrest of erythropoeises that results in a severe drop in hemoglobin and virtual absence of reticulocytes on peripheral smear (reticulocytes < 1%). You see in sickle cell and Parvovirus B19. Aplastic anemia: pancytopenia, low retieculocytes and hypoplastic bone marrow.

Explain serioal cardiac biomarkers

Initial cardiac enzymes may be normal if has happened within 6 hours, cuz it may take up to 6 hours for cardiac troponin levels to be elevated. So a single troponin usually can't be used to exclude MI.

HIV screening

Initial screening -Anyone 15-65 -TrGetting treatment for TB -Getting treatemet for other STD ANNUAL screening (or more frequent) -IV drug userrs, -men who has sex with men homeless sex for money drugs, parter of HIV posotive ADDITIONAL SCREENING -pregnancy, occupational exposure, any new STD symptoms

How to treat malnutrition patient in hospital?

Initial treatment of patients with severe malnutrition should address temperature control (warming), possible infection, dehydration and feeding. Dehydration should be treated with oral rehydration in malnourised patients whenever possible. IV rehydration should be used only if there is severe dehydration resulting in shock because it can result in heart failure and edema in malnourished patients.

Pleural rub?

Inspiratory and expiratory "rubbing" or scratching breath sounds heard when inflamed visceral and parietal pleurae come together.

What is the likely pathophys behing non-alchoholic fatty liver diasese?

Insulin resistance--->lead to increased peripheraly lipolysis, triglyceride syntheiss and hepatic uptake of fatty acids--->the intrahepatic fatty acid acids gets oxidized and causes damage

Dysentery definition?

Intestinal infection resulting in severe bloody diarrhea with mucus

What are characteristis imaging findings of patients of head of pancreas tumor?

Intra- and extrehaptic biliary tract dilation findings on imagin Patients with tumors there have abdmonial pain, weight loss, jaundic, and distended NONTENDER gallbladder

Kid who had appendicits surgery had it alreayd preforated when surgery was done. now a week later and he still ahs a fever, what you worried about?

Intra-abdominal abscess or infection.

Keloid treatment

Intralesional glucocorticoids. Surgery if that doesn't work.

Cystometry use?

Investigating bladder function in setting of incontinete or urgency? Bladder is fillied with water via catheter then emptied into measuring device and the pressure is recorded in the process

Whats the use of voiding cystourethrogram

Investigating structural or functional abnormalities of bladder and ureters Contrast medium is placed into the bladder via catheter and visualized with x-ray during active micturition

What is the major concern of Guilliain-Barré syndrome?

Involvement of respiratory muscles and subsequent respiratory failure. You use spirometry in these patientes to look at FVC to monitor respiratory funciton.

H

Ir

Atrial fibrillation

Is it A-fib w/RVR or not? Etiology: PIRATES Pulmonary disease, ischemia, rheumatic heart disease, anemia, thyrotoxicosis, ethanol, sepsis Signs: -palpitations or skipped beats -light-headedness: this is due to fact that without atrial "kick", the cardic output falls -thrombus can develop and lead to TIA or stroke Treatment Hemodynamially STABLE: Rate control: slow rate down with digoxin, calcium channel blocker, or beta blocker. You just slow down rate without affecting rhythm, this can control symptoms. Rate contral can often convert AF back to sinus rhythm too. **BBs conraindicated or use with caution CHF, hypotension, bronchospasm, and bradyarrhtymias. **Digoxin can be used as rate control in although less effective than BBs or CCB. BUT in the event that those are contraindicated, you can use (think CHF and/or low BP which are common). Its effect can take several hours to become apparent. Rhythm control for maintaining sinus rhythm should be considered in patients unable to achieve adequate rate control, with recurrent symptomatic episodes (palpitations, lightheadedness, dyspnea, angina), or with heart failure symptoms in the setting of underlying left venrticular systolic dysfunction. If you wanna convert back to sinus rhythm. Shock (cardioversion) then amiodarone and beta blockers can help maintain rhythm. Hemodynamically UNSTABLE patients: immediate cardioversion Use the CHADVASC score to decide whether neeeds to be on anticoagulation. Good explanation: There are 2 strategies in the treatment of persistent or paroxysmal atrial fibrillation: controlling the ventricular response to atrial fibrillation (rate control) and using antiarrhythmic drugs to maintain sinus rhythm (rhythm control). There is no survival advantage associated with iether of these strategies, but for older patients (>70yrs) rate control is associated with improved qualituy of life scores. More hospitilizations and adverse drug reactions occuin in patients receiving rhythm control compared with rate control. The use of anticoagulation for stroke prevention is not affected by choice of approach. ----------------------- A-fib origin? Ectopic foci within the pulmonary veins. Most commonly ------------------------------- What heart condition is hyperthyroidism associated with? What the treatment? A-fib. --- In patientw with hyperthyroidism-related tachysystolic A-fib, beta blocker is the drug of choice. It also helps diminsh other symptoms of hyperthyroidism. -------------------------- CHA2DS2 VASC?? ...Calculates ischemic stroke risk in patients with A-fib CHF 1 Hypertesnion 1 Age >75 2 Diabetes Mellitus 1 Prior stroke or TIA 2 Vascular disease 1 Age 65-74 1 Sex category: female 1 **KNOW THIS..use warfarin or other t target specific anticoagulants (rivaroxaban, apixaba, dabigatran) to reduce the risk of thromboemoblism in patients with score GREATER or EQUAL to 2. Patinets with "lone AF" (score 0) have an extremely low risk, and anticoagulant therapy is NOT indicated. -if score of 1 you can do antioagulation (preferred) or aspirin **ALSO KNOW: Target specidic oral anticoagulants (dabigatran, rivaroxaban, apixaban, edoxaban) are approved for therapy in patients with NON-VALVULAR A-FIB. They are NOT recommended for use in patients with mistral stenosis, prosthetic heart valves, end-stage renal disease (since they are renally excreted) and severe decombensated valvular disease likely to require valve replacement.

White patch in back of throat that is scrapale? that is not scrapable?

Is scrapable= Candidiasis oral thrush Is not scrapable=Leukoplakia. This is a reactive precancerous lesion that represents hyperplasia of squamos epithelium. Risk factors are smoking and drinking. Develoment of areas with induration and/or ulceration should prompt biopsy to rule out malignancy.

Gastric varices vs splenic vein thrombobsis, vs portal vein thrombosis vs Budd-Chiari syndrome.

Isolated gastric varices (without evidence of esophageal varices): suggestive of splenic vein thrombosis. Can be complication of recurrent chronic pancreatitis. Splenic vein runs along the posterior surface of pancreas and can get direclty inflamed and thrombosed due to recurrent inflammation of pancreas. Aapart from gastric varices, patients with chronic splenic vein thrombosis may develop noncirrhotic portal hypertension, ascited, and massive splenomegaly w/features of hyperslpenism (anemia, thrombocytopenia, and leukopenia). Portal vein thrombosis: cliniclal consequence of portal vein thrombosis are similar to that of splenic vein thrombosis, but patients with portal vein thrombosis have both gastric and esophageal varices. Budd-Chiari syndrome: due to thrombosis of hepatic veins or intra/suprahepatic inferior vena cava. Acutely , present with RUQ pain, hepatomegaly, jaundice and rapidly developing ascites. Chronic Budd-Chiari syndrome usually presents with ascites, cirrhosis, and portal hypertension.

Indications for 24-hour Holter monitor?

It documents continous recordings of 2 or 3 leads on EKG for a given period of time. Current guidelines recommend it for unexplained syncope, near-syncope, episodic dizziniss and recurrent palpiations.

What is the usefulness of wireless video endoscopy (small pills that record as they pass through GI system)?

It has been proven effective to diagnose small bowel disease because visualization of majority of small bowel mucosa is not possible with push endoscopy. But endoscopy is still preferred for diagnosis of esophageal and stomach disease.

Wh

It.

Most comon cause of SCA (sudden cardiac arrest) outside of hospital?

Its V-tach or V-fib due to acute myocardia ischemia or infarction. This is why adequate CPR, prompt rhythm analysis and defibrillation is the most impportant stuff to do quickly. Rescue breathing not as important.

Acute bronchitis presentation and management?

Its a common cause of blood-tinged sputum and usually viral in etiology (so no antibiotics needed) If person afebrile, new onset blood tinged sputusm without signs of more serious disease...best thing to do is observe closely. Wheezing common finding on physical exam.

Atelectasis in surgery?

Its a common postoperative complication that results from shallow breathing and weak cough due to pain. It is most common on postoperative DAYS 2 AND 3 following abdominal or thoracoabdominal surgery. Pain and changes in lung complicance can cause ipaired cough and shallow breathing. Shallow inhalations limit recruitment of alveoli at lung bases, and weak cough predisposes to small-airway mucus plugging. This results in hypoxa--> RR increases---> low Pc02. *ABG usually shows hypoxiemia, hypocapnea, and respiratory alkalsosis. Large areas of atelectaiss may bause significant V/P mismatch, leading to hypoxemia and increased work of breathing. What happens is as compenation for the hypoxemia, patients usually hyperventilate and develop resp alkalosis and decreased Pc02. Adequate pain control, deep breathing excercises, directed coughing, early mobilization and INCENTIVE SPIROMETERY decrease the incidience of atelectasis.

In what patients are you worried about using succinycholine?

Its a depolarizing neuromuscular blocker that can cause life-threatening hyperkalemia. It should not be used in patients with or at high risk for hyperkalemia, such as burn and crush injury patients and patients with prolonged demyleination.

why is abdominal waist circumference important?

Its a measure of central obesity, a surrogate estimate for visceral fat. Visceral fat is a more metabolically active fat that releases free fatty acids into the portal system, which contributes to hyperlipidemia, hyperinsulinemia and atherogenesis.

Inferior wall MI signs?

Its a right ventricular infarct that shows signs of Right sided heart failure. Hyptension, JVP distention, clear lung fileds whouls raise suspicion for right ventricular infarction. Avoid things that drop preload like nitrates and diuretics, treat with IV fluids. Tx: treat right ventricular myocardial infarction with normal saline infusion. Volume expansion is the primary supportive treatment for the hemodynamic abnormalities. This is in addition to reperfusion therapy for STEMI.

How to prevent the Jarish-Herxheimer reaction in syphillis treatment?

Its an acute fever that develops within 24 hours after initiation of treatment. No effective prevention is available.

what is hemophilic arthropathy?

Its an eventual consequence of recurrent hemarthrosis. You see this with Hemophilia people. Associated with hemosiderin depostiong leading to synovitis and fibrosis within the joint. The risk for this can be signifacnty reduced by prophylcactic treatment with factor concentrates. A major source of morbidity from Hemophilia.

What is chylothorax?

Its drainage of lymphatic fluid into the pleural space secondary to disruption or blockage of the thoracic duct or one of its lymphatic tributaries. Malignancy is the most common cause, trauma is the second most common cause. Other causes are pulmonary tuberculosis, chronic mediastinal infections, sarcoidosis, lymphangioleiomyomatosis, and radiation fibrosis.

Explain fibromusclur dysplasia

Its the one associated with renal artery stenosis. Fibromuscluar dysplasia is a noninflammatory and nonatheroscelrotic condition that presents most commonly in women age 15-50. The condition affects primarily the renal arteries and causes hypertension. Renal artery most affected but can commonly affect carotid and vertebral arteries which can cause ysomtpoms of brain ischemia (TIA, stroke,) or nonspeicif symptoms like headache, tinnitus, dizziness.

describe vertebral osteomyelitis

Iv druge users, sickle cell anemia patients, and immunosuppresse d patients are at highest riskfor oseomyelitis. Spine is a frequent site of osteomyelitic infection in injection drug users. Staph aureas is most common pahtogen. TENDERNESS to PERCUSSION over the spinous process if most important clue. Pain not relieved with rest. Fever and leukocytosis are unreliable findings. The ESR is elevaetd. MRI is what to do. A very high index of supspicion for vertebral osteomyelitis should be present for patients with history of injection drug use or recent distant site infection (UTI). If you suspect vertebral osteomyelitis, a microbiologic dianoses must be established to guid antibiotc therapy. Because the infection is often hematogenous, blood cultures should be obtained initially in all patients.

Strongest known risk factor formale breat cancer?

Klinefelter's syndrome. Has 50-fold increase in risk.

Primary care: hyperlipidemia

LDL: -about 2/3 of total cholesterol. CAD risk is primarily due to LDL component because LDL is thought to be the most atherogenic of all lipoproteins. -levels about 160 significantly increase CAD risk -LDl cholesterl not directly measured. Calculates as follows: LDL=total cholesterol-HDL-TG/5. Total cholesterol: Ideal is <200. high is >240. LDL: ideal is <130. high is >160. *goal for LDL in diabetic patient is <100. All diabetics with LDL above 100 should be started on statin. If patient has CAD AND DM, goal for LDL is<70. Triglycerides: ideal is <125. high is >250. Clinical features: severe hyperlipidemia can get you xanthelasma (yellow plaques on eyelids), xanthoma (hard, yellowish masses found on tendons), pancreatitis can occur Dx: - mesaure TC and HDL. if either abnormal, then order full lipid profile. -consider checking Lab tests to exclude secondary causes of hyperlipidemia: a. TSH (hypthyroidism) b. LFTS (chronic liver disease) c. BUN and Cr, urniary proteins (nephrotic syndrome) d. glucose levels (diabetes) Statins: lowers LDL. Monitor LFTs. Harmless evelations in muscle enzymes (CPK ) may occur. Niacin: Best for incraeasing HDL and lowering TG levels. Do not use in diabetic patients cuz may worsen glycemic control. You might have flushing effect, pruritis. Check LFTs and CPK levels as with statin drugs. Bile acid-binding resins: Lowers LDL. Effective whn used in combination with statins or niacin to treat severe disease in high-risk patients. Adverse GI effects. Fibrates (gemfibrozil): primarily for lowering TG levels.

Tx of choice for metastatic prostate cancer

LHRH agonists (leuprolide) are the initial treatment of choice in patients with metastatic prostate cancer. Cuz it leads to decrease in LH which leads to decrease tesosterone. The concurrent administration of an antiandrogen (flutamide) for a week prior to LHRH therapy reduces the initial sy8mptoms flare. cuz if blockes the initial testosterone surge.

Classifications of acute diverticulitis?

LLQ patin, leukkocytosis, fever. CT scan is imaging procedure of choice for diagnosis. Colonoscopy in contraindicated. Uncomplicated (75%) -Tx: -stable patient: outpatient setting with bowel rest, oral antibiotics, and observation. -Hospitialization, treatment iwith IV antibiotics and obseration is recommended for patients who are elderly, are immunosuppressed, have high fever or significant luekocytosis and with significant comorbidities. - Complicated (25%). CT scan helps identifiy these. -refers to associated abscess, perforation, obstruction, or fistula formation. *fluid collection <3cm can be itreated with IV antibiotics. If >3cm, should to CT guided percutaneous drainage. If that doesn't work, surgery for drainage and debridement is the next step. *Fistulas can occur between the sigmoid colon and bladder, vagina, skin, or anothers segment of bowel. Tx: resection of sigmoid colon, escision of fistulous tract, and repair or resection of other involved organ. ---Diverticulitis is most common cause of GI tract fistulas *For just asymptomatic diverticuli in GI system (diverticulosis), only thing you recommend is increase fiber in diet.

Patient has hip fracture, what should you start them on? when should have surgery?

LMWH is considered prophylactic therapy of choice for preventing DVP in patieht with hip fracture and shoud be started on admission, even if the patient is scheduled for surgery. THis can be stopped 12 hours before the surgery. Surgery should be done WITHIN 48 HOURS cuz that is associated with lower risk of pressure ulcers andpneumonia. Nonoperative management is reserved for those who are nonambulatory, have advanced dementia, or are medically unstable.

Clincial features of acute decompensated HF

LV systolic dysfunction and/or diastolic dysfunction is most common cause of ADHF. other causes include coronary ischemia, ACS, acute valvular abnormalities (mitral or aortic regurg), sever hypertension, and severe renal disease. Goal of initial management of ADHF is to 1. ensure HDS stability 2. maintain adequate ventilation and oxygenation 3. provide rapid symptomatic relief 4. ongoing evaluation to identify predisposing and/or precipitating causes. Initial tests to order: urgent pulse ox, chest x-ray, and ECG should be obtained. Then improve symptoms by REDUCING PRELOAD by ordering DIURETICS. Also add IV VASODILATORS (nirtoglycerine, nitroprusside, nesiritide) in selected patients with bad hypertension and pulm edema. An echo should be obtained in all patients with pulm edema to assess ventricular function and r/o valvular heart disease. **BB are an important part of therapy in COMPENSATED heart failure 2/2 LV systolic dysfunction. but their use in acute DECOMPNESATED HF can cause worsennig of symptoms and is not recommended. **fyi: IV morphine reduces central sympathetic outflow, causing venous and arteriolar dilation and potential drop in cardiac preload. but don't use in ADHF not established w/data.

APproach to childhool lead poisoning

Lead toxitiy required early diagnosis and identification as most effects are permanent if undetected and untreated. You can get cognitive impaiment, language delayn and hearing loss. Conspitation/ileus can also occur at high levels. Due to frequent mouthing and oral habits of young childrn, screeenig for risk factors should be perofrmed during outing health visits. *Painted toys and deocrations made beofer 1976 or outside the US may be overlooked at sources of lead. Lab eval is finger stick and if that is elevated you need to get a confrimatory venous sampling. If venous level >orequal5 then lead poisoing.

Wha

Left

Tricuspid atresia findings?

Left axis deviation Hypoplast right ventriclen Atrial and ventricular septal defects are necessary for survival

Criterion for implantable cardioverter-defibrillation (ICD) for prevention of sudden cardiac death in setting of heart failure?

Left ventricular ejection fraction less than 35%, regardless of the presence or absence of coronary disease or the occurrence of arrhythmia.

Explain how dipyridamole can be used in myocarcial perfusion scanning

Let say exercise stress test not possible cuz patient is amputee. Myocardial perusion scanning can be employed intstead using dipyridamole to reveal the areas of restricted myocardial perfusion through the "coronary steal" phenomenon. Dipyridamole and adenosine are coronaly vasodilators. Infustion of these in patients without coronary artery disease will increase coronary blood flow 3 times baseline levels. But w/ patients with coronarly artery idsease,, the disease vessesl distal to the obstruction are already maximally dilated and their ability to increase myocardial perfusion is limited...so redistribution of coronarly blood flow to "non-diseased" areas occurs and the perfusion of "diseased" segments diminishes. This is called coronary steal and is used to diagnose ischemic heart disease.

CREST syndrome?

Limited form of systemic scleroris. Calcinosis cutis-deposition of calcium in skin and manifests as subcutanous pink-to-white nodules tpically on upper extremeities. Raynaud phenomenon Esophageal dysmotility Sclerodactyly-this is skin tightening limited to hands, wrists, and face. Telaniectasias *if you see skin tightening in other areas like trunk, proximal extremeites..this is most likely NOT CREST (which is limited SSc) but its probably DIFFUSE systemic scleroris which has worse prognosis. You see other manifestations here, like INTERSTITIAL FIBROSIS, which happens in 40% of patients. ------------------------------ Scleroderma presentation? Thickening of skin with edema that transitions to sclerosis that obliterates hair follicles, sweat glands and causes flexion contractures. Common complications are -kidney involvement leads to HTN and before ACE inhibitors this was most common cause of deat -PAH ultimatley results in RHF -Esophageal and gastric dysmotility cause these patients to suffer GERD. Labs: anti centromere antibodies, ANA antibodies, anti-topoisomerase-I antibodies,

PAD

Lipid lowering therapy is indicated for ALL patients with symptomatic PAD. Also, all patients with symptomatic PAD should be taking aspirin or clopidogrel to reduce risk of stroke, MI, cardiovasc death. Also do BP control and DM screening. ABI Ankle-brachial index Calculated by dividing the higher ankle (dorsalis pedis or posterior tibial) systolic pressure in each lower extremity by the higher brachial artery (left or right) systolic pressure ABI <.90= abnormal (diagnositc of ABI) 0.91-1.30= normal >1.30=suggestive of calcified and uncompressibnle vessels; additional vascular studies should be considered. *Arterial ultrasound is less sensitive and less specific than ABI for initial diagnoses of PAD. Generally done in symptomait patients with abnoraml ABI who are being considered for interventialn procdues.

Cardiovasuclar screenin

Lipid profle starting at age 25, every 5 years Blood pressure every 2 years

Bronchiectasis

Localized: usuallly result of previous pneumonia Severe of bilateral: CF, Karganeres, immunodeficiency, HIV, etc Resulting airway damage allows bacterial colonization, buildup of secretions and continued bronchial destruction Signs: Chronic nasty productive cough, hemoptysis, wheezing, FTT Dx: CT scan will detect broncial dilatation and destruction in most cases

Hypoparathyroidism tx

Long term management of patients with chronic hypoparathyroidism is usually high doses of vitamin D and calcium. Vitamin D is generally preferred over 1,25-dihydroxy vitamin D for chronic management in most patients because it is cheaper and effective. Usual dose of vitamin D varies from 25000 to 100000 units per day. High doses of vitamin D are required in hypoparathyroid patients because of defective conversion of 25-hydroxyvitmain D to 1,24-dihydroxyvitamin D in kidneys resulting from low PTH levels. After starting treatment with VITAMIN D and CALCIUM, majority of the patietsn will have an increase in theri urinary calcium excertion due to low PTH levels. If patient has low serum calcium and high urinary calcium, add a THIAZIDE cuz it will decrease rinary calcium and increase serum calcium levels. Vitamin D=calciferol 1,25 dihydroxyvitamin D=calcitriol cholecalciferol: Vitamin D3

what are you looking at with diaphragm on xray?

Look for free air under right hemidiaghrapgm (suggests bowel perforation). Look for stomach, bowel, or nasogastric tube (NGT) above diaphram (suggests diaphragmatic rupture).

Lung cancer screening?

Low dose CT chest yearly in patients who are.. age 55-80 + have a >30 pack year smoking history + are currently smoking or quit within past 15 years

Pericardial effusion EEG findings?

Low-volage QRS complexes. Electrical alternans (beat-to-beat variation in the amplitude of QRS axis) can be seen with large effusions

Most common cause of brain mestastis?

Lung cancer, then breast

Most commmon causes of secondary clubbing

Lung malignancies Right-to-left cardiac shunts Lung abscess Empyema Bronchictasis Chronic cavitary infection CF Asbestosis, pulmonay fibrosis, arterio-venous malformations COPD (with or without hypoxemia) does not cause digital clubbing, and the presence of clubbing should prompt a search for occult malignancy. Hypertrophic osteoarthropathy refers to digital clubbing along with painful joint enlargement, periostosis of long bones, and synovial effusions. -commonly affects wrist and hang joints. Often associated with lung cancer so development of clubbing and suddent onset joint arthropathy in a chronic smoker is suggestive of this. You wanna get X-ray to rule out malignancy if you suspect this.

Granular immunoglobulins found on immunofluorescence microscopy from renal biopsy?

Lupus nephritis or post streptococcoal glomerulnoeprhitis

What kind of stuff do you think about when deciding if a lymphadenopathy is worrisome or not?

Lympadenopathy is uaully evaluated in patients with systemic symptoms, progressively enlarging lymph nodes, or persistently enlarged nodes for greater than 2 weeks. If someone has had a viral illness recently, that can suggest reactive lymphadenopathy.

Pneu

M

Consequences of renal failure mnemonic

MAD HUNGER Metabolic Acidosis Dyslipidemia Hyperkalemia Uremia Na/H20 retention Growth retardation/developmental delay in children Epo deficiency Renal Osteodystrophy

Steps into knowing what to look for for MCVs anemias..

MCV<80: ---> now check iron studies. a. Fe and TIBC decreased---> Anemia of chronic disease b. Fe decrease and TIBC increase-->Iron deficiency anemia c. Fe normal to high, TIBC normal or decrease--> Lead poisoning, thalassemia d. Fe high, ferritin high, TIBC low--> sideroblastic anemia. INH can cause. *I think if you have thallasemia and its symptamobit then you have a minor thalassemia. There are beta and alpha thalassemia minor. Beta-thalassemia: meditarreanea ppl, increased hemoglobin A2 on electrophoresis. ALpha thalassemia: southeas asian ppl. **Thalassemia minor often is confused with iron deficiency anemia. Beta-thalssemia trait has microscytosis out of proporation to the degree of anemia, hemoglboin >10 and high RBC count. Iron deficiency usually has a low RCB counta nd rarely ecomes mircorycit until hemoglobin is <10. Normocytyc: here you look at decreased or increased reticulocyte count. -Decreased: -Leukemia, -aplastic anemia, (coul be hereditary as in Fanconi's anemia, may ahve autoimmuen or viral etioloty (HIV, parvovirus) may result from toxins or radiation. Tx: Blood transufion and stem cell transplantation to repleace absent cells. INfections are a major cause of mortality and shouldb e treated aggressively. -infection, - medication side effect -Increased: Hemorrhage, hemolysis ---within hemolysis threre is intrinsic defects of hemoglobin, membrane or enzymes. then there is extrinsic (autoimmune (coombs +), PNH (Coombs negative)). Macrocytc--->check B12 and folate levels--> if they're normal suspect liver disease (you see spur cells on smear for liver disease) high methylmalonic acid=B12 deficiency hypersegmented neutrophils=B12 defieincy high homocysteine=both B12 and folate deficiency have *alchohol abuse is the most common cause of folate deficiency in the United States. Other causes of folic acid defieicny besides poor diet and/or alcoholism Drugs: drugs that can impar absoprtio of folic acid (phenytoin) or antagonize its physiolgic effects (methotrexate, trimethoprim). -Extremely high yield quesiton for USMLE -also other causes of macrocytis are myelodyplasitc syndrome, hypothyroidism, drug induced (MTX and Hydroxyurea are two). *high ferritin and high transferrin start thinking hemachromatosis.an

MEN syndromes

MEN 1: para-pan-pit --pancreatic endocrine tumors can be: Zollinger Ellison, insulinoma,s VIP omas TX: ppl with MEN1 have parathyroid hyperplasia and require removal of 3.5 parathyroid glands or total parathyroidectomy with autotransplantation. MEN 2: MPH -meduallry tryoid carcinoma (secretes calcitonin) -pheo -hyperplasia of parathryoid MEN 2B: MMMP -medullary thryoid, pheo, mucosal neuromas (GI, oral), marfaonid habitus *genetic testing (RET proto-oncogen germline mutaiton) is more sensitive than biochemicl measurement (serum calcitonin) and is the recommended screening test for suspected MEN 2 syndrome

Complicaitons of aortic dissection

MI, Storke, AR, tamponade. All these through dissection or obstruction of coronary arteries, or caroitids, aortic root, or pericardium.

Causes of ST elevation:

MI, pericarditis, LV aneurysms, also Pizmental angina can cause

ACS treatment

MONA+ Beta blocker : morphine (last medication, in severe pain circumstances, helps achieve analgesia which decreases levels of catecholamines, thus reducing myocardial oxygen comsumption), oxygen, nitrate, aspirin

Explain methotrexate?

MTX is the initial disease-modifying antirheumatic drug of choice in patients with rheumatoid arthritis. common side effects of MTX include GI symptoms, oral ulcers or stomatitis, rash, alopecia, hepatotoxicity, pulmonary toxicity, and bone marrow suppression. Macrocytic anemia is a common side effect. Folic acid supplementation has been shown to reduce the incidence of adverse effects of MTH therapy without loss of efficacy. FOLINIC acid (Leucovorin) is more potent than folic acid in "rescuing" RBCs from the folate deficiency. A DMARD **other drugs to know what cause intefer with folate metabolism and result in macrocytic anemia: Trimethoprim, Phenytoin.

Back pain categories

MUSCULOSKELETAL (MAJORITY) -mechanical (muscle strain, spasm, degenerative arthritis). Clinical clues: normal neurologic examination, negative straight leg raise, possible paraspinal tenderness -herniated disk. clinical clues: radiculopathy, positive straight leg raise, possible NEUROLOGIC DEFICITS. sitting, driving, or lifting worsens leg pain they all are forward flexion. -Spinal stenosis: (neuropathic claudication), low back pain with neuro symptoms (weakness, sensoary problems) that is better with spine flexion, worse with extension. OLDER AGE. Shopping cart sign. -Compression fracture: OLDER AGE, TRAUMA, more common in women INFLAMMATORY Anklysoing spondylitis, reactive arthritis, psoriatic arthritis, inflammatory bowel disease. Clinical clues:better with activituy or exercise, no improvement with rest, gradual onset, HLA-B27 present. MALIGNANCY -metastatic cancer to bone History of malignancy, age >50, worse at night, weight loss. Cauda equina syndrome (weakness, urine retention/incontinentce, saddle anesthesia). INFECTIOUS -Osteomyelitis, discitis, abccess. IV DRUG USE, FEVER, EXQUISITE POINT TENDERNESS, diabetes, recent infection. ***in the case of epidural abscess you get a triad of fever, severe localized back pain, and nerologic deficits (motor weakness, parasthesias, bowel/bladder dysfunction). ***in the case of vertebral osteomyleitis, leukocyte may be normal, but ESR and CRP are usually eleveated. plain x-rays can be normal in the first 2-3 weeks so MRI is the modality of choice. VERTEBRAL COMPRESSION FRACTURE -common complication of osteoporosis. these patients can develop a compression fracture with following miminal trauma. there is POINT TENDERNESS here too, no neuro problems.

Marfan's syndrome

Main cause of morbidity and mortaily in patients with Marfan syndrome is aortic root disease manifestating as aneurysmal dilation. All Marfan's patient shoul dhave routine screening for aortic root disease with TTE or chest CT.

Duke's criteria for endocarditis? managment of infective endocaridits? possible complications of endocarditis?

Major: 1. sustained bacteremia (blood culture positive for typical bacteria: strept virid, staph aurea, enteroccos) 2. echo showing valvular vegetation Minor: -predisposing condition -fever -vascular phenomeona (janeway lesions, septic emboli, septi infarcts, mycotic aneurysm) -immunolgic phenomena (osler nodes, orths spot, nephritis) -microbioligical evidence that does not meet major criteria ) Definite: 2 major OR 1 major and 3 minor MOst common valves: Most common valve is mitral valve, causing regurgitation. Aortic valve is 2nd monst common cardiac valve involvd in IE, usually in patietns with prior history of bicuspid aortic valve with stenososis. For IV drug users, its the tricuspid valve that is monst common. Microorganisms: STAPH AURES: prostehtic valves, intravasc catheters, injection drug users, implanted devices VIRIDANS STREPT: dental proceudres, procedures involving incision and biopsy of repiratory tract COAGULASE NEGATIVE STAPH: intravasc cathteers, prostetic valves, pacemakers or defibrillaters ENTEROCOCCI: nocosomical UTIs STREPT BOIS: Colon cancer, IBD FUNGl: immunocomprised host, chronic indwelling catheters, prolonged antibiotic therapy MANAGEMENT OF INFECTIVE ENDOCARDITIS? 1st empiric IV vancomycin to cover Staph (MRSA and M-senstivitie), Strept, and enterococci after obtaining blood cultures. If it turns out to be a viridans groud strept. (mutans or sanguis) then the Tx is IV penicillin G or IV ceftriaxone. **Blood cultures from separate venipuncture sites should be obtained over a specified period in al lpatients with suspected infective endocarditis prior to initiating antibiotic therapy. **Fragments of the vegetation can embolize to the lungs, causing the characteristic nodular infiltrate with cavitation. ----This is septic pulmonary emboli. Are common in Tricuspid endocarditis, occurring in up to 75% of patients. Can lead to pneumonia. ---Can also embolize to brain and cause stroke. Development of an AV block in a patient with infective endocarditis should raise suspicion for what? -perivalvular abscess extending into the adjacent cardiac conduction tissues -AORTIC VALVE endocarditis (so can cause aortic regurg as a result of infection) and IV drug abuse are associated with increased risk of periannular extension of endocarditis. Person with infective endocarditis has triad of fever, lekuoctyosis, left upper quadrant pain? -Splenic abscess. -This is most commonly associated with infective endocarditis.

Clinincal features of acute bronchitis

Majority of acute bronchitis cases are due to viruses (influenza A and B, parainfluenza, rhinovirus), rarely is the cause bacterial. Purulent sputum here does NOT indicate bacterial infection. Physical exam can show wheezing due to bronchospasm and rhonci (that clera with coughing) due to airway secretions and may show chest wall tenderness from muscle strain due to coughing.

Hemoglobin

Male 13.5-17.5 Female 12.0-16.0

What do you think of with PAINLESS jaundice with hyperbilirubinemia, elveated alk phosh, and systemic signs?

Malignant obstruction of biliary system, likely due to pancreatic cancer or cholangiocarcinoma. Other biliary obstruction stuff like stones with cause PAIN.

Upper GI bleeds causes

Mallory's Vices Gave An Ulcer mallory weis tear varices gastritis/esophagitis av malformation ulcer: peptic/duodenal Signs: hematemesis (bright red or coffee grounds, hypotension, tachycard, black tarry stool (melena), Do a nasogastric tube to determine whether bleeding is active. Irrigate with water or saline until gastric aspirates are clear. Then do upper GI endoscopy establishes Dx in most cases. **Upper GI endoscopy is great cause it also has therapeutic applications like photocoagulation or local injection of vasoconstrictor agents. Surgery indicated if bleeding not stopping. **Studies show that most stable patient with upper GI bleed have better outcomes if you transfuse at Hb <7 instead of a level <9. However, patients with risk of morbidity in setting of severe anemia (unstable coronary artery disease) may benefit from maintaining hemoglobin level >9.

Post nasal Drip syndrome. explain it.

May be caused by a mucus hypersecretory phenotype that develops floowing chronic exposure of respiratory tract to particular matter, allergen, irritant, or pathogen. The mechanical actin of secretions dripping into the hypopharynx triggers the cough reflex. Etiology: All causes of rhinosinusitis like common cold, bacterial sinusitis, allergic rhinitis, environmental irritant rhinitis. Single most common cause of cough in both acute (< 3 weeks) and chronic cough.

Carcinoid tumours

May cause appendidcitis. May cause carcinoid syndrome ( increased serotonin, vasomotor disturbances, or bronchoconstriction)

Cardiothoracic ratio on x-ray

Measure largest width of heart and divide by largest diameter of chest. A normal ratio is <0.5. Cardiomegaly on Xray is suggestive of volume overlaod.

What is TIBC?

Measure of transferrin molecules in the blood

What is RDW?

Measures variation in RBC size. RDW usually abnormal in iron deficiency but is generally normal in all of other microcytic anemias.

Ulnar nerve entrapment? Radial nerve?

Median nerve is carpal tunnel. Ulnar nerve: tingling and numbness of one and half fingers on ulnar aspect of hand Radial nerve: Konwn as the "great extensor nerve. sensory abnormalities during radial nerve involement are lcoated on the dorsal aspect of the forearm and hand.

What is neutropenic fever?

Medical emergency. Are at high risk for developing overwhelming bacterial infection due to blunted neutrophil response. Most common organism if Pseudomonas. Empiric monotherapy with anti-pseudomonal agent is recommended. Intern boot camp:what is neurophenia: ANC<500 OR ANC expected to decrease <500 during next 48 hours. ANC= WBCtotal (% neutrophil + %band). febrile neutropenia: imagine you get a page, with new fever, very important to go and see the patient. get cultures (at least 2 sets of blood cultures). If central venous catheter, culture each lumen. before you administer Abx. CBC, CMP, LFTs. Tip: you will get commonly paged at night for new fever on patient. No need for cultures for every fever or every day. Get blood cultures on first fever then every 24 hours after if fever continues. UA with reflex culture just prob once. commonly get chest X-ray too. Abx course for febrile neutropenia: cefepime + zosyn montherapy. Vanc is not part of empiric treatment. If persistent fevers but lclincialy stable, do not change Abx. If fevers persists >4 days, consider fungal.

Medications in recent MI

Medications at discharge for patients with ACS This for STEMI, NSTEMI and Unstable angina i think Aspirin forever Betal blocker forever ACE-inhibitor forever -(lesses ventricular remodeling that happens after an MI) Statin to maintain LDL<70 Clopidogrel (Plavix) if a stent was placed *Uworld says clopidogrel shjould be included as secondary prevention following unstable angina/ NSTEMI for at least 12 months. It should also be prescribed for thirty days (bare metal stents) to one year (drug eluting stents) foollowing PCI, as it has been shown to help prevent subacute stent thrombosis.

How much alchohol is sufficient to cause cirrhosis generally?

Men: 6 drinks/day/10 years Women: 3 drinks/day/10 years

Hepatocellular carcinoma vs metastasis

Metastases to the liver are 20x more common than hepatocellular carcinoma. Liver is the second most common site of metastatic spread (after the lymp nodes) because of large size, dual blood supply, high perfusion rate, etc. most common primary tumors to metstasize to liver include malignancies of GI tract, lung, breast, and skin. -Clinical presentation is variable. Hepatocellular carcinoma: tyupically accompanied by an elevation of alpha-fetoprotein. imaging of HCC usualy revelase one lesion with porrly defined margins instead of several masses of varying sizes as you see in metastasis. --remember that patients with chronic Hep B in absence of cirrhosis may develop hepatocellular carcinoma and should undergo periodic screening

Diabetes medications points to remember

Metformin -initial therapeutica agent for most type 2 -weight neutral, low risk of hypoglycemia -lactic acidosis is a life threatening complication -should not use in renal insufficiency **usually held on the day contrast is given in hospital and restarted at least 48 hours after documenting stable renal function Sulfonylurea (glipizide, glyburide) -generally added to patients with metformin failure -weight gain and hypoglycemia are main side effects Overdose: dextrose is 1st line. Octreotide is a somatostain analog that decreases insulin in patients with severe sulfonylurea overdose. TZDs (Pioglitazone, Rosiglitazone,) -used if unable to tolerate metformin or sulfonylureas -side effects: weight gain, edema, CHF, bone racture, bladder cancer -low risk of hypoglycemia when used alone or with metformin -can be used in renal insufficency Insulin -added as 2nd agent in metformin failure with A1C>8.5 -usurally you have a prandial short acting insulin combo'd with oral antidiabetic drugs and basal insulin -weight gain and hypoglycemia are main concerns DPP-IV inhibitors (sitagliptin). (newer) -low risk of hypoglycemia, weight neutral, can be used in renal insufficneyc GLP-rectpor agaonist (newer) -possible second agent for metformin failure, especially if weight loss desired. -low risk of hypoglycemia SGLT2 inhibitors (newer) Diabetes management point from Dr. Chadha -Lifestyle goal should be 5%-10% loss If starting meds: -Metformin first, if creatinine above 1.4 or GFR<30 then don't give metformin. It's a good drug, 1-2% reduction in A1c. Also don't give in//be sure to discontinue in condition of acute renal failure, liver failure, and sepsis..cuz all these conditions increase risk of lactic acidosis. THEN... -Sulfonylureas: cheap, high risk of hypoglycemia though. THEN.. -TZDs: decreases insulin resistance. Biggest contraindication is heart failure cuz causes fluid retention. -or Lantus Remember the main goal with therapy is lowest A1c WITHOUT hypoglycemic events Interesting that effect of intensive glycemic control in type 2 diabetes decreases the risk of microvascular complications (retinopathy, nephropathy) but benefits in preventing macrovascular complications (MI, stroke, PAD) have not been firmly established. Lantus is the long acting. Remember the longest fasting period glucose value, usually before breakfast, represents how good the dose is. So if that glucose level is high, don't go after any short acting insulin he's taking, go after the long acting, increase the dose maybe. Sliding scale insulin only really useful if all sugars are very high. Otherwise its a "flawed system" according to Dr. Chadha. Also MKSAp says "Sliding scale regular insulin has been associated with increased hyperglycemic and hypoglycemic excurions and has been found to result in inferior glycemic control compared to basal-bolus correction regmine in hostpitlized patients". So best way is basal-bolus regimen consisting of a long-acting insulin and a rapid -acting insulin analogue before meals for hospitilized patients with uncontrolled diabetes. Also, remember that there is NO AGENT that raises HDL that decreases risk of cardiovascular events. There is no "goal" as in number anymore for LDL, just risk profile BP goal is 140/90 or below in diabetics now Main goal should be getting below 8.0 A1C cuz you see the biggest decrease in getting below that.

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ABGs in asthmatic. What is mild asthma and what is severe asthma

Mild asthma: 7.48/30/60 (respiratory alkalosis) Severe asthma: 7.4/40/55 ( the "normalization" of the pH and Pc02 in presence of continued symptoms and hypoxia indicate that the patient is getting fatigued and no longer able to mainatin Co2 balance. He is tiring out. So you wanna intubate.

Dehydration Tx guidleline?

Mild dehydration: history of decreased intake or increased fluid loss with minimal or no clnical symptoms Moderate dehydration (6-9%) presents with decreased skin turor, dru mucum membranes, decreased urine output, tachycardia, etc. Severe dehydration (10-15%), all before plus sunken eyes, sunken fontanelle, minimal or no urine output. Mild and MOderate: Tx is oral rehydration. Moderate to severe: Tx immediately given IV fluids. Isotonic saline is the ONLY thing you give.

Kinds of Nephrotic

Minimal Change Membranous nephropathy FSGS Diabetic

2nd degree heart block

Mobitz 1 -causes: inferior wall MI, digitalis toxicity, increased vagal tone -PR prolongs progressively until a beat is dropped Mobitz II-more dangerous -causes: inferior wall or septal MI, conduction system disease -fixed PR interval, No QRS following P wave at a beat, -always place pacemaker and important to treat quickly distinction between Mobitz type 1 and type II AV block cannot be readily made from ECG. Certain ECG features and maneuvers (atropine, exercise, carotid sinus massage) are useful in differentiating between Mobitz 1 and 2. **atropine and exercise stress testing worsen Mobitz type II **carotid sinus massage worsens Mobitz type I and can parodixically improve Mobitz type II. **in absence of reversible causes, both symptomatic Mobitz type 1 and asymptomatic or symptomatmic Mobitz type II should get a permanent pacemaker.

What should you know about Trastuzumab?

Monocloncal antibody commonly used to treate breast cancer that is HER2+. It has benefit both in adjuvant situations as well as in the case of metastatic disease. An echo is recommended before beginning treatment as there is a risk of developing cardiotoxicity, particularly in patients with baseline low ejection fractions.

What is enlarged cardiac sillhouette on xrya?

More that 1/2 thoracic width at base of heart

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Cat scratch disease complications

Most common complication is suppuration of lymph nodes. Other complications are: visual loss due to neuroretinits, encephalopathy, fever, hepatosplenomegaly.

oSteophytes seen in what conditions?

Most common finding on cervical radiography in patients with cervical spondylosis, but specificity of these findings is low. Osteophytes are also bony growths often seen around the joints of patients with OA. *also see in gouty arthritis, other things as well. there are likely more conditions but these are 3.

What is postoperative endopthalmitis?

Most common form of endophthalmitis. Usually occurs within six weeks of surgery. Patients usually present with pain and decreased visual acuity. You get swollen eyelids and conjunctiva, hypopyon, cornea edema and infection.

Stuff to know about scuba diving

Most common injury associated with scuba diving is ear barotruma. You can have increased susceptibility to ear and sinus barotrauma because of h/o allergic rhinitis, which can block drainage due to mucosal edema and discharge. Studies have shown that the use of non-sedating decongestants (specifically pseudoephedrine) before diving reduces the incidence of ear and sinus barotraumas by 75%.

Most common site of GI cancer metastsasis and presentation?

Most common site of colon cancer metastasis is the liver. Liver metastases manifests as RUQ pain, milldy elevated liver enzymes (its gonna be mild and be more cholestatic in nature), and firm hepatomegaly. Dx: confirmred by CT of the abdomen.

How do you diagnose MG and what should you screen for after?

Most common symptoms relate to weakness of muscles that lift up lid (ptosis) or move eyes (double fistion). SOB and difficulty swalloing may be very serious symptoms. MG doesn't produce pain or numbness, so if you have those think of something else. The elctromyogram (EMG) and acetylcholine receptor antibody test are used to confirm the diagnosis. After establishing the diagnosis, screening for a thymoma using CT is highly recommended. Edrophonium (Tensilon) test isn't really that good.

How to stop epistaxis

Most epistaxis originates from Kiesselbach's plexus (anterior nasal septum). Nostril pinching is the first step in management. A topical vasoconstrictor (oxymetazoline) can be applied if direct compression does not stop the bleeding. Cauterization and nasal packing are additional nonsurgical measures for persistent bleeding.

Signs of adrenal failure, or Addison's disease?

Most have nausea, vomiting, abdominal pain, etc. Hyponatremia is most common, cuz of mineralcorticoid deficiency Hyperkalemia is also common due to dcreased activation of aldsoterone receptors. You get hyperkalemic, hyperchloremic, acidosis. Weight loss, hyperpigmentation, low blood pressure and vitilitgo as well

Thyrotoxicosis with low radioactive iodine uptake causes?

Most important causes 1. subacute painelss thydoitis (most common, most cases occur during post partum period) 2. subacute granulmonatous thyroiditis 3. iodine-induced thyroid toxicosis 4. levothyroxine overdose 5. struma ovarii

how do you diagnose Histoplasma? Tx?

Most rapid and sensitive test to diagnose disseminated histoplasmosis in immunocompromised patients is urein or serum assay for Histoplasma antigen. Tx: Itraconazole.

Hypothyroidism can cause what metabolic abnormliaties?

Mostly hypercholestolemia. Hypertriglyceridemia. Can also cause HYPOnatremia, asymptomaitic elvetionas of cratinine kinase and serum transaminases.

Pericardial effusion

Mot comonly idiopathic (thought to be likely from viral illness) , or bacteria, neoplasma, trauam, post MI, autoimmune, etc. Appear on x-reay as ENLARGED AND GLOBULAR cardiac silhourette "water bottle" with CLEAR LUNG FILEDS. Physical exam: inability to palpate point of maxima apical impulse. Patients with cardiac tamponade may also have Bec's triad of hypotension, JVP, and muffled heart sounds.

Behcet's syndrome

Multi systemic inflammatory condition: Recurrent oral and genital ulcers, skin lesions. Seen most commonly in the Turkish, Asian, and Middle Easter population.

What is a concer about long-term PPI use?

My increase the risk for osteoporosis through reducing bone mineral density.

MG vs Lambert-Eaton vs polymyositis

Myastheia Gravis: autoantibodies agasint post synaptic receptors. The more you use the weaker you get. Lambert-Eaton: autoantibodies against voltage Ca channels in presynaptic. The more you use the better you get. ALSO, associated with small cell carcinoma of the LUNG. Polymyositis-immunse mediate muscle inflammation. Presents as proximal weakness clibing stairs, combing hari, kneeling down, etc. CPK level is typically high.

What are the atypical pneumonias and whic is most common? how do yo distinguish them from one another?

Mycoplasma pneumoniae, Chlamydia, Legionella, Coxiella, and influenza. Different types of atypical pneumonia can present similarly and are at times challenging to distinguish. Mycoplasma is the most common. Look for erythema multiforme with mycoplasma, that can help distinguish it.

Opiate withdrawal

Mydriasis nausea, vomiting, diarrhea, piloerection, muscle pai

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NGT tube vs PEG tube

NGT tube can be a transitory vehicle for food and fluid andministration, however, it is uncomfotable, can aggravate dypsnea, and can lead to sinusitis. PEG tube (percutaneous gastrostomy) is more comfotable, does not lead to sinusitis, and does not affect patient's breathing or speech. Other ways for nutrition are enteral and TPN.

What is AERD?

NON-IGE mediated aspirin exacerbated respiratory disease, a condition commonly assoicated with the development of NASAL POLYPS. This is what you have: chronic rhinosinusitis +asthma, +apirin or NSAID induced bronchospasm. Symptoms are frequently symptoms of bilateral nasal obstruction, nasal discharge, and anosmia. Its not due to IgE reaction but from aspirin induced prostaglandin/leukotriene misbalance.

How do you treat Dresslers?

NSAIDS

Pupil sieze is not as reliable as recognition of bradypnea in opiod intoxication. How do you treat?

Naloxone.

Paralytic ileus

Nausea, vomiting with soft distended abdomen, dcreased bowel sounds, and gaseous distension of small and large owels shown on x-ray suggest ileus. Presence of gas in the colon and rectum and ABSENCE of air fluid levels is evidence against SBO. In the absence of obvious obstruction and no history of surgery, metabolic causes of ileus are most likely. Hypokalemia can cause. Common causes of hypokalemia are perisstent vomiting and loop diuretic use. Use parenteral potassium replacment to replace cuz can't tolerate oral replacment with the ileus. Diuretic induced hypokalemia is a common complication of antihypertensive/congestive heart failure therapy, especially with loop diuretics.

Gout

Negatively bifringent, yellow, needle shpaed crystals. NSAIDs are 1st line therapy and effective for .90% of patients. Oral colchicine is alternalte therpy for ppl with contraindications to NSAIDs like indomethacin is contraindicated in patients with renal failure or a history of GI bleed. Intrarticular steroids can be used in acute gout for patients with 1 or 2 inflamed joints and contraindications to NSAIDs or colchicine. Gout can result from overproduction or underexcretion of uric acid. Induction chemotherapy results in rapid tumor cell lysis and releases uric acid into the circulation. It is important to distinguish between the prevention and treatment of gout. For prevention, allopurinol and probenecid are used For treatment, colchicine, NSAIDs and steroids are used during acute attacks Dx: Arthrocentesis. If unable to have arthrocentesis, can be diagnosed clnically with classic findings (acute onset, 1st toe involvement, elevated serum uric acid, tophi). However, clinical features are not as good as arthrocentesis and many patients can have a normal or even low serum uric acid level during acute gouty attack. Gout begins as asymtpomatic hyperuricemia and progresses to monoarticular arthritis. Great toe most commonly affected; severe swelling and pain in the great toe due to deposition of monosodium urate cyrstals is referred to as podagra. Uric acid crystals form in the renal tubules and collecting system resulting in nepholithiasis. In chronic disease, urate crystals may deposit in the soft tissues forming tumors known as tophi. Tophi can ulcerate and drain a chalky material. the DDx of tophi includes rhematoid noducles and calcinosis cutis. So in chronic tophaceous gout: urate crystals can be deposited in the skin resulting in the formation of tumors with a chalky white apperance. *Myeloproliferative disorders are common cause of uric acid overproduction and thus gout because of increased turnover of purines. *You wnna have people avoid alchohol, stay on a low purine diet, and avoid drugs such as diuretics and pyrazinamde.

Types of edema usually seen in nephritic vs nephrotic?

Nephrotic: periphearl edema due to hypoalbuminemia but doesn't usually cause pulmonary edema. Alveolar capillaries have higher permeability to albumin at baseline (reducing oncotic pressure difference) and greater lymphatic flow than skeletal muscle, proteting the lungs from edema. Nephritic: here the edema comes from decreased GFR and you get significant volume overload (ppulmonary edema, distended neck veins, anasarca).

Neuroleptic malignant syndrome vs serotonin syndrome?

Neuroleptic malignant sndrome is a life-threatening disorder caused by an idiosyncratic reaction to neuroleptic tranquilizers (D2 receptor antagonists) and some antipsychotic drugs. The most common offending ones are haloperidol and fluphenazine. Serotonin syndrome: like neuroleptic malignant syndrome this presents with high fever, muscle rigidity, and cognitive changes. Findings unique to the serotonin syndrome are shivering, hyperreflexia, myoclonus, and ataxia.

How can you distinguish between Vit B12 deficiency and folate deficiency on physical exam?

Neuropathy hapens in B12 defieincy. Do you get dmyelination in tracts. So neurologic finds are found like posotion/vibratory sensation loss.

What do you never do a patient with diverticulitis

Never do colonoscopy , risk of perforation

Pediatric sepsis

Newborns are prone to overwhelming bacterial infection due to their immature immune systems. FEVER can be the first and only sign of serious bacterial infection in neonates. Look for POOR APPETITE and LASSITUDE. *Ceftriaxone and sulfonamides should be avoided due to risk of hyperbilirubinemia in infants <28 days.

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WHen does a snoring patient need formal testing for OSA

No indication for special tests in a snoring patient if the patient doesn't have associated symtoms and clinical findings of oSA, like daytime hypersomnolence, nocturnal choking, gasping apena with desaturation, and hypertension. Patients who snore but have no other signs or symptoms of OSA should be advised to lose weigh, stop smoking, and void alcohol near bedtime.

Bladder outlet obstruction clinical picture

Nocturnal urinary frequency, dribbling, weak stream. Commonly caused by BPH. Post-void residual volume is usually >50ml in significant bladder outle obstruction.

what is the use of NPPV in obstructive pulmonary disease patients?

Noninvasive positive pressure ventilation can be used basically after medications aren't quite cutting it and before you decide to intubate w/mechanical ventilation. If a patient fails a 2-hour trial of NPPV then go to intubation w/mechanical ventilation.

What should you give patients with small nonbleeding varices as prohpylaxis against future bleeding?

Nonselevtive beta blockers. If have contraindications to beta blocker therapy, endoscopic variceal ligation can be used as alternative.

UA-specific gravity?

Normal is 1.002-1.035 High (>1.010) indicates dehydration Inability to concentrate urine in the setting of dehydration indicates renal disease

UA-Nitrite

Normal is negative. Positive indicates bacteria in urine, usually Gram - rods.

Lung Physical exam principles. Normal lung? Consolidation? Pleural effusion? Pneumonthorax? Emphysema? interstitial lung disease?

Normal lung: Auscultation will reveal VESICULAR breath sounds: which consist of a quiet inspiratory phase and an almost inaudible expiratory phase. -If there is a consolidated region, you will get BRONCHIAL breath sounds, which are louder and have a more prominent expiratory component. IMPORTANT: this holds true oonly if airways are patent! If the airways are blocked, the breath sounds over the consolidated lung tissue would be decreased. increased sound transmission over the consolidated lung region can also be assessed by the egopony thing (have patient say E). Crackles also heard with consolidation. ---so with consolidation expect dullness to percussion, bronchial breath sounds (assuming patent airways) and egophany, increased tactile fremiuts Pleural effusion: dullness to percussion, decreased breath sounds, decreased tactile fremitus - (presence of fluid or air outside the lung interrupts the transmisison of sound, resulting in decreased fremitus in pleural effusion and pneumothorax....while fluid inside the lung gives you increased fremitue (pneumonia)) Pneumontroax-hyperresoncnce on percussion and decreased breath sounds, decreased tactile fremitus Emphysema: hyperresonance bilaterally, breath sounds are vesicular and intesity of breath sounds is significantly decreased. wheezing may be present. Interstitial lung disesase: resonant on percussion and vesicular breath sounds. Fine crackles heard at end of inspiration.

Normal urinary output? Oliguria ??

Normal: 2-4 ml/kg/hr Oliguria: <0.5 ml/kg/hr

Joint fluid lab characteristics for normal and diseases

Normal: Clear, WBCs<200, PMNs < 25% Non-inflammatory (like OA): Clear, 200-2000, 25% Infammatory (crystals, RA,): Translucent of opaque, 2,000-100,000, > 50% often, Septic joint: Opaque, 50,000-150,000, Often >80% Gout-needleshaped, yellow cyrstals when paralel to polarizing axis and blue if perpendicuar to polarizing axis, are negatively birefrignent Pseudogout- Compared to urate crystals, CPPD (calcium pyrophosphate dihydrate deposition) crystals are smaller, RHOMBOID SHAPED, positively birefringent. Attacks of pseudogout often occur in the setting of trauma, surgery, or medical illness. **Lok for history of hemochromatosis or hyperparathyroidism. **Pseudogout causes chondrocalcinosis-calcifieid articualr cartilage on x-ray cuz its due to the calcium crystals depositing on tissues. You also gonna see this in Hemachromatosis.

Hodgkins lympphma

Normally have NORMAL blood msmears Reed Sternberg cells are seen in the lymph node biopsy

Foodborne disease algorithm

Norovirus is most common cause of epidemic gastroenteritis and now the most common cause of all gastroenteritis in adults and children. Spread via fecal-oral and virus can be transmitted from food and water, fomites, or airborne droplets from vomitus. Norovirus outbreaks are common and occur in institiutionalized settings such as nursing homes, health care facilities, restaurants, cruise ships. Norovirus can cause the following: 1. Asymptomatic infection 2. Fever with watery diarrhea--non-inflammatory small bowel process 3. Severe illness: fever, VOMITING, headache, other systemic symptoms. Symptoms usually start and last 48-72 hours. If needed, diagnoses can be confirmed by PCR or nucleic acid based testing.

Bladder cancer screening?

Not recommended, even in patients who are at risk of devleoping disease

Alternative medicine stuff

Not regulated by government and are generally classified as food or dietary supplements, enabling manufacturers to avoid the same scientific scrutiny that prescription drugs reieve. What limited data there is, it's often flawed data. Saw palmetto: popular herb preparation most often used by med to treat BPH. HAS NOT been shows to improve urinary symptoms, flow measures, or affect PSA or prostate size. Kava kava: herbal preparation that may help with symptoms of anxiety and insomnia. However, its use is not recommended due to potential risk of severe liver toxicity. St. John's wort: frequently used in depression treatment. Inconssitent evidence supporting its efficacy. Fish oil supplementation can be effective in treatment of refractory hypertriglyceridemia Osteoarthritis is often treated with glucosamine and chondroitin. Although these agents appear to be safe, studies demonstrating their clinical benefit are limited. Ephedra: has been banned by FDA These give increased POST OPERATIVE BLEEDING risk due to platelet dysfunction: saw palmetto, gindgo biloba, ginseng, black cohosh, garlic.

Lidocaine is used in what?

Not used prophylatially in patients with ACS. Althought it suse decreases the risk of V-fib, it may increase the risk of asystole.

Ear infections: Primary Care:

OTITIS EXTERNA -infection of external auditory canal -ear pain and itching sometimes -exam shows an inflamed, swollen, external ear canal, often with exudates. Movement of ear can be painful. Tympanic membrane usually uninvolved. -staph, strept, psuedomonas ("swimmers ear) . -irrigation and topical antibiotics, frequently combined with steroids, usually successful -patiends with diabetes are at risk fo invasive external otitis (MALIGNANT OTITIS EXTERNA). caused by pseudomona, IV cipro is empiric treatment. Unrelenting pain, purulunt drainage, conductive hearing loss. can spread to skull and cause osteomyelitis, pain with chewing, and invovlve CNs. Typically seen in elderly, diabetic patients and presence of granulation tissue on floor of canal is ppathognomonic. OTITIS MEDIA -infection of middle ear -Strept pneumoniae, H. influenzae, Moraxela mot common bacterial caues -Can be viral too. Viral infection with serous otitis may predispose to acute bacterial otitis media. Infection of middle ear space, caused by upper respiratory tract pathogens, is promoted by obstructino to drainage through edematous, congested eustachian tubes. -On exam the TM may appear red, but the presence of decreased membrane mobilitiy or fluid behind the tympanic membrane are necessary for the diagnosis. -Most cases of acute OM will resolve spontaneously. -If prolonged or recurrent, Amoxicillin is for initial therapy. Alternative treatments are amoxicillin-clavulanic acid, TMP/SMX, 2nd or 3rd gen cephalosporins. * the inflammatory response during acute OM also leads to mucosal response of the mastoid air cells. an exclusive complication of otitis media (although uncommon nowadays) that process may result in accumulation of pus within mastoid cavities and you get acute mastoiditis. this usually resolves quickly with effective Abx Tx of acute OM. *exposure to cigarettes smoke is one of the most important risk factors for developing acute OM. parents sould be urged to quit smoking. *while adults have wide, steeply angled Eustachian tubes, infants have shorter, almost horizontal Eustachian tubes. The fact makes fluid accumulation and infection quite common in young children.

What to know about adverse events

Occr in 5%-1% of hospitilized patienets. 4 broad categories. 1. operative and post-procdure -wound infections, bleeding, DVT. These are most common in hospitlized patients, are related to surger. 2. adverse drug event.: Most common in patients not having surgery. Comonly related to hypoglycemic agents, anticoagulatns, antibiotics, or analgesic. 3. general care (fall, pressure ulcer, etc) 4. hospital acquired infections

Psoriatic arthritis

Occurs in 5-30% of people with psoriasis. The classic presentation involves the distal interphlangeal joints. Morning stiffness, deformity, dactylitis "sausage digit" and nail involvement are common. Current treatment options for psoriatic arthritic include nonsteroidal anti-inflammatory agents, methotrexate, and anti-tumor necrosis factor agent. No lab tests available for psoriatic arthritis. Untreated HIV infection is associated with the occurrent of explosive onset, widely distributed psoriasis and up to 40% of these can go on to develop psoriatic arthritis.

What is the hallmark of ischemic hepatic injury?

Occurs in the setting of hypotension and causes rapid and massive increase in Transaminases with modest accompanying elevations in total bilirubin and alkaline phosphatase. In patients who survive the underlying cause of their hypotension (septic shock, heart failure) liver enzymes typically return to normal iwthin one to two weeks.

Ankylosing spondylitis

Occurs most often in adults aged 20-30 years. Patients suffer from limited spine mobility and progressive back pain or greater than 3 months duration. The pain and stiffness are worse in the monring and improve with exercise. Bilateral sacroilitis on plain film of a patient with the above symptoms is diagnostic. The most prominent extraarticular manifestiation of AS is anterio uveitis. Patients with this for 20 YEARS OR longer are at increased risk of vertebral fracutre. Osteopenia/osteoporosis is the reusult of increaed osteoclast activity in this state. 3 mont important clinical criteria for diagnosis: 1. Presence of low back pain and stiffness for more than a three month duration that improves with exercise or activity. 2. Limitation of the range of mothion of the lumbar spine 3. Limitation of chest expansion relative to the normal values. Plain X-ray of the sacroiliac joint is the next best step in the management of a patient who is suspected with ankylosing spondylitis. Other radiographic abnormaltiies suggesting the diagnosis inclue erosions of the ischial tuberosity and iliac crest. Early in course of disease, squaring of the vertebral bodies on plain x-ray may also suggest the diagnosis. How to monitor: X-ray and ESR used to monitor disesae progression. *Most common and important extraarticular manifestations of anklyosing spondylitis are acute anterior uveitis, aortic regurgitation, apical pulmonary fibrosis, IgA nephropathy, and restrictive lung disease.

Who gets anoscopy/proctoscopy?

Office based anoscopy/proctoscopy should be the initial procedure in patients less than 50 years old who present with minimal bright red blood per rectum and do not have any risk factors for colon cancer. Blood intermixed with stool is not included in this category.

Glucagonoma explain it

Often presents with nonspecific symptoms and requires high index of supsicion to make the Dx. Suspct it in patients with midl diabetes mellitus or hyperlgycemia with necrotic migratoy erythema, diarrhea, anemia, and weight loss. GLucagon >500 usually confirms diagnosis.

Hereditary Hemachromatosis

Only a small percentage present with the classic triad of cirrhosis, diabetes mellitus, and skin pigmentatin (bronze diabetes) seen in later stages of the disease. You also get arthropathy (associated with PSEUDOGOUT), hypognadism, restricted cardiomyopathy, and conduction abnormalities. Remember these other manifstations cuz you probably won't get the classic triad on a test cuz that's too easy. Cardiac dysfunction associated with hemachromatosis can be reversed with early idenfitication of the disease and treatment. Tx: Preferred treatment is therapeutic phlebotomy, which ential removing about 1 unit of blood each week until iron stores normalize.

Lab values on osteoporosis? osteopetrosis? Paget disease? Osteomalacia/Rickets? Hypervitaminosis D?

Osteoporosis: Calcium and PTH are normal. everything normal. Low bone mass but adequate mineralization. Osteopetrosis: -bad osteoclasts don't do their job-->dense brittle bones. - Mostly normal lab values, in severe disease decreased calcium. Paget disease: -bad bone REMODELING by osteoblasts and osteoclasts--> bones are weak and fracture. abnormal "mosai" patter of bones. -femoral BOWING characteristic on x-ray -commonly get cranial enlargement (increased hat size) and hearing loss -Lab: only increased ALP. *most common presentation is asymptomatic and increased ALP found incidentally on routine blood tests. Osteomalacia/Rickets -Vit D deficiency causes increased pTH secretion which excretes a lot of phosphate. You get soft bones. -problem is increased deposition of poorly mineralized osteoid. -Lab: decreased Calcium, decreased Phosphate, Increased ALP, Increased PTH. -Bone pain and muscle weakness. -x0ray findings unclude PSEUDOFRACTURES (looser zones). *its 25-hydrovit D that converts to 1,25-hydroxyvit D in response to PTH. Although 25-hydroxyvit D levels are very sensitive markers for Vit D intake, 1,25-hihydroxyvit D levels may remain normal until late stages of Vit D defieincy due to upregulation of 1-alpha-hydroxylae in kidneys. Hypervitaminosis D -caused by oversupplmentation or granulmonatous disese (sarcoidosis) Lab-increased vit D leads to increased Ca and Phosph. PTH is decreased -Symptoms are similar to that of hypercalcemia: constipation, polyuria, polydipsia, abdominal pain **ALP is a marker of bone turnover (bone fraction) as well as biliary tract disease (liver fraction).

Hypertrohpic cardiomyopathy

Outflow obstruction in hypertrophic cardiomyopathy due to what? 2 things 1. hypertrophied interventruicular septum 2. abnormality in the motion of the mitral valve leaflets referred to as systolic anterior motion (SAM). SAM results in nincreased outflow obstruction and in some patients may be of greater clinical consequence than septal hypertrophy. *good thing to know is that hypertrophic cardiomyopathy murmur increases when less blood is going through it, so anything that decreases preload. whereas AS murumr will increase with more preload. also, hypertrophic cardiomyopathy like the only murmur that decreases with increased SVR (hand grip). Causes of paradoxical splitting of S2; hypertrophic cardiomyopathy aortic setnosis LBBB Tx of hypertrophic cardiomyopathy: Beta blockers or cardiac Ca channel blocker like diltiazem cuz promote diastolic relaxation Tx: ICD is put for SCD prevention if patients who have increased risk for SCD. IMPORTANT: if young athlete suddenly collapses and dies, don't think its 100% a HCM case. Anomalous origin of the coronary artery is a common cause of sudden cardiac death in young athletes. With these patients, the ECG and ECHO will be normal, with HCM that is unlikely.

Explain premature atrial beats?

P waves that are premature relative to sinuse cycle and differ in morphology form sinus "P" waves. normal QRS. Premature atria beats may be completely normal or due to anxiety, CHF, hypoxia, caffeine or electrolyte abnormalities. Never requires treatment and is totally benign. Premature atrial complexes (PAC) (I'm not sure if differnet thing or same), according ot uworld: most likely benign but can be symptomaitc. Beta blockers are standard treatment for smptomatic PACs.

Go over basic seizure stuff. page 485 First AId.

PARTIAL (focal)-affect 1 area of brain. 1.Simple partial-consciounsness intact . 2. Complex partial-brief episodes of impaired consciousness, failure to respon to stimuli during episodes, staring spells, automatisms (lip smacking, swallowing, picking movements of hand) and post-ictal confusion. the EEG patter is usually normal or may show brief discharges. GENERALIZED SEIZURES (always loss of awareness, always bitemporal ) 1. Typical absence: brief impaired consciousness, no post-ictal state, may have automatisms. Hyperventilation during EEG reveals a 3 Hz spike and wave patter on normal background. 2. Atypical abscence: Lasts longer. EEG pattern is slow spike and wave with frequency less than 2.5 Hz. 3. Myoclonic-quick, repetitive jerks -early 20s cuz of sleep deprivation, alchohol, stress 4. Tonic clonic (grand mal)-alternating stiffening and movement 5. Tonic- stiffening 6. Atonic-"drop" seizures (falls to floor); commonly mistaken for fainting

HIV prophylaxis

PCP: -Prophy: TMP/SMX, dapsone alternative. -CD4 count: <200 cells. Oropharyngeal candidiasis. Toxoplasma gondii: -Prophy: TMP/SMX -CD4 count <100 Mycobacterium avium (you see increased ALP, splenomegaly, fever, diarrhea, cough). -Prophy: Azithro -CD4 count <50 Histoplasma capsulatum -Prophy: Itraconazole -CD4 count<150

Test for Whipples? Treatment

PCR for T whippeli in salivea, stool, or blood Tx: antibiotic therapy . Fatal if untreated, curable if treated. patients prsent with fevers, arthralgia,s and CNS symptoms,

V/Q scan can rule out what? whwen do you use?

PE When do you use? in most paitnets CT angio is best choice. But in patients with contrast allergy or renal insufficeicny, contrast cannot be given, making the V/Q scan the test of choice.

Diabetic neuropathy?

PERIPHERAL NEUROPATHY usually presents with alterations in sensation (pain, temp, etc) including loss of proprioception. Motor findings may be a late mainfestation in severe cases. Its a LMN process though so you shouldn't see UPM lesion signs such as hyperactive reflexes or upgoing Babinski! TReatmnet:A systematic review of the literature found that pregabalin is established as effective and should be offered for relief of painful diabetic neuropathy. Agents deemed "probably effective" include venlafaxine, duloxetine, amitriptyline, gabapentin, valproate, opioids, and capsaicin. **another uworld question said that TCAs are the drug of choice for diabetic neuopropathy. And if ur having problems with side effects like urinary symptoms or orthostatic hypotension, Gabapentin is an alternative. AUTONOMIC NEUROPATHY MONONEUROPATHY -Divided into crainal and somatic. -Among the cranial, CN III is affected most often. ------In diabetes, the CNIII neuropahty is ischemic. Somatic and parasympathetic fibers of CN III have separate blood supplies. For this reason, diabeteic CN III neuropathy affects onluy somatic fibers, leaving parasympathetic fibers intact. Symptoms are ptosis and "down and out" gaze. Accomdoation and pupil's response to light remain intact. (Alternatively, if nerve compression causes CN III neuropathy, both the somatic and parasympathetic fibers will be affected. Patients wiill have ptosis, "down and out" gaze, a fixed dilated pupil, and no accomodation reflex. Also on this note, the pupilloconstrictor fibers of the 3rd nerve lie superficially on the nerve, so lesions impinging here will affect these before they affect the ocular motor fibers. -diabetes is the most common cause of mononeuritis multiplex. In this disorder, individual nerves are transiently disabled. The neuropathy usually develops over the course of minutes to days, and the recovery of function may require weeks to months.

Diagnosis of TB, screeing of it,

PPD stands for purified protein derivative. It indicated INFECTION, not ACTIVE disease. TB skin test 1. plant .1mL of PPD intradermally. 2. Wait 48-72 hours. 3. Measure INDURATION, NOT ERYTHEMA. ---if induration >15 mm, person is considered infected ---If induration >10 mm, person is considered infected if he is one of the high prevalence groups ---if induration is >5mm and person has HIV, or clost contact, or abnormal CXR, or immunocompromised. The that person is considered infect. If positive PPD test..then the patient should recieve a chest X-ray to exclude ACTIVE disease. ------- If X-ray is negative, you gotta treat for latent TB infection which is prophylaxis with isoniazid (and pyridoxine to prevent possible neuropathy) for 9 months -------If X-ray is positive for ACTIVE TB: standard therapy is at least 6 months of 3 to 4 drug therapy (isoniazid, rifampin, pyrazinamide, and ethambutol). False positive: -BCH vaccination will give a false positive on PPD for 10-15 years after getting it. So immigrants who got is a child shold not be giving false positives as adults over 25-30 yrs of age. -A nontuberculosis mycobacterial infection False neagtive: -10-25% of patients with infection give a false negative -this is reason of two step TB skin test. *if a person is planning on taking a TNF-alpha inhibitor and has a tuberculin skin test of 5 mm or more induration OR a positive interferon-gamma release assy...then CDC recommends Tx of latent TB infection (the 9 months of isoniazi) **sputum microscopy for acid-fact bacilli can serve as surrogate mareker for infectivity for TB. patients with 3 NEGATIVE SPUTUM SAMPLES are considered noninfectious for TB. but these patients may still have active infection which requires treatment. **When is TB patient considered non-infectious? Sputum positive pulmonary TB patients are rendered non-infectious if they are receiving effective antituberculous therapy and have had 3 consecutive negative results on sputum acid-fast smears permoed on different occasions.

Hyperaldosteronism

PRIMARY -Conn syndrome: adrenal adenoma. Results in hypertension, hypokalemia, metabolic alkalsos, and LOW plasma renin. Normal Na+ due to alodsterone escape. Tx:surgery and spironolactone (acts as an aldoserone antaognist too) Initial screening test: Ratio of plasam aldosterone to plasma renin. PAC/PRA ratio >20 with plasma aldosterone >15 ng/dl suggests it. You need further testing to confirm; adrenal suppression test (salt loading and documenting inability to suppress serum aldosterone) SECONDARY -renal pereception of low intravsacular volume results in an overactive RAAS system. Causes are renal artery stenosis (commonly from fibromuscular dysplasia in young women), CHF, cirrhosis , or nephrotic syndroem. HIGH PLASMA renin. Also have hypertension, hypokalemia, metabolic alklaosis. Tx: spironolacotne.

No

PRIMARY CLINICAL H

Kinds of nephritic syndrome

PSGN IgA nephropathy (Berger's disease) MPGN Rapidly progressive GN (RPGN) (also called crescentic) ---a. Puaci-immune RPGN ---b. immune complex RPGN ---c. Anti-glomerular basement AB disease -remember, any glomerulonephritis that progresses can subsequently become a RPGN. Like PSGn, Ig Nephropathy, MPGN can all cause leter b.

You can get PSGN from throat or skin infection. With rheumatic fever, you can get from pharyngitis or skin infections as well. Also with PSGN, successfully treating prior strept infection with antibiotics doesn't do anything to ensure PSGN not happening. Pharnygitis=sore throat Pharyngitis + sandpaper rash = scarlet fever PHaryngitis + 2-3 weeks afterwards JONES criteria stuff happpens= Rheumatic fever

PSGN mediated by immune complexes so complement levels gonna be low. ASO is almost elevated.

PTH and Vit D

PTH -bone-resorption of both calcium and phosphate -kidney-excretes phosphate and resorps calcium Vit D -kidney retention of calcium and phosphate -renal failure results is VIt D deficiency so the resulting low Ca---> increased PTH

Common causes of hemoptysis

PULMONARY bronhitis, PE, bronchiectasis, lung cancer CARDIAC mitral stenosis/acute pulmonary edema INFECTIOUS TB, lung abscess, aspergillus HEMATOLOGIC coagulopathy VSCUALAR av malformations SYSTEMIC Wegener's , Goodpastures, SLE -most commonly encountered causes of hemoptysis in ambulatory in ambulatory patients are infection (bronchitis or pneumonia) and malignancy. All patients with hemoptysis should have a chest x-ray.

Postoperative urinary retention

PUR is a common complication of surgery and anesthesia. A precpitating event (bladder distention during general anesthesia, epidural anesthesia use) can lead to inefficient detrusor muscle activity and acute urinary retention. Postoperative olugira requires immediate assessment with initial portable bladder scan toi assess bladder volume. Patietns with significant urinary retention and likely distal obstruction require FOley catheterization to restore normal urine output and resolve or prevent hydronehprosis, tubular atorphy, and renal injury.

Metabolic alkalsos respiratory compensation equation?

PaC02= (.9 x HCO3) + 16 +- 2 Used to determine the degree of respiratory compensation. Which is how well the lungs adapt to the alkalemia and retain PaC02 through hypoventialtion.

Breast cancer. Know pathoma stuff.

Paget's disease of the breast should be suspected in a aptient with no prior history of skin disease who presents with an eczematous rash near thenipple that does not improve with topical treatments. The majority of patients with Paget's disease have an underlying breast aenocarcinoma.

Evaluation of bone metastasis

Pain from bone metastasis is typically dull and aching or boring in character, and symptoms often occur at night. *Malignancies from osteolytic metastases are poorly visible on radioisotope (technetium-99 MDP) bone scans as the labeled technetium is preferentially taken up in areas of new bone formation (thats why its good for osteoblastic metastases)

Herpes simplex keratitis

Pain, photobphosbia, decresaed vision. Dendritic ulcer is most commone presentation.

Spermatocele

Painless, fluid-filled cyst of head of the epididymis. Thy are located on the superior pole of the testis and contain nonviable sperm. They are distinguishable on physical examination os a moass outside of the testis that does not change with position.

Describe Tinea versicolor?

Pale, velvety pink or whitish, hypopgimented macules THAT DO NOT TAN and do not appear scaly, but scale on scraping. Topical treatment with SELENIUM SULFIDE lotion and ketoconazole shampoo is recommended. Extremely high yield for Step 2

Mixed essential cryoglobulinemia signs?

Palpable purpura, glomerulonephritis, athralgias, hepatosplenomegaly, peripheral neuropathy, LOW complement. Also patient has HCV!

Fanconi's anemia presentation?

Pancytopenia + Characateristis congenital anomalies like hyperpigmentation of trunk, neck, and intertrignous areas and/or cafe-au-lait spots, short, limb abnormalities, hypognadism, skeltala problems, eye problems, renal problems.

Panic disorder?

Panic disorder is characterized by recurrent, unexpected panic attacks that feature the abrupt onset of numerous somatic symptoms, such as palpitations, sweating, tremulousness, dyspnea, chest pain, nausea, dizziness, and numbness. Symptoms typically peak within 10 minutes of onset, and attacks usually last from 15 to 60 minutes. The most appropriate treatment for panic disoerder is cognitive-behavorial therapy and a SSRI.

ED management of asthma exacerbation

Parenteral magnesium sulfate is bronchodilator. It is indicated when PEF <40% despite >1 hour of intesive therapy with inhaled SABA and glucocorticoids. Has not been shown to benefit patients with mild to moderate exacerbations.

Treatment of stones

Passage: -95% of stones <5 mm will pass by itself -15% of stones 5-8 mm will pass -5% of stones >8 mm will pass For stones that are unliley to pass -Extracoporeal shock wave lithotripsy (ESWL) is pretty good. with 85% success rate. Don't use in unstable patients, go straith no percutaneous nephrolithotomy. -Percutaneous nephrolithotomy, which establisehs a tract from skin to collectying system is used when ESWL doesn't cut it. It drains obstruction portion of urinary tract. You can also do retrograde ureteral stent, but generlaly percutaneous nephrolithotomy preferred. These procedures preferred for ppl who are UNSTABLE or have very large stones. Hydration: Drink GREATER THAN 2L daily. THis helps a lot. Stones less than 5mm typically pass. Pain control: narcotics and NSAIDS: equally effective in relieving the pain, but in patients with normal renal function NSAIDS are preferred because narcotics can exacerbate nausea and vomiting

Differential diagnosis of delayed gastric emptying

Patient with nausea, bloating, postprandial fullness, and a succussion splash (splashing sound auscultated with a stethoscope placed over the LUQ and is suggestive of retained gastric material). These are clinical features of impaired gastric emptying related to gastric outlet obstruction or delayed gastric motiliy First step: exclude mechanical obstruction with upper GI endoscopy. 2nd step: if obstruction ruled out, do tests for gastric motility disorders, like scintigraphic gastric empyting study.

Oral lesion in old person?

Patients who wear dentures all the time are prone to develop oral lesions. The most appropriate inital step for such patients is to simply advise them to remove their dentures for a couple of weeks. If lesion does not subside, the patient should have a biopsy to rule out malignancy.

Tetanus prophylaxis

Patients with DIRTY (eg, dirt, feces, saliva) or SEVERE (punctures, avulstions, crush injuries, burn, frostibe) wounds have a higher risk for Clostridium tetani due to favorable anaerobic growth environement. Early doses of tetanus toxoid only prime the immune system but DO NOT confer immediately.

Who should get a carotid endarterectomy?

Patients with Symptomatic carotid artery stensos of 70%-99%. Men w/Asymptomatic carodi artery stenosis of 60-99% may also benefit from CEA compared to medical management alone. Patients with lesster degrees of stenosis should do medical management of antiplatelt agents and statins with optimization of risk factors (smoking cessation, diabetes mellitus, and hypertension control). Ppl with <50% stenossis are typically monitered with annual Duplex ultrasound.

How often should you screen for cancer in UC patient?

Patients with UC are at an increased risk for the development of colorectal cancer. Most guidelines state that patients should begin colonoscopy surveillance 8 years after diagnosis. Once a surveillance program is started, colonoscopy should be repeated every 1-2 years to assess for development of colonic dysplasia.

What is the role of antibiotic prophyslaxis in rhematic heart disease?

Patients with a history or rheumatic fever have an increased risk or recurrent episodes and progression of rheumatic heart disease with repeated infection with group A pharyngitis. All such patients whould receive CONTINOUS ANTIBIOTIC PROPHYLAXIS to prevent recurrent Strep phrayngitis and limit the progression of rheumatic heart disease. Preferred regimen is IM penicillin ever 4 weeks. Duration of prophylaxis: depends on severity. something like 5 to 10 years or until 21 years old (whichever is longer.).

Person traveled to mexicao comes back with liver mass. what should you think?

Patients with a liver mass who have traveled in endemic area should be evaluated for amebic liver abscesses with serologic testing and receive empiric treatment with oral metronidazole. Because of its associated risks, cyst aspiration is NOT typically recommended unless patient fails therapy. cause is Entamoebea Histolytica, is usually a SINGLE cyst and causes BLOODY DIARRHEA . tx is metronidazole. Pyogenic (bacterial) liver abscess shoudl be considered in DDx but its usually secondary o surgery, GI infection, or appendicits. Also presentation mroe severe than with amebic liver abscess.

Person traveled to mexicao comes back with liver mass. what should you think?

Patients with a liver mass who have traveled in endemic area should be evaluated for amebic liver abscesses with serologic testing and receive empiric treatment with oral metronidazole. Because of its associated risks, cyst aspiration is not typically recommended unless patient fails therapy. Pyogenic liver abscess shoudl be considered in DDx but its usually secondary o surgery, GI infection, or appendicits. Also presentation mroe severe than with amebic liver abscess. These you initially treat with perutaneous catheter drainage and antibiotics against gram-negative and anaerobic organisms.

What is ERCP generally reserved for?

Patients with cholestasis (like from tumor compressing biliary system) who may require an intervention (like stenting) ERCP with spincterotomy is indicated for patients with biliary obstruction due to choledocholithiasis. It has no role in removing nonobstructing stones from the gallbladder. (MKSAP) ERCP with spinceterotomy and stone extraction is the initial treatment of choice for gallstone pancreatitis.

Compartment syndrome

Patients with compartment syndomre may develop rhabdomyolysis and release myoglobin. Heme pigment from myoglobin is nephrotoxic; patients may develop acute renal failure, especially if they are volume depleted. Pressure >30 mmHg or delta pressure (diastolic-compartment pressure) <20-30 mmHg indicates CF. If compartment pressures are improving, patients may be observed closely. If not, need fasciotomy to avoid permanent loss of function from nerve and muscle injury. SIgns and symptoms like absence of pulse, elevated CK, etc are unreliable indicators of CS severity A high index of suspicion and timley fasciotomy are the most important factors predicting complete functional recovery. CS is commonly from traumatic injuries, BUT can also occur in nontraumatic settings like arterial occlusion and reperfusion. This is Postischemic CS: due to interstitial edema and possibley intracellular swelling following tissue ischemia and subsequent reperfusion.

Gastroparesis

Patients with gastroparesis often have labile diabetic control and frequent hypoglycemia as it is difficult to time thier insulin dose to correspond with the delayed intestinal absorption of glucose. In evaluating patients with delayed gastric emptying, first step is to rule out mechanical obstruction. This is usually done with UPPER GI endoscopy or barium swallow. Unfortunately, this does not assess motility. If diabetic gastroparesis or another motility disorder is suspected, the patient will require a NUCLEAR GASTRIC EMPTYING study to confirm the diagnosis. Foundation of managing gastroparesis is DIETARY MODIFICATION. if this is insufficiency, promotility agents like ERYTHRYOMYCIN or METOCLOPRAMIDE may be needed.

What type of infection are people with demential at risk for?

Patients with impiared consciousness, advanced dementia, and other neurologic deficits are at risk for aspiration pneumonia due to impaired epiglottic function.

Platelet transfusions are given to who?

Patients with plateley count <10,000 (increased risk of spontaneous hemorrhage) or.. active bleeding and plateleys <50,000 *DIC treatment is reverse underlying cause, RBC transfusion, platelet transfusion and shock management.

Explain signs and who gets Niacin deficiency

Pellagra is due to Niacin deficiency. Commonly found among people eating corn-based diets in Pinda, Africa and Chinla. Also seen in alchoholics, cacinoid syndrome, and Hartnup's disease. 3 D's, Diarrhea, Dermatitis, and Dementia and if untreated eventually leads to Death (4th D). The skin rash is present in sun-exposed areas.

What do you expect to see with perofrated peptic ulcer

Perforates and stuff goes into peritoneum, like air and contents. It iritiates wht peritnesum and causes chemical peritonitis. So suddent onset of severe epigastric pain that spreads over entire abdomen. Also, on X-ray you're gonna be able to see free air under the diaphragm.

After cardiac surgery infant shows up in bad shape with x-ray that shows big heart, what is it?

Pericardial effusion. This is part of "post pericardiotomy syndrome" which is a pleuropericardial disease that occurs days or months after cardiac surgery or injury. Inflammation from surgical intervention can lead to reactive pericarditis, pericardial effustion, or even cardiac tamnponade. Remember tamponade characterized by "Beck's triad". distant heart sounds, distended jugular veins, and hypotension. Chest x-ray shows enalred cardiac sillhouette from fluid accumulation. Tachycardia gonna happen to mainatin cardiac output. Also pulsus paradoxus.

Common side effect of calcium channel blockers?

Peripheral edema

Pvd vs Acute arterial occlusion?

Peripheral vascular disease -intermitten claudiction, rest pain (OFTEN prominent at night, awakens person from sleep), decreased pulses, ischemic ulcers, -Dx: arteriogram -Tx: claudication-conservative treatment. rest pain- surgery. So you start on LOW DOSE ASPIRIN and STATINs. Then endroll patient in SUPERVISED EXERCISE PROGRAM. The goal is to reproduce claudication symptoms each session. This has been shown to reduce symtpoms and improve max walking ditance. If this fail then go to cilostazol and percutaneous or surgical revasculariation. Acute arterial occlusion -6 Ps: pallor, pain, pulselessness, paresthesias, paralysis, polar (cold) -Dx: arteriogram -Tx: anticoagulation, emergent surgery

Patient has megalobalstic anemia, atrophic glossitis (shiny tongue), thyroid disease, nerulogic abnormalities.

Pernicious anemia, most common cause of Vit B12 deficiency of whites of northern European background . These patients frequently have other associated autoimmune disease, including autoimmune thyroid disease and vitiligo Dx of pernicious anemia can be confirmed by detection of anti-intrinsic factor antibodies. Remember: patients develop chronic atrophic gastritis with decreased production of IF by parietal cells. This atrophic gastritis increases the risk of gastric cancer. So patients with pernicious anemia need to be monitered for development of gatric cancer (periodic stool testing for blood). HIGH YIELD: Three main components of AMAG (which is associtaed with pernicious anemia) are glandular atrophy, intestinal metaplasia, and inflammation. Atrophy affects mainly the gastric body and fundus. Typically, little changes are observed in the gastric antrum. Tx: patients with moderate to severe megaloblastic anemia can have severe hypokalemia during the first 48 hours of treatment with vitamin B12. Close monitoring and supplementatino of patassium is requred during this period.

When do you start thinking resistant hypertension?

Persistnet hyueprtension depsite using >orequal 3 antihypertensive agents (1 being diuretic). All patients with resistant hypertension should be evaluated for secondary causes. Secondaryu causes: Renovascular disease (renal stenosis most common) **there is atherosclerotic renal artery stenosis you wanna look out for in older adults. **there is also renal artery stenosis caused by fibromuscular dypslasia. **Evaluate for this with renal Duplez, or CT, or MR angio. Due to risk of contrast-induced nephropathy and nephrogenic fibrosis when using contrast, CT or MR angio should be avoided in patients with renal insufficency. Renal parenchymal disease Primary aldosternishm Pheo Cushings Hypothyroidism Primary Hyperparathyroidsism Coarctation of aorta **Renal parenchymal disease is an IMPORTANT cause of secondary hypertension in children and young adults, and may cause severe or resistant hypertension.

Dx of COPD

Physical exam: barrel chest, decreased air entry with prolonged expiration, wheezes. Chest x-ray: 1. Hyperinflated lungs. 2. Low, flattened diaphragm. PFTs: low FeV1. Later stages of COPD often have "airt trapping" (increasd residual volume) and progressive huyperinflation (increasd total lung capacity). Lung hyperinflation preserves max expiratory airlfow as the higher lung volume increases elastic recoid pressure. The enlarged airways decrease overall airway resistance. Hyperinflation is what flattens the diaphrragm. However, large lung volumes and diaphrragmatic flatttening make it aharder to decrease intrahoracic pressure during inhalation and so work of breathing increases. Lung volume reduction surgery involves reducing lung volume via excision of emphysematous tissue. **Pulonary compliance i increased in COPD due to loss of alveolar and elastic tissue. In contrast, patients with restrictive lung disease have decreased lung compliance. COPD patients have significant airflow limiation with reduced inspiratory and exiratory flow rates. HOME OXYGEN COPD patients with Pa02<55 or Sa)2<88% are candidates for long-term home oxygen treatment. Patient with signs of pulmonary hypertension or hematocrit >55% should be started on home oxygen when the Pa02 <60 mmHg.

Remember that patients with acute, severe pain should recieve the same starndard of pain management regardless of drug addictino history. IV morphine is most appropriate treatment of acute, severe pain.

Physicians should nver undertreat pain, even if there is a risk for abuse. In case of concern for abuse, frequent reassessment, outpatient follow-up, and referall to a pain specialist is appropriate.

What is Nelson's snydrome

Pituitary enlargement( due to loss of feedback by adrenal glucocorticoids), hyperpigmentation, and visual field defect following bilateral adrenalectomy. Usually, these tumors are rapidly growing and can be treated with surgery and/or local radiation.

What vaccine for HIV infected patients?

Pneumococcal vaccine is recommended for all HIV-infected patients unless they were vaccinated wtihin the previous 5 years. It should be repeated once after 5 years. If the CD4 count is <200cells/microliters at the time of vaccination, patients should be revaccinated when the CD4 count is > 200/ul.

Chr

Po

Lab

Po

Most common cause of polyarticular septic arthritis. Most common cause of just a random septic arthritis

Polyarticular:Neisseria gonorrhea Random joint: Staph. aureus

Explain different things that can cause polycythemia. Also list chronic myeloproliefeative disorders.

Polycythemia by itself techincally is only a Hb level higher than 16.5 in a woman and 18.5 in a man. When you see this a good test to order is a serum erythropoietin. A low level suggests polythemia vera whereas a high one suggests a secondary cause, like chronic hypoxia (this very common, secondary to pulmonary or cardiac disease) or hormon causing neoplasm (commonly renal cell carcinoma) Chronic hypoxia is most common cause. Consider getting carboxyhemoglobin levels in patients who smoke, as carbon monoxide toxicity can happen. Sleep apnea is another common cause. Plasma volume loss can cause polycythemia, so things like diarrhea, vomiting, diuretic use, and poor oral intake Pulmonary hypertension and polycythemia are conditions that commonly co-exist. AV shunting can cause polychtemia. Pulmonary conditionsthat cause hypercarbia, like COPD often cause polycythemia. CHRONIC MYELOPROLIFERAIVE DISORDERS Polycythemia vera: often intense itching after shower, increase in ALL THREE blood lines (wbc, rbc, plateltes), rare but classic symptoms is severe buring pain and reddis or blush coloration due to episodic blood clots in vessels. *Levels of erythropoietin may be useful in distinguishing PCV, in whic levels are LOW, from other causes of polycythemia. JAD2 mutations tests often confirm the diagnosis. Essential thrombocytosis: overpdoruction of abnromal plateltes--> bleeding, thrombosis. Bone marrow contains enlarged megakarycotyes. Myelofibrosis: Bone marrow gets fibrotic obliteration. TEARDROP RBCs. Spleen gets hugh b/c or extramedullary hematopoesis.

Person has RUQ and just had cholecystectomy but pain is sitll there?

Postcholecystectoy sydnrome Spincter of Oddi dysfunciton, common bile duct stones, or functional etiology (diagnosies of exclusion) Sphincter of Oddi dysfunction is characterized by RUQ pain, elveation of liber enzyems during pain attack which resolve when attacks subside. -elevated biliary spincter pressure highly specific for it -ERcp with a spincterotomy is the treatment of choice **Another postcholecystectomy thing that can happen is bile salt-induced diarrhea, occurs in 5-10% of patients following cholecystectomy and in patients with short bowel syndrome. Treatment of choice is bile salt-binding resins such as cholestyramine. **Another postcholecystectomy things is that they do NOT need to change their dietary habits. Half of them may have transiet and mild episodes of diarrhea, flatulence or bloating that will be self-limited.

Guy has jaundice after a surgery that needed blood trasnfused?

Postoperative cholestasis, a benign condition that often develops after a major surgery characterized by.. 1. hypotension 2. Extensive blood loss 3. Massive blood replacement the jaundic is caused by.. a. increased pigment load (from transfuision) b. decreased liver functionality (caused by hypotension) c. decreased renal bilirubin excretion (caused by tubular necrosis) You will prob see high bilrubin levels, alk pohsop can be elevated, AST and ALT are mostly normal or mildy elevated

Post-op urinary retention

Potential compliation of surgery and anesthesia . A preciipitating event (general or epidural anesthesia) can lead to inefficient detrusor muscle activity and acute urinary retention. Bladder distension may also be caused by rapid IV fluid boluses and blood transfusion in hypotensive patients. Patients should void 2-3 hours after surgery. If not voiding, likely bladder is over-distended and now cannot void spontanesously. Post-op oliguria/anuria requires bladder scan to assess bladder volume. Patients with significant urine retention require urinary catheterization to restore normal urine output and resolve or prevent hydronephrosis, tubular atrophy, and renal injury. If a large amount of urine is drained from the bladder, the catheter may be kept in place for one day, followed by voiding trials.

What is refeeding syndrome?

Potentially fatal complication of nutritional rehabilitation in anorexia nervosa. Happens as a result from surge in insulin activity as body resumes anabolism. Carb intake stimulates insulin acivity, which in turn promotes cellular uptake of phosphorus, potassium, and magnesium. Clincial manifestations inculde arrhythmias and cardiopulmonary failure, seizures, and Wernickes encephalopathy. So aggressive initiation of nutrition without adequate electorly repletion can lead to problems.

Describe viral myocarditis

Potentially lethal inflammatory disorder of myocardium. Causes of myocarditis in general are infections, toxins, and automimmune. For viral pathogens, Coxsackie B and Adenovirus are the main pathogens. Patho: Direct viral injury and autoimmune inflammatio that leads to mycocyte necrosis with subsequent impariment of systolic and diastoli funciton. Presentation: usually you have a URI then followed by worsening RESPIRATOYY DISTRESS (tachypnea, dyspenea, wheezing, and/or crackles ) from Left Heart Failure and pulmonary Edema. You can gaet a holosystolic murmur due to dilated cardiomyopathy and resulting mitral regurg and heaptomegaly can results from Right heart failure. Acute Rheumatic fever can cause myocarditis (usually 2-4 weeks after untreated or badly treated Group A strept pharyngitis) but remember that no comon under age of 3 cuz these kids have fewer epithelial cell attachment sites in throat.

Heparin action. Indications for use

Potentiates action of antithrombin to inchit clotting factors 2a and 10a . So it prolongs PTT. 1. DVT, PE 2. ACS: unstable angina, MI 3. Low dose heparain or LMWH for DVT prophylaxis 4. A-fib in acute setting 5. After vascular bypass grafting

Complications of untreated severe acute/chronic sinusiis

Pre septal or orbital cellultilsi Cerebral abscess Meningitis Dural sinus venous thombosis. **cavernous sinus thrombosis can sometimes be difficult to distinguish from orbital cellulitis. Headache is a common and early symptoms and can become unberagle. Fundoscopy typically reveals papillee

Explain urinary sodium in setting of pre-renal and intrinsic

Pre-renal: low urine sodium and high urine osmolarity. FeNa<1%, best indicator. Intrinsic: FeNa>2% because kidneyrs are unable to concentrate urine. high urine sodium and low urine osmolarity.

Stages of Change Model

Precontemplation, contemplation, preparation, action, maintenance, addressing relapse or relapse prevention

Most common cause of a stent thrombosis after getting a stent put in post-MI ?

Premature discontinuation of DUAL antiplatelet therapy (aspirin and clopidogrel)

Conditions where one may have increased BUN/creatinine ratio

Prerenal renal failure GI bleed-cuz bacterial breakdwon of hemoglobin in GI tract results in urea absorption Steroid administration-elevates BUN without increase in creatinine

Causes of hearing loss in elderly population

Presbycusis: age related sensorineural hearing loss usually associated with both selective high-frequency loss and difficulty with speech discrimination. Most common form of hearing loss in elderly. Diagnosis of exclusion. Decreases ability to discriminate speech in a noisy, distracting environemnet is especially obvious in presbycussi. **One of the most frequent causes of social withdrawal and isolation in the elderly. It must be differentiated from depression and dementia. Screening can be accomplished through simple hearing tests in the office. Speech discrimination score may be normal in these patients, however, introducing background noise can reveal the hearing loss. Noise-induced hearing loss:essentially a wear and tear phenomenon that can occur with either industrial or recreational noise exposure. Typically presents with tinnitus, difficulty with speech discrimination, and problems hearing background. Cerumen impactation: external auditory canal is common, may produce a transient, mild conductive hearing loss. Otosclerosis: an AD disorder of bones of inner ear. Onset most commonly in late twenties to early forties. Central auditory processing (CAPD): general term for conditions involving hearing impairment that results from CNS dysfunction. Patient with CAPD will have difficulty understanding spoken language, but may be able to hear sounds well.

Pulseless electrical activity (PEA)

Presence of an organized electrocardiographic rhythm without succicient CO to produce a palpable pulse or measurable blood pressure. Immedicate chest compressions should be started. Defib or cardioversion are not a component of PEA management.

Acute limb ischemia dx? tx?

Present with "five Ps": pain, pulselessness, parasthesia, poikilothermia (coldness) and paollor. Angiogram will typically show an abrupt cutoff of arterial blood flow. IV heparin should be started immediately upon suspicion. The definitive treatment is surgical embolectomy or intra-arterial fibrinolysis/mechanical embolectomy. A bit more stuff to know... acute limb ischemia from arterial occulsion is typiaclly caused by cardaic emboli, thrombosis (vasc stens, hypercoagulable states) or trauma. Majore sources of cardiac sources of arterial emboli include 1. LV thrombus 2. Thrombus (usually left atria) formation due to atrial fibrillation 3. Aoritc atheroscleoris. *ppl who just had a STEMI are at highestes risk of LV thrombus..so if u think this is goin on you wnat to immediately anticoagulate, get vasc surgery, and make sure to get a TTE FOR LV THROMBUS to screen for thrombus.

Hyperthryoid causes and complications

Presentations: warm most skin, tachycardia o A-fib, fine TREMOR, LID LAG, hyperactive refelexes. Only graves has exophalmos, pretibial myxedema and thyroid bruits. -Untreated hyperthyroid patients are at risk for RAPID BONE LOSS loss resulting from increased osteoclastic activity in the bone cells. -Untreated hyperthyroid partiens are also at risk for CARDIAC tachyarrhythmias, including atrial fibrillation. TOXIC MULTINODULAR GOITER r: you have patches of hyperfuncitoning follicular cells making a lot of T3 and T4 independent of TSh due to a mutation in TSH receptor. GRAVES : Autonantiboides stimulate TSh receptors. Tx: radioactive iodine therapy. Contraindications to this are pregnancy and very sever opthalmopathy. Surgery also optoin. Radioactive iodine therapy is associated with potential development or worsening of opthalmopathy initially. -Antithyroid drugs are used primarily in the treatment of hyperthyroidism during pregnancy and in preparation for surgery or radioactive iodine therapy. iN management, propranolol is generally used for sympnotomaiic releif until the underlying cause is identifited and definitively treated. HIGH YIELD FOR USMLE ***most serious side effect for anti-thyroid drugs is agranulocytosis. If you see sore throat and fever be sure to check white cout -also remember that Graves' opthalmopathy is NOT due to increased thryoid hormones but due to the SAME anti-TSh recepter autoantibodies acing on the orbital fibroblasts resulting in increased volume of retro-orbital tissues THYROID STORM : infection, surgery or trauma induces catehcolamine surge seen as serious coplication of Graves and other hyperthryoid disorders. So its usually triggered by a single EVENT. 3P treatment: Propanlol, Propylthiouracil, Prednisone. SUBACUTE THYROIDITIS: (de Querviains' thyroiditis) may have high ESR with significant thyroid TENDNERESS. Due to release of preformed thyroid hormone from the inflamed gland. Lasts < 8weeks. RAI percent uptake is low. Tx: is NSAIDS for pain relief, BBs for symptoms, self-limited. POSTPARTUM or SILENT SPORADIC THYROIDITIS: autoimmune conditions with significnantly lower titers of antibodies than Hashimotos' thyroidisit. Alos its preformed thyroid hormone thats release. Lasts < 8 weeks. RAI percent uptake is low. TSH-SECRETING PITUITAARY ADENOMAS: Present with hyperthyrodism and are due to INCREASED ALPHA SUB UNITS. Have normal or elevated TSH, elevated T3 and T4. IODINE-INDUCED THYROTOXICOSIS:occurs in mainly patients with nodular goiter, wehree excess iodine can serve as a subtrate for excessive thyroid hormone formation. Can happen secondary to iodine administration during coronary angiography (so if symptoms happen few weeks after coronary angiography, this this). EXOGENOUS HYPERTHYYROIDISM: should be suspected in patients who have non-enlarged thyroid glands and admit to taking dietary supplements which may contain thyroid hormone. The 24 hour radioiodine uptake (RAIU) should be low cuz thyroid gland is making lower level of thyroid hormone as a response. They thyroglobulin should also be low since there is no inflammation or destruction of native thyroid gland, helping to distinguish this problem from thyroiditis. *high RAIU, high serium thyroglublin: Graves *low RAIU, high thyroglublin: struma ovarii and various causes of thyroiditis like postpartum thyroiditis an dDeQuervian's thyroiditis. *normal RAIU, high serum thyroglobulin: thyroid cancer *high RAIU, low thyrogluclin: toxic adenoma and toxic multinodular goiter where there are nodules of autonomosuly hyperfunctioning thyroid tissue. *low RAIU, low thyroglobulin **sublinical thyrotoxicosis: low TSH with normal T4 and T3. common causes are graves, levothyroxine treatment, nodular thryoid disease, thyrodidits. if no symptoms, just re-check in 6-8 weeks cuz high chance of TSH normalizing. **apathetic thyrotoxicosis: atypical presentation of hyperthyroidism in older patients characterized by lethargy, confustion, and depression. Often misdiangosed as dementia. REMEMBER with TX: -PROPANOLOL is used for initial symptoamatic relief until underlying cause is identified and definitliey treated. -PTU inhibits hormone synthesis and also conversion of T4 to T3, but in most cases, hyperthyroidsism comes back within 6 months. So PTU generally only used when radioactive iodine is contraindicaated, like in pregnancy. -Methimazole:inhibits peroxidase only, has fewer side effect than propythioruracil and results in quicker ahcievement of the euthyroid state in patients with hyperthyroidism

Atrial Myxoma

Presents with signs and symptoms of mitral valve obstruction (diastolic murmur and "tumor plop"), heart failure rapidly worsening in otherwise healthy young ppl, and new-onset A-fib. Myxomas frequently embolize systemically, leading to acute arterial occlusion in otherwise healthy patients.

Presence of aura in seizure?

Presnnce of an aura always indicted a focal onset of the seizure. PHysiologically, an aura is simply the earliest conscious manifestation of a seizure and corresponds with area of brain involved.

You see symmetric duskiness and coolness of ALL fingertips and patient is on vasopressors?

Pressors such as norepinephrine can cause ischemia of distal finger and toes secondary to vasospasm. Norepi has alpha 1 agonist properties which can cause vasoconstriction, uself when trying to incresae blood pressure of hypotensive patients. But in some patients with decreased blood flow, vasoconstriciton can result in ischemia and necrosis of distal fingers and toes.

Evaluation of chest pain algorithm

Pretest probability of CAD Exercise ECG sress testing is prefererd initial testing modality for diagnosis and risk stratification in most patients with no contraindications (severe hypertension), normal baseline ECG, and ability to achieve adequate workload during exercise. PHarmacologic stress test: use adenosine or regadenoson as vasodilator. this is done as an alternate to exercise ECG who are unable to achieve adequate workload during exercise due to osteoarthritis or peripiheral vascular disease. **remembe Adenosine is CONTRAindiated in a patient with asthma or history of BRONCHOspasm.

Sodium bicarb uses

Prevenitng arrhythimas with TCA overdose: it increases serum ph and extracellular sodium. The increased ph modifies TCAs to their neutral (non-ionized) form, making them less available to bind to the rapid sodium channels. Salicylate toxicity: alkalinizes urine which enhances salicylate excretion by kidney. Correcting severe lactic acidosis with severe acidemia (ph <7.1) and serum bicarb <6). Adjunctive therapy for treating significant hyperkalemia or rapidly increasing potassium w/ECG changes.

Dec

Pri

Common causes of priapism

Priapism is persitent, painful erections that develops without secual stimulation and has long duration. Begins as a nonischemic state and progresses to veno-occlusion, acidosis, anoxia and finally ischemia. Common causes, remember them. 1. Sickle cell disease and leukemia-usually in children or adolescents 2. Perineal or genital trauma-results in laceration of the cavernous artery 3. Neurogenic lesions-susuch as spinal cord injury, cauda equina compression etc 4. Medications-such as trazodone and prazosin. Tx: Should be treated first conservativley (ice pack application), if that fail then injection of alpha-adrenergic agonist such as phenylephrine or epinephrine every 5 minutes until detumescence is achieved. this should be done within first several hours to prevent long-term damage.

Anti-mitochondrial antibodies?

Primary biliary cirrhosis

Primary care: Primary care headache

Primary headache syndrome: tension, cluster, migraines Secondary causes of headache "VOMIT" -Vascular: subarachnoid hemorrhage, subdural hematoma, epidural hematoma, intraparenchymal hemorrhage, temporal arteritis -Other causes: malignant HTN, pseudomotor cerebri, postlumbar puncture, pheochromocytoma -Medication/drug related: nitrates, alchohl withdrawal, chronic analgesic use/abuse -Infection: meningitis, encephalitis, cerebral abscess, sinusitis, herpez zoster, fever -Tumor

Causes of hypercalcemia

Primary hyperparathryoidism is most common cause in outpatient Malignany is most comon cause in inpatient -hypercalcemia of malignancy have cerum calcium levels gnerally much higher (>13) than those with primary hyperparathyroidism CHIMPANZEES Calcium supplementation Hyperparathrydoisism/Hyperthyroidism Immobility/Iatrogenic: excessive bone resorption after immobilization leads to hypercalcemia. This is usually seen in patients with a very high bone turnover (adolescent patients and older patients with Paget's disease) Metastasis Paget's disease Addison's/Acromegaly Neoplasm Zollinger-Ellison Excessive Vit A Excessive Vit D Sarcoidosis -----sarcoidosis causes hypercalcemia through increased production of 1-alpha-hydroxylase and can be treated with prednisone Clinical signs: CONSTIPATION (due to altered intestinal smooth muscle tone), anoreaxia, vomiting, weakness, POLYURIA, and CONFUSION First thing you wanna do with elevated corrected calcium levels that is confirmed with repeat testing is...measure pTH levels to know whether this is PTH independent or dependent. If High to normal (PTH dependent)..think primary or tertiary hyperparathyoidism, familial hypercalcemic hypocalciuria, lithium induced **Primary hyperthryoid etiologies are mostly adenomas. These are also where MEN 1 and 2a come in. Treatment is parathyroidectomy for symptomatic patients or selected asymptomatic patients. If PTH is suprressed (PTH independent) , then measure PTHrP and Vit D. Long list of potential causes. *most commonly malignancy, Vit D toxicity, or granulmoatous disease (sarcoid). alos interesting that immobilization can cause hypercalcemia due to high bone turnover whereas rhabdo leads to hypocalcemia due to phosphorous binding to calcium in blood initially but hypercalcemia can occur in he diuretic/recovery phase of illness. *Hyperparathryoidism is also associated with certain well-described cardiovascular effects, including increased prevalence of hypertension, left ventricular hypertrophy, and calcifications of th emyocardium and mitral and aortic valves. **Various things all contribute to the hypercalemia seen in malignancy..cancer cells make PTHrP production, they can make more 1,25 Vit D, they can be bone lytic when metastasize, and make PTH as well. But by far, 80% of malignancy-induced hypercalemia, its the PTHrP production that contributes to most of it.

Polyuria and low urine osmolality. What is Ddx and how to do differentiate?

Primary polydipsia -serum Na<137 Central DI -serum Na may be >150 due to significant thirst impairment Nephrogenic DI -serum Na 142-150 due to intact thirst mechanism

Pneumothorax etiologies, signs, tx

Primary spontaneous: Male smokers, tall for weight patients Secondary spontanous: COPD (chronic desturction of alveolar sacs lead to formation ofdilated alveolar blebs that rupture air into the pleural space) , CF, Pneumonia, Cancer Signs and symptoms: chest pain, dyspnea, hyperresonance on affected side, decreased breath sounds on affected side, tracheal devation away from affected side (tension pneumothroax) Tx: 100% oxygen, if >20% of lung volume do thoracostomy to remove air

Trea

Prol

What prophylaxis and vaccinations should renal transplant person have?

Prophylaxis: Oral TMP/SMX for PCP prophy Vaccines: patietns should be vaccinated against influenza, pneumococcus, and Hep B and Hep A (if they don't have documented immunity)

UA-protein?

Proteinuria indicates glomerualr dysfunciton Protein loss in urine of >3g/day is nephritis syndrome Proteinuria is significant beginning at levels 500-1000mg.

Nephrotic stuff

Proteinuria> 3 gday Triad of proteinuria, hyperlipidemia, and peripheral edema (loss of albumin causes edema) -also hyperocagulability due to loss of proteins C adn S and antithrombin III renal vein thrombosis is an important complication of nephrotic syndrome due to hypercoagulability, memnbranous glomerulonephritis is most common cause CLINICAL ASSOCIATIONS Focal segmental glomeruloscelrosis : Black, hispanic, HIV and heroin use Membranous: Adenocarinconoma, NSAIDS, hep B, SLE Membranoproliferative glomerulonephritis: HEp B & C, -type 2 caused by persistent activation of alternative complement pathway Minimal change: NSAIDS, lymphoma IgA nephrophathy: Upper respiratory tract infection

Alkaline urine suggest infection of what?/

Proteus or Ureaplasma

What are the 5 common side effects of Amiodarone?

Pulmonary toxicity: Pulmonary fibrosis. *chronic interstitial pneumonitis is the most common presentation of amiodarone-induced toxicity. It is characterized by presence of nonproductive cough, fever, pleuritic chest pain, weight loss, dyspneia on excerion and a focal or diffuse intersitial opacity on x-ray. Usually seen after months to years of amiodarone therapy. Tx: discontinue of amiodarone. steroids can be used in patients with severe or life threatening disease. Thryoid dysfunction: mostly hypothyroidism. improves with time, no treatment is necessary. Hepatoxicity Corneal deposits Skin change: blue-gray skin discoloration, typicaly most prominent on face

Empyema?

Purulent infection in the pleural space; may be associated with chest pain, dyspnea, or fever; usually senn in conjunction with bacterial pneumonia or pulmonary abscess

Chr

R

Explain waht the RAAS system does

RAAS activation leads to increased angiotensin II. Angiotensin causes numerous things including the following... 1. Vasoconstciotionc of both the afferent and efferent glomerulat arterioles, leading to an increase in renal vascular reistance and aa ned DECREASE in RENAL BLOOD FLOW. 2. PREFERENATIONL VASOCONSTRTION OF EFFERENT RENAL ARTERIOLES, which increases intraglomerular PRESSURE in an attempt to maintain adequate GFR. 3. Direct sitimulation of sodium resoprtion in the proximal tbuules and increased secretion of aldosterone from adrenal galnds, which in turn promotes further sodium resorption in the collecting duct. These actions lead to DECREASED SODIUM DELIVERY to the distal tubule and an increase in extracellular fluid volume.

Radiation induced cardiotoxicity vs Anthracylcine (chemo) cardiotoxicity

RADIATION INDUCED CARDIOTOXICITY -long term survivors of cancer who got radiation are and risk for this. Radiation therapy causes fibrosis in the myocardium along with the pericardial layers, conducting cells, and cusps of the valves. ALSO it causes injury to the artererial intimal layer of the coronary vessels. This leads to... 1. MI!! 2. restrictive cariomyopathy with DIASTOLIC DYSFUNCTION 3. Constrictive pericarditis 4. Valvular abnormalities 5. Conduction defects (sick sinus, heart blocks) ANTHRACYCLINE -leads to DILATED CARDIOMYOPATHY -NOT associated with valvular disease or coronary artery disease.

UA-casts

RBC casts-glomerularnephritis WBC casts-pyelonephritis OR interstitial nephritis Muddy brown casts: ATN Broad and waxy casts: Chronic renal failure Fatty casts: nephrotic Hyaline casts: pre-renal azotemia *extremely high yield question for USMLE

Main toxicities of cyclosporine, tacrolimus, azathioprine, mycophenolate

REally high yield for USMLE Cyclosporine-increases uric acid serum levels by decreasing urate excretion from kidneys so increased risk for gout, nephrotoxicity, hyperkalemia, gum hypertrophy, hirsutism, tremor Tacrolimus-same thing as cyclosporine, excet no gum hypertrophy or hirsutism. Azathioprine- dose-related diarrhea, leukopenia, hepatotoxicity Mycophenolate-bone Marrow suprresion

Primary care: dyspepsia

REfers to a spectrum of epigastric symptoms, including heartburn, indigesttion, bloating, and epigastric pain/discomfort PUD, GERD, nonulcer dyspepsia (functional dyspespia), gastritis are big causes PUD; two most common causes are NSAIDs and H. pylori. Functional dyspepsia: defined as chronic or recurrent discomfort in the epigastrium with no organic cause determined. Upper endoscopy is necessary to rule out organic causes, and only after this is performed can the diagnosis of functional dyspepsia be distinguished from organic dyspepsia (dyspepsia caused by PUD, reflux, malignancy) endoscopy if test of choice for evaulation but it should NOT be routinely performed in all patients, only in certain situations like alarming symoptoms, vomiting , not responding to the empiric therapy of H2 blocker, PPIs, antacids, systemic ilness. Another test you wanna do is test for H. pylori.

Explain gallbladder carcinoma

Rare malignancy that most often arises in Hispanic and Southwestern Native American females who have a history of gallstones. Typically diagnosed during or after cholecystectomy due to the vauge and nonspecific symptoms (pain, vomiting, anorexia).

Chronic A-fib

Rate control with Beta blocker or calcium channel blocer Antioagulation: patiens with Afib in absence of other heart disease or risk factors and UNDER AGE 60 do not require anticoagulation because they low risk -treat all other patiends with chronic anticoagulation

Upper loabe infiltrate with cavities on chest x-ray is likely what?

Reactivation TB

Suspect HUS in a child with what symptoms?

Recently recovered from diarrheal illness, presnts with acute renal failure, hemolytic anemia, fever, thrombocytopenia and characteristc peripheral smear finding of schistocytes, helmet cells. EXTREMELY HIGH YIELD FOR USMLE. Associated with E.coli O157:H&, Shigella, and Salmonella. Looks like management IS NOTantibiotics but supportive with monitroning of renal and hematoloic parameters. *Routine stool cultures only test for salmonella, shigella, and campylobacter. Therefore, in patients with bloody diarrhea, stool should also be sent specifically for E.coli O157:H& testing . But the diagnosis is based on presence of microangiopathic hemolytic anemia and thrombocytopenia.

When do you screen for diabetes and what tests are there?

Recommended in patients.. ..w/ BP >135/80 ..considered in patients over 45 ..also with those with risk factors for diabetes Options include fasting plasma glucose, 2-hour oral glucose tolerance test, HgB A1c Type II diabetes is diagnosed when fasting plasma glucos i>126, random plsasma glucose is >200, or after 2 hour glucose tolerance test the glucose is > 200, or A1C 6.5% or greater *Prediabetes -Impaired fasting glucose (IFG): defined as fasting plasma glucose in range of 100-125 -Impaired glucose tolerance (IGT): fasting plasma glucase of 140-199 -Diet and exercise is the best way to treat this. Maybe Metformin can be used in patients with IFG or IGT who are in a higher risk group.

Recurrent bacterial infections in adule?

Recurrent bacterial infections in adule point to humoral immunity problem. Recurrent fungal and viral i think its a T cell problem.

Why are ACE inhibitors so good for diabetics?

Reduces blood pressure as well as the direct effect on reducing intraglomerular pressure which helps slow down the progression of renal damage.

Atrioventricular nodal reentry tachycardia cause origin?

Reentrant circuit formed by 2 separate conducting pathways within the AV node.

In primary care setting, remember to refer diabetic to who annually?

Refer all diabetic patients to an opthalmologist for annual funduscopic examination

Stess ulcers?

Refers to acute gastric or duodenal erosive lesions that occur following shock, sepsis, major surgery, trauma or burns. Are superficial and multiple sites. Unlike chronic benign gastric ulcers, which are generally lesser curvature and antrum, acute erosive lesions usually invovle the body and fundus and spare the antrum. These people do not have increased gastric secrtion but rather have decreased splanchnic blood flow. So ischemic damage to the mucosa may play a role.

Primary Care: Fatigue

Refes to lack of energy or a sense of being tired. Not muscular weakness. Not directly related to exertion. DDx: depression (most common), anxiety, endocrine problems, hematologic/oncologic, metabolic, infectious, cardiopulmonary (OSA, CHF), medications, other-chronic fatigue syndrome, fibromyalgia, sleep disturbances Lab studies in fatigue workup: CBC (anemia) TSH (hypthyroidism) Fasting glucose (diabetes mellitus) BMP (electrolyte abnormalities) UA, BUN/creatinine (renal disease) LFT (liver disease) Chronic fatigue syndrome: profound fatigue for longer than 6 months that not due to medical or psychiatric disorder. cuase is unknown. diagnosis of exclustion. depression is common in patients with CFS. -criteria: fatigue not alleviated by rest, not due to exerction, unexplained cause, significantly affects quality of lie. -4 or more of following symptoms for at least 6 months: memory problems, muscle pain, sore throat, tender lymph nodes, unrefreshing sleep, join pain, headaches, postexertional malaise for longer than 24 hours.

Mi complications timeline

Reinfarction (hours-2 days) Ventricular septal rupture (hours -1 week) --presents with sudden onset hypotension, CHF (right heart failure), and loud holosystolic murmur Free wall rupture (hours - 2 weeks). ----------Present with acute chest pain and shock with rapid progression to to pulselessness and death. Postinfarction angina (hours-1 month) Papillary muscle rupture (2 days-1 week) Pericarditis (1 day - 3 months) Left ventricular aneurysm (5 days-3 months)

Distended neck veins, cirrhosis, ascites

Remember to keep in mind constrictive pericarditis. Can present similar to liver problems Basically can presnt 2 ways: with volume overload signs or through decreased cardiac output signs

Hepatorenal syndrome

Renal failure in ppl with advanced liver disease. Due to systemic hypoperfusion of renal system. This is thought to be secondary to generation of NO in splanchnic circulation due to portal hypertenion---> systemic vasodilation---> hypoperfusion of kidneys Characterized by renal failure that does NOT respond to volume resuscitation. Dx; Urine sodium < 10 mEq/L (very low) Hyponatremia . Should be considered a diagnosis of exclusion. A fluid bolus is needed to confirm that the renal failure is not due to intravascular volume depletion. Type 1: rapidly progressive, most patients die within 10 weeks Type 2: progresses more slowlsy, with average survival of 3-6 months. most common causes of death are infection and hemorrhage. Tx: none proven effective. ALbumin commonly infused but never has been proven effective. Liver transplanation is only intervention with established benefit. **a combination of midodrine and octreotide along with albumin seems to be preferred treatment of choice.

UA-crystals

Renal stones, ethylene glycol intoxication

What is porcelain gallbladder?

Results from chronic cholecysitis and its the intramural deposition of calcium salts that happens. Its usually diagnosed on abdominal imaging Associated with increased risk of gallbladder cancer so for this it requires surgical resection.

Heart failure stuff

Results from impaired or inadequate ventricular emptying (systolic dysfunction) or impaired ventricular relaxation (diastolic dysfunction). Most common cause of CHF is ischemic heart disease. Other known etiologies are hypertension (13%), valvular disease (10-12%), renovascular disease and very rare causes like OSA myocarditis, alcohol, cocaine abuse. etc. When trying to identify etiology of CHF, do cardiac stress test (as ischemic heart disease is most common), objective here is to quickly identify presence of ischemia to address the need for coronary angiography (for possible revascularization). Dx based on 2 major criteria and 2 minor. provided the minor can't be explained by other illness. MAJOR: paraoxysmal nocturnal dyspnea, orthopnea, raised JVP, pulmonary rales, presence of third heart sound, increased cardiac silhouette, pulmonary vasc congestion on x-ray. MINOR: b/l lower extremity edema, nocturnal cough, dyspnea on exertion, tachycardia, presence of pleural effusion, hepatomegaly. Chest x-ray findings of CHF: cardiomegaly. pulmonary vascular congestion (espeically upper lobes), Kerley B lines, bilateral pleural effusions. This stuff will help differentiate it from dyspnea secondary to primary pulmonary pathology. CHF medications that have actuallhy been shows to improve mortaility? What lab value is an independent predictor of adverse clinical outcomes? ACE inhibitors Beta blockers ARBs Spironolactone **Hyponatremia in patients with CHF parallels the severity of heart failure and is an independent predictor of adverse clinical outcomes . It is cased by increased levels of renin, norepinephrine, and ADH. Free water is retained and leads to DILUTIONAL HYPONATREMIA. Angiotensin II and presence of low CO also stimulate thirds, leading to increased water intake and worsening hyponatremia. WATER INTAKE RESTRICTION is the mainstay of therapy for CHF hyponatremia patients. -Correction of hyponatremia does not improve outcomes and is only indicated in patients who develop symptoms 2/2 hyponatremia or have severe asymptomatic hyponatremia (<120). If water restriction doesn't work, try vasopressin receptor antagonists like Tolvaptan to raise the serum sodium above 120. Cardiac resynchronization therapy with biventricular pacing recommended for whao? *Patients in sinus rhythm with severe LV systolic dysfunction and -EF <35% and -NYHA class 2, 3, or 4 heart failure symptoms and - LBBB (with QRS >150 msec). Criterion for implantable cardioverter-defibrillation (ICD) for prevention of sudden cardiac death in setting of heart failure? -Left ventricular ejection fraction less than 35%, regardless of the presence or absence of coronary disease or the occurrence of arrhythmia. **LV dysfunction (low EF) is a common problem. many ppl will have symptoms of heart failure but many will not, studies show that asymptomatic LV dysfunction (low EF) is at least as prevalent as symptomatic heart failure. Asymptomatic LV dysfucntion can come from prior MI (if absence of a regional WMA on echo then prior MI unlikely) but in ppl without a clear cause, need to evaluate futher cuz many will progress to symptomatic heart failure. -The MOST important med for patients with asymptomatic LV dysfuncion is an ACE inhib, which can delay the onset of symptomatmic heart failure. BB can also be added but data not as strong.

Incrreased aldosterone causes what to get excreted in urine?

Results in increased H+ and K+ losses in the urine and serum alkalosis. Contraction alkalsos occurs in state of volume contraction where increased aldosterone functions to restore intravascular volume but also causes more loss of urinary protons.

APproach to GI bleeding

Resusciation -IV access and tranfuse fluids and blood if needed -Evaluate for hypotension, tachycardia, orthostatis -Type and crossmatch, CBC, coag studies Determine source of bleeding-upper GI vs Lower GI -H&P, Rectal exam, Stool exam for melana/guaiac, Nasogasstric lavage looking for bright red blood or coffe grounds (this procedure r/o UGI bleed)

5Hs and 5Ts?

Reversible causes of asystole/pulseless electrical activity 5Hs Hypovolemia Hypoxia Hydrogen ions (acidosis) Hypo or hyperkalemia Hypothermia 5Ts Tension pneumothorax Tamponade, cardiac Toxins (narcotics, benzos) Thrombosis (pulmonary or cronoary) Trauma

Basophillic stippling?

Ribosomoal precipitaes which appear as blue granules dispersed through cytoplasm of RBC. Often seen with thalassemias, as well as lead or heavy metal poisoning.

A common complication of endotracheal intubation?

Right mainstem bronchus intubation buecause it diverges from the trachea at a relatively non-acute angle, so an ETT advanced too far will preferentially enter into the right main bronchus. This results in overinlfation of the right lung, underventilation of left lung and asymmetric chest expansion. Repositioning the endotracheal tube by pulling back slighlty will move the tip between the carina and vocal cords and solve the problem.

Bugs that cause UTI mnemonic?

SEEKS PP S. saprophyticus E. coli Enterobacter Kliebsiella Serratia Proteus Pseudomona (especially with GU instrumentaiton)

m

SHiP

SIRS, Sepsis, severe sepsisk, septic shock

SIRS (systemic inflammatory response syndrome): 2 or more of....high temp, tachycardia, high RR, high WBC Sepsis: SIRS and a nidus of infection Severe sepsis: Sepsis with evidence of organ hypoperfusion Tx: administer activated protein C; improved survival rates with people w/ APACHE score >25. Septic shock: severe sepsis w/ hypotension despite adequate fluid resuscitation requiring vasopressors to mainatin blood pressure Tx: most commonly used vasopressor is norepinephrine

Sustained monomorphic ventricular tachycardia?

SMVT. WIDE COMPLEX TACHY with 2 FUSION BEATS.

THe triad of back pain, muscle weakness, and loss of bowel or bladder control is suggestive of what? What do you do?

SPinal cord compression. You worry about metastases causing spinal cord compression. Give dexamethsaseone 10mg IVx1, followed by dexamethasone 4mg IV/PO q6 hours. This in addition to good neuro exam (for when you consult neurosurg), get STAT MRI back.

ECG info: ST depression? T wave inversion? poor R wave progression? QT interval prolongation? LBBB? RBBB?

ST depression >1mm: commonly caused by ischemia, "stratin", digitalis effect, and hyopkalemia or hypomangensemia. T wave inversion: commonly occurs in MI, angina, and ventricular hypertrophy. However, T wave inversion rarely indicates ischemia if the QRS is also negative in those leads. Poor R wave progression: occurs when R wave in leads V1 and V4 remains the same size or increases very little. Common pathologic causes of poor R wave progression include LVH, RVH, COPD, anterior infarction, conduction defects and cardiomyopathy. QT interval is considered prolonged if it measures more than half the R-R interval. Common caiuses are drugs (antiarrhtymic agents, TCAs,) electrolyte imabalances (hypokalemia), CNS catastrophes (stroke seizure). W pattern in V1-V2 and M pattern in V3-V is LBBB. V1: wiLLiaM V6. M pattern in V1-V2 and W in V3-V6 in RBBB. V1: MaRRow V6.

DIC menmonic

STOP Making New Thrombi Sepsis Trauma Obstetric stuff Pancreatitis Malignancy Nephrotic syndrome Transfusion Lab: schistocytes, Increased fibrin split products (D-dimer) .

Tibial stress fracture

STRESS or FATIGUE FRACTURE -complete fracture resulting from repetitive applicatin of minor trauma -most occur in lower extremities and in people involved in sports or military "march fracture" -2nd metatarsal is the one that is most commonly injured. -tibia is the most common bone in body to be affected. classicaly occurs in anterior part of the middle third of the tibia. patient usually develops medial tibial stress syndrome ("shin splints" with no tibial tenderness on palpation) which can progress with further activity to a complete or incomplete fracture, resulting in pain to palpation of the tibia. -x-ray likely to be NORMAL if seen within first 2 weeks of symptoms -pain with activity only. Tx: decrease physical activity. Comon in athletes and nonathletes who suddenly increase their physical activity. Clnicila features include pain, localized tenderness, swelling. Tibial stress fractures can be managed in most cases with pneumatic splinting, reduced weightbearing, and a graduated exercise program. Most patients may resume full-intensity exercise within 12 weeks, but the program may need to be delayed if the patient develops recurrent pain.

Celiac Disease

Screening for celiacs is performed by checking the anti-ENDOmysial antibody and anti-TISSUE transglutaminase antibody. Gold standard for diagnosis is SMALL intestinal biopsy. young patient with MULTI-NUTRIENT malabsorption, most likely explanatino is celiac disease. although classicaly associated with prominent GI symptoms like diarrhea, a substantial subset of patient develops malabsoprtion with minimal or no GI symptoms. **Important to remember that these people are at increased for developing T cell lymphomas.

How to screen for pheochromotcytoma? What should you remember NOT to do when treating pheochromocytooma?

Screening tool:PLASMA FREE METANEPHRINE levels or a 24 hour urine collectino for measurement of catecholamine and metanephrine CT or MRI is next step for localizing a pheo after biochemical confirmation of the tumor. Patients with negative abdominal imaging usually require futher testing, such as the metaiodobenzylguanidine scan. Removal of tumor is performed only after adequate preoperative blood pressure control for 10-14 days withalpha blocker, IV fluid repletion. BBs are only given to patients with adequate and complete alpha blockade. DO NOT give beta blocers without alph blockers. Blocking beta-receptors leads to unopposed stimulation of vascular alpha-receptors by circulating catecholamines, which may result in a rapid, catastrophic increase in blood pressure. Alsways give an alpha blocker first, followed by a beta blocker; doing this in the wrong order can lead to a dangerous increase in blood pressure. *this is also important to remember when treating cocaine toxicity it seems **intraopertaive hypotension in patients with pheo usually responds to IV bolus of NS. Only use IV bolus of phentolamine with severe hypERtension (not hypo) during surgery for pheochromocytoma.

What else can you see with RCC besides the triad of hematuria, flank pain, and palpable mass?

Scrotal varicoceles (left sides): it fails to empty when a patient is recumbent Also paraneoplastic-anemia or erythroctysos, fever, thrmobocytosis, hypercalemia, cachexia. REMEMBER THIS. CT scan of the abdomen is the best thing to do for diagnosing RCC

Management of slow-transit chronic constipation

Secondary causes: hypothyroidism, medications (TCAs or other med with anticholinergic affects, certain hypertensives (like verapamil) I think at some point early on you want to have a colonoscopy to exclude malignancy and structural disorders Psyllium: increase stool bulk, maintain stool water content, and soften the stool. This is why preferred initiallly.

UA-presence of eosinophils?

Seen in AIN

Positive Nikolsy's sign?

Seen in Stevens Johsnons Syndrome, Toxic Epidermal Necrosis, Pemphis vulgaris, staphylcoccal scalded skin sndrome

Define acute liver failure

Seevere liver injury with encephalopathy and INR <1.5 in a paitent without cirrrhosis or underlying liver disease. (cirrhoitic patients have decreased funcitonal liver tissue, as a result, severe hepatic injury may elevate the AST and ALT only midly) Acute liver failure most commonly due to drugs (acethominophen) and viral hepatitis (hep A). Also sepsis or isechmia ("shock liver"), automimmune hepatitisna nd malignant infiltration. Patients with rapidly progressing liver failure can have decreasing transaminases with WORSENING PT/INR and bilirubin.

Hyperphosphatemia

Serum >5 Renal failure , tumor lysis syndrome, iatrogenic (too much given) Tx: Calcium carbonate (binds phosphate in gut and decreases absorption),

How do you diagnose CHRONIC pancreatitis?

Serum amylase and lipse may be a bit elevated but are mostly normal as there is only patchy inflammation and fibrosis seen (unlike widespread inflammation in acute pancreatitis). So CT looking for PANCREAS CALCIFICATION is considered diagnostic. Its charactereized by recurrent bouts of upper abdominal pain, diarrhea/steatorhhea, and weight loss. Chronic pancreatitis causes? Recurrent episodes of acute pancreatitis, usually from alchohol abuse Dx: pancreatic calcifications on x-ray or Ct, diabetes and steatorrhea due to pancreatic insufficiency Person with chronic pancreatitis who develops abdominal pain and weightl loss? Concern for pancreatic cancer. Dx: US is useful to exclude biliary obstruction in patients with jaundice. In patients who don't have jaundice, do abdominal CT. so most ppl complain of abdomnal pain which is insidious, knaing, ansd WORSE AT NIGHT . But some patients don't have pain and jsut have PAINLESS JAUNDICE. Another CLASSIC ASSOCIATION is MIGHRATORY THROMBOPHLEBITIS (TROUSSEAU SIGN). **chronic pancreatitis can cause islet cell damage which can lead to PANCREATOGENIC DIABETES. many patients with mild hyperglycemia can be managed with metformin, but most wiill eventualy require insulin therapy.

Hypophosphatemia

Serum phosphate <2.5 Usually alchoholism or malnutrion the cause. *in chronic alchoholics that show up to hospital....despite total body phosphorus depletion, these patients may have normal serum phosphorus levels on admission to hospital. Severe hypophosphatemia often develops over the first 12 to 24 hours after admission, usually because of IV glucose administration, which stimulates insulin release and causes phosophate to shift into cells. The suddes development of hypophosphatemia may cause confusion, rhabdo, hemolytic anemia, and severe muscle wakness that can lead to respiratory failrue. Neuro symptoms and muscle weakness. Treat with phsophate supplementation ALSO: hypophosphatemia is not very recognized in hospitilized patients. Continous glucose infusions are the leading cause of hypophosphatemia in hospitilized patinets. Hypophasphetmia is a jor cause of RESPIRATORY muscle weakness and can lead to failure of being able to wean a patient off ventilator.

Serum sickness

Serum sickness-like reaction may occur on to two weeks after administartion of certain drugs, such as penicillin, amoxicillin, or cefaclor in the setting of viral inlness. Prominent symptoms include fever, urticarial rash, polyarthralgia, and lymphadenopathy. The condition derives its name from its similarities to true serum sickness, an immune-complex mediated by hypersensitivity reaction to non-human proteins. Serum-sickness like reaction is a clinical diagnosis and should resolve with withdrawal of the offending agent; it does not represent a true drug allergy.

Acute bacterial cholangitis presentation?

Severe jaundice, fever, RUQ pain, and leukocytosis.

Bloody stool infectious etiology mnemonic?

Shigella Salmonella E.coli, Entomoeba histolyca C. dif Campylo bact. Yersinia "SSECCY" (sexy)

What medications should be held before cardiac stress testing?

Should be held: beta blockers, Ca channel blockers, nitrates Should be continued: ACE inhibitors, ARBs, Digoxin, Statins, Diuretics.

How does Gastrinoma (Zollinger Ellison syndrome present?

Should be suspected in patients with multiple stomach ulcers and thickened gastric folds on endoscopy. Dx is strongly suggested by a FASTING SERUM GASTRIN LEVEL of >1000 pg/ml. Patiens with non-diagnositc serum gastrin levels should be evaluated with a secretin stimulation test. Most common cause of the condition is gastrin-producing pancreatic tumor. As result of uncontrolled gastrin secretion, parietal cell hyperplasia develops and STOMACH ACID production is significantly INCREASED. Multiple duodenal ulcers are typical and a jejunal ulcer is almost pathognomic fort this condition. STEATORRHEA may develop, because increased production of stomach acid inactivates pancreatin enzymes.

Toxoplasmosis treatemtn

Shows up as multiple ring enhancing lesions on CT. Administration of empirical sulfadiazine and pyrimethamine is both diagnostic and therapeutic.

GERD signs, dx, tx

Signs -substernal burning pain -dysphagia -hypersalivation, with SOUR tase in mouth -cough (particularly nocturnal), hoarseness -wheezing Dx; Often, you go first with a trial run of PPi and see if symptoms are relieved. But, if you have alarm signals for cancer...weight loss, advanced age, nausea, refractory symptoms, guaiaic positive, or dysphagia, vomiting, GI bleeding... a ENDOSCOPY to r/o cancer is required. --i think you should do a barium swallow before the endoscoy here but am not sure. I just know that when you're evaluation for esophageal cancer you do barium swallow followed by endoscopy. Tx: Phase 1: Lifestyle modicitaion: Elevate head of bed, discontinue foods that decreases LED tone, avoid food <3 hours before bed. Antacids Phase II: add H2 blocker Phase III: switch to PPI Phase IV: add a promotility agent like metoclopramide (dopamine blocker) Phase V: combination of medications Phase VI: surgery correction *surgery for those who have persistent or progressive disease despite maximal medical therapy or with structureally defective LES. Goald of surgery is to return normal sphincter length and function and return the physiologic swallowing function of the esophagus. Procedure of choice is a fundoplication-wrapping the fundus of the stomach around the distal portion of the esophagus to create a sphincter, called the Nissen procedure. PHarmocologic: H2 blocker, PPI Complications of GERD. Know. -Recurrent pneumonia due to pulmonary aspiration: cytologic apsirate findings on broncho that can dignose aspiration of gastric contents are LIPID LADEN MACROPHAGES (from phagocytosis of fat). -Esophagitis - Esophageal (peptic) stricture: dysphagia to solids -barret's esophagus; rmember, Barret's does NOT regress, even if GERD is successfully treated -esophageal cancer;: upper two thirds is isuallu squamos cel and lower one thir is usually adenocarcinoma

Admission vs discharge in asthma exacerbation

Signs and symptoms of imprending respiratory failure and status ashtmaticus should be recognzed early in asthma exacerbation. These patients should be intubated immediately to secure the airways. Inhaled beta agonists, inhaled ipratropium, IV glucocorticoids, and IV magnesium should also be given.

Simple renal cyst vs malignant renal cyst

Simple: Almost always benign, do not require further evaluation. Very common. Malignant: Multilocular mass, irregular walls, thickened septae, contrast enhancement **If clinical suspicion is low for malignancy, can do an ultrasound to differentiate simple renal cyst from a solid mass. If suspicion is high, go to CT scan. **Increase in hematocrit and hemoglobin support diagnosis of renal malignancy. So pts. with renal mass, plycythemia, flank pain, and h/o smoking are likely to have renal cell carcinoma. High Yield: Surgical management is the only chance of cure for patients with renal cell carcinoma. If the renal mass is confined within the renal capsule (stage 1), partial nephrectomy can be offered. If the process extends through the renal capsule but not beyond Gerota's fascia (stage II), radical nephrectomy is the best treatment option.

Common cutaneous signs of insulin resistance?

Skin Tags: skin tags are associated with obesity, insulin resistance, overt diabetes, and metabolic syndrome. Aconthosis nigricans Xanthelasma

CLL

Smudge cells on smear are characterisitc, Older patients. Staging system directly related to prognosis. 0 Lympcytosis only. Prognosis good 1 Lymphocytosis +adneopathy 2 Splenomegaly 3 Anemia 4 Thrombocytopenia Prognosis bad CLL is a B-cell disease

Perioperative medication management

Some meds should be continued through the perioperative period, cuz they are cardioprotective and reduce risk of cardiovascular event, or because disontinuation can cause withdrawwal. On the ohter hand, some meds carry increased risk and should be discontinued prior to surgery.

Rheumatoid arthritis

Spares DIP joint , unlike osteoarthritis. DIP=distal interphlanagleal joints Labs that may be abnormal: -positive anti-CCP antibodies (more specific than RF and also a positive anti-CCP may precede the clinical manifestation of disease by many years), -high IgM Rheum factor. BUT does not need to be positive, abscence of Rheum factor does NOT exclude diagnosis. About 20% of patients will have negative RF factor. -elevated ESR/CRP -anemia (she anemia of chronic disease kind). **Anti-TNF-alpha agents like infliximab improve ACD in these patients. -thrombocytosis -low albumin: level os hypoalbuminemia usually correlates with the severity of the disease Rheumatoid nodules (especially on elbows) Can cause cervical joint involvement can lead to spine subluxation--> spinal cord compression. are at INCREASED risk for osteoporosis and fractures. most ppl suggest a low threshold for starting bisphophonate therapy in these patients. RA is a clinical diagnosis. If have symptoms and has radiologic presentation but negative RF, still most likely diagnosis is RA. Tx algorithm: If using MTX and persistent symptoms for >6 months either "add anticytokine agent (TNF inhibitor) or add another non-biolic agent (sulfasalzine, hydroxychloroquine..if these are inadquate then go to anticytokine agent)--->if inadeuqate response still then switch to alternative TNF inhibitor and continue MTX NSAIdS Glucocorticoids DMARDS: methotrexate, sulfasalazine, ANticytokines: infliximab, etanercept Topical analgesics **if erosive joint disease seen on X-ray then that is clear cut indication to use DMARDs even if symptoms resolve with NSAIDs to slow progression of bony erosions. MTX is initial drug for this. **TNF inhibitors (etaternecpt and infliximab) are highly effective in patients who have refractory disease with methotrexate. They are clasified as biologic DMARDs as opposed to nonbiologic like MTX. Very expensive and are not indicated as first line drugs of treatment. PPD test is indicated before the treatment with TNF inhibitors.

Erysipelas

Specific ofrm of cellulitis. Lower extremeities are the most common sites of involvement. Lesion is usually characteristic: it is red, painful, edematous and elevated. A shapr demarcation from the univovled skin is isually present. Abrupt oncset and systemic symptoms (fever, chills, malaise, etc). Group A strept is typcailly etiologic agent.

Splenic sequestration crisis vs autosplenectomy in SCC?

Splenic sequestration: sudden pooling of blood into spleen results in rapid development of splenomegaly and hypovolemic shock. Repeated splenic infarctions--->autosplenectomy as the spleen is reduced to a small, calcified remnant.

Patient has cirrhosis and ascites. Then gets fever or change in mental status, what should you consider?

Spontaneous bacterial peritonitis and HE. SBP superimposed on cirrhosis can be a subtle presentation, require a low threshold of suspicion. Fever and suble changes in mental status are the most common signs, with abdonial pain often less prominent than in peritoniti of other etiologies. A diagnostic paracentesis is the test of choice for making the diagnoses, wich a positive ascites fluid culture and PMN level of greater than 250/mm3 being the main diagnostic criteria. The paracentesis should be done before antibiotic therapy is initiated because antibiotics often result in negative ascites cultures. You also wanna calculate the SAAG to make sure portal hypertension as the cause of ascites which makes SPB more likely. SAAG>orequal to 1.1 indicates portal hypertension as the cause. Enterics like E. coli and Klebsiella are the msot common culture organisms. They go from GI system to ascites fluid and cause infection.

Diabetic nephropathy tests to know.

Spot urine colection and timed urine colection for measurement of urine MICROALBUMIN TO CREATINE RATION are generally accepted as GOOD SCREENING methods for microalbuminuria. Although 24-hour urine colllection is slightly more acccurate in screening for microalbuminuria, its inconvenience to patients makes it less preferred by physicians. Development of nephropathy is preceded by development of escessive protein excretion, the initial states of which is termed micoalbuminuria. Patients with microalbuminuria typically have a urine albumin excretion value between 30-300mg/24hr. Normal urine protein is <30 mg/24hr. -during the initial pahses of diabetic nephoropathy, there if glomerular hyperfiltration and an increase in creatinine clearance. First year. - Creatinine clearance then declines with progression of diabetic nephropathy; however it can still be realtively normal with proteinuria (micro and macroalbuminuria) due to high initial values. First 5 years. - Low creatinine clearance occurs when the renal damage is fairly advanced. Due to these reasons, creatinine clearance is not used as a screening tool for diabetic nephropathy. 5-10 years. ---the glomerular hyperfiltration is the major mechanisms by which THICKENING OF THE GLOMERULAR BM happens. the effectiveenss of ACE inhibitors for diabetic nephropathy is related to their ability to reduce intraglmoerular hypertension and, therby, decrease glomerula damage. Dipstick testing can only detect excessive urinary protein when the level is >300mg/24hr (macroalbuminuria). Most beneifical theray to reduce progression of diabetic nephrophaty is strict blood pressure contorl. Patients with diabeteic mnephorpahty should be treated toward a target blood pressure of 130/80.

Sprain vs Strain

Sprain: A stretching or tearing injury of a ligament Strain: A stretching or tearing injury of a muscle or tendon

Explain esophageal cancer

Squamos cells (smoking and drinking) and adenocacrinoma (this one related to barrets esopagus) To diagnose: BARIUM SWALLOW FOLLOWED by ENDOSCOPY Surgery can be done that is curative if the metastasis present. If metastiss then go with chemo and radiation for palliative treatment becase disease usually not curable.

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Who gets packed RBCs?

Stable patients without significant comorbid conditions < 7 Hgb A higher threshold of HgB <9 is considered for patient with symptomatic anemia or ACS w/active ischemia.

Anginas

Stable: chronic, predictable, due to temporary myocardial ischemia. Resolves with rest or medicaiton. - Tx: Beta blocker (reduces myocardial oxygen demand), aspirin, nitroglycerin. Calcium blockers can be used in place of beta blockers if patient cant use beta blockers, or it can be added to beta blocker use if symptoms difficult to manage. -All patients with chronic stable angina should carry either a sublingual or a spray form of nitroglycerin for emergency use - Ranolazine should be only considered in patietns who remain symptomatic despite optimal dose of beta blockers, calcium channel blockers, and nitrates. Unstable angina: 1. new pain 2. anginal pain that accelerates or changes in pattern location or severity 3. anginal pain at rest Pizmental angina-angina due to vasospam, not linked to exertion. Chronic and intermittent. Can cause ST elevations. Tx: Calcium blockers and nitrates

You think someone has aortic dissection cuz of tearing chest pain and different blood pressures in each arm, what do you do?

Start IV beta blocker stat (to lower HR and reduce left ventricular contractility) *Nitroprusside should only used in addition o BBs if systolic blood pressure remains above 100-120 mm Hg after adequate blockade. Order CT angiogram to confirm aortic dissection. Type A dissections typically require surgery and medical therapy. Type B usually be managed with medical therapy.

Penicillin allergy alternatives

Strept throat: if pt. has penicillin allergy use erythromycin Syphillis: if pt. has peniicllin allegery and is nonpregnant use doxycycline for 14 days. If patient is pregnant then pt. should undergo penicillin densitization therapy before penicillin.

Most comon cause of pneumonia in nursing home patients

Streptococcus pneumoniae

Stress hyperglycemia

Stress hyperglycemia is defined as transiently elevated blood glucose levels in the context of severe illness in patients without known diabetes mellitus. During illness and stress, hyperglycemia can results from the release of high levels of stress hormone (cortisol, catecholamines, pro-inflammatory cytokines). Associated with increased morbidity in critically ill patients.

Key Lung Exam Findings

Stridor -Due to airway narrowing above the thoracic inlet. Usually heard with inspiration, but can be biphasic if obstruction is severe. Wheezing -Typically due to airway narrowing below the thoracic inlet. With mild airway obstruction, wheezing is usually heard only in expiration. With increasing obstruction, wheezing may become biphasic and may even disappear altogether when obstruction is severe. Although typically diffuse, focal wheeze may be heard in some settings such as mucus plugging. Wheezing can also be characterized as polyphonic or monophonic: Polyphonic wheeze is characterized by multiple pitches and is typical of asthma; monophonic wheeze is characterized by only a single pitch and is typical of focal airway obstruction. Rhonchi -Coarse, low-pitched rattling sounds heard best in expiration. Thought to be due to secretions and narrowing of airways. Crackles -Finer breath sounds heard on inspiration. Associated with either fluid in the alveoli or with opening and closing of stiff alveoli (as in interstitial disease). Sometimes described as either coarse or fine. (Coarse crackles are usually thought to be associated with purulent secretions in the alveoli as with pneumonia; fine crackles are often associated with pulmonary edema or interstitial lung disease. Air entry -The amount of air entry should be noted during every lung exam. Decreased air entry can be a sign of consolidation, atelectasis, pneumothorax, pleural effusion or airway obstruction. Bronchial breath sounds -Lower in pitch and more hollow-sounding than normal breath sounds. Caused by air moving through areas of consolidated lung.

Repetitive overhead motions might give you what?

Subacromial bursitis is the result of repetitive overhead motions. Patietns complain of pain with active range of motion of the shoulder, and passive internal rotation and forward flexion at the shoulder also elicitys tenderness.

You see rapidly developing hyperandrogenism with virilization, what do you think and do?

Suggestive of androgen secreting neoplasm of the ovary or adrenal. Order serum testosterone and DHEAS. -elevated testosterone with normal DHEAS indicate an ovarian source -elevated DHEAS with normal tesosterone indicated an adrenal source

A nonhealing, painless, bleeding skin ulcer that develops with a chronic scar?

Suggests squamos cell carcinoma

Sun screen guidelines?

Sunscreen with SUN PROECTION FACTOR 15-30 or HIGHER should be applied 15-30 MINUTES PRIOR TO SUN EXPOSURE to allow time for development of a protective film.

4 basic types of Melanoma

Superficial Spreading Melanoma -Most common type -raised borders and brown lesions with pinks, whites, grays, or blues Lentigo Maligna -Least common of four types. When found, its most often found in the eldely. -Tan to brown Acral Lentiginous Melanom -Most common type found in Africans Americans and Asians. Usually found under nails, soles of feet, palms of hand. Nodular Melanoma -Most agressive and 2nd most common type. -Brown to black lesions that arise from nevi or normla skin. *Melanoms less than 1mm thick have a low rate of metastasis *Microstaging of melanomas (prognostic indicator i think): Breslow method (more accurate than clark ethod) is based on depth of invasion:vertical height of melanoma from granular layer to the area of of deepest penetration. Tx: surgery is primary theerapy for patients with nodal involvement. margins are important. like you want a 1-2 cm margin for a lesion 1-2 cm in thickness. And 3 cm margin for legions >4 cm in thickness. no role for radiation therapy pre or post operatively for melanoma.

Only therapy proven to extend life for COPD?

Supplemenatal oxygen.

What do you do to treat ascending cholangitis?

Supportive care and broad-spectrum antibiotics. Patients who do not respond to this treatment regimen should undergo biliary drainage with endoscope: ERCP (endoscopic retrograde cholangiopancreatography). This is an emergency. Cholangitis is an infection of the common bile duct secondary to onstruction of CBD by sotne or stricure or tumor. You see Charcot's triad of fever, severe jaundice, and RUQ. REynolds pentad is wosre prognoisis= Charcot's triad + shock + altered mental status Biliary system becomes superinfected and without drainage the patient becomes septic and may die without immediate intervention. So biliary drainage is necessary. *Biliary injuries from laparascopic cholecystectomy can present with either biliary leak or obstruction.

Alcoholic smoker presents with palpable cerviceal lymph node?

Suspect squamos cell carcinoma of the mucosa of the head and neck. Best initial test is pandendoscopy (triple endoscopy=esophagoscopy, bronchoscopy, laryngoscopy) You should also keep in mind breat cancer and if the lymph node bioopsy shows metastatic adenocarcinoma then breast cancer should be considered.

V-tach

Sustained vs nonsustained Vtach Sustained: LASTS LONGER THAN 30 SECONDS and iS ALWAYS SYMPTOMATIC , life threatening and can progress to Vfib if untreated Non-sustanied: brief self limited runs of Vtach, usually asymptomatmic, ppl should be evaluated for underlying heart disease EKG: WIDE AND BIZZARE QRS

Primary care: barret's esophagus screening

Symptomatic GERD patient for at least 5 years should be screened with endoscopy w/biopsy. If patient has documented Barret's esophagus without any dysplastic changes, every 3 years do another.

Physical exam findings of renal artery stenosis, the leading cause of secondary hypertension?

Systolic-diastolic abdominal bruit.

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LDL=?

TC-HDL-VLDL = LDL

Thalassemias

THALASSEMIA MINOR PRESENTATION Microcytic anemia with Target cells and Teardrop cells on periphearl smear. RDW, TIBC, Serum iron, and FErritin levels are typically normal. alpha-thalassemia minor-normal Hemoglobin electrophoresis. southeaseter asian ppl. beta-thalassemia-elevated hemoglobin A2 on electrophhoreses. mediterreanean ppl. **Thalassemia minor often is confused with iron deficiency anemia. Beta-thalssemia trait has microscytosis out of proporation to the degree of anemia, hemoglboin >10 and high RBC count. Iron deficiency usually has a low RCB counta nd rarely ecomes mircorycit until hemoglobin is <10. HOW DO YOU DISTINGUISH irone deficiency anemia from Thalassemia? Iron deficiency has elevated red cell distribution width, which is typically >20% in iron deficiency. Elevated RDW commonly occurs in nutritional defieicences as nutrient level available for RBC synthesis vary throughout the day, resulting nin cells of varying size.

Hereditary spherocytosis signs, dx,

THe sphere spahed RBCS are not flexible and get trappend in the fnestrations of spleen's red pulp. increased MCHC (due to membrane loss and RBC dehydration, know this for spherocytosis), hemolytic anemia, jaundice, splenomegaly. Hyperbilirubnemia due to hemolysis which gives dark urine, jaundice and pigment gallstones. Acute cholecystitis from pigmented galstones is acommon complication. Patiets will need folate supplemenation as chronic hemolgysis consumes folates and many require SPLENECTOMY to minimze hemolysis.

Bactram

TMP-SMX,

Important prognositc features of breast cancer

TNP staging-MOST important then..in order of decresing significance... -ER+ and PR + are good prognositc features -Her-2/neu oncogen overexpression is related to worse prognosis -Histological grade of tumor; poorly differentiated is worse outcomes

Everything about blood transfustions

TRANSFUSION REACTIONS Seconds-Minutes: Anaphylaxis ---IgA deficient individuals are at risk due ot presence of anti-IgA IgG antibodies. Minuntes-hour: Acute hemolytic (also febrile). TRALI. THIS ONE BAD, STOP TRSNFUSTION and GIVE FLUIDS. -antibodies against donor erythroctyes ---Careful cross matching of blood prevents this but sometimes ABO mismathcing can occur due to clerical errors..whci presents with fever, chills, flank pain and hemoglobinuria within an hour of transfustion. Can progress to renal failoure and DIC. The direct antiglobulin test (Coombs) is positive and plasma free hemoglobin is >25 mg/dl. UA also shows hemoglobinuria. Tx: Stop transfusion and give acetinompheon. also there is Minor Allergic Reaction in which there is prominent urticaria. -antibodies against donor protiens. Tx: antihistamines and if necessary, stop transfusion. but blood transfusion may be continued if it is confirmed that the patient has only an urticarial reactino to the transfustion (hives) without serious reactions. 1 hour-6 hours: Febrile nonhemolytic. ---febrile hemolytic: when red cells and plasma are separted from whole blood, small amounts of residual plasma and/or leukocyte debris may remain in the red cell concentrate. During blood storage, these leukocytes release CYTOKINES which when transfused can cause transient fevers, chills, and malaise, withouth hemolysis. --most common Tx:stop trnsfusion and give tylenol. 2 days-10 days: Delayed hemolytic ----causes low grade hemolysis, rquires no treatment in most cases. Result from an anamnestic antibody response to a red blood cell antigen to which the patient was previously sensitized. The antibody is undetectable prior to transfusion but reappears rapidly following transfusion. also.. -premedication with antihistamines and acetaminophen does not prevent blood transfusion reactions -calcium gluconate infustion is used to avoid or treate severe hypocalcemia following massive blood transfusion. What happens is prior to storage, whole blood (for transfusions) is generally mized with solutions containing citrate anticoagulant. Packed cells derived from these whole blood collections also contain citrate. Infused citrate can chelate serum calcium, causing hypocalcemia. Generally not a problem cuz normal ppl can metabolize the citrate well but ppl with hypothermia or shock can't do it well. In these patients (renal failure, hepatic failure, shock, lactic acidosis) prprophlyactic administration of at least 10 cc of 10% calcium gluconate is reommended for ever 500 ml of packed red blood cells transfused. -Warming blood is recommended only during rapid massive transfusion to prevent hypothermia. -Whole blood contains numberous leukocytes and increases the risk of febrile reaction. There, it is rarely used except in cases of acute massive hemorrhage (trauma). -stored RBCs gradually lose intracellular potassium in to the surrounding solution. This has the potential to cause hyperkalemia. -there is also urticarial/alergic transfusion reaction: within 2-3 hours, caused by recipient IgE antibodies and mast cell activation -there is also transfusion-related acte lung injury: respiratory distress and signs of noncardiogenic pulmnoary edema. Within 6 hours. Caused by donor anti=leukocyte antibodies.

Patients with new-onset AF should have what measured?

TSH and free T4 levels measured to screen for occult hyperthyroidism as an underlying cause

What do you do to investigate suspicious murmurs?

TTE. Suspicious murmurs being diastolic and continuous and loud systolic murmurs. Midsystolic soft murmus (I-II) in asymptomatic young person need no further workuup. Chest X-ray or EKG too non-specific.

Primary care: migraines

TYPES -migraine w/aura: "classic migraine", 15% of cases -migraine w/o aura " common migraine", 85% of cases -menstural migraine -status migrainosus-last over 72 hours Followin can provoke a migraine: -hormonal alteration (mensturation) -stress, anxiety -sleeping disturbances -certain drugs/foods: chocholate, cheese, alchohol, smoking , OCPs -weather changes Clinical features; severe, throbbing, unilateral. lasts 4 to 72 hours. Tx: -analgesics, NSAIDs -DHE: serotonin 5-HT1 receptor agonist -Sumatriptan: more selecive 5-HT1 agonist -if noe of the avialbe migraine meications work, it is unlikely that the patient is suffereing from a migraine headahce prophylaxis: must be taken daily -TCAs and propanolol

Difference in acute mitral regurg and chronic mitral regurg?

Table is of ACUTE MR Acute MR presents with sudden onset of pulmonary edema, hypotension, and HYPERDYNAMIC PRECORDIUM with a systolic murmur. The murmur can be soft and/or inaudible (SILENT MR) in up to 50% of patients with acute, severe MR. Patients with acute MR typically have a dramatic presentation (due to lack of time for left heart adaptiation) compared to hose with chronic MR. Dx typically confirmed by TTE or TEE. **massive PE can cause sudden onset dyspnea, hypotension, right heart failure and syncope. Patients do NOT typically develop acute pulmonary edema. Acute you see a rise in left atrial pressure without much change if left atrial size cuz the heart atrium hasn't had time to accomodate. Chronic you see incrased left atrial size as it dilates to accomodate chronically increased left atrial pressures.

What is tamoxifen and what should you remember about the side effects?

Tamoxifen is a mixed agonist and antoaginst activity on estrogen receptors. Estrogenic effects of tamoxifen increase the risk of endometrial cancer and venous thrombosis. Its used ER+ and /or PR +

How to remove a tick?

Technique recommended by CDC is grasp the tick with tweezers as close to skin as possible and then remove the tick using steady upward pressure. Some studies suggest that mouthparts that break off and remain in the skin can be left alone because the infective body of the tick is no longer attached.

Signs and symptoms of hereditary telangiectasia (Osler Weber Rendu syndrome)

Telangiectasias blanche under pressure. You see diffuse telangiectassias, recurrent bloody nose, and widespread AV malformations (AVMs). AVMs in lung can shunt blood from right side to left side, causing chronic hypoxemia and reactive polycythemia.

Heat stroke

Temp > 105, Altered mental status, Hypotension, tachycardia, tachypenea In heat stroke, the thermoregulatory center fails to dissipate heat at the rate necessary to maintain a euthermic state. so person is exposed to sun for a long time but doens not sweat enough to dissipate the heat A body temperature of 105.8, may cause rhabdomyolysis and organ system damage. Large blood on dipstick with no RBCs by microscopy on urinalysis suggests rhabdomyolysis, the result of muscle breakdown. Tx: Evaporative cooling. Naked patient hsould be sprayed with a tepid water mist or covered with a wet sheet while large fans circulate air to maximize evaporative heat loss.

Testing for Cushings syndrome

Tests: -24hr cortisol on urinalysis -midnight salivary cortisol (normal people: low at night, high in morning) -overnight low-dose dexmethsone suppresion test ---First you measure ACTH. If that is low then you either have an adrenal tumor (MRI to confirm) or you're using exogenous steroids. If the ACTH is elevated then that means you further have to distinguish between Cushing disease and ectopc ACTH . Dexamethsasone is glucocorticoid analog that can inhibit ACTH secretion from pituiatary. If you do the suppression test now, if ectoic secretion ACTH will not decrease with dexamethasone because the source if resistant to negative feedback. If ACTH does decrease then that points to Cushings disease.

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What is the goal of HR when using beta blocker?

The Beta Blocker dose should be titrated to achieve a resting heart rate 55-60 and approximatley 75% of theheart rate that produces angina with exertion.

what do you see in G6PD deficiency

The G6PD deficient erythrocytes cannot bind oxidative metabolites which causes membrane instability and leads to ACUTE EPISODIC HEMOLYSIS in the spleen. Drugs, infection, fava beans, etc are common causes Clnical signs: pallor fatigue (anemia), jaundice/dark urine (from hemolysys) and abdominal/back pain (from severe hemolysis). Lab: Hemolysis-low Hgb, increased indirect bili, increased LDH, decreased haptoglobpin. Periphearl smear shows BITE CELLS with Heinz bodies. Remember: G6PD activity can be uased as a screening test, but has REDUCED SENSITIVITY during an acute hemolytic epidose cuz most erythroctes that are severely G6PD deficient are hemolyzed early in the episode...and reticulocytes which have normal G6PD levels are circulating at abnormally high levels. So its best to wait 3 months before retesting. Tx: supportive, with removal or management of insult

Describe what happens with a PE that kills someone? (massive PE)

The PE causes RIGHT HEART STRAIN (which itself has signs of JVP distention and RBBB on ECG) which progresses rapidly to right ventricular dysfunction-->decreased return to left side of heart---> decreased cardiac outpu ---> left heart pump failure---> resultant bradyardia. This results in cadriogenic shock and causes CNS effects and then death. So if you see HYPOTENSION and RIGHT HEART STRAIN, think PE.

How does carcinoid syndrome present?

The carccinoid tumors release products like histamine, serotonin, VIP that are released in blood but liver metabolizes. If liver gets meatstasized and starts to fail with the metabolizeing, the products go out to systemic circulation. Episodic flushing Secretyory diarrhea Wheezing Murmur of tricuspid regurgitation-pathognomonic plaque-like deposits of fibrous tissue occur most cmmonly on ednocardium on right side of heart, leading to tricuspid regurg and right sided heart failure Dx; elevated 24 hour urinary 5-hydroxyindoleacetic acid can confirm diagnoses

Syncope Differential Diagosis

The cause of syncope can often be established by careful history taking, PE, simple lab tests and ECG. ----- ---Examples of significant diagnostic clues in history are preliminary nausea or lightheadhedness (vasovagal), convulsions, chest pain, dyspnea, palpitations, etc. ---PE findings that also provde important clues are orthostatic blood pressure changes, abnormal cardiac exam, response to carotid meassage, etc. ---ECG helps to reveal brady- or tachyarrhythmias and conduction abnromalities as well as provide other clues to the presence of organic heart disease. UP to 70% of patients can be diagnosed with these. Ventricular tachycardia Pulmonary embolism Sick sinus syndrome, bradyarrhythmias, AV block : sinus pauses on monitor, prolonged PR interval or QRS Common causes 1.Vasovagal (also known as situational syncope, also known as neurocadiogenic syncope)-prolonges standing, emotional ditress, painful stimulit. Prodrome: nausea, warmth, diaphoresis. Typical situations is middle aged man who loses conscouisuness after urination or during coughing fit. 2. Orthostatic-postural changes in heart/blood pressure after standing suddenly. 3. Medications Other causes Torsades de pointes-hypokalemia, hypomagnesemia, medications causing prolonged QT Tx: IV magnesium sulfate, regardless of patient's baseline serum magnesium levels. Temporary transvenous pacing should be used in patients who do not respond to IV mag. Aortic stenosis or Hypertrophic cardiomyopathy or MI- syncope with exertion cuz of systemic hypotension causing decreased cerebral perfusion. Congenital Long QT- family history of sudden death, prolonged QT on EEG, syncope with triggers. Long QT syndrome can be congenital or acquired and increases risk for SCD due to torsades. A QTc>450 msec in men or >470 msec in women in considered prolonged QT. Seziure

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The obyd obatins Vit K exogenously from intestinal absorption of dietary Vit K and endogenously from bacterial produciton of VIt K in the intestine. Vit K deficiency is most commonly due to inadeuqate dietary intake, intestinal malabsorption, or hepatocellulaur disease that causes loss of storage sites. An ill patient ( prolonged lack of oral intake, antibiotics) can become Vit K deficcient in 7-10 days. Lab studies show prolonged PT>>> prolonged PTT.

How does valsava affect murmur?

The valsava maneuver and the squat-to-stand maneuver transiently decrease venous return with the septum and anterior mitral leaflet brought closer together. Turbulent flow-and the murmur-are increased.

Primary care: COPD -stages of COPD and Tx

There are 4 stages of COPD *all have Fev1/FVC <0.7 STAGE 1 (Mild) Fev1 >orequal 80% predicted Tx: short acting bronchodilators -albuterol and ipratropium STAGE 2 (Moderate) Fev1 50-80% predicted Tx: Long acting bronchodilators -salmeterol and tiotropium STAGE 3 (Severe) Fev1 30-50% predicted Tx: Inhaled steroids STAGE 4 (Very severe) Fev1 <30% predicted or Fev1 <50% predicted with chronic hypoxemia Tx: Longer term oxygen therapy and consider surgical interventions *oxygen therapy is O2 sat <orequal 88% *oxygen therapy is the only intervention that has been shown to decrease mortality and must be worn for at least 15 h/d **age and FEV1 are two most important prognostic factors

Tx of Pneumonia

There are best choices for empiric cov

Lymphadenopathy

There are multp.e cause so f cervical lymphadneopathy, but it most commonly edevelops int he setting of an upper respiratory infection. The physical exam often helps to distinguish between benign etiologies and more serious ones. Small, rubber lymph nodes are rarely pathologic and are often found in healthy children and young adults. Nodes less than 1.0 cm in diamter are almost always due to a benign process. IN contrast, nodes associated with cancer tend to be firm and immoblie. A nodal diameter > 2.0 cm is associated with a greater likelihood of malignancy or granulmoatiose disease.

Types of cystic leisons on pancreas. How to evaluate?

There are pseudocysts, non-neoplastic, and neoplastic. Endoscopic ultrasound with aspiration is the best test to evaluate a pancreatic cyst to differentiate malignancy from nonmalignant. *Pancreatic cystic neoplasms account for nearly 50% of pancreatic cysts and can be asymptomatic. Further analysis with biopsy is required to identify malignant potential. Serial CT scans in 3-6 months are used to monitor benign lesions.

From wards: lines and catheters

There are two types of IV, peripheral IV and central IVs. Peripheral: IV that doesn't go to IVC, SVC, or subclavian. They are easy to displace. NEed to be changed every 96 hours for concern for infection. -"midline" is a type of peripheral that is a bit more stable and longer than other peripheral Central IV: Goes to IVC, SVC or subclavian. types: Cordis, PICC, vascular catheter, Triple Lumen Catheter. Cordis: Short and large. Purpose is quick fluid rescusciation. PICC: enters peripherally but catheter goes all the way to central line areas. Done for long term stuff. Some medications you can only do through this type of central access cuz they would hurt smaller vessells...like chemo, vasopressors, TPN Vascular catheter Triple Lumen Catheter (TLC): femoral, suclavian, jugular. Multiple lumens allow different stuff to be pushed through/sucked out at once CATHETERS -suprapubic: directly in bladder -Foley: sometimes you leave in for a long amount of time -straight catheter-usually person does it every 4 hourse, goes into bladder and drains the urine

C dif

There can be recurrent C dif infection after successful treatment. Nearly 255 of CDI treated with metronidazole or vanc will recure, usually within 1-3 weeks. Recurrent CDI should be confirmed with stood studies for C dif (either C dif toxin or PCR for toxigenic strains of C dif). Once confirmed, the treatemtn for a 1st recurrence is same for initial infection. -Oral metronidazole for nonsevere -Oral vanc for severe disease (fever, WBCs >15000, Cr >1.5x baseline

Valsava, carotid massage, cold water immerson do what?

They are Vagal maneuvers, they increase vagal tone and decrease conduction through the AV node. This slows the heart rate and can often breakt the rhythm (commonly PSVT) Adenosie is a very short acting AV-nodal blocker that is often used as well.

Nucleated RBCs present in periphery show what?

They are immature RBCs typically found in bone marrow and not in periphery of normal patients. Presence of them in peripheral bloodsstream is indicative of significant bone marrow stress and is seen in conditions such as mylofibrosis and severe hemolysis.

What should you remember when dealing with electolyte abnormalities in chronic alcohohlics?

They typically present with multiple electrolyte abnormalities such as hypokalemia, hypmagnesemia, and hypophsophatemia. Remember that hypomagnesemia causes refractory hypokalemia therefore it is important to correct the magnesium along with the potassium levels to be able to correct the electrolyte abnormlaities of such patients.

Drug therapy for Hypertension

Thiazides are first choice Then ACE inhibitors, Ca channel blockers, or beta blockers 8th Joint National Committee rec as of 2014. i think the goal BP for diabetics has since changed

Cause of death in hypertrophtic cardiomyopathy

Thick intraventricular septum obstructs blood flow out of the heart and can cause sudden death by arrhtyhmia.

Scleroderma presentation?

Thickening of skin with edema that transitions to sclerosis that obliterates hair follicles, sweat glands and causes flexion contractures. Common complications are -kidney involvement leads to HTN and before ACE inhibitors this was most common cause of deat -PAH ultimatley results in RHF -Esophageal and gastric dysmotility cause these patients to suffer GERD. -Raynauds phenomenon is another complication Labs: ANA antibodies, anti-topoisomerase-I antibodies,

How do you know whether the hyperbilirubinemia is conjugated or unconjugated?

This can be evaluated by urine dipstick. Normally 95% of circulating bilirubin is the unconjugated fraction which is highly insoluble in water and tightly bound to albumin. When bound, its not filtered by glomeruls and is therefore not excreted in the urine. In contrast, the conjugted bilirubin is water soluble, loosely bound to albumin, and excreted in urine when present in excess. Therefore, the presence of bilirubin in urine is indicative of a conjugated hyperbilirubinemia. Like Rotor syndrome. Rotor syndomre is benign condition in which there is a defect of hepatic storage of conjugated bilirubin, resulting in its leakage into the plasma. LFTs are normal, and no treatment is required. Normal BILI pathway: following hemoglobin breakdown, majority (95%) of bilirubin is in the unconjugated form, whjich undergoes hepatic conjugation. Conjugated bilirubin then goes into the intestines, where it is predominantly deconjugated and receycled (enterohepatic circulation) to be reconjugated in th eliver. Alternatively, some of its metabolism produces are excreted in feces as urobilinogen, with around 1% of urobilinogen being renally excreted. When were' not talking about the excess conjugated bili spilling into plasma and being renally excreted, the normal amount of conj. bili goes intestines where is is degraded. Normally it gets degraded and so NO BILIRUBIN is seens on UA (NEGATIVE URINE BILLIRUBIN ASSAY). This is cuz there isnothing abnormla causing the conj. bili to spill into plasma and thus leak into urine, stuff life hepatic dysfunction, biliary obstruction, or defect in hepatic bilirubin storage or buildup of conju bili. if that abnormal stuff is happening then the results is DARK URINE AND A POSITIVE URINE BILIRUBIN (NOT UROBILINOGEN) assay. When you have excess unconjugate bili (like in hemolysis), resultant excess gets conjugated and can end up in higher than usual excretion in feces and urine as urobilinogen. so you gets POSITIVE URINE UROBILINOGEN asssay. Both types of hyperbilirubinemia cause jaundice. ?

Explain what you see with sideroblastic anemia

This condition results drom defective heme synthesis usually manifests as microcytic/hypochromic anemia simulating iron-deficiency anemia, but iron studies reveal elevated serum iron level and decreased TIBC (which differentiates it from iron deficiency) -usually you can see hypochromic and normochromic RBCs on microscopy ("dimorphic" RBC population) -bone marro sampling can confirm the diagnosis by demonstrating "ringed sideroblasts" but is not necessary every time In patients with an identifabiel cause of Vit B6 deficiency (alcoholism, drugs (INH)), administration of pyridoxine can easily correct the problem.

What lab test should a person newly diagnosed with hypertension get?

This helps look for possible secondary cause even though most cases are essential. Also helps look for risk for coronary artery disease. 1. UA for occult hematuria and urine protein/creatinine ratio 2. Chem panel 3. Lipid profile 4. Baseline ECG

Management of testicular cancer?

This is the tumor we kill first and investigate later. So remove the testis and associated cord before anything else.

Isolated hypercholesterolemia

Those genetic diseases

Most common adverse effect of inhaled cortiosteroid therapy?

Thrush (oral candidiasis) inhaled corticosteroid therapy is a cornerstone for asthma therapy

Most common bone affected by stress fracture?

Tibia.

4-2-1 IVF Rule?

To determine rate in milliilters per hour use 4 (for first 10 kg) x 10 kg + 2 (for second 10 kg) x 10 kg + 1 (for remaineder) x remaining kg . in other words... 0-10 4/kg 11-20 40 + 2/kg over 10 >20 60 + 1/kg over 20 This is for Milliliter/Hour for maintenance fluids. If you wanna calculate maintenance fluids required per day you use Holliday-Segar method to determine IVF requirements... -Give 100ml/kg of water for first 10 kg -For child over 10 kg but under 20 kg, give 1000ml + 50/kg over 10 -For child over 20 kg, 1500 + 20/kg over 20

Medical management of brain dead organ donor

To maintain euvolemic, normotensive, and morothermic state. Common misconeption is that the body temperature should be kept low to improve viability of organs. IN contrast, normothermia should be maintained passively in all brain dead patients using blankets. Can use warm IV fluids too. Normotension is critical too.

SIADH

Too much ADH, causes hyponatremia TREATMENT: Asymptomatic or mild symptoms (forgetfulness, unstable gait): Fluid restriction, possible oral salt tablet Moderate symptoms (confusion, lethargy): Hypertonisc saline to increase sodium above 120, then treat as if "asymptomatic or mild" Severe symptoms: (seizures, inability to communicate, coma): Hypertonic solution, possibly conivaptan (vasopresson recepetor antagonists) *demecyclocine causes kidneys to be resistent to ADH (nephrogenic DI) but is rarely used as treatment of SIADH cuz kinda nephrotoxic

Varicoceles are what?

Tortuous dilation of the pempiniform venous plexus surrounding the spermatic cord and testis in the scrotum. They usually result from left renal venous compression between aorta and superior mesenteric artery. Examination shows a soft left-sided scrotal mass "bag of worms" that worsens with standing and Valsalva maneuvers but regresses when the patitne is supine.

You think patient has IBD but seems like worsening symptoms w/signs of sepsis, what do you think?

Toxic megacolon. Patient will look bad and have distended, tympatnitic abdomen. Do X-ray to confirm diagnoses. The most widely used criteria to Dx toxic megaolon includes x-ray evidence of it + 3 of the following Fever>38 Heart rate >120 Neutrophili leukocytes >10,500 Anemia Tx: medical emergency that requires prompt IV steroids, nasogastric decompression, antibiotics, and fluid management. **Note that management depends on underlying cause, you're not gonna give steriods to someone with toxic megacolon due to C. dificile or other infection.

Pleural effusion. Types? Dx?

Transudative-CHF, Cirrhosis, Nephrosis. Due to incrased hydrostatic pressure or decrased oncotic pressure. *hepatic hydrothorax common transudative cause in cirrhosis patients, usually located on right. Exudative-due to increased capillary permeability, usually due to inflammatory process. -Infection (pneumonia, TB), --tumor, --trauma, (may be hemorrhagic) -- pulmonary embolism *effusions from PE can be either exudatieve (75%) or transudative (25%) asand associated with a pulmonary infarction. However, pleural fluid ph and glucose are usually normal in these. Management: Any pleural effusion should be tapped for analysis. Except if there are signs of CHF, in which a trial of diuretics is warranted. For analysis do total and differnetial cell count, protein, glucose, LDH, and ph (if there is suspicion for empyema). 2. AFter you use that to decide if transudative or exudative... if exudative now u gotta decide if its uncomplicated, complicated, or empyema. -Complicated: involve persistent bacterial invasion of pleural space which decrased glucoe <60 and incraeases LDH (from lysis of neutrophils. The culture is usually negative and effusion resolves with antibiotics -Empyema: when FRANK PUS is in plerual space, requires chest tube drainage. if empyema is really bad and has thick rim, only surgery is the answer. -Ph <7.2 and/or glucose <60 is indication for thoracostomy. LDH and protein can point to exudative causes but are not absolute indications for thoracostomy. -why low glucose? due to high metabolic activity of leukocytes and bacteria within the pleural fluid. Light's critera: Effusion is exudate if one or more more is present. The reasons is because the increased capillary permeability lets more protein and LDH through to reach the pleural space -Ratio of pleural to serum protein > 0.5 -Ratio of pleural to serum LDH >0.6 -Plerual fluid LDS> 2/3 upper normal limit of serum LDH -also if ph is pretty normal that helps point to transudative because the transudative fluid is just normal body fluid -low glucose usually seen in complicated parapneumonic effusions, malignancy, TB, or rheumatoid arthritis. Parapneumonic effusion devleops in the setting of pneumonia. This specturm. A simple can become 'complex" and 'complicated" with the other end being empyema in which frank pus can be aspirated. Empyemas ALWYAS require CHEST TUBE. - On x-ray you see a loculated abnormally contoured effusion WITH ADJACENT pulmonary consodliation. If empyema is complex and has a thick rim, only surgery is the answer. The thick peel can be removed through surgery.

Acute glaucoma treatment?

Treat acute glaucoma with mannitol, acetozaolamide, timolol, or pilocarpine.

Criteriato diagnose rheumatic fever

Two major of JONES or.....1 Jones Major + 2 Minor (athralgia, fever, elevated CVR, prolonged PR) REMEMBER THAT THE ARTHRITIS IN JONES IS A MIGRATORY ARTHRITIS

Hemodialysis

Two most commonly used vascular access sites are arterovenous fistulae (AVF) usually in the foream and artificial grafts inserted between an artery and a vein. Dialysis needles are placed directly into the graft. A tunneled dialysis catheter (TDC) is usually placed in the right internal jugular vein and serves as a bridge that allows hemodialysis to take place until AVF or graft is palced.

BPH vs prostate cancer

Tx for BPH: alpha 1 blockers (doxazosin or tamsulosin) prefferred alone or in combination with 5-alpha reductase inhibitors (finastreide) for symptoms relief. PSA antigen can screen for prostate cancer. However, PSA can also be elevated (>4ng/dl) in BPH. Prostate cancer is more peripheral in growth and rectal exam shows NODULES. BPH is more central and rectal exam is smooth. Remember, all patients with suspected BPH should hav e UA (to look for blood) and serum creatinine tested. You wanna make sure you're not having bladder outlet obstruction that is causing renal failure. Generally, creatinine is not elevated by unilateral urinary obstruction but wil be elevated due to bilateral obstruction. As a result, patients with elevated creatinine require imaging (renal US) to assess for hydronephrosis and other causes of obstruction. PSA screening controversy: USPSTF (US preventative services task force) does not recommend any population screening using PSA. But American Cancer Society and American urological association disagree with this. *interesting thing from uworld: if a pt. has severe pain with couhghing and movement from like a back injury, he might be unable to generate suffiicient intraabdominal pressure to overcome resistance to flow caused by BPH, so he might get urinary retention secondary to pain.

Features and managment of TCA overdose

Tx: Sodium bicarb is preferred for treating arrhythmias. Patients who are refractory to sodium bicarb may response to adjuvant magnesium or lidocaine.

Alchohol withdrawal

Tx: with Benzos DT: tachycardia, fever, hallucionations,

Types of esophageal rupture/perforation

Types of esophageal rupture/perforation Boerhaave's syndrome: A full thickness tear. Due to forceful vomiting, cough, trauma. *can occur during episodes of vomiting, particularly when the patient is resisting the vomiting reflex. Cuz high intraabdominal pressures are transmitted into the mediastinal esophagus. -Mallory-Weiss syndrome: A partial-thickness tear. Due to forceful vomiting/wretching. Common presentation is self-limited hematemesis. **hiatal hernia is most well known anatomical predisposing factor for Mallory-Weiss syndrome (40-100% of patients w/Mallory Weiss). During retching/vomiting, the pressure is greateer within the hernia therby making this locatino most likely to susatin a tear. -Foreign body: like endoscopy can perforate the esophagus. iatrogenic cause is most common cause. *esophageal perforation is a surgical emergency. Signs: pain in chest, dysphagia, dyspnea. SUBCUtANEOUS EMPHYSEMA, mediastinal emphysema hear as a "crunching sounds" with heartbeat. (Hammon's crunch) Pneumomediastinum: air within mediastinal space. X-ray finding of radiolucent band adjacent to the cardiac border is typical of pneumomediastinum. Dx: -ESOPHAGRAM w/ water-soluble contrast (KNOW). Water-soluble contarst is preferred during the initial examination because it causes less mediastinal irritation than barium if a large leak is discovered. **note this is not upper GI endoscopy which has no role here. -X-ray-left sided PLEURAL EFFUSION (pleural fluid analysis is low ph and very HIGH AMYLASE (cuz of salivary amylase)) , mediastinal or subcutaneous emphysema Tx: Full thickness tear: surgery. Partial thickness: may resolve spontaneously Full thickness tears: surgical closure of full-thickness tears within 24 hours: 80-90% survival rate -drain the contaminated mediastinum -monitor for recovery from sepsis *urgent management is needed because of risk of mediastinitis for full thjickness tears, which carries a mortality rate of more than 40% if not properly diagnosed within first 24 hours. *In patients with and unerlying motility disorder, stricture, or malignancy, surgical intervention must address both the perforation and the esophageal abnormality. For patients with a distal esophageal carcinoma, treatment usually requires esophagectomy. Esophageal exclusion or proximal diverstion (with a cervical esophagostomy or "spit fistula") are typically reserved for patients in whom a late diagnosis of esophageal perforation was made.

Explain metabolic syndrome

Typical presentation: hypertension, impaired fasting flucose, dyslipidemia. Patietns are characteristically overweight with predominantly abdominal fat districution. Insulin resistance plays a central role in the pathogenesis of metabolic syndrome. Dx is 3 or 5 criteria; 1. Abdominal obesity 2. Fasting glucose >100 3. Blood pressure >130/80 4. Triglycerides >150 5. HDL, men<40, women <50. Most health care providers believe that insulin resistance if the first even in the development of DM2. However, DM2 dose not develop without a beta cell secretory defect. Increasd insulin secrtion from the beta cells is required to cope with increased insulin resistance. If beta cells are able tco compensate for the incread insulin resistance, subjects generally remain normoglycemic at the xpence of very high insulin levels; however, if beta cells are unable to cppensate fully, glocse intolerance and thnype 2 DM result. So insuline resistance typical for patients with central-type obesity is the key pathogenic factor in the development of DM3 and associated abnormalities (heyprtension, dyslipidemia) *Extermely high yield topi for USMLE

What are some well-known ATYPICAL presentations of ACS?

Typical- chest pain, Atypical-dyspnea,nausea, vomiting, epigastric pain -so women, elderly, diabetics are more likely to have the atypical symptoms

Trichinellosis

Typically presents with GI complaints (abdominal pain, nausea, vomiting) followed by the characteristic triad of periorbital edema, myositis, and eosinophilia (hallmark of disease). Other findings include fever, subungual splinter hemorrhages, and conjunctival or retinal hemorrhages.

Explain small bowel obstruction

Typically presents with colickly abdominal pain, vomiting, no BM and no gas, abdominal distention, and diffuse tenderness. Patients can also have increased pain with hyperactive bowel sounds during peristaltic rush. Depending on the level of obstruction, X-ray can reveal DILATED BOWEL LOOPs with multipe air fluid levels. A mild leukocytosis and modest increase in amylase are expected in any bowel obstruciton. Most SBO patients can be managed initially with conservative measures, including complete bowel rest, decompression with nasogastric tube placement, pain control, fluid resuscitation, and correction of metabolic deragnements. Patietns who do not imporove with conservative measures and/or develop syymptoms or signs of strangulation should be referred for urgent surgical intervention.

What are the acute phase reactants, which are elevated and which are downregulated

UPREGULATED -Serum amyloid A: prolonged elevation can lead to amyloidosis -C-reactive protien: Opsonin; fixes complememnt and facilitates phagocytosis. -Ferritin: Binds and sequesters iron to inhibit microbial iron scavenging -Fibrinogen: coagulation factor;correlates with ESR -Hepcidin: prevents release of iron boud by ferritin--> anemia of chronic disease DOWNREGULATED - Albumin: reduction conserved amino acids for positive reactants -Transferrin: internalized by macrophages to sequester iron

Tx of UTI

Uncomplicated UTI-3-5 days of oral antibiotics Complicated UTI requires longer duration Bacteruria in pregnancy isalways treated COnsider hospitilization and IV antibiotic for high risk patients---elderly, ummunocompmosieed, indwelling catheters,

UTI classifications

Uncomplicated UTI-healthy, nonpregnant females COmplicated UTI- all the rest

Malignant hyperthermia?

Uncontrolled efflux of calcium from the sarcooplasmic reticulum is the underlying pathophys of malignant hyperthermia, a rare autosomal disorder. It occurs in genetically susceptbiel patients after administration of the anesthetic drugs halothane and succinylcholine and may be associated with severe hyperthermia ( up to 113).

Pancreatic cancer screening?

Unfortunatley, no serologic or radiographic test has proven effective in screening for pancreatic cancer in asymptomatic adults.

what is the "honeymoon" phase of diabetes?

Up to 75% of newly dignosed diabeteics have a progressive decrease in the daily insulin requirement in the months after their diabetes diagnosis; a few patients temporarily require no insulin. This "honeymoon" period usually lasts a few months, and then an insulin requirement returns. Patiens are told that the "honeymoon" period is not a cure and that they should expect a return to insulin requirement.

Dx of UTI

Urine dipstick tha tmeasures leukocyte esterase and nitrites. UA that you can vicualize pyuria Urine culture is definite test. A + is >10,000 colony forming units.

How do you predict mortality in patients with chronic liver diseease?

Use the Model for End-Stage Liver Disease (MELD) scoring system. Can be used to determine a patient's 90 days survival. 3 values you use are bilirubin, INR, and serum creatitine. MELD scoring system is used to select patienets for placement of a transjugular intrahepatic portosystemic shunts (TIPS). MELD score also used to calculate a patient's priorty on the liver transplant list, with patients that have a higher MELD score taking precedence.

Amiodarone

Used for atrial and ventricular tachycardia.

What is sputum AFB stain used for?

Used in making the diagnosis of pulmnnonary tuberculosis. CXR also shows cavitary lesions.

What is carotid massage used for?

Used to determine paraoxysmal supraventricular tachycardia.

What is sputum cytology used for?

Useful in making a histologic diagnosis of pulmonary malignancy.

Complex regional pain syndrome

Usually occuring after an injury, CRPS presents with pain out of proportion to the injury, temperature change, edema, and brnomal skin color. Pathogenesis is likely die to an injury causing increasd sensitivity to sympathtiec nerves, an abnormal response to and sensation of pain, and increased neuropeptide release causing burning pain to touch (allodynia). Dx: can be confirmed by either autonomic testing that measures inccreased resting sweat output or MRI that looks for the above changes. Tx: regional sympatetic nerve block or IV regional anestehsia.

GI webs and rings

Usually presents as dysphagia to solids, an anatomical problem. Plummer Vinson syndrome: Webs (thin mucosal structures protruding into lumen) associated with iron deficiency anemia. Schatzki's ring: A narrow lower esophageal ringlike outgrowth associated with dysphagia Dysphagia to solids AND liquids often indicated a motility problem (like achalasia, DES). Dysphagia to ONLY solids indicated mechanical obstruction

Transposition of great vessels

Usually presnts with cyanosis in first few hours of life. Typica phisical exam findings include cyanosis and a single loud second heart sound, usually with no murmur.

Hepatic encephalopathy

Usually reversible mental status change associated with hepatocellur dysfunction Cirrhoitc patients, can happen anytime in them Cause unclear, prob related to increased NH3 and increased GABA Signs: mental status changes, asterixis (flapping of hands when arms extended), Fetor hepaticus (peculiar breath smell) may be presetn *remember cirrhotics are really likely to bleed, so a spontatneous intracranial bleed can happen and mimic HE with the mental status changes. so really think about getting a head scan. Part of management is identifying and treating precipitating cause. Common causes of HE are 1. GI bleed 2. hypokalemia (usually from loop diuretics) 3. hypovolemia 4. Hypoxia 5. Sedative 6. Hypoglycemia 7. Metabolic alkalosis 8. Infection (including SBP) Tx: you wanna treat precipitating cause (volume depletion, electrolye abnormalities) and loweronig serum ammonia. Tx: protein restriction , lactulose, noemycin (kills urease producing bacteria in gut) In early liver disease, patients are placed on a high-protein diet because the general state of protein malnutrition puts the body at a disadvantage to fight other stresses such as infection. In end stage liver disease the liver cannot break down protein, and the excess accumulation can cause encephlopathy. At this stage, the patient is protein restricted.

Pseudomembranous colitis?

Usually seen in elderly patients who reside in nursing homes and other long term care facilities. Patients usually present with abdominal pain, fever, and non bloody diarrea. Can have elevated white count. Stool Clostridium dificile toxin assay is positive. Prior history of antibiotic use is also present in majority of patients. THe pseudomembranes are raised yellow/off-white plaques scattered over the colonic mucosa.

Dr. Corbridge acidosis/alkalosis lecture during medicine clerkship

Uworld: first look at arterial ph to know if acidemia or alkalemia. Then look at Pc02 and bicarb, this helps you decide if resiratory or acidotic. This is important for me cuz there are questions where pac02 is 40. If serum HC03 is low then metabolic acidosis probably. When you look at Pc02 you wanna know if it represents effecitve respirtory compensation, cuz if it's not the value you'd expect then there is something else going on. This is where you use Winters formula or the trick coorbridge says. Lets say your pc02 is higher than expected pc02, then there is respiaroy acidosis going on. So after identifying a primary acid base disorder, the caclulated expected pc02 OR hc02 should be compared to measured values to distinguish between appropriate compensation and a mixed disorder. MAcid: use winters formule to look at expected pc02. Malk: expected c02 should reflect a .7 increase in pc02 for every 1 rise in bicarb. -if ur actual Pc02 is higher then i guess you have respiratory acidosis goin on as well. Acute resiratory acidosis: expected bicarb should refelct a 1 increase in bicarb for every 10 rish in Pac02. Acute respiraory alkalosis: expected bicarb should reflect a 2 decrease in bicarb for ever 10 decrease in Paco2. Acute respiratory acidosis/alkalosis things to remeber -For every 10 Co2 changes, ph should change in opposite direction by .08 for ONLY RESPIRATORY conditions. If you don't see that then (im guessing) you have anohter metabolic process -for acute respiratory stuff, bicarb changes around 1 or 2 for every 10 Co2, .08 ph changes. Bicarb doesn't change drastically so not that important. You're only going to see big changes in bicarb when your kidney and/or GI tract is involved like in metabolic processes. Compensated respiratory acidosis/alkalosis things to remember -Bicarb takes some days to compensate for respiratory process Metabolic things to remember -with metabolic you don't have the acute or compensated stuff to remember as with respiratory. The question is was their effective respiratory compensation? -AG MA: use Winters or that rule that says is Pco2 number matches the number at right side of decimal point, then their was effective respirtaory compensation. Like 7.20ph and 20 Pco2. remember too its around that area, you don't need exact matching. -General idea of NG MA is bicarb wasting -General idea of AG MA adding ions -Delta Delta: idea is added ions get buffered by bicarb, so bicarb levels should go down by same amount that anion gap is. So the math is AG-10(always 10) =x. then add x to your bicarb you have and if its around 24 then no other process going on. If its considerably over then that means you have extra bicarb and you have a concomittant met. alkalosis going on. If its under 24 then you have a concomitant bicarb wasting state (NG MA) going on. -with ABG they get the bicarb level by calculating it by Henderson Hasselbach. The bicarb in venous samples is the bicarb direclty measured. -every decrease in albumin by 1 your AG should decrease by around 2.5. Hypoalbuminemia is common cause of low AG. With metabolic alkalosis you have Chloride responsive and Chloride unresponsive. -Cloride responsive (saline responsive): Vomiting a big cause. When you vomit you lose Cl-, Na+ and volume so your kidney gonna be grabbing to to Cl-, Na+ so you're not going to see much Cl- in urine. But if you get Cl- deplete your kidneys gonna want an anion to hold on to with the Na+ grabbing so if Cl- not there, its gonna start grabbing Bicarb (it's anion). That's why saline responsive, if you give NaCl then your kidney can pee out bicarb. -For chloride unresponsive the big ones are hypokalemia, and steroid excess. Also..UAG Basically used to decide between RTA or diarrhea as cause of NG Metabolic Acidosis. The idea is cations must equal anions in urine. So UNa + UK+ Unmeasured cations (NH4+ being the important one) = UCl + Unmeasured anions If you rearrange the equation you get... Urine Anion Gap=UNa + UK -UCl = U. anions - U. cations. If UAG>0 that means decreased NH4, so its RTA If UAG <0 that means incraesed NH4 generated in kidneys. Normal or GI loss (diarrhea).

Charcot joint (neurogenic arthropathy)

VIt B12 defieicny, Diabetes, tertiary syphillis, peripheral nerve damage, Normal neurologic input is lost, patients unknowlingly traumatize thier weight bearing joints. manifests with functional limitation, deformity, and degenerative joint disease and losse bodies on joint imaging. Management of a Charcoit joint involves treating the underlying disease and providiing mechanical devices (special shoes) to assist in weight bearing and decrease further trauma.

Holosystollic murmur at left lower sternal border?

VSD. Echo should be done to determine location and size of defect. Most small VSDs close spontaeously and require no treatment.

Things DDAVP is used to treat

VWF deficiency= high PTT and increased bleeding time. Normal platelet count. Tx: DDAVP Central DI: DDAVP Abnromal bleeding in chronic renal failure: Tx: DDAVP Old child peeing the bed Hemophilia too i think

Vaccine with people who get splenectomy?

Vaccinations : Pneumocococssu: PCV13 then PSV23 8 months later. Give PV 23 again 5 years later and at 65 yrs old. H.influenczae: Give 1 dose of vaccine Meningococsus: Give 1 dose. Revaccinate vevery 5 years INfluenza: INACTIVATED influenze vaccine annually Others: HAV, HBV, Tdap once as substitute for Td, then Td every 10 years Vaccinations against each of these organissms should be administered either >14 days before scheduled splenectomy or >14 days after splenectomy.

Who gets varicella vaccine and who gets the VZIG (varicella zoster immunoglobulin). in terms of exposure prohylaxis

Vaccine: live vaccine, all who are asymptomatic, nonimmune, and immunocompetent should get for post-exposure prohylaxis whithin 3-5 days of exposure. Because its live vaccine avoided in pregnant women and immunocomprised. VZIG: asymptomatic, nonimmune and immunocompromised should get the VZIG within 10 days of expsoure. May not prevent infection, but can reduce disese severity.

In elderly patient with abdominal pain, always consider what?

Vascular causes, like -AAA -Mesenteric Ischemia -MI

How do diagnose vasovagal syncope?

Vasovagal (also known as situational syncope)-prolonges standing, emotional ditress, painful stimulit. Prodrome: nausea, warmth, diaphoresis. Typical situations is middle aged man who loses conscouisuness after urination or during coughing fit. -triggers lead to increased parasympathetic tone, causing a drop in heart rate and blood pressure; decreased sympathetic tone causing vasoidialtion and hypotentsion or a combo of the two. This increased parasympathetic tone ty[pically causes a prodrome of nausea, diaphoresis and pallor. Its a clinical diagnoses and does not need further testing if history and physical examination point strongly toward the diagnosis. However, in uncerain cases, upright tilt table testing is used to establsih the diagnoses. During the upright tilt table test, the patient lies down strapped on table. Continous ECG and blood pressure monitoring are used throgughout test. Table is passively moes the patient from a supine to a head-up position between 60 and 90 degrees. The patient is held in this position for 20-45 minutes. If there are signs of unconscoiusness (syncope, inability to mainatin posure due to fall in blodd pressure pulse), the test is considered posiitve and sotpped. Tilt-table testing is reserved for patients who have been ruled out for heart disease (structural or conductive).

"Dizziness" characterizations

Vertigo: rotational sensation in which room spins around the patient Orthostasis: refers to light-headedness upon arising, common with orthostatic hypotension. Presyncope: is a feeling of impending faint Disequilibrium: sensation of unsteadiness, or loss of balance. If asked whether the problem is in the head or feet, patients often respond by saying the problem is in the feet. Lightheadedness: is often vaguely described as a "floating" sensation

What are risk factors for polyp progressing into malignancy

Villous adenoma, sessile (opposited of pedunculated)adenoma, and size >2.5cm. Polyps classified as following 1. Hyperplastic: Most common non-neoplastic kind, no further workup needed. 2. Hamartomatous: Include juvenile polyp (non-malignant) and Peutz Jeghers poly (non-malignant) 3. Adneoma: Most commont type. Potentially premalignant, but <1% are malignant. Most are asymptomatic. Adenomas... can be sessile or stalked (pedunculated) Can be tubular, tubulovillous, or villous And various sizes.

Pericarditis

Viral ( most common), bacteria infection, heart surgery complications, Signs:Precordial pain with radiation to shoulder and neck (often relieved by standing), PERICARDIAL FRICTION RUB on asucultation, signs of cardiac tamponade,

The most common predisposing factor for actue bacterial sinusitis is what?

Viral URI. Contaminating bacteria cannot be cleared by mucociliary clearance due to mucosal inflammation from viral infection, leading to secondary bacterial infection. First line treatment for actue bacterial sinusitis is amoxicillin plus clauvanic acid.

What to look for to differentiate URI vs influenza vs strept pharyngitis.

Viral URI: onset of symptoms is slow, stepwise. respiraroty symptoms like rhinorrhea, sneezing, coryz, mild pharyngitis are prominent. systemic symptoms are usually mild. Influenza: onset of symptoms is abrupt and often dramatic (out of proprortion to the relatively mild nasal and respiraroty symptoms), bam! sytemic feautres like high fever, headache, and myalgias are prominent. Strept: pharyngitis: Centor Criteria >2 or equal. systemic symptoms are variable but can have fever, mylagias.

Myocarditis

Viral: Cox B most common, bunch of other viruses Bacterial: Strept. pyoegens, and bunc of other bacteria Systemic disease: SLE, inflammatory conditions, kawasaki. Autoimmune mechanisms often accompanied by rash. Drugs: cocaine, ephedra Findings can be: chest pain, fever, recent URI, signs of CHF Dx: Auscultation : Typically AUDIBLE S3, PULMONARY VSCULAR CONgestion, fircition rub if pericardium involved, S4 may be heard Labs: elevaed cardiac enyzmes, elevated ESR, leukocytosis

Common features of viral versus bacterial URIs

Viral: fever, cough, headache, myalgias, rhinorrhea Bacterial: fever, cough, yellow sputum *although yellow sputum doesn't clinch it, like if yellow sputum but clear chest x-ray (no signs of pneumonia), probably still viral

Primary care: Acute Bronchitis

Viruses account for majority of casese Lab tests are usually not indicated. tx: antibiotics are usually not necessary. cough suprressants (codeine containing cough medication) are effective for symtomatic relief. bronchodilators may help.

Cystoscopy use?

Visualize inside of bladder, can also be therapeutic, for crushing bladder stones. Just a scope that goes into bladder

Renal Ultrasound uses?

Visualize kidney. First step in investigating kidney failure. Atrophic kidneys suggest kidney dmage.

Warm agglutinin AIHA vs Cold agglutinin AIHA AiHA=automminue hemolytic anemia

WARM -drugs -viral infections -autoimmune (SLE) -immunodefieicny -lymphoproliferative (CLL) -Coombs + with ANTI IgG, anti C3 or both. Tx: corticosteroids, splenectomy for reractory disease COLD -infections (ex. mycplsama pneumoniae and infetious monoclucleiosis) -lymphoproliferateive disease -livedo reticularis and acral cyanosis with cold exposure that disappear with warming -Coombs + with ANTI IgM (not IgG, anti C3 Tx: avoid cold temeratures, rituximamb +/- fludarabine *spherocytes can bee seen in AIHA as well as in hereditary spherocytosis. AIHA give positive Coombs test while Herediary spherocytosis gives negative Coombs test. *PNH gives negative coombs test

what is pyuria?

WBC >10/hpf

What do you need to rmember when starting warfarin therapy about the first few days

Warfarin has an initial PROCOAGULAnT effect. It inhibits protein C earlier than other factors. So to prvenet clot formation in the initial days use HEPARIN as a bridge until warfarin takes full effect.

How to differentiate between central diabetes insipidius and nephrogenic diabetes insipidus

Water restriction test: in central and nehprogenic DI, patients excrete a high volume of innappriopatiely DILUTE urine. -in primary (psychogenic polydipsia), the urine osmoloariyty INCREASES. -DDAVP test is the last part of water restriction test i think. After you've ruled out psychogenic polydipsia then you administer DDAVP to distinguish between central and nephrogenic DDAVP (ADH analog test) replaceemnt test: CEntral DI: urine output decreases and urine osmolarity increases by 50-100%. Nephrogenic DI: No effect is seen on urine output or urine osmolairy ( or just small increase) ALso: Central DI Tx: Intranasala DDAVP, hydration Nephrogenic: HCTZ, indomethacin, amiloride, hydration

What is the most effective nonpharmacologic thing to do for someone to lower their blood pressure? say the person is fat, sedentary, diabetes, and smokes.

Weight loss is the most effective. After than comes DASH diet, exercise, dietary sodium alchohol intake

Eye problems:

What are signs of orbital cellulitis and what is cmost common predisposing factor? Bacterial sinusitis most common predisposing factor. Symptoms: proptosis, opthalmoplegia, diplopia, pain with extraocular movements. Proptosis, ohthalmoplegia and decreased vision differentiate it from preseptal ceullultis (periorbital cellulitis). Perioorbital cellulutis Inflammation of eyelids and periorobital tissue anterior to septusm. Etiology: extension of local infections like URI, sinusitis, facial scellulutis or eyeld infection. Trauma: Skin trauma is most liekly etiology. Signs and smptoms: erythema, edema, no pain with extraocular movement. Can lead to orbital cellulutis. most common causes of preorbital and orbital cellulits SHiP Diabetic retinopahty: 3 main categories: 1. simple retinopathy: microaneurysms, hemorrhages, exudeates, retinale edema 2. pre-prolieferative: cotton wool spots 3. prolieferative or malignant retinoapthy: consists of newly formed vessels. -patients are normally asymptoamtic at first despite early signs of retinopathy (microaneurysms). Visual impairment occurs with developmend of macular edema. Argon laser photocoagulati ois the suggested treatemnt. Central retinal artery occlusion: painless, nilatral blindness. Cherry red spot on fovea. pupil sluggishly reactive to light. Tss: intra-arterial thrombolysis within 8 hours. Cnetral retinal vein occlusions: painless. suddent unialteral visual impairment. You have disc swelling, venous dilation, retinal hemorrhages, cotton wool spots. Tx: laser photocoagulation has variable results. Macular degeneration : Affects central visions. Characterized by distorted vision and central scotoma. Cigarrete smoking increases risk . There is dyry and wet. Dry you have multiple sores in macular region. Wet is new blood vessesl that may leak, bleed, and scar the retina. **One of the earliest findings of macular degeneration is distortion of straight lines such that they appear wavy. Dry (Atrophic) Tx: none Wet (Exudative) : VEGF inhibitor, laser therapy Open angluse glaucoma: gradual loss of peripheral vision resulting in tunnel vision. You see patholoci cupping of optic disc. Tx: B blockers (decrease aqueous humor production), pilocarpine (increases aqueos humor flow), carbonicc anydrase inhibotrs. Closed Angle gluacoma: prolonged pupillary dilation often triggered by dark places or medications. characterized by sydden onset of symptoms such as blurred vision, severe eye pain, nausea, and vomiting. Examination reveals a red eye with a hazy cornea and a fixed, dilated pupil. --Acute glaucoma treatment? Treat acute glaucoma with mannitol, acetozaolamide, timolol, or pilocarpine. Optic neuritis: acute unilateral vision loss , severe pain, and afferent pupillary defect. Often initial presentation os mutipl scleroris. Treat with IV methlyrednisone. Amaurosis fugax: usually caused by atheroemboli from the carotid arteries and causes TEMPORARY vision loss as opposed to the persistent . Cataracts: patients usually complain of blurred vision, problems with nigttime driving, and glare. Definitive treatment is lens extraction. What is postoperative endopthalmitis? Most common form of endophthalmitis. Usually occurs within six weeks of surgery. Patients usually present with pain and decreased visual acuity. You get swollen eyelids and conjunctiva, hypopyon, cornea edema and infection. Herpes simplex keratitis ? Pain, photobphosbia, decresaed vision. Dendritic ulcer is most commone presentation and corneal vesicles. Bacterial keratitis? usually seen in contact lense weareers and following corneal trauma. Cornea ppears hazy with central ulcer and adjacent stromal abscess. Gram negatives like Pseudomona usually involveed, medical emergency. Hordeolum or stye: common staphyloccocal abscess of eyeld. Usulally responds to warm compresses. IF doesn't work in 48 hours do incision and drainage. Chalazion: granulmoatous inflammation of meibomian gland. Inicision and curettage is treatment of choice. Dacrycystitis: infection of lacrimal sac. use systemic antibiotics.

Woff-Parkinson White syndrome, explain it

What happens is that there is an accessory pathway that allows the electrial signal to travel from sinus node to ventricle bypassing the AV node. This results in abnormal delta watve and gives you risk for arryhtmias. Signs: delta wave on ECG, slurred QRS, Dx: patients suspected should have electrophysciolog testing to find the abnormal electrical tract in the cath lb and ablation of that detected bypass tract Remember, DONT give ABCD (adenosine, Beta-blockers, Calcium channel blockers, or digoxin) with someone with WPW. PROCAINIMIDE is the classic choice.

treatment for graves

What is used to assess function after RAI (radioactive iodine) treatment? Thyroid stimulating hormone levels may remain suppressed for weeks or even months following RAI treatment and do not reliably reflect thyroid functional status.

Explain a fecal occult blood test

When the reagent of the fecal occult blood test combines with hemoglobin, a blue color appears. Test is very sensitive.

treatment of multiple brain metastases

Whole radiation therapy is the mainstay of treatment of multiple brain metastases. Also, corticosteriods help to increase patient survival by up to two months. Chemo is currently not recommended for brain metastases due to poor penetration of most chemotherapeutic drugs through the hemato-encephalic barrier.

How to diagnose pheochromocytoma?

With abdominal CT scan.

When and with what doyou treat Hep B?

With acute liver failure or clinical cirrhosis and HIGH serum hep B virus DNA Treatment aslo recomended for patients without cirrhosis but with positive HBeAg, Hep B DNA>20,000, and serum alanine transaminases >2x upper limit of normal. ENTECAVIR and TENOFOVIR have become preferred therapies due to lower drug resistance and ability to be used in decompensated cirrhosis.

Primary biliary cirrhosis

Women, autoimmune diseases IgM antibodies.Anti-mitochondrial antibodies pruitis, jaundice, xanthomas (deposits of cholesterol in skin) Most common cause of loss of intrahepatic bile ducts. Remember you DON"T see loss of bile duct in primary sclerosing cholangitis, just fibrosis and stensos of extra- and intrahepatic bile ducts. Tx:ursodeoxycholic acid is drug of choice, slow down the symptoms. Advanced disease you need transplantation. **Osteomalacia and osteoporosis are important complications of long-standing cholestatic disease, and of PBC in particular. Screening with bone densitometry, calclium supplementation, and eventual treatment with vitmain D and/or bisphosphonates are essential in these patients' follow-up. Cholestyramine does what? forms a nonabsorbable complex with bile acids in the small intestine, thereby increaseing the ffecal loss of bile salts and cholesterol. helpful in reducing severe pruriti and hypercholesterolemis seen in patienns with primary biliary cirrhosi **another use of cholestyramine: postcholecystectomy thing that can happen is bile salt-induced diarrhea, occurs in 5-10% of patients following cholecystectomy and in patients with short bowel syndrome. Treatment of choice is bile salt-binding resins such as cholestyramine.

Pneumonia

Workup of Pneumonia -Chest X -ray ***On X-ray.. Viral: hyperinflation, hilar adenopathy, perihilar infiltrate. Adenovirus prob out of viruses. Bacterial: alverolar consoldiation Mycoplasma: interstistial infiltrates Most common cause of community aquired pneumonia: Strept. pneumoniae, H. influenz is 2nd most common. -Gram stain of sputum -Culture of sputum culture. Once oransim is identified, antiobiotics should be tailored to cover the organism. DAVID most reliable sign is tachypnea among lots of other signs Tx: Inpatient: see below Outpaitient: patients should hav normal 02 sat and be able to take oral fluids in order to be outpatients. tx: see below. Tx is oral therapy with Betal lactam plus macrolide or flouroquinolone. Community pneumonia with co-morbidites you treat with macrolide + cephalospronn or just a fluorquinolone. Community pneumonia without co-morbidies you treat with macrolide (azithromycin) or doxycyline Aspiration pneumonia: clindamycin or combination beta-lactam w/beta lactamase inhibitor Healthcare associated-within 90 days of visiting longterm nursing place, dialysis center, NOT a normal outpatient center tho Hosptial acquired: symptoms < 48 hrs after leaving hosptial Ventilator axxociated: occur within >48 hours after intuabation and presetns with fever, purulent secretions, and abnormal Chest x0ray. Patients should then have lower respiratory tract sampling (gram stain and culture) and receive epmpiric antibiotics). PCP pneumonia: TMP-SMX is initial treatment of choice for all patiets with suspected or documented PCP. IV done early and can transition to PO when better. If patient is intolerant of TMP-SMX, IV pentamidine can be used. **how to diagnose: bronch with lavage ICU: -assess risk for Psueomdona or MRSA -anti pseudomona Beta lactam + aminoglycoside + FQ or macrolide -if MRSA concern add vancomycin or linezolid PATHOGENS; After influenza pneumonia: Staph. aurea. Pneumonia w/ GI symptoms, hyponatremia, LFT abnormalities: Legionella. Most common hospital acquired: Pseudomonas, then Saph. Most common community atypical: Chlamydia. CURB-65 Assesses severity of pneumona. Confusion bUn >19 RR>30 blood pressure low Age>65 Each one gives you a point. 0-1 point: low risk, outpatient treatment 2 points: Consider short hospitilzation or close outpatientl. 3-5 points: Hopitalization strongly recommended, consider ICU care if higher score. *Another prediction rule used besides the CURB-67 is PSI, pneumonia severity index. Immunocompsomsed: Add TMP-SMZ to cover for PCP ***Many patients will get inital worsening in pulmonary funciotn with possible respiratory failure when antibiotic therapy is started, likely due to inflammatory effects of dead organisms in lung tissue. Corticosteroid steroid has been shown to minimize the worsening respiraory function. Corticosteroid should be given with antibiotics in patients with Pa02<70 mm HG on room air or an A-a gradient>35 to minimize pulmonary complications.

Human Bites microbiology and managment. Also animal bites.

Wound should be debrided and irrigated. With the exception of facial injuries (where cosmetic outcome is important and risk of infection is relatively low), primary closure should be avoided. Most wounds are left open to heal by secondary intention. Amoxicillin/clavulanate is the drug of choice for significant wound infections due to mammalian bites, including human bites. Provides coverage against oral aerobic and anaerobic flora, including Eikenella. A person who has sustained an animal bite should be treated with.. 1. local wound management 2. rabies prophylaxis 3. tetanus prophylaxis 4. measures to prevent or control bacterial infection. (amoxicillin/clavulanate for 5 days). RABIES Post-exposure prophylaxis (for rabies) for animal bites? If it is healthy-appearing domesticated animals (dogs, cats, ferrets), the animal can observed for 10 days without PEP. Unvaccinated individuals who are bitten by animals that could have rabies should receive PEP with active and passive immunization. TETANUS -Tetanus toxoid (active immunization) should be given to 1. ppl w/dirty wounds + reveiced booster more than 5 years ago. 2. ppl w/clean wounds +received booster more than 10 years ago. **2nd dose of toxoid is given at 1 month, and 3rd dose is igiven at 12 months. -Tetanus immune globulin (passive immunization) should be given to any individual with a dirty would and unclear or insufficient immunization history.

What imaging should be done frist in evaluation of painful joint?

X-ray. Must include at least two views at 90degress to each other.

Heart complications of Marfans?

You can get Aortic dissection which can subsequently cause aortic regurgitation. You can also get MVP

What do you gotta remember about Isoniazid liver toxicity

You can get a mild hepatotoxicity or severe INH hepatitis . Patient should have a baseline and monthly monitoring of aminotransferases. Mild hepatoxicity-you see mild LFT elevations but the prognosis is really good and condition is self limited. Don't stop tieh INH therapy in this case. severe INH hepatitis: Clinical manifestations similar to viral hepatitis. can happen more in people who drink alcohol daily, already have liver disease, or are >50 yrs old. If this is what is going on, INH should be discontinued immediately. INH should be d/c in patients who have aminotransferases >5 times upper limit of normal or develop symptoms with >3 time the upper limit of normal The other major side effect is peripheral neuropathy. Also, it can cause sideroblatic anemia. But giving B6 along with INH typically prevents neurotoxicity.

What happens in beta blocker toxicity?

You get bradycardia, AV block, hypotension, and diffuse wheezing. Calcium channel blockers, digoxin, and cholinergic agents would cause some of the above symptoms, but wheezing is indicative of beta-blocker toxiity. Most common presentation is bradycardia and hypotension which can lead to cardiogenic shock. Other effects are bronchospasm (beta 2 blockade) which can lead to diffuse wheezing, neurological affects (delirium and seizures), and hypoglycemia. Medicaiton: First give atropine and IV fluids, then if blood pressure is not improved then go to glucagon. It leads to increase in intracellular calcium--> increased contractility.

Wolff Parkinsons White

You have an accessory AV bypass tract. Short PR interval, delta wave, wide QRS. Although patients with WPW can be completely asymptomatmic, some develop TACHYARRHYTHMIAS which is then symptomatmic. Parosyxmal SV tachyardica is most common. Developmend of atrial fibrillation can be dangerous as it can result in V-fib and cardiac arrest. Tx: Catheter ablation therapy is recommended therapy in symptomatic patients with WPW. Has a nearly 90% efficacy rate.

Mnemonic for dehydration?

You know a ppatient is dehydrated when he or she is PARCHED Pee, Pressure (blood) Anterior Fontanel Crying Heart rate Elasticity of skin Dryness of mucous membranes

PFT stuff to remember from lecture with Dr. Chadha

You know the FEV1/FVC stuff. Know this as well. DLCO-low in COPD, pulmonary hemorrhage, interstitial fibrosis. DLCO-normal to high in asthma TLC-normal to high in obstructive TLC-decreased in restrictive Need to correlate Fev1/FVC w/TLC to see if it agrees. If not, maybe there is obstructive AND restrictive going on. RV: increase in obstructive RV: decrease in restrictive I think low VC is seen in both obstructive and restrictive. Pulmonary compliance is increased in COPD. Pulmonary compliance is decreased in restrictive. COPD airtrapping explained (increased RV) and progressive hyperinflation (increased TLC). Lung hyperinlfation preserved max Expiraotry airflow as the higher lung volume increases elastic recoild pressure. The enlarge airways decrease overall airway reisance. Hyperinlfaiont also flattens the diaphragm. Large lung volumes and diaphragmatic flattening make it more difficult to decrease intrahtoracic pressure during inhalation and thus increase the work of breathing. DLCO: measures the ability of lungs to transfer gas from alveoli to RBCc in pulmonary capillaries. Low in conditions characterized by loss of lung tissue or barriers to gass diffustion (for exaple, interstiial edema, intersittial infiltrates, tissue fiborsis) or loss of lung tissue (emphysema).

What are things you think about with ADPKD?

You normally see hypertension, palpabple bilateral abdominal masses, and microhematura Many patients with APKD have a progressive decline in renal function. THe ideal goal for blood pressure control in any patient with CKD, including ADPKD, is lees than 130/80mmHg. **Extremely important questions for USMLE step 3. Ultrasound is the procedure of choice fror screening asymptomatic family members of a patient with ADPKD. Presence of at least 3-5 cysts in each kidney is required to make the diagnosis. *Before considering peritoneal dialysis as a treatment option in patients with adulte polycysitc kidney disease, it is important to rule out diverticulosis. Extra-renal complications 1. Hepatic cysts-most common extrarenal manifestations 2. Valvular heart disease-most often mitral valve prolapse and AR 3. Berry aneurysms-danger for intracranial bleed 4. Colonic diverticula 5. Abdominal wall and inguinal hernia **Hypertension technically NOT an extrarenal manifestation of ADPKD cuz its the RAAS system activated that causes it. **Extremely important questions for USMLE step 3.

If a person gets an infection after any instrumentation of upper aiwray or esophagus what do you expiect to see?

You suspect that it's an anaerobic lung infection. Patients with pnemonia caused by anarobic organissm typically present with systemic symptoms such as fever, malaise, as well as a characteristic foul-smelling sputum. Clindamycin is the drug that you use.

Approach to platelet abnormalities

You wanna think first is it a quantitative (high or low) problem or qualitative (normal count but abnormality in function) QUANTITATIVE 1. Thrombocytopenia DECREASED PRODUCTION -viral infctions (EBV, HEp C, HIV) -Chemo -Myelodysplaisa Alchohol use -Congenital (Fanconi syndrome) -Vit B12 or folate deficienty INCREASED DESTRUCTION -SLE -Meds (heparin) -ITP, DIC, TTP/HUS -Antiphospholipid OTHER ---Sequestration from splenomgaly, dilutional due to massive RBC transfusion. 2. Thrombocytosis ---Reactive or autonomous

You know its anion gap MA but wanna know if its ethlyene glycol, methanol, or ethanol intosication.

You will see a high osmolar gap in these as well. So you calculue osmolarity for serum and compare that to observed osmolarity. Normal osmolar gap is <10. If observed osmolarity-calculate osmolarity is greater than 10 then you have a high osmolar gap and the cause of your AG MA is one of those three. WIth ethlyne glycol poisoning (anti-freeze) you also might see CALCIUM OXALATE (rectangular, envelope shaped crystals) in urine. TX: giving Fomepizole (a competitive inhibitor of alchool dehydrogenase) or ethanol prevents further breakdown of ethylene glycol into its toxic metabolites and is integral part of treatment. Hemodialysis may be required. Methanol damages the eye, wherease ethylene glycol damages the kidneys.

A positive PPD test means..

You've been infected or are currently infected. Doesn't go positive from exposure. This is why the next step is X-ray. This is why if you've had a positive PPD in the past, you don't do new ones cuz its always gonna be positive

Multiple episodes of thrombosis without a clear precipitating factor should raise concern for what in younger patient? older patient?

Younger: genetic defect. Older: malignancy.

Acute epididymitis in younger patients? older patients?

Younger: usually caued by sTDs like C. trachomatis or N. gonorrhewa Older: usually non-sexually transmitted and is caused by GRAM NEGATIVE RODS, like E.coli. Not staph aures.

DDX of myopathies

a clue could be the patient has the inability to comb hair with difficulty holding arms up cuz that indicatd a proximal muscle weakness and likley a myopathy. GLUCOCORTICOID INDUCED MYOPATHY -proressive proximal muscle WEAKNESS and trophy WITHOUT pain or tenderness -ESR and Creatine kinase are normal POLYMYALGIA RHEUMATICA -Muscle PAIN AND STIFFNESS in the shoulder and pelvic girlde -NO WEAKNESS -RESPONDS rapidly to GLUCOCORTICOIDS -ESR is HIGH, Creatine kinase is normal INLAMMATORY MYOPATHIES (polymyositis, dermatomyositis) -WEAKNESS if more prominent than pain. -SKIN RASH AND INFLAMMAOTRY ARTHRITIS may be present -ESR is HIGH and Cratine Kinase is HIGH -Muscle biopsy is the best test. STATIN INDUCED MYOPATHY: -muclpe pain/tendnerss with or witout wakness -rare rhabdo -ESR is normal, Creatine kinase is HIGH HYPOTHRYOID MYOPATHY -Mucle pain, cramps and weakness involving proximal muscles -Delayed tendon relfexes and myodemea -FEATURES OF HYPOTHYROIDISM -ESR is normal, Creatine kinase is HIGH HYPERTHYROID MYOPATHY -weakness of proximal muscles of upper extremities-es. **aldolase and creatine kinase are markers of myocyte injury and are used to r/o myopathies like polymyositis.

Explain anemia of chronic disesae?

aAnemia associated with chronic inflammation (autoimmune for example) or cancer. Precise etiology not fully understood but is generally thought to be due to suppression of hematopoiesis by inflammatory cytokines. Iron is locked away in the macrophages to prevent bacteria from accessing iron. So ferritin increases, TIBC decreases, serum Fe decreases (if bone marrow can't use iron from macrophage, it will start to take it from serum). Common complication of rheumatoid arthritis. Foundation of treatment for ACD is addressing the underlying inflammatory disorder.

Sarcoidosis?

affects blacks more. Pulmonary sarcoidosis is often diagnosed incidenctally on routine CXR by presence of BILATERAL HILAR ADEONPATHY(mediastinal widening suggests this). On biopsy you see NONCASEATING GRANULOMAS. up to 30& present with extrathoracic manifestations such as erythema nodosum, uveitis, polyarthralgia elevated ACE enzyme often seen Definitive diagnosis of sarcoidosis can be made from the biopsy of the easily accessible lesions, including: 1. any palpable lymph node 2. subcutaneous nodule except erythema nodosum 3. enlarged parotid 4. lacrimal gland If there is no easily accessible lesion, fiberoptic bronchosocopy with transbroncial lung biopsy is the procedure of choice.

sick sinus syndrome

also called sinoatrial node dysfunction Comprises a collectin of pathologic findings that result in bradycardia. These include sinus arrest, sinus exit block, and sinus bradycardia. About 50% of patients with sick sinus aalso have associated supraventricular tachycardia, most often A-fib or A-flutter. The tachy-brady syndomre is characterized by rapid ventricular conduction during episodes of A=fib, but resting bradycardia between episodes.

Thrombosis, history of miscarriages in a patient suscpeted of SLE suggests?

antiphospholipid syndrome. APS characterized by 1. Venous thromboemoblism OR recurrent early miscarriages 2. Presence of antiphospholipid antibody such as the lupus anticoagulant, anticariolipin antibody, or beta 2 glycoprotein antibody. * the lupus anticogulant, is a pro-thrombotic immunoglobulin that causes a spuriosly prolonged partial thromboplastin time (PTT) in vitro. So what you see on testing is a positive VDRL, prolonged PTT, and thrombocytopenia. Prophylaxis with low dose aspirin and LMWH are recommended to avoid pregnancy loss.

Failure of a prosthetic aortic valve often leads to what?

aortic insufficiency

Anti-smooth muscle antibodies

autoimmune hepaitits.

Avascular necrosis.

avascular necrosis of the femoral head usually presents as progressive hip or groin pain without restriction of motion range and normal radiograph on early stages. Although a variety of things can cause it, corticosteroid use and excessive alcohol intake account for about 90% of of cases. Other ccauses are sickle cell, trauma, alchohl abuse, gout and hypercoagulable state MRI is the GOLD STANDARD for the dagnosis of avascular necrosis of hip. REMEMBER, X-rays are NORMAL in early stages so they aren't that useful for avascular necrosis. Tx: -rest, partial weight bearing, and analgesics for early disease -core decompression offers a chance to preserve the native join in early stage 1 or 2 disease (positive X-ray without femoral head collapse). -total hip replacement is therapy of choice for stage 4 disease (flattening of femoral head with joint space narrowing). **discontinuing prednisone does not halt progress of disease.

What is brain death?

basically Neuro tests are negative and Apnea test shows absent respiratory responce when disconnected from ventilator. Its defined as the irreversible loss of function of the whole brain, including the brainstem. Its a LEGALLY ACCEPTABLE DEFINITION OF DEATH and the hospital can remove person from ventilator legally without taking any other further steps with family. Although its a good idea to have family involved, family permission is not legally required to dicontinue mechanical ventilation in a patient with brain death.

signs of inlammatory etiology of back pain?

better with activituy or exercise, no improvement with rest, gradual onset, HLA-B27 present. Anklysoing spondylitis, reactive arthritis, psoriatic arthritis, inflammatory bowel disease *Enthesitis: inflammationand patin at sites where tendons and ligaments attach to bone. Most commmonly seen in HLA-B27 associated arthropathies like AS, psoorriatic arthritis and reactive arhtirirs. Particulalary prominent in AS and classically maniefsts with heel pain due to tenderness at the insertion of the Achilles tendon. Tibial tuberosities and iliac crests are also common sites of smptoamtic enthesisi.

Primary care: hypertension

birth control pills are the most common secondary cause of secondary HTN in yoiung women Pathophys of HTN effects on heart: 1. incrased afterload--> concentric LVH-->decreased LV function--> chamber dilates and you get signs of heart fialure 2. HTN accelerates atherosclerosis, leading to high incidence of CAD Where it damages: -CNS: intracerebral hemorrhage, encephlopathy -Eyes: hemorrhages, exudates, papilledema -Aorta; arotic dissection -Heart: CHF, CAD, MI -Kidneys: renal failure Tx: 1st line montherapy: Thiazides, long acting Ca channel blocker, and ACE inhib or ARB. Betablockers are not commonly used as initial montherapy, they come after. other medicaionts that can come after: alpha blockers, hydralazine. *remember in reproducive age woman get a pregnancy test because thiazides, ANE inhib, CA channel blockers and ARBs are contraindicated. Can use beta blockers or hydralazine. GOal of Tx: BP should be lowered to <140/90, with 135/85 be MINIMUM goal in people with diabetes or renal insufficiency. The ideal goal it to lower <120/80 but that is not always practical.

Teardrop cell

bone marrow infilration (myelofibrosis)

Pleural effusion causes?

can be transudate or exudate dpending on results of fluid analysis for protein and lactate dehydrogenase; origins include CHF, infectious (mycobacgterial pneumonia), and malignant (lymphoma)

Primary care: tension headache

cause unkown, but precipitants include anxiety ,stress, depression pain is "visorlike", encircles entire head. can be acccompanied by tender muscles, tightness in neck muscles

VZV: varicella-zoster virus

causes 2 different disease...varicella and herpes zoster Varicella - is what chicken pox is...all states oflesions over body. in adults chickenpox is more sever, with systemic complications like pneumonia and encephalitis. Zoster -called shingles, represents teh recurrent of VZV in a specific nerve, in dermatomaos disribution. Older patients may develop POSTHERPETIC NEURALGIA. Post hherpectic neuralgia can be prevents and/or treated with TCAs like amitryptyline or nortriptyline along with acute antiviral therapy. -remember that pain from shingles may PRECEDE the onset of vesicular rash by several days, during with the diagnosies may not be obvious. TX: Valacyclovir is drug of cohice. But acyclovier is less expensive and is also effective. **Herpes zoster opthalmicus -Caused by VZV. Characterized by dendriform corneal ulcers and a vesicular rah in trigeminal distribution. -You have fever, malaise, burning, itching in periorbital region **The diagnosis of herpes zoster or varicella is made clnically. If patient is immunosuppressed (HIV) the rash can be atypical and can be confused with herpes simplex. In this case if patient is critical and antiviral therpay needs to be started, lesions can be scraped for PCR or immunofluorescence studies.

What is Nelson's snydrome

characterized by pituitary enlagement, hyperpigmentation, and visual field defect following bilateral adrenalectomy. Usually, these tumors are rapidly growing and can be treated with surgery and/or local radiation.

Most consistent reversible risk factor for pancreatic cnacer?

cigarettes

what are dipsticks for?

commercially available kits that dtect presence of lekocyte esterase and nitrite in the urine of patients with suspected UTI.

3rd egre heart block

complete heart block -independent atrial and ventricular activity -emergency, pacemaker treatment -causes : inferior wall MI, digitalis toxicity, conduction system disease

the types of bad hypertension

continuation of photo -Acute coronary syndrome: Nitroglycerin -Aortic dissection: Labetalol. HYPERTENSIVE URGENCY -Severe, usually >180/120 with no sympoms or acute end-organ damage. HYPERTENSIVE EMERGENCY -Severe hypertension with acute, life-threatening, end-organ complications 1. Malignant hypertension: has papilledema, retinl hemorrhages, or exudates 2. Hypertensive encephalopathy: has cerebral edema TX for hypertensive emergency: You wanna lower MAP ((2DP + SP)/3) by no more than 20%, cuz there is risk of reduction in coronary and cerebral perfusion with IV blood lowering agents. Kinda risky. Common IV agents are -Labetalol -Nitroprusside -Phentolamine if pheo is cause

Culters obtained before empiric antibiotic therapy

endocarditis meningitis osteomyeltisi central line infection cellulitis around central line septic arthritis *pneumonia is the opposite it seems... "Sputum culture is optional in outpatient setting due to low yield of culture results and high success rate of empiric antibiotics" maybe in inpatient setting its different *also, you get cultures before antibiotic therapy for complicated cystitis, uncomplicated and complciated pyelo. Don't need to worry about getting culture before antibiotic therapy when you have uncompliated cystitis.

Goiter cause

enlarged thyroid gland caused by excessive stimulation of TSH receptors. Graves disease and iodine deficiency common causes.

What raises suspicion for necrotizing fascitits?

erythema and swelling, servere pain out of proprootion to phycial exam, signs of tissue necrosis such as crepitus, pururlent drainage, or radiographic evidence of gas in deep tissues. When skin or soft-tissue infection is suspected, rapid progression of physical examination findings or severe systemic signs such as hypotension should raise suspicion for necrotizing fascititis. 2 types of clinicaly distinct necrotizing fascitis have been described. The most common form (type II) usually occcurs in ppl w/o concurrent medical ilness. Typically GROUP A strept. In contrast , type 1 is usually seen in ppl with underlying diabetes and PVD. Generally polymicrobial. ***Crepitus is more commmon in anaeraobic organisms, like C. perfringes or B fragilis.

Pericarditis

etiology: -Viral: recent viral URI, defiinitve cause not known -Bacterial: TB, strept. , (rheumatic fever causes pancarditis) , staph -Metastasis -Immediate post MI -Dresslers syndrome (autoimmune resposne to infarcted myocardium -Uremia (>60). Tx w/hemodialysis. Dx: Ausuclation: Friction rub on expiration, on EKG: St elevation and PR depression. Diagnosed by presence of at least 2 of the 3 classic features: 1. pleuritic chest pain 2. friction rub 3. diffuse concordant ST segment elevation on ECG Tx:: Most cases are self limitied and resolve, treat underly9ing cause if known, NSAIDS are mainstay of therapy for pain.

Primary care: cluster headaches

excruciating periorbital pain "behind the eye": almost always unilateral usually begins a few hours after patient goes to bed and lasts 30 to 90 minutes: awakens patient from sleep. attacks occur nightly for 2 to 3 months and then disappear. remissions may last from several months to several years. Tx: sumatriptan and O2 inhalation are helpful.

magnesium IV used for ?

first line therapy for conscious and stable patients in Torsades. If they are hemodynamically unstalbe then first line therapy is immediate defibrillation.

Ch

for

Sinus bradycardia

heart rate < 60 Ppl with symptomatic bradyarrhythimas in inferior MI should be treated with IV atropine. If has persistent hypotension, give IV fluids. Temporary cardiac PACING is indicated only in patients with persistent and symptomatic bradyarrhythmias that are not responsive to IV atropine. If R-R distance is at least one inch, consider: "One Inch" Overmedication Inferior wall MI (most common arrhtyhami in patients with inferior wall MI due to increase in vagal tone after MI.) Normal variant Carotid sinus hypersentivity Hypothyroidism

Nephritic:

hematuria with RBC casts, mild proteinuria often include hypertension, edema, and azotemia (large amounts of nitrogen containing compounds in blood due to decreased renal filtration, like urea, creatinine. )

Spherocyte

hereditary spherocytosis autoimmune hemolysis

Causes of paradoxical splitting of S2

hypertrophic cardiomyopathy aortic setnosis LBBB

most common cause of persistently stiff, painful, or unstable joints following sprains is...

inadeuqate rehabilitation.

Acute pancreatitis :

inflammation of pancrease due to parenchyman autodigestion by proteolytic enzymes GETSMASHED Gallstones, ethanol, trauma, steroies, mumps, autimmune, scorpion sting, hypercalemia/hypertiglyceridema (>1000), ERCP, drugs (comon drugs are diuretics, (anti convulsants) valproic acid, and (antibiobitcs) metronidazole. -hypercalemia can cause pancreatitis and pancreatitis can cause hypocalcemia a. acute pancreatitis can generate free fatty acids that avidly helate insoluble calcium salts in the pacreatic bed, resuling in hypocalcemia Signs: -constant midepigastric or LUQ pain that radiates to back, fever, vomiting, tender abdomen, The GREy TURNER signs (flank discoloration) and CULLEN SIGN (perumbilical discoloration) suggests RETROPERITONEAL HEMORRHAGE -remember that US should be peformed in ALL patients with acute pancreatitis once the Dx has been confirmed to look for gallstones Dx: requires 2 of the following: -acute epigastric abdominal pain often radiating to back -increased amylase/lipase >3 times normal limit -CT scan scan showing it or US showing it. **REMEMBER: you only need 2 out of three so imaing not required for diaagnosis if you have other 2. Also, after diagnosis, you ALWAYS do ultrasound to look for gallstones. **also, all patients with pancreatitis should also have triglycerides and calcium checked as these etiologies may be missed otherwise. Tx: IV hydration, Bowel rest, Antibiotics (can develop infection with gut-derived bacteria). **antibiotics are indicated only in patients with clninical or tissue evidence (by CT scan) of infection of necrotic pancreatic tissue or evidence of extrapancreatic infection. NOt indicated in patients with mild attacks of acute panreatitis. ***which antibiotics to use: imipenem, metronidazole, or flouroquinoles are preferred for both for empiric and targeted coverage. If Gallstones the cause then do cholecystectomy. Sequelae: < 48 hours: usually isolated pleural effusion containing high amylase peripancreatic fluid 1-4 weeks: Pseudocyst: best diagnosed by US and often resolves sponteneously. 4-6 weeks: Abscess; required surical drainage Complications: pleural effusion, ARDS, ileus, and renal failure Prognosis: "GA LAW", Ransons's criteria that predict risk of mortality. its the oldest scoring system for panreatitis severity but the predictie value is low and can only be calculated completely after patient hospitizlied for 48 hours. In contrast, the APACHE II scoring system is better for prognostic value, it was originally creatied for critically ill patients in ICU, has been studied extensviely in acute pancreatitis and has been found to be real good negative predicitve value and modest positive predictive value. Can be calculated on admission and on a daily basis. Patients with score>8 should undergo CT scan at 72 hours to evaluate degree of pancreatic necrosis. **Hemorrhagic pancreatits is a severe, life-threatening illness characterized by retroperitoneal hemorrhage and pancreat necrosis. Physical examination findings may include a bliush disocolration of flangs (Grey Turner) or periumbileeical region (culles sign) resulting from blood accmulation. **INfected pancreatic necrosis is the diffuse infection of necrotic pancreatic tissue, usually occuring 1-2 weeks after an episode of acute pancreatitis. These people are gravely ill. Surgical debridement is the treatment of choice. **Pancreatic ascites results from rupture of the pancreating duct or leakage of psuedocyst into peritoneal cavity. Abdominal distention and shifting dulnes are typically observed. Significant pain is uncommon. **Lipase is more sensitive and specific than serum amylase. Amylase is nonspecific as it also elevated in a number of other conditions, like acute parotitis, intestinal disorders, kidney disease, cholecystitis, and fallopian tube disease.

Explain LMWH (enoxaprin (Lovenox) is one)

inhibit 10a like heparin but don't inhibit as much 2a or plateley aggregation can't be monitored by PT or PTT cuz don't affect either Longer half life than heparin but also nothing exists to reverse effects examples are enoxaparin (Lovenox) Are being used more now because of better conveniance than heparin and decreases risk of side effects (HIT, ostoporosis). -given subq, PTT monitoring not necessary, eeasire to use as outpatient. Patient may be discharged if stable and the patient can continue LMWH until the level of long-term anticoagulation (warfarin) is therapeutic (check INR for this). excreted in kidneys so use cautiously in patient with renal fucntions

Glossitis

iron defieincy anemia

Stj

j

norm

j

Maternal hyperglycemia results

macrosomia hypocalcemia hypoglycemia hyperviscosity due to polycythemia respiratory diffultieis cardiomyopathy and CHF due to excessive glycogen deposition in the fetal myocardium

ESR range

male 0-15 female 0-20

Primary sclerosing cholagnitis

men, ulcerative colitis Chronic progressive disorder of unkown etiology with inflammation, fibrosis and stricutring of medium and large sized intrahepatic and extrahepatic bile ducts. Continued bile duct destruction leads to end-stage liver disease and portal hypertension. Frequently associated with UC. Labs usually show unexplained elevated LFTs in a cholestatic pattern. (elevated ALT and AST, severely elevated Alk phosph and bilirubin. Dx: Not US. Cholangiogram shows multifocal narrowing and duct dilataion "beading". Also "onion" skin fibrosis. Tx: Only cure is liver tranplant

Isolated hypertriglyceridemia

more genetic diseases

Primary care: Sinusitis

most cases are complications of common cold or other URIs. May also be caused by nasal obstruction due to polyps, deviated septum, or foreign body. -acute bacterial sinusitis: usually due to Strept pneumoniae, H. influenzae, or anaerobes other types: viral, fungal, or allergic -most common sinuses involved are the maxillary sinuses. maxillary sinusitis (most common) pain over the cheeks that may mimic pain of dental caries. -if a patient has a cold beyond 8 or 10 days, or if the cold symptoms improve and then worsen after a few days "double sickening" consider acute bacterial sinusitis (may be a secondary bacterial infection after a primary viral illness). -chronic sinusitis: symptoms should be present for at least 2 to 3 months. on exam: - look for purulent discharge draining from one of the turbinates. - perform transillumination of maxillary sinuses (note impaired light transmission) the room must be completely dark with a strong light source. -palpate over the sinuses for tenderness (not reliabe finding) imaging studies: - conventional sinus radiograph: lok for air-fluid levels in acute disease -a CT scan is superior to radiograph, for complicated disease complications: mucocele, orbital cellulitis, osteomyelitis, cavernous sinus thrombosis Acute sinusitis Tx -General measures: saline nasal spray, avoid smoke -Decongestants (pseudoephedrine): facilitate sinus drainage, give no more than 3 to 5 days -Antibiotics -Antihistamines: reserve for patients with allergies; use discriminately because of the "drying effect" (can make secretions thicker and can worsen congestion) Chronic sinusitis Tx -treate with a broad spectrum penicilinase resistant antibiotic -refer to ENT; endoscopic drainage may be necessary

Lumbosacral strain?

most common cause of acute back pain . Typically back pain after physical exertion..if absence of radiation, paravertebral tenderness, negative straigt leg raise and normal neurologic examination.

Osteomyelitis

most of hhematogenous reason is Staph aureus. elevated WBCs, ESR, Crp DDx: septic arthritis, rheumatic fever, Ewing's sarcoma Tx: Medical: IV antibiotics after obtaining culture specimen. monitor temp, swelling, pain, joint motility and WBCs Surgical: open drainage of abscess if antibioitcs fail or signs of abscess appear. After surgical drainage, wound is left open to heal by secondary intention. *Chronic osteomyelitis often seen in extremities of diabetic patients usually polymicrobial Tx: extensive debrdiement of all necrotic and granulation tissue along with reconstruction of bone and soft tissue defects with concomitant antibiotics

Hypothermia: lab abnromalities

most of the lab abnormlaties will improve with normalization of core temperature.

demand ischemia

myocardial oxygen demand. serum trops are increased in a number of clnical settings: sepsis, septic shock, SIRS, hypotension or hypovolemia, A-fib or other tachyarrhythmias. --how to know if trop elevation is 2/2 ACS? factors that suggest ischemia are ECG changes, chest pain, WMA on echo and other atherosclerotic risk fators.

CKD, patho, Tx:

nephrons are lost and remaining healthy ones try to compensate by increasing their GFR. This damages them as well. You decrease syntehsis of activeaed VIt D, ammonia, and erythropoeitin. usually asymptomatic until GFR<30 Tx: ACE-inhibitors may slow progression, treat reversible causes, diet: protein restriction, dialysis (decision is CLINICAL, no absolute lab value that requires dialysis)

Howel Jolly bodies

nuclear remnants found in RBCs. Normally removed by spllen but if have hyposplenai or asplenia its not gonna be removed.

How do you diagnose Chlamydia urethritis in men?

nucleic acid amplifiaction testing of a first-catch urine sample what is more common etiology of urethritis in men? 1. Gonorrhoeae 2. Chlamydia

Explain HIT

occurs with heparin. Not much with LMWH but STILL CAN OCCUR WITH LMWH (enoxaprin). its a drop in platelets a few days after heparin administration. Platelets clump leading to DVT or PE. Decrease in plateltey count by 50% suggests HIT There is actually Type 1 HIT and Type 2 HIT Type 1 HIT; non-immune mediated, not really significant, 1-4 days after heparin, platelet count rarely below 100,000. Type 2 HIT: 5-10 days after heparin, platelet count >20,000, increased risk of thrombosis, necrotic skin lesions at ijectino sites. Dx: gold standard confirmatory test: serotonin release assay. Tx: stop heaprin, use other anticoagulatnt such as direct thrombin inhibitor (argatroban ) or fondaparinux.

Most common cause of vertebral compression factor is ?

osteoporosis and osteomalacia.

Hypertension definition

over 140/90 on TWO seprrate occasions. 90% is primary, idiopathis 10 % is secondary: -renal parenchymal disease (chronic pyelonephritis) -renal artery stenosis -primary hyperaldosteronism (cushings and conn's syndrome) -pheochromocytoma

Patients with very high TGs, >1000, are at risk for

pancreatitis

Explain PNH

paraoxysmal nocutrnal hemoglobinuria. Autoimmune hemolytic disorder characterized by intravscular and extravascular hemolysis and hemoglobinuria. Lack proteins CD55 and CD59 that normally stop complement from attacking RBCs. You get hemolysis, cytopenias, and HYPERCOAGULABLE state (portal vein thrombosis). Patients with autoimmune hemolytic anemia have a tendency for venous thomboembolism but those with PNH are at particular risk, especially for intraabdominal or cerebral veins. Dx: Flow cytoometery tests Tx: iron and folate supplementation, Eculizumab (monoclonal antibody that inhibits complement activation).

Tinea capitas

scaly erthematous patch on scalp, hair loss, possible lymphadenopathy, "shared combs" transmission Dx: KOH to document spores Tx: ORAL GRISEOFULVIN

Most common bacteria that cause epiglottis?

speicially in the adulte population, is Haemohpilus influenczae and Stretpooccus pyogenes. Its a medical emergency and rapid treatment must be initiated in order to prevent obstruction of the airway.

AIN

sually associated with exposure to medications such as beta lactams and proton pumop inhibitors. However, AIN usually occurs 7-10 days after drug exposure. Patients can develop findings that include skin rash, eosinophilia, esoinophiluria, and pyuria.

Dermatomyositis

symmetrical proximal muscle weakness and erthematous rash on the dorsum of the fingers (Gottron's sign) and/or upper eyelids (heliotrope eruption). Diagnosis based on clnical features and serum antibody testing but is usually confirmed by muscle biopsy. Over 15% of adulte patients will develop internal malignancy, so age-appropriate cancer screening is essential in these patietns. *interstitial lung disease with progressive pulmonary fibrosis and secondary pulmonary arterial hypertension is one of the leading causes of death in patients with polymyositis and dermatomyositis.

Primary care: Common Cold

synonymous with acute rhinosinusitis: inflammation and congestion of mucous membranes of nasal and sinus passages caused by viruses: mostly rhinoviruses most resolve within 1 week but symptoms may last up to 10 to 14 days Clinical features: rhinohrrea, sore throat, malaise, nonproductive cough, nasal congestion. Fever is uncommon in adults (suggests a bacterial complication or influenza) but is not unsual in children. Tx (symptomatic) -adequate hydration -rest and analgesics -cough suppressant (dextromethorphan, codeine) -nasal decongestant spray for less than 3 days -oral 1st generation antihistamines for rhiorrhea/sneezing

Primary care: sore throat

think of folllowing: virus (by far most common cause), tonsiliitis, strep throat, mononucleiosis viral versus bacterial infection-often difficult to distinguish, but if patient has a cough and runny nose, virus is more likely remember that tonsillopharyngeal exudate does not differential viral and bacterial causes Dx: -throat culture:takes 24 hours but is more accurate than rapid strept test -rapid strep test: results within 1 hour, but wiill not indicate wheter sore throat is caused by bacterium other than Strept. -if mononucleiosis suspected: obtain appropriate blood tests (monospot) Tx -if strep throat: penicillin for 10 days (erythromcyin if patient has penicillin allergy) -if viral -symptomatic treatment -if mononucleosis-advise rest and acetaminophen/ibuprofen for symptoms -symptomatic treatemnt of sore throat a. acetaminophen or ibuprofen b. gargling with warm salt water c. use of humidifier d. sucking on throat lozenges, hard candy, flavored frozen dessert

Diagnosis of epilepsy requires ?

two or more unprovoked seizures.

C. dif diarrhea is usually how many times a day? Also what are risk factors?

up to 10 or 15 times days Risk factors: advanced age, recent antibiotic use, hospitiatlzation, comorbid ilness..AND if you have prolonged gastric acid suppression with PPis or H2 antagosniss that can aslo increase your risk.

ICP

usually presnts as headache, nausea, vomiting, diplopia, personality change Can present as bulging fontanelle, impaired upward gaze in infants Presentation depends also on rate at which the ICP inrcreases. If increases slowly, then intraanial structures have time to accomadoate for the change. Coughing or Valsalva maneuver tends to make pain worse yby increasing ICP further. Papilledema-think increasd ICP Classic presntation of pressing of brainstem is Curhings triad= decreased RR, decreased HR, increased BP

Bacterial keratitis

usually seen in contact lense weareers and following corneal trauma. Cornea ppears hazy with central ulcer and adjacent stromal abscess.

Acute ischemic colitis presentation?

usually seen in patients who have evidence of atherosclerotic disease and is usually manifestated by acute abdominal pain followed by bloody diarrhea. Most vulnerable areas are watershed areas, which include splenic flexure and rectosigmoid junction. Patients usually have elevated white count. X-rays and sigmoidoscopies usually show mucosal edema and mucosal ulcerations.

Primary care: Laryngitis

usually viral, common cause of hoarseness, typically self limiting, patient should rest voice until laryngitis resolves to avoid formation of vocal nodules

In syphillis, what does VDRL and RPR test? FTA-ABS?

veneral disease research laboratry and rapid plasma reagin are rapid screening assays, referred to as nontreponoemal testing ; measure antibody to cells affected by Treponema pallidum. may be false positisve. fluorescent treponemal antibody absorption; referred to as treponemal testing; measures specific antibody to Treponema pallidum

What is not affected with conjunctivitis?

vision

What are rales?

wet or 'crackly' inspiratory breath sounds due to alveolar fluid or debris; usually heard in pneumonia or CHF

Leukemoid reaction vs CML, how do you tell the difference?

what leukemoid reaction is a marked increase in leukocytes to to a severe infection or inflammation. These 2 are indistinguishable on peripherlal smear. You see sudden elevation in total leukocytes and marked increase of granulocyte precursos (left shift). Its the leukocyte alkaline phosphatase test (LAP) that is used to distinguish these two. Its high in leukemoid and low in CML.

Explain stress teset

you have exercise or pharmacologic, while ECG monitors changes. Considered positive for CAD if patient develops: -ECG changes (ST elevation or depression) -decreased blood pressure -failure to exercise more than 2 minutes due to cardiac symptoms Dobutamine stress echo is an appropriate choice in patients who are unable to excercise and are not hypertensive at rest.

DDx for anterior mediastinal mass

"4Ts" thymoma, teratoma (and other germ cell tumors), thyroid neoplasm, terrible lymphoma.

Target cell

"HALTS said the hunter to his Target" HbC disesase Asplenia liver disease Thalassemia Sickle

Explain clopidogrel

(Plavix) Blocks ADP binding to platelets when they be trying to aggregate so increases bleeding time Used for ACS and if any stent put in for any indiction patient should recieve for at least 1 year.

Evaluation of Chest Pain in the ED

****patient presenting to ED w/ chest pain and suspected ACS should be a ADMINISTERD ASPIRIN as soon as possible. Early antiplatelty therapy with aspirin reduces the rate of MI and overally mortaliy in patients with ACS

Vitamin D deficiency

**Gastric bypass causes malabsoprtion in majority of patients. this is one of the vitamins will need to supplement.

other stuff about iron defiency anemia

**Iron deficiency has elevated red cell distribution width, which is typically >20% in iron deficiency. Elevated RDW commonly occurs in nutritional defieicences as nutrient level available for RBC synthesis vary throughout the day, resulting nin cells of varying size. **Ferritin levels in iron deficiency anemia? Ferritin is low. Its the most reliable test available. Its the primary iron storage protein of body. Iron stores in macrophages and the liver. **Almost all patients with serum ferritin concentrations of less than traditional cutoff of 15ngm/Ll are iron deficient. However, the sensitivity using this cutoff is only modest at best and it cannot be used to exclude the diagnosis of iron defiency since a majority of patients with a level of 15-30 are also iron deficient. **Most common reason for iron deficiency anemia in older people? GI bleed. Next step would be colonoscopy. A single negative occult blood test DOES NOT exclude the possibility of GI bleed. **Whats a common cause of iron deficiency andemia? NSAIDS and aspirin. Can cause gastritis and/or gastric ulcers leading to chronic GI blood loss and depletion of iron stores.

AKI genral stuff

*ATN is responsible for most cases of acute renal failure in hospitlized patients. the etiopathology generally involves a perfusion deficit due to hypovolemia, hypotension, shock, sepsis, or lwo CO states. typical presentation is oliguria following hypotensive episode, with eelvated BUN adn creatinine levels (though the ratio is typically normal) and AG acidosis. You get muddy brown cases too. *Prerenal azotemia is assoicated w/ decreased fractional excretion of sodium; however, once ATN sets in, the fractional excretion of sodium increases (usually >2). Response to a FLUID CHALLENge is the gold standard in distinguishing prereanl azotemia (which responde to a fluid challenge with improved urine output) from ATN. *remember that fluid OVERLOAD can can occur in patients who are oliguric or anuric. If no hypovolemia findings on physical exam and no ongoing volume loss, there is no indication for volume exapnsion with IV saline..even if patient is oliguric. Excess saline infusion can worsen clinical status by causeing volume overload (pulm edema) and hyperchloremic metabolic acidosis (non AG met acidosis). ---a trial of loop diuretics is generally indicated if there is evidence of fluid overload (like pulmonary edema). ---IV albumid can expand intravascular volume. IT albumin is used for volume expansion in cirrhotic patients w/ hepatorenal syndrome or SBP, as they are at risk for this spacing of fluid. **what is third spacing? Third-spacing occurs when too much fluid moves from the intravascular space (blood vessels) into the interstitial or "third" space-the nonfunctional area between cells. This can cause potentially serious problems such as edema, reduced cardiac output, and hypotension

Anaphylaxis

*At the first supsicion of anaphylaxis, -aqueous epinephrine 1:1000, in a dose of 0.2 to 0.5 mL is injected subcu or intramuscl. Repeated injections can be given every 15 to 30 minutes when necessary. -Rapid IV infusion of fluids is essential to replace loss of IV plasma into tissues. -Endotracheal intubation may be required due to airway obstruction caused by larnyx edema or by bronchospasm. Bronchospasm shouls respond to subcu ephinephrine or terbutaline. - antihistamines can be useful to treat cutaneous manifestations of urticaria, angioedema (painless deep subcutaneous swelling that often is periorbita, circumoral, and facial), and pruritis.

Restless leg syndrome

*Persistent/moderate to severe symptoms -First line: Dopamine agonists (pramipexole) -Second line: Alpha-2-delta calcium channel ligands (gabapentin enacarbil) RLS is more common in older people. Nearly half of ppl with idiopathic RLS have positive family history, clinical diagnosis. RLS characterzed by spontaneous, repeated leg movements (to provide relief) in association with unpleasant sensations that occur while at rest. It is associated with IRON DEFICIENCY and iron supplementation improves symptoms. A serum ferritin level should be obtained as iron deficiency is frequently present in absence of anemia. *Levodopa has been shown to cause "augmentation" in RLS patients, which is PARADOXICAL WORSENING (occuring earlier in the day, spreading

Hypothermia: classification and treatment

*bradycardia is a physiologi response to hypothermia and resolves with rewarming. atropine or cardiac pacing is not required unless bradycardia persists after temperature is corrected. *patients with hypothermia should be handles gently as rough physical handling can precipitate serious ventricular arrhthmias. even the myocardial irritation that could occur during the placement of jugular or subclavian lines can cause ardiac arrhthmias. If central line placement is required, femoral lines are preferred. *pulmonary edema is common in significant hypothermia, and does not necessarily indicate additional pathology. should improve with rewarming. *the usual increase in core temperature with external warming is around 1-2C/hr

Primary care: hemorrhoids tx:

*in patients with bleeding from hemorrhoids, blood is usually on the SURFACE of stool as opposed to mixed in with stool 1. General measures to ease symptoms -sitz bath -applicatino of ice packs to anal area and bed rest -stool softeners to reduce strain -high-fiber, high-fluid diet -topical steroids 2. rubber gand ligation for internal hemorrhoids: rubber bands applied to hemorrhoidal bundles leads to necrosis and sloughing of lesion 3. surgical (hemorrhoidectomy)

Recurrent pneumonias

*nearly 90% of ppl with Parkinson's suffer from dyshpagia and resulting aspiration pneumonia is leading cause of death. THe dysphagia and aspiratino may be silent and undetected. Diagnosis is confirmed with a videofluososcopic swallowing study. Multidiscplinary intervention required to address nutrition and reduce risk of recurrent aspiration pneumonia. *Aspiration pnuemonia treatment: 1. Blood and sputum cultures with initiation of broad-spectrum antibiotics w/anaerobic coverage (clindamycin). What shoiuld you think in the case of recurrent pneumonia in same anatomic location Its a red flag for bronchial obstruction. Most common cause is bronchogenic carcinoma. Do CT SCAN FIRST..., THEN bronchoscopic or CT guided biopsy may be performed for any suspected lesion seen on CT scan.

Signs and symptoms of hypocalcemia? How do you go about figuring out hte cause of hypocalcemia?

-Circumoral paresthesia usually first symptoms T-hen comes muscular tetany: which can be observed by Chvostek's sign (facial muscle spasm with tapping of the facial nerve) and Trousseau's sign (Carpal spasm after occluding blood flow in forear with blood pressure cuff) -Acute severe hypocalcemia will cause seizures, confustion, cardio collapse, etc Dx: looks for signs of prior neck surgery (postoperative hypoparathyroidism). ECG Prolonged QT and ST TO Figure out cause... Repeat testing Then see if low magnesium level? Due to drug? Recent blood transfusion? rhabdo? If those are no, then measure PTH. PTH high: stuff like Vit D deficiency, CKD, tumor lysis, pancreatitis, sepsis PTH low: parathryoid surgery, autoimmune, cancer ***Remember that calcium in blood is bound to albumin (45%), present as ionized calcium (40%), or is bound to inorganic and organic ions (15%). Patients with hypoalbuminemia can have decreased total plasma calcium. However, the ionized serum calcium (physiologically active form) is hormoally regulated and remains stable. As a result, these patients may be asymptomatic as teh measured total plasma calcium does not correlate with they physiologically active calcium. So for hypocalcemia, always consider hypoalbuminemia. Since a large amount of calcium is bound to albumin, patient with hypoalbuminemia (liver failure, nephrotic syndrome) have low total calcium levels but normal ionzed calcium levels. You can calculate a corrected alcium as follows for an estimate of effective calcium level, or you can check an ionzed calcium level to be sure. Corrected calcium=measured total calcium + 0.8(4.0 g/dL - measured serum albumin in g/dL) **normal serum albumin is 4.0g/dL **serum calcium decreased by 0.8 mg/dL for every 1 g/dL decresae in serum albumin. Also, increased p (like in respiratory alkalosis) can cause an increase in affinity of serum albumin to calcium, threby decreasing the levels of free ionized calcium---> hypocalcemia manifestations. So although corrected calcium is usually accurate in most patients, direct measurement of ionized calcium is usually more accurate in patients with acid base disorders (acidosis increases ionized calcium, alkalosis decreases ionized calcium), primary hyperparthyroidism, CKD, and multiple myeloma (elevated proteins can increase corrected calcium). -Hypocalcemia: remember it can occur during or immediately after surgery in patients requireing blood transfusions. Hyperactive DTRs -Hypermagnesemia: Decreased DTRs. -Hypomagnesemia: Increased DTRs

Low glucose in pleural effusion?

-Complicated parapneumonic effusion and empyema -RA ( glucose extremely low, usually <15) -Tumor -Tuberculosis

Signs and symptoms of post nasal drip. Then Tx?

-Cough that is more on lyind down and more at night when patient sleeps. -nasal dischare or obstruction -dripping sensation or tickle in throate. Tx: First generation antihistamin and a decongestant. Nonsedating antihistamin have been shown to be less effective. -you can use intrasal cortiosteroids are used in cases where PNDS is seconary to allergic rhinits or symptoms are more persistent.

EKG- pattern of evaluation

-HR -Rhythm -Axis-do the two thumb test. Look at P waves- best lead to look at is II (should be upright), then I, then V1 (should be biphasic). Interval-look at P first, then PR, then QRS, then QT (should be less than QRS) -Look at Q waves-III, ave you can have "free" Q waves -Look for chamber enlargement -Look for ST segment changes. -Look for peaked T waves (a T wave you would not want to sit on). Will be more obvious on pericardial leads.

Options for DVT prophylaxis

-LMWH -LOW dose unfracitonated heparin -Complression boots

Dia

-Lif

What tests do you do the diagnose MS?

-MRI cuz you can see the white matter lesions -CSF analyusis will show normal pressure and presence of ologclonal IgG bands in >95% of patients

Therapy for STEMI

-Prompt reperfusion (percutaneous coronary interventions (PCI)) with cardiac cath. BEFORE 90 minutes is ideal. --------Fibrinolysis may be administered within 12 hours of symptoms onset for STEMI patients who cannot undergo PCI but is associated with higher rates of recurrent MI, intracranial hemorrhage, and mortality compared to cardiac cath. -Oxygen -nitrates -Antiplateley therapy- apsirin +P2y12 receptor blocker (clopidogrel) -Anticoagulation-unfractionaled heparin, LMW heparin, or bivaluridin -Beta blockers-contraindicated in heart failure

Colon cancer screening

-Rectal exam yearly after age 50 years (uworld i think). But MKSAP says annual rectal examination with office FOBT is not considered adeuqate screening cuz of poor sensitivity. -Occult blood in stool yealry after age 50 years. This is the home high-sensitivity FOBT, sampling 2 to 3 consecutive specimens. -Colonoscopy every 8-10 years -Patients with an affected first degree relative should begin screening (colonoscopy) at age 40 or 10 years before the age of relative's diagnosis. -Patient with UC should get colonoscopy after 8 years of diagnosis and then eVERY 1-2 years after. Risk factors for colorectal cancer: family history, polyposis syndromes like FAP, IBD, African American race, ALCOHOL INTAKE (cuz interferss with folate absorption), smoking, obesity Protective factors: high fiber diet, regular NSAID use, hormone replacement therapy, regular exercise.

Diagnoses of stones

-Urinary Ph can help differentiate -X-ray will reveal only radiopaque stones, not radiolucent. -Intravenous PYELOGRAM is gold standard. It can clearly outline the entire urinary sstyem making it easy to see hydronephrosis and presence of any type of stones.. a. NONCONTRAST helical abdominal CT has replaced IV pyelography as the gold standard for diagnosing kidney stones. However, noncontrast helical abdominal CT is expensie and has a higher radiation exposure than other imaging studies. IV pyelography has high sensitiviy and specificy for diagnoses of stones, however this study requires bowel perparation and the use of IV iodinated contrast agents, which are contraindicated in patients with acute kidney injury and chronic kidney disease. -If patient pregnant then do ABDOMINAL ULTRASOUND. Ultrasound is preferred in patients with a low likelihood of alternate diagnosis and pregnant patients too.

Primary care: diarrhea pearls:

-acute dirrhea is usually due to infection (virus, bacteria, and parasite) or medications - if nausea and vomiting are present: suspect viral gastroenteritis or food poisoining. if food poisoning the cuase, diarrhea appears within hours of the meal -remember that occult blood in the stool MAY be present in all types of acute infectious diarrhea, but it is much less common to have gross blood -a finding of fever and blood together is typical of infection with SECCCY -no fever and no blod is typical of infection with viruses (rotavirus, norwalk viruse), ETEC, and food poisoning (staph aureas, clostridium perfringes) Lab test to consider : -CBC -stool WBCs -stool for ova and parasites -stool culture -stool for C dif culture -stool for C dif toxin -stool for Giardia antigen

What is Zendker's divericulum signs? risk for? diagnoses?

-elderly -dyshpagia and regrurgitation -halitosis -at risk for aspiration pneumonia -occurs due to posterior herniation between fibers of the cricopharyngeal muascle Dx: A contrast (barium) esophgram Tx: surgical

Hypothyroidism

-fatigue, cold intolerance, constipation, dry skin, amenorrhea, periobital puffiness, When using levothyroxine to treat, rmember patient should be instructed to take on empty stomach, preferably in the morning, separately from other medications. common medications, such as calcium and iron, can impair its absoprtion. -remember between total T4 leves and free T4 levels, free T4 levels the better test -you can get myxedema coma here: treatment is IV levothyroxine, IV hydrocortixone and go to ICU. HASHIMOTOS -autimmune, +antithyroglobulin and antimicromoal (anti-TPO antibodies) that preciipate thyroid destruction. --High TSH, Low T3 and T3 **important: high titers of anti-TPO antibody is diagnostic of Hashimoto's. BUT if you suspect a thyroid lymphoma (all thyroid lymphomas occur in patients with preexisting Hashimoto's thyroiditis), large needle aspiration biopsy can be done. a rapid increase in thyroid size w/comppressive symptoms suggests thyroid lymphoma in patients with Hashimotos. **Pemberton's sign is the presence of facial plethora or neck vein disention when the arms are raised and confirms an enlarged thyroid gland as the cause of esophageal obstructive symptoms. SUBACUTE, POSTPARTUM, AND VIRAL AND AMIODARONE: -these intially present hyperthyroid but can have a hypothyroid phase that comes after. -subacute is painful but all others have painless goider SICK EUTHYROID SYNDOME NORMAL TSH, low T3 and normal T4 after being sick?? Thought to be due to caloric deprivation and increase in cyokine levels. "low T3 syndrome" Any patient with an acute, severe illness can have abnormal thryoid funcion tests. Thyroid function tests often normalize after recovery. SUBCLINICAL PRIMARY HYPOTHYROIDISM -mildy increased TSH, normal T4 and T3. Patients do not have clincial features of overt hypothyroidism. **doesn not require treatment if asymptomatic. Treatment is warranted in presence of 1. antithyroid antibodies 2. an abnormal lipid profile 3. symptoms of hypothyroidism 4. ovulatory and menstrual dyfunction CENTRAL HYPOTHYROIDISM -Normal TSh, normal T3, increased T4 SECONDARY AND TERTIARY HYPOTHYROISM -low everything. Hypothyroidism can cause what metabolic abnormliaties? -Mostly hypercholestolemia. Hypertriglyceridemia. -Can also cause HYPOnatremia, asymptomaitic elvetionas of cratinine kinase and serum transaminases. Hypothyroid patient has wrist pain? Carpal tunnes syndrome occurs in approximatley 30% of patients with hypothyroidism. Deposition of mucopolysaccharide protein complexes within the perineurium and endoneurium of the median nerve is though to be primarily responsible for its pathogenesis. *Patients with coronary artery disease are at risk of MI when levothyroxine is first started and the medication should be started very slowly in these patients. **Patients with primary hypothyroidism are predispose to get other autoimmune diseases such as pernicious anemia. Hypothyroidism during pregnancy ?Because a fetus depends on meaternal thyroid hormone for the first 10 to 12 weeks of gestation, the thyroid levels of pregnant women with hypothyroidism should be carefuly montired. Because of estrogen eleveation during pregnancy, TBG levels increase. Levothyroxine requirements may increase 30% to 50% during first trimester

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Tx of hypercalcemia

-if calcium>12 or asymptomatic you really don't even need to treat but if not... SHORT TERM IV fluids +/- Lasix (use diuretics if volume overload present ) Calcitonin LONG TERM Bisphophonates (pamidoronate, alendronate, zolendronate) ----binsphosonates bind to bone, get engulfed by oseteoclasts and kill thems. Side effects: pill esophagitis, osteonecrosis of jaw *apparently tho bisphosphonates are the initial drugs of choice for hypercalcemia of malignancy. also good for osteoporosis. *Parathyroidectomy is recommended for asymptomatic hypercalcemia patients who have at least one of the following features.. -serum calcium level >1.omg/dl above the upperlimit of normal -young age (<50 yrs) -bone mineral density <T-2.5 at any site -reduced renal function (GFR<60) **all patients under consideration of parathyroidectomy should undergo preoperative localication study to determine feasibility of minimum invasive parathyroidectomy or unilateral explorations. Some common ones are ultrasound, sestambi scan (nuclear imagin), MRIs, and CTs.

OSA dx?

-made with polysomonography (sleep study) -defined by >5 episodes of apnea and hypopnea per hour of sleep Tx: lateral sleeping position. CPAP is very good if used consistently. Surgery also can be done. Complications: Hypoxemia--> increased pulmonary resistance--> pulmonary HTN--> cor pulmonale

Victims of abuse presentatinon

-obvious bruises, scars, etc -depression, anxiety, panic, suicide attempts -victims of abuse may present to doctors frequently for health copmlains or have physical symptoms that cannot otherwise be explained

Priary Care: Knee pain

-osteoarthritis ANTERIOR KNEE PAIN DDX -patellofemoral pain: very common cause of anterior knee pain, worse with climbing and descending stairs. you do the PATELLOFEMORAL COMPRESSION TEST (pain elicited by extending the nkee while compressing the patella) and if you get pain that is highly suggestive. PHysical therapy is very effective. typical patient is young female athlete. -Osgood Schlatter Disease : preadolescent/adolsecent athelete, recent growth spurt. Pain incearesase with sports, relieved by rest. Tenderness at tibial tubercule. -Patellar tendinitis "jumpers knee"" common caus of anterior knee pain. running and jumping sports can cause, an oveuse injury. OTHER TYPES OF PAIN -degeneration or tear of meniscus: you see recurrent knee ieffusions, tendnerness, positive McMurray test. -rheumatoid arhtritis, psioratic arthritis, SLE -acute monoacruticuar arthritis: septic arhtritis, gonorrhea, gout, lyme, etc. *if patient has monoarticular red swollen joint, you MUST do a joint aspirate because you need to r/o infected joint. This is very important because cartilage can be destroyed within the first 24 hours of infection. -osteochondritis dissecans (OCD): area of necrotic bone and degenerative changes in overlying cartilage. The bone/catilage piece may separate from the underlying bone and beomce a loose body in the joint. Pain, catching and popping. Tx options are limited but arthroscopic surgery can help. -Baker's cyst: caused by intra-articular pahtology (meniscus tear). Majority resolve spontaneously. -anserine bursitis: this bursa is located anetomedially over the tibial plateau just below the joint line. inflammation can be from overuse, injury or abnormal gait. There is tenderness on palpation. -plica syndrome: typically seen in athletes or with oveuse injuries, sometimes after trauma. *fyi: none of these are "shin splints", that is called medial tibial stress sydnrome

Paraoxysmal SVT

-paroxysmal supraventricular tachycardia (PSVT) sometimes called AV nodal reentrant tachycardia. is its >150, narrow complex regular, unidentifiable P waves..gonna be SVT. a.adenosine commonly used for this and carotid massage commonly used There are different types of SVT, including atrioventricular nodal reentrant tachycardia (most common), AV reentrant tachycardia, and atrial tachycardia. The term PSVT excludes A-fib and atrial flutter, other common forms of supraventricular arrhythmias. These patients typically have lightheadhendess, SOB, diaphoresis, chest pain, presyncope, or syncope. If stable, use IV adenosine or vagal maneuvers (carotid sinus massage or Valsava). If hemodynamically unstable, do urgent cardioversion. *Sinus tacycardia often has a gradual onset compared to PSVT, which starts suddently. also, sinus tach has normal P waves w/narrow QRS complex.

Multifocal atrial tachycardia (MAT)

-presence of 3 or more P waves of different morpohologies -QRS narrow -variable PR and RR intervals -HR can reach up to 200 bpm Hypoxia and COPD are most common etiologies. Others are hyokalemia, hypomagnesemia, coronary/hypertensive/valvular disease, meds (aminophylline, theophylline, isoproterenol). Tx: correct underlying cause. if therapy not effective and no contraindications to BBs, you can use BB. If patient has asthma or COPD, use Verapamil instead.

1st degre heart block

-prolonged pR interval >.20s -no treatment required

Preferred rhythm control drugs for A-fib depending on situation

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Antimicrobial therapy of the initial streptococcal infection does NOT prevent the onset of PSGN (as opposed to rheumatic fever).

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Blood in the chest, if not evacuated, can get infected. This can happen in an accident fo example. majority of patiients witll present with fever, dyspnea, and chest pain.

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Coombs test telss you if autoimmune process likelY?

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Cyclosporine: immunosuppressive medication that is most commonly used after transplatation to prevent organ rejection. Predisposes to viral infections and lymphoma, and can be nephrotoxic.

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Depsite the favorable portrayal of CPR in the media, only about 15% of all patients who undergo CPR in the hospital survive to hospital discharge.

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Excessive alcohol intake is associated with increased incidence of hypertension.

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Fanconi anemia is a type of aplastic anemia

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Fol

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Folic acid and B12 deficiencies can cause pancytopenia, also SLE

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From wards: remember when dealing with hypercalcemia by mets. Renal, lung, breast mets can go to bone and be lytic--> hypercalemia. But prostate cancer that mets to bone is blastic, does NOT cause hypercalcemia.

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From wards: when looking at bacteria susceptibility from labs. Use the medication with most narrow coverage.

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HE is

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Hep A-AST and ALT are usually greater than 500U/L.

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Heparin does not dissolve already existing clots, rather it prevents futuer ones from forming.

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I guess anytime you see a person not vaccinated against Hep A or Hep B, you wanna go ahead and do it

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If AST/ALT stand out as the most abnormal, the defect is usually parenchmal liver damage. If the alkaline phosphatase stands out as most abnormal, it is usually obstructive.

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If you have a guy angina and clnical manifestations of new onset heart failure--just go straight to cardiac cath, don't even need to do stress test. But for examle of the patient has intermediate likelihood of CAD and no angina, go with exercse stress test if has normal ECG.

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KNow cardiac drugs

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Kernig's sign: Resistance to extension of the knee (C) Brudzinski's sign:Involuntary flexion of hip and knee in response to flexion of the neck by the examine

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Know Bacterial endocarditis and Rheumatic fever, was too lazy for flashcards. Page 47 First aid step 2

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Know first aid stuff COPD, Asthma.

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Know the Valve diseases. pg 272 step 1 first aid, pg 32 first aid medicien.

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Know what tubule cells do, Pg 548 First Aid

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Look at OB/GYN cards for -stages of labor -what fetal heart tracings can happen -what tests are done when -vaginitis -contraception

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MIC concentrations...better to have lower number.

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OCPs can cause hypertension, and discontinuing its use can correct the problem in most patients.

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Oral estrogen preparations increse levels of TBG, patients on thyroid replacemetn may need a higher dose to saturate the increased number of thyroxine binding globuline (TBG) binding sites.

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PT is prolonged by warfarin. PTT is prolonged by heparin. Bleeding time: reflects platelet function.

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Pica is pretty indicative or iron deficiency anemia/

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Put bone cancer stuff from peds here...

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Remember exercise treadmill stress testing not useful in someone who already has a diagnosis of coronary artery disease.

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Remember that diffusing capacity of lung (DLCO) is decreased in emphysema (due to alveolar destruction). and normal in chronic bronchitis.

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Remember that infection cause elevated persistent blood glucose levels.

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Remember that you can see hemoptysis with PEs

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Remember that you see hypotension due to increased vasciular permeability in severe pancreatitis.

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Remember to not treat hyponatremia too fast or you're gonna give person central pontine myelinolysis.

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STIs or other reportable conditions (like TB) MUST be reported by the physician or physician's designated appointee to the state health department. Also, it is mandatory that the information be disclosed to partners. However, the law does not require discolure of sensitive medical information to parents. Like is minor has STD and doesn't want parents to know. "emancipation" of a minor implies that the minor is able to make decisions regarding health-related isues but does not give the patient the right to voite, consume alchohol, or use tobacco. 14/50 states currently allo a minor to have an abortion without the consent of or notification of parents.

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Severe pain in a patient with mild urinary obstruction, such as BPH, may cause urinary retention due to inability to Valsava.

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The association between diabetes and mucormycosis is frequently tested on the USMLE. The most common cause of mucomycosis is Rhizopus.

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Under normal conditions, body temperature is maintained 96.8-99.5 by dissipation of heat, primarily in the form of sweat.

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When someone lies on their left side, the left lung gets more perfusion and ventilation. Same goes for right side. This principle comes is relevant because with consolidation you can see worsening O2 sat if someone with left lobe consolidation leands on left side, its like exaggerating the problem cuz now you have more perfusion and ventilation going there. Convsersely, if you were to lie on right side with left lobe consolidation, your hypoxia will get better cuz more ventialtion and perfusion are going to the good lung and the shunt is minimized.

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good thing to know: Post nasal drip, asthma, and GERD account for nrealy 100% of causes of chronic cough in nonsmokers with normal CXR who aren't on Ace inhibitors.

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s

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Elderly person with bone pain, renal failure, and hypercalcemia?

..has multiple myelopma until proven otherwise. About 50% of multiple myeloma patients develop some degree of renal insufcciency; this is most likely due to obstruction of the distal and collecting tubules by large laminated cases containing paraproteins (mainly Bence Jones protein).

Normal Serume Creatinine range

.6-1.2

Age ranges of the leukemias

0-14 ALL 15-39 AML 40-59 CML/AML 60+ CLL

Contrast nephropathy usually resolves in? Tx?

1 week Adeuqate IV hydration with isotonic bicarbonate or normal saline and administration of acetylcysteine help to minimze the risk of contrast-induced nephropathy.

Alchohol abuse treatment

1. AA: best treatment 2. Disulfiram: person gonna vomit and feel like crap for about 90 minutes if drinks alchohol. Lasts about 90 minutes. Good for short term but should not be taken chronically. 3. Naltrexone (Trexan): Has been shown to improve abstinence rates. It reduces te craving for alcohol. 4. Drugs for withdrawal: benzos (best to use is long-acting agents like diazepam) 5. Correction of fluid imbalance, vitamin supplementation (thiamine, folate, multivitamin).

X-ray reading:

1. AP( front to back) or PA (back to front)? -generally PA view is best, normally you get lateral view with it. this is the kind you get when patient is ambulatory. you won't get magnification and you'll get a better view. -generally in a hospital when patient is sick in bed you get AP view, which is susceptible to magnification of heart and vessels -generally we like to have patients inspire for x-ray, gives us better view. a few exceptions: PTX, air trapping. these will be accentuated on exhalation. 2. comment on penetration 3. rotation? 4. lung field descriptors *linear *reticular: spider webs * fluffy: pulm edema * nodules A-look at trachea. looking to see if something is moving it, like in atelectasis (pulls it to its side) or pleural effusion (pushes trachea to opposite side). also if patient is intubated, you wanna check and see if ETT is 2-3 cm above carina. B-look at claviccles, ribs, look for lytic lesions, look at spinal processes C-if cardiac sillouhette greater than half of distance from side to side then you're worried about CHF *if right heart border gets hazy then you know you have RML pneumonia. if left heart gets hazy, then pneumonia in lingula which is part of left upper lobe D-if right hemi diaphgram gets hazy then RLL pneumonia. if left hemi diaphragm gets hazy then its LLL pneumonia. look for free air under diaphragm, blunting of costophrenic angle. E: -you wanna look at edges of lung fields and make sure lung markings go out to edges to make sure there isn't a pneumonthorax anywhere -westermark sign for PE -cephalization: normally the pulmonary vasculature on x-ray, the bottom ones are bigger. but with cardiopulmonary congestion (CHF), the upper ones can be big (hence the name cephalization). another thing you look for in CHF, are Curly B lines (caused by fluid in lungs), you look for these at edges -air bronchogram 1. Black-air 2. Dark grey-fat 3. Light grey-soft tissue 4. Off white -bone 5. Bright white -metal

Secondary hyperparathyroidism

1. Bad kidney-> can't excrete phosphate--> hyperphosphatemia---> this binds calcium and lower free calcium in serum---> PTH incrased---> more PTH releasing calcium from bone 2. Bad kidneu--> can't make calcitriol--> Brain sees this and increases PTH to help kidney out to make calcitrio---> extra PTH releases calcium frome bone 3 types of bone lesions associated with secondaru hyperparathyroidism 1. Oseitis fibrosa cystica: bone replaced by fibrous tissue, woven bone, 2. Osteomalacia: Assoaciated with Vit D deficiency, characterized by defective oseiod mineralization 3. Adynamic bone disease: cause unknown. Tx: goal is to normalize calcium-phosphate balance. Do things like dietary phosophate restriction. Take Vit D with calcitriol. *there is also tertiary hyperparathryoidism which results from chronic renal disease. This is autonomous hypersecrtion of pTH even after correction of hyopcalecmia.

Dietary recommendations for patients with renal calculi?

1. Decreases dietary protein and oxalate ---high protein diet is associated with increased predispostion to stone formation 2. Decreased sodium intake 3. Increased fluid intake 4. Increased dietary calcium ---limiting calcium intake actually has a pradoxical effects, and has been associated with enhanced tendency towards stone formation. Most common causes of calcium stones are 1. Idiopathic hypercalciuria: this is characterized by hypercalciuria, normal serum calcium levels, and absent metabolic disease. ITs the most common form of hypercalciuria. 2. Hypercalciuria due to systemic disorders 3. Hyperuricosuria 4. Hyperoxaluria

Primary Care: Obesity Tx:

1. Diet, exercise 2. Drugs: Orlistat is first line agent and can be used for up to 4 years 3. Bariatric surgery. Best evidence if for patients with BMI over 40 (morbidly ovese ). Most common procedure is the laparoscopic gastric bypass. The the laparoscopic adjustable gastric banding (LapBand) has fever complications, is reversible, but is not as effecting in achieving weight loss as compared to the gastric bypass.

Three major pathological stages of alcoholic liver disease

1. Fatty liver (steatosis) 2. Alcohohlic hepatitis. 3. Alcohholic fibrosis/cirrhosis Mallory bodies, infiltration by neutrophils, liver cell necrosis and perivenular distribution of inflammation all characterize alcohol hepatitis. *The histological pattern (I think) is pretty much indistinguishable from non-alchoholic steatosis or hepatitis. NASH. So they both have the same stuff. -in a diabetic patient, metformin can improve NASH. What is reversible? Fatty liver and alcohholic hepatitis can be COMPLETELY REVERSIBLE with the cessation of alcohol intake. True cirrhosis (with regenerative nodules) is irreversible, regardless of alcohol abstinecne.

2 most common causes of end stage renal disease and their type of damage?

1. Hypertension: arteriosclerotic lesions of afferent and efferent renal arterioles and glomerular capillary tufts are the most common renal vascular lesions seen. As hypertension progresses, there is progressive decrease in renal blood flow and GFR. The sequence of kidny damage evolves from nephrosclerosis to glomerulosclerosis. Nephrosclerosis is characterized by hyperterophy and intimal medial fibrosis of renal arterioles; whereas, glomerulosclrosis is characterized by progressive loss of glomerlay capillary surface area with glomerular peritubular fibrosis. 2. DM: you get increased extracellular matrix, BM thickening, mesangial expanision, and fibrosis.

What are complications of a variceal bleed that you gotta watch out for during hospitlization?

1. Infection (most common, up to 50% in hospitilized variceal bleed patients). Usually occurs as UTI, SBP, respiratory ifnection, aspiration pneumonia or bacteremia. The patients should be treatd with PROPHYLACTIC antibiotics: preferred regimen is fluoroquinolone agent for 7-10 days. 2. Hepatic encephalopathy 3. Renal Failure: ATN (ischemic or toxic), or precpitation of hepatorenal syndrome. but not as common as infection.

What questions do you ask yourself in the case of an arthritis?

1. Is it an inflammatory (elevated WBC count) process? 2. Is it monoarticular or polyarticular? 3. Is it symmetric or asymmetric? 4. What is the duration of symptoms? VIRAL ARTHRITIS: is symmetric. Distinguished by other types cuz it resolves within two months. . Tx involves NSAID use. **Common causes are parvovoirus (ppl that have frequent contact with children), rubella, HeB, C, and HIV. *this can mimic inflammatory arthritistis like RA. Its morning stiffness last less thatn 30 minutes and there shouldn't be any joint swelling which you see in RA. And ESR is increased in RA but not in viral arthritis. Also, Arthritis must be present for at least 6 weeks in order to diagnose RA. SEPTIC ARHTIRIS and CRYSTALLINE ARTHRITIS tend to be monoarcitualr and most commonly affect the knee Joint aspiration is important for differentiating the ttwo. *a septic joint will have a VERY LIMITED ROM due to pain coupled with joint effustion and fever. However, a nearby cellulitis, bursitis, or osteomyeitis will usally maintain ROM of a joint. ***Gonococcal septic arthritis: mar present with asymmetric polyarthralgiaas (most often associated ith tenosynoviti and skin rash) or an isolated purulent mono-or-oligoarthritis. Roughtly 75% of cases are "silent", meaning that the preceding genitourinary or pharyngeal infection goes unnotied. IMPORTANT: purulent arthritis in a sexually active person is gonococcal arthritis until proven otherwise. ***Non gonococcal septic arthritis: more classic case would be someone with chronic disease (diabeted, OA, etc) who has single joint involvement (rather than migratory polyarthralgias) and dever. Gram stain and blood cultures necessary for dx. ***Gouty arthritis-Synovial fluid is critical to diagnose because cannot be reliably distinguished from septic arthritis or pseudogout. Most common cause of polyarticular septic arthritis.?Polyarticular:Neisseria gonorrhea Most common cause of just a random septic arthritis?Random joint: Staph.aureus RA AND SLE are chronic and do not resolve quickly. these are symmetric inflammatory arthritides. **Remember, RA diagnosis CAN"T be made unless it;s been going on for >6 weeks. OA: ;non-inflammaotry REACTIVE ARTHRITIS, PSORIATIC ARTHRITIS: asymmetric arthritis. --Reactive: urethritis, conjunctivitis/uveitis, arthritis --inflammatory *morning stiffness presnet in all inflammatory arthritis: RA, psoriatic arthritis. OA has it too just for not as long. REACTIVE ARTHRITIS: usually develops within 1-4 weeks of inciting infeciton Preceding infection: ---Gastroenteritis: salmonella, shigella, yersinia, campylobacter, C-diff ---Genitourinary infection: Chlamydia **affects DIP joints, spares MCP joints. MSK: asmmetric, peripheral oligoarthritis, enthsitis, dactylitis Extraarticular symptoms: uveitis, conjunctivitis, urethritis, cervicitis, prostattis, keratoderma blennorrhagicum, circinate balanitis, oral ulcers Management: Antibiotics for chlamydia or non-self-limiting GI infection , NSAIDS. -if NSAIDs fail or contraindicated, go to intraarticulat steroids, then systemic steriods, then DMARDS. **Circinate balanitis (painless, shallow ulcers of glans penis) is an extraarticular manifestation of ReA that is painless, resolves after several months, and is not associated with inguinal lymphadenopathy. It resolves after several months unlike painless lesions of lymphogranulmoa venereum (resolves within few days) or syphillis (resolves within 3-6 weeks). Reavtive arthritis vs gonococcal septic arthritis? Type of seronegative spondyloarthropathy resulting from enteric or genitourinary infection. Classic reactive arthritis is triad of urethritis, oligoarthritis, and conjunctivits. Also, mucocutaneous lesions and tendon pain are common. NSAIDs are first line therapy. **remember that hemochromatosis can cause an arthropathy. tpicallly affects the second and third MCP joints, and causes osteoarthritis changes (hook-like osteophytes). CPPD crystals (pseudogout) can be found on synovial fluid analysis in 50% of cases. Usual age of presentation is between 50 and 60.

Primary care: osteoporosis tx?

1. Nonpharmacologic therapy: -get plenty of calcium -get plenty of vitamin D -weight bearing exercise -smoking cessation is critical 2. Pharmacologic -bisphosphonates -PTH therapy or human recombinant PTH therapy. Not a first line drug due to high cost and safety concerns for long term use. -Calcitonin: useful as short term therapy. Less popular and not commonly used -Estrogen-progestin therapY: no longer a first line approach for tx of osteoporosis because of increased risk of breast cancer, stroke, venous thromboembolism and perhaps CAD *just fyi relief of hot flushes is the primary (aruably the only) indication for estrogen replacement therapy, although it also reduced the rate of bone densitly loss...but the risks include increased rates of breat cancer, thromboembolism, and cardiac events **Bone density screening should begin at AGE 65 in women without risk factors. Risk factors are low body weight, chronic steriod use, smoking malabsorptive disorders, h/o of frctures. Bone antiresoprtive agents (bisphosophonates, raloxifene) are approved for osteoporosis prevention in high-risk women.

Primary care: Bursitis

1. Olecranon bursitis: swelling a dnpain at elbow, "bag of fluid" over olecranon (due to effusion into the olecranon bursa) 2. Trochanteric bursitis-Very common cause of lateral hip pain. Greater trochanter is exquisitely painful on palaption. These eople have trouble with sleeping caused by pain on lateral hip. -Causes include trauma, overuse, weakness of hip musculuatre. In many causes, onset is gradual. -Tx is NSAIDS and activity modification. If symptoms persists, local corticosterone injections can provide relief.

Drug-induced pancreatitis accounts for 5% of cases of pancreatitis. Most cases of drug-induced pancreatitis are mild. The common conditions which involve the use of drugs (important for USMLE) that can cause pancreatitis are:

1. Patient on diuretics: furosemide, thiazides 2. Patient with IBD: sulfasalazine, 5-ASA 3. Patient on immunosuppressant: azathioprine, L-asparaginase 4. Patient with h/o seizures or bipolar disorder: valproic acid 5. AIDS patient-think about didanosine, pentamidine 5. Patient on antibiotics: metronidazole, tetracycline

To determine cause of thrombocytopenia

1. Peripheral smear. 2. Bone marrow biopsy.

Primary care: nausea and vomiting approach

1. Questions to ask: food intake? time of onset of vomiting in relation to food intake? anyone else eat food? symptoms related to meals? ask about medications and recent changes/additions? history of abdominal surgery or recent sugery? family members with similar ilness? 2. Define the vomitus: -bilious: obstructin ois distal to ampulla of Vater -feculent: distant intestinal obstruction, bacterial overgrowth, gastrocolic fistula -vomiting of undigested food: esophagel problem more likely (achalasia, stricture, diverticulum) -projectile vomiting: increased ICP or pyloric stenosis -coffee ground material or blood: GI bleeding 3. Accompanying symptoms: -diarrhea dn fever: point to an infectious process (gastroenteritis) -abdominal pain point to obstruction, acute inflammatory condictions (peritoniits, cholecystitis) -headace, visual disrubances and other neurlogic findings point to increased ICP or increased IOP

Indications for hemodialysis:

1. Refractory hyperkalemia 2. Volume overload or pulmonary edema not responding to diuretics. 3. Refractory metabolic acidosis (ph <7.2) 4. Uremic pericarditis 5. Uremic encephalopathy or neuropathy 6. Coagulopathy due to renal failure

2 major types of ACS

1. STEMI. Most dangerous kind. Addisitonal treatment needed to MONA+B. They need urgen opening of blockage...can be done with thrombolytics and/or cardiac catheritization + stent. -Coronary angiography to diagnose degree and location of blockage followed by prompt reperfusion (percutaneous coronary interventions (PCI) or possibly CABG). BEFORE 90 minutes is ideal. if that can't be done....then do Fibrinolysis (tpa, retplase, streptokinase) may be administered within 12 hours of symptoms onset for STEMI patients who cannot undergo PCI but is associated with higher rates of recurrent MI, intracranial hemorrhage, and mortality compared to cardiac cath. So make sure there are no contraindications to thrombolysis (history of hemorrhagic stroke, recent ischemia sroke, severe heart failure, cardiogenic shock) *coronay angiography refers to one of the procedures that can be done by a cardiac cath. small amounts of dyeare injected into the arteries in the heart. This always for the anatomy of these blood vessels to be visualized and blockages or other problems to be diagnosed. Thrombolytic therapy indications: if they present within 12 hours of smptoms, if ECG demonstrates ST elevations >1mm in TWO contiguous leads. Another candicate for thromboltic therapy includes ppl with persistent symptoms of new LBBB. **important to give nitroglycerin to these patients before perofrming ECG to rule out coronary vasospams. 2. Unstable angina and NSTEMI. Difference between these is that NSTEMI is severe enough to cause myocardial damage and cause enzyme leakage, whereas unstable angina doesn't. *for NSTEMI: Do CORONARY ANGIOGRAPHY w/in 48hrs to determine need for intervention. • PCI w/ stenting is standard (drug eluting or bare metal) • CABG if: L main dz, 3 vessel dz (especially involving proximal LAD), 2 vessel dz + DM, >70% occlusion, refractory angina despite max medical therapy, or post-infarction angina also.. cocaine cause cause MI. Tx of cocaine related chest pain is similar to chest pain management in general population with a few key exceptions..BENZOS early cuz that decreases neuropsychiatric manifestations and thus improves the hypertension and tachycardia. Also avoid BBs to avoid coronary vasospasm. If BP doesn't improves with BBs, then go with PHENTOLAMINE. -if no patient improvment, do coronary angiography to check for thrombus. vasospasm is the main way cocaine leads to myocardial ischemia and may lead to coronary artery thrombosis. and there is a Inferior wall MI- special case. Affects right ventricle, so MAJOR danger of dropping preload. Tx must maintain preload and AVOIDANCE of nitrates (these drop preload). so i think you're going to see st depression in V1 V2 and V3, right sided MI.

What sort of screening stuff should be done with cirrhotic patient?

1. Screening endocscopy to exclude varices, indicate risk of variceal hemorrhage, determine strategies to prevent it (beta blockers). Esophageal varices are the major cause of morbitidiy and mortailiy and can occur in up to 50% of patients. 2. Also everyone should undergo surveillance for HCC with US every 6 months, regardless of etiology of cirrhosis.

What kind of things are you looking for with these tests? 1. Serial evaluation of Hgb and Hematocrit 2. RBC indices 3. Hgb electrophoresis 4. Blood smear 5. Bone marrow biopsy

1. Serial eval of Hgb and hematocrit is helpful in determining the cause of anemia in some patients. Rapid falls suggest hemolysis or blood loss, wheras gradual falls are consistent with a halt in RBC production. 2. RBC indices include MCV, MCH, and MCHC. These values are helpful in determining if an anemia is microcytic or macrocytic, or whether thalassemia or spherocytosis is present. 3. Good for sickle cell 4. Great value in identifiygin unusually shaped RBCs or the presents of parasites such as malaria or babesiosis. 5. Bone marrow biopsy most often incitated in patients iwith pancytopenia or blast forms in circulation.

What things should you remember when treating with phosphodiesterase inhibitors?

1. Sildenafil is contraindicated in patients being treated with nitrates 2. Sildenafil is used with caution in conditions predisposing to priapism 3. Concurrent use of drugs which interfere with the metabolism of sildenafil (erythromycin, cimetidine) may predispose to adverse reactions by prolonging its plasma half life 4. While combining with an alpha-blocer, it is important to give the drugs with at least a 4-hour interval to reduce the risk of hypotension.

Primary care: Tendinitis

1. Supraspinatus (rotator cuff) tendinitis-impingment syndrome 2. Lateral epicondylitis at elbow "tennis elbow" 3. Medial epicondylitis "golfer's elbow" 4. De Quervan's disease -pain at radial aspect of wrist in region of radial styloid due to inlammation -Positive Finkelsteins test: Have the patient clench the thumb under the other fingers when making a fast. Then ulnarly deviate the wrist. The test is posivie if pain is reproduced. -Tx: is thumb spica splint and NSAIDS. Surgery can be done.

A patient comes in vomiting blood, what do you do?

1. Two large bore IVs and fluid. 2. Type and crossmatch blood 3. Endocscopy for Dx and Tx

DDx of hypoxia

1. V/Q mismatch -COPD, CHF, Pulmonary fibrosis, asthma, -PE 2. R to L shunt - consolidation, congeintal heart defect 3. Diffusion defect -interstial lung disease 4. Anemia -has a normal Pa02, dut decreased Pv02 due to increased extraction from tissues 5. IMproper utilization of delivered oxygen in tissues -cyanide poisoning, diptheria toxin 6. Low inspired oxygen 7. CO poisoning 8. Hypoventilation -occurs with obesity, neurmosuclar disorders (like guillian Barre, MG, ALS)

INdications for aortic valve replacement are:

1. all symptomatic patients with AS 2. patients with severe AS undergoing CABG or other valvular surgery 3. asymptomatic patients with severe AS and either poor LV systolic function, LV hypertrophy >15 mm, valve area <0.6cm2 or abnormal response to exercise.

DDx of cola-colored urine following exercise?

1. exercise induced hematuria 2. myoglobinuria from rhabdomyolysis 3. march hemoglobinuria form RBC trauma All of these entities may results in a positive resuls for blood on UA, although identifying intact RBCs on microscopy excludes myoglonuria and hemoglobinuria. The absence of RBC casts also makes a glomerular cause of hematuria less likely. Up to 24% of participants in marathons may have exercise induced hematuria. This hematuria may be caused by repetitive up and down movments of the bladder during running. In contact sports, direct trauma to kidneys or bladder may resuls in hematuria. Shunting of blood flow towards muscles and away from kidneys may also contribute. Even when an appropatie history is present, exercise hematuria should be considered a diagnosis of exclusion and repeat urinalysis should be done in ONE WEEK to ensure resolution.

IV potassium must be given immediately when hypokalemia found in these situations?

1. hepatic encephalopathy 2. ventilatory failure 3. cardiac arrhythmias in these cases, fast potassium replacement is critical to patient's recovery and prognosis.

Important causes of hypoglycemia in non-diabetc patients with eleveated insulin levels

1. insulinoma (beta cell tumor) 2. surreptitious use of insulin or sulfonylureas (sulfonylureas cause increased insulin output from beta cells) Proinsulin gets cleaved off from insulin peptide when they leave the secretory granules. C-peptide stays on insulin peptide and proves that the insulin is not exogenous.

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Go over some major neurocutaneous syndromes

1.NF1- most well known. Café-au-lait spots, axillary freckles, Lisch nodules of iris, neurofibromas, and bony lesions. 2.NF2-brain tumors (especially bilateral acoustic neuromas) -patients with NF have tendency to form tumors in CNS, PNS, skin and viscera. Other neurocutaneous.. 3.Sturge-Weber: port wine stains in V1 nerve distribution, seizures, hemiparesis 4. Tuberous Sclerosis: ash leaf hypoigmentaiton, cardiac rhabdomyomas, kidney angioleiomyomas, mental retardation, seizures.)

Types of lung cancer:

1.Small cell lung cancer: central, senstive to chemo, NO surgery, poor prognosis. most paraneoplastic stuff associated with small cell. 2.Non-small cell lung cancer: squamos cell, large cell, adenocarcinoma. poor response to chemo. Treated with surgery if early stage Squamos cell: central. Only paraneoplastic associated with non-small cell is PTH related peptide (presents with hypercalcemia, classically in squamos subtype). -hypertrophic osteoarthropathy usually associated with adenocarcinoma. -adenocarcinoma is most common type of lung cncer in both smokes and nonsmokers as is the predominant type seen in nonsmokers. squamos, large cell, small cel are rarely seen in nonsmokers. Presents peripheraly. Large cell: Peripheral. Gynceomastial and galactorrhea.

what raises serum K by 1.0 mEq/L

10 mEq infusion

Normal Pt (prothrombin time)

11-15 sec

Treatment for patient with syphillis if allergic penicillin?

14 days of doxycyline--unless of pregnant

Platelet count

150000-400,000

What do you gotta wory about with smoke inhalation?

1st you woorry about airway edema from irritation from smoke 2nd you worry about cyanide and CO that you absorb. These people should be suspected to have an acute carbon monoxide poisoning and are treated with 100% oxygen via a facemask. Early symptoms are nerulogical and include agitation, confustion, and somnolence. Dz confirmed clinically and by documenting en elevated carboxyhemoglobin level (through C0-oximetry). Pulse ox is unreliable cuz can't differnetiale carboxyhemoglobin from oxyhemogloin. *Methemoblobin if Fe3+ iron in hemoglobin. Fe3+ is unable to bind oxygen, and it also increases the affinitiy of Fe2+ to oxygen, causing a LEFT SHIFT in oxygen dissociation curve. Result is functional anemia due to reduced oscygen delivery to tissues. Methemoglobinemia occurs after expsorue to oxidizing agents (DAPSONE, nitrates, TOPICAL/LOCAL ANESTHESTICS)

From wards: Apprach to treating sepsis

1st. Volume Control 2nd. Treat source of infection

Causes of QT prolongation and treatment

2 Categories of causes, Acquired and Congeintal. Acquired: 1. Electrolyte derangments (low calcium, potasssium, or magnesium) 2. Medication induced-bunch of crap Inherited: 1. Jervell and Lange-Nielson (AR) 2. Romano-Ward syndrome (AD) TX Beta blockers with pacemaker can prevent cardiac arrest Patients with prolonged QT intervals are at risk for syncope, ventricular arrythrmias (torsades), and sudden cardiac death.

Lead poisoning

2 things it does: lead inhibits and enzyme necessar for heme synthesis AND inhibits rRNA degradation (which is why you see basophilic stippling). LEAD Lead Line on gingivae (Burton lines) and on metaphyses of long bones Encephalopathy and Erthrocyte basophilic stippling Abdominal colic and sideroblastic Anemia Drops: wrist and foot drop. Dimercapol and EDTA used 1st line treatment.

Normal Ptt (activated partial thromboplastin time)

25-40 sec

Serum osmolarity normal values and equation

280-300 mOsm/kg Serum osmolarity=2(Na+K) + Glucose/18 + BUN/2.8

Rapid strept. antigen test is reasonable strategy for patient w/ pharyngitis who have what critera filled?

3 of 4 Centor criteria. -fever, tonsillar exudates, tender anterior cervical lymphadenopathy, and absence of cough Presence of at least three of these criteria has a roughly 50% positive predictive value for streptococcal pharyngitis (only minimally helpful) but there is an 80% negative predictive value for streptococccal pharyngitis if the patheitn has less than three of these criteria. Diagnostic testing is generlaly recommended to confirm the diagnosis in patieht with at least two Centro criteria.

Definition of microscopic hematuria:

3 or more RBCs per HPF

B12 stores in body lasts?

3-4 years

Potassium range

3.5-5.0

Normal HDL

30-100

BOlus = 20mg/kg up to 1 liter in kids. Don't go over 1 liter. Maintenance fluids: once vitals stabilize and most importantly URINARY OUTPUT through boluses, here is where maintenance fluids com in.

3:1 rule: Only about 25% of crystalloid will remaine in intravascular space; thus, you may need to administer three times the estimated fluid loss. When doing boluses.

Lyme carditis can cause what kind of block?

3rd degree block.

How long it take for warfarin to go in affect?

4-5 days. Its a vitamin K antagonist, "1972" clotting factors are reliant on Vit K.

Folic acid stores in body lasts?

4-5 months

UA-low ph? high ph?

4.5-7.5 Alkaline urine indicates type 1 RTA or UTI w/proteus or ureaplasma or you could be in respiratory alkalosis and the body is secreting bicarc to compensate Acidic urine can bee seen with aspirin overdose or type 2 RTA?? (even though the problem is reabsorption of bicarb, i guess the kidney is still able to acidify the urine)

Leukocyte range in serum

4500-11,000

Thyroid hormone mnemonic and stuff to know

4Bs Brain maturation Bone growth Beta-adrenergic effects Basal metabolic rate increase TBG: bind most T3 and T4 in blood. Only the free hormone is active. -decreased TBG: seen in hepatic failure -increased TBG: in preganncy or OCP use (cuz increased estrogen). So a normal person will increase thyroxine production to saturate the increased number of TBG binding sites. If you're hypothyroid however, you can't compensate and will result in decreased free thyroince and icnreased TSH. This is why hypothyroid pregnant person needs increased dosing of levothyroxine. Primarily what comes out of thyroid is T4. This is converted to T3 in the peripheral tissue by 5-deiodinase. T3 has greater affiniiy for recpetors than T4. Woff-Chaikoff effect: excess iodine temporarily inhibits thyroid peroxidase--->decrased iodine organification-->decreased T3/T4 production. Propythiouracil: inhibits both peroxidase in thyroid and 5-deiodinase Methimazole:inhibits peroxidase only, has fewer side effect than propythioruracil and results in quicker ahcievement of the euthyroid state in patients with hyperthyroidism

Primary Care: Urinary incontinence

5 types: urge, stress, overflow reflex, functional Male is usually due to BPH or neurlogic disease. Female is usually due to hormonal changes, pelvic floor dysfunction or laxity, or uninhibited bladder contractions (detrusor contractions) due to aging Most common cause of incontinence in elderly patients is urge incontinence. In women <70 years of age, most common is stress. Urge (detrusor instability) -involuntary detrusor conractions results in involuntary loss of urine -sudden urge to urinate (patients can't make it to bathroom), loss of large volumens of urine with small postvoid resudual , nocturnal wetting - Tx: bladder training exercises. If unsuccessful, antigholinergics (oxybutinin) and TCAs. Stress: Occurs in mostly women (after multiple deliveries of children). involuntary urine loss during activities that increase intra-abdomonal pressure (coulg, lauge, sneeze, exercise). -Tx: kegel exercises to stregnthen pelvic floor musculature Overflow: common in diabetics, and neurologic disorders. -Urine leakage. Noctunral wetting, frequent small amount of rine, large postvoid residual (usually more than 200cc on bladder ultrasound suggest presence of detrusor muscle weakness or obstruction, which can lead to overflow incontinentnce) -causes: neurogenic bladder (diabetics, lower motor neuron lesions), medications, Obstruction to urine flow (like BPH, prostate caner) Reflex: spinal cord injury most common cause. Patient cannont sense need to urinate Functional incontinence:: secondary to disabling and debilitating disease.

Acute Limb Ischemia

6Ps Pain, pallor, paraesthesia, pulselsenssness, poikilothermia, paralysis All patients with clinical signs and symptoms of ALI should receive ANTICOAGULATIOn (IV heparin bolus followed by continous heparin infustion) while awaiting further interventions. This prevents thrombus propagation and formation of new distal thrombus due to statis. Patients with an immediatly-threatened extremity are at increased risk for IRREVERSIBLE MYONECROSIS within 4-6 hours and should have emergency surgical revascularization.

Normal BUN range

7-18

Normal ABG

7.4/40/90/24/98

Desribe the rash associated with Neisseria meningitis

75% present with peechial rash that is prominent on axilla, wrists, flanks, and ankles. Appears within 24 hours of infection.

ALT range

8-40

AST range

8-40

Calcium serum range

8.4 - 10.2

Normal Cl range

95-105

DIlute urine lab value?

< 1/2 plasma osmolality.

Hypomagnesemia

<1.8 -Drugs (loop diuretics, amphotericin) -Low magnesium causes hypokalemia and hypocalcemia that WILL NOT RESPOND to replacement if magnesium not fixed first -ECG changes similar to hypokalemia

Normal JVP

<3cm above sternal angle

Hypermagnesemia

>2.3 Iatrogenic, magnesium contatinin druges (some laxative, antacids) if given to a patient with renal failure Tx: IV fluids, calcium if there are ECG changes, dialysis if refractory

Breast cancer screening guidelines

>40 yrs -monthly brest exam -clinical breast exam yearly -mammogram every 1 or 2 years (controversial whether 1 or 2 years) 50-64 yrs -monthly self breast exam -clinical breast exam every year -Mammogram annually 65 years and over -monthly self breast exam -clinical breast exam every year -mammogram every 2 years *Uworld says the USPTF recommends EVERY 2 YEARS screening mammography for women age 50-74.

Whats a good level of HDL

>60 is cardioprotective

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What can Chagas disease cause?

A CHRONIC disease that can cause megaclon, and/or cardiac dysfunction. The protozoan Trypanosoma cruzi, endemic to Latin America, is responbile

Hydroxychloroquine

A DMARD. Can be used for SLE. common adverse effects are Gi distress, visual disturbances, and hemolysis in G6PD defieincy. Most serious side effect is retionpathy, eye examinations every 6 months are the only form of routine screening required with it .

what is pretty indicative of aspergilloma clinically?

A MOBILE cavitary mass in the lung, whic presents with intermittent hemoptysis. Mobile meaning that the cavitary nodule may move as patient changes position. Lab findings: Positive IgG PLUS radiographic evidence.. like cavities (with or without fungus ball, this is whyppl with who may have had TB with cavity in lungs can get a fungus ball in that caviry), consolidation, peribronchial infiltrates

Septic Arthritis presentation and stuff to remember

A bacterial joint infection that is often preceded by skin or URI. Lab findings: Elevated WBC, Elecated ESR and CRP, Synovial fluid WBC> 50,000 To treat remember you wanna start empiric antibiotics AFTER an arthrocentisis because if you stgarted before the antibiotics would mess up your findings to isolate the bacteria. Tx: Birth to 3 months: Staph, GBS, Gram - . Naf or Vanc PLUS gent or Cefotaxime. Older than 3 months: Staph: Group A strept. Strep pneumoniaae. Antibiotics: Naf, clinda, cefazol, or vanc.

Polycythemia?

A central hematocrit of 65% or higher, which can lead to blood hyperviscosity.

Poor inhlaer technique is a major reason why patient with asthma don't respond well to medications. How can you find out if it happens?

A clue suggesting poor inhaler technique is the patient's rapid improvement in FEV1 after the supervised use of a bronchodilator.

What is de quervain tenosynovitis?

A condition that classsically affects new mothers who hold their infants with the thumb outstretched (abducted/extended). The abductor pollicis longus and extensor pollicis brevis tendons are affected; passive stretch of these tendons elicits pain.

Cystinuria

A group of disorders characterized by impaired amino acid transport and several modes of inheritance. Problem is with defectie transport of cystine, lysine, arginine, and ornithine by the tubular cells. Cystine is poorly soluble in water and leads to fomration of hard, radiopaque renal stones. Look for a personal history of recurrent kidney stones from childhood and a positive family history. The characteristic stones are hard and radiopaque. UA shows typical hexagonal crystals. The urinary cyande nitroprusside test is widely used as a qualitative screening procedure.

What is Trousseau's syndrome?

A hypercoagulable disorder that usually presents with unexplained superficial venous thrombosis at unsual sites (arm, chest). Usually is associated with cancer involving pancreas (MOST common), lung, prostate, stomach, and colon and leukemias. Patho likely is that tumor releases mucins that react with platelets to form palately-rich microthrombi.

What is small-intestin bacterial overgrowth ?

A malabsorption syndrome due to anatomic or dysmotility disorders. Abdominal bloating, flatulence, and diarrhea. Endoscopy with jejunal aspirate showing >10^5 organisms/ml is gold standard. Anatomic causes can be strictures, surgery. Motility causes can be diabetes, scleroderma. there are other causes. Lab values usually normal but nutitional defiiencies can happen.

What is ursodeoxycholic acid?

A medication used to dissolve small gallstones in patients with normal functional gallbladders who are poor surgical candidates. However, this medication is crey costly and associated with ah high risk of relapse when therapy is halted.

Person has hypertension and benign essential tremor, how do you treat?

A non selective beta blocker.

Ranolazine?

A novel antianginal agent that is approved for the treatment of chronic stable angina. It should only be used, however, in addition to baseline therapy with a Beta Blocker, a Ca channel blocker, and a long-acting nitrate.

What is the "sucussion splash?

A physical exam maneuvier in which the you place stehoscope over upper abdomen and rocking the patient back and forth at his you can hear a splash sounds, indicating the presence of a hollow viscous filleed with fluid and gas. Can indicate gastric outlet obstruction.

what is hemothorax?

A pleural effusion with hematocrit >50% of serum hematocrit. A surgical emergency!! Causes include trauma and aortic dissection.

Explain VIPoma

A rare tumor affecting the pancreatic cells that produce VIP. Most patients develop VIPoma syndrome (pancreatic cholera) with 1. watery diarrhea 2. muscle weakness/cramps (due to HYPOKALEMIA due to increased intestinal secrietion)) 3. hypo-or achlorydria (due to decreased gastric acid secrtion). Also get flushing, lethargy, mausea, vomiting, Stool studies are consistent with secretory diarrhea and show decreased stool osmotic gap; a VIP level >75pg/ml confirms VIPoma diagnsoes. Most of time its in the pancreatic tail. Abdominal CT can find it.

What is erysipelas and what causes it?

A specific type of cellulitis, characterized by inflammation of superficial dermis. Classic finding is sharply demarcated, erythematous, edematous, tender skin lesion with raised borders. Sudden onset. Group A streptococcus most frequently implicated organism.

What is Mean corupscular hemoglobin concentration?

A value calculated by dividing the hemoglobing by hematocrit and is a measure of hemoglobin concentration of each erythrocyte. Decreased: iron deficiency, thalassema Increased: in patients with hereditary spherocytosis secondary to loss of RBC surface area

Causes of cardiac emboli

A-fib Prior h/o of MI or LV dysfunciton Endocarditis Valvular disease Atrial Myxoma Prosthetsi aortic valve