Final COMLEX/USMLE STEP 1 Study Set

Hypertriglyceridemia

Fibrate

Breast tumor (benign, young woman)

Fibroadenoma

Iliohypogastric nerve: a. Sensation to what areas b. Motor to what?

L1 a. Sensation to suprapubic and gluteal regions b. Motor: anterolateral abdominal wall muscles

Genitofemoral nerve: a. Sensation to what areas? b. Motor to what?

L1-2 a. Sensation to upper anterior thigh b. Cremasteric reflex in men, mons pubis in women?

Lateral femoral cutaneous nerve: a. Sensation to what areas

L2-3 Sensation to skin on lateral thigh

Femoral nerve: a. Sensation to what areas? b. Motor?

L2-4 Sensation: Upper thigh and inner leg Motor: muscles that extend knee (quads)

Coronary artery involved in thrombosis

LAD > RCA > Circumflex

Smoking

LBW, preterm labor, placental problems, IUGR, ADHD

Primary biliary cholangitis: pathological findings?

Lymphocytic infiltrates and destruction of small and mid-sized intrahepatic bile ducts. Similar to GVHD.

Schizophrenia (positive symptoms)

Typical and atypical antipsychotics

Growth hormone: Through what intermediate does it have its effect? What pathway?

Via IGF-1 from liver. GH binds to receptor and leads to IGF-1 production through JAK-STAT pathway.

Enlarged hardened left supraclavicular node

Virchow node (abdominal metastasis)

Hypercoagulability, endothelial damage, blood stasis

Virchow triad (elevated risk of thrombosis)

Sudden Cardiac Death

Most commonly d/t vfib

Sporothrix schenckii

Itraconazole, oral potassium iodide

Strongyloides and Onchocerca tx

Ivermectin

Prostate adenocarcinoma/uterine fibrinoids

Leuprolide, GnRH (continuous)

Infertility

Leuprolide, GnRH (pulsitile), clomiphene

Alcohol withdrawal

Long-acting benzodiazepines

Frameshift mutation: how to detect?

Look for number of bases that is not divisible by 3.

Furosemide

Loop diuretic. SE = Ototoxicity

Huntington disease

Loss of GABA-containing neurons

Phentolamine: MOA

Mnemonic: phentoequalamine alpha-1=alpha-2 antagonist

Sensitivity

Sn = TP / (TP + FN)

Bounding pulses, wide pulse pressure, diastolic heart murmur, head bobbing

Aortic regurgitation

Heart nodules (granulomatous)

Aschoff bodies (rheumatic fever)

Rifaximin: indications, MOA?

- Indications: traveler's diarrhea, hepatic encephalopathy to decrease ammonia production (generally used in addition to lactulose*) - MOA: rifaximin is non-absorable abx a. In HE: decreases intestinal production of ammonia by bacteria b. In traveler's diarrhea: inhibits bacterial RNA synthesis through binding with DNA-dependent RNA pol *Lactulose: catabolized by intestinal bacteria to short-chain fatty acids, lowering colonic pH and increasing conversion of ammonia to ammonium for excretion.

Type II pneumocyte function

- Surfactant production - Regeneration of alveolar lining after injury - Act as progenitor cells for type I pneumocytes (type I pneumocytes cannot regenerate on their own)

ACEi

-Pril medications.

Glands: Compare and contrast between apocrine, holocrine and merocrine glands in terms of how each releases contents. Provide examples for each type.

1. Apocrine glands: release contents via membrane-bound vesicles. Example = mammary glands. 2. Holocrine glands: release contents via cell lysis. Example = sebaceous glands ( to hair follicles) and Meibomian glands (rim of eyelid) 3. Merocrine glands: release contents via exocytosis. Examples = sweat glands (eccrine and apocrine types). Note: apocrine sweat glands are really merocrine. This is misnomer.

Insulin: types? Which are basal long-acting? Which are post-prandial short-acting?

1. Basal (long-acting) a. NPH: give twice daily (good for about 18 hours) b. Glargine and detemir: once daily (good for 24 hours) 2. Post-prandial (short-acting) a. Regular insulin: peak is 2-4 hours. Best for IV use (to prevent DKA) b. Lispro, Aspart, Glulisine: peak is 45-75 mins (fast acting). Best to prevent post-meal hyperglycemia

Pediatrics: patent processus vaginalis leads to

1. Communicating hydrocele 2. Indirect inguinal hernia Not testicular torsion (result of trauma or congenitally-horizontal positioning of the testes aka bell clapper deformity)

Cholecystitis: Describe steps of inflammation in acute calculous cholecystitis.

1. Gallstone obstruction of cystic duct 2. Mucosal disruption by lysolecithins, bile salt irritation of luminal epithelium, PG release with transmural inflammation 3. Gallbladder hypomotility 4. Increased intraluminal pressure causing ischemia 5. Bacterial invasion

Polyhydramnios: causes?

1. Impaired fetal swallowing: GI obstructioen, anencephaly (eg. d/t use of folic acid antagonists such as anti-epileptics and trimethoprim) 2. Increased fetal urine output: high cardiac output d/t anemia or twin-twin-transfusion syndrome

Repro: Derivatives of aortic arch

1. Mnemonic = First is Max = Maxillary artery 2. Mnemonic = Second is Stapedial = Stapedial artery 3. Mnemonic = 3rd letter in alphabet = C = Common carotid artery and proximal internal carotid artery 4. Mnemonic = fOUR rhymes with AOR = aortic arch. Also = fouRS = right subclavian (UW says that subclavian arteries come from 4, but FA says just Right). 5. Obliterated 6. Mnemonic = 6 looks like lungs = pulmonary arteries + ductus arteriosus

Complete hemithorax opacification: causes? How to distinguish?

1. Pleural effusion: trachea deviates away 2. Collapsed lung d/t bronchial obstruction (eg. tumor): tracheal deviates toward. Why? Air trapped in lung is absorbed into the blood = alveoli collapse = pulling trachea and thoracic organs toward the side of collapse.

Follicular lymphoma translocation

14; 18 = bcl-2 from 18 now under Ig heavy chain enhancer on 14

Bipolar treatment

1st line = lithium, valproate and 2nd generation antipsychotic quetiapine.

Congenital adrenal hyperplasia, hypotension

21-hydroxylase deficiency

tRNA sites and function

3' = amino acid binding site T-loop/arm = TPsiC (aka ribothymidine, pseudouridine and cytidine) = binding of tRNA to ribosomes Anticodon loop/arm = complementary to RNA, ensures proper placement of AA into polypeptide chain D-loop/arm = correct tRNA recognition by proper aminoacyl tRNA synthetase

Bile acid synthesis

7-alpha hydroxylase

Hernias

736875

Rheumatic fever: What is the primary cause of morbidity in acute RF? Long term complication in heart?

Acute rheumatic fever = severe pancarditis Long term = mitral stenosis years to decades after infection

Somatomedin C: What is it?

Aka IGF-1. It is directly correlated with GH. When GH rises, IGF-1 rises. Causes differentiation and proliferation of chondrocytes at epiphyseal growth plate = gigantism.

HMP Shunt: what is it?

Aka Pentose Phosphate Pathway, which serves to generate NADPH (to fight oxidative stress and other things) + ribose-5-phosphate for nucleotide synthesis.

Hawthorne Effect

Aka observer effect. Tendency of study subjects to change their behavior as a result of their awareness that they are being studied.

Phenylephrine: MOA

Alpha agonist

Mydriasis

Alpha-1 agonist

Essential fructosuria: A. Defect B. Finding with copper reduction test and glucose oxidase test

A. Defect = fructokinase B. Positive copper reduction test (indicates fructose, a reducing sugar is present). Glucose oxidase is negative (no glucose in urine).

BRAF V600E mutation: associated with what cancer

Melanoma. V = valine to E = glutamic acid at position 600.

Eosinophils: How do they participate in host defense against parasite?

ADCC: Antibody-dependent cell-mediated cytotoxicity. Eg. Parasite coated with IgG and E. Eosinophils bind to these via their Fc receptors. This triggers eosinophil degranulation.

Anion gap calculation

AG = Na - (Bicarb + Chloride). Nml = 10-14.

Malignancy (kids)

ALL, medulloblastoma (cerebellum)

Age Ranges of ALL/CLL/AML/CML

ALL: child CLL: adult > 60yo AML: adult ~65yo CML: adult 45-85yo

Auer rods are associated with what? What is the translocation?

AML M3 (APML) variant is associated with translocation = 15;17

Isosorbide dinitrate: Why is dosing so high compared to sublingual nitro?

Absorbed via GI tract and undergoes 1st pass metabolism in liver prior to release in systemic circulation. Sublingual nitro is rapidly absorbed from oral mucosa directly into venous circulation and has rapid onset of action within 2-5 minutes.

Red currant jelly stools

Acute mesenteric ischemia (adults), intussusception (children)

Cavernous hemangioma: histology

Most common benign liver tumor Don't biopsy, as procedure causes fatal hemorrhage.

Mitral stenosis: What is the best and most reliable auscultatory indicator of the degree of mitral stenosis?

A2-opening snap interval Shorter = more severe stenosis. Why? Left atrial pressure increases d/t impaired movement of blood into left ventricle. Higher pressure in left atrium causes mitral valve to open more forcefully resulting in shorter interval. Current standard for diagnosing severity of MS = mean transvalvular pressure gradients via 2D doppler echo.

ACEi side effects

ACE: angioedema, dry cough, hypotension. Other SE = hyperkalemia, decreased GFR (efferent arteriole doesn't constrict as much d/t less AT II), fever, altered taste.

Lithium: Drug interactions

ACEi, NSAIDs (not ASA), Thiazides

Anterior drawer sign

ACL injury

Tuberous sclerosis

AD Angiomyolipomas (BVs, fat, muscle), cortical tubers, subependymal hamartomas, cardiac rhabdomyomas, facial angiofibromas, leaf-shaped patches on skin lacking pigment (Ash-Leaf patches) Brain lesions = seizures, cognitive disability

NF2

AD Bilateral acoustic neuromas (Schwannomas), may also develop multiple meningiomas, gliomas, ependymomas of spinal cord

VHL

AD Cerebellar hemangioblastomas, retinal hemangiomas, liver cysts. Increased risk for bilateral RCC.

NF1

AD Neurofibroma (plexiform or solitary), optic gliomas, pigmented nodules of iris (Lisch nodules), cutaneous hyperpigmented macules (Cafe-Au-Lait spots)

"Spontaneous intracranial hemorrhage: Most common cause in young adults?"

AV malformations, ruptured cerebral aneurysms (patients w/coarctation more likely), or abuse of sympathomimetic drugs such as cocaine

Atherosclerosis: What arteries are most affected by atherosclerotic plaques, in order of first to last affected?

Abdominal aorta > coronary > popliteal > ICA > circle of Willis

Site of atherosclerosis

Abdominal aorta > coronary artery > popliteal artery > carotid artery

Cocaine

Abnormal fetal growth, fetal addiction, placental abruption

Migraine

Abortive therapies (eg. sumatriptan, NSAIDS), prophylaxis (eg. propranolol, topiramate, CCBs, amitriptyline)

Hypoparathyroidism

Accidental excision during thyroidectomy

Fatty acid synthesis

Acetyl-CoA carboxylase (ACC) (+) insulin, citrate (-) glucagon, palmitoyl-CoA

WBC cases in urine

Acute pyelonephritis

Branching gram (+) rods with sulfur granules

Actinomyces israelii

Permissiveness vs Synergistic vs Additive Effects

Additive: Drug A produces X effect, Drug B produces Y effect. Combination of drugs produce X + Y effect. Synergistic: Combination of drug A and B produces greater effect than would be expected if you added their effects together. Permissiveness: Drug A does not generate the effect of B at all. When combined with drug B, it allows drug B to increase its effect. Eg. Cortisol increases vascular and bronchial smooth muscle reactivity to catecholamines and increases glucose release by liver in response to glucagon.

NE: Which receptors does it have affinity towards? Which doesn't it?

Affinity predominantly on alpha and beta-1 Little affinity on beta-2.

Pancreatitis (chronic)

Alcohol (adults), cystic fibrosis (kids)

Liver disease

Alcoholic cirrhosis

Pediatrics: What supplements do breastfed infants require?

All vitamins and trace elements are found in breast milk except adequate vitamin D and K. Vit K given as shot at birth. All should receive vit D supplements as they shouldn't be exposed to sun. Breast milk also has low iron content, but bioavailability is higher than in a supplement and sufficient til age 4 months. Iron content decreases over time and > 4 months, supplementation of iron required.

Acute promyelocytic leukemia (M3)

All-trans retinoic acid

Dementia

Alzheimers disease, multiple infarcts (vascular dementia)

Streptomycin

Aminoglycoside. MOA = inhibition of protein synthesis through inactivation of 30S ribosomal subunit.

MI: Drug of choice in acute management of ventricular arrhythmias in setting of MI?

Amiodarone Second-line = Lidocaine (1B antiarrhythmic that binds preferentially ischemic or depolarized Purkinje and ventricular tissue / inactivated Na channels and rapidly dissociates) 1B mnemonic = 1B is Best post-MI

Tx of choice for listeria

Ampicillin

Mixed (UMN + LMN) motor neuron disease

Amyotrophic lateral sclerosis

TTP-HUS: Classic pentad

Anemia, Thrombocytopenia, Fever, Neurologic Sx, Renal failure

Chest pain on exertion

Angina (stable: with moderate exertion; unstable: with minimal exertion or at rest)

Bamboo spine on x ray

Ankylosing spondylitis (chronic inflammatory arthritis: HLA-B27)

Affect of anorexia on hypothalamic-pituitary-ovarian axis

Anorexia leads to functional hypothalamic amenorrhea. Thought that decrease in leptin starts this process off via inhibition of GnRH. Impaired GnRH = low LH, FSH = low E

Chemotherapy-induced vomiting

Antagonists to 5-HT3 and NK1 are useful in treating chemo therapy-induced vomiting

RA: most specific antibodies?

Anti-CCP (citrullinated peptides/proteins). RF factor: anti-Fc on IgG have poor specificity.

Pseudomonas aeruginosa

Anti-pseudomonal penicillins, aminoglycosides, carbapenems

Acute rheumatic fever: what do antibodies cross-react with?

Antibodies cross-react between bacteria (M proteins) and self, specifically toward: myosin (cardiac protein), lysoganglioside (neuronal cell surface protein)

C. tetani

Antitoxin

Clostridium botulinum

Antitoxin

Presentation: diastolic decrescendo blowing murming (best heard at left sternal border), bounding femoral and carotid pulses, head bobbing with carotid pulsations. What is the diagnosis?

Aortic regurgitation Regurg into LV = increase LVEDV = LV enlargement w/eccentric hypertrophy = increase SV (felt as sense of pounding or uncomfortable feeling of heartbeat esp when lying on left) with abrupt distension and rapid falloff of peripheral arterial pulses = Bounding pulses and wide pulse pressure. Some patients exhibit head bobbing w/carotid pulsations (de Musset sign) d/t transfer of momentum from large LV SV to head and neck.

Ejection click

Aortic stenosis

Systolic ejection murmur (crescendo-decrescendo)

Aortic stenosis

Methimazole

Aplasia cutis congenita: absence of skin, typically circular portion missing on scalp This is hyperthyroidism drug

Breast cancer in postmenopausal women

Aromatase inhibitor (anastrozole)

Capitation: what is it?

Arrangement in which payor pays fixed, predetermined fee to provide all the services required by the patient.

Epidural hematoma

Associated with lucid interval followed by loss of consciouness

Light microscopy findings post MI

At 2 weeks, will see well developed granulation tissue with neovascularization

Pulmonary vascular resistance: At what point on a lung capacity / volume graph is pulmonary vascular resistance (PVR) lowest?

At FRC: functional residual capacity. Lowest point of TV. When you are fully inhaled, the alveolar capillaries are longitudinally stretched by expanded alveoli leading to increased PVR. When you are fully exhaled, the alveolar capillaries are narrowed d/t decreased radial traction from adjacent tissues and compression by positive intrathoracic pressure leading to increased PVR. FRC is midpoint between these.

Aortic aneurysm, abdominal

Atherosclerosis

Chronic arrhythmia

Atrial fibrillation (associated with high risk emboli)

Meds with anticholinergic side effects

Atropine, TCAs, H1 receptor antagonists (eg. diphenhydramine), neuroleptics, antiparkinsonian drugs

Warfarin

Bone deformaties, fetal hemorrhage, abortion, ophthalmologic abnormalities

Muffled heart sounds, distended neck veins, hypotension

Beck triad of cardiac tamponade

Cardiac tamponade: triad, cause?

Beck's triad: hypotension with pulsus paradoxus (decrease in SBP > 10 on inspiration), elevated JVP and muffled heart sounds. Cause: any cause of pericardial dz (infectious, autoimmune, neoplasm, cardiac, trauma, metabolic, radiation, drugs)

CYP 450 Inducers

Barbiturates, rifampin, carbamazepine, griseofulvin, chronic etoh consumption

GERD: histologic findings?

Basal zone hyperplasia, elongation of lamina propria papillae and scattered eosinophils (don't get confused with eosinophilic esophagitis).

Denial

Behaving as if an aspect of reality does not exist

Tetrodotoxin (Pufferfish): MOA

Binds VG Na channel in nerve and cardiac tissue preventing Na influx, preventing AP conduction.

Tennis racket shaped cytoplasmic organelles (EM) in Langerhans cells

Birbeck granules (Langherhans cells histiocytosis)

Death in CML

Blast crisis

Coronary steal phenomen

Blood flow in ischemic areas is reduced d/t arteriolar vasodilation in non-ischemic areas leading to worsening of ischemia in the original area.

Abdominal pain, ascites, hepatomegaly

Budd-Chiari syndrome (post hepatic venous thrombosis)

Recurrent inflammation/thrombosis of small/medium vessels in extremities

Buerger disease (strongly associated with tobacco smoking)

t(8;14)

Burkitt lymphoma (c-myc fusion, transcription factor)

Sheets of medium-sized lymphoid cells with scattered pale/tingible body-laden macrophages (starry sky histology)

Burkitt lymphoma (t8:14 c-myc activation, associated with EBV; starry sky made up of malignant cells)

Bluish line on gingiva

Burton line (lead poisoning)

Pelvic inflammatory disease

C trochomatis, N gonorrhoeae

Hypertension, hypokalemia, metabolic acidosis

Primary hyperaldosteronism (Conn syndrome)

Drug clearance

CL = rate of elimination of drug / plasma drug concentration = Vd x Ke (elimination constant)

Prolactinoma

Cabergoline/bromocriptine (dopamine agonists)

Trigeminal neuralgia (tic douloureux)

Carbamazepine

Fatty acid oxidation (beta-oxidation)

Carnitine acyltransferase I (-) Malonyl CoA

Glucocorticoids: Anabolic and catabolic effects

Catabolic: lipolysis (w/altered fat distribution), adrenal cortex atrophy, osteoporosis, immune suppression/T cell apoptosis, skeletal muscle atrophy, skin thinning/stria/impaired wound healing Anabolic: liver only (increased gluconeogenesis and glycogenesis)

Maternal Diabetes

Caudal regression syndrome (anal atresia to sirenomelia, which is Mermaid syndrome), congenital heart defects, NTDs

TH1 cells

Produce and express IFN-gamma

Cystinuria: Cause? SSx? What does UA show?

Cause = defective dibasic amino acid transport in intestinal and proximal renal tubular cells. SSx: recurrent stone formation at young age d/t increased reabsorption of cysteine from urine UA: elevated urinary cysteine levels (aminoaciduria), Na-cyanide-nitroprusside test detects presence of urinary cystine. Cystine stones.

Neisseria gonorrhoeae

Ceftriaxone (add doxycycline to cover likely concurrent C. trochomatis)

Phases of gastric acid secretion

Cephalic and gastric phases stimulate secretion of gastric acid. Intestinal phase tends to reduce gastric acid secretion.

Cardiomegaly with apical atrophy

Chagas disease (trypanosoma cruzi)

Large granules in phagocytes, immunodeficiency

Chediak-Higashi disease (congenital failure of phagolysosome formation)

Chi-squared vs t-test vs ANOVA

Chi-squared: use with categorical data (not means) to evaluate expected frequency of occurrence is consistent with observed frequency of occurrence. Eg. comparing the percentage of members of 3 different ethnic groups who have essential HTN = chi-squared. Not comparing the mean BPs. T-test: compare the means of 2 groups of subjects ANOVA: compare the means of 3 different groups of subjects

Malaria

Chloroquine, mefloquine, atovaquone/proguanil (for blood schizont), primaquine for liver hypnozoite)

Right heart failure due to pulmonary cause

Cor pulmonale

Fat, female, forty, and fertile

Cholelithiasis (gallstones)

Nutmeg apprearance of liver

Chronic passive congestion of liver due to right heart failure or Budd-Chiari syndrome

Hereditary hyperbilirubinemias: Which of these presents with kernicterus? What is the defect?

Crigler-Najjar syndrome type I Absent UDP-glucuronosyltransferase (inability to conjugate bilirubin)

Palpable purpura on buttocks/legs, joint pain, abdominal pain (child), hematuria

Henoch-Schonlein purpura (IgA vasculitis affecting skin and kidneys)

Drug of choice for anticoagulation during pregnancy

Heparin

Clostridium tetani: SSx

Clinical diagnosis (trismus, sardonic smile, muscle spasms, no vaccine)

Patent Ductus Arteriosus

Close: indomethacin Keep open: PGE analogs

Painful blue finger/toes, hemolytic anemia

Cold agglutinin disease (autoimmune hemolytic anemia caused by Mycoplasma pneumoniae, infectious mononucleosis, or CLL)

Metastases to liver

Colon >> stomach, pancreas

Craniopharyngiomas

Composed of calcified cysts containing cholesterol crystals. Derived from remnants of Rathke's pouch, an embryonic precursor of the anterior pituitary.

Concentric vs eccentric hypertrophy: which conditions contribute to each of these structural changes in the heart?

Concentric (increase in muscle fibers in parallel): LVH = long-standing hypertension, aortic stenosis d/t increased afterload. Also hypertrophic cardiomyopathy. Eccentric (increase in muscle fibers in series): myocardial inflammation leads to dilation and enlargement of heart chambers with decreased ventricular contractility.

Chorioretinitis, hydrocephalus, intracranial calcifications

Congenital toxoplasmosis

Eosinophilic globule in liver

Councilman body (Viral hepatitis, yellow fever), represents hepatocyte undergoing apoptosis)

Assessing attention and concentration

Counting down backwards from 100 by 7 or 3, reciting months of year in reverse order, spelling world backwards.

Myocarditis

Coxsackie B virus

Steeple sign on frontal CXR

Croup (parainfluenza virus)

Acyclovir: Side effects

Crystalline nephropathy. Can be avoided if adequate hydration is provided.

Renal clearance

Cx = (Ux . V) / Px Ux = urine concentration of X (mg/ml) V = urine flow rate (ml/min) Px = plasma concentration of X (mg/ml)

Granulomatosis with polyangiitis (Wegener)

Cyclophosphamide, corticosteroids

Colonies of mucoid Pseudomonas in lungs

Cystic fibrosis (autosomal recessive mutation in CTFR gene -> fat-soluble vitamin deficiency and mucous plugs)

Anion gap metabolic acidosis

Decreased bicarb + increased AG = AG metabolic acidosis secondary to lactic acidosis

Howell-Jolly Bodies: seen in what?

Decreased or absent splenic function

Clear cell adenocarcinoma of the vagina

DES exposure in utero

Which artery runs with the radial nerve along the posterior humerus?

Deep brachial artery

Disease with DNA mismatch repair issue? Disease with DNA excision repair issue?

DNA mismatch repair issue = HNPCC / Lynch DNA excision repair issue = xeroderma pigmentosum

Primase: What type of polymerase is this?

DNA-Dependent-RNA-Polymerase. Meaning that you can see Uracil being laid down in areas where this enzyme has been active.

Valproic acid

DOC (drug of choice) for absence and TC seizures combined. Ethosuximide will only tx absence seizures, not TC.

Genetic defect: Down Syndrome vs Turner Syndrome in terms of dysmorphic features

DS: epicanthal folds, upslanting palpebral fissures, protruding tongue, excessive skin at nape of neck, cardiac defects Turner: low-set ears, webbed neck, wide-spaced nipples, cardiac defects (aortic coarctation)

Heinz Bodies: seen in what?

Denatured Hb seen after oxidant stress in G6PD deficiency. These will become bite cells.

Phenytoin

Depends on P450 oxidases. Inducer of P450

Melanocytes

Derived from neural crest cells

Diabetes insipidus

Desmopressin (central); hydrochlorothiazide, indomethacin, amiloride (nephrogenic)

Diabetes mellitus type 1

Dietary intervention (low carbohydrate) + insulin replacement

Diabetes mellitus type 2

Dietary intervention, oral hypoglycemics, and insulin (if refractory)

Tetracyclines

Discolored teeth, inhibition of bone growth

Mitochondrial inheritance

Disease occurs in both males and females, inherited through females only

PSNS activation

Does not lead to pupillary dilation, but rather constriction (miosis)

Single palmar crease

Down syndrome

Decreased AFP in amniotic fluid/maternal serum

Down syndrome or other chromosomal abnormalities

Intellectual disability

Down syndrome, fragile X syndrome

Rickettsia rickettsii

Doxycycline, chloramphenicol

"Down Syndrome: Most common GI complication?"

Duodenal atresia (double-bubble sign = dilated stomach and proximal duodenum). Present with bilious emesis in first few days of life.

Genetic heterogeneity

Dz phenotype can be caused by one of several different genotypes. For example: OI can result from mutations affecting either of the genes coding for type 1 collagen (COL1A1 or COL1A2)

UTI

E coli, S. saprophyticus (young women)

Onion skin periosteal reaction

Ewing Sarcoma (malignant small blue cell tumor)

Lactose fermenting gram negative: what bacteria?

E.coli, Klebsiella, Enterobacter

Atypical lymphocytes

EBV

Ejection fraction

EF = SV / EDV = (EDV - ESV) / EDV

Lyme disease: Tx of early and late Lyme dz

Early Lyme: doxycycline Late Lyme: PCN-type abx (eg. Ceftriaxone recommended)

Lithium

Ebstein anomaliy (atrialized right ventricle)

Lithium: teratogenic effects

Ebstein anomaly (atrialized Rt ventricle, ASD potentially), NDI, hypothyroidism

Polished ivory-like appearance of bone at cartilage erosion

Eburnation (osteoarthritis resulting in bony sclerosis)

Infant with microcephaly, rocker bottom feet, clenched hands, and structural heart defect

Edwards syndrome (trisomy 18)

Osmotic diuretic: SE

Eg. mannitol Pulmonary edema = severe SE. Use cautiously in high risk patients such as those with pre-existing CHF or pulmonary edema.

Elastic skin, hypermobility of joints, increased bleeding tendency

Ehlers-Danlos syndrome (type V collagen defect, type III collagen defect seen in vascular subtype of ED)

Pink complexion, dyspnea, hyperventilation

Emphysema (pink puffer, centriacinar [smoking] or panacinar [alpha-1 antitrypsin deficiency])

Gynecologic malignancy

Endometrial carcinoma (most common in US); cervical carcinoma (most common worldwide)

PCOS: Which cancer are these patients at greatest risk for developing and why?

Endometrial hyperplasia/carcinoma Why: anovulatory cycles, chronic E stimulation (proliferation of endometrium) w/ decreased P secretion

Enoxaparin: MOA

Enoxaparin = LMWH that functions like heparin - binds and activates AT III = binds to factor Xa and stops it from converting prothrombin to thrombin (IIa).

Helminthic infection (US)

Enterbius vermicularis, Ascaris lumbricoides

Pediatrics: most common cause of death in Hirshsprung's dz patients?

Enterocolitis

Dubin-Johnson: What causes the liver to be black?

Epinephrine metabolites

Neonate with arm paralysis following difficult birth

Erb-Duchenne palsy (superior trunk [C5-6] brachial plexus injury; "waiter's tip")

Erosions vs. Ulcers

Erosions: mucosal defects that don't fully penetrate through muscularis mucosa (ie. limited to mucosal layer) Ulcers: penetrate through muscular layer and into the submucosal layers.

Large rash with bull's eye appearance

Erythema chronicum migrans from Ixodes tick bite (Lyme disease, Borrelia)

Amino acids: Which are essential? Which are glucogenic? Which are ketogenic?

Essential = PVT TIM HALL = phe, val, thr, try, iso, met, his, arg, leu, lys Glucogenic = all except leu and lysine Ketogenic: leu and lys

Absence seizures

Ethosuximide

SIADH: Describe in terms of plasma Na, plasma osmolality compared to urine osmolality, body fluid volume

Euvolemic hyponatremia Plasma Na: low Plasma osmolality compared to urine osmolality: concentrated urine compared to serum Body fluid volume: normal body fluid volume

Acting out

Expressing unacceptable feelings through actions

Homocystinuria: What is the enzyme deficiency? What supplement can dramatically improve this condition?

Ez deficiency = cystathionine synthase (B6 requiring ez) Supplement w/B6

Meckel diverticulum: Cause? SSx?

Failed obliteration of vitelline duct (omphalomesenteric duct) - connection between intestines and yolk sac. Ssx: painless lower GI bleeding most commonly

Thousands of polyps on colonoscopy

Familial adenomatous polyposis (autosomal dominant, mutation of APC gene)

Achilles tendon xanthoma

Familial hypercholesterolemia (decreased LDL receptor signaling)

Short stature, cafe-au-lait spots, thumb/radial defects, Increased incidence of tumors/leukemia, aplastic anemia

Fanconi anemia (genetic loss of DNA crosslink repair; often progresses to AML)

Polyuria, renal tubular acidosis type II, growth failure, electrolyte imbalances, hypophosphatemic rickets

Fanconi syndrome (Multiple combined dysfunction on the proximal convoluted tubule)

Type 1 Diabetes Mellitus: what is the best test to diagnose this?

Fasting BGL not the OGTT

Cystic Fibrosis: What vitamin deficiency are CF patients at risk for?

Fat-soluble vitamins ADEK.

Triglyceride accumulation in liver cell vacuoles

Fatty liver disease (alcoholic or metabolic syndrome)

Iron containing nodules in alveolar septum

Ferruginous bodies (asbestosis: elevated chance of mesothelioma)

Phenytoin

Fetal hydantoin syndrome: IUGR, microcephaly, craniofacial dysmorphisms, limb defects (hypoplastic nails and distal phalages). Some with growth problems, developmental delay and intellectual disabilities Like carbamazepine

Enterobiasis (pinworm) tx

First line = albendazole. Second line = pyrantel pamoate

Antidote to arsenic poisoning

First-line chelating agent = dimercaptol

Generalized anxiety disorder

First-line tx = SSRIs / SNRIs. Benzos = 2nd line d/t dependence and tolerance and potential for rebound and withdrawal with abrupt cessation.

Bulimia nervosa

First-line tx = fluoxetine (SSRI) + nutritional rehab and psychotherapy

Nephrolithiasis: Cystine stones

Flat, yellow, hexagonal

Cryptococcus neoformans

Fluconazole (in AIDS patients)

SIADH

Fluid restriction, IV hypertonic saline, conivaptan/tolvaptan, demeclocycline

Diabetic ketoacidosis

Fluids, insulin, K+

Ethylene glycol/methanol intoxication

Fomepizole (alcohol dehydrogenase inhibitor)

Schistocytes: seen in what?

Fragments of RBCs seen when they are mechanically lysed/sheared. Seen in HUS, TTP and DIC.

Gq mechanism

G protein activates PLC, which cleaves PIP2 into IP3 and DAG. IP3 causes increase in Ca, which activates PKC.

Gi mechanism

G protein inhibits process of Gs (see Gs)

CMV

Ganciclovir, foscarnet, cidofovir

Multiple colon polyps, osteomas/soft tissue, impacted/supernumerary teeth

Gardner syndrome (subtype FAP)

Pernicious anemia: Location of parietal cells

Gastric body and fundus. More specifically, they are in upper glandular layer. Deeper layer contains chief cells that synthesize and secrete pepsinogen

Lysosomal storage disease

Gaucher disease

Hepatosplenomegaly, pancytopenia, osteoporosis, aseptic necrosis of femoral head, bone crises

Gaucher disease (glucocerebrosidase deficiency)

Hilar lymphadenopathy, peripheral granulomatosis lesion in middle or lower lung lobes (can calcify)

Ghon complex (Primary TB, Mycobacterium bacilli)

Soap bubble in femur or tibia on x ray

Giant cell tumor of bone (generally benign)

Mucosal bleeding and prolonged bleeding time

Glanzmann thrombasthenia (defect in platelet aggregation due to lack of GpIIa/IIIB)

Pseudopalisading tumor cells on brain biopsy

Glioblastoma multiforme

RBC casts in urine

Glomerulonephritis

Sucrose: this is a disaccharide composed of what monomers?

Glucose and fructose

Linear appearance on IgG deposition on glomerular and alveolar basement membranes

Goodpasture syndrome

Antiglomerular basement membrane antibodies

Goodpasture syndrome (glomerulonephritis and hemoptysis)

Needle shaped (-) birefringement crystals

Gout (monosodium urate crystals)

Elevated uric acid levels

Gout, Lesch-Nyhan syndrome, tumor lysis syndrome, loop and thiazide diuretics

Sudden swollen/painful big toe joint, tophi

Gout/podagra (hyperuricemia)

Arteriovenous [] gradient

Gradient reflects tissue solubility of an anesthetic. High tissue solubility = large AV gradient and slower onset of action.

Chloramphenicol

Gray baby syndrome

Ischemic-Hypoxic Encephalopathy

Gross histology: bilateral wedge-shaped strips of necrosis over cerebral convexity, parallel and adjacent to longitudinal cerebral fissure.

Bacterial meningitis (newborns and kids)

Group B strep/E coli (newborns) S. pneumoniae/N. meningitidis (kids/teens)

Lactation: although prolactin secretion increases as pregnancy progression, what inhibits lactation from occuring?

HIgh progesterone levels through -ve feedback on prolactin in ant pituitary. After delivery, precipitous drop in P allows prolactin to stimulate lactation.

Cholesterol synthesis

HMG-CoA reductase (+) insulin, thyroxine, estrogen (-) glucagon, cholesterol

Ketogenesis

HMG-CoA synthase

Viral encephalitis affecting temporal lobe

HSV-1

Renal biopsy findings: widespread narrowing of renal arterioles with deposition of homogenous, glassy material in subendothelial space that stains with PAS pink. What is the underlying condition?

HTN (that is poorly controlled or untreated) Diabetes mellitus

Indurated, ulcerated genital lesion, painful chancroid with exudate

Haemophilus ducreyi

C.diff: contact precautions

Handwashing with soap and water, gown, non-sterile gloves. Etoh sanitizers don't kill bacterial spores.

Nitrates: Major SEs

Headaches, cutaneous flushing, lightheadedness, hypotension and reflex tachy.

Loop diuretics: SEs

Hypokalemia, hypomagnesemia, hypocalcemia and ototoxicity

Fatty acid breakdown defect: How can this be detected?

Hypoketotic hypoglycemia (no evidence of ketone bodies). Ketone bodies = acetoacetate, beta-hydroxybutyrate, acetone)

Prostate: Prostate Cancer: How does it spread to the spinal column bone?

Hematogenously via the prostatic venous plexus

Describe breakdown of heme

Heme = biliverden via ez: heme oxygenase Biliverdin = unconjugated bilirubin via ez: biliverdin reductase

Raltegravir: MOA

Integrase inhibitor, which disrupts HIV's genome from integrating with host's, thereby preventing host cellular machinery from being used to synthesize HIV mRNA.

Infection secondary to blood transfusion

Hepatitis C

AFP: Marker of?

Hepatocellular carcinoma (HCC), germ cell tumor

Neurophysin II mutation

Hereditary hypothalamic diabetes insipidus

Temporal arteritis

High-dose steroids

Hemoglobin-O2 dissociation curve: a. What does the body do when hemoglobin has affinity for o2 that is too high?

Higher affinity for o2 = reduced ability to release o2 within peripheral tissue = renal hypoxia = increased EPO synthesis = compensatory erythrocytosis

Atrial myxoma

Histology: scattered cells within mucopolysaccharide stroma, abnormal BVs and hemorrhaging

Malignancy associated with noninfectious fever

Hodgkin lymphoma

VSD

Holosystolic, low pitched murmur accentuated during maneuvers that increase afterload (ie. handgrip maneuver).

Circular grouping of dark tumor cells surrounding pale neurofibrils

Homer-Wright rosettes (neuroblastoma, medulloblastoma)

Chorea, dementia, caudate degeneration

Huntington disease (autosomal dominant CAG repeat expansion)

Hepatitis C: Transmission?

IV drug use, transfusion Rarely: sexually!

Suppression

Intentionally putting unwanted feelings aside to cope with reality vs. Repression: involuntarily withholding an idea or feeling from conscious awareness

"Scurvy: Where does hydroxylation of proline and lysine take place?"

Hydroxylation of proline and lysine occurs in RER. Necessary for collagen to attain its maximal tensile strength.

Sickle cell disease

Hydroxyurea (increases fetal hemoglobin)

Brown tumor of bone

Hyperparathyroidism or osteitis fibrosa cystica (deposited hemosiderin from hemorrhage gives brown color)

Aortic dissection

Hypertension

Cold intolerance

Hypothyroidism

Myopathy

Hypothyroidism is a common cause of elevated CK d/t hypothyroid myopathy. See for other sx to suggest hypothyroid.

Retinal artery: from what does it receive its blood?

ICA to Ophthalmic artery

Celiac disease

IgA against tissue transglutaminase

Anaphylaxis following blood transfusion

IgA deficiency

Chronic myelogenous leukemia

Imatinib

Post-strep glomerulonephritis: what type of hypersensitivity is this?

Immune complexes (Type III)

Berkson's bias

Selection bias created by choosing hospitalized patients as control group

TTP: etiology

Impaired function of ADAMTS13 (vWF-cleaving protease). Normally, large vWF in circulation are cleaved to regular size by this protease. In TTP, these uncleaved vWF multimers are more prothrombotic resulting in microvascular thrombosis = platelet-rich thrombi. Thrombocytopenia and hemolytic anemia (w/schistocyte formation) occurs.

"Down Syndrome: At risk complications?"

Imperforate anus, Hirschprung dz, tracheoesophageal fistula, Celiac disease and duodenal atresia (most common GI complication).

No lactation postpartum, absent menstruation, cold intolerance

Sheehan syndrome (pituitary infarction)

Effect of concurrent use of NSAID and loop diuretic

In addition to inhibition of Na-K-2Cl symporter in loop of Henle, loop diuretics also stimulate PG release. PG increases RBF leading to increased GFR and enhanced drug delivery. NSAIDS block PG releae leading to decreased diuretic response

Hormone Sensitive Lipase

In adipose tissue, HSL drives breakdown of TGLs into FFAs and glycerol during times of starvation providing substrates for gluconeogenesis and ketone body formation

Antidepressants

In susceptible patients (ie. bipolar patients who haven't been diagnosed), these can induce mania.

Thiazide diuretics: Effect on calcium, glucose, uric acid, cholesterol, TGLs, sodium, K and mag levels

Increase: calcium, uric acid, glucose (via decrease in insulin secretion), cholesterol and TGLs Decrease: sodium, potassium, magnesium (chronic)

"Coarctation of aorta: Most common morbidities associated with this?"

Increased risk for ruptured intracranial aneurysm d/t increased incidence of congenital berry aneurysms of Circle of Willis + aortic arch HTN

Nitrates: why avoid with RV infarct? Why avoid with HCM?

Infarct of RV: Reduction in preload = impaired CO HCM: increased outflow tract obstruction. Heart relying on volume.

Heterophilic antibodies

Infectious Mononucleosis (EBV)

Malingering: diagnostic criteria?

Intentional falsification of sx for personal gain (time off work, financial benefit etc.)

Brain tumor in children

Infratentorial: medulloblastoma (cerebellum) or Supratentorial: craniopharygioma

Effect of antimuscarinic agents on cutaneous BVs and skin?

Inhibition of eccrine sweat glands = fever with compensatory cutaneous vasodilation.

Valproate

Inhibition of maternal folate absorption = NTDs

5-FU: MOA

Inhibits thymidylate synthase, which converts THF back into DHF, while converting dUMP to dTMP. Used in thymidine DNA synthesis pathway.

Conjugate horizontal gaze palsy, horizontal diplopia

Internuclear ophthalmoplegia (damage to MLF, may be unilateral or bilateral)

Honeycomb lung on x ray or CT

Interstitial Pulmonary Fibrosis

PI3K/Akt/mTOR pathway

Intracellular signal pathway important for anti-apoptosis, cellular proliferation and angiogenesis

Mycobacterium tuberculosis: a. Intracellular or extracellular infection?

Intracellular. Macrophages (alveolar initially).

Renal epithelial casts in urine

Intrinsic renal failure (eg. ischemia or toxic injury)

Breast cancer

Invasive ductal carcinoma

Type IV Hypersensitivity

Involves macrophages, CD4 T cells, and CD8 T cells

Microcytic anemia

Iron deficiency

Mitochondrial vacuolization: sign of reversible or irreversible cell injury

Irreversible (not simple swelling)

TCA cycle

Isocitrate dehydrogenase (+) ADP (-) ATP, NADH

Aflutter radiofrequency ablation site

Isthmus between IVC and tricuspid annulus

"Fructose: why is it metabolized faster than other non-glucose monosaccharides"

It enters the glycolytic pathway via glyceraldehyde-3-phosphate after the RLS. Others enter before PFK-1, the major rate-limiting step.

Nodular hyaline deposits in glomeruli

Kimmelstiel-Wilson nodules (diabetic nephropathy)

Red currant jelly sputum in alcoholic or diabetic patients

Klebsiella pneumoniae pneumonia

Hyporeflexia, hypotonia, atrophy, fasiculations

LMN damage

Unilateral facial drooping involving forehead

LMN facial nerve (CN VII) palsy; UMN lesions spare the forehead

Neisseria meningitidis: what factor is responsible for toxic effects and increased M&M?

LOS (lipooligosaccharide) is responsible for toxic effects seen in meningitis and correspond to morbidity and mortality

Anaerobic antibiotics

Lactamase/PCNase sensitive Beta-lactams + beta-lactamase inhibitors, metronidazole, carbapenems and clindamycin (most cases).

Pediatric: Anatomical pathological feature seen with midgut malrotation?

Ladd's fibrous bands

Cuboidal alveolar cells under EM with decreased numbers of granules containing parallel stacks of membrane lamellae. What is the diagnosis?

Lamellar bodies of type II pneumocytes store and release pulmonary surfactant into alveoli to line surfaces. Lamellar contents release by exocytosis into alveolar space where lamellar contents unravel and spread along alveolar lining. Surfactant deficiency = diagnosis = atelectasis in neonatal respiratory distress syndrome.

Methotrexate: teratogenic effects

Limb and craniofacial abnormalities, NTDs, abortion

Thalidomide

Limb defects: phocomelia and micro melia = flipper limbs

Thrombi made of white/red layers

Lines of Zahn (arterial thrombus, layers of platelets/RBCs)

Cephalosporin resistant organisms

Listeria, MRSA, Enterococci, Atypicals (eg. Myco, Chlamydia - these all have no cell wall)

Klinefelter's

Low testosterone d/t damaged Leydig cells = lack of feedback inhibition = increase in FSH/LH = increase E = gynecomastia

Metastases to brain

Lung > breast > genitourinary > melanoma > GI

Death in SLE

Lupus nephropathy

Lung transplant: a. Histological features of chronic rejection b. Spirometry findings

Lymphocytic inflammation, fibrosis and destruction of bronchioles (bronchiolitis obliterans) FEV1/FVC reduction (including FEV1 reduction) = obstructive pattern

Atypical depression

MAOIs = first line

Triptan

MOA = serotonin (1B and 1D) agonists

Cilostazol: MOA, indications?

MOA: phosphodiesterase inhibitor that inhibits platelet aggregation and acts as a direct arterial vasodilator. Indications: peripheral arterial disease (PAD). Tx for PAD = cilostazol, graded exercise. Give antiplatelet agent such as ASA or clopidrogel for secondary prevention of coronary heart disease and stroke.

S. aureus

MSSA: nafcillin, oxacillin, dicloxacillin (antistaphylococcal penicillins) MRSA: vancomycin, daptomycin, linezolid, ceftaroline

Legionella pneumophila

Macrolide

Subarachnoid hemorrhage

Major cause of morbidity and mortality is vasospasm 4-12 days after SAH. Tx with nimopidipine, a CCD to prevent this. CT may fail to show the vasospasm.

Overdose deaths: what is majority of deaths d/t?

Majority of overdose deaths in US from opioids.

Eosinophilic cytoplasmic inclusion of liver cell

Mallory body (alcoholic liver disease)

Vomiting blood following gastroesophageal lacerations

Mallory-Weiss syndrome (alcoholic and bulimic patients)

Spikes on basement membrane, dome-like subepithelial deposits

Membranous nephropathy (nephrotic syndrome)

Episodic vertigo, tinnitus, hearing loss

Meniere disease

Effect of maneuvers on preload, afterload: Describe how these changes affect HCM

Maneuvers that increase preload or afterload = decrease murmur intensity by increasing LVEDV and lessening outflow tract obstruction

Cardiac manifestations of lupus

Marantic/thrombotic endocarditis (nonbacterial)

Arachnodactyly, lens dislocation (upward), aortic dissection, hyperflexible joints

Marfan syndrome (fibrillin defect)

Aortic aneurysm, thoracic

Marfan syndrome (idiopathic cystic medial degeneration)

Foramen ovale: contents

Mnemonic = foramen ovalee = Vthree

Sublimation

Mature defense mechanism Channeling impulses into socially acceptable behaviors

Chronic exercise intolerance with myalgia, fatigue, painful cramps, myoglobinuria

McArdle disease (skeletal muscle glycogen phosphorylase deficiency)

Fever, cough, conjunctivitis, coryza, diffuse rash

Measles

Lymphatic drainage: a. Describe drainage of the LEs and foot lesions

Medial track = drainage to superficial inguinal nodes. Therefore medial foot lesions drain to superficial inguinal nodes Lateral track = drainage to popliteal LNs and inguinal areas. Therefore lateral foot lesions drain to popliteal LNs and inguinal areas.

Anteromedial humeral supracondylar fracture has risk of damaging

Median nerve and brachial artery. Median nerve damage = sensory loss over first 3 digits and wrist. Brachial injury = pulseless hand.

SVC syndrome: What type of mass causes this?

Mediastinal mass (most commonly lung cancer (bronchogenic carcinoma) followed by non-H lymphoma). Rarely Pancoast tumor - these typically cause Horner's syndrome.

Friedrich ataxia

Most common cause of death = hypertrophic cardiomyopathy

MEN2B

Medullary thyroid cancer, pheochromocytoma, mucosal neuromas and marfanoid habitus

Hypersegmented neutrophils

Megaloblastic anemia (B12 deficiency: neurologic symptoms; Folate deficiency: lack of neurologic symptoms)

Psammona bodies

Meningiomas, papillary thyroid carcinoma, mesothelioma, papillary serous carcinoma of the endometrium and ovary

Hypercalcemia presentation

Mental status changes, muscle weakness, constipation, polyuria, polydipsia and dehydration.

Cyclophosphamide-induced hemorrhagic cystitis

Mesna

CAIs diuretic: SEs

Metabolic acidosis

X-rays

Microcephaly, intellectual disability

Isotretinoin: teratogenic effects

Microcephaly, thymic hypoplasia, small ears, hydrocephalus

Antineutrophil cytoplasmic antibodies (ANCAs)

Microscopic polyangiitis and eosiniphilic granulomatosis with polyangiitis (Churg-Strauss syndrome) (MPO-ANCA/p-ANCA); granulomatosis with polyangiitis (Wegener; PR3-ANCA, c-ANCA)

Cardiac tumor (adults)

Metastasis, myxoma (90% in left atrium, "ball and valve")

ADHD

Methylphenidate, CBT, atomoxetine, guanfacine, clonidine

Antibiotics: Which abx can cause a disulfiram-like effect?

Metronidazole

Trichomonas vaginalis

Metronidazole (patient and partner)

Carpal bones: name them? In which direction are they named?

Mnemonic: Some Lovers Try Positions That They Can't Handle - Lateral to medial, proximal row then distal row - Scaphoid, Lunate, Triquetrum, Pisiform (ball), Trapezium, Trapezoid, Capitate, Hamate (hook)

Blood vessel: What BV lies at the junction of the frontal, parietal, sphenoid and temporal? What does it branch from? Through what foramen does it course? Damage to this will cause what?

Middle meningeal Branches from maxillary off of external carotid Foramen: spinosum Damage = epidural hematoma

Atypical depression: SSx

Mood reactivity, leaden paralysis (parent's arms and legs feel extremely heavy), rejection sensitivity, increased sleep and appetite

Bipolar disorder

Mood stabilizers (eg. lithium, valproic acid, carbamazepine), typical antipsychotics

Classification of diverticula

Morphologically: true (all gut layers) vs false (not all gut layers) Pathogenesis: traction (true) vs pulsion (false) - Traction = diverticula created by inflammation and subsequent scarring of gut wall, which results in pulling and outpouching of all gut wall layers (true). - Pulsion = increased intraluminal pressure causes mucosa and submucosa to herniate through areas of focal weakness in muscularis creating false diverticula.

Nephrolithiasis: Most common stone? What does it look like?

Most common = calcium stone (calcium oxalate or phosphate) Oxalate = octahedron (square with X in center) Phosphate = elongated, wedge-shaped, forms rosettes (see another card)

Pediatrics: most common neoplasm in children? Second most?

Most common = leukemia (ALL) Second most common = brain tumors (1. Pilocytic astrocytomas, 2. Medulloblastomas, 3. Ependymomas)

Black eschar on face of patient with diabetic ketoacidosis

Mucor or Rhizopus fungal infection

Hemochromatosis

Multiple blood transfusions or hereditary HFE mutation (can result in heart failure, bronze diabetes, and increased risk of HCC)

Lytic punched out bone lesions on x ray

Multiple myeloma

Primary bone tumor (adults)

Multiple myeloma

Monoclonal antibody spike

Multiple myeloma (usually IgG or IgA) Monoclonal gammopathy of undetermined significance (MGUS consequence of aging) Waldenstrom macroglobulinemia (M protein = IgM) Primary amyloidosis

Demyelinating disease in young women

Multiple sclerosis

Erythroderma, lymphadenopathy, hepatosplenomegaly, atypical T cells

Mycosis fungoides (cutaneous T cell lymphoma) or Sezary syndrome (mycosis fungoides and malignant T cells in blood)

Pus/sputum: what causes the green discoloration seen in pus/sputum during common bacterial infections?

Myeloperoxidase (blue-green heme-based enzyme from neutrophils)

Signs of reversible cell injury

Myofibril relaxation (in cardiomyocytes), disaggregation of polysomes (rRNA dissociating from mRNA), disaggregation of granular and fibrillar elements of nucleus, clumping of nuclear chromatin, TGL droplet accumulation (in hepatocytes, striated muscle cells and renal cells), glycogen loss, simply mitochondrial swelling (not vacuolization)

Daptomycin: side effect

Myopathy and CPK elevation Note: inactivated by pulmonary surfactant (ineffective at tx pneumonia)

Cutaneous/dermal edema due to connective tissue deposition

Myxedema (caused by hypothyroidism, Graves disease [pretibial])

NE vs EPI Which receptors does each work on? Which do they not work on? Affinity towards receptors?

NE: alpha-1>alpha-2>beta-1 agonist (no affinity for beta-2) EPI: beta>alpha agonist - relatively beta-1 (heart) selective at low doses (Mnemonic = B1 = B1ow = B1 affinity at low doses). Alpha effects at high doses.

Number needed to harm

NNH = 1/attributable risk

Negative Predictive Value (NPV)

NPV = TN / (FN + TN)

Acute Gout Attack

NSAIDs, colchicine, glucocorticoids

Folate antagonists (eg. MTX)

NTDs

Valproate: teratogenic effects

NTDs

Carbamazepine

NTDs, craniofacial defects, fingernail hypoplasia, developmental delay, IUGR Like phenytoin

Phenytoin: teratogenic effects

NTDs, orofacial clefts, microcephaly, nail or digit hypoplasia

Mitral stenosis: Describe how the following parameters are changed in this condition: a. Left atrial pressure b. Pulmonary venous pressure c. Pulmonary capillary wedge pressure d. Pulmonary artery pressure e. Pulmonary vascular compliance f. Right ventricular pressure and volume g. Changes at the tricuspid valve h. LV diastolic pressure Which one of these parameters would indicate aortic valve dysfunction?

Narrowing in mitral valve means more blood is left in atria after diastole is complete = a. Left atrial pressure increased Pressure is transmitted retrograde towards the lungs b. Pulmonary venous pressure increased c. PCWP increased d. Pulmonary artery pressure increased Prolonged increased lung pressure results in pulmonary edema and alveolar hemorrhage resulting in pulmonary HTN e. Pulmonary vascular compliance decreases d/t vessel constriction and obliteration Pressure is transmitted retrograde from lungs towards right heart f. Right ventricular volume increases (cannot pump all the volume into high pressure lung space) = right ventricular pressure increases Eventual right heart failure leads to g. Tricuspid regurg = increase JVD and peripheral edema h. Usually near normal or even decreased with severe stenosis. Increase in LV diastolic pressure would indicate aortic valve dysfunction such as aortic regurg.

Warfarin: teratogenic effects

Nasal hypolasia, stippled epiphysis

Tumor of the adrenal medulla (kids)

Neuroblastoma (malignant)

Sphingolipidoses: Compare and contrast Niemann-Pick and Tay-Sachs in terms of a. Presentation and b. Deficient ez and Accumulated substance

Niemann-Pick a. Presentation: HSM, neurologic regression and cherry-red macular spot in infancy b. Deficient ez: sphingomyelinase Accumulated substance: sphingomyelin Tay-Sachs: a. Presentation: neurologic regression, cherry-red macular spots. No HSM like Niemann-Pick. b. Deficienc ez: Beta-hexosaminidase A Accumulated substance: GM2 ganglioside

Trypanosoma (Chagas) tx

Nifurtimox

Reid index

Nml = 0.4

Type of Hodgkin lymphoma

Nodular sclerosing (vs. mixed cellularity, lymphocytic predominance, lymphocytic depletion)

Fasting: What reactions occur to sustain normoglycemia? Time frame?

Normoglycemia sustained by glyconeolysis and gluconeogenesis. Glycogen stores last for about 12-18 hours. Thereafter gluconeogenesis occurs.

Anorexia

Nutrition, psychotherapy, mirtazapine

Gestational Diabetes: best test to diagnose this?

OGTT

Flow vs Lung Volume Graphs: Describe for normal, obstructive and restrictive defect. Describe for tracheal stenosis. What are the obstructive lung diseases? Restrictive? Describe how the indices change.

Obstructive: COPD (chronic bronchitis -> emphysema), CF, asthma, bronchiectasis - FEV 1 decreased, FVC decreased, FEV1/FVC ratio decreased, RV increased, FRC increased, TLC increased Restrictive: interstitial lung dz (incl. fibrosis), atelectasis, poor breathing mechanics (neuromuscular issues, scoliosis, obesity) - FEV 1 decreased, FVC decreased more than FEV1, FEV1/FVC increased or normal, RV decreased, FRC decreased, TLC decreased

Carcinoid syndrome

Octreotide

Odds ratio (for case-control studies)

Odds ratio = (a/c) / (b/d) = ad/bc

Mitral stenosis

Opening snap in early diastole

Pupillary light reflex: describe the reflex pathway

Optic nerve (CN II) responsible for afferent limb and oculomotor nerve (CN III) is responsible for efferent limb

Dexamethasone

Or Betamethasone administered to pregnant women at risk for premature delivery. Helps accelerate fetal lung maturation through surfactant production.

C. difficile

Oral metronidazole; if refractory, oral vancomycin

Enlarged thyroid cells with ground glass nuclei with central clearing

Orphan Annie eyes nuclei (papillary carcinoma of the thyroid)

Influenza

Oseltamivir, zanamivir

Painful, raised red lesions on pads of fingers/toes

Osler nodes (infective endocarditis, immune complex deposition)

Telangiectasias, recurrent epistaxis, skin discoloration, arteriovenous malformation, GI bleeding, hematuria

Osler-Weber-Rendu syndrome

Osmolality vs Osmolarity What is meaning of high vs low osmolality in terms of concentrated or dilute?

Osmolality = amount of osmoles of solute / kg solvent Osmolarity = amount of osmoles of solute / L solution HIgh osmolality = concentrated Low osmolality = dilute

Swollen hard painful finger joints

Osteoarthritis (osteophytes in PIP [Bouchard nodes], DIP [Heberden nodes])

CA125: Marker of?

Ovarian

Diabetic Autonomic Neuropathy

Overflow incotinence d/t inability to sensory when bladder is full and incomplete emptying. PVR (post void residual) confirms inadequate emptying.

Enlarged cells with intranuclear inclusion bodies

Owl eye appearance of CMV

MDR1 function

P-glycoprotein TM ATP-dependent efflux protein pump. Can reduce the influx of chemotherapeutic drugs and increase efflux from cytosol preventing efficacious therapy.

Winters Formula

PCO2 = 1.5 [HCO3-] + 8 +/- 2

Positive Predictive Value (PPV)

PPV = TP (TP + FP)

Pulmonary vascular resistance

PVR = (Ppulm artery - Pleft atrium) / CO Ppulm artery = pressure in pulmonary artery Pleft atrium = pulmonary wedge pressure

Posterior pituitary: ADH and oxytocin from the hypothalamus are packaged with what? Function of this? Why do I care about this?

Packaged with neurophysins Involved in post-translational hormone processing and stabilization Why care? Neurophysin I is paired with ADH. Defect in that leads to hereditary diabetes insipidus

Bone pain, bone enlargement, arthritis

Paget disease of bone (increased osteoblastic and osteoclastic activity)

Red itchy swollen nipple/areola

Paget disease of the breast sign (sign of underlying neoplasm)

SLE: What cellular changes can be seen in SLE patients?

Pancytopenia is common in pts with SLE. Occurs d/t formation of autoantibodies against cells (type 2 HS rxn). Note: Type 3 HS rxn is cause of lupus nephritis.

Differentiate between: PaO2, SaO2 and CaO2

Pao2 = partial pressure of o2 in arterial blood determined by pressure of inhaled o2 (PIO2). Affected then by disturbances in lung (VQ abnormality, diffusion block, shunt). Sao2 = percentage of available binding sites on Hb that are bound with oxygen in arterial blood. Affected by PaCO2, body temp, pH and other factors. Not affected by hemoglobin, therefore anemias don't affect this. You can have an anemia with a normal Sao2. CaO2 = content of arterial oxygen. CaO2 reflects the total number of o2 molecules in arterial blood both bound and unbound to Hb. This depends on hemoglobin content, SaO2 and the amount of dissolved oxygen. For more on this: http://www.ucdenver.edu/academics/colleges/medicalschool/departments/medicine/intmed/imrp/CURRICULUM/Documents/Oxygenation%20and%20oxygen%20therapy.pdf

Thyroid cancer

Papillary carcinoma (childhood irradiation)

Depigmentation of neurons in substantia nigra

Parkinson disease (basal ganglia disorder: rigidity, resting tremor, bradykinesia)

Resting tumor, rigidity, akinesia, postural instability, shuffling gait

Parkinson disease (loss of dopaminergic neurons in substantia nigra pars compacta)

Hamartomatous GI polyps, hyperpigmentation of mouth/feet/hands/genitalia

Peutz-Jeghers syndrome (inherited, benign polyposis can cause bowel obstruction; increased cancer risk, mainly GI)

Fibrous plaques in soft tissue of penis with abnormal curvature

Peyronie disease (connective tissue disorder)

Red urine in the morning, fragile RBCs

Paroxysmal nocturnal hemoglobinuria

Partial mole vs complete mole

Partial mole: more than normal karyotype owing to maternal and paternal DNA. Fetal tissue. Complete mole: normal karyotype owing to paternal DNA only. No fetal tissue.

Buprenorphine

Partial opioid agonist with high affinity, but low intrinsic activity. Displaces other opioids and precipitates withdrawal from opioids.

Contact precautions with respirator mask w/filter: for what organisms?

Particles < 5 microns: bacteria (TB), viruses (varicella)

Dog bite bacterium

Pasteurella multocida

Dermatitis, dementia, diarrhea

Pellegra (niacin [Vitamin B3] deficiency)

Anti-desmoglein (anti-desmosome) antibodies

Pemphigus vulgaris (blistering)

Bladder carcinomas: major determinant of prognosis in these cancers?

Penetration of bladder wall

Treponema pallidum

Penicillin

Streptococcus bovis

Penicillin prophylaxis; evaluation for colon cancer if linked to endocarditis

Electrical alternans (alternating amplitude on EKG)

Pericardial tamponade

SLE: most common CV manifestation

Pericarditis (sharp pleuritic chest pain that is relieved by sitting up and leaning forward)

Tumor of the adrenal medulla (adults)

Pheochromocytoma (usually benign)

t(9;22)

Philadelphia chromosome, CML (BCR-ABL, activation, tyrosine kinase oncogene)

Glycolysis

Phosphofructokinase-1 (PFK-1) (+) AMP, Fructose-2,6-BP (-) ATP, Citrate

Brachial plexus block: Injection between the anterior and middle scalene muscles has the potential to damage what other nerve?

Phrenic nerve, which passes through the interscalene sheath.

Tx of Beta-lactamase producing bacteroides fragilis

Piperacillin-tazobactam, which is a combo extended-spectrum PCN with beta-lactamase inhibitor (tazobactam)

Hypopituitarism

Pituitary adenoma (usually benign tumor)

Dysphagia (esophageal webs), glossitis, iron deficiency anemia

Plummer-Vinson syndrome (may progress to esophageal squamous cell carcinoma)

Dysphagia, Anemia, Koilonychia and Shiny-Red tongue. What is diagnosis?

Plummer-Vinson syndrome d/t iron deficiency anemia. Dysphagia d/t esophageal web formation Koilonychia = spoon-shaped nails

Opportunstic infections with AIDS

Pneumocystis jirovecii pneumonia

Fanconi Syndrome: presentation

Polyuria, acidosis and hypophosphatemia

Myopathy (infantile hypertrophic cardiomyopathy), exercise intolerance

Pompe disease (lysosomal alpha 1,4 glucosidase deficiency)

Ecological study: What is it?

Population data = unit of study

Acute hepatitis A: histology? Presentation?

Presentation: Self-limited that presents acutely with prodromal sx (fever, malaise, anorexia, N/V and RUQ pain). Followed by signs of cholestasis (jaundice, pruritus, dark-colored urine (increased conjugated bili levels), clay-colored stool - lack of bilirubin).

Influenza virus: what antibodies prevent re-infection?

Re-infection of influenza virus prevented with anti-hemagglutinin abs, not anti-neuraminidase

Fluoroquinolones

Possible damage to cartilage

Lumpy bumpy appearance of glomeruli on immunofluorescence

Poststreptococcal glomerulonephritis (due to deposition of IgG, IgM, and C3)

Back pain, fever, night sweats

Pott disease (vertebral TB)

Most common presentation of ARPKD neonates

Potter sequence d/t oligohydramnios: flattened facies, limb deformities, pulmonary hypoplasia Clinical findings in general for ARPKD patient = renal insufficiency, nephromegaly, HTN. Note: HTN usually not present at birth, but instead develops over the first few months in those with ARPKD who survive the neonatal period.

Schistosoma, Clonorchis and Paragonimus tx

Praziquantel

Peptic ulcer disease drugs: Difference between -prazole and -tidine drugs

Prazoles = PP inhibitors (H/K ATPase inhibitors) Tidines = H2 (histamine) receptor blockers

Neural tube defect prevention

Prenatal folic acid

Adenomyosis: What is it?

Presence of endometrial glandular tissue in myometrium. SSx = menorrhagia, dysmenorrhea, uniformly enlarged uterus with normal-appearing endometrial tissue on biopsy.

Skin hyperpigmentation, hypotension, fatigue

Primary adrenocortical insufficiency (eg. Addison disease) causes elevated ACTH and alpha-MSH production

Lacunar infarct

Primarily caused by chronic HTN predisposing to lipohyalinosis, microatheroma formation and occlusion (hypertensive arteriolar sclerosis).

Xanthelasma: conditions associated with it

Primary or secondary hyperlipidemia. Secondary includes cholestatic processes including obstructive biliary lesions and primary biliary sclerosis, which result in subsequent hypercholesterolemia.

Indurated, ulcerated genital lesion, nonpainful chancre

Primary syphilis; Treponema pallidum

TB: Distinguish between primary, secondary (reactivation TB)

Primary: formation of Ghon focus in MID-LOWER lungs. Then spreads to hilar LNs forming a Ghon complex = latent infection (dormant bacteria walled off), cleared by immune system w/scar formation OR failed immune system results in progressive lung consolidation and necrosis. Secondary: patients with primary TB infection that never cleared completely. Occurs most often in immunosuppressed pts and is characterized by apical cavitary lesions and hemoptysis, cough and weight loss.

Pituitary tumor

Prolactinoma, somatotropic adenoma

Composition of RPGN (rapidly progressive glomerulonephritis)

Proliferated glomerular parietal cells, monocytes, macrophages that have migrated into Bowman's space, and abundant fibrin between cell layers of crescents. Note: essential pathologic step in crescent formation = deposition of fibrin. Also note: fluorescent microscopy that diagnosis is d/t antibodies against fibrin.

Organ of Corti

Prolonged exposure to loud noises causes hearing loss d/t damage of stereociliated hair cells of organ of Corti

Urethritis, conjunctivitis, arthritis in a male

Reactive arthritis associated with HLA-B27

Metastases to bone

Prostate, breast > lung > thyroid

Prostatectomy can lead to what other major dysfunction? How?

Prostatectomy leads to erectile dysfunction. Prostatic plexus lies within fascia of prostate and innervates corpus cavernosa of penis facilitating penile erection.

Male cancer

Prostatic carcinoma

Heparin reversal

Protamine sulfate

Acute tubular necrosis: histological findings

Proximal tubular cell ballooning and vacuolar degeneration

Ureters: blood supply

Proximal: branches of renal artery Distal: superior vesical artery

Rhomboid crystals, (+) birefringement

Pseudogout (calcium pyrophosphate dihydrate crystals)

Indwelling bladder catheters UTIs: bacteria?

Pseudomonas aeruginosa

Osteomyelitis with IV drug use

Pseudomonas, Candida, S. aureus

HLA-B27

Psoriatic arthritis, ankylosing spondylitis, IBD-associated arthritis, reactive arthritis (formerly Reiter syndrome)

Psoriasis: complications

Psoriatic arthritis, nail pitting, uveitis

Symptoms of CN III palsy

Ptosis (paralysis of levator palpebrae), unopposed action of LR (CN VI) and SO (CN IV) = down and out gaze

ASD: surgical repair of ASD is required to prevent what irreversible change?

Pulmonary vascular sclerosis resulting in Eisenmenger and reversal of shunt (from right to left) Right heart changes are reversible.

Base Excision Repair: Purpose? Steps?

Purpose = correct single-base DNA defects induced spontaneously or by chemicals Steps = Glycosylases remove defective base, empty sugar phosphate site removed by endonuclease and lyase, DNA pol replaces missing nucleotide and ligase seals nick

Autonomic nervous system: downstream pathways of alpha1, 2, beta1, 2

QISS: alpha-1, alpha-2, beta-1, beta-2 Q: IP3 increase I: cAMP decrease S: cAMP increase

Resistance

R = (driving pressure (deltaP)) / (flow (Q)) R = 8n (viscosity) x length / (pi x r ^4)

Renal blood flow

RBF = RPF / (1 - Hct) RPF = renal plasma flow

Mycobacterium tuberculosis

RIPE (rifampin, isoniazid, pyrazinamide, ethambutol)

GFR and RPF: how are these estimated?

RPF is estimated with: - PAH: both filtered and actively secreted in the proximal tubule. Nearly all PAH entering the kidney is excreted. GFR is estimated with: - Inulin: freely filtered and neither reabsorbed nor secreted - Creatinine: approximate measure of GFR. It is freely filtered and moderately secreted by renal tubules.

Anterolateral humeral supracondylar fracture has risk of damaging

Radial nerve = wrist drop

Cellular crescents of Bowman capsule

Rapidly progressive crescentic glomerulonephritis

Pure red cell aplasia: what is it? Diseases associated with it?

Rare form of marrow failure characterized by severe hypoplasia of marrow erythroid elements in setting of normal granulopoiesis and thrombopoiesis. Associated with thymoma, lymphocytic leukemias and parvo B19 infection

Painful fingers/toes changing colors from blue to white to red with cold or stress

Raynaud phenomenon (vasospasm in extremities)

Nephrolithiasis: Magnesium ammonium phosphate stones

Rectangular prism (coffin lids)

Tourette syndrome: SSx

Recurrent motor and verbal tics (ranging from coughing/throat clearing/grunting to obscenities/other comments/words)

Vancomycin: side effect

Red man syndrome Nephrotoxicity

NADPH: function

Reducing glutathione (oxidative damage protection), biosynthesis of cholesterol, FAs, steroids

Hodgkin Lympoma: What is the cell type? What does it look like? Compare to CMV infected cell?

Reed-Sternberg Cell. Owl-Eye apperance. CMV also has owl-eye, typically single eye.

Vomiting reflex

Regulated by M1, D2, H1, 5-HT3 and neurokinin receptors

Rectangular, crystal-like cytoplasmic inclusions in Leydig cells

Reinke crystals (Leydig cell tumor)

Relative risk

Relative risk = a/(a+b) / c(c+d)

EPI: effect on HR, SBP and DBP

Remember: beta>alpha agonist with relative beta-1 selectivity at low doses HR: beta-1 = increase HR SBP: beta-1 and alpha-1 = increase SBP DBP: - Low dose = beta-1 > beta-2 > alpha = heart effects > vasodilation > vasoconstriction = overall decrease in DBP - High dose = alpha > beta = vasoconstriction = overall increase in DBP

PE: Results in what type of acid-base disturbance?

Respiratory alkalosis

Hypertension, secondary

Renal artery stenosis, chronic kidney disease (eg. polycystic kidney disease, diabetic nephropathy), hyperaldosteronism

Renal tumor

Renal cell carcinoma: associated with von Hippel-Lindau and cigarette smoking; paraneoplastic syndromes (EPO, renin, PTHrP, ACTH)

ACEi

Renal damage

ACEi: teratogenic effects

Renal dysgenesis, oliogohydramnios

Amphotericin B: Side effects

Renal toxicity (renal vasoconstriction and direct toxin on renal epithelial cells) - severe hypokalemia and hypomagnesemia commonly seen. Requires daily supplementation.

Reaction formation

Responding in a manner opposite to one's actual feelings

Iron deficiency anemia effect on pregnancy

Restriction of fetal growth

Regression

Reverting to earlier developmental stage

Cardiac primary tumor (kids)

Rhabdomyoma, often seen in tuberous sclerosis

Mitral valve stenosis

Rheumatic heart disease

Anti-IgG antibodies

Rheumoatoid arthritis (systemic inflammation, joint pannus, boutonniere deformity)

H. influenzae (B)

Rifampin (prophylaxis)

Meningococcal dz: most frequently used chemoprophylaxis drug?

Rifampin. Other choices include cipro, IM ceftriaxone (not widely used d/t painful mode of administration. Give within 24 hrs.

AV node location

Right atrium near insertion of septal leaflet of TV and orifice of coronary sinus

Triglyceridemia

Risk factor for pancreatitis because TGLs metabolized to FFAs via pancreatic lipase.

Temporal arteritis

Risk of ipsilateral blindness due to occlusion of ophthalmic artery; polymyalgia rheumatica

"Why is coadministration of MAOI and SSRI contraindicated? Procedure to switch from MAOI to SSRI? What is happening?"

Risk of serotonin syndrome (restlessness, altered mental status, hyperreflexia, clonus, diaphoresis, tremors). Why? SSRIs prevent reuptake and MAOIs would also increase amount of 5HT available. Patients must wait atleast 2 weeks after MAOI discontinuation before initiating SSRI therapy. This allows sufficient time for regneration of MAO enzyme.

Retinal hemorrhages with pale centers

Roth spots (bacterial endocarditis)

Stacks of RBCs

Rouleaux formation (high ESR, multiple myeloma)

Severe RLQ pain with palpation of LLQ

Rovsing Sign (acute appendicitis)

Hematoma - subdural

Rupture of bridging veins (crescent shaped)

SDH

Rupture of cortical bridging veins. Gradual onset. Crescent-shaped mass.

Hematoma - epidural

Rupture of middle meningeal artery (trauma; lentiform shaped)

TCA

SEs = Anticholinergic toxicity (fever, cutaneous flushing, oral dry mucosa, dilated poorly responsive pupils, confusion), cardiac arrhythmias, hypotension

Lithium

SEs = hypothyroidism and nephrogenic DI. Monitor serum TSH and renal function (BUN and Cr) regularly.

Antinuclear antibodies (ANAs: anti-Smith & anti-dsDNA)

SLE (type III hypersensitivity)

Antioxidant enzymes: Which are the antioxidant enzymes in the body that neutralize free radicals?

SOD, glutathione peroxidase and catalase. Not NADPH oxidase, found in phagocytic cells. This catalizes reduction of o2 to superoxide free radicals and destroys bacterial. Myeloperoxidase in neutrophils converts hydrogen peroxide to hypochlorous acid, which is bactericidal.

Lead poisoning: SSx, Lab findings

SSx: colicky abdominal pain, constipation, lead lines on gum, peripheral neuropathy (wrist drop, foot drop) Labs: microcytic anemia (w/nml iron studies), smear = basophilic stippling. Ringed sideroblasts may be seen in bone marrow, which is excess iron in mitochondria surrounding nucleus.

Cauda equina syndrome. SSx? Which nerve root is affected?

SSx: low back pain radiating down both legs, saddle anesthesia and loss of anocutaneous reflex (pinprick to perianal region), bowel and bladder dysfunction, loss of ankle-jerk reflex Nerve root affected: S2-S4 (S4 is right on the butt)

Stroke volume

SV = EDV - ESV

Osteomyelitis in sickle cell disease

Salmonella

Bilateral hilar adenopathy, uveitis

Sarcoidosis (noncaseating granulomas)

Strawberry tongue

Scarlet fever, Kawasaki disease

Giant cell arteritis: histologic findings? What other vasculitis are these findings identical to? Compare these findings to polyarteritis nodsa.

Scattered, focal granulomatous inflammation within the media with intimal thickening, elastic lamina fragmentation and giant cell formation. Identical histology = Takayasu arteritis, which typically involves aortic arch and affects younger patients. Polyarteritis nodosa: transmural inflammation of arterial wall with fibrinoid necrosis. Occurs in young adults and presents with intermittent episodes of manifestations including abdominal pain, peripheral neuropathy, renal insufficiency and severe HTN.

Glomerulus-like structure surrounding vessel in germ cells

Schiller-Duval bodies (yolk sac tumor)

Anticentromere antibodies

Scleroderma (CREST)

Splitting

Seeing others as all bad or all good

Basophilic stippling: seen in what?

Seen in lead poisoning, anemia of chronic disease, alcohol abuse, thalassemias, myelodysplastic syndromes.

Theophylline: toxicity side effects

Seizures (major cause of M&M), tachyarrhythmias

Lymphatic drainage: a. Describe drainage of scrotum and testes

Scrotum drains to superficial inguinal LNs Testes drains to paraaortic LNs

Swollen gums, mucosal bleeding, poor wound healing, petechiae

Scurvy (vitamin C deficiency: can't hydroxylate proline/lysine for collagen synthesis)

Acne: what glands are involved? What types of glands are these?

Sebaceous glands. These are holocrine glands, meaning cell lysis releases entire contents of cytoplasm and cell membrane.

Athlete with polycythemia

Secondary to erythropoietin injection

Breast tumors: Distinguish between the following on histology: a. Fibroadenomas b. DCIS c. Medullary carcinoma d. Paget dz of the nipple e. Scerlosing adenosis

See Shotgun histology

"Adrenal steroid synthesis pathway Describe each of the CAH conditions"

See diagram in study packet

Testicular tumor

Seminoma (malignany, radiosensitive), elevated placental ALP

Extracellular amyloid deposition in gray matter of brain

Senile plaques (Alzheimer disease)

Ovarian tumor (malignant)

Serous cystadenocarcinoma

Ovarian tumor (benign, bilateral)

Serous cystadenoma

DIC

Severe sepsis, obstetric complications, cancer, burns, trauma, major surgery, acute pancreatitis, APL

Mycoplasma pneumoniae: how does this cause hemolytic anemia?

Shares antigens with human RBCs. When body mounts immune response, Igs formed against RBCs lead to hemolytic anemia. The antibodies that do this are called cold agglutinins.

Nitroprusside effect and use

Short-acting balanced veno and vaso dilator - therefore decreases LV preload and afterload allowing for adequate CO to be delivered at lower LV EDP. Used for hypertensive heart failure.

Confidence interval: In order for CI to be statistically significant, it shouldn't contain what value?

Shouldn't contain the null value of 1.0. If this is contained, then p not < 0.05 (if 95% CI) or p not < 0.01 (if 99% CI) and data not significant.

Autosplenectomy (fibrosis and shrinkage)

Sickle cell disease (hemoglobin S)

Site of diverticula

Sigmoid colon

Pulmonary arterial hypertension (idiopathic)

Sildenafil, bosentan, epoprostenol

Erectile dysfunction

Sildenafil, tadalafil, vardenafil

Dry eyes, dry mouth, arthritis

Sjogren syndrome (autoimmune destruction of exocrine glands)

Osteitis fibrosa cystica: What is it? Condition it is found it? Findings?

Skeletal disorder caused by hyperparathyroidism. Surplus PTH stimulates osteoclasts. Findings = bone pain, subperiosteal erosions affecting hands, salt and pepper skull and brown tumor bone cysts.

Lymphatic drainage: a. Describe drainage of skin of penis and glans penis

Skin of penis drains to superficial inguinal LNs Glans penis drains to deep inguinal nodes

Alternating areas of transmural inflammation and normal colon

Skip lesions (Crohn disease)

SIADH

Small cell carcinoma of the lung

Cytochrome P450: Where is it found to metabolize drugs?

Small intestine and Liver

Beurger disease

Smoking cessation

Specificity

Sp = TN / (TN + FP)

Patient-centered medical home: what is it?

Specific model of primary care where patients have access to personal physician who coordinates care and sees patient through all aspects of care, including preventive services and acute and chronic dz mgmt. Payment for these services may be capitated or fee-for-service.

Hyperaldosteronism

Spironolactone

"Which diuretic has anti-androgenic effects?"

Spironolactone (aldosterone antagonist). Can cause gynecomastia, decreased libido and impotence. Eplerenone w/fewer side effects.

Watershed areas in gut? Clinical importance?

Splenic flexure and rectosigmoid junction. In hypotensive states, ischemic damage can occur to these areas. Result = ischemic colitis.

Sickle cell anemia

Splenic infarctions lead to fibrosis and atrophy of spleen

Eczematous dermatitis: histologic finding

Spongiosis: accumulation of edema fluid in intercellular spaces of epidermis

Keratin pearls on skin biopsy

Squamous cell carcinoma

Esophageal cancer

Squamous cell carcinoma (worldwide); Adenocarcinoma (US)

Pharyngeal arches

Stapes is derived from 2nd pharyngeal arch

Heart valves: what is the nidus for colonization between Staph Aureus and Strep?

Staph aureus: damaged or normal endothelial cells Strep: colonize damage pre-existing lesions that specifically have fibrin-platelet nidus on damaged / disrupted endothelial surface

Butterfly facial rash and Raynaud phenomenon in a young female

Systemic Lupus Erythematous

Hypercholesterolemia

Statin (first line)

S4 heart sound

Stiff/hypertrophic ventricle (aortic stenosis, restrictive cardiomyopathy)

Carotid sinus massage: effect?

Stimulates baroreceptors increasing firing rate from carotid sinus = increase PSNS activity = inhibition of SA node activity, slowing of AV node conduction and prolongation of AV node refractory period = decrease in HR, CO and termination of PSVT.

LH

Stimulates production/release of testosterone in Leydig cells

Tumor of infancy

Strawberry hemangioma (grows rapidly and regresses spontaneously by childhood)

Narrowing of bowel lumen on barium x ray

String sign (Crohn disease)

ER (+) breast cancer

Tamoxifen

Dermatomyositis: Disease associations

Strong association with malignancy, particularly lung, colorectal and ovarian cancers

Bloody or yellow tap on lumbar puncture

Subarachnoid hemorrhage

Worst headache of my life

Subarachnoid hemorrhage

Stable angina

Sublingual nitroglycerin

TCA cycle: which rxn in TCA cycle yields GTP

Succinyl-CoA --> Succinate (ez: succinyl-CoA thiokinase aka succinyl-CoA synthetase)

Toxoplasma gondii

Sulfadiazine + pyrimethamine

Gluteus maximus, medius and minimus innervation

Superior gluteal nerve innervates the gluteus medius and minimus. Inferior innervates the glut max.

Axillary Nerve

Supplies teres minor and deltoid and skin over lateral shoulder

FOOSH often results in what fracture at humerus

Supracondylar fracture

Brain tumor in adults

Supratentorial: metastasis, astrocytoma (including glioblastoma multiforme), meningioma, schwannoma

Cystic Fibrosis

Sweat contains high concentration of Na and Cl. Hypovolemia not d/t excessive free water loss, but d/t excessive Na loss and intravascular volume contraction.

Polyarteritis nodosoa: SSx? Associated viral infection? Histologic findings?

Systems involved = renal, nervous, GI and MSK Renal: glomerulonephritis, HTN Nervous: peripheral neuropathy, mononeuritis multiplex GI: mesenteric ischemia/bowel infarction, bleeding MSK: myositis, arthritis Typically occurs in young adults, episodic sx Associated viral infection = Hep B Histology: transmural inflammation of vessels with fibrinoid necrosis

Constrictive pericarditis

TB (developing world); idiopathic, viral illness (developed world)

Degeneration of dorsal column fibers

Tabes dorsalis (Tertiary syphilis), subacute combined degeneration (dorsal columns, lateral corticospinal, spinocerebellar tracts affected)

UTI prophylaxis

TMP-SMX

Pneumocystis jirovecii

TMP-SMX (prophylaxis and treatment in immunocompromised patients)

Hypocapnia Cerebral Blood Flow

Tachypnea causes hypocapnia = cerebral vasoconstriction = less blood flow to brain. Can be induced when there is risk for / increased ICP.

Appendix: best landmark to identify the appendix in surgery

Teniae coli, which are 3 separate smooth muscle ribbons that converge at root of appendix at their cecal base origin

Aminoglycosides

Teratogen (? defect - CN VIII toxicity mentioned in another quizlet set)

Griseofulvin

Teratogenic

Ribavirin

Teratogenic

Aortic aneurysm, ascending or arch

Tertiary syphilis (syphilitic aortitis), vaso vasorum destruction

Boot shaped heart on x ray

Tetrology of Fallot (due to RVH)

Tetanus: What is the vaccine composed of?

Toxoid component. Tetanus disease is not d/t the bacterium itself, but rather d/t to the protein toxin.

Ring-enhancing brain lesion on CT/MRI in AIDS

Toxoplasma gondii, CNS lymphoma

"Diuretic to decrease incidence of calcium stones"

Thiazide. Increases Calcium reabsorption (resulting in hypercalcemia).

Ringed sideroblasts: seen in what?

These are precipitates of Fe granules in RBCs d/t defect in heme synthesis pathway including enzymatic inhibition induced by lead poisoning

Nitrates: do these have an effect on arterial blood vessels?

They are primarily venodilators (increase venous capacitance) = reduce cardiac preload and LV EDV and pressure. Have modest effect on arteriolar dilation, causing a decrease in systemic vascular resistance and therefore cardiac afterload.

Air in biliary tree after gallstone

Think cholecystenteric fistula leading to gallstone ileus. Ileum is narrowest portion of intestine where stone is likely to lodge.

Displacement

Transferring feelings to a more acceptable object

Primary Osteoporosis

This is osteoporosis not caused by a medical disorder. Serum PTH, Ca and phosphorus are normal.

"Sharp chest pain that increases on inspiration but relieved by sitting up and leaning forward"

This is pleuritic (inspiration worsens) and relived by sitting up and leaning forward (postural) is indicative of pericarditis

Abdominal aortic aneurysms: Pathogenesis

Transmural aortical wall inflammation, abnormal collagen modeling and cross-linking, and loss of elastin and smooth muscle cells.

"Holosystolic murmur that increases in intensity on inspiration"

Tricuspid regurg. Other holosystolic murmurs typically don't.

Linezolid: side effect

Thrombocytopenia Optic neuritis High risk for serotonin syndrome

Myasthenia gravis: associated with abnormalities in what organ?

Thymus (eg. thymoma, thymic hyperplasia)

Pharyngeal pouch: derivative of third pharyngeal pouch?

Thymus, inferior parathyroid glands Note: superior parathyroid glands come from 4th pharyngeal pouch.

Acute Stress Disorder vs PTSD

Time frame ASD: >3 days < 1 month PTSD: > 1 month

Brief psychotic disorder vs schizophreniform vs schizophrenia vs schizoaffective disorder vs schizotypal personality disorder vs schizoid PD

Time frame Brief psychotic disorder: > 1 day < 1 month Schizophreniform: > 1 month < 6 months Schizophrenia: > 6 months (including at least 1 month of active sx) Schizoaffective disorder: at least 2 weeks of stable mood with psychotic sx + major depressive, manic or mixed episode. 2 subtypes: depressive or bipolar. SchizoTypal PD (mnemonic = magical Thinking): perceptual distortions, eccentric behavior and appearance, odd beliefs or magical thinking, detached and unemotional and prefer to be alone. SchizoiD PD (mnemonic = Distant): voluntary social withdrawal, limited emotional expression, content with social isolation. Don't confuse with avoidant PD: hypersensitive to rejection, socially inhibited, timid, feelings of inadequacy, desires relationships with others.

HER2/neu (+) breast cancer

Trastuzumab

Clozapine

Treatment-resistent schizophrenia

Paroxysmal nocturnal hemoglobinuria: a. Classic triad? b. Most likely pathologic renal finding?

Triad = thrombosis (at unlikely sites) d/t release of prothrombotic factors, hemolytic anemia, pancytopenia Renal pathology = hemosiderosis (chronic hemolysis leads to iron deposition in kidney)

Hypercoagulability (leading to DVTs and vasculitis)

Trousseau syndrome (adenocarcinoma of pancreas and lungs)

Streak ovaries, congenital heart disease, horseshoe kidney, cystic hygroma at birth, short stature, webbed neck, lymphedema

Turner syndrome (45 XO)

Lead pipe appearance of colon on abdominal imaging

Ulcerative colitis (loss of haustra)

Exercise: How does exercise affect arterial Po2 and PCo2? Venous?

Unchanged arterial Po2 and PCo2 Venous Po2 will be decreased (more o2 extracted by muscle) and PCo2 (greater Co2 produced) will be increased

Pediatrics: most common cause of unilateral fetal hydronephrosis? Bilateral?

Unilateral: Inadequate canalization of the ureteropelvic junction (connection between kidney and ureter) Bilateral: posterior urethral valves (persistent urogenital membrane at junction of bladder and urethra).

Physiologic dead space

VD = VT x [(Paco2 - Peco2) / paco2] VT = tidal volume Paco2 = arterial PCO2 Peco2 = expired air PCO2

Intellectualization

Using intellect to avoid uncomfortable feelings

MI: Chordae Tendineae Rupture

Usually early complication of MI, usually within ~ 10 days

Congenital cardiac anomaly

VSD

Pediatrics: most common congenital heart lesion? Presentation?

VSD Presentation: small VSD = loud, blowing holosystolic murmur at mid to lower left sternal border w/no sx. Becomes audible around 4-10 when PVR declines enabling left-to-right shunting. Most are hemodynamically insignificant and close spontaneously. Moderate to large VSDs usually present with heart failure, FTT, diaphoresis with feeding. Have no murmur as RV pressures are similar to those of LV. Large VSDs rarely close spontaneously and can result in chronic pulmonary HTN and cyanosis (Eisenmenger syndrome) is not closed early in life.

Holosystolic murmur

VSD, tricuspid regurgitation, mitral regurgitation

DES

Vaginal clear cell adenocarcinoma, congenital Mullerian anomalies

Enterococci

Vancomycin, aminopenicillins/cephalosporins

Volume of distribution

Vd = amount of drug in the body / plasma drug concentration

MI: Most common cause of sudden cardiac death within first 2-3 days after MI?

Ventricular arrhythmias

Hydrocephalus ex vacuo

Ventricular enlargement d/t brain atrophy, not accompanied by increase in CSF pressure.

Osteomalacia/rickets

Vitamin D supplementation

Acid-Base: What acid-base change happens with Mallory-Weiss tears?

Vomiting leads to this mucosal tear. Vomiting = metabolic alkalosis (loss of H+).

Urinary tract infections: Distinguish between upper and lower? Pathognomonic finding of upper tract infection?

WBC casts are pathognomonic for acute pyelonephritis (upper tract) Pyuria (pus) and bacteriuria are found in both upper and lower

Tetralogy of Fallot: Describe the embryological error.

Waiting from Matz

Long term anticoagulation

Warfarin, dabigatran, rivaroxaban and apixaban

Adrenal hemorrhage, hypotension, DIC

Waterhouse-Friderichsen syndrome (meningococcemia)

Atrophy of the mamillary bodies

Wernicke encephalopathy (thaimine deficiency causing ataxia, ophthalmoplegia, and confusion)

Dilated cardiomyopathy, edema, alcoholism or malnutrition

Wet beriberi (Thiamine deficiency [Vitamin B1])

Caudal regression syndrome. What is it? SSx? Common maternal comorbidity associated with development of this?

What: rare condition affecting 1/60K births with agenesis of sacrum and occasional lumbar spine SSx: flaccid paralysis of legs, dorsiflexed contractures of feet and urinary incontinence. Comorbidity associated with = poorly control maternal diabetes

Weight loss, diarrhea, arthritis, fever, adenopathy

Whipple disease (Tropheryma whipplei)

Golden brown rings around peripheral cornea

Wilson disease (Kayser-Fleischer rigns due to copper accumulation)

Low serum ceruloplasmin

Wilson disease (hepatolenticular degeneration)

Recurrent infections, eczema, thrombocytopenia

Wiskott-Aldrich syndrome

Cavernous hemangiomas

Within brain parenchyma. Increased risk for intracerebral hemorrhage, not sub/epi dural.

Delta wave on EKG, short PR interval, supraventricular tachycardia

Wolff-Parkinson-White syndrome (bundle of Kent bypasses AV node)

Chronic gout

Xanthine oxidase inhibitors (eg. allopurinol, febuxostat); pegloticase; probenecid

Yellowish CSF

Xanthochromia (eg. due to subarachnoid hemorrhages)

Nephrolithiasis: Uric acid stones

Yellow or red-brown diamond or rhombus

Diverticulum in pharynx

Zenker diverticulum (diagnosis by barium swallow)

Aplastic anemia: a. Pathogenesis b. Causes c. SSx d. Diagnosis

a. Bone marrow failure d/t HSC deficiency (CD34) b. Autoimmune, infections (parvo B19, EBV), drugs (carbamazepine, chloramphenicol, sulfonamides), exposure to radiation/toxins (benzene, solvents) c. Sx result from pancytopenia: No splenomegaly (characteristic)! - Anemia (fatigue, weakness, pallor) - Thrombocytopenia (mucosal bleeding, easy bruising, petechiae) - Leukopenia (recurrent infections) d. Bone marrow biopsy shows hypocellular bone marrow composed mainly of fat and stromal cells

Embryology: a. What does the ureteric bud give rise to? b. ... metanephric mesoderm (blastema)?

a. Ureteric bud = collecting system of kidney including collecting tubules, collecting ducts, major and minor calyces, renal pelvis and ureters b. Metanephric mesoderm = glomerulus, Bowman's space, PCT, loop of Henle, DCT

Pheochromocytoma

alpha-antagonists (eg. phenoxybenzamine)

Benign prostatic hyperplasia

alpha1-antagonists, 5-alpha reductase inhibitors, PDE-5 inhibitors

Heme synthesis

delta-ALA synthase (+) glycine, hypoxia, barbiturates (-) glucose, heme

Cross sections of spinal cord identification

http://neuroscience.uth.tmc.edu/s2/chapter03.html

Glycogenolysis: regulation

https://classconnection.s3.amazonaws.com/677/flashcards/142677/png/glycogen_regulation1341010491564.png

Thiazide diuretic: SEs

hypokalemia, hyponatremia, hyperuricemia, hypercalcemia

Ventricular Volume Pressure Loop - Increased Preload

or: www.easynotecards.com/uploads/1087/4/_53022d86_13d85ffda7d__8000_00001444.jpg

Henderson-Hasselbach equation (for extracellular pH)

pH = 6.1 + log [(HCO3-) / (0.03 x pCO2)]

Half-life

t1/2 = (0.693 x Vd) / CL CL = drug clearance Vd = volume of distribution

Renal cell carcinoma (bilateral), hemangioblastomas, angiomatosis, pheochromocytoma

von Hippel-Lindau disease (dominant tumor suppressor gene mutation)

Hereditary bleeding disorder

von Willebrand disease

Best indicator of severity of mitral regurg

" Presence of audible S3. S3 gallop reflects an increased rate of left ventricular filling d/t large volume of regurgitant flow re-entering the ventricle mid- diastole"

Lactase deficiency: causes

"1. AR disorder (congenital) 2. Progressive non-persistence of lactase expression in adulthood 3. Inflammatory disorder affecting the intestinal brush border"

"Features of UC-related colorectal CA versus sporadic colorectal CA"

"1. Arises from non-polypoid dysplastic lesions 2. Be multifocal in nature 3. Develop early p53 lesions and late APC mutations 4. Be of higher histological grade"

Gallstones: types & contents.

"1. Cholesterol: too much cholesterol for bile salts to solubilize. These are hard and yellow to pale gray in color. 2. Pigmented: calcium salts of unconjugated bilirubin. These are soft and are dark brown to black. 3. Mixed"

Failure of urachus obliteration

"3 weeks gestation, yolk sac forms protrusion known as allantois that extends into urogenital sinus. Upper part of UG sinus becomes bladder and allantois now becomes urachus (duct bw bladder and yolk sac). Failure of urachus obliteration before birth leads to: 1. Patent urachus (straw-colored urine discharge from umbilicus). 2. Urachal sinus (failure of distal part of urachus to close) w/periumbilical tenderness and purulent umbilical discharge d/t infection. 3. Failure of central portion of urachus to close = urachal cyst."

MDD: diagnostic criteria?

">=2 week period with >=5 of following: depressed mood, loss of interest, sleep disturbance, appetite disturbance, loss of energy, psychomotor agitation or retardation, impaired concentration, guilt or suicidal thoughts. Don't diagnose adjustment disorder if the patient meets full criteria for MDD. MDD often precipitated by psychosocial stressors."

Myotonic dystrophy

"AD disorder caused by increased number of TNRs on myotonia-protein kinase gene. Sustained muscle contraction (myotonia) along with weakness and atrophy is common. Cataracts are seen in almost all patients. Frontal balding and gonadal atrophy are other common features."

PKU

"AR. Deficiency in phenylalanine hydroxylase. Normally this ez converts Phe to tyrosine, which serves as precursor to DOPA (precursor to melanin and catecholamines). Sx: intellectual disability, seizures, light pigmentation and musty odor."

Structures associated with third part of duodenum

"Abdominal aorta, IVC, superior mesenteric vessels lie anterior. Infiltration of duodenal mass past gut wall would compromise superior mesenteric vessels."

Intraerythrocytic inclusions: think what organisms? How to tell difference?

"Acute febrile illness + this finding = Malaria or Babesiosis. Use epidemiology to make diagnosis. NE US w/outdoor exposure = Babesiosis. Organism transmitted by ixodes tick. Inclusion is Maltese cross shape (was not present in the question I saw)."

Functional heart murmur

"Acute hemodynamic changes can produce these types of murmurs in absence of any fixed valve lesion. Example: dilation of left ventricle in response to increased preload can result in functional mitral regurg, which can be eliminated by preload reduction and reduced by afterload reduction."

"Addison's dz: Describe electrolyte abnormalities"

"Addison's: aka primary adrenal insufficiency. Loss of cortisol feedback = high ACTH (high pigmentation) No aldosterone, no cortisol, no sex hormones Aldosterone = retain Na, secrete K and H (compensatory increase in HCO3), compensatory decrease in Cl- Therefore labs = hyponatremia, hyperkalemia, retain H, low bicarb, compensatory hyperchloremia to maintain net neutrality in non-anion gap metabolic acidosis"

Coronary steal medications

"Adenosine and dipyridamole = selective vasodilators of coronary vessels. When MI present, these drugs cause redistribution of blood flow and reduce collateral flow to areas with already maximal flow. This is coronary steal phenomenon."

Hepatic encephalopathy

"Ammonium is converted into glutamine in the astrocytes resulting in hyperosmolarity and mitochondrial dysfunction causing swelling and impairment. In addition, it is taken up into neurons where it consumes alpha keto glutarate and with glutamate DH is converted into glutamate. Conversion into glutamine depletes glutamate stores decreasing excitatory neurotransmission. Depletion of alpha keto glutarate depletes energy metabolism in neurons (supposed to be used in Krebs cycle)."

Corynebacterium diphtheriae: pathogenicity? What does capsule contain?

"Antiphagocytic capsule required for pathogenicity. Capsule contains D-glutamate instead of polysaccharide. Also note: this organism forms long chains described as serpentine or medusa head on appearance under microscope, aka Chinese letters/characters"

Gallstones: causes of pigmented stones

"Arise secondarily to bacterial infection (E.coli) or helminthic infection (Ascaris lumbricoides or Clonorchis sinensis liver fluke) of the bile duct tract. The infection results in release of beta-glucuronidase by injured hepatocytes and bacteria, which hydrolyzes bilirubin into unconjugated. Chronic hemolytic anemia can also cause pigmented stones. C.sinensis is common cause of pigmented stones in East Asia"

Aspergillus fumigatus vs Rhizopus and Mucor: morphology

"Aspergillosis: Septated hyphae, branching at narrow angles (acute-V) *mnemonic: LL in Aspergillus reminds me of the septations Rhizopus & Mucor: non-septated hyphae, branching at wide angles"

Dantrolene

"Blocks ryanodine receptors and prevents release of Ca into cytoplasm of skeletal muscle fibers. Used to tx malignant hyperthermia (sx = fever, muscle rigidity soon after surgery)."

Bortezomib

"Boronic-acid containing dipeptide. MOA = proteasome inhibitor, resulting in accumulation of toxic intracellular proteins. Proteasomes also regulate balance of pro and anti apoptotic proteins, inhibition of these proteasomes leads to excess pro-apoptotic proteins and induce apoptosis. Used in multiple myeloma to induce apoptosis of malignant plasma cells."

Syringomyelia

"Central cystic dilation in c-spine that slowly enlarges characteristically causing damage to VWC (ventral white commissure) and anterior horns. Sx: fixed segmental loss of UE pain and temp sensations, UE LMN signs and LE UMN signs in setting of scoliosis (d/t weakness of paraspinal muscles)"

Friedrich ataxia

"Characterized by cerebellar ataxia (d/t spinocerebellar tract degeneration) and loss of position/vibration sensation (dorsal column/dorsal root ganglia degeneration), kyphoscoliosis and hypertrophic cardiomyopathy. Food abnormalities and diabetes are common. AR disorder with mutation in FXN gene. Gene codes for essential mitochondrial protein involved in assembly of iron-sulfur enzymes. Increase in TNRs (GAA) seen in the gene."

First generation anti-histamines

"Chlorpheniramine and diphenhydramine have antimuscarinic, anti-alpha adrenergic and anti-serotonergic properties. Anti-cholinergic effects on ciliary muscles impair accommodation and cause blurring of vision for close objects"

Milrinone: Class, Indications, MOA, contra

"Class = PDE3 enzyme inhibitor Indications = refractory heart failure MOA = decreases rate of cAMP degradation in myocardium = more calcium stays around = inotrope = increase FOC. In vascular smooth muscle, it vasodilates. Contraindications: d/t vasodilatory action, be careful in hypotensive patient"

Pioglitazone: Side Effects

"Class = TZDs (thiazolidinedione). Other meds in this class = rosiglitazone. Main SEs = fluid retention, weight gain, edema. This excess fluid can exacerbate underlying CHF."

Diphenoxylate: Class, Indications, MOA

"Class = mu opioid agonist MOA = slows motility Indications: diarrhea (anti-diarrheal) Note: usually combined with atropine, which induces side effects: dry mouth, blurry vision and nausea to prevent abuse (morphine-like euphoria)."

"Vaughn-Williams classification: a. Describe including names of drugs b. MOA"

"Class I: Na-channel blocking agents (affect phase 0 upstroke) Ia = quinidine, procainamide, disopyramide Ib = lidocaine, mexiletine Ic = flecainide, propafenone Class II: beta-blockers Class III: K-channel blocking agents (affect 3): amiodarone, sotalol, dofetilide Class IV: Ca-channel blocking agents (affect phase 2): DHP (-dipines) and non-DHP (verapamil, diltiazem). Note: non-DHP selective for heart."

Femoral nerve (L2-4)

"Comes out between iliacus and psoas. Compromise from fracture or mass involving either of these = inability to flex thigh or extend leg and loss of sensation to anterior thigh, medial knee and medial leg / gastroc."

TCA

"Common cause of death with OD = cardiac arrhythmias and refractory hypotension. This is d/t inhibition of fast Na channels in cardiac myocytes and the His-Purkinje system."

Junctional complex

"Comprised of three components: 1. Tight junctions (aka zonula occludens): at apices of glandular cells consisting of two adherent cytoplasmic membranes without an intervening space 2. Intermediate junctions (aka zonula adherens) 3. Desmosomes: circular adherent patches"

Factitious disorder: diagnostic criteria?

"Conscious and deceptive production of physical or psychological sx to obtain attention and medical care. Absence of obvious reward. Assume sick role. Eg. Injecting fecal matter to produce abscess."

Atrial myxoma

"Constitutional sx (fevers, weight loss d/t IL-6 produced by tumor), mid-diastolic rumbling murmur (best heard at apex), positional dyspnea, large pedunculated mass in left atrium. These are the most common primary cardiac neoplasm (80% arise from left atrium)"

DDAVP: What is it? Function in uncontrolled bleeding events? Which bleeding diseases can it be used for?

"DDAVP = desmopressin, synthetic form of ADH 2 mechanisms used in uncontrolled bleeding: 1. Induces release of VWF from endothelial cells 2. Increases circulating factor VIII. Diseases: hemophilia A (not severe and not for B), Von Willebrand Disease and thrombocytopenia

Function of DNA pol III and I

"DNA Pol III: replicates DNA by polymerizing DNA in 5 - 3 prime direction, with exonuclease in 3 - 5 prime direction DNA Pol I: replicates DNA by polymerizing DNA in 5 - 3 prime direction, with exonuclease in 3 - 5 prime direction. Also has 5 - 3 prime exonuclease to remove primer left by RNA primase"

Cori dz (type III) defect? SSx?

"Debranching enzyme deficiency (inability to degrade alpha-1,6-glycosidic linkages) resulting in accumulation of glycogen with abnormally short chains in hepatocytes SSx: hypoglycemia, ketoacidosis (indicates fat degradation is working fine), hepatomegaly, muscle weakness and hypotonia"

Thiazolidinediones: MOA

"Decrease insulin resistance by binding to PPAR-gamma, a transcriptional regulator of genes involved in glucose and lipid metabolism. Effect = increased FA uptake, increased insulin sensitivity. Because it alters gene transcription, it takes several days to a few weeks to observe significant reduction in glucose."

AD

"Decreased levels of Ach in nucleus basalis of Meynert and hippocampus. Cause is diminished activity of choline acetyltransferase in these structures."

Diastolic heart failure

"Decreased ventricular compliance and characterized by normal LV ejection fraction, normal LV EDV and elevated LV pressures. Causes = HTN, obesity, and infiltrative disorders (such as transthyretin-related amyloidosis, sarcoidosis)"

Charcot-Bouchard aneurysm rupture

"Deep intraparenchymal hemorrhage commonly caused by HTNsive vasculopathy of small deep penetrating branches of cerebral arteries. Compared to saccular aneurysms, which typically cause subarachnoid hemorrhage."

Pompe Disease (GSD Type II)

"Defect = acid alpha glucosidase (aka acid maltase), ez responsible for breaking down glycogen. Classic presentation in early infancy with cardiomegaly, generalized hypotonia, macroglossia and hepatomegaly. Key distinguishing feature from other GSDs = muscle biopsy shows glycogen in lysosomes."

SCID

"Defect in T cell development (either defective IL2R gamma chain, which is XR or adenosine deaminase deficiency, which is AR) = loss of both cellular and humoral immunity. Presentation = infancy recurrent bacteria, viral, fungal and opportunistic infections + failure to thrive + chronic diarrhea"

Maple Syrup Urine Disease

"Defect in breakdown of BCAAs (LIV: leucine, isoleuc. And valine). Branched-chain alpha-ketoacid DH requires Tender Loving Care For Nancy (Thiamine, Lipoate, Coenzyme A, FAD and NAD) to work. Some patients with MSUD, improve with high dose thiamine (B1). Burned sugar smell in diaper = MSUD."

Attack Rate

"Defined: number of those that became ill divided by the number of individuals at risk for contracting that illness. Example of people who go to a BBQ and eat potato salad alone or in combination with other things. Attack rate among all attendees who ate potato salad is calculated as: Total number of attendees who had potato salad = number of attendees who ate potato salad only + those who ate potato salad in various combinations with other things. Find out the number of those in the various categories who became ill eating the various combinations. Attack rate is then this number divided by total number of attendees who at potato salad." Basically: Attack rate = #ppl who get sick / #ppl who are exposed.

Delirium v Psychosis

"Delirium (a disorder) is a disturbance in attention or awareness along with a change in baseline cognition. It can include psychotic symptoms like hallucinations or delusions, but doesn't always. It develops quickly, and often fluctuates over the course of hours. Psychosis is the presence of hallucinations, delusions, or disorganized thought or behavior. Psychosis itself is a symptom, not a disorder - a whole variety of disorders, including delirium, can include psychotic symptoms. In a primary psychotic disorder, like schizophrenia, the psychotic symptoms do not fluctuate over the course of hours, and attention or awareness may be unimpaired. "

Delirium vs Dementia

"Delirium = Reversible, acute-onset, fluctuating LOC with deficits in attention, memory and executive function. Dementia = gradual onset, is irreversible, does not involve fluctuations in consciousness. Note: cognitive impairment does increase vulnerability to delirium, but delirium itself indicates unstable medical condition that must be identified and treated."

Dandy-Walker malformation

"Developmental anomaly = hypoplasia/absence of cerebellar vermis and cystic dilation of 4th ventricle with posterior fossa enlargement. Presentation: infants with developmental delay, progressive skull enlargement. Cerebellar dysfunction can result in unsteadiness and impaired muscle coordination. Hydrocephalus results in elevated ICP and infant will have irritability, vomiting etc."

Schizophrenia: diagnostic criteria?

"Diagnosis: >= 2 of following: delusions, hallucinations, disorganized speech, grossly disorganized behavior and negative symptoms. One of them must be from first three options (delusions, hallucinations and disorganized speech). Total illness duration >= 6 months with >= 1 month of active sx"

Aortic regurgitation

"Diastolic murmur (Early, Mild = early distolic; Advanced = Holodiastolic) Best heard at right sternal border"

DRESS syndrome

"Drug reaction with eosinophilia and systemic sx: occurs 2-8 weeks of exposure to high-risk drugs such as anticonvulsants (phenytoin, carbamazepine), allopurinol, sulfonamide and abx (minocycline and vanc). Sx = fever, generalized LAD, facial edema, diffuse skin rash, eosinophilia, internal organ dysfunction."

Pancreas: embryologic development

"Duodenum gives rise to ventral and dorsal buds. Ventral gives rise to inferior posterior head, major pancreatic duct (of Wirsung) and uncinate process Dorsal gives rise to most of pancreas: tail, body, most of head Failure of fusion = pancreas divisum"

Mitral regurg

"Effect on hemodynamics: increase in preload, decrease in afterload, increase in ejection fraction (much of it going wrong way, thus forward SV and CO decreased) Systolic murmur"

Prinzmetal's angina

"Episodic, transient attacks of coronary vasospasm at rest or during midnight-early morning hours. They produce temporary transmural MI with STE. Ergonovine can provoke this vasospasm aiding in diagnosis. Tx with nitrates and CCBs, which vasodilate."

Decerebrate posturing

"Extensor posturing. Occurs w/damage to brainstem at / below level of red nucleus (in midbrain tegmentum and pons). Why? Loss of descending excitation to UE flexors (via rubrospinal tract) and predominance of extensors (controlled by vestibulospinal tract). Decorticate posturing from damage above red nucleus. With this, flexors predominate."

Akathisia: what is this? Caused by what meds?

"Extrapyramidal side effect of antipsychotic meds (esp. first generation) characterized by inner restlessness and inability to sit or stand in one position. Often misdiagnosed / misinterpreted as worsening psychotic agitation. The antipsychotic dose is often increased exacerbating the akathisia."

"Urea cycle: What is the enzyme that produces urea? From what?"

"Ez = Arginase Rxn = arginine + H2o = urea and ornithine Note: urea cycle for catabolism of amino acids"

Filtration fraction

"FF = GFR/RPF. With hypovolemia, GFR and RPF decrease. Lowering of GFR activates RAAS system. Ang II = efferent renal arteriole vasoconstriction = attempt to restore GFR to normal. GFR is raised, but not to normal levels. Therefore GFR decreased, but not as much as RPF, overall FF increases."

FSH: function

"FSH binds to FSH R on Sertoli cells resulting in Inhibin B. This feedsback on pituitary to decrease FSH release. FSH also stimulates Sertoli cells to produce androgen-binding protein. This concentrates testosterone in seminiferous tubules, which with FSH is necessary for spermatogenesis to occur."

Haloperidol

"First generation antipsychotic and potent D2 receptor blocker. Frequent SE = drug-induced parkinsonism. Used central acting antimuscarinic to tx if patient cannot be taken off this med. This includes benztropine or trihexyphenidyl."

Erythroid precursors

"Found in liver and spleen are sign of extramedullary hematopoiesis stimulated by EPO and hyperplastic marrow cell invasion of extramedullary organs. Extramedullary hematopoiesis is most frequently caused by chronic hemoloytic anemias such as Beta-thalamssemia"

Gs mechanism

"G protein activates adenylate cyclase, which causes a rise in cAMP. cAMP activates PKA = increase in Ca in heart, and blocks smooth muscle via MLCK (myosin light-chain kinase)"

Krukenberg tumor

"Gastric tumor metastasized to ovary. Presents with: weight loss, epigastric pain, adnexal masses. Histologically: large amounts of mucin with apically displaced nuclei resulting in signet ring appearance."

Neonatal tetanus: when is this seen? How is it treated?

"Generally from unhygienic deliveries or cord care. Prevention focused on vaccinating women who are pregnant or may become pregnant. Vaccinated women provide transplacental IgG to fetus. Tx of neonatal tetanus (if prevention didn't happen) = abx and administration of tetanus Ig to neutralize unbound toxin."

"Golgi tendon organ vs Intrafusal muscle fiber function"

"Golgi: monitor tension in muscle when active contraction and increased tension is transmitted through tendon. Serves to regulate and maintain muscle tension. When muscle exerts too much force, GTOs inhibit muscle via their 1b afferent connect to inhibitory interneuron that synapses onto alpha motor neuron that innervates the muscle. Arranged in series. Intrafusal: sensitive to changes in muscle length and mediate the stretch reflex. When muscle is stretched, there is monosynaptic reflex activation of alpha motor neuron (to same muscle) which causes a contraction to resist the stretch."

Pseudogout vs Gout

"Gout: Most common joint = 1st MTP. Crystals = negatively birefringent = when crystal aligned on axis of slow ray of compensator, they are yellow. When perpendicular, they are blue. Crystals are needle-shaped and it is monosodium urate (salt of uric acid). Pseudogout: Most common joint = knee. Crystals = rhomboid (diagnostic) & positively birefringent = when crystals aligned on axis of slow ray of polarizer, they are blue. When perpendicular, they are yellow. Crystals are calcium pyrophosphate."

Gardnerella vaginalis: disease? Morphology of bacterium?

"Gram-variable rod, anaerobic. Responsible for BV"

S4

"Heard at end diastole just prior to S1. It results from decreased left ventricular compliance at atrial kick and is often associated with restrictive cardiomyopathy d/t left ventricular hypertrophy."

Metabolic Alkalosis

"High pH, HCO3- and pCO2. To determine metabolic vs respiratory, look at pCO2. If low, then respiratory alkalosis d/t blowing off CO2. If high, then metabolic. Common causes of metabolic alkalosis = vomiting/NG suctioning (removes H and Cl), thiazide/loop diuretic use = increase in K and H losses as Na is retained; hyperaldosteronism (Conn syndrome). Botton line in these cases is to determine patient's volume status and measure urinary chloride concentration to determine cause. Low urine Cl in cases of vomiting/NG suctioning, ongoing use of thiazides/loop. High urine Cl in cases of hyperaldosteronism."

Use Dependence

"Higher rates of depolarization lead to increase Na channel blockade d/t channels spending less time in resting state. Class I antiarrhythmics, Na channel blocking strength = 1C > 1A > 1B. 1C = most use dependence. 1B with least."

Insulin Receptor Intracellular Cascade

"IR has intrinsic tyrosine kinase. When phosphorylated, activates PI3K pathway leading to glycogen, lipid and protein synthesis and glut-4 receptor translocation to membrane. Also acts on the RAS/MAP kinase pathway leading to cell growth and DNA synthesis."

Projection: what is this?

"Immature defense mechanism involving misattributing one's unacceptable feelings or thoughts to another person who does not actually have them. This relieves the person of the internal conflict that would occur with self-expression of the feelings."

Thromboangiitis obliterans (Buerger's dz)

"Immune hypersensitivity to component of tobacco smoke leads to vasculitis of medium and small-size arteries, principally in tibial and radial arteries. Histologically: acute and chronic inflammation of arterial walls, often with thrombosis of lumen, which undergoes organization and recanalization. This vasculitis often extends into contiguous veins and nerves (rarely seen in other vasculitis). Seen w/heavy cigarette smokers in Israel, Japan and India. Sx = calf, foot or hand intermittent claudication may be seen as well as superficial nodular phlebitis and cold sensitivity (Raynaud's). Severe distal pain, event at rest, can result and may be d/t neural involvement. Later complications = ulcerations, gangrene of toes, feet or fingers. Tx = smoking cessation."

Ubiquitination

"Impairment of ubiquitin-proteasome system can contribute to the development of neurodegenerative disorders, including PD and Alzheimer's. Ubiquitin labels protein in cell for degradation."

Viridans streptococci: morphology and growth? Tropism?

"In pts with pre-existing heart valve lesions, viridans adhere to fibrin-platelet aggregates via the dextrans they produce from sucrose Gram pos: catalase -ve, alpha-hemolytic"

Vaccines

"Inactivated viral vaccines induce humoral immune response (ultimately preventing infection via neutrolizing antibodies), whereas live/attenuated induce cell mediated response in addition to humoral"

Levodopa

"Increase of DA = behavioral changes (anxiety, agitation, insomnia, confusion, delusions, hallucinations.) as SE. Carbidopa decreases peripheral conversion making more DA available in brain."

Linezolid

"Indication: used to tx gram pos bacterial infections (particularly VRE and MRSA). Contraindications: has MAOI activity and can precipitate serotonin syndrome when used comcomitantly with an SSRI "

IL-12 R deficiency

"Individuals suffer from mycobacterial infections as they aren't able to stimualte TH-1 response. Tx these patients with IFN-gamma, which is secreted by TH1 cells normally, but lacking in these patients d/t R deficiency"

Thiamine deficiency

"Infusion of glucose without thiamine in a patient with chronic thiamine deficiency precipitates encephalopathy. Thiamine is a cofactor for enzymes responsible for glucose metabolism. Wernicke's encephalopathy: confusion, ataxia, ophthalmoplegia = triad. Hemorrhage into mamillary bodies is characteristic."

Lactase deficiency: tests to diagnose

"Lactose is not converted into galactose and glucose. This leads to attraction of excess water into lumen. Bacteria ferment lactose to produce short-chain FAs with lower stool pH and hydrogen gas emission (flatulence). Therefore: 1. Breath test shows increased hydrogen content 2. Elevated stool osmotic gap"

Electrical Impulse Axon

"Length constant = measure of how far along an axon an electrical impulse can propagate. Low = less distance an impulse can travel. Time constant = time it takes for a change in membrane potential to achieve 63% of new value. Low = increase in axonal conduction speed. With MS, length constant = decreased and time constant = increased = overall decrease in axonal conduction speed. Layman's: in MS, impulse cannot travel far and it takes a long time to travel any distance"

Bipolar type I: diagnostic criteria

"Lifetime hx of >=1 episodes of mania. Mania = elevated/irritable mood, hyperactivity, decreased need for sleep, pressure speech, grandiosity and may include psychotic features (delusions, hallucinations). DIGFAST mnemonic = distractibility, impulsivity, grandiosity, flight of ideas, activity increase, sleep decrease, talkativeness"

"Name Glycogen storage diseases List enzymes defective SSx"

"Listed by order of defect in glycogenolysis (deficient ez) Type II: Pompe - acid alpha glucosidase aka acid maltase SSx: normal glucose levels, severe cardiomegaly, glycogen accumulation in lysosomes Type V: McArdle - muscle glycogen phosphorylase SSx: weakness and fatigue with exercise, no rise in blood lactate levels after exercise Type III: Cori - debranching enzyme (alpha-1,6-glucosidase) SSx: hepatomegaly, ketotic hypoglycemia, hypotonia and weakness, abnormal glycogen with very short outer chains Type I: Von Gierke - glucose-6-phosphatase SSx: hepatomegaly & steatosis, fasting hypoglycemia, lactic acidosis, hyperuricemia & hyperlipidemia"

Osteocytes

"Long intracanalicular processes that extend through ossified bone matrix. Through these processes, they send signals, nutrients, exchange waste with osteocytes neighbouring lamellae via gap junctions."

MI

"Loss of cardiomyocyte contractility occurs within 60 seconds after onset of total ischemia. Although total ATP levels remain relatively normal during first few minutes, ATP is rapidly depleted from areas of cell with high metabolic demand such as cytosol surrounding contraction fibers and electrolyte transport pumps. "

Rett Syndrome

"Loss of speech, motor skills, deceleration of head growth, stereotypic hand movements after a period of normal development. Affects mainly girls and associated with mutations in MECP2 gene."

I-Cell Disease

"Lysosomal storage disease. Specifically disease d/t defects in protein targeting. Proteins destined for lysosome require phosphorylation of specific mannose residues to ensure proper transit through Golgi."

"Multiple endocrine neoplasia: Distinguish the types from each other"

"MEN1: primary hyperparathyroidism, pituitary tumors, pancreatic tumors (mnemonic = 3Ps) MEN2A: medullary thyroid cancer, pheochromocytoma, parathyroid hyperplasia MEN2B: medullary thyroid cancer, pheochromocytoma, mucosal (oral and intestinal) neuromas, marfinoid habitus"

Physostigmine

"MOA = AChE inhibitor with tertiary amine structure. Reverses both CNS and peripheral sx of severe atropine toxicity. Neostigmine and edrophonium have quaternary structure limiting CNS penetration."

Fibrates

"MOA = activation of LPL = converts TGLs into VLDLs and VLDLs into IDLs. Also activates PPAR alpha (peroxisome proliferator-activated receptor alpha) = decreases VLDL production."

TNF-alpha Induces Insulin Resistance

"MOA = activation of serine kinases, which phosphorylate serine residues inhibiting phosphorylation and induction of PI3K and RAS/MAP kinase pathways. Therefore no glycogen, lipid and protein synthesis occurs. No GLUT-4 receptor translocation occurs onto membranes and no cell growth and DNA synthesis occurs. Note: catecholamines, glucocorticoids and glucagon induce insulin resistance via this same mechanism."

Benzodiazepines

"MOA = bind to BZP (benzodiazepine) binding site (not location where GABA binds), allosterically modulating binding of GABA = increased frequency of Cl channel opening = inhibition of AP"

Niacin

"MOA = increases HDL, decreases LDL and TGLs SEs = cutaneous flushing (mediated by PGs), can be disipated by pre-treatment with ASA"

Fibrates

"MOA = inhibition of cholesterol 7alpha hydroxylase (RLS in bile acid synthesis). Reduced bile acid production and increased cholesterol excretion = decreased cholesterol solubility and favors formation of cholesterol gallstones"

Metformin

"MOA = inhibition of hepatic gluconeogenesis and increase glucose utilization. SE: lactic acidosis (decreased use of lactic acid). Check serum Cr prior to use to see for renal insufficiency."

Phenoxybenzamine

"MOA = irreversible alpha-1 and 2 antagonist Indications = pheochromocytoma Pharmacology: since irreversible antagonist, it reduces the affinity of NE for receptors (predominantly alpha-1) regardless of concentration (pheos can produce a lot of NE)"

Ivabradine

"MOA = selective inhibition of funny Na channel = prolonged slow wave depolarization (phase 4) and slowing of SA firing rate, therefore -ve chronotropic effect. No inotropic (contractile) or lusitropic (relaxation) effect."

Acute rheumatic fever: SSx

"Manifestations: J(heart)ONES: - Joints: Polyarthritis - (heart): Carditis - Nodules (subcutaneous) - Erythema marginatum (faint erythematous circular lesions with central clearing to trunk and extremities) - Sydenham chorea (non-rhythmic movements of hands, feet, face, often with sudden changes in pitch and volume) Cause = S. pyogenes (GAS, but beta-hemolytic)"

Fetal anomalies

"Maternal serum AFP elevated in multiple gestations, open NTDs, abdominal wall defects. Low AFP and unconjugated estriol are associated with DS. Low AFP also seen with other aneuploidies."

Neprilysin inhibitors

"Meds = Sacubitril. MOA = inhibition of neprilysin. Neprilysin functions as MMP to inhibt bradykinin, enkephalins, glucagon and natriuretic peptides. When inhibited, more ANP available. ANP secreted by atrial cardiomyocytes and causes = peripheral vasodilation and increased excretion of Na and water."

Class III antiarrhythmic

"Meds = amiodarone, sotalol, dofetilide MOA = block K channels, inhibit outward K currents during phase 3 = prolonging repolarization and total AP duration."

Antineoplastic agents that inhibit DNA synthesis

"Methotrexate inhibits DHFR (normally converts folic acid to DHF and then into THF) 5-FU inhibits thymidylate synthetase (functions to convert dUMP to dTMP) Rescue agent to overcome inhibition of DHFR and therefore lack of THF = folinic acid (aka leucovorin)"

Heteroplasmy

"Mitochondrial disease severity dependant on how many ""bad"" mitochondria one inherits from mom. This explains why boy can have severe phenotype and his sister may not. Mitochondrial diseases = LHON (bilateral vision loss), myoclonic epilepsy with ragged-red fibers (associated with exercise) and mitochondrial encephalomyopathy (lactic acidosis and stroke-like episodes)."

Negative sense ssRNA viruses: which are they?

"Mnemonic = Always Bring Polymerase Or Fail Replication Doofus Arena, Bunya, Paramyxo, Orthomyxo, Filo, Rhabdo, Delta (requires HBV co-infection)"

Cardiac AP Conduction Speed vs Rate of Depolarization

"Mnemonic = Park At Venture Avenue (Conduction speed) (Fastest) Purkinje > Atrial muscle > Ventricular muscle > AV node (slowest) Impulses travel fastest through Purkinje and slowest through AV node vs rate of intrinsic depolarization rate: SA > AV > bundle of His/Purkinjes/Ventricles"

Non-enveloped viruses: which are they?

"Mnemonic = give PAPP smears and CPR to NAKED Heppies Papilloma, Adeno, Polyoma, Parvo, Calici, Picorna, Reo, Hepe"

Positive sense ssRNA viruses: which are they?

"Mnemonic = i went to a RETRO TOGA party where i drank FLAVored CORONA and ate HEPpy CALIfornia PICkles Retro, Toga, Flavi, Corona, Hepe, Calici, Picorna"

Intraductal papilloma

"Most common cause of blood/serosanguinous nipple discharge. This is proliferation of papillary cells in cyst wall / duct that may contain focal atypia. Presents without breast masses or skin changes."

Cerebral amyloid angiopathy

"Most common cause of spontaneous lobar hemorrhage particularly in elderly. Most common sites = P and O areas. Hemorrhages tends to be recurrent."

Neuroblastoma

"Most common extracranial childhood cancer. Develops from neuroblasts located in adrenal medulla. Opsoclonus-myoclonus is a paraneoplastic syndrome associated with neuroblastoma. Associated sx with this = non-rhythmic conjugate eye movements and myoclonus."

Paraneoplastic cerebellar degeneration.

"Most commonly associated with small cell lung cancer. Also breast, ovarian and uterine. Caused by immune response against tumor that cross-reacts with Purkinje neuron antigens. Anti-Yo, anti-P/Q and anti-Hu most commonly detected."

Aspiration pneumonia

"Most dependent part of lung = superior regions of lower lobes and posterior regions of upper lobes. Infiltrates in these areas = high suspicion for aspiration pneumonia. Especially in setting of dementia or hemiparesis patient with dysphagia = risk factors for aspiration."

Loop diuretics

"Most potent diuretic used for first line. MOA = inhibiting Na-K-2Cl cotransporter in thick ascending limb = increase Na and H2o excretion. Provides rapid relief in acute decompensated heart failure."

Subacute combined degeneration

"Myelopathy associated with vit B12 deficiency. Degeneration of both ascending dorsal columns and descending corticospinal tract. Therefore loss of position and vibration sense, ataxia and spastic paresis."

NNT calculation

"NNT = 1/ARR ARR (absolute risk reduction) = control rate - treatment rate"

Heparin

"Naturally present in mast cells. MOA = heparin binds to AT III, resulting in a conformational change in AT III, which allows it to bind to Xa neutralizing thrombin and preventing coagulation. ATIII is a naturally occuring anticoagulant and giving heparin stimulates this process."

Supinator canal injury: What nerve is injured? How? SSx?

"Nerve = radial nerve. How = repetitive pronation, supination; direct trauma, subluxation of the radius SSx = weakness during finger and thumb extension without wrist drop (higher up injury like in humerus) and no sensory deficits. Why no sensory deficits: superficial branch that does sensation to dorsal radial half of hand has already left and only deep branch under."

AD

"Neuritic plaques: Extracellular deposits found in medial temporal lobe often composed of amyloid beta core surrounded by dystrophic neurites. This is histopathologic for AD."

MS Pathogenesis

"Neurologic manifestations result from characteristic sclerotic plaques throughout white matter. Main process in plaque formation is demyelination of axons. This impairs saltatory conduction down axon resulting in conduction blockade/slowing of neuronal signal transmission."

Gout

"Neutrophils = primary cells responsible for intense inflammatory response seen in gout. These phagocytoze the urate crystals leading to inflammation. NSAIDs inhibit prostanoid biosynthesis ultimately inhibiting neutrophils. Colchicine impairs neutrophil migration by interfering with microtubule formation. Used in patients allergic to NSAIDs."

"Effect of nitrites on cellular respiration? How does PaO2 change in blood?"

"Nitrites cause methemoglobinemia, where Fe2+ is converted into Fe3+, which has no affinity and doesn't bind o2. As a result, o2 carrying capacity by RBCs is decreased. PaO2 is normal"

C.albicans: where does it normally colonize?

"Normal colonizer of GI tract (including oral cavity). In cases where you suspect TB and do a sputum study and it reveals budding yeast that form germ tubes, it is because of contaminant from oral cavity."

Antisocial PD: at what age is it diagnosed? Diagnostic criteria?

"Not diagnosed under age 18. < 18 = conduct disorder Involves pattern of violation of basic societal rights and rules and requires hx of some sx of conduct disorder < 15 yo."

GVHD

"Note: GVHD affects other systems other than the organ itself. The donors T cells from graft survive and migrate into host tissue recognizing foreign host MHC antigens. T cells participate in destruction not B cells. Skin, liver and GI are most commonly affected organs. Skin: palms and soles usually early signs - they desquamate."

Gliosis

"Occurs in setting of irreversible neuronal damage. This is proliferation of astrocytes in area of neuron degeneration. Leads to scar that compensates for volume loss from neuronal death."

Ankylosing spondylitis

"Part of larger group of diseases (AS, reactive arthritis, arthritis with IBD, psoriasis) under umbrellas seronegative spondyloarthropathies. Sx for AS = inflammation of SI joints and axial skeleton. These are associated with HLA-B27 (class I MHC)."

Conduct disorder: diagnostic criteria?

"Persistent pattern of violating major societal norms or rights of others. Usually childhood diagnosis. Behaviors include: aggression towards others including animals, theft, deceitfulness, destruction of property and serious violation of rules."

Borderline personality disorder: diagnostic criteria

"Persistent unstable relationships, mood lability, impulsivity. May also exhibit suicidal ideation or behavior in context of interpersonal crisis in which they feel rejected or abandoned. Both histrionic and borderline characterized by attention-seeking. Excessive anger and self-destructive behavior more characteristic of borderline personality."

"What is phenelzine? What other meds are in its class?"

"Phenelzine = MAOI. Other meds = selegiline and tranylcypromine. MOA = inhibition of monoamine oxidase to allow monamines (DA, NE, 5-HT) to remain high. Used for depression."

PCP

"Phenyclidine is N-Methyl-D-Aspartate R Antagonist. Dissociative and anesthetic effects and may cause psychosis and severe agitation leading to violent trauma. Ataxia, horizontal and vertical nystagmus, and delirium can also be present."

Skewed distribution

"Positive vs negative skew = where the tail extends. If tail extends away from zero towards right, it is positively skewed. If tail extends away from zero towards left, it is negatively skewed. Mode = most frequent value; median = central value; mean = average. With positively skewed distribution = mean > median > mode With negatively skewed distribution = mode > median > mean"

Somatic symptom disorder: what is it? How to manage?

"Preoccupation with unexplained medical sx and excessive health care use. Mgmt = schedule regular visits with PCP who can monitor and avoid unnecessary diagnostic testing and specialist referral. "

Septic abortion

"Presentation = fever, abdominal pain, uterine tenderness and / or foul-smelling discharge following a pregnancy termination Common pathogens = S. aureus and E. coli, which become seeded in uterine cavity."

Inhibin B

"Produced by Sertoli cells via stimulus of FSH. In patients with single testicle, insufficient mass of Sertoli cells exist and less inhibin B is produced. Will see high FSH in these indivdiuals"

HIV-associated dementia

"Progressive cognitive decline. Histopath findings = microglial nodules (groups of activated macrophages / microglial cells formed around small areas of necrosis that may fuse to form multinucleated giant cells)"

Sex hormones: Effect on the growth plate

"Promote both growth at epiphyseal plate and closure of plate. In those with precocious puberty, they will experience both an increase in growth, where they exceed others on the charts yet will be shorter as the growth plate closes before others without precocious puberty."

Schizoaffective disorder: what is this?

"Psychosis in absence of major mood episodes, but mood sx present for most of illness. In MDD or bipolar with psychotic features, psychotic sx occur exclusively during mood episodes."

Creutzfeldt-Jakob

"Rapidly progressive dementia + myoclonic jerks. Microscopy: multiple vacuoles in gray matter of brain (spongiform encephalopathy)."

Subacute sclerosing panencephalitis (SSPE)

"Rare complication of measles occuring several years after apparent recovery. CSF shows oligoclonal bands of measles virus antibodies. When you see RNA virus containing hemagluttinin, think measles."

Bulimia nervosa: SSx? How to differentiate from anorexia nervosa?

"Recurrent binge eating, concerned about body weight and shape, binge eating followed by compensatory changes to maintain normal body weight, able to maintain normal body weight. Note: binge eating disorder = recurrent binge eating w/o compensatory changes. Also body dysmorphic not diagnosed with someone preoccupied with weight gain that has eating disorder. Can sometimes look similar to anorexia nervosa, but with anorexia nervosa, BMI is always low. With bulimia, body weight often maintained."

Acute intermittent porphyria

"Reddish-brown urine. Tx of AIP = IV glucose or heme preparations, which downregulate the ALA synthase activity."

IL-12

"Released by macrophage APCs & B cells Function: Induces differentiation of TH-0 cells into TH-1 (cell-mediated), inhibits TH2. Mnemonic: 1 before 2 to read 12 Activates NK cells"

IL-4

"Released from non-macrophage APCs, TH2 cells Function: Induces differentiation and growth of TH-0 cells into TH-2 (humoral immunity) Stimulates growth of B cells Isotype switching of B cells (particularly to IgE, but also to IgG)"

"Standard error. What is this? How is it calculated?"

"SE = SD/sqrtn (where n = sample size). Most research is done on samples instead of on entire population. To account for variability between samples, SD (standard deviation) must be divided by sqrtn. SD reflects spread in a normal distribution."

Arginase deficiency: SSx and Tx

"SSx = excess arginine in plasma and CSF, progressive spastic diplegia, growth delay, abnormal movements Tx = arginine-free diet, low protein diet Note: unlike other urea cycle disorders, patients with arginase deficiency have mild or no hyperammonemia"

Q fever: cause? SSx? Exposure?

"SSx: non-specific illness (myalgias, fatigue, fever), retroorbital HA w/nml leukocyte count, thrombocytopenia, increased LFTs. Exposure: farm workers with exposure to cattle/sheep waste = Coxiella burnetii"

Dermatomyositis: SSx

"SSx: proximal muscle weakness, heliotrope rash (periorbital area), Gottron's papules (raised plaques over joints and bony prominences of hands), muscle biopsy with mononuclear perimysial infiltrates, perifascicular atrophy and patchy necrosis."

Bulimia nervosa: SSx

"SSx: recurrent binge eating, preoccupation with weight, excessive exercises; self-induced vomiting (pharyngeal erythema, parotid enlargement, hypokalemia and hyperamylasemia. "

Olanzapine

"Second-gen antipsychotic to tx psychotic and mood disorders. SE = weight gain, dyslipidemia, hyperglycemia, increased risk for DM. Greatest risk with olanzapine, clozapine."

IFN-gamma

"Secreted by TH1 cells Function: Activates NK cells to kill virus-infected cells Increases MHC expression and antigen presentation in all cells (ie. stimulates macrophages)"

Serpentine growth: What organism? Why?

"Serpentine (parallel chain, ropelike cord growth) seen in mycobacterium tuberculosis. This is due to cord factor, compound composed of two mycolic acid molecules bound to disaccharide trehalose. Presence of this factor contributes to virulence. Those without this factor, don't correlate with disease. Cord factor effect: inactivates neutrophils, damages mitochondria, and induces release of TNF-alpha"

Cluster headache

"Severe, episodic, unilateral periorbital and temporal pain associated with lacrimation, nasal congestion and ptosis. More common in males and occur classically same time each day."

Thiopental

"Short acting barbiturate for anesthesia induction. Equilibrates with brain then redistributes into skeletal muscle and adipose tissue resulting in rapid recovery from anesthesia."

Hyperthyroidism

"Specific features that hyperthyroidism are d/t Graves = pretibial myxedema and exophthalmos. These are caused by autoimmune response against TSH receptor resulting in accumulation of GAGs within affected tissues (fibroblasts and adipocytes have this receptor too)."

Hereditary spherocytosis

"Spherocytes seen on peripheral blood smear (more densely hemoglobinized, more dense at periphery, often zone of central pallor). Defect in ankyrin and spectrin. Common presentation = hemolytic anemia, jaundice, splenomegaly."

Acute intermittent porphyria

"Sx = recurrent non-specific abdominal pain + neuro sx (tingling, difficulty concentrating etc.). Defect in PBG deaminase (AD) combined with ALA synthase induction = accumulation of ALA (aminolevulinate) and porphobilinogen. Mgmt w/glucose or hemin inhibits ALA synthase activity."

Candida

"T lymphocytes prevent superficial candida infections. Neutrophils prevent from spreading via hematogenous route/systemically preventing formation of candidemia. Localized superficial candidiasis more common in low CD4 T cell count HIV patients, while systemic candidemia more common in neutropenic patient."

Negative Predictive Value (NPV)

"The probability of being free of disease if the test result is negative. Note: this varies with pre-test probability. Pt with high pre-test probability will have low NPV with a negative test. Conversely, pt with low pre-test probability will have high NPV with a negative test."

Herpes viruses: enveloped or not? Where do they acquire their envelope?

"These viruses are part of the enveloped viruses, but are unique in that their envelope is obtained from the nuclear membrane from host and not the plasma membrane as the others."

Carpal Tunnel Syndrome

"Things that reduce carpal tunnel space = pregnancy, hypothyroidism (GAG buildup), DM (CT thickening), RA (tendon inflammation), hemodialysis (deposition of beta-2 microglobulin = dialysis-associated sarcoidosis)"

Axonal reaction

"This happens after axon is severed. Cell body shows edema. Nucleus is displaced to periphery. Nissl substance becomes fine, granular and dipsersed throughout cytoplasm."

Normal pressure hydrocephalus (NPH)

"Triad = ataxic gait, UI, dementia (wacky, wobbly and wet). Cause = distortion of periventricular white matter. Bladder control is influenced by descending cortical fibers that run in distended paraventricular area."

Wiskott-Aldrich syndrome

"Triad = eczema, thrombocytopenia, combined B and T-Cell deficiency (recurrent infections). Repeated infections by encapsulated organisms. Pathogenesis: Mutation in WAS gene (XR) = T cells unable to reorganize actin cytoskeleton. Mnemonic = WATER: Wiskott-Adrich, Thrombocytopenia, Eczema, Recurrent infections"

Muscle fiber types

"Type 1 (slow twitch): postural muscles, produce low-level sustained force, aerobic, high Mb content, high mitochondrial count, red Type 2: rapid forceful movement 2b: anaerobic 2a: ""fast twitch"", intermediate between type 1 and 2b"

Wegener's syndrome

"Type of crescenteric glomerulonephritis with triad = pulmonary dz, URT/upper airway dz and renal dz. Saddle nose, recurrent nosebleeds. Ab = c-ANCA (cytoplasmic antineutrophil cytoplasmic antibody)."

Translation Termination

"UAA, UAG and UGA = stop codons found in mRNA. No tRNA charged with amino acids. Last tRNA to come into the ribosome comes in for the codon prior to the stop. The tRNA has an anticodon region that is complementary to the codon. Eg. 5-UUG-3, tRNA anticodon will be 3-AAC-5"

PID

"Untreated or inadequate treatment of PID = fallopian tube scarring leading to infertility. Tx = third gen cephalosporin (eg. Ceftriaxone) + azithro or doxycycline"

Antiphospholipid syndrome

"Up to 30% of SLE patients have antiphospholipid syndrome. Presents with prolonged aPTT in vitro; however in vivo results in hypercoagulability predisposing to PE, DVT, ischemic stroke/TIA and recurrent pregnancy losses."

Ureter relationship

"Ureter posterior to gonadal vein and artery. Crosses anterior to external and internal iliac artery and medial to ovarian vessels Ureter crosses posterior to uterine artery (water under bridge)"

Cholinergic agonist

"Use: Urinary retention, paralytic ileus, glaucoma. SEs = nausea, vomiting, abdominal cramps, diarrhea, dyspnea, and increased secretions (lacrimation and salivation), sweating."

Cause of intestinal atresia distal to duodenum

"Vascular accident. ""Apple Peel"" or ""Christmas Tree"" deformity = blind ending proximal jejunum, a length of absent bowel and mesentery and finally a terminal ileum spiraled around an ileocolic vessel."

Syringomyelia

"Ventral white commissure = Carries pain and temperature from dorsal horn to contralateral lateral spinothalamic tract. This is damaged in syringomyelia (formation of cavity within cervical spinal cord = loss of pain/temp detection in arms hands)."

Vitamin E deficiency

"Vit E protects againsts oxidative injury. Most susceptible cells = neurons with long myelinated axons and RBCs. Defects = neuromuscular defects and anemia. CF patients have pancreatic insufficiency. Pancreatic enzymes necessary for absorption of ADEK vitamins. CF patients can be subject to deficiencies in these vitamins."

Linkage disequilibrium

"When two alleles are inherited together at higher frequency that if either were to be inherited alone. Example: frequency of inheriting A = 0.2, while frequency of inheriting B = 0.3. Frequency of inheriting both together = 0.2 x 0.3 = 0.06. What is actually seen in the population is frequency of inheriting AB = 0.4, then this is linkage disequilibrium. Note: this can be d/t physical linkage of c/s or genes on separate c/s."

Elimination of Drugs

"Zero-Order: Same/Constant amount of drug eliminated per unit time (straight line going down on concentration/time graph) First-Order: Same/Constant proportion of drug eliminated per unit time (exponential decay/reduction curve on concentration/time graph) *Note: on rate of metabolism graph w/hyperbolic response curve (similar to Michaelis-Menten curve): first-order is climbing part of graph, zero-order is plateau"

Autonomic receptors that affect CV system

"alpha-1 = vasoconstriction alpha-2 = decreased SNS outflow beta-1 = heart (increased contractility and HR) beta-2 = vasodilation"

Osteoporotic fractures: Meds associated with these?

- Anticonvulsants that induce CYP450 (phenobarb, phenytoin, carbamazepine) - Aromatase inhibitors - Medroxyprogesterone - GnRH agonists - PPIs - Glucocorticoids - Unfractionated heparine - Thiazolidinediones

ANS: Effect of Beta-1 receptor blocking

- Decreased HR, decreased contractility, decreased renin release, decreased lipolysis

Anemia: a. Lab values with intravascular hemolysis of RBCs

- Decreased serum haptoglobin (being use to bind free Hb) - Increased unconjugated bili - Increased LDH Note: no significant change in iron.

Hyperkalemia: Meds that cause this?

- Non-selective beta-blockers: interfere with beta-2 mediated K uptake - ACEi: decrease aldosterone secretion - K-sparing diuretics: aldosterone antagonist and ENaC blockers - Cardiac glycosides: inhibition of Na/K ATPase - ARBs: block AT1 receptor = less aldosterone secretion - NSAIDs: impaired PG synthesis leads to reduction in renin and aldosterone production

B1 (Thiamine): what rxns does it run?

- Pyruvate DH: pyruvate into acetyl-CoA in TCA cycle - Alpha-ketoglutarate DH: alpha-KG to succinyl-CoA in TCA cycle - BC alpha-ketoacid DH: catabolism of LIV AAs - Trankelotase: converts ribulose 5-P (derived from glucose) into glycolysis intermediates (glyceraldehyde) in the PPP pathway.

Capacity to refuse tx: Requires?

1. Ability to express choice, 2. Understanding of relevant medical information, 3. Appreciation of consequences of tx options, 4. Rationale given for decision

Nevi progression: describe histologic and gross findings

1. Junctional nevi - Gross: flat, black->brown pigmented macules w/darker coloration in center than periphery, preserved skin markings - Histology: aggregates of nevus cells along dermal-epidermal junction (but within epidermis) 2. Compound nevi - Gross: raised papules w/uniform brown->tan pigment - Histology: aggregates of nevus cells extend into dermis with now epidermal and dermal involvement 3. Intradermal nevi - Gross: skin->tan colored, dome-shaped and sometimes pedunculated - Histology: epidermal nests of nevus cells lost, dermal nevus cells present, but lost tyrosinase activity therefore producing little to no pigment

Melanocytic Nevi vs Melanoma: Compare and contrast the microscopic and gross appearance

1. Melanocytic nevi: - Gross: < 6mm, regular outline sharply demarcated border, symmetrical, homogenous surface - Histology: round uniform melanocytes (nevus cells) that are mitotically quiescent (few mitotic figures), inconspicuous nucleoli 2. Melanoma: - Gross: irregular, asymmetric border, variable coloration, > 5 mm - Histology: cells larger than nevus cells, larger nuclei with prominent nucleoli, greater mitotic activity

PSC vs PBC: Describe in terms of: a. What it is? What is affected? b. Presentation? c. Associations?

1. PSC: Unknown etiology. Diffuse inflammation/fibrosis of large intra and extra hepatic bile ducts with periduct concentric onion-skin pattern fibrosis and obstruction of small ducts (beading appearance with ERCP) Presentation: fatigue and high alk phos in a man with long hx of UC Associations: hyperIgM, pANCA pos, increased risk for cholangiocarcinoma 2. PBC: Autoimmune liver dz w/ destruction of intrahepatic interlobular bile ducts by granulomatous inflammation. Presentation: insiduous onset, pruritus, fatigue, middle-aged women, signs of cholestasis (jaundice, pale stool, dark urine), hypercholesterolemia Association: autoimmune diseases, anti-mitochondrial antibodies

Gluconeogenesis: Describe the reactions Which is RLS? What are the substrates?

1. Pyruvate = oxaloacetate (ez: pyruvate carboxylase)***RLS 2. Oxaloacetate = malate (ez: malate DH) -- Malate exits mitochondria and converted to oxaloacetate via cytosolic malate DH. This is malate shuttle. 3. Oxaloacetate = phosphoenolpyruvate (ez: PEP carboxykinase) **These enzymes: pyruvate carboxylase and PEP carboxykinase bypass pyruvate kinase. 4. PEP to glucose via reverse glycolysis mostly except fructose-1,6-bisphosphatase (bypasses phosphofructokinase) and glucose-6-phosphatase (bypasses hexokinase) Purpose of these steps are to bypass hexokinase, phosphofructokinase and pyruvate kinase, which are all unidirectional. RLS = pyruvate carboxylase Substrates = pyruvate, glycerol-phosphate, glucogenic amino acids (all except for leu and lys)

Down syndrome: Genetic causes

1. Trisomy d/t non-disjunction (most common, over 95% of cases) 2. Unbalanced Robertsonian translocation (3 copies of 21, extra copy attached to another c/s) 3. Mosaicism: some cells have an extra copy of c/s 21 d/t non-disjunction in early embryonic life.

Spliceosomes: what nucleotides are recognized at the beginning and end of the intro in order for the splicing to be done?

5' splice site = GU 3' splice site = AG

MI: Free wall rupture: how long after MI can it occur?

5-14 days w/transmural MI. Responsible for < 10% of all deaths in patients with acute MI.

Ulcerative colitis

5-ASA preparations (eg. mesalamine), 6-mercaptopurine, infliximab, colectomy

HIV: Opportunistic infections at <200, <100 and <50 cell/microLiter CD4 count? What are the treatments?

< 200: pneumocystis jirovecii - tx with TMP-SMX < 100: toxoplasma gondii - tx with TMP-SMX < 50: MAC and M. intracellulare - tx with Azithromycin Note: < 150 and in OH and MS river valleys = H. capsulatum - tx with itraconazole

Meconium ileus: Presentation? Specific finding for what condition?

Abdominal distension, bilious emesis, x-ray findings (air-fluid levels, small bowel dilation) = bowel obstruction. In surgery: green inspissated mass (dehydrated meconium) in distal ileum = source and diagnosis. Specific findings for CF.

Erythrocytosis: Causes of absolute vs relative

Absolute = a. Polycythemia vera b. Hypoxia induced EPO release (Sao2 < 92%, PaO2 < 65) and tumor induced EPO release Relative = nml RBC mass w/plasma volume contraction a. Dehydration b. Excessive diuresis

TH1 response

Activates CMI (cytotoxicity and delayed hypersensitivity) via mediators: IL-2, IFN-gamma, lymphotoxin beta that act on macrophages and cytotoxic T cells

TH2 response

Activates humoral immunity (class-switching, secretion of antibodies) via mediators: IL-4, IL-5, IL-10, IL-13 that act on B cells

Cholecystitis: acute acalculous subtype: What is it? In what patients does it occur?

Acute inflammation of GB in absence of gallstones. Typically occurs in critically ill patients (eg. sepsis, severe burns, trauma and immunosuppression) d/t GB stasis and ischemia. SSx may be subtle: fever, RUQ pain, leukocytosis

Gastric cancer

Adenocarcinoma

Primary hyperaldosteronism

Adenoma of adrenal cortex

Primary hyperparathyroidism

Adenomas, hyperplasia, carcinoma

Agents that induce IgE-independent mast cell degranulation? Mechanism? Result?

Agents: opioids, radiocontrast, some abx (eg. vancomycin) Mechanism: activation of Protein kinase A and PI3 kinase Sx: diffuse itching / pain, bronchospasm, localized swelling (urticaria) Note: IgE-dependent = environmental, foods, insect stings, beta-lactam and sulfonamide abx. Opioids can cause this, but it is very rare (more common for IgE-independent).

Raised periosteum (creating a Codman triangle)

Aggressive bone lesion (eg. osteosarcoma, Ewing sarcoma, osteomyelitis)

Hereditary nephritis, sensorineural hearing loss, cataracts

Alport syndrome (mutation in collagen IV)

Anterior pituitary derivation

Ant. Pituitary from surface ectoderm. Ectoderm gives surface ectoderm, neural tube and neural crest. Post. Pituitary from neural tube neuroectoderm. Remember: Ectoderm divides into surface ectoderm, neuroectoderm (of which their are neural tube neuroectoderm and neural crest neuroectoderm). Neural tube neuroectoderm = brain (including neurohypophysis/aka post. pituitary), retina, optic nerve, spinal cord Neural crest neuroectoderm = PNS, melanocytes, chromaffin cells of adrenal medulla, parafollicular C cells of thyroid, pia and arachnoid, bones of skull, odontoblasts, aorticopulmonary septum

Innervation

Anterior 2/3rd tongue general sensation = trigeminal V3, taste = chorda tympani (VII). Posterior 1/3rd general sensation and taste = IX

Syphilis: when does neurosyphilis occur?

Any stage of infection.

Myxomatous changes with pooling in media layer of large arteries. What is diagnosis?

Aortic aneurysm

Aorta: Traumatic Aortic Rupture: Where is most likely site?

Aortic isthmus. Why? Tethered to ligamentum arteriosum and relatively fixed/immobile.

COX 1 and 2: Function of each pathway? Where do ASA, NSAIDs and celecoxib work?

Arachidonic acid cleaved = 1. constitutive PGs and 2. Inducible PGs 1. Constitutive PGs = gastric mucosal protection, increased renal perfusion, platelet aggregation 2. Inducible PGs = increased renal perfusion, vasodilation, tissue repair + increased pain sensitivity ASA and NSAIDs block the constitutive PGs, while celecoxib blocks the inducible PGs.

Global payment: what is it?

Arrangement in which an insurer pays provider a single payment to cover all the expenses associated with an incident of care. This is most commonly done for elective surgeries, in which the global payment covers the surgery as well as any pre and post-op visits needed.

"Insecticide use presenting with garlic breath"

Arsenic poisoning

Glomerulus

Ascending limb impermeable to water, not descending.

Horseshoe kidney

Ascent limited by IMA

Congenital hypothyroidism: SSx? If untreated, what are these infants at high risk for?

Asymptomatic at birth (maternal thyroxine via placental transfer). After thyroxine wanes = slowing physical and mental activity (lethargy, poor feeding, constipation, hypotonia), accumulation of matrix substances cutaneously and internally resulting in non-pitting edema (puffy face), umbilical hernia, protruding tongue and large anterior fontanelle. High risk for irreversible intellectual disability

Chronic mesenteric ischemia: a. SSx b. Similar to what other pathologic process

Atherosclerosis of mesenteric arteries resulting in diminished blood flow to intestine after meals a. SSx: postprandial epigastric pain (intestinal angina) with associated food aversion/weight loss, does not respond to antacids, normal upper endoscopy b. Pathogenesis: similar to angina pectoris

Attributable risk

Attributable risk = a/(a+b) - c/(c+d)

Projection

Attributing one's own feelings to others

Schizophrenia (negative symptoms)

Atypical antipsychotics

Azurophilic peroxidase (+) granular inclusions in granulocytes and myeloblasts

Auer rods (AML, especially the promyelocytic M3 type)

Passive aggression

Avoiding conflict by expressing hostility covertly

Xanthine oxidase inhibitors: effect on azathioprine metabolism. Describe azathioprine use?

Azathioprine = purine analog, active metabolite MOA = undergoes non-enzymatic conversion to 6-MP (mercaptopurine), then converted to active metabolite 6-thioguanine (see below) = action: decrease de novo purine synthesis - Activated to active metabolite by HGPRT - Inhibited by thiopurine methyltransferase (TPMT) and xanthine oxidase XOIs increase azathioprine activity, resulting in increased conversion of azathioprine to its active metabolite

Fever, night sweats, weight loss

B symptoms (staging) of lymphoma

Hepatitis: B vs C histological differences

B: cytoplasm fills with hep B surface antigen - finely granular, dull eosinophilic (pink), ground glass appearance C: lymphoid aggregates within portal tracts and focal areas of macrovesicular steatosis

Obstruction of male urinary tract

BPH

Toe extension/fanning upon plantar scrape

Babinski sign (UMN lesion)

Splinter hemorrhages in fingernails

Bacterial endocarditis

Slow, progressive muscle weakness in boys

Becker muscular dystrophy (X-linked misense mutation in dystrophin; less severe than Duchenne)

Glomerulonephritis (adults)

Berger disease (IgA nephropathy)

Bleeding disorder with GpIb deficiency

Bernard-Soulier syndrome (defect in platelet adhesion to vWF)

Delirium

Best tx for behavioral (agitation) and psychotic manifestations of delirium = haloperidol.

Isoproterenol

Beta-1 and 2 receptor agonist = increase in FOC and decrease in TPR

Uterine tocolysis

Beta-2 agonist

Where does beta oxidation take place in the cell? Fatty acid synthesis?

Beta-oxidation (in mitochondria) Fatty acid synthesis (in cytoplasm)

Beta-oxidation: most common enzyme defect?

Beta-oxidation = fatty acid breakdown Most common ez defect: acyl CoA dehydrogenase

Hemoglobin A2 increased

Beta-thalassemia (minor or major)

Target cells

Beta-thalassemia (minor or major). RBCs have less hemoglobin in them and thus it is like you are taking air out of a ball, membrane blebs out somewhat creating target cell appearance.

Hair on end (Crew cut) appearance on xray

Beta-thalassemia, sickle cell disease (marrow expansion)

Adherence to meds in adolescence

Better tx adherence rates with close peers with complementary behavioral practices

What anticholesterol medication raises TGLs?

Bile acid-binding resins such as cholestyramine, colestipol and colesevalem.

Bohr-Haldane effect: Describe what is moving into and out of RBCs with each.

Bohr = CO2 and H being loaded into RBCs facilitates O2 unloading out of RBCs Haldane = loading of O2 facilitates the unloading of H and CO2

Neuroleptic malignant syndrome vs Serotonin Syndrome? What drugs cause these?

Both present with mental status change, hyperthermia, autonomic instability. NMS: diffuse, lead-pipe-like rigidity, bradyreflexia. Caused by antipsychotics. Serotonin syndrome: neuromuscular hyperactivity (shivering, clonus, hyperreflexia). Caused by: SSRI.

Hexagonal double pointed, needle-like crystals in bronchial secretions

Bronchial asthma (Charcot-Leyden crystals: eosinophilic granules)

Male child, recurrent infections, no mature B cells

Bruton disease (X linked agammaglobulinemia)

Sexually transmitted disease

C trochomatis (usually coinfected with N gonorrhoeae)

Abdominal pain, diarrhea, leukocytosis, recent antibiotic use

C. difficile infection

CHF: Pathogenesis? Why is the bodies response potentially deleterious?

CHF = structural or functional cardiac disorder that impairs cardiac filling or ejection of blood ultimately causing REDUCED CARDIAC OUTPUT. This reduced CO is detected initially as a drop in BP and therefore causes (with results): 1. SNS activation = increase HR, contractility, vasoconstriction 2. Stimulation of RAAS = vasoconstriction, increase extracellular fluid volume 3. Release of ADH = increase extracellular fluid volume Deleterious: - Increased afterload (d/t vasoconstriction) = impeded CO = extra fluid retention d/t poor renal perfusion - High RAAS = increased fluid retention = peripheral edema and pulmonary congestion - Deleterious cardiac remodeling occurs secondary to hemodynamic stress (increased preload and afterload) and long-term ang II, aldosterone and catecholamine exposure - All these effects add to a vicious circle.

WBCs that look smudged

CLL (almost always B cell)

Philadelphia chromosome t(9;22) (BCR-ABL)

CML (may sometimes be associated with ALL/AML)

Cardiac output

CO = rate of o2 consumption / (arterial o2 content - venous o2 content) CO = SV x HR

Most chemical carcinogens enter body in inactive state (as pro-carcinogens). How are these converted into active carcinogens?

CP450 oxidase (microsomal monooxygenase) system

McCune Albright syndrome

Café-au-lait macules (CALMs), fibrous dysplasia (osteolytic lesions of hip, pelvis), endocrine abnormalities.

Kidney stones

Calcium - radiopaque Struvite - ammonium, radiopaque (formed by urease (+) organisms such as Klebsiella, Proteus species, and S saprophyticus) Uric acid - radiolucent Cystine - radiolucent

Crystals seen with ethylene glycol ingestion

Calcium oxalate

Osteoporosis

Calcium/vitamin D supplementation (prophylaxis); bisphosphonates, PTH analogs, SERMs, calcitonin, denosumab (treatment)

Disarrayed granulosa cells arranged around collections of eosinophilic fluid

Call-Exner bodies (granulosa cell tumor of the ovary)

Painless jaundice

Cancer of the pancreatic head obstructing bile duct

CYP 450 Inducers

Carbamazepine, Phenobarbital, Phenytoin, Rifampin, Griseofulvin

Urea cycle

Carbamoyl phosphate synthetase I (CPS-I) (+) N-acetylglutamate

De novo pyrimidine synthesis

Carbamoyl phosphate synthetase II (CPS-II)

Cutaneous flushing, diarrhea, bronchospasm

Carcinoid syndrome (right sided cardiac valvular lesions, increased 5-HIAA)

Carcinoid tumor: How to differentiate b/w localized and metastatic?

Carcinoid tumor = enterochromaffin (endocrine) cells of intestinal mucosa that secrete vasoactive substances such as serotonin, bradykinins and PGs. When confined to intestine, secretory products metabolized by liver and no effect seen. If in liver and elsewhere, sx seen. SSx = flushing, watery diarrhea, bronchospasm etc. Labs = 5-HIAA in urine

Digoxin: side effects

Cardiac arrhythmias (brady, junctional escape beats d/t AV nodal block), non-specific GI (nausea, vomiting), neurologic (confusion, weakness), visual symptoms, elevated K. Classic = GI disturbances and visual changes

Helicobacter pylori: what type of ulcers does it cause? Why?

Cause of duodenal ulcers. Typically found in greatest concentration in prepyloric area of gastric antrum.

Anti-transglutaminase/anti-gliadin/ anti-endomysial antibodies

Celiac disease (diarrhea, weight loss)

Giant cell arteritis: Pathogenesis? What cell types are responsible? What is the most important molecular mediator?

Cell-mediated immune process involving CD4+ T cells, macrophages and multinucleated giant cells. Production of IL-6 seems to be important. Ab against IL-6 (tocilizumab) has proved effective.

Cerebellar tonsillar herniation

Chiari II malformation

hCG elevated

Choriocarcinoma, hydatidiform mole (occurs with and without embryo, and multiple pregnancy)

Small cell carcinoma

Chromogranin stain

Hypoxemia, polycythemia, hypercapnia

Chronic bronchitis (hyperplasia of mucous cells, "blue bloater")

Waxy casts with very low urine flow

Chronic end stage renal disease

Obesity hypoventilation syndrome: SSx, pathophysiologic changes

Chronic fatigue, dyspnea, difficulty concentrating, evidence of hypoventilation (PaCO2 > 45 mmHg while awake), hypoxemia with normal alveolar o2 gradient. Pathophys changes: increased CO2 production d/t increased mass and surface area, sleep-disordered breathing, reduced lung volumes and compliance

Thyroid-like appearance of kidney

Chronic pyelonephritis (usually due to recurrent infection)

HCG: Marker of?

Chroriocarcinoma, germ cell tumor

Facial muscle spasm upon tapping

Chvostek sign (hypocalcemia)

CYP 450 Inhibitors

Cimetidine, Ciprofloxacin, Erythromycin, Azole antifungals, Grapefruit juice, INH, Ritonavir (protease inhibitors)

Hepatocellular carcinoma

Cirrhotic liver (associated with hepatitis B and C and with alcoholism)

QT prolongation: which meds cause this?

Class IA and III antiarrhythmics, antipsychotics (eg. haloperidol), abx (macrolides and fluoroquinolones)

Antiarrhythmics: which cause QT prolongation?

Class IA: quinidine, procainamide, disopyramide & Class III: sotalol, ibutelide specifically, rarely amiodarone

Arrhythmia in damaged cardiac tissue

Class IB antiarrhythmic (lidocaine, mexiletine)

Dofetilide: class of antiarrhythmic and MOA

Class III (w/amiodarone, sotalol): block K and inhibit outward K currents during phase 3

"Antiarrhythmics with reverse use dependence"

Class III. Reverse use dependence = more prolongation of QRS/QT with lower HR.

Antiarrhythmics with use dependence

Class Ic. Use dependence = more prolongation of QRS/QT with higher HR. These agents are the slowest to dissociate from their sodium channels.

Gas gangrene #1 cause

Clostridium perfringens (Gram pos, anaerobe)

Stippled vaginal epithelial cells

Clue cells (Gardenella vaginalis)

Rib notching (inferior surface, on x rays)

Coarctation of the aorta

Streptococcus bovis bacteremia

Colon cancer

Apple core lesions on barium enema x-ray

Colorectal cancer (usually left sided)

Aortic regurgitation

Common causes in developed countries = aortic root dilatation or bicuspid aortic valve

Pediatrics: Trisomy 21: What is the most common congenital cardiac anomaly associated with DS? Auscultatory findings?

Complete AV canal defect: ASD (ostium primum type), VSD and common AV valve Auscultatory findings: AV valve regurg (holosystolic -- best heard at apex) and increased pulmonary venous return (mid-diastolic rumble)

Sarcoid granulomas: Composition? What substances do these produce?

Composition = non-caseating, CD4 + TH cells Produce ACE and active Vit D, resulting in hypercalcemia

Spontaneous Retroperitoneal Hematoma

Compresses psoas muscle

Smooth, moist, painless, wart like white lesions on genitals

Condylomata lata (secondary syphilis)

Iodide

Congenital goiter of hypothyroidism

Describe the work of breathing vs RR graph Describe what happens with increased elastic resistance. Describe what happens with increased airflow. Which diseases have increased elastic resistance? Which have increased airflow? What changes can these patients make to minimize the work of breathing.

Consider graph where minute ventilation (product of RR and TV) is the same as RR increases. At a high TV and low breathing frequency, most of the total work is d/t elastic work, energy required to maximally inflate the lung with each TV. When breathing frequency is high and TV is low, most of the work of breathing is frictional work because of the rapid breathing rate and thus friction of air against airways. Most of the elastic work here is small as TV has been reduced. There is an optimal point where sum of elastic and friction work is lowest. Overall: - Higher TVs = work of breathing d/t elastic work dominates - Higher RR = work of breathing d/t frictional work dominates Patients with pulmonary fibrosis, pulmonary edema, ARDS have stiff lungs d/t increased elastic resistance. These patients can minimize their work of breathing when RR is high and TV is low - shallow, rapid breaths. Patients with asthma, COPD have high airflow resistance. These patients can minimize their work of breathing when RR is low and TV is high - slow, deep breaths.

Case-Control study: what should control be?

Control subjects = estimation of exposure frequency among non-diseased general population. Example: - Community with increased incidence of AML - Concern about some households being exposed to chemical waste contributing to increased incidence of AML - Control = children who don't have AML (which is the outcome of interest) regardless of exposure status to chemical waste - Case group = children with AML

Infant with hypoglycemia, hepatomegaly

Cori disease (debranching enzyme deficiency) or Von Gierke disease (glucose 6 phosphatase deficiency, more severe)

Crohn disease

Corticosteroids, infliximab, azathioprine

Jaundice, palpable distended non-tender gallbladder

Courvoisier sign (distant malignany obstruction of biliary tree)

Intranuclear eosinophil droplet-like bodies

Cowdry type A bodies (HSV or VZV)

Rash on palms and soles

Coxsackie A, Secondary syphilis, Rocky mountain spotted fever

Vitamin A overdose effect on pregnancy

Craniofacial abnormalities, posterior fossa defects, auditory defects, abnormalities of the great vessels. Similar to those in DiGeorge syndrome.

Hypertrophic cardiomyopathy: Describe heart sound. Differentiate from AS.

Crescendo-Decrescendo systolic murmur at apex and left sternal border. Accentuates with standing. Note: AS = crescendo-decrescendo sytolic murmur loudest at heart base and radiates to carotids. Sx = syncope, angina and dypnea on exertion. Murmur decreases with standing (decreased preload).

Severe jaundice in neonate

Crigler-Najjar syndrome (congenital unconjugated hyperbilirubinemia)

Acute gastric ulcer associated with severe burns

Curling ulcer (greatly reduced plasma volume results in sloughing of gastric mucosa)

Desquamated epithelium cases in sputum

Curschmann spirals (bronchial asthma; can result in whorled mucus plugs)

Acute gastric ulcer associated with CNS injury

Cushing Ulcer (increased intracranial pressure stimulates vagal gastric sloughing of gastric mucosa)

Maintenance dose

D = (Cp x CL x tau) / F Cp = Target plasma concentration at steady state F = Bioavailability Tau = dosage interval (time between doses), if not administered continuously

High level of D-dimers

DVT, PE, DIC

Malignant hyperthermia

Dantrolene

Increased AFP in amniotic fluid/maternal serum

Dating error, anencephaly, spina bifida, (neural tube defects)

Left ventricular failure: what happens to compliance in lungs? Why?

Decreased compliance Increased backflow into lungs = increased hydrostatic pressure in pulmonary circulation = transudation of fluid from pulm capillary into interstitium = swelling of tissue = increased resistance to movement (decreased lung compliance)

Reaction formation: what is this?

Defense mechanism that involves replacing unacceptable feelings and impulses with their extreme opposites.

HLA-DR3

Diabetes mellitus type 1, SLE, Graves disease, Hashimoto thyroiditis, Addison disease

HLA-DR4

Diabetes mellitus type 1, rheumatoid arthritis, Addison disease

Kimmelstiel-Wilson Nodules

Diabetic Nephropathy - Progressive proteinuria, nephrotic syndrome, renal failure Presence of these indicates irreversible damage

Deep labored breathing/hyperventilation

Diabetic ketoacidosis (Kassmaul respiration)

Diastolic heart failure (isolated): a. What happens to EF, EDV and LV filling pressure (EDV pressure) b. Causes? Compare with systolic heart failure

Diastolic HF a. EF normal/near normal EDV normal/near normal LV filling pressure (LV ED pressure) increased b. Causes = decreased compliance of LV d/t ischemia or stiffness from amyloid deposition or LV wall hypertrophy d/t HTN Systolic HF a. EF decreased Chamber dilates = EDV increased, LV filling pressure (LV ED pressure) increased b. Causes = decrease in myocardial contractility

Loa loa and Wuchereria bancrofti (filariasis) tx

Diethylcarbamazine

Type of Non-Hodgkin lymphoma

Diffuse large B cell lymphoma

Wire loop glomerular capillary appearance on light microscopy

Diffuse proliferative glomerulonephritis (usually seen with lupus)

Anti-topoisomerase antibodies

Diffuse systemic scleroderma

Digoxin: MOA for use in atrial fibrillation with rapid ventricular response?

Digoxin indications: a. Heart failure (inhibition of Na/K ATPase results in increase Na in the cell = increased in intracellular Ca = increased contractility). b. Afib ventricular rate control: decreases AV nodal conduction by increasing PSNS vagal tone.

Hyperphenylalanemia + hyperprolactinemia. What is the deficiency?

Dihydrobiopterin reductase deficiency (BH4 converted to BH2 in Phe-Tyr and Tyr-DOPA rxns. Reductase reduces back to BH4 for re-use).

Coombs Test: Direct vs Indirect Describe each

Direct (= bound Abs) - Looking for Abs bound to RBCs - Use patient's blood/RBC mass and add Coomb's Reagent (abs against autoimmune abs) - Used to see if RBCs of neonate/fetus are being destroyed by abs created by mother Indirect (= unbound Abs) - Looking for unbound Abs that will react with RBCs - Use patient's serum and add reagent RBCs (that will be targeted by unbound Abs) - Add Coomb's Reagent (abs against autoimmune abs) - Used to see if mother contains abs (prenatally) that will react against fetus' RBCs

Multiple sclerosis

Disease-modifying therapies (eg. B-interferon, natalizumab); for acute flares, use IV steroids

Alcoholism

Disulfiram, acamprosate, naltrexone, supportive care

Chloramphenicol side effects

Dose-dependent reversible cytopenias and dose-independent irreversible aplastic anemia requiring bone marrow transplantation.

Chlamydia trachomatis

Doxycycline (+ ceftriaxone for gonorrhea coinfection), erythromycin eye drops (prophylaxis in infants)

Common cardinal veins

Drain into sinus venosus. In adult, this structure is the SVC.

Lymphatic drainage: a. Describe drainage of prostate gland

Drains to internal iliac LNs

Chest pain, pericardial effusion/friction rub, persistent fever following MI

Dressler syndrome (autoimmune mediated post MI fibrinous pericarditis, 2 weeks to several months after acute episode)

Antihistone antibodies

Drug induced SLE (eg. hydralazine, isoniazid, phenytoin, procainamide)

Echinocandins: Name the drugs that are part of this class. MOA?

Drugs = caspofungin and micafungin MOA: antifungals, inhibit synthesis of polysaccharide glucan (component of fungal cell wall)

Direct/selective arterial vasodilators: examples of these drugs? Indications? Side effects that limit their use long term?

Drugs = minoxidil and hydralazine Indications = used acutely for patients with severe high BP Side effects = drop in BP stimulates baroreceptors with resulting increase in SNS. Amongst other things, it activates RAAS resulting in Na and fluid retention leading to peripheral edema. Rarely used as monotherapy. Given with other drugs, ie. sympatholytics and diuretics.

Congenital conjugated hyperbilirubinema (black liver)

Dubin-Johnson syndrome (inability of hepatocytes to secrete conjugated bilirubin into bile)

Child uses arms to stand up from squat

Duchenne muscular dystrophy (Gowers sign)

Celiac disease

Duodenal biopsy shows villus flattening, intraepithelial lymphocyte infiltration

Effective renal plasma flow

ERPF = Upah x (V / Ppah) = Cpah Upah = urine concentration of PAH V = urine flow rate Ppah = plasma concentration of PAH Cpah = clearance of PAH

Renal calculations: What is effective renal plasma flow (ERPF)? How is it calculated?

ERPF is an estimate of RPF (amount of plasma that flows through kidneys per unit time as RPF is difficult to measure in practice). Use PAH, which is freely filtered and secreted. ERPF = (Urine [] PAH x Urine flow rate)/Plasma [] PAH ERPF = U.V/P

Late cyanotic shunt (uncorrected left to right becomes right to left)

Eisenmenger syndrome (caused by ASD, VSD, PDA; results in pulmonary hypertension/polycythemia)

S3 heart sound

Elevated ventricular filling pressure (eg. mitral regurgitation, HF), common in dilated ventricles

Clarithromycin

Embryotoxic

Chocolate cyst of ovary

Endometriosis (frequentyly involves both ovaries)

Lead poisoning: Which enzymes are affected? SSx of presentation?

Enzymes blocked in heme synthesis pathway = ferrochelatase and delta-aminolevulinic acid (ALA) dehydratase SSx: neurotoxicity (behavioral problems, developmental delay/regression), anemia.

Lucid interval after traumatic brain injury

Epidural hematoma (middle meningeal artery rupture)

Thumb sign on lateral neck x ray

Epiglottitis (Haemophilus influenzae)

Child with fever later develops red rash on face that spreads to body

Erythema infectiosum/fifth disease (slapped cheeks appearance caused by Parvovirus B19)

Poison Ivy: What does the rash look like?

Erythematous papules, vesicles or bullae that often form linear patterns. Intensely pruritic.

Secretin: effect on gastrin from gastrinomas?

Exogenous secretin stimulates gastrin release from gastrinomas. Normally secretin inhibits gastrin release physiologically. Therefore use this to distinguish from hypergastrinemia d/t ZES syndrome vs other causes (atrophic gastritis).

Elastin: what structural properties give elastin its rubber-like property?

Extensive cross-linking between elastin monomers by lysyl oxidase. Lysyl oxidase requires Cu and deaminates some lysine residues on of tropoelastin, facilitating formation of desmosine cross-links.

Bladder: is it peritoneal or extraperitoneal? Why do we care? What is pierced during suprapubic cystostomy?

Extraperitoneal. Only superior surface has peritoneum. During cystostomy, the tube pierces through abdominal layers, but not peritoneum.

Tetrahydrobiopterin (BH4) deficiency. Where is this enzyme needed? Resulting deficiency? SSx?

Ez required for synthesis of catecholamines, serotonin and DOPA specifically in the hydroxylation steps. Deficiency in catecholamines, serotonin and DOPA with buildup in phenylalanine. SSx = intellectual disability (hallmark), other sx = developmental delay, hypotonia, dystonia and seizures

Alcohol: characteristic findings in FAS

FAS: short palpebral fissures, smooth philtrum, thin vermillion border

Filtration fraction

FF = GFR / RPF GFR = glomerular filtration rate RPF = renal plasma flow

Renal calculations: How to calculate FF if given renal blood flow and GFR?

FF = GFR/RPF Note: RPF does not equal RBF. RPF is used instead as it takes out RBC mass, which cannot be filtered. RPF = RBF * (1-Hct) Now you can calculate FF.

DS features: face, ears, tongue, eyes, neck, hands, feet

Face: flat facial profile Neck: short w/excess skin Ears: small, low set Tongue: protruding furrowed tongue Eyes: Brushfield spots, upslanting palpebral fissures Feet: sandal toe deformity (increased space bw toe 1 and 2) Hands: sgl palmar crease (Simian crease), hypoplastic incurved 5th digit

Vitamin A, Isotretinoin

Facial: Cleft palate, small or no ears, micrognathia, depressed nasal bridge, hypertelorism Cardiac abnormalities: transposition of great arteries CNS: hydrocephalus, microcephaly

Alcohol

Facies: microcephaly, smooth philtrum, thin vermillion border, shortened palpebral fissures CNS deficits: cognitive and developmental delay

Tetralogy of Fallot: Describe failure that occurs resulting in this anomaly?

Failure = deviation of the infundibular septum Note, infundibular septum = membranous portion of interventricular septum. This is where three parts (aorticopulmonary septum, muscular growth of intraventricular septum and endocardial cushions need to meet to make the complete interventricular septum).

HAV transmission: transmission? Where are outbreaks seen?

Fecal-Oral transmission common in areas with overcrowding and poor sanitation. Outbreaks frequently seen from contaminated water or food and raw / steamed shellfish are common culprits in US

Mammary gland, blue domed cyst

Fibrocystic change of the breast

Breast mass

Fibrocystic change, carcinoma (in postmemopausal women)

Niacin: SEs

Flushing, hyperglycemia, hepatotoxicity, decreases renal excretion of uric acid leading to increased risk for acute gouty arthritis.

Prostate adenocarcinoma

Flutamide

Nephrotic syndrome (Adults)

Focal segmental glomerulosclerosis

Vitamin deficiency (US)

Folate (pregnant women are at high risk; body stores only 3-4 month supply; prevents neural tube defects)

t(14;18)

Follicular lymphoma (BCL-2 activation, anti-apoptotic oncogene)

Benzodiazepines

For patients with impaired hepatic metabolism, use the LOT benzos = lorazepam, oxazepam, temazepam

What are internal ribosome entry sites (IRES)?

For translation, eukaryotic initiation factors recognize the 5' cap on mRNA. During apoptosis, caspases result in eIF degradation resulting in interruption of translation. Proteins necessary for apoptosis are still necessary, so they use an alternative method for translation. IRES attract ribosomes to mRNA and allow translation to begin in middle of mRNA sites. These are located in 5' untranslated region.

PAH: How is it handled in the kidney?

Freely filtered from blood in glomerular capillaries and enters into tubular fluid Secreted from blood into tubular fluid by proximal tubular cells through carrier-mediated process. This can be saturated at high blood concentrations Note: because it is freely filtered and secreted, it can be used to estimate renal plasma flow.

Warfarin reversal

Fresh frozen plasma (acute), vitamin K (non-acute)

Gluconeogenesis

Fructose-1,6-bisphosphatase (+) ATP, acetyl-CoA (-) AMP, Fructose-2,6-BP

Kinesin

Function = anterograde transport of NT-containing secretory vesicles toward synaptic terminals

Rough endoplasmic reticulum

Function = synthesis of secretory proteins, integral membrane proteins of nucleus and cell membrane, proteins within ER, Golgi and lysosomes

Renal calculations: How to calculate GFR from Inulin's information?

GFR = (Urine [] inulin x Urine flow rate) / Plasma [] inulin GFR = U.V/P Note: inulin is freely filtered, not reabsorbed or secreted. Don't get confused with PAH, which is used to estimate RPF in a calculation that is called ERPF.

Glomerular filtration rate

GFR = Uinulin x (V/Pinulin) = Cinulin GFR = Kf [(Pgc - Pbs) - (pi gc - pi bs)] Uinulin = urine concentration of inulin V = urine flow rate (ml/min) Pinulin = plasma concentration of inulin Cinulin = clearance of inulin Kf = filtration constant (capillary permeability) Pgc = glomerular capillary hydrostatic pressure Pbs = Bowman space hydrostatic pressure pi gc = glomerular capillary oncotic pressure pi bs = Bowman space oncotic pressure

Ureteral constriction or obstruction

GFR decreases and FF decreases

Insulin: What glut channels does it act on? Which tissues are insulin-dependent? Which glut channels do not respond to it? Therefore which tissues are insulin-independent?

GLUT-4: insulin-sensitive. Expressed on skeletal muscle cells and adipocytes. GLUT-1, 2, 3 and 5: insulin-insensitive - 1: RBCs, BBB - 2: hepatocytes, pancreatic Beta cells, renal tubules and small intestinal mucosa - 3: placental and neuronal glucose transport - 5: fructose transporter found in spermatocytes and GI tract

Huntington's disease: Is it due to a gain-of-function or loss-of-function? Explain disease pathogenesis/molecular nature?

Gain-of-function AD dz with increase in CAG repeats. Expansion of polyglutamine region results in gain-of-function that leads to pathological interaction with other proteins, including various transcription factors. Silencing (transcriptional repression) is one of the mechanisms by which mutated huntingtin protein is thought to cause disease. Abnormal huntingtin causes increased histone deacetylation, silencing the genes necessary for neuronal survival. One of the tx being investigated includes histone deacetylase inhibitors that upregulate survival genes.

Neisseria meningitidis: how does it gain access to CNS?

Gains access to CNS: pharynx => blood => choroid plexus => meninges

Wilson's Disease Neuropsych Sx

Gait disturbance, dysarthria, depression, personality changes. Almost all patients with these manifestations will have Kayser-Fleischer rings.

Pancreatitis (acute)

Gallstones, alcohol

CEA (carcinoembryonic antigen): Marker of?

Gastrointestinal (eg. Colorectal)

Hereditary harmless jaundice

Gilbert syndrome (benign congenital unconjugated hyperbilirubinemia)

Panic disorder

Give benzo for rapid relief. SSRI/SNRI for longer term management.

HMP shunt

Glucose-6-phosphate dehydrogenase (G6PD) (+) NADP+ (-) NADPH

De novo purine synthesis

Glutamine-PRPP amidotransferase (-) AMP, IMP, GMP

"Second generation sulfonylureas Which are long-acting? Why is this bad?"

Glyburide, glipizide and glimepiride. Glyburide and glimepiride are long-acting and has highest incidence of hypoglycemia in glucose-independent manner.

Glycogenolysis

Glycogen phosphorylase (+) AMP, epinephrine, glucagon (-) insulin, ATP, G6P

Glycogen synthesis

Glycogen synthase (+) G6P, insulin, cortisol (-) epinephrine, glucagon

Staphylococcus epidermidis: morphology growth? Who is susceptible?

Gram pos, Coag negative, novobiocin sensitive, seen in: immunocompromised, prosthetics, Ivs

Necrotizing vasculitis (lungs) and necrotizing glomerulonephritis

Granulomatosis with polyangiitis (Wegener; PR3-ANCA/c-ANCA) and Goodpasture syndrome (anti-basement membrane antibodies)

Resting membrane potential: a. How does resting membrane potential line up with equilibrium potential for each individual ion? b. Correspond this information to conductance capacity for each ion?

Greater permeability of a membrane for an ion, closer to that ions equilibrium potential the RMP will be. Example: RMP of -70 mV (like in most human cells). Equilibrium potential for K = -80. Equilibrium potential for Na + = +60. This membrane has higher conductance for K and smaller conductance for Na. Therefore closer to equilibrium potential for K.

Rapidly progressive limb weakness that ascends following GI/Upper respiratory infection

Guillain-Barre syndrome (acute inflammatory demyelinating polyradiculopathy subtype)

Bacteria associated with gastritis, peptic ulcer disease, and gastric malignancies (eg. adenocarcinoma, MALToma)

H. pylori

Primary liver cancer

HCC (chronic hepatitis, cirrhosis, hemochromatosis, alpha1-antitrypsin deficiency, Wilson disease)

Hypertrophic cardiomyopathy: What medications should be avoided and why?

HCM = LVOT obstruction. Worsens with decreased LV volume caused by reduction in preload and afterload. Don't give meds that decrease preload and afterload. This includes nitroglycerin (venodilator) and DHP CCBs (decrease systemic vascular resistance and therefore afterload).

Most common cause of sudden cardiac death in athletes age < 35? What is the histologic findings in this condition? Etiology?

HCM: massive myocyte hypertrophy and myofiber disarray Etiology: AD genetic disorder caused by mutation in one of several sarcomere genes.

Immediate anticoagulation

Heparin

Increased osmotic fragility on acidified glycerol lysis test = what diagnosis?

Hereditary spherocytosis: findings = hemolytic anemia, jaundice, splenomegaly

Airway resistance in LRT: where is it the highest? Why? Lowest? Why?

Highest in medium-sized bronchi d/t highly turbulent airflow. Lowest in terminal bronchioles

Ptosis, miosis, anhydrosis

Horner Syndrome (sympathetic chain lesion)

Basophilic nuclear remnants in RBCs

Howell-Jolly bodies (due to splenectomy or nonfunctional spleen)

Recurrent cold (noninflammed) abscesses, unusual eczema, high serum IgE

Hyper IgE syndrome (Job syndrome: neutrophil chemotaxis abnormality)

ENAc diuretic: SEs

Hyperkalemia (K-sparing)

Aldosterone antagonist diuretic: SEs

Hyperkalemia, gynecomastia, antiandrogen effects

Osmotic diuretic: SEs

Hypernatremia, pulmonary edema

Secondary hyperparathyroidism

Hypocalcemia of chronic kidney disease

What happens to Na levels with DKA? Why?

Hyponatremia Osmotic gradient created by high BGL results in water movement from ICF to ECF (dilutes Na). Also, hyperglycemia induces diuresis, which isn't just loss of free water, but also of Na.

Chronic hepatitis B or C

IFN-alpha (HBV and HCV); ribavirin, simeprevir, sofosbuvir (HCV)

Cavernous sinus: contents Compare to contents of superior and inferior orbital fissures

III, IV, VI and V (V1 and V2) Superior: III, IV, V1 and VI Inferior: V2, infraorbital vessel and branches from sphenopalatine ganglion

Superior orbital fissure: contents

III, V1 branches (including nasociliary = sensory of cornea), IV, VI and superior ophthalmic vein

Isoniazid: How do mycobacterium become resistant?

INH's MOA = inhibition of mycolic acid synthesis enzyme. Needs processing by mycobacterial catalase peroxidase to become activated. Resistance accomplished by non-expression of catalase-peroxidase enzyme OR genetic modification of INH binding site on mycolic acid synthesis enzyme.

CYP 450 Inhibitors

INH, cimetidine, macrolides, azoles, grapefruit juice

Kawasaki disease

IVIG, high dose aspirin

Cushing syndrome

Iatrogenic- from corticosteroid therapy Adrenocortical adenoma - secretes excess cortisol ACTH secreting pituitary adenoma - Cushing disease Paraneoplastic - due to ACTH secretion by tumors

Antiplatelet antibodies

Idiopathic thrombocytopenic purpura

Compare and contrast IgA nephropathy, Henoch-Schonlein Purpura and PSGN in terms of a. What it is? b. Presentation? c. Findings? 2. How to tell difference between IgA nephropathy and PSGN?

IgA nephropathy a. Nephritic syndrome - IgA immune complex deposition in mesangium of glomeruli (most common nephropathy worldwide) b. Presents during childhood as episodic gross or microscopic hematuria with RBC casts usually following mucosal infections (eg. gastroenteritis or URI). Why? IgA production is increased during infection. Slow progression to renal failure c. RBC casts LM - mesangial proliferation EM - mesangial immune complex deposits IF - IgA deposits in mesangium HSP a. Vasculitis d/t IgA immune complex deposition (most common vasculitis in children) b. Triad (below) following URTI often 1. Skin: palpable purpura on buttocks/legs 2. Arthralgias 3. GI: pain, melena, multiple lesions Can occur w/hematuria (IgA nephropathy component). Dz self-limited, but may recur. c. Same as IgA nephropathy PSGN a. Nephritic syndrome arises after Group A beta-hemolytic strep infection of skin (impetigo) or pharynx. It is type III HS rxn. Not URI or GI infection as in HSP or IgA nephropathy. b. 2-3 weeks after infection w/hematuria, oliguria, HTN and periorbital edema. Usually seen in children, may occur in adults. c. RBC casts, increase anti-DNase B titers and decreased complement levels LM - glomeruli enlarged and hypercellular IF - starry sky, granular appearance (lumpy - bumpy) d/t IgG, IgM and C3 deposition along GBM and mesangium EM - subepithelial immune complex humps 2. IgA nephropathy, the kidney involvement overlaps or occurs very shortly after the infection. PSGN happens 2-3 weeks after.

Estrogen: effect on thyroxine-binding globulin and T3/T4 levels?

Increases thyroxine-binding globulin This leads to increase in total thyroid hormone levels (total T4/3), but feedback control remains normal (TSH normal) and free T3 and T4 remain the same. Note Michael: T3 is most active.

Methimazole: Indication, MOA?

Indication = hyperthyroidism MOA = inhibition of thyroid peroxidase (ez responsible for both iodine organification and coupling of iodotyrosinases)

Thiazolidenediones: MOA

Indication: Type 2 DM Activates PPAR-gamma = overall increase in insulin sensitivity. How: increase in GLUT-4 translocation to membrane, increase in adiponectin production (increase in responsiveness to insulin and uptake of FAs for beta-oxidation). Other responses: decrease leptin production, decrease TNF-alpha.

Foscarnet: a. Indications? b. SEs?

Indications = ganciclovir-resistant CMV SEs = chelator of Ca = hypocalcemia and nephrotoxic leading to hypomagnesemia. These electrolyte abnormalities can lead to seizures.

Relationship between afterload and contraction velocity

Indirectly proportionate As afterload decreases, contraction velocity increases

Uremia: effect on bleeding

Induces qualitative bleeding disorder with = increased bleeding time w/nml PTT, PT and platelet count

What part of renal, urogenital system is injured in pelvic fracture? SSx?

Injury to posterior urethra. Anterior urethra damage in straddle injuries. SSx: full bladder sensation, high-riding boggy prostate, blood in urethral meatus. Foley cath contraindicated here.

Cells adhere to the ECM via what?

Integrin-mediated binding to fibronectin. Integrin attaches to the cell via actin (intracellularly) and then EC to fibronectin, which is linked to collagen. Differential expression of integrin subtypes affects adhesion properties and has been found to correlate with malignant behavior in a number of tumors.

Edwards syndrome: features

Intellectual disability, rocker-bottom feet, MICROGNATHIA, low-set ears, CLENCHED HANDS, PROMINENT OCCIPUT, congenital heart disease, OMPHALOCELE, HORSE-SHOE KIDNEY

Patau syndrome: features

Intellectual disability, rocker-bottom feet, MICROOPHTHALMIA, MICROCEPHALY, cleft liP/Palate, holoProsencephaly, Polydactyly, congenital heart disease, CYSTIC KIDNEYS

Epistasis

Interactions between multiples genes combine to create a new phenotype or they mask/modify the phenotype of one of the genes. Example: sickle cell anemia pt with mutation causing persistence of high fetal Hb levels often have less severe clinical course.

Shingles: histologic finding of rash

Intranuclear inclusions in keratinocytes and multinucleated giant cells (pos Tzanck smear) on light microscopy

Cretinism

Iodine deficit/congenital hypothyroidism

Hypochromic, microcytic anemia

Iron deficiency anemia, lead poisoning, thalassemia (fetal hemoglobin sometimes present)

Painless erythematous lesions on palms and soles

Janeway lesions (infective endocarditis, septic emboli/microabscesses)

Fever, chills, headache, myalgia following antibiotic treatment for syphilis

Jarisch-Herscheimer reaction (rapid lysis of spirochetes results in endotoxin release)

Rationalizaton

Justifying behavior to avoid truths

EGFR: what intracellular pathway does it use?

K-RAS (GTP-binding protein) that regulates cell division.

Diuretics: Which are K-sparing? Where do they work?

K-sparing = aldosterone receptor antagonists (spironolactone, eplerenone) and epithelial sodium channel antagonists (amiloride and triamterene) Both work at late DCT and collecting duct. Note: board prep states both late DCT and collecting duct, but I believe collecting duct is best choice.

Neuron migration failure

Kallman syndrome (hypogonadotropic hypogonadism and anosmia)

Dark purple skin/mouth nodules in a patient with AIDS

Kaposi sarcoma, associated with HHV-8

Situs inversus, chronic sinusitis, bronchiectasis, infertility

Kartagener syndrome (dynein arm defect affecting cilia)

Cervical lymphadenopathy, desquamating rash, coronary aneurysms, red conjuntivae and tongue, hand-foot changes

Kawasaki disease (Treat with IVIG and aspirin)

Sulfonamides

Kernicterus

Digoxin: cleared where?

Kidney

Hyperphagia, hypersexuality, hyperorality, hyperdocility

Kluver-Bucy syndrome (bilateral amygdala lesion)

Koilocyte: what is it indicative of? What does it look like?

Koilocyte = sign of HPV infection. Looks like: immature squamous cell with dense, irregularly staining cytoplasm and perinuclear clearing resulting in a halo. It also has enlarged pyknotic nucleus where chromatin has condensed as part of apoptosis process giving it a raisinoid appearance.

Dysplastic squamous cervical cells with raisinoid nuclei and hyperchromasia

Koilocytes (HPV: predisposes to cervical cancer)

Small, irregular red spots on buccal/lingual mucosa with blue-white centers

Koplik spots (measles [rubeola] virus)

Bilateral ovarian metastases from gastric carcinoma

Krukenburg tumor (mucin-secreting signet ring cells)

Breathing Patterns: Kussmaul, Cheyne-Stokes and OSA. Causes?

Kussmaul: deep-labored breathing with = TV throughout. Causes = KUSSMAUL (metabolic acidosis) = ketoacidosis, uremia, sepsis, salicylates, methanol, aldehydes, u = nothing, lactic acidosis Cheyne-Stokes: low to high to low TVs then apneic spell - repeat. Causes = advanced CHF, neurological dz (CVA, brain tumor, TBI) OSA: TVs heights constant mostly, then apneic spell, then repeat.

Measure of fetal lung maturity

L/S ratio = Lecithin (aka phosphatidylcholine) / sphingomyelin ratio >= 2 = inadequate surfactant production L increases after 30 weeks gestation. S remains approximately constant.

Ilioinguinal nerve: a. Sensation to what areas:

L1 Accompanies spermatic cord through superficial inguinal ring. Sensation to upper and medial thighs and parts of external genitalia

Obturator nerve: a. Sensation to what areas b. Motor to what?

L2-4 Sensation: skin of medial thigh Motor: adductor muscles of LE

Loading dose

LD = (Cp x Vd) / F Cp = Target plasma concentration at steady state F = Bioavailability

Basophilic stippling of RBCs

Lead poisoning or sideroblastic anemia

ACEi: Why are these bad in patients with bilateral renal artery stenosis?

Leads to severe reduction in GFR. Why? Ang II acts to vasoconstrict efferent arteriole leading to increased GFR and FF (decreased RBF) when low BP detected. ACEi blocks this response = low GFR = acute renal failure. Same thing with ARBs.

Eisenmenger Syndrome

Left-to-right shunt (VSD, ASD, PDA) reverse right-to-left over time. Pathognomonic: differential clubbing and cyanosis without BP or pulse discrepancy are pathognomonic for a large PDA complicated by Eisenmenger.

Tumor in women

Leiomyoma (estrogen dependent, non precancerous)

Gout, intellectual disability, self mutilating behavior in a boy

Lesch-Nyhan syndrome (HGPRT deficiency, X-linked Recessive)

Visual Tract Lesion

Lesion in optic tract = contralateral (to lesion) homonymous hemianopia and RAPD in contralateral eye.

Rescue agent for methotrexate use as it kills bone marrow

Leucovorin

Tonic-clonic seizures

Levetiracetam, phenytoin, valproate, carbamazepine

Eosinophilic cytoplasmic inclusion in neuron

Lewy body (Parkinson disease and Lewy body dementia)

Pruritic, purple, polygonal planar papules and plaques (6 P's)

Lichen planus

Nephrotic syndrome: why is it a hypercoagulable state?

Loss of anticoagulant factors, esp. antithrombin III.

Antipsychotics: a. Name the first generation antipsychotics according to potency (low and high). b. What are the side effects of the low potency? High potency?

Low potency = chlorpromazine and thioridazine SEs = 1. Sedation (anti-histaminergic) 2. Anticholinergic: "dry" 3. Orthostatic hypotension (alpha-1 blockade) High potency = haloperidol and fluphenazine SEs = extrapyramidal sx (mnemonic = Potency = extraPyramidal) = acute dystonia, akathisia, parkinsonism

Mean arterial pressure

MAP = CO x TPR MAP = 2/3 DBP + 1/3 SBP

Hereditary spherocytosis: What are the MCV and MCHC values in this disease?

MCV: normal to low MCHC: spherocytes are smaller (mild dehydration of RBC) and therefore have an increased MCHC.

Pancreatic, pituitary, parathyroid tumors

MEN 1 (autosomal dominant)

Thyroid and parathyroid tumors, pheochromocytoma

MEN 2A (autosomal dominant RET mutation)

Thryoid tumors, pheochromocytoma, ganglioneuromatosis

MEN 2B (autosomal dominany RET mutaiton)

"Multiple endocrine neoplasia: Type with marfinoid habitus?"

MEN2B

Adenosine: MOA?

MOA = A1 receptor, acts on phase 4 of cardiac pacemaker cells opening K channels allowing for K to efflux from the cell prolonging phase 4. Also blocks Ca2+ L-type channels. Ultimately: sinus rate slowed with increase in AV conduction delay.

Fenoldapam: MOA: Indications:

MOA = D1 agonist = arteriolar dilation, increased renal perfusion and promotion of diuresis and natriuresis Indications: IV to lower BP in HTNsive emergency esp in patients with renal insufficiency

Zidovudine (aka AZT). MOA

MOA = NRTI = competitively binds to reverse transcriptase and is incorporated into viral genome as a thymidine analog. AZT has an azido group instead of a hydroxyl group on the free 3' end, therefore preventing DNA chain elongation.

D-Penicillamine

MOA = chelation to remove excess loosely bound serum Cu

Succinylcholine: MOA? SEs?

MOA = depolarizing paralytic agent SEs: hyperkalemia, arrhythmias. Especially at risk for this are patients with burns, myopathies, crush injuries, denervation injuries as they upregulate nAChR. Also causes malignant hyperthermia, brady from SNS effects and tachy from SNS effects. In patients mentioned above, use rocuronium or vecuronium instead. These are non-depolarizing agents.

Benzodiazepines

MOA = increase frequency of opening of GABA-A Cl channels, not duration.

Acyclovir

MOA = this drug is nucleoside analog incorporated into new viral DNA leading to termination of DNA synthesis.

Describe MOA, indications for the following meds: - Acyclovir - Famciclovir - Valacyclovir - Ganciclovir - Valganciclovir - Foscarnet - Cidofovir Note which require activation via viral and host kinases.

MOA: - Cy(i)clovir drugs are viral-dependent nucleosides meaning they rely on first viral kinase and then host kinase. Once they have passed this process, they inhibit DNA pol and cause chain termination. Famciclovir is a prodrug that is first metabolized to penciclovir and then same process as above. - Val- drugs have increased oral bioavailability. - Foscarnet inhibits viral DNA pol without requires activation by viral kinases. - Fovir- drugs (incl. tenofovir) requires host cell kinase (not viral kinase). Indications: HSV: use acyclovir or valacyclovir. If resistant, use Foscarnet or cidofovir. Note: famciclovir can be used for HSV infections. CMV: use ganciclovir or valganciclovir. If resistant, use Foscarnet or cidofovir. VZV: famciclovir (preferential for VZV / zoster), can use other acyclovir or valacyclovir too (but more for HSV). If resistant (per UW), use foscarnet or cidofovir.

Dobutamine: MOA, indication

MOA: Beta-1 (heart) primarily: inotropic > chronotropic. Minimal beta-2 effect = mild vasodilation, weak effect on BP overall Indication: stress testing, refractory heart failure associated with severe LV failure and cardiogenic shock (does increase myocardial O2 activity, but drawback accepted given improvement in CO and end-organ perfusion).

Atropine: MOA, indication, toxicity

MOA: Muscarinic antagonist Indication: tx bradycardia and for ophthalmic applications Toxicity = hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter (disoriented) = increased temp (less sweating), decreased secretions, flushed skin/dry, mydriasis and cycloplegia (loss of accommodation d/t paralysis of ciliary muscles), disorientation (disruption of ACh, much like Alzheimer's), constipation, urinary retention ** Can cause acute angle-closure glaucoma in elderly (d/t mydriasis)

Methotrexate: MOA, what builds up in the cell when using MTX

MTX = folate antagonists that inhibits DHFR reductase. It is structurally similar to folic acid. Normally, Folic acid converted to DHF and then to THF using DHFR reductase. This is blocked and DNA, RNA and some amino acid synthesis pathways don't occur. When folic acid enters cell, it is kept in cell via polyglutamation. Therefore, when MTX is used, DHF polyglutamate builds up.

Prostacyclin: Where is it made? Function? Which molecule does it's effect directly oppose?

Made by: vascular endothelial cells Function: vasodilates, inhibits platelet aggregation and increases vascular permeability. Directly opposes effect of thromboxin A2 to ensure vascular homeostasis.

Severe RLQ pain with deep tenderness

McBurneys sign (acute appendicitis)

Cafe-au-lait spots (unilateral), polyostotic fibrous dysplasia, precocious puberty, multiple endocrine abnormalities

McCune-Albright syndrome (mosiac G-protein signaling mutation)

Tram-track appearance of capillary loops of glomerular basement membranes on light microscopy

Membraneoproliferative glomerulonephritis

DDx for bilious emesis in newborn

Midgut volvulus, intestinal stenosis and atresia

Medical abortion

Mifepristone

HCG

Mimics LH surge and used in infertility tx

Nephrotic syndrome (Kids)

Minimal change disease

Podocyte fusion or effacement on electron microscopy

Minimal change disease (child with nephrotic syndrome)

Hemiglobinopathy: What type of mutation results in Hb S and Hb C? Describe banding pattern on electrophoresis.

Missense mutation Hb S: Glut (-vely charged) -> Val (non-polar) Hb C: Glut -> Lys (polar +vely charged) Speed of movement from -ve to +ve = Hb A > Hb S > Hb C

Heme synthesis: What organelle is required?

Mitochondria

HMG-CoA Lyase: function

Mitochondrial enzyme necessary for ketogenesis Also responsible for metabolism of the ketogenic AA leucine.

Heart valve in bacterial endocarditis

Mitral > aortic (rheumatic fever), tricuspid (IV drug abuse)

Holosystolic murmur best heard at apex and radiates to axilla

Mitral regurgitation

Opening snap

Mitral stenosis

Heart murmur, congenital

Mitral valve prolapse

Retroperitoneal organs

Mnemonic = SAD PUCKER Suprarenal glands (adrenals) Aorta & IVC Duodenum* (except 1st part) Pancreas* (head and body) Ureters and bladder Colon* (ascending and descending) Kidneys Esophagus Rectum (mid-distal) *secondarily retroperitoneal: developed intraperitoneal and migrated retro.

Foramen rotundum: contents

Mnemonic = foramen rotwodum = V2

Isoproterenol: MOA

Mnemonic: Iso-Bro (beta1=beta-2 agonist)

Abx to avoid in pregnancy

Mnemonic: SAFe Children Take Really Good Care Sulfonamides Aminoglycosides Fluoroquinolones Clarithromycin Tetracyclines Ribavirin Griseofulvin Chloramphenicol

Branchial/Pharyngeal Arch Derivatives and Innervation

Mnemonic: when at the restaurant of the golden arches, children tend to first CHEW (1), then SMILE (2), then SWALLOW STYLishly (3), or SIMPLY SWALLOW (4), and then SPEAK (6). 1: CHEW = Mastication = M derivatives = Meckel cartilage, Mandible, Malleus, incus, spheno-Mandibular ligament, Muscles of Mastication (temporalis, masseter, lateral and medial pterygoids), Mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini Innervation = CN V2 and V3. Just remember mastication and that trigeminal does that. 2: SMILE = S derivatives = Reichert cartilage, Stapes, Styloid process, lesser horn of hyoid, Stylohyoid ligament, Stapedius, Stylohyoid, platySma, posterior belly of digastric Innervation = VII. Just remember smiling is controlled by VII. 3: SWALLOW STYLishly = Stylo- words = greater horn of hyoid, STYLOPHARYNGEUS Innervation = IX (glossoPHARYNGEUS). Just remember styloPHARYNGEUS innervated by glossoPHARYNGEUS 4. SIMPLY SWALLOW = thyroid cartilage, epiglottic cartilage, most pharyngeal constrictors, cricothyroid muscles, levator veli palatini Innervation = X. Just remember vagus (superior laryngeal branch) for SWALLOWING. 6: SPEAK = cricoid, arytenoids, corniculate and cuneiform cartilages, all intrinsic muscles of larynx except cricothyroid Innervation = X. Just remember vagus (recurrent laryngeal branch) for SPEAKING.

Retinal artery occlusion: most common cause

Most common cause = thromboembolic occlusion of atherosclerosis in the internal carotid

S.aureus: most common site of colonization?

Most common site of colonization = anterior nares including MSSA and MRSA

Fibrates

Most effective agents for tx of hypertriglyceridemia

Nystagmus, intention tremor, scanning speech, bilateral internuclear ophthalmoplegia

Multiple sclerosis

Osler-Weber Rendu (aka hereditary hemorrhagic telangiectasias)

Multiple telangiectasias of skin and mucosa. Presentation classically = recurrent epistaxis or GI bleeding (melena)

Pancreas a. What G-protein receptors does it have? b. What is the effect of activating these receptors on insulin release?

Muscarinic M3 = Gq = increase insulin secretion Glucagon = Gs and Gq = increase insulin secretion **pay attention here. Glucagon induces release of glucose into serum via glycogenolysis and gluconeogenesis. Some insulin must be around for cells to be able to use glucose. Beta-2, GLP-1 and H2 = Gs = increase insulin secretion Alpha-2 and somatostatin D = Gi = decrease insulin secretion

Calf pseudohypertrophy

Muscular dystrophy (most commonly Duchenne, due to X-Linked recessive frameshift mutation of dystrophin gene)

Defect in Beta-thal

Mutations result in defective transcription, processing and translation of beta-globin mRNA

Highest oxygen extraction

Myocardium oxygen extraction exceeds that of any other tissue or organ in body.

HIV drugs: NNRTIs vs NRTIs

NNRTIs = non-nucleoside reverse transcriptase inhibitors. These act in the cytoplasm without first being phosphorylated. Drugs = nevirapine and efavirenz NRTIs = nucleoside reverse transcriptase inhibitors. These must first be phosphorylated by cellular thymidine kinase. Drugs = zidovudine and emtricitabine

Number needed to treat

NNT = 1/absolute risk reduction

NNH: equation

NNT = 1/attributable risk Attributable risk = adverse event rate in tx group - adverse event rate in placebo/other group

How is calcium removed following contraction within cardiac myocyte?

Na/Ca exchanger (NCX) and SR Ca-ATPase pump (SERCA) Not CALMODULIN, which functions in SM cells that don't have troponin.

Eosinophilic inclusion bodies in cytoplasm of hippocampal and cerebellar neurons

Negri bodies of rabies

Periorbital and/or peripheral edema, proteinuria (> 3.5g/day), hypoalbuminemia, hypercholesterolemia

Nephrotic syndrome

Small cell carcinoma

Neuroendocrine origin, therefore stain for neural cell adhesion molecule (NCAM aka CD 56)

Protein aggregates in neurons from hyperphosphorylation of tau protein

Neurofibrillary tangles (Alzheimer disease) and Pick bodies (Pick disease)

Cafe-au-lait spots, Lisch nodules (iris hamartomas), cutaneous neurofibromas, pheochromocytomas, optic gliomas

Neurofibromatosis type 1

Bilateral acoustic schwannomas

Neurofibromatosis type 2

Pupil accomodates but doesn't react

Neurosyphilis (Argyll Robertson pupil)

MI: histologic change immediately after MI?

No change/minimal. Earliest signs of coagulative necrosis = 4 hrs after onset. Change = early coag necrosis, edema, hemorrhage and wavy fibers

Highest risk factors (coronary heart disease equivalents) for coronary heart dz

Non-coronary atherosclerotic dz, DM and CKD

Polyps: Which microscopically are non-neoplastic? Which are neoplastic (have greatest risk for progressing from adenoma to carcinoma)?

Non-neoplastic: hyperplastic, inflammatory (UC & Crohn's), submucosal (lipomas and lymphoid aggregates), mucosal polyps (folds of colonic mucosa) Neoplastic: serrated, adenomatous (villous > tubular / mnemonic = villain), size > 2 cm, sessile growth (no on pedunculated stalk)

Digitoxin toxicity SSx

Non-specific GI sx, neurologic (fatigue, confusion, weakness), changes in color vision (rarer finding), life-threatening arrhythmias

Propanolol: MOA

Non-specific beta antagonist (beta-1=beta-2) AMEBA = specific beta-1 antagonist

Pringle maneuver: what is it?

Occlusion of the hepatoduodenal ligament containing the hepatic artery, CBD and portal vein to distinguish source of liver injury bleed. If this is occluded and bleeding persists, it is most likely damage to IVC or hepatic veins.

Medication for carcinoid syndrome

Octreotide MOA: synthetic analog of somatostatin with a longer half-life. Inhibits secretion of many of the hormones involved in carcinoid syndrome and VIPomas.

Malignant HTN: describe pathologic histological lesion to blood vessels as a result of this.

Onion-like concentric thickening of arteriolar walls This is DBP in excess of 120/130 Lower levels of HTN results in homogenous deposition of hyaline material in intima and medial of small arteries and arterioles known as hyaline arteriosclerosis.

Which of these tests are influenced by disease prevalence: Sn, Sp, PPV, NPV, +ve LR, -ve LR?

Only PPV and NPV are influenced by prevalence.

Primary hyperparathyroidism: most common skeletal manifestation? Which bone is affected? Which is preserved?

Osteitis fibrosa cystica Affected: cortical bone Preserved: trabecular bone

Blue sclera

Osteogenesis imperfecta (type 1 collagen defect)

Pediatrics: Osteomyelitis: what area of bone is most likely affected? Ewing's Sarcoma: what area of bone is most likely affected? Osteosarcoma: what area?

Osteomyelitis: Metaphysis: slower blood flow and capillary fenestrae in this region Ewing's: Diaphysis Osteosarcoma: Physis

Vertebral compression fracture

Osteoporosis (type I: postmenopausal woman; type II: elderly man or woman)

Retinoblastoma: familial retinoblastoma patients are at increased risk for what secondary tumors?

Osteosarcomas

Vitiligo: What other conditions has vitiligo been correlated with?

Other autoimmune disorders such as type I DM, pernicious anemia, Addison's dz, autoimmune hepatitis, Graves', autoimmune thyroiditis

Neonatal respiratory distress syndrome: What treatment causes retinopathy (specifically neonatal neovascularization)?

Oxygen therapy. Local hyperoxia is thought to induce up-regulation of angiogenic factors such as VEGF upon return to room air ventilation. Retinal vessel proliferation and detachment of retina may occur. This is referred to as retinopathy of prematurity or retrolental fibrodysplasia.

Alveolar gas equation

PAo2 = PIo2 - (Paco2 / R) PIo2 = Po2 in inspired air Paco2 = arterial PCO2 R = respiratory quotient = CO2 produced / O2 consumed

Continuous machine like heart murmur

PDA (close with Indomethacin; keep open with PGE analog)

Cyanosis: How can you tell the difference between cyanosis d/t PDA, coarctation of aorta and tetralogy of fallot

PDA: cyanosis more pronounced in lower extremities as PDA is distal to left subclavian artery Coarctation: differential cyanosis and pulses between upper and lower extremities Tetralogy of Fallot: whole body cyanosis

Pyruvate kinase deficiency: effect of this disease on spleen?

PK deficiency results in hemolytic anemia d/t failure of glycolysis and resultant failure of ATP to maintain RBC including structurally. Splenic hyperplasia of red pulp occurs d/t increased work of splenic parenchyma, which must remove these deformed RBCs from circulation.

Amaurosis fugax: What is it?

Painless, transients loss of monocular vision caused by small emboli to the opthlamic artery. Doesn't last much longer than a few seconds.

Bronchogenic apical lung tumor on imaging

Pancoast tumor (can compress cervical sympathetic chain and cause Horner syndrome)

CA19-9: Marker of?

Pancreatic

Thyroid: Clusters of overlapping cells with large nuclei containing sparse, finely dispersed chromatin. Numerous intranuclear inclusion bodies and grooves. What is the diagnosis?

Papillary thyroid cancer Most common thyroid cancer Large cells with nuclei containing finely dispersed chromatin with a ground glass apperance = Orphan Annie Eyes Note: laminated calcium bodies (aka Psammoma bodies) can be found in this tumor

Contact precautions with simple face mask: for what organisms?

Particles > 5 microns: bacteria (N. meningitidis, B.pertussis, M.pneumoniae) and viruses (influenza, RSV)

Dog or car bite resulting in infection

Pasteurella multocida (cellulitis at infection site)

Mouse-Like Odor: what bacteria?

Pasteurella multocida, odor = indole positive.

Infant with cleft lip/palate, microcephaly or holocephaly, polydactily, cutis aplasia

Patau syndrome (trisomy 13)

Salmonella typhi: what finding is pathognomonic?

Pathognomonic: rose spots on abdomen.

Klinefelter syndrome: Lab findings?

Patient has primary hypogonadism Low T = high FSH and LH production Note: no sperm exist

Neisseria meningitidis

Penicillin/ceftriaxone, rifampin (prophylaxis)

Streptococcus pneumoniae

Penicillin/cephalosporin (systemic infection, pneumonia), vancomycin (meningitis)

Teratogenic medications

Phenytoin Lithium Valproate Isotretinoin MTX ACEi Warfarin

Silver-staining spherical aggregation of tau proteins in neurons

Pick bodies (Pick disease: progressive dementia, changes in personality)

Hereditary spherocytosis: complications?

Pigmented gallstones and aplastic crises from parvo B19

Cerebellar tumor in child: what are the two types? How are they differentiated?

Pilocytic astrocytoma (most common brain tumor in children) Medulloblastoma (most common malignant brain tumor in children) Differentiate on brain imaging. Pilocytic astrocytoma: cystic and solid components. Medulloblastoma: solid always.

Net filtration pressure

Pnet = [(Pc - Pi) - (pi c - pi i)] Pc = capillary hydrostatic pressure Pi = interstitial hydrostatic pressure pi c = capillary oncotic pressure pi i = interstitial oncotic pressure Jv = net fluid flow = (Kf) (Pnet) Kf = filtration constant (capillary permeability)

Pediatrics: most common cause of death in CF patient in US?

Pneumonia, bronchiectasis and cor pulmonale

Poison Ivy: What cell type is responsible for causing damage?

Poison ivy causes a contact dermatitis. This is a type IV hypersensitivity. Main effector cell = CD8+ T lymphocyte.

Actinic (solar) keratosis

Precursor to squamous cell carcinoma

Chronic atrophic gastritis (autoimmune)

Predisposition to gastric carcinoma (can also cause pernicious anemia)

Syphilis: Name the lesions seen in primary vs secondary vs tertiary

Primary = chancre (painless ulcerated lesion with raised indurated borders. Secondary = diffuse macular rash encompassing palms and soles. Condyloma lata (not acuminata as seen with HPV) are large gray wartlike growths typically appearing in genital/perianal region. Tertiary (late) = gummas (painless, indurated granulomatouse lesions that progress to white-gray rubbery lesions that may ulcerate) found in cutaneous tissue (incl. genitals), but also subQ, bones, liver and other organs.

Antimitochondrial antibodies (AMA)

Primary biliary cirrhosis (female, cholestasis, portal hypertension)

Acidosis Patient has chronic acidosis, how does kidney excrete acid? What amino acid is involved in this process?

Process of renal ammoniagenesis where rental tubular cells do the following reactions: glutamine -> (ez: glutaminase) glutamate + NH4 -> (ez: glutamate DH) alpha-ketoglutarate + NH4 NH4 is excreted into tubular lumen and alpha-ketoglutarate is converted somehow into bicarb that is then released into circulation

b-HCG

Produced 6-7 days after fertilization and detectable in serum 8 days after fertilization. Implantation takes place 6 days after fertilization.

"Opioid side effect: How does it cause abdominal pain and where?"

RUQ pain. It causes SM contraction in sphincter of Oddi leading to increased pressure in common bile duct and GB.

Giant B cells with bilobed nuclei with prominent inclusions (Owls eye)

Reed-Sternberg cells (Hodgkin Lymphoma)

Sickle cell anemia: what causes the major chronic pathologic changes in spleens in these patients? Gross appearance?

Repetitive splenic infarctions causes by splenic microvessel occlusion. Appearance = fibrosis, brownish discoloration (hemosiderosis).

Pyrrolidonyl arylamidase: which organism is + ve for this?

Replaces bacitracin test. Bacitracin sensitive organisms = S. pyogenes, which is pyrrolidonyl arylamidase positive. Note: enterococcus is also PYR positive.

Point-of-service plans: what is it?

Requires patients to have a PCP and obtain referrals for specialty consults. Differs from HMO in that they allow patients to see providers outside the network, albeit at higher out of pocket costs.

Pygmalion effect

Researcher's belief in efficacy of treatment can potentially affect the outcome.

Osteomyelitis

S. aureus (most common overall)

Food poisoning (exotoxin mediated)

S. aureus, B. cereus

Infection in chronic granulomatous disease

S. aureus, E coli, Aspergillus [catalase (+)]

Nosocomial pneumonia

S. aureus. Pseudomonas, other enteric gram (+) rods

Bacterial meningitis (adults and elderly)

S. pneumoniae

Bulimia nervosa

SSRIs

Depression

SSRIs (first line)

Generalized anxiety disorder

SSRIs, SNRIs (first line); buspirone (second line)

Hepatitis B: SSx of acute infection? Transmission?

SSx: joint-pain, LAD, pruritic urticarial rash, RUQ pain, hepatomegaly, elevated hepatic transaminases Transmission: sexually, parenterally, vertically

Novobiocin response

Sensitive: S. epidermis Resistant: S. saprophyticus

Optochin response

Sensitive: S. pneumoniae Resistant: Viridans streptococci (S. mutans & S. sanguis)

Bacitracin response

Sensitive: S. pyogenes (group A); Resistant: S. agalactiae (group B)

Mucin-filled cell with peripheral nucleus

Signet ring (gastic carcinoma)

Sturge Weber syndrome

Sporadic Congenital vascular disorder. Facial port-wine stain (V1/V2 distribution), leptomeningeal (pia, arachnoid) capillary-venous malformation

Acute tubular necrosis: Describe 3 changes and features associated with each.

Stage 1 = Initiation stage: - Ischemic injury d/t hemorrhage, acute MI, sepsis, surgery etc. Stage 2 = Maintenance stage - Decrease UOP = fluid overload, increase Cr and BUN, hyperK (watch for peaked T waves), retention of H and anions (high AG metabolic acidosis), hypoNa, hypoCa (deposition of calcium phosphate and reduced vit D), hyperMag and hyperphosphatemia Stage 3 = Recovery phase - Slowly recovering tubular function = gradual increase in UOP = high-volume diuresis = electrolyte abnormalities including hypoK (most problematic), hypoMg/PO4/Ca.

Complications of obstructive sleep apnea

Systemic HTN, pulmonary HTN and right heart failure. Not hypertrophic cardiomyopathy.

Cherry red spots on macula

Tay-Sachs (ganglioside accumulation) or Niemann-Pick (sphingomyelin accumulation), central retinal artery occulsion

Beta-lactamase inhibitors

Tazobactam, clavulanic acid and sulbactam

Cyanosis (early; less common)

Tetrology of Fallot, transposition of great vessels, truncus arteriosus

Candida albicans

Topical azoles (vaginitis); nystatin, fluconazole, caspofungin (oral/esophageal); fluconazole, caspofungin, amphoteracin B (systemic)

Types of proteinuria

Tubular: presence of LMW proteins such as beta-2 microglobulin, Ig light chains, AAs, retinol-binding protein. These are normally filtered by glomerulus and then almost completely reabsorbed in PCT. They appear in urine when proximal tubular function is disrupted (ie. tubulointerstitial nephritis). Overload: presence of LMW that are overproduced in cases such as multiple myeloma (Ig light chains are produced). Functional: change in blood flow through glomerulus. Precipitating factors include exercise, high fever, emotional stress, cold exposure. Common cause in young adults with nml renal function and disappears with repeat testing. Selective: LMW (such as albumin and transferrin) loss with minimal loss of more bulky proteins (such as IgG and macroglobulin). Happens in nephrotic syndromes eg. MCD. Orthostatic: increased protein excretion in upright position, but nml protein excretion in the supine position. Occurs in older, tall, thing adolescents. Isolated: incidental finding in an asymptomatic individual with nml renal function and nml urinary sediment. No systemic diseases.

Primary amenorrhea

Turner syndrome (45,XO or 45XO/46XX mosaic)

Hyperreflexia, hypertonia, Babinski sign present

UMN damage

What mechanism do cells use to process and present pathogenic antigens on MHC1?

UPP

Upper respiratory tract vs lower respiratory tract: describe anatomy

URT: nasal passages, mouth, pharynx and larynx LRT: trachea, bronchi, bronchioles

What mechanism do cells use to process and present pathogenic (eg. viral) antigens on MHC1?

Ubiquitin proteasome pathway

SA node location

Upper anterior right atrium at opening of SVC

Inferior orbital fissure: contents

V2, infraorbital vessels and branches from sphenopalatine ganglion. Note: these structures just pass through, but don't enter into the orbit.

MRSA: Abx used to tx and MOA

Vancomycin, Daptomycin and Linezolid Vancomycin: blocks glycopeptide polymerization by binding to D-Ala D-Ala Daptomycin: depolarizes cellular membranes by creating transmembrane channels Linezolid: inhibits bacterial protein synthesis by binding to 50S subunit

Syphilis: Pathogenesis of tertiary syphilis? What structure is affected?

Vasa vasorum (blood vessels that supply the blood vessels) endarteritis and obliteration, resulting in inflammation, ischemia and weakening of the aortic adventitia.

Cocaine's effect on pregnancy

Vasoconstrictive = insufficient blood flow = spontaneous abortion, IUGR, placental abruption and / or prematurity

Which infections are profound neutropenic patients (less than 500) who present with febrile neutropenia most at risk for? Which are the most common fungal infections?

Viral and fungal infections Most common fungal infections = Aspergillus and Candida

Infectious mononucleosis: What is the virus that causes this infection? What cell type is affected? What is the bodies response against this cell type? If blood smear is done, what is seen?

Virus = EBV Cell type infected = B lymphocytes Response = CD8+ T cell lymphocytosis Seen on smear = atypical lymphocytes, which aim to destroy infected B cells

Refractory peptic ulcers and high gastrin levels

Zollinger-Ellison syndrome (gastrinoma of duodenum or pancreas), associated with MEN1

Primary immunodeficiency: IgA deficiency a. What is the defect? b. Presentation?

a. **Most common Ig deficiency** Defect = low serum and mucosal IgA. b. SSx = increased risk for mucosal infections especially viral. Most patients asymptomatic.

Microscopic changes with ischemia to brain: Describe time course?

a. 12-24 hrs: red neurons (eosinophilic cytoplasm, pyknotic nuclei, loss of Nissl (RER)) b. 24-72 hrs: neutrophilic infiltration c. 3-7 days: macrophage/microglia infiltration & phagocytosis begins d. 1-2 weeks: reactive gliosis & vascular proliferation around necrotic area e. > 2 weeks: glial scar formation

CML: a. Translocation? b. Gene product?

a. 9;22 translocation b. ABL proto-oncogene transported from 9 to 22 where it is placed adjacent to BCR. The resulting oncogene = BCR-ABL = fusion protein with constitutive tyrosine kinase activity. Imatinib targets this.

Hereditary Pulmonary Arterial Hypertension a. Inheritance pattern and gene involved b. Describe pathogenesis c. SSx

a. AD with variable penetrance. Gene = BMPR2. b. Patients with this mutation are predisposed to dysfunctional endothelium and smooth muscle cell proliferation. Second insult (infection, drugs, ion channel defect etc.) activates the disease process. Result = SM proliferation, intimal thickening and fibrosis and increase pulmonary vascular resistance with progressive pulmonary HTN. c. Dyspnea, fatigue -- eventually -- cor pulmonale (RV failure) w/ exertional angina, elevated JVP, hepatic congestion and peripheral edema. Accentuation of P2 heard on auscultation. NB: suspect in young, otherwise healthy women.

Chediak-Higashi Syndrome a. Defect and pathogenesis? b. SSx?

a. AR disorder of neutrophil phagosome lysosome fusion. Causes abnormal giant lysosomal inclusions that are visible on light microscopy of a peripheral smear. Leads to recurrent pyogenic infections most commonly from staph and strep. Abnormal melanin storage in melanocytes cause partial oculocutaneous albinism. b. SSx: neurologic abnormalities (including nystagmus and peripheral/cranial neuropathies), partial albinism, immunodeficiency

Wolffian ducts: a. Aka? b. What structures does it give rise to?

a. Aka the mesonephric ducts b. Gives rise to the epididymis, ductus deferens, seminal vesicles and ejacualtory ducts

Mullerian ducts: a. Aka? b. What structures does it give rise to?

a. Aka the paramesonephric ducts b. Gives rise to fallopian tubes, uterus, cervix and upper vagina

Intoxication/Poisoning: a. Toxin found in some mushrooms? b. What does this toxin do? Inhibits what?

a. Amatoxin in variety of poisonous mushrooms (Amanita phalloides known as death cap) b. Concentrated in liver and inhibits RNA pol II halting mRNA synthesis.

Leukemoid reaction: a. What is it? b. What is meaning of LAP (leukocyte alkaline phosphatase) beingnormal or increased? c. How to tell difference between leukemoid rxn d/t infection vs that d/t malignancy?

a. Benign leukocytosis (> 50 K WBCs) that occurs in response to severe infection, hemorrhage, malignancy (leukemia) or acute hemolysis. b. Granulocytes fight infection with LAP. If normal or increased, indicates infection. If -ve, then malignancy (eg. CML). LAP +ve = Dohle bodies (light blue basophilic peripheral granules in neutrophils). c. In malignancy: LAP -ve, with increase in immature cells (promyleocytes and myeloblasts). Specific for CML: LAP -ve, increased basophils, 9;22 translocation. With infection: LAP +ve, increased bands and early mature neutrophil precursors (eg. myelocytes).

Exercise: Effect on: a. CO b. LV ED pressure c. Pulmonary artery systolic pressure d. Systemic BP e. Total systemic vascular resistance

a. CO increases b. LV ED pressure increases c. Pulmonary artery systolic pressure increases d. Systemic BP increases e. Total systemic vascular resistance decreases. Note: while still overall rise in systemic BP, it would be much higher if vasodilation to muscles didn't occur. Vasodilation in muscles d/t local release in adenosine, K, ATP, CO2 and lactate.

Pediatrics: Compare and contrast between the heart defects found in: a. DS b. DiGeorge c. Marfan d. Friedrich ataxia e. Turner syndrome f. Edwards g. Patau h. Williams

a. DS: Complete AV canal defect: ASD (ostium primum type), VSD and common AV valve b. DiGeorge: Tetralogy of Fallot, truncus arteriosus, transposition of great arteries c. Marfan: cystic medial necrosis of aorta resulting in dissecting aortic aneurysms and aortic valve regurg. MVP is also common. d. Friedrich ataxia: HCM e. Turner: bicuspid aortic valve (most common), coarctation of aorta f. Edwards: "structural heart dz" - E = ears (low set), clenched hands, prominent occiput g. Patau: "congenital heart dz", P = cleft liP/Palate, holoProsencephaly, Polydactyly, cutis aplasia (focal skin defect on scalp), omPhalocele h. Williams: supravalvular aortic stenosis, elfin facies, extroverted personality

Inguinal rings a. Deep inguinal ring is physiologic opening in what layer of abdomen? b. Superficial inguinal ring is physiologic opening in what layer of abdomen?

a. Deep inguinal ring = opening in transversalis fascia b. Superficial inguinal ring = opening in external oblique muscle aponeurosis

Primary immunodeficiency: Wiskott-Aldrich Syndrome a. What is the defect? b. Presentation?

a. Defect = X-linked defect in WASP protein = defective humoral and cell-mediated immunity b. SSx = Mnemonic = WATER = Wiskott-Aldrich, Thrombocytopenia, Eczema, Recurrent infections

Homocystinuria a. Defect b. SSx

a. Defect = cystathionine synthase most commonly. Can also occur with B6 deficiency. b. SSx: hypercoagulability and thromboembolic occlusion, ACS, ectopia lentis (lens displacement) and intellectual disability. Note: homocysteine is prothrombotic.

Primary immunodeficiency: SCID a. What is the defect? b. Presentation?

a. Defect = defective T and B cell mediated immunity d/t three etiologies: 1. ADA deficiency: buildup of adenosine and deoxyadenosine waste products that are toxic to lymphocyte 2. Cytokine receptor defect 3. MHC class II deficiency b. SSx = susceptibility to fungal and viral infections (d/t T cell deficiency) and bacterial, enterovirus and protozoal infections (d/t B cell deficiency). Includes susceptibility to opportunistic infections and live vaccines.

Primary immunodeficiency: DiGeorge Syndrome a. What is the defect? b. Presentation?

a. Defect = developmental failure of 3rd and 4th pharyngeal pouches b. SSx = Lack of thymus (T cell deficiency = increased risk for viral and fungal infections), parathyroid glands (hypocalcemia and SSx associated with that) and abnormalities in great vessels of heart, heart itself and face.

Primary immunodeficiency: Hyper-IgM syndrome a. What is the defect? b. Presentation?

a. Defect = ineffective/lack of 2nd activation signal to B cell d/t mutated CD40L (on helper T cell) or CD40 receptor (on B cell). Most common defect = CD40L deficiency (X-linked recessive). Result = cannot switch Ig = elevated IgM with lack of IgA/D/E. b. SSx = recurrent pyogenic infections (d/t poor opsonization) especially at mucosal sites

Primary immunodeficiency: CVID a. What is the defect? b. Presentation?

a. Defect = low Ig d/t B or helper T cell defects b. SSx = increased susceptibility to bacterial, enterovirus and G. lamblia infections usually in late childhoo.

Primary immunodeficiency: X-Linked Agammaglobulinemia a. What is the defect? b. Presentation?

a. Defect = mutated BTK (Bruton tyrosine kinase) = pre- and pro-B cells (naive B cells) cannot mature leading to absence of immunoglobulins b. After 6 months of live = increased susceptibility to bacterial, enterovirus and Giardia lamblia infections. Avoid live vaccines.

S cells: a. Where do these cells reside? b. What do they secrete and in response to what?

a. Duodenum b. 1. In response to increasing H+, it releases secretin. - Secretin acts to increase pancreatic bicarb secretion. Note: chloride concentration on pancreatic secretions decreases in proportion to bicarb concentration increases. - Secretin inhibits release of gastrin from normal gastrin cells in stomach. Gastrin normally results in parietal cell hyperplasia and stimulates gastric acid secretion.

Atrial fibrillation: a. EKG findings b. What regulates the number of atrial impulses that reach the ventricle and determines ventricular contraction rate?

a. EKG: absent P waves, irregularly irregular R-R intervals, narrow QRS complexes, frequently see are low amplitude fibrillatory waves b. AV node refractory period regulates number of atrial impulses that reach the ventricle and determines the ventricular contraction rate

Appendicits: a. Pathogenesis of acute appendicitis b. Typical cause in children vs adults

a. First event in pathogenesis of acute appendicitis = obstruction of lumen d/t fecalith, hyperplastic lymphoid follicles, FBs, tumors b. Children = hyperplastic lymphoid follicles. Adults = fecalith.

Tropheryma whippelii: a. Gram-staining b. Classic histologic finding of Whipple disease c. Classic presentation of Whipple dz

a. G+ actinomycete b. Small intestine: mucosa contain enlarged, foamy macrophages packed with both rod-shaped bacilli and PAS-pos diastase resistant granules c. Presentation: middle-aged Caucasian males presents with malabsorption with diarrhea, weight loss, arthropathy, polyarthritis and psych and cardiac abnormalities may also be observed.

Antifungals: MOA of: a. Griseofulvin b. Flucytosine c. Caspofungin d. Amphotericin B e. Nystatin f. Azoles

a. Griseofulvin = inhibits mitosis (via interacting with fungal microtubules) b. Flucytosine = Converted to 5-FU and interferes with fungal RNA and protein synthesis c. Caspofungin = inhibits synthesis of glucan (component of fungal cell wall) d and e. Amphotericin B and nystatin = bind to ergosterol molecules in fungal cell membranes creating pores and causing cell lysis f. Azoles = inhibit synthesis of ergosterol

Renal papillary necrosis: a. Presentation? b. In what patient group is this seen?

a. Gross hematuria, passage of tissue fragments in urine. May have acute flank pain. b. Most commonly seen in patients with sickle cell dz or trait, DM, analgesic nephropathy or severe obstructive pyelonephritis.

Bloom Syndrome: a. SSx b. Defect

a. Growth retardation, facial anomalies, photosensitive skin rash, immunodeficiency (d/t chromosomal instability and breakage) b. Mutation in BLM gene encoding helicase (responsible for unwinding DNA) = chromosomal instability and breakage)

Calculations a. Half-life calculation b. Loading dose calculation c. Maintenance dose calculation

a. Half life = (Vd x 0.7) / Cl b. LD = (Cpss x Vd) / Bioavailability c. MD = (Cpss x Cl) / Bioavailability Vd = volume of distribution = (amount of drug in body) / (plasma [] of drug) Cl = clearance Cpss = plasma concentration of drug as steady state Bioavailability: IV = 1.

Equilibrium movements of charged ions a. Which ions are of higher concentration outside of the cell? b. Inside the cell? c. If at RMP of -70 mV, in what direction will Na, Cl, Ca and K move if their channels are open?

a. Higher [] outside the cell: Ca, Na, Cl b. Higher [] inside the cell: K c. See table

Halothane a. Indications b. Side effects and presentation

a. Indication = inhaled anesthetic for surgeries b. Highly lethal fulminant hepatitis - SSx: fever, anorexia, nausea, myalgias, arthralgias, rash, tender hepatomegaly, jaundice, marked elevated aminotransferases, prolonged PT time (d/t factor VII deficiency and its short half-life), leukocytosis, eosinophilia. Note: no decrease in albumin, as it has a long half-life (~20 days).

Clozapine: Indications, MOA, Side effects?

a. Indications: tx-resistant schizophrenia, schizophrenia associated with suicidality b. MOA: 2nd gen antipsychotic, mechanism not completely known, but has affinity for multiple dopamine and 5-HT receptors c. SEs: agranulocytosis (lesser extent neutropenia), seizures, myocarditis, metabolic syndrome. Must regularly monitor patients absolute neutrophil count through centralized program.

Hereditary angioedema: a. What is the defect? b. SSx? c. Avoid what drug?

a. Inherited AD condition with low serum C1 esterase inhibitor. C1 usually leads to angioedema. It also normally inactivates kallikrein. In the absence, kallikrein leads to increase of bradykinin, resulting in further angioedema. b. SSx = angioedema of face, neck, lips, tongue, but also internal organs and tracheobronchial tree. c. ACE normally breaks down bradykinin. Avoid ACE inhibitors (-prils).

Granulosa cell tumor of ovary: a. Clinical features b. Histology

a. Large, unilateral adnexal mass, increased estrogen (endometrial hyperplasia, precocious puberty), increased inhibin b. Call-Exner bodies (cuboidal granulosa cells in Rosette pattern with coffee bean nuclei), yellow theca cells with lipid - From UW: small cuboidal cells in sheets with gland-like structures containing acidophilic material. Cells arranged in microfollicular pattern around pink-eosinophilic center.

a. Layers of spermatic cord. What does each layer arise from? b. Layers of scrotum. What does each layer arise from?

a. Layers of spermatic cord: From internal to external Internal spermatic fascia = transversalis fascia Cremasteric muscle and fascia = internal oblique External spermatic fascia = external oblique b. Layers of scrotum: Mnemonic: Some Damn Englishman Called It The Testes Skin Dartos fascia and muscle External spermatic fascia Cremasteric fascia Internal spermatic fascia Tunica vaginalis Tunica albuginea

Transesophageal echo a. When pointing anterior, which part of heart are you looking at? b. When pointing posterior, what vessel are you looking at?

a. Left atrium b. Descending aorta

Heparin: a. MOA? b. treatment for overdose? c. Is vit K or FFP effective?

a. MOA = increases effect of naturally occuring anticoagulant ATIII, which is to inhibit activated forms of factors 1972 + 12, 11. b. Protamine sulfate = heparin-specific antidote. It binds to heparin forming a complex w/no anticoag activity. c. Vit K is ineffective FFP is ineffective as it contains antithrombin III therefore enhancing heparin effect.

Warfarin: a. MOA? b. treatment for overdose?

a. MOA = inhibition of epoxide reductase and therefore blocking recycling of vit K, which is needed to activate factors. b. Vit K (takes days). FFP (contains all blood clotting factors and proteins). Can also give prothrombin complex concentrates (PCCs), which contain vit-K dependent factors 1972.

True vs False Diverticula a. Meckels' b. Zenker's c. Diverticulosis

a. Meckel's: true b. Zenker's: false c. Diverticulosis: false

Acute interstitial nephritis a. What meds cause this? b. SSx? c. Histological findings?

a. Meds = NSAIDs, sulfonamides, rifampin, diuretics, beta-lactams b. SSx = fever, rash, acute renal failure (elevated Cr, oliguria) that occurs a few weeks (sometimes days) after starting meds. Look for eosinophiluria or eosinophilia. Can be a type IV hypersensitivity or an IgE mediated hypersensitivity depending on the drug. c. Histologically: interstitium is affected, not glomerulus.

Drug-Induced SLE: a. What drugs cause it? b. What antibody is associated with it?

a. Most common = hydralazine, procainamide, isoniazid. Others = minocycline and quinidine. b. Antibodies = ANA (specifically anti-histone). Rarely, anti-dsDNA seen.

Pancreatitis: a. Most common causes of acute pancreatitis? b. Less common causes?

a. Most common causes (80%) = gallstones and chronic alcoholism b. Less common (20%) = - Recent ERCP - Drugs (azathioprine, sulfasalazine, furosemide, valproic acid) - Infections (mumps, Coxsackie virus, Mycoplasma pneumoniae) - Hypertriglyceridemia (>1000): concentration of FFAs > binding capacity of albumin and leads to direct injury of pancreatic acinar cells - Structural abnormalities of pancreatic duct - Surgery - Hypercalcemia

Pancreatic adenocarcinoma: a. SSx of this cancer at head of pancreas. Compare to pancreatic cancer involving body and tail. b. Risk factors. Which is most important?

a. Non-tender GB (Courvoisier's sign), weight loss, obstructive jaundice (pruritus, dark urine, pale stools) Note: cancers of body and tail don't obstruct the CBD. They typically invade the splanchnic plexus causing midepigastric abdominal pain. b. Risk factors: age, smoking, DM, chronic pancreatitis, genetic predisposition. Most NB = smoking (doubles risk).

Compare and contrast the following: serum sodium, urine osmolality after water deprivation test, urine osmolality after vasopressin injection a. Normal b. Central DI c. Nephrogenic DI d. Primary (psychogenic) polydipsia Lastly, describe tx.

a. Normal - Serum Na = normal - Water deprivation = urine osmolality increased - After vasopressin = no further increase b. Central DI - Serum Na = high - Water deprivation = no change or mild increase. - After vasopressin = large increase Tx = desmopressin (synthetic ADH) c. Nephrogenic DI - Serum Na = high - Water deprivation = no change or mild increase - After vasopressin = mild increase (or no change?) Tx = thiazide diuretic (to induce mild hypovolemia leading to increased proximal tubule Na and water reabsorption) OR indomethacin (decreases synthesis of PGs, which inhibit ADH - so any that is working will stop) d. Primary (psychogenic) polydipsia *looks similar to normal except serum Na low to begin with - Serum Na = low* - Water deprivation = increased - After vasopressin = no further increase

AS: a. Is RF factor positive in these patients? b. Extraskeletal complications?

a. Not positive b. Involvement of costovertebral and costosternal junctions leading to hypoventilation. Monitor ventilation regularly in these patients. Most common CV complication = ascending aortitis leading to dilation of aortic ring and aortic regurgitation. Eye: anterior uveitis.

Emphysema: a. Restrictive or obstructive? b. FEV1/FVC - increased or decreased? c. TLC - increased or decreased? d. DLCO - increased or decreased?

a. Obstructive b. Decreased c. Increased d. Decreased (destruction of alveoli and adjoining capillary beds). Not all obstructive patterns have decreased DLCO. Depends on etiology. Asthma has increased DLCO d/t increased pulmonary capillary blood volumes.

Tracheal deviation: What direction is the trachea deviated in the following: a. Pleural effusion b. Collapsed lung d/t bronchial obstruction c. Tension pneumothorax d. Spontaneous pneumothorax

a. Pleural effusion: trachea away b. Collapsed lung d/t bronchial obstruction: trachea towards c. Tension pneumo: trachea away d. Spontaneous pneumo: trachea toward

T-Cell maturation: a. Positive selection: describe. Where does it occur? What other cell type is used? b. Negative selection: describe. Where does it occur? What other cell type is used?

a. Positive = process by which only T cells expressing TCR that is able to bind self MHC are allowed to survived. Takes place in thymic cortex with thymic cortical cells expressing self MHC. b. Negative = process by which T cells possessing TCRs that bind with high affinity to self antigen or self MHC I or II are eliminated via apoptosis. Takes place in thymic medulla with thymic medullary and DCs.

Ehlers-Danlos syndrome: a. What is the defect? b. Presentation?

a. Procollagen peptidase deficiency resulting in impaired cleavage of terminal propeptides in the EC space. b. Presentation: joint laxity, hyperextensible skin, tissue fragility d/t formation of solluble collagen that doesn't crosslink.

Leptin: a. Where is it produced? b. Function? c. Result in leptin receptor knock-out mice?

a. Produced primarily in adipocytes. b. It decreases food intake via: - Decrease in production of neuropeptide Y, potent appetite stimulate, in arcuate nucleus of hypothalamus - Stimulates production of POMC in arcuate nucleus. Alpha-MSH is produced through cleavage of POMC and inhibits food intake c. Hyperphagic and profoundly obese mice. - Note: mice who have leptin knocked out, will have low leptin and high BMI. Mice who have leptin receptors knocked out, will have high BMI with high leptin.

6-mercaptopurine (6-MP). a. MOA b. Which enzyme activates this drug? c. Which enzyme inactivates this drug?

a. Purine analog that inhibits de novo purine synthesis. Note: same MOA for 6-TG. b. Activated by HGPRT c. Inactivated by xanthine oxidase and thiopurine methyltransferase (TPMT).

Celiac disease a. What is the rash associated with this? b. Histological findings of these rashes? c. Histological findings in intestines?

a. Rash = dermatitis herpetiformis (erythematous pruritus papules, vesicles and bullae bilaterally on extensor surfaces such as knees and elbows) b. Histology of rash = microabscesses containing fibrin and neutrophils at dermal papillae tips. c. Intestinal histology = increased intraepithelial lymphocytes, variable loss of villi height, crypt hyperplasia.

Primary immunodeficiency: Selective IgA deficiency a. Presentation b. What happens to these patients when transfused?

a. Recurrent sinopulmonary & GI infections as well as autoimmune dz (eg. celiac) is common. b. Transfusion = anaphylaxis rxn. Blood products that contain small amounts of IgA. These individuals have IgE antibodies directed against IgA.

Renal cancer: a. Most common type? b. Histological findings? c. Most common site of metastasis?

a. Renal cell carcinoma, specifically clear cell carcinoma (specifically from proximal renal tubules) b. Rounded, polygonal cells with abundant clear cytoplasm (high glycogen or lipid dissolves on preparation) c. Lungs

S3: a.) Why is it heard? b.) Cause? c.) When is it best heard and why?

a. S3 results from limitation of ventricular movement d/t rapid passive filling phase. b. Cause = normal finding in healthy children and young adults, decompensated heart failure, chronic severe mitral regurg, chronic aortic regurg. c. Best heard when patient is in left lateral decubitus at end expiration

Lac Operon a. What is it? b. What is the structure? What are the genes involved and their function? c. Describe induction.

a. Sequence of genome in E.coli required for metabolism of lactose b. Lac I (regulatory gene), P (promoter), O (operator region), three structural genes = Z (beta-galactosidase), Y (permease), A (beta-galactoside transacetylase) Z = hydrolysis lactose -> gal and glucose Y = increase permeability of cell to lactose A = transfer acetyl groups to ez beta-galactosidase. Unnecessary for lactose metabolism c. Lactose induces this process. Normally, repressor molecule binds O preventing binding of RNA pol. Lactose binds to repressor resulting in transcription and translation of genes.

Adrenal crisis: a. Presentation? b. Treatment? c. Which patients are at risk for this?

a. Severe hypotension, abdominal pain, vomiting, weakness and fever. Patients with adrenal insufficiency are not able to increase glucocorticoid production in response to acute stress such as illness and surgery b. Tx requires immediate glucocorticoid supplementation in addition to aggressive fluid resuscitation c. Those with established adrenal insufficiency, but also those with other autoimmune endocrinopathies such as hypothyroidism.

Subclavian steal syndrome a. What is it? b. SSx?

a. Severe stenosis of proximal subclavian artery = reversal in blood flow from contralateral vertebral artery to ipsilateral vertebral toward distal stenotic subclavian region. b. SSx: Sx related to arm ischemia (exercise-induced fatigue, pain, paresthesias) or vertebrobasilar insufficiency (dizziness or vertigo) There is something known as coronary-subclavian steal phenomenon. In pt with coronary artery bypass where internal mammary artery has been used, blood flow can reverse through IMA leading to steal from coronary during times of increased UE demand. Sx related to coronary ischemia.

Thyroid: a. What BVs supply it? From where do they arise? b. Superior laryngeal nerve branches? What do they innervate? Which branch courses with the superior thyroid artery? c. Recurrent laryngeal nerve. What does it innervate?

a. Superior and inferior thyroid arteries. Superior from external carotid. Inferior from thyrocervical trunk (off subclavian). b. Branches into internal and external branches of superior laryngeal nerve. External (courses with superior thyroid artery) and innervates cricothyroid muscle. This muscle tenses the vocal cords to create high pitch sound. Damage results in low pitch hoarseness. Internal provides supraglottic / laryngeal mucosa sensation above vocal folds c. Recurrent laryngeal (left runs under aorta, right runs under right subclavian) innervates all intrinsic larynx muscles (except the cricothyroid muscle as above). These muscles all end in -arytenoid. They function to provide sensation to the larynx and also open/close the vocal cords. The posterior cricothyroid is the only one that opens the vocal cords.

Paget's disease of bone: a. Sx b. Pathogenesis c. What causes differentiation of osteoclasts

a. Sx = long bone pain, hearing loss b. Path = excessive osteoclast bone resorption followed by increased bone formation c. Osteclasts arise from mononuclear phagocytic lineage. In Paget's, Osteoclasts are particularly large with up to 100 nuclei. Differentiation of osteoclasts involves M-CSF (macrophage colony stimulating factor) and receptor for nuclear factor kappa-B ligand (RANK-L).

A-a o2 gradient a. What is normal range? b. Etiology of hypoxemia in context of normal A-a o2 gradient? c. Etiology of hypoxemia in context of elevated A-a o2 gradient?

a. This is difference between partial pressure of oxygen in alveolar air space and arterial system. Normal = 5-15 b. 1. Hypoventilation: obesity hypoventilation syndrome, neuromuscular disorder 2. Low inspired fraction of o2: high altitude c. 1. Right-to-left shunt: cardiac septal defects, pulmonary edema 2. VQ mismatch: PE, COPD 3. Impaired diffusion: interstitial lung dz

ASA: a. What type of acid-base abnormality does an overdose cause? How? b. What are the lab values seen? c. Tx of ASA intoxication/overdose?

a. Type: Causes 2 acid-base disturbances: 1. Respiratory alkalosis (early < 3 hours) and 2. Anion gap metabolic acidosis (late > 3 hours) 1. Respiratory alkalosis: directly stimulates respiratory centers causing hyperventilation and loss of CO2. 2. AG metabolic acidosis: stimulates lipolysis, uncouples oxidative phosphorylation and inhibits TCA cycle. Therefore causing ketoacidosis. b. pH normal d/t opposing processes, paCO2 low (resp. alkalosis), HCO3- low (metabolic acidosis) c. ASA is a weak acid and is trapped in the renal tubules when in alkaline environment. Give bicarb to eat up the protons and force it into deprotonated form and thus to be excreted out of body.

Pulmonary gas values: What are the partial pressure values of o2 and co2 in the trachea (upon inspiration), the alveoli (after equilibration with blood), incoming lung venous capillary and outgoing lung arterial capillary? How can you tell if there is poor perfusion?

https://classconnection.s3.amazonaws.com/184/flashcards/1904184/jpg/picture511352142493414.jpg https://classconnection.s3.amazonaws.com/990/flashcards/777990/jpg/picture31318436800146.jpg If the alveolar gas concentration is exactly or similar to that of the tracheal air concentration, then no blood entered into the capillary and no equilibration took place and the partial pressure of the alveolar air matches that in the trachea (ie. inspired).

Respiratory tree - Describe cell types and how it changes - When do goblet cells end? - When does smooth muscle end? - What is the conducting vs respiratory zone?

https://upload.wikimedia.org/wikipedia/commons/c/c8/Respiratory_Tract_Histological_Differences.png https://classconnection.s3.amazonaws.com/184/flashcards/1904184/jpg/picture251352060657462.jpg - Goblet cells extend to end of bronchi - Smooth muscle ends at end of terminal bronchi - Conducting = Nose to terminal bronchioles - Respiratory = Respiratory bronchioles, alveolar ducts, alveoli. Note: alveolar macrophages here too.

Hypertrophic cardiomyopathy H&E

https://www.google.com/search?q=hypertrophic+cardiomyopathy+h%26e&espv=2&biw=1366&bih=643&site=webhp&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiwqNK9i_TMAhUPK1IKHbUrD_wQ_AUIBigB

Colonic adenomas: Villous vs tubular vs tubulovillous Which is more likely to undergo malignant transformation?

image.slidesharecdn.com/neoplasticpolyps-140220125421-phpapp01/95/neoplastic-colonic-polyps-colonic-adenoma-familial-syndromes-11-638.jpg?cb=1392900978 Link shows tubulovillous Villous = more like to undergo malignant transformation

Hardy-Weinberg equation

p^2 + 2pq + q^2 = 1 p + q = 1