Medical Council Step exam for International Medical Graduates / ECFMG Certification USMLE Step 1 & Step 2: Organ Systems Pathophysiology Flashcards

24 sample cards from the USMLE Step 1 & Step 2: Organ Systems Pathophysiology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. How do you use the Henderson-Hasselbalch approach to classify acid-base disorders?

   Determine pH (acidemia <7.35, alkalemia >7.45). Metabolic acidosis: low HCO3 (split by anion gap = Na − [Cl + HCO3]; normal ~12). Metabolic alkalosis: high HCO3. Respiratory acidosis: high PaCO2. Respiratory alkalosis: low PaCO2. Check Winter's formula for compensation: expected PaCO2 = 1.5×HCO3 + 8 ± 2.

2. Give the high-anion-gap metabolic acidosis mnemonic and an example each for hyper/hyponatremia.

   MUDPILES: Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates. Hyponatremia (e.g., SIADH) risks osmotic demyelination if corrected too fast; hypernatremia (e.g., diabetes insipidus) risks cerebral edema if corrected too fast.

3. Contrast uncomplicated UTI organisms with the composition/risk factors of the common kidney stones.

   UTIs: most commonly E. coli, also Staph saprophyticus (young women), Proteus (urease, alkaline urine). Stones: calcium oxalate (most common, radiopaque), struvite (Mg-NH4-PO4, urease organisms, staghorn), uric acid (radiolucent, acidic urine, gout), cystine (genetic).

4. Map diuretics to their site of action and a key adverse effect: acetazolamide, furosemide, thiazide, spironolactone, mannitol.

   Acetazolamide: proximal tubule (carbonic anhydrase), metabolic acidosis. Furosemide: thick ascending limb (Na-K-2Cl), hypokalemia/ototoxicity. Thiazide: distal convoluted tubule (Na-Cl), hyperGLUC (hyperglycemia, lipid, uric acid, calcium). Spironolactone: collecting duct aldosterone antagonist, hyperkalemia/gynecomastia. Mannitol: osmotic.

5. Distinguish central from nephrogenic diabetes insipidus and the water deprivation/desmopressin test result.

   Central DI: deficient ADH production; urine osmolality rises after desmopressin. Nephrogenic DI: renal ADH resistance; no response to desmopressin. Both present with polyuria, dilute urine, and hypernatremia. SIADH is the opposite (excess ADH, concentrated urine, hyponatremia).

6. Compare hyperthyroidism vs. hypothyroidism lab patterns and name Graves vs. Hashimoto antibodies.

   Primary hyperthyroidism: low TSH, high free T4 (Graves: TSI/anti-TSH receptor antibodies, exophthalmos). Primary hypothyroidism: high TSH, low free T4 (Hashimoto: anti-TPO and antithyroglobulin antibodies, lymphocytic infiltrate with germinal centers).

7. Differentiate primary, secondary, and tertiary hyperparathyroidism by calcium, phosphate, and PTH.

   Primary: adenoma → high PTH, high Ca, low phosphate. Secondary: chronic kidney disease/low Ca → high PTH, low/normal Ca, high phosphate. Tertiary: autonomous gland after prolonged secondary → very high PTH and high Ca.

8. Contrast Type 1 and Type 2 diabetes mellitus pathophysiology and acute decompensation (DKA vs. HHS).

   Type 1: autoimmune beta-cell destruction, absolute insulin deficiency, prone to DKA (ketoacidosis, high anion gap, fruity breath). Type 2: insulin resistance with relative deficiency, prone to HHS (extreme hyperglycemia, hyperosmolarity, minimal ketones).

9. Distinguish Cushing syndrome, Addison disease, Conn syndrome, and pheochromocytoma.

   Cushing: excess cortisol (central obesity, striae, hyperglycemia). Addison: primary adrenal insufficiency (low cortisol/aldosterone, hyperpigmentation, hyperkalemia, hypotension). Conn: primary hyperaldosteronism (hypertension, hypokalemia, metabolic alkalosis). Pheochromocytoma: catecholamine excess (episodic hypertension, headache, sweating; elevated metanephrines).

10. Outline the menstrual cycle hormonal control and the LH surge trigger.

    Follicular phase: FSH drives follicle growth, rising estrogen. Mid-cycle: high estrogen exerts positive feedback → LH surge → ovulation. Luteal phase: corpus luteum secretes progesterone (maintains endometrium). Without fertilization, corpus luteum regresses, hormones fall, menses occurs. hCG (from blastocyst) rescues the corpus luteum.

11. What are the key physiologic changes of pregnancy and the classic features of preeclampsia?

    Pregnancy: increased plasma volume/CO, dilutional anemia, respiratory alkalosis, increased GFR. Preeclampsia: new hypertension + proteinuria after 20 weeks; eclampsia adds seizures; HELLP = Hemolysis, Elevated Liver enzymes, Low Platelets. Definitive treatment is delivery.

12. Match endocrine/reproductive drugs to use: metformin, levothyroxine, methimazole, clomiphene, finasteride.

    Metformin: decreases hepatic gluconeogenesis (first-line type 2 DM). Levothyroxine: T4 replacement for hypothyroidism. Methimazole: inhibits thyroid peroxidase (hyperthyroidism; PTU preferred in first trimester). Clomiphene: SERM inducing ovulation. Finasteride: 5-alpha-reductase inhibitor (BPH, alopecia).

13. Classify anemias by MCV and give the leading cause in each category.

    Microcytic (MCV <80): iron deficiency, thalassemia, anemia of chronic disease, sideroblastic, lead poisoning. Macrocytic (MCV >100): B12/folate deficiency (megaloblastic), alcohol/liver disease. Normocytic: split by reticulocyte count into hemolytic (high) vs. underproduction (low).

14. Distinguish intravascular from extravascular hemolysis findings.

    Both: elevated LDH, indirect bilirubin, low haptoglobin, reticulocytosis. Intravascular: hemoglobinemia, hemoglobinuria, schistocytes, very low haptoglobin (e.g., mechanical valve, microangiopathy, PNH). Extravascular: splenomegaly, spherocytes, no hemoglobinuria (e.g., hereditary spherocytosis, warm AIHA).

15. Differentiate hemophilia, von Willebrand disease, and DIC by PT, PTT, platelets, and bleeding time.

    Hemophilia A/B: prolonged PTT, normal PT/platelets (deep joint/muscle bleeds). von Willebrand: prolonged PTT and bleeding time, normal platelet count (mucosal bleeding, most common inherited disorder). DIC: prolonged PT and PTT, low platelets, low fibrinogen, high D-dimer, schistocytes.

16. Name a key thrombophilia and contrast acute leukemias (ALL vs. AML) and which lymphoma has Reed-Sternberg cells.

    Factor V Leiden is the most common inherited thrombophilia (resistance to protein C). ALL: lymphoblasts, children, TdT+, good prognosis. AML: myeloblasts with Auer rods, adults. Hodgkin lymphoma is defined by Reed-Sternberg (CD15+/CD30+) cells; non-Hodgkin lacks them.

17. Differentiate multiple myeloma from the myeloproliferative neoplasm polycythemia vera.

    Multiple myeloma: malignant plasma cells → monoclonal M-spike (IgG), lytic bone lesions, hypercalcemia, renal failure, anemia, Bence Jones proteinuria, Rouleaux. Polycythemia vera: JAK2 mutation → increased RBC mass (also WBC/platelets), pruritus after bathing, low EPO.

18. Match blood/anticoagulant drugs to mechanism: heparin, warfarin, aspirin, clopidogrel, alteplase.

    Heparin: activates antithrombin III (monitor PTT, reverse with protamine). Warfarin: inhibits vitamin K epoxide reductase, factors II/VII/IX/X (monitor INR/PT, reverse with vitamin K/FFP). Aspirin: irreversible COX inhibition. Clopidogrel: P2Y12 ADP receptor blocker. Alteplase: tPA thrombolytic.

19. Contrast ischemic vs. hemorrhagic stroke and name the artery for a classic MCA stroke deficit.

    Ischemic (~85%): thrombotic/embolic occlusion, treat with tPA if within window. Hemorrhagic: intracerebral/subarachnoid bleed (worst headache of life in SAH from berry aneurysm). MCA stroke: contralateral face/arm weakness and sensory loss, with aphasia (dominant) or neglect (non-dominant).

20. Contrast the protein pathology of Alzheimer, Parkinson, and the demyelination of multiple sclerosis.

    Alzheimer: beta-amyloid plaques and tau neurofibrillary tangles, cortical atrophy. Parkinson: alpha-synuclein Lewy bodies, dopaminergic neuron loss in substantia nigra (resting tremor, rigidity, bradykinesia). MS: autoimmune CNS demyelination, oligoclonal bands in CSF, periventricular plaques, relapsing-remitting.

21. Differentiate the CSF profiles of bacterial, viral, and fungal/TB meningitis.

    Bacterial: high neutrophils, very high protein, low glucose, high opening pressure. Viral: lymphocytes, normal/slightly high protein, normal glucose. Fungal/TB: lymphocytes, high protein, low glucose. Partial seizures arise focally; generalized involve both hemispheres with loss of consciousness.

22. Distinguish common adult vs. child CNS tumors and a neurocutaneous syndrome.

    Adults (supratentorial): glioblastoma (pseudopalisading necrosis), meningioma (psammoma bodies), schwannoma. Children (infratentorial): pilocytic astrocytoma, medulloblastoma, ependymoma. Neurofibromatosis type 1: café-au-lait spots, neurofibromas, Lisch nodules (chromosome 17).

23. Differentiate rheumatoid arthritis from osteoarthritis and name the antibody in SLE and scleroderma.

    RA: autoimmune, symmetric small-joint inflammation, morning stiffness >1h, pannus, anti-CCP/RF, ulnar deviation. OA: degenerative, weight-bearing joints, worse with use, Heberden/Bouchard nodes, no systemic inflammation. SLE: anti-dsDNA/anti-Smith. Diffuse scleroderma: anti-Scl-70; limited (CREST): anti-centromere.

24. Contrast basal cell carcinoma, squamous cell carcinoma, and melanoma of the skin.

    Basal cell carcinoma: most common, pearly papule with telangiectasias/rolled borders, palisading nuclei, rarely metastasizes. Squamous cell: ulcerated/scaly, keratin pearls, from actinic keratosis. Melanoma: pigmented (ABCDE criteria), depth (Breslow) predicts metastasis, S-100 positive, most deadly.

What this deck covers

USMLE Step 1 & Step 2: Organ Systems Pathophysiology flashcards FAQ