Examius

🇺🇸 Medical Council Step exam for International Medical Graduates / ECFMG Certification · subject

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

The USMLE Step 1 & Step 2: Organ Systems Pathophysiology syllabus for Medical Council Step exam for International Medical Graduates / ECFMG Certification in full: 7 chapters, 41 topics and 10 sub-topics, every one listed below, plus 58 USMLE Step 1 & Step 2: Organ Systems Pathophysiology flashcards with answers.

7Chapters
41Topics
10Sub-topics
58Flashcards

USMLE Step 1 & Step 2: Organ Systems Pathophysiology syllabus: all 7 chapters

Expand any chapter to see its topics and sub-topics.

  1. Cardiovascular System

     6 topics
    • Cardiac Physiology
      • Cardiac cycle, pressure-volume loops
      • Cardiac action potentials and conduction
      • Cardiac output and preload/afterload regulation
    • Vascular & Ischemic Disease
      • Atherosclerosis and arteriosclerosis
      • Ischemic heart disease and myocardial infarction
      • Hypertension and its complications
    • Heart failure and cardiomyopathies
    • Arrhythmias and ECG interpretation
    • Valvular disease and congenital heart defects
    • Cardiovascular pharmacology

  2. Respiratory System

     6 topics
    • Pulmonary Physiology
      • Lung volumes, compliance, and ventilation/perfusion
      • Gas exchange and oxygen-hemoglobin dissociation
    • Obstructive lung disease (asthma, COPD)
    • Restrictive and interstitial lung disease
    • Pulmonary infections and tuberculosis
    • Lung neoplasia and pleural disease
    • Pulmonary embolism and respiratory failure

  3. Gastrointestinal & Hepatobiliary System

     6 topics
    • Esophageal and gastric disorders
    • Small and large bowel pathology including IBD
    • Hepatitis, cirrhosis, and liver failure
    • Biliary and pancreatic disease
    • GI malignancies and screening
    • GI pharmacology and nutrition

  4. Renal & Genitourinary System

     6 topics
    • Renal Physiology
      • Glomerular filtration and tubular transport
      • Acid-base and electrolyte regulation
    • Glomerular and tubulointerstitial disease
    • Acute kidney injury and chronic kidney disease
    • Fluid, electrolyte, and acid-base disorders
    • Urinary tract infections and nephrolithiasis
    • Diuretics and renal pharmacology

  5. Endocrine & Reproductive Systems

     6 topics
    • Hypothalamic-pituitary axis disorders
    • Thyroid and parathyroid disease
    • Diabetes mellitus and adrenal disorders
    • Male and female reproductive endocrinology
    • Pregnancy physiology and complications
    • Endocrine and reproductive pharmacology

  6. Hematologic & Lymphoreticular Systems

     5 topics
    • Anemias: microcytic, macrocytic, hemolytic
    • Coagulation disorders and thrombophilia
    • Leukemias and lymphomas
    • Plasma cell disorders and myeloproliferative neoplasms
    • Blood transfusion and hematologic pharmacology

  7. Neurologic, Musculoskeletal & Integumentary Systems

     6 topics
    • Cerebrovascular disease and neuroanatomy
    • Neurodegenerative and demyelinating disorders
    • Seizures, headache, and CNS infections
    • CNS tumors and neurocutaneous syndromes
    • Bone, joint, and autoimmune connective tissue disease
    • Dermatologic pathology and skin malignancy

Medical Council Step exam for International Medical Graduates / ECFMG Certification USMLE Step 1 & Step 2: Organ Systems Pathophysiology flashcards — 58 questions with answers

  1. What is the Fick principle equation for calculating cardiac output?

    CO = VO2 / (CaO2 − CvO2), where VO2 is oxygen consumption and (CaO2 − CvO2) is the arteriovenous oxygen content difference. Equivalently, CO = HR × stroke volume.

  2. List the three primary determinants of myocardial oxygen demand.

    Heart rate, contractility, and wall tension (which depends on preload/ventricular radius and afterload). Wall stress is described by Laplace's law: T = (P × r) / (2 × wall thickness).

  3. In stable angina vs. unstable angina vs. NSTEMI vs. STEMI, what distinguishes them?

    Stable angina: exertional pain, no troponin rise, no ST elevation. Unstable angina: rest pain, no troponin rise. NSTEMI: troponin elevated, ST depression/T-wave changes, no ST elevation. STEMI: troponin elevated with ST-segment elevation (transmural infarct, full vessel occlusion).

  4. What is the timeline of histologic changes after a myocardial infarction (0–24h, 1–3d, 3–14d, >2wk)?

    0–24h: coagulative necrosis begins, wavy fibers, contraction bands. 1–3d: neutrophil infiltration (risk of fibrinous pericarditis). 3–14d: macrophages, granulation tissue (highest rupture risk ~day 5–7). >2wk to months: collagen scar formation.

  5. Differentiate systolic (HFrEF) from diastolic (HFpEF) heart failure.

    HFrEF: reduced ejection fraction (<40%), impaired contractility, dilated ventricle (eccentric hypertrophy). HFpEF: preserved EF (≥50%), impaired ventricular relaxation/filling, concentric hypertrophy, often from hypertension.

  6. Compare dilated, hypertrophic, and restrictive cardiomyopathy by ventricular morphology and systolic/diastolic function.

    Dilated: dilated chambers, systolic dysfunction (low EF). Hypertrophic: thick septum/wall, diastolic dysfunction, often outflow obstruction. Restrictive: stiff/non-compliant walls, diastolic dysfunction with preserved EF (e.g., amyloid, sarcoid, hemochromatosis).

  7. On ECG, how do you distinguish first-, second- (Mobitz I and II), and third-degree AV block?

    First-degree: PR >200ms, all beats conduct. Mobitz I (Wenckebach): progressive PR lengthening until a dropped QRS. Mobitz II: constant PR with sudden dropped QRS (risk of progression). Third-degree (complete): P waves and QRS completely dissociated.

  8. What ECG findings characterize atrial fibrillation, and what is its main embolic complication?

    Irregularly irregular rhythm with absent discrete P waves and a fibrillatory baseline. Risk of left atrial thrombus formation leading to cardioembolic stroke; stratify with CHA2DS2-VASc and anticoagulate accordingly.

  9. Describe the murmurs of aortic stenosis vs. aortic regurgitation vs. mitral regurgitation vs. mitral stenosis.

    Aortic stenosis: crescendo-decrescendo systolic murmur radiating to carotids. Aortic regurgitation: early diastolic decrescendo murmur, wide pulse pressure. Mitral regurgitation: holosystolic murmur radiating to axilla. Mitral stenosis: opening snap followed by mid-diastolic rumble.

  10. Which congenital heart defects cause right-to-left shunts (cyanotic), and name the 5 Ts.

    Cyanotic = right-to-left shunt. The 5 Ts: Truncus arteriosus, Transposition of great vessels, Tricuspid atresia, Tetralogy of Fallot, Total anomalous pulmonary venous return.

  11. What are the four components of Tetralogy of Fallot?

    Pulmonary stenosis (right ventricular outflow obstruction), right ventricular hypertrophy, overriding aorta, and ventricular septal defect. Severity of cyanosis is determined by the degree of pulmonary stenosis; "boot-shaped" heart on X-ray.

  12. Classify the major antihypertensive/antianginal drug classes and one key mechanism of each.

    ACE inhibitors/ARBs: block angiotensin II (reduce afterload, renoprotective). Beta-blockers: reduce HR/contractility/O2 demand. Calcium channel blockers: vasodilation (dihydropyridines) or rate control (non-dihydropyridines). Nitrates: venodilation reducing preload. Diuretics: reduce volume.

  13. State the alveolar gas equation and what it is used for.

    PAO2 = FiO2 × (Patm − PH2O) − (PaCO2 / R), typically PAO2 = 150 − PaCO2/0.8 on room air at sea level. Used to calculate the A-a gradient to distinguish causes of hypoxemia.

  14. What are the five causes of hypoxemia, and which correct with supplemental oxygen?

    Hypoventilation (normal A-a gradient), high altitude/low FiO2 (normal A-a), V/Q mismatch, diffusion limitation, and right-to-left shunt (all increase A-a gradient). All correct with O2 except a true shunt, which does not.

  15. Contrast asthma and COPD in terms of reversibility, pathology, and DLCO.

    Asthma: reversible bronchoconstriction, airway hyperresponsiveness/inflammation (eosinophils), normal/increased DLCO. COPD: largely irreversible obstruction; chronic bronchitis (mucus, Reid index increase) or emphysema (alveolar destruction, decreased DLCO).

  16. How do FEV1/FVC ratio, lung volumes, and DLCO differ between obstructive and restrictive lung disease?

    Obstructive: decreased FEV1/FVC (<0.7), increased TLC/RV (air trapping). Restrictive: normal/increased FEV1/FVC, decreased TLC/RV/FVC. DLCO decreases in emphysema and interstitial fibrosis but is normal/elevated in chronic bronchitis and chest-wall restriction.

  17. What is the classic histology and presentation of idiopathic pulmonary fibrosis (usual interstitial pneumonia)?

    Patchy fibrosis with temporal heterogeneity, fibroblastic foci, and honeycombing (subpleural, basal predominance). Presents with progressive dyspnea, dry cough, and inspiratory "velcro" crackles; restrictive pattern with low DLCO.

  18. Compare primary (Ghon) tuberculosis with secondary (reactivation) TB location and findings.

    Primary TB: Ghon complex (lower/mid-lobe subpleural lesion + hilar node), usually asymptomatic, forms latent granuloma. Secondary/reactivation: apical (upper lobe) cavitary disease due to high O2 tension; caseating granulomas with Langhans giant cells; risk of miliary spread.

  19. Distinguish small cell lung carcinoma from non-small cell types in location, smoking link, and treatment.

    Small cell: central, strong smoking link, neuroendocrine origin, paraneoplastic syndromes (SIADH, Cushing, Lambert-Eaton), treated with chemo/radiation (not surgery), aggressive. NSCLC (adeno-peripheral, squamous-central, large cell): surgery possible if localized.

  20. Differentiate transudative from exudative pleural effusions using Light's criteria.

    Exudate meets ≥1 of Light's criteria: pleural/serum protein >0.5, pleural/serum LDH >0.6, or pleural LDH >2/3 upper normal serum limit. Transudate (none met): from CHF, cirrhosis, nephrotic syndrome. Exudate: infection, malignancy, PE, inflammation.

Show the other 38 USMLE Step 1 & Step 2: Organ Systems Pathophysiology flashcards

  1. What is the classic triad and characteristic ABG finding in acute pulmonary embolism?

    Classic features: sudden dyspnea, pleuritic chest pain, and tachycardia/hypoxia. ABG shows hypoxemia with respiratory alkalosis (low PaCO2 from hyperventilation) and an increased A-a gradient. ECG may show S1Q3T3; CT angiography is the diagnostic test of choice.

  2. Distinguish the Berlin definition / hallmark of ARDS (acute respiratory failure).

    ARDS: acute onset (within 1 week), bilateral pulmonary infiltrates not from cardiac failure (PCWP <18), and PaO2/FiO2 <300. Caused by diffuse alveolar damage with non-cardiogenic pulmonary edema and hyaline membranes; managed with low-tidal-volume ventilation.

  3. Differentiate GERD, Barrett esophagus, and the two main esophageal cancers.

    GERD: acid reflux, can erode mucosa. Barrett esophagus: metaplasia from squamous to nonciliated columnar epithelium with goblet cells (premalignant). Adenocarcinoma: distal esophagus, arises from Barrett. Squamous cell carcinoma: upper/mid esophagus, linked to smoking/alcohol.

  4. What organism causes most peptic ulcers, and how do gastric vs. duodenal ulcers relate to meals and malignancy risk?

    H. pylori (also NSAIDs). Duodenal ulcers: pain improves with food, increased acid, almost never malignant. Gastric ulcers: pain worsens with food, can be malignant—biopsy required. H. pylori is associated with gastric adenocarcinoma and MALT lymphoma.

  5. Compare Crohn disease and ulcerative colitis in distribution, depth, and complications.

    Crohn: any GI segment (skip lesions, often terminal ileum), transmural inflammation, non-caseating granulomas, fistulae/strictures, cobblestoning. UC: continuous colonic involvement from rectum, mucosal/submucosal only, crypt abscesses, toxic megacolon, higher colon cancer risk.

  6. What are the key serum markers and complications of cirrhosis?

    Cirrhosis (irreversible fibrosis with regenerative nodules) causes portal hypertension (varices, ascites, splenomegaly, caput medusae), hepatic encephalopathy (high ammonia), coagulopathy (low synthesis), hypoalbuminemia, jaundice, and increased hepatocellular carcinoma risk (elevated AFP).

  7. Compare hepatitis A, B, C, D, and E by transmission and chronicity.

    HAV: fecal-oral, acute only. HBV: blood/sexual/perinatal, DNA virus, can become chronic and cause HCC. HCV: blood-borne, RNA, frequently chronic, HCC risk. HDV: requires HBV coinfection/superinfection. HEV: fecal-oral, acute, dangerous in pregnant women.

  8. Distinguish the classic causes and presentation of acute cholecystitis, choledocholithiasis, and ascending cholangitis.

    Acute cholecystitis: cystic duct stone, RUQ pain/fever, positive Murphy sign. Choledocholithiasis: common bile duct stone, jaundice. Ascending cholangitis: CBD obstruction + infection, Charcot triad (RUQ pain, jaundice, fever) ± Reynolds pentad (+hypotension, confusion).

  9. What are the two leading causes of acute pancreatitis and the diagnostic enzyme findings?

    Gallstones and alcohol are the top causes (also hypertriglyceridemia, drugs, scorpion sting, ERCP). Diagnosis: epigastric pain radiating to back plus elevated lipase (more specific) and amylase; complications include pseudocyst, necrosis, and ARDS.

  10. What are the screening recommendations and key precursor lesion for colorectal cancer?

    Average-risk screening begins at age 45 (colonoscopy every 10 years or stool-based tests). Most colorectal cancers arise from adenomatous polyps via the adenoma-carcinoma sequence (APC → KRAS → p53). CEA is used for monitoring, not screening.

  11. Match these GI drugs to mechanism: omeprazole, ranitidine, ondansetron, metoclopramide, octreotide.

    Omeprazole: proton pump inhibitor (blocks H+/K+ ATPase). Ranitidine: H2-receptor antagonist. Ondansetron: 5-HT3 antagonist (antiemetic). Metoclopramide: D2 antagonist prokinetic (risk of tardive dyskinesia). Octreotide: somatostatin analog (variceal bleeding, secretory tumors).

  12. Write the equations for GFR estimation via clearance and for filtration fraction.

    Clearance of substance X: Cx = (Ux × V) / Px. GFR is estimated by inulin or creatinine clearance. Renal plasma flow (RPF) ≈ PAH clearance. Filtration fraction = GFR / RPF (normal ~0.20).

  13. Contrast nephritic and nephrotic syndromes by hallmark findings.

    Nephritic: hematuria, RBC casts, hypertension, mild proteinuria, oliguria (inflammatory, e.g., post-strep GN, IgA nephropathy). Nephrotic: proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia (e.g., minimal change, FSGS, membranous).

  14. Differentiate prerenal, intrinsic (ATN), and postrenal acute kidney injury using BUN/Cr ratio and FENa.

    Prerenal: BUN/Cr >20, FENa <1% (intact tubules reabsorbing Na). Intrinsic/ATN: BUN/Cr 10–15, FENa >2%, muddy brown granular casts. Postrenal: obstruction; early prerenal-like, later intrinsic pattern. CKD = GFR <60 for ≥3 months.

  15. 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.

  16. 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.

  17. 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).

  18. 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.

  19. 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).

  20. 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).

  21. 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.

  22. 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).

  23. 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).

  24. 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.

  25. 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.

  26. 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).

  27. 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).

  28. 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).

  29. 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.

  30. 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.

  31. 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.

  32. 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.

  33. 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).

  34. 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.

  35. 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.

  36. 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).

  37. 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.

  38. 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.

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

What is in the Medical Council Step exam for International Medical Graduates / ECFMG Certification USMLE Step 1 & Step 2: Organ Systems Pathophysiology syllabus?

Medical Council Step exam for International Medical Graduates / ECFMG Certification USMLE Step 1 & Step 2: Organ Systems Pathophysiology is split into 7 chapters: Cardiovascular System, Respiratory System, Gastrointestinal & Hepatobiliary System, Renal & Genitourinary System, Endocrine & Reproductive Systems, Hematologic & Lymphoreticular Systems and Neurologic, Musculoskeletal & Integumentary Systems. Together they contain 41 topics and 10 sub-topics.

How many chapters are in Medical Council Step exam for International Medical Graduates / ECFMG Certification USMLE Step 1 & Step 2: Organ Systems Pathophysiology?

7 chapters, containing 41 topics and 10 sub-topics. The largest chapter is Cardiovascular System, with 6 topics.

Are there flashcards for Medical Council Step exam for International Medical Graduates / ECFMG Certification USMLE Step 1 & Step 2: Organ Systems Pathophysiology?

Yes — a 58-card USMLE Step 1 & Step 2: Organ Systems Pathophysiology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.