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

USMLE Step 1 & Step 2: Organ Systems Pathophysiology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for USMLE Step 1 & Step 2: Organ Systems Pathophysiology in Medical Council Step exam for International Medical Graduates / ECFMG Certification, not a summary of it.

1. 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. 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. 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. 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. 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. 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. 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

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

19 of 58 cards from the USMLE Step 1 & Step 2: Organ Systems Pathophysiology deck — real questions with worked 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.

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