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Preparation for candidates sitting:

USMLE

USMLE Step 1

1,200 questions12 mock exams6 months

Practice with exam-style questions, detailed rationales, timed mock exams, and tracking that shows your weak topics.

  • Mapped to the blueprintEvery question sits under an official outline heading — not a scraped MCQ dump.
  • A rationale on every answerWhy the key is right, and why each distractor was written to tempt you.
  • Timed mock examsSame clock, same length, same question style as the real sitting.
  • One bank, several authoritiesValid preparation for the regulators listed on this page.

2,400 practitioners have studied with this bank

Written as preparation for

USMLEUnited States Medical Licensing Examination
1,200
Questions
12
Mock exams
2,400
Subscribers
6 months
Access
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Sample questions

Same stem length, same distractor style, same rationale you get inside the bank.

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Read the USMLE Step 1 sample questions

  1. 1.A 62-year-old man is brought to the emergency department with crushing substernal chest pain radiating to his left arm that began 90 minutes ago. An ECG shows ST-segment elevation in leads II, III, and aVF. Which coronary artery is most likely occluded?
    • A.Left anterior descending artery
    • B.Left circumflex artery
    • C.Right coronary arteryCorrect
    • D.Left main coronary artery

    Why: ST elevation in the inferior leads (II, III, aVF) indicates an inferior wall myocardial infarction, which in most patients is supplied by the right coronary artery. The RCA also supplies the SA and AV nodes in most individuals, explaining the association with bradyarrhythmias in inferior MI.

  2. 2.A 55-year-old woman with a long history of poorly controlled hypertension is found to have concentric left ventricular hypertrophy on echocardiography. At the cellular level, which change best explains the increased ventricular wall thickness?
    • A.Hyperplasia of cardiac myocytes
    • B.Addition of sarcomeres in parallel within existing myocytesCorrect
    • C.Addition of sarcomeres in series within existing myocytes
    • D.Interstitial deposition of amyloid protein

    Why: Pressure overload from chronic hypertension causes concentric hypertrophy through the addition of sarcomeres in parallel, increasing myocyte width and wall thickness. Cardiac myocytes are terminally differentiated and cannot undergo hyperplasia. Adding sarcomeres in series (volume overload) causes eccentric hypertrophy with chamber dilation.

  3. 3.A 24-year-old man collapses during a basketball game and dies. Autopsy reveals asymmetric septal hypertrophy with myofiber disarray. This condition is most commonly caused by a mutation affecting which structure?
    • A.Sarcomeric proteins such as beta-myosin heavy chainCorrect
    • B.Cardiac sodium channels
    • C.Dystrophin
    • D.Lamin A/C

    Why: Hypertrophic cardiomyopathy is most often caused by autosomal dominant mutations in sarcomeric proteins, especially beta-myosin heavy chain and myosin-binding protein C. The resulting asymmetric septal hypertrophy and myofiber disarray predispose young athletes to sudden cardiac death from ventricular arrhythmias.

  4. 4.A 70-year-old man with heart failure is started on a medication that blocks the effects of angiotensin II. He develops a persistent dry cough. Which mechanism best explains this side effect?
    • A.Decreased aldosterone secretion
    • B.Reflex bronchoconstriction from hypotension
    • C.Increased bradykinin levelsCorrect
    • D.Direct irritation of bronchial mucosa

    Why: ACE inhibitors block angiotensin-converting enzyme, which normally degrades bradykinin. The resulting accumulation of bradykinin causes the characteristic dry cough and can also produce angioedema. This distinguishes ACE inhibitors from angiotensin receptor blockers, which do not raise bradykinin and rarely cause cough.

  5. 5.A researcher measures the pressure-volume relationship of a patient's left ventricle. During which phase of the cardiac cycle does the aortic valve open?
    • A.Isovolumetric contraction
    • B.At the onset of ventricular ejection when LV pressure exceeds aortic pressureCorrect
    • C.During rapid ventricular filling
    • D.Isovolumetric relaxation

    Why: The aortic valve opens when left ventricular pressure rises above aortic pressure at the end of isovolumetric contraction, marking the beginning of the ejection phase. During isovolumetric contraction all valves are closed and volume is constant as pressure builds.

  6. 6.A 3-day-old infant develops cyanosis. Echocardiography shows the aorta arising from the right ventricle and the pulmonary artery arising from the left ventricle. This defect results from failure of which embryologic process?
    • A.Fusion of the endocardial cushions
    • B.Closure of the ostium secundum
    • C.Spiraling of the aorticopulmonary septumCorrect
    • D.Formation of the ductus arteriosus

    Why: Transposition of the great arteries results from failure of the aorticopulmonary (spiral) septum to spiral normally, producing parallel rather than crossing outflow tracts. Survival depends on a shunt such as a patent ductus arteriosus, patent foramen ovale, or VSD to allow mixing of oxygenated and deoxygenated blood.

  7. 7.A 68-year-old woman presents with exertional chest pain and syncope. Cardiac examination reveals a harsh crescendo-decrescendo systolic murmur best heard at the right upper sternal border that radiates to the carotids. Which valvular lesion is most likely?
    • A.Mitral regurgitation
    • B.Aortic stenosisCorrect
    • C.Aortic regurgitation
    • D.Mitral stenosis

    Why: Aortic stenosis produces a crescendo-decrescendo systolic ejection murmur at the right upper sternal border radiating to the carotids. The classic triad of angina, syncope, and heart failure reflects the fixed obstruction to left ventricular outflow. In the elderly it is most often due to calcific degeneration.

  8. 8.A 45-year-old man with a history of intravenous drug use develops fever and a new holosystolic murmur at the left lower sternal border that increases with inspiration. Blood cultures grow Staphylococcus aureus. Which valve is most likely affected?
    • A.Aortic valve
    • B.Mitral valve
    • C.Tricuspid valveCorrect
    • D.Pulmonic valve

    Why: In intravenous drug users, infective endocarditis most commonly affects the tricuspid valve because venous blood carrying organisms reaches the right heart first. Staphylococcus aureus is the most common pathogen. A right-sided murmur classically increases with inspiration (Carvallo sign) due to augmented venous return.

  9. 9.A physiologist studies the electrical activity of the SA node. The spontaneous depolarization (phase 4) that gives the SA node its automaticity is primarily due to which ionic current?
    • A.Rapid inward sodium current through fast sodium channels
    • B.Outward potassium current
    • C.Inward calcium current through L-type channels
    • D.Funny current (If) carried by inward sodium flowCorrect

    Why: The gradual phase 4 depolarization of SA nodal cells is driven largely by the funny current (If), a slow inward flow of sodium through HCN channels activated by hyperpolarization. This spontaneous drift toward threshold underlies the pacemaker automaticity. The upstroke (phase 0) in nodal cells is then carried by L-type calcium current, not fast sodium channels.

  10. 10.A 58-year-old man is started on a calcium channel blocker for hypertension. The drug preferentially acts on vascular smooth muscle with little effect on the heart. Which agent was most likely prescribed?
    • A.Verapamil
    • B.Diltiazem
    • C.AmlodipineCorrect
    • D.Digoxin

    Why: Dihydropyridine calcium channel blockers such as amlodipine act preferentially on vascular smooth muscle, producing vasodilation with minimal direct cardiac effect. Non-dihydropyridines (verapamil, diltiazem) have greater negative inotropic and chronotropic effects on the heart. Digoxin is not a calcium channel blocker.

What you get

Why candidates choose this bank

Written like the exam

Single-best-answer items in the exam's own phrasing and length — clinical vignette first, then the lead-in question.

Rationales, not answer keys

Each explanation says why the key is correct and why the other options were built to look correct.

Full-length timed papers

Complete papers under the real clock, scored by topic so you can see where the marks leaked.

Weak-topic tracking

Your dashboard ranks topics by accuracy and pushes the weakest ones back into your next session.

Updated with the blueprint

When the authority revises the outline, the bank is revised. Updates are free for your whole term.

Built for gaps in the day

Works on phone, tablet and desktop; progress syncs, so ten minutes between patients still counts.

Available exams

12 timed mock exams

60 minutes each • 70% target score

MockQuestionsTime
Quiz 1Free sample — 10 questions10060 minSee sample questions
Quiz 210060 minIncluded with full access
Quiz 310060 minIncluded with full access
Quiz 410060 minIncluded with full access
Quiz 510060 minIncluded with full access
Quiz 610060 minIncluded with full access
The plan

Your 4-step preparation plan

1

Subscribe

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2

Sit a baseline mock

A timed paper on day one. You need a real score before you build a plan.

3

Drill your weak topics

Work the lowest-scoring topics until they move.

4

Rehearse the real thing

A full timed mock in the final week, so exam-day pressure is already familiar.

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Frequently asked questions

No. Real exam questions are confidential and we do not reproduce them. These are original questions written to the same style, difficulty and blueprint as the exam, so practising them prepares you for the real paper.

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