(3 Sets) Question Bank (Latest 2026/2027 Edition) –
Questions, Answers & Detailed Rationales
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SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY
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Question 1
A 68-year-old male with a 40-pack-year smoking history presents with crushing
substernal chest pain radiating to the left arm. Troponin I is elevated at 4.2 ng/mL.
Which pathophysiologic mechanism best explains the myocardial injury in this patient?
A. Coronary vasospasm without underlying plaque rupture
B. Rupture of atherosclerotic plaque with subsequent thrombus formation and vessel
occlusion
C. Demand ischemia from sustained tachycardia without coronary obstruction
D. Coronary artery dissection with intramural hematoma formation
Correct Answer:
B — Rupture of atherosclerotic plaque with subsequent thrombus formation and vessel
occlusion
Rationale:
Acute coronary syndrome in patients with significant smoking history typically results
from plaque rupture exposing thrombogenic core material, triggering platelet
aggregation and thrombus formation leading to vessel occlusion and myocardial
necrosis. Option A describes Prinzmetal angina, which is less common and not
associated with elevated troponins; option C describes type 2 MI without plaque
,rupture; option D is rare and typically seen in younger patients or those with connective
tissue disorders.
Question 2
A 72-year-old female with chronic hypertension develops progressive dyspnea on
exertion, orthopnea, and bilateral lower extremity edema. Echocardiography reveals
concentric left ventricular hypertrophy with preserved ejection fraction. Which cellular
mechanism primarily drives this pattern of cardiac remodeling?
A. Eccentric hypertrophy with increased sarcomeres in series
B. Concentric hypertrophy with increased sarcomeres in parallel
C. Myocardial cell apoptosis leading to chamber dilation
D. Replacement fibrosis with collagen deposition and scar formation
Correct Answer:
B — Concentric hypertrophy with increased sarcomeres in parallel
Rationale:
Chronic pressure overload from hypertension stimulates parallel addition of
sarcomeres, resulting in concentric hypertrophy with increased wall thickness and
preserved or reduced chamber volume. Option A describes volume overload patterns
seen in aortic regurgitation; option C describes the mechanism in dilated
cardiomyopathy; option D describes post-infarction remodeling rather than hypertensive
heart disease.
Question 3
A 55-year-old male with atrial fibrillation presents with acute onset left-sided weakness
and aphasia. CT scan shows no hemorrhage. Which pathophysiologic mechanism is
most likely responsible for this cerebrovascular event?
A. Embolization from left atrial thrombus due to blood stasis
,B. Hypertensive intraparenchymal hemorrhage
C. Atherosclerotic thrombosis of the middle cerebral artery
D. Venous sinus thrombosis with venous infarction
Correct Answer:
A — Embolization from left atrial thrombus due to blood stasis
Rationale:
Atrial fibrillation causes ineffective atrial contraction leading to blood stasis, particularly
in the left atrial appendage, promoting thrombus formation that can embolize to
cerebral circulation causing ischemic stroke. Option B is ruled out by negative CT for
hemorrhage; option C typically occurs in patients with significant carotid or intracranial
atherosclerosis; option D presents with different clinical features and risk factors.
Question 4
A 45-year-old female presents with fatigue, dyspnea, and a holosystolic murmur at the
apex radiating to the axilla. Echocardiography shows severe mitral regurgitation with left
atrial enlargement. Which hemodynamic consequence is most likely to develop first in
this patient?
A. Right ventricular pressure overload and pulmonary hypertension
B. Left ventricular volume overload with increased preload
C. Systemic hypotension and cardiogenic shock
D. Left ventricular outflow tract obstruction
Correct Answer:
B — Left ventricular volume overload with increased preload
Rationale:
Mitral regurgitation allows blood to flow backward into the left atrium during systole,
causing volume overload of both the left atrium and left ventricle with increased preload
as the primary initial hemodynamic consequence. Option A develops later as pulmonary
, venous hypertension leads to pulmonary arterial hypertension; option C occurs only in
acute severe regurgitation; option D is unrelated to mitral valve pathology.
Question 5
A 60-year-old male with diabetes mellitus presents with intermittent claudication in the
right calf. Ankle-brachial index is 0.65. Which pathophysiologic process best explains
his peripheral arterial disease?
A. Vasculitis with immune-mediated vessel wall inflammation
B. Atherosclerotic plaque formation with progressive luminal narrowing
C. Hypercoagulable state with recurrent in-situ thrombosis
D. Arterial wall calcification with loss of vascular compliance
Correct Answer:
B — Atherosclerotic plaque formation with progressive luminal narrowing
Rationale:
Peripheral arterial disease in diabetic patients primarily results from accelerated
atherosclerosis with plaque formation causing progressive stenosis and reduced distal
perfusion, clinically manifesting as claudication with ABI <0.90. Option A describes
vasculitic disorders; option C describes thromboembolic phenomena; option D
describes Monckeberg medial calcific sclerosis which does not typically cause
flow-limiting stenosis.
Question 6
A 28-year-old female presents with sudden onset tachycardia, palpitations, and
syncope. ECG shows wide-complex tachycardia with a rate of 220 bpm. Which
electrophysiologic mechanism is most consistent with this presentation?
A. Re-entry circuit involving the atrioventricular node
B. Enhanced automaticity in the sinoatrial node
C. Triggered activity from early afterdepolarizations