NURS 611 / NURS611 Exam 3: Advanced Pathophysiology –
Maryville University Actual Exam Complete Questions &
Rationales | Complex Disease Processes | Pass Guaranteed -
A+ Graded
Cardiovascular Pathophysiology
Q1: A 58-year-old male with a 20-pack-year smoking history and dyslipidemia is found to
have elevated blood pressure. Biopsy of his renal artery shows intimal thickening and
inflammation. This patient most likely has which form of hypertension?
A. Primary essential hypertension from increased SVR
B. Secondary hypertension from renal artery stenosis activating RAAS [CORRECT]
C. Pheochromocytoma-mediated hypertension from catecholamine excess
D. Primary aldosteronism from adrenal adenoma
Correct Answer: B
Rationale: The best answer is B. Renal artery stenosis reduces perfusion pressure to the
kidney, tricking the juxtaglomerular apparatus into releasing renin and activating the
RAAS cascade — that drives angiotensin II-mediated vasoconstriction and
aldosterone-mediated sodium retention, producing secondary hypertension.
Q2: A patient with long-standing hypertension develops left ventricular hypertrophy and
mildly reduced ejection fraction. At the cellular level, sustained elevation in afterload
leads to myocyte hypertrophy primarily through which mechanism?
A. Increased preload stretching the ventricular wall
B. Pressure overload triggering parallel sarcomere addition and concentric remodeling
[CORRECT]
C. Volume overload causing eccentric remodeling with chamber dilation
D. Apoptosis of cardiomyocytes from ischemic injury
Correct Answer: B
Rationale: The best answer is B. Chronic pressure overload from hypertension causes
individual myocytes to add sarcomeres in parallel, leading to concentric left ventricular
,hypertrophy — the wall thickens but the chamber size stays relatively normal, at least
initially.
Q3: A 67-year-old patient has crushing substernal chest pain that radiates to the jaw.
Troponins are elevated. At autopsy, the myocardium shows coagulative necrosis with
neutrophilic infiltration. Which pathophysiologic event initiated this process?
A. Coronary vasospasm without thrombosis
B. Rupture of an atherosclerotic plaque with thrombus formation and vessel occlusion
[CORRECT]
C. Gradual stenosis without acute thrombotic event
D. Embolization from an atrial mural thrombus
Correct Answer: B
Rationale: The best answer is B. Most acute myocardial infarctions start with rupture of
a vulnerable atherosclerotic plaque — the fibrous cap tears, exposing thrombogenic
material to the bloodstream, and a platelet-rich thrombus forms that occludes the
coronary artery, cutting off oxygen supply and causing coagulative necrosis.
Q4: A patient with coronary artery disease experiences chest pain when climbing stairs
that resolves completely with rest. There is no troponin elevation. This pattern
represents:
A. Unstable angina from plaque rupture and non-occlusive thrombus
B. Stable angina from fixed atherosclerotic plaque causing supply-demand mismatch
[CORRECT]
C. Prinzmetal's angina from coronary vasospasm at rest
D. Non-ST-elevation myocardial infarction
Correct Answer: B
Rationale: The best answer is B. Stable angina is predictable — it happens when
myocardial oxygen demand exceeds the fixed supply through a hemodynamically
significant stenosis, and it reliably resolves when demand drops. There's no plaque
rupture or cell death, which is why troponins stay normal.
Q5: A patient with an acute anterior wall STEMI develops hypotension, pulmonary
edema, and an S3 gallop 48 hours after presentation. The NP understands that
extensive myocardial necrosis has led to:
A. Acute right ventricular failure from inferior wall damage
, B. Cardiogenic shock from loss of contractile function and decreased cardiac output
[CORRECT]
C. Hypertrophic cardiomyopathy from compensatory remodeling
D. Cardiac tamponade from ventricular free wall rupture
Correct Answer: B
Rationale: The best answer is B. When a large territory of myocardium infarcts, the
viable muscle mass drops, stroke volume falls, and the heart can't maintain perfusion
despite compensatory vasoconstriction — that's cardiogenic shock, with backup into the
lungs causing pulmonary edema and the S3 reflecting rapid ventricular filling into a
failing ventricle.
Q6: A 72-year-old patient with heart failure has an ejection fraction of 30% and dilated
left ventricular cavity. Another patient with heart failure has an ejection fraction of 55%
but severely thickened, stiff ventricular walls with impaired relaxation. Which statement
best describes the key pathophysiologic distinction between these two patients?
A. Both have systolic dysfunction from reduced contractility
B. The first patient has HFrEF with reduced contractility; the second has HFpEF with
diastolic dysfunction and impaired ventricular filling [CORRECT]
C. The first patient has primary valvular disease; the second has infiltrative
cardiomyopathy
D. Both have restrictive cardiomyopathy from amyloid deposition
Correct Answer: B
Rationale: The best answer is B. HFrEF is a forward failure problem — the heart can't
contract effectively, so ejection fraction drops and the chamber dilates. HFpEF is a
backward failure problem — the heart can't relax and fill properly during diastole
because the walls are stiff, so pressures back up into the lungs despite a preserved
ejection fraction.
Q7: A patient with HFrEF develops peripheral edema, JVD, and hepatomegaly. Which
compensatory mechanism, while initially adaptive, ultimately contributes to disease
progression?
A. Decreased sympathetic nervous system activity
B. RAAS activation causing vasoconstriction, sodium retention, and adverse myocardial
remodeling [CORRECT]
C. Decreased preload from venodilation
Maryville University Actual Exam Complete Questions &
Rationales | Complex Disease Processes | Pass Guaranteed -
A+ Graded
Cardiovascular Pathophysiology
Q1: A 58-year-old male with a 20-pack-year smoking history and dyslipidemia is found to
have elevated blood pressure. Biopsy of his renal artery shows intimal thickening and
inflammation. This patient most likely has which form of hypertension?
A. Primary essential hypertension from increased SVR
B. Secondary hypertension from renal artery stenosis activating RAAS [CORRECT]
C. Pheochromocytoma-mediated hypertension from catecholamine excess
D. Primary aldosteronism from adrenal adenoma
Correct Answer: B
Rationale: The best answer is B. Renal artery stenosis reduces perfusion pressure to the
kidney, tricking the juxtaglomerular apparatus into releasing renin and activating the
RAAS cascade — that drives angiotensin II-mediated vasoconstriction and
aldosterone-mediated sodium retention, producing secondary hypertension.
Q2: A patient with long-standing hypertension develops left ventricular hypertrophy and
mildly reduced ejection fraction. At the cellular level, sustained elevation in afterload
leads to myocyte hypertrophy primarily through which mechanism?
A. Increased preload stretching the ventricular wall
B. Pressure overload triggering parallel sarcomere addition and concentric remodeling
[CORRECT]
C. Volume overload causing eccentric remodeling with chamber dilation
D. Apoptosis of cardiomyocytes from ischemic injury
Correct Answer: B
Rationale: The best answer is B. Chronic pressure overload from hypertension causes
individual myocytes to add sarcomeres in parallel, leading to concentric left ventricular
,hypertrophy — the wall thickens but the chamber size stays relatively normal, at least
initially.
Q3: A 67-year-old patient has crushing substernal chest pain that radiates to the jaw.
Troponins are elevated. At autopsy, the myocardium shows coagulative necrosis with
neutrophilic infiltration. Which pathophysiologic event initiated this process?
A. Coronary vasospasm without thrombosis
B. Rupture of an atherosclerotic plaque with thrombus formation and vessel occlusion
[CORRECT]
C. Gradual stenosis without acute thrombotic event
D. Embolization from an atrial mural thrombus
Correct Answer: B
Rationale: The best answer is B. Most acute myocardial infarctions start with rupture of
a vulnerable atherosclerotic plaque — the fibrous cap tears, exposing thrombogenic
material to the bloodstream, and a platelet-rich thrombus forms that occludes the
coronary artery, cutting off oxygen supply and causing coagulative necrosis.
Q4: A patient with coronary artery disease experiences chest pain when climbing stairs
that resolves completely with rest. There is no troponin elevation. This pattern
represents:
A. Unstable angina from plaque rupture and non-occlusive thrombus
B. Stable angina from fixed atherosclerotic plaque causing supply-demand mismatch
[CORRECT]
C. Prinzmetal's angina from coronary vasospasm at rest
D. Non-ST-elevation myocardial infarction
Correct Answer: B
Rationale: The best answer is B. Stable angina is predictable — it happens when
myocardial oxygen demand exceeds the fixed supply through a hemodynamically
significant stenosis, and it reliably resolves when demand drops. There's no plaque
rupture or cell death, which is why troponins stay normal.
Q5: A patient with an acute anterior wall STEMI develops hypotension, pulmonary
edema, and an S3 gallop 48 hours after presentation. The NP understands that
extensive myocardial necrosis has led to:
A. Acute right ventricular failure from inferior wall damage
, B. Cardiogenic shock from loss of contractile function and decreased cardiac output
[CORRECT]
C. Hypertrophic cardiomyopathy from compensatory remodeling
D. Cardiac tamponade from ventricular free wall rupture
Correct Answer: B
Rationale: The best answer is B. When a large territory of myocardium infarcts, the
viable muscle mass drops, stroke volume falls, and the heart can't maintain perfusion
despite compensatory vasoconstriction — that's cardiogenic shock, with backup into the
lungs causing pulmonary edema and the S3 reflecting rapid ventricular filling into a
failing ventricle.
Q6: A 72-year-old patient with heart failure has an ejection fraction of 30% and dilated
left ventricular cavity. Another patient with heart failure has an ejection fraction of 55%
but severely thickened, stiff ventricular walls with impaired relaxation. Which statement
best describes the key pathophysiologic distinction between these two patients?
A. Both have systolic dysfunction from reduced contractility
B. The first patient has HFrEF with reduced contractility; the second has HFpEF with
diastolic dysfunction and impaired ventricular filling [CORRECT]
C. The first patient has primary valvular disease; the second has infiltrative
cardiomyopathy
D. Both have restrictive cardiomyopathy from amyloid deposition
Correct Answer: B
Rationale: The best answer is B. HFrEF is a forward failure problem — the heart can't
contract effectively, so ejection fraction drops and the chamber dilates. HFpEF is a
backward failure problem — the heart can't relax and fill properly during diastole
because the walls are stiff, so pressures back up into the lungs despite a preserved
ejection fraction.
Q7: A patient with HFrEF develops peripheral edema, JVD, and hepatomegaly. Which
compensatory mechanism, while initially adaptive, ultimately contributes to disease
progression?
A. Decreased sympathetic nervous system activity
B. RAAS activation causing vasoconstriction, sodium retention, and adverse myocardial
remodeling [CORRECT]
C. Decreased preload from venodilation
