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NSG 3850 Exam 2 Patho 2 Exam Questions and
Answers Practice Questions with Solutions Newest
| Already Graded A+
SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY (Questions 1-15)
1. A patient with chronic hypertension develops left ventricular hypertrophy. Which of the following
best explains the pathophysiologic mechanism of this adaptation?
A. Increased afterload leads to concentric hypertrophy of the left ventricle
B. Increased preload leads to eccentric hypertrophy of the left ventricle
C. Decreased contractility leads to ventricular dilation
D. Increased heart rate leads to myocardial fibrosis
✅ Correct Answer: A
RATIONALE:
Chronic hypertension increases afterload—the resistance the left ventricle must overcome to eject
blood. The ventricle adapts by adding sarcomeres in parallel, resulting in concentric
hypertrophy (thickened ventricular wall with normal or reduced chamber size). This preserves cardiac
output initially but eventually leads to diastolic dysfunction and heart failure with preserved ejection
fraction (HFpEF). Eccentric hypertrophy (B) occurs with volume overload (e.g., aortic regurgitation,
dilated cardiomyopathy), where sarcomeres are added in series, leading to chamber dilation.
HIGH-YIELD MARKUP: Pressure overload → Concentric hypertrophy (thick wall). Volume overload →
Eccentric hypertrophy (dilated chamber).
2. A patient with acute coronary syndrome has elevated troponin I and CK-MB. Which of the following
cellular events is the PRIMARY cause of these elevated biomarkers?
A. Reversible myocardial ischemia causing transient membrane dysfunction
B. Irreversible myocardial necrosis with release of intracellular proteins
C. Coronary artery vasospasm without myocyte injury
D. Stunned myocardium with temporary contractile dysfunction
✅ Correct Answer: B
RATIONALE:
Troponin I and T and CK-MB are intracellular proteins released into the bloodstream only when
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myocardial cells undergo irreversible necrosis (cell death). This occurs after 20-40 minutes of sustained
ischemia, when ATP depletion leads to sarcolemmal membrane disruption. Reversible ischemia (A)
causes functional changes (e.g., wall motion abnormalities) but does not release these
biomarkers. Vasospasm (C) may cause transient ischemia. Stunned myocardium (D) refers to prolonged
but reversible contractile dysfunction after reperfusion.
HIGH-YIELD MARKUP: *Troponin = Myocyte necrosis. Rises 2-4h after MI, peaks 12-24h, remains
elevated 7-14 days. CK-MB rises 4-6h, peaks 18-24h, normalizes in 48-72h.*
3. A patient with chronic heart failure has elevated B-type natriuretic peptide (BNP). Which of the
following best explains the pathophysiologic stimulus for BNP release?
A. Increased ventricular wall stretch due to volume overload
B. Decreased renal perfusion activating the renin-angiotensin system
C. Increased sympathetic nervous system activity
D. Myocardial ischemia causing cellular injury
✅ Correct Answer: A
RATIONALE:
BNP is a hormone synthesized and released by ventricular myocytes in response to increased wall
stretch from volume or pressure overload. Its physiologic effects include vasodilation, natriuresis, and
inhibition of the renin-angiotensin-aldosterone system (RAAS)—essentially counter-regulatory
mechanisms. Elevated BNP is a key diagnostic marker for heart failure, with levels correlating with
severity. Decreased renal perfusion (B) stimulates renin release. Sympathetic activation (C) releases
norepinephrine. Myocardial ischemia (D) releases troponin.
MARKUP NOTE: *BNP = Ventricular stretch. ANP = Atrial stretch. Both cause natriuresis and
vasodilation. BNP >100 pg/mL suggests HF.*
4. A patient with long-standing, poorly controlled hypertension develops proteinuria and a rising
serum creatinine. Which of the following pathophysiologic processes best explains the renal injury?
A. Hyaline arteriosclerosis of afferent and efferent arterioles leading to glomerular ischemia
B. Immune complex deposition in the glomerular basement membrane
C. Acute tubular necrosis from renal hypoperfusion
D. Obstructive uropathy from ureteral compression
✅ Correct Answer: A
RATIONALE:
Chronic hypertension causes hyaline arteriosclerosis—thickening and hyalinization of the walls of small
arteries and arterioles, particularly the afferent and efferent arterioles of the kidney. This narrows the
vessel lumen, reducing glomerular perfusion and causing ischemic glomerulosclerosis (nephrosclerosis).
The result is progressive loss of nephrons, proteinuria (usually <2 g/day), and rising creatinine. This is the
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most common cause of end-stage renal disease in older adults. Immune complex deposition (B)
describes glomerulonephritis. Acute tubular necrosis (C) is from acute ischemia or nephrotoxins.
Obstructive uropathy (D) causes postrenal AKI.
HIGH-YIELD MARKUP: Hypertensive nephrosclerosis = Benign nephrosclerosis. "Flea-bitten" kidney
appearance (granular surface).
5. A patient presents with crushing substernal chest pain radiating to the left arm, diaphoresis, and
nausea. ECG shows ST-segment elevation in leads V1-V4. Which of the following describes the
underlying pathophysiology?
A. Transmural myocardial ischemia due to complete occlusion of a coronary artery
B. Subendocardial ischemia due to partial coronary artery occlusion
C. Coronary artery vasospasm without atherosclerotic plaque
D. Myocardial oxygen demand exceeding supply without coronary occlusion
✅ Correct Answer: A
RATIONALE:
ST-segment elevation myocardial infarction (STEMI) indicates transmural ischemia—ischemia
extending through the full thickness of the ventricular wall. This is almost always caused by complete
thrombotic occlusion of an epicardial coronary artery, usually at the site of a ruptured atherosclerotic
plaque. The ECG leads correspond to the affected myocardial territory: V1-V4 indicates anterior
wall (left anterior descending artery territory). Subendocardial ischemia (B) causes ST-
segment depression (NSTEMI/unstable angina). Vasospasm (C) causes Prinzmetal angina. Demand-
supply mismatch (D) causes type 2 MI.
HIGH-YIELD MARKUP: *STEMI = Transmural = ST elevation. NSTEMI = Subendocardial = ST depression
or T-wave inversion. Anterior MI (V1-V4) = LAD occlusion → highest mortality.*
6. A patient with aortic stenosis develops syncope during exertion. Which of the following best
explains the pathophysiologic mechanism?
A. Fixed obstruction to left ventricular outflow prevents an increase in cardiac output to meet exercise
demands
B. Arrhythmia from myocardial ischemia causes sudden loss of consciousness
C. Reflex bradycardia from baroreceptor stimulation
D. Embolization of valvular vegetations to the cerebral circulation
✅ Correct Answer: A
RATIONALE:
In aortic stenosis, the stenotic valve creates a fixed obstruction to left ventricular outflow. During
exercise, peripheral vasodilation occurs in skeletal muscle, but the obstructed valve prevents a
compensatory increase in cardiac output. This leads to exercise-induced hypotension and cerebral
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hypoperfusion, causing syncope. The classic triad of severe aortic stenosis is: Angina, Syncope, and
Dyspnea (heart failure). Arrhythmias (B) may occur but are not the primary mechanism. Baroreceptor
reflex (C) would cause vasodilation and bradycardia in other conditions. Embolization (D) occurs in
infective endocarditis.
HIGH-YIELD MARKUP: Aortic Stenosis Triad = Angina, Syncope, Dyspnea. Syncope is exertional due to
fixed outflow obstruction.
7. Which of the following best describes the pathogenesis of atherosclerotic plaque rupture?
A. Smooth muscle cell proliferation and collagen synthesis stabilize the plaque
B. Inflammatory cell infiltration and matrix metalloproteinase degradation weaken the fibrous cap
C. Calcification of the plaque core increases its structural integrity
D. Endothelial cell regeneration covers and stabilizes the plaque surface
✅ Correct Answer: B
RATIONALE:
Plaque rupture is the precipitating event in most acute coronary syndromes. It occurs when the fibrous
cap overlying a lipid-rich atherosclerotic core becomes thin and weak. This weakening is driven
by inflammatory cells (macrophages, T-lymphocytes) that release matrix metalloproteinases (MMPs) ,
enzymes that degrade collagen and other extracellular matrix proteins. The result is cap rupture,
exposure of thrombogenic material (tissue factor, collagen), and acute thrombus formation. Smooth
muscle proliferation (A) and calcification (C) contribute to plaque growth and stenosis but not acute
rupture. Endothelial regeneration (D) is protective.
HIGH-YIELD MARKUP: "Vulnerable plaque" = Large lipid core + Thin fibrous cap + Inflammation. MMPs
degrade the cap → Rupture → Thrombosis.
8. A patient with chronic heart failure develops pitting edema, jugular venous distention, and
hepatomegaly. Which of the following best explains these findings?
A. Left ventricular failure causing pulmonary congestion
B. Right ventricular failure causing systemic venous congestion
C. Biventricular failure causing both pulmonary and systemic congestion
D. Pericardial constriction limiting diastolic filling
✅ Correct Answer: B
RATIONALE:
The triad of pitting edema, jugular venous distention (JVD), and hepatomegaly are classic signs
of right-sided heart failure. Right ventricular failure impairs the heart's ability to pump blood forward
into the pulmonary circulation, causing blood to "back up" into the systemic venous system. This
increases hydrostatic pressure in systemic capillaries, leading to peripheral edema, and causes
congestion of the liver (hepatomegaly) and jugular veins (JVD). Left-sided failure (A) causes pulmonary
NSG 3850 Exam 2 Patho 2 Exam Questions and
Answers Practice Questions with Solutions Newest
| Already Graded A+
SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY (Questions 1-15)
1. A patient with chronic hypertension develops left ventricular hypertrophy. Which of the following
best explains the pathophysiologic mechanism of this adaptation?
A. Increased afterload leads to concentric hypertrophy of the left ventricle
B. Increased preload leads to eccentric hypertrophy of the left ventricle
C. Decreased contractility leads to ventricular dilation
D. Increased heart rate leads to myocardial fibrosis
✅ Correct Answer: A
RATIONALE:
Chronic hypertension increases afterload—the resistance the left ventricle must overcome to eject
blood. The ventricle adapts by adding sarcomeres in parallel, resulting in concentric
hypertrophy (thickened ventricular wall with normal or reduced chamber size). This preserves cardiac
output initially but eventually leads to diastolic dysfunction and heart failure with preserved ejection
fraction (HFpEF). Eccentric hypertrophy (B) occurs with volume overload (e.g., aortic regurgitation,
dilated cardiomyopathy), where sarcomeres are added in series, leading to chamber dilation.
HIGH-YIELD MARKUP: Pressure overload → Concentric hypertrophy (thick wall). Volume overload →
Eccentric hypertrophy (dilated chamber).
2. A patient with acute coronary syndrome has elevated troponin I and CK-MB. Which of the following
cellular events is the PRIMARY cause of these elevated biomarkers?
A. Reversible myocardial ischemia causing transient membrane dysfunction
B. Irreversible myocardial necrosis with release of intracellular proteins
C. Coronary artery vasospasm without myocyte injury
D. Stunned myocardium with temporary contractile dysfunction
✅ Correct Answer: B
RATIONALE:
Troponin I and T and CK-MB are intracellular proteins released into the bloodstream only when
,2
myocardial cells undergo irreversible necrosis (cell death). This occurs after 20-40 minutes of sustained
ischemia, when ATP depletion leads to sarcolemmal membrane disruption. Reversible ischemia (A)
causes functional changes (e.g., wall motion abnormalities) but does not release these
biomarkers. Vasospasm (C) may cause transient ischemia. Stunned myocardium (D) refers to prolonged
but reversible contractile dysfunction after reperfusion.
HIGH-YIELD MARKUP: *Troponin = Myocyte necrosis. Rises 2-4h after MI, peaks 12-24h, remains
elevated 7-14 days. CK-MB rises 4-6h, peaks 18-24h, normalizes in 48-72h.*
3. A patient with chronic heart failure has elevated B-type natriuretic peptide (BNP). Which of the
following best explains the pathophysiologic stimulus for BNP release?
A. Increased ventricular wall stretch due to volume overload
B. Decreased renal perfusion activating the renin-angiotensin system
C. Increased sympathetic nervous system activity
D. Myocardial ischemia causing cellular injury
✅ Correct Answer: A
RATIONALE:
BNP is a hormone synthesized and released by ventricular myocytes in response to increased wall
stretch from volume or pressure overload. Its physiologic effects include vasodilation, natriuresis, and
inhibition of the renin-angiotensin-aldosterone system (RAAS)—essentially counter-regulatory
mechanisms. Elevated BNP is a key diagnostic marker for heart failure, with levels correlating with
severity. Decreased renal perfusion (B) stimulates renin release. Sympathetic activation (C) releases
norepinephrine. Myocardial ischemia (D) releases troponin.
MARKUP NOTE: *BNP = Ventricular stretch. ANP = Atrial stretch. Both cause natriuresis and
vasodilation. BNP >100 pg/mL suggests HF.*
4. A patient with long-standing, poorly controlled hypertension develops proteinuria and a rising
serum creatinine. Which of the following pathophysiologic processes best explains the renal injury?
A. Hyaline arteriosclerosis of afferent and efferent arterioles leading to glomerular ischemia
B. Immune complex deposition in the glomerular basement membrane
C. Acute tubular necrosis from renal hypoperfusion
D. Obstructive uropathy from ureteral compression
✅ Correct Answer: A
RATIONALE:
Chronic hypertension causes hyaline arteriosclerosis—thickening and hyalinization of the walls of small
arteries and arterioles, particularly the afferent and efferent arterioles of the kidney. This narrows the
vessel lumen, reducing glomerular perfusion and causing ischemic glomerulosclerosis (nephrosclerosis).
The result is progressive loss of nephrons, proteinuria (usually <2 g/day), and rising creatinine. This is the
,3
most common cause of end-stage renal disease in older adults. Immune complex deposition (B)
describes glomerulonephritis. Acute tubular necrosis (C) is from acute ischemia or nephrotoxins.
Obstructive uropathy (D) causes postrenal AKI.
HIGH-YIELD MARKUP: Hypertensive nephrosclerosis = Benign nephrosclerosis. "Flea-bitten" kidney
appearance (granular surface).
5. A patient presents with crushing substernal chest pain radiating to the left arm, diaphoresis, and
nausea. ECG shows ST-segment elevation in leads V1-V4. Which of the following describes the
underlying pathophysiology?
A. Transmural myocardial ischemia due to complete occlusion of a coronary artery
B. Subendocardial ischemia due to partial coronary artery occlusion
C. Coronary artery vasospasm without atherosclerotic plaque
D. Myocardial oxygen demand exceeding supply without coronary occlusion
✅ Correct Answer: A
RATIONALE:
ST-segment elevation myocardial infarction (STEMI) indicates transmural ischemia—ischemia
extending through the full thickness of the ventricular wall. This is almost always caused by complete
thrombotic occlusion of an epicardial coronary artery, usually at the site of a ruptured atherosclerotic
plaque. The ECG leads correspond to the affected myocardial territory: V1-V4 indicates anterior
wall (left anterior descending artery territory). Subendocardial ischemia (B) causes ST-
segment depression (NSTEMI/unstable angina). Vasospasm (C) causes Prinzmetal angina. Demand-
supply mismatch (D) causes type 2 MI.
HIGH-YIELD MARKUP: *STEMI = Transmural = ST elevation. NSTEMI = Subendocardial = ST depression
or T-wave inversion. Anterior MI (V1-V4) = LAD occlusion → highest mortality.*
6. A patient with aortic stenosis develops syncope during exertion. Which of the following best
explains the pathophysiologic mechanism?
A. Fixed obstruction to left ventricular outflow prevents an increase in cardiac output to meet exercise
demands
B. Arrhythmia from myocardial ischemia causes sudden loss of consciousness
C. Reflex bradycardia from baroreceptor stimulation
D. Embolization of valvular vegetations to the cerebral circulation
✅ Correct Answer: A
RATIONALE:
In aortic stenosis, the stenotic valve creates a fixed obstruction to left ventricular outflow. During
exercise, peripheral vasodilation occurs in skeletal muscle, but the obstructed valve prevents a
compensatory increase in cardiac output. This leads to exercise-induced hypotension and cerebral
, 4
hypoperfusion, causing syncope. The classic triad of severe aortic stenosis is: Angina, Syncope, and
Dyspnea (heart failure). Arrhythmias (B) may occur but are not the primary mechanism. Baroreceptor
reflex (C) would cause vasodilation and bradycardia in other conditions. Embolization (D) occurs in
infective endocarditis.
HIGH-YIELD MARKUP: Aortic Stenosis Triad = Angina, Syncope, Dyspnea. Syncope is exertional due to
fixed outflow obstruction.
7. Which of the following best describes the pathogenesis of atherosclerotic plaque rupture?
A. Smooth muscle cell proliferation and collagen synthesis stabilize the plaque
B. Inflammatory cell infiltration and matrix metalloproteinase degradation weaken the fibrous cap
C. Calcification of the plaque core increases its structural integrity
D. Endothelial cell regeneration covers and stabilizes the plaque surface
✅ Correct Answer: B
RATIONALE:
Plaque rupture is the precipitating event in most acute coronary syndromes. It occurs when the fibrous
cap overlying a lipid-rich atherosclerotic core becomes thin and weak. This weakening is driven
by inflammatory cells (macrophages, T-lymphocytes) that release matrix metalloproteinases (MMPs) ,
enzymes that degrade collagen and other extracellular matrix proteins. The result is cap rupture,
exposure of thrombogenic material (tissue factor, collagen), and acute thrombus formation. Smooth
muscle proliferation (A) and calcification (C) contribute to plaque growth and stenosis but not acute
rupture. Endothelial regeneration (D) is protective.
HIGH-YIELD MARKUP: "Vulnerable plaque" = Large lipid core + Thin fibrous cap + Inflammation. MMPs
degrade the cap → Rupture → Thrombosis.
8. A patient with chronic heart failure develops pitting edema, jugular venous distention, and
hepatomegaly. Which of the following best explains these findings?
A. Left ventricular failure causing pulmonary congestion
B. Right ventricular failure causing systemic venous congestion
C. Biventricular failure causing both pulmonary and systemic congestion
D. Pericardial constriction limiting diastolic filling
✅ Correct Answer: B
RATIONALE:
The triad of pitting edema, jugular venous distention (JVD), and hepatomegaly are classic signs
of right-sided heart failure. Right ventricular failure impairs the heart's ability to pump blood forward
into the pulmonary circulation, causing blood to "back up" into the systemic venous system. This
increases hydrostatic pressure in systemic capillaries, leading to peripheral edema, and causes
congestion of the liver (hepatomegaly) and jugular veins (JVD). Left-sided failure (A) causes pulmonary
