NUR 2063 Pathophysiology Exam 3 – Practice Test Bank with Verified Answers & Detailed Rationales |
2026/2027
Section 1: Cardiovascular Disorders (Questions 1–35)
1. What is the primary pathophysiologic mechanism in atherosclerosis?
A) Accumulation of lipid-laden macrophages in arterial walls forming plaques
B) Acute inflammation of the pericardium
C) Decreased systemic vascular resistance
D) Valvular stenosis
Answer A: — Accumulation of lipid-laden macrophages in arterial walls forming plaques
Rationale: Atherosclerosis involves endothelial injury, inflammation, and cholesterol deposition, leading to
plaque formation, vessel narrowing, and reduced blood flow. ---
2. What distinguishes stable angina from unstable angina?
A) Stable angina occurs at rest; unstable angina occurs with exertion
B) Stable angina occurs predictably with exertion and is relieved by rest; unstable angina occurs at rest and
is unpredictable
C) Stable angina is caused by coronary spasm; unstable angina is caused by anemia
D) Stable angina indicates infarction; unstable angina indicates ischemia
Answer B: — Stable angina occurs predictably with exertion and is relieved by rest; unstable angina
occurs at rest and is unpredictable
Rationale: Unstable angina indicates plaque rupture or thrombosis and may precede myocardial infarction. -
--
,3. What is the main consequence of left-sided heart failure?
A) Peripheral edema and jugular venous distention
B) Pulmonary congestion leading to dyspnea, orthopnea, and pulmonary edema
C) Hepatomegaly and splenomegaly
D) Ascites and peripheral edema
Answer B: — Pulmonary congestion leading to dyspnea, orthopnea, and pulmonary edema
Rationale: Left ventricular dysfunction increases pulmonary venous pressure, causing pulmonary
congestion. ---
4. What is a common sign of right-sided heart failure?
A) Pulmonary crackles
B) Peripheral edema and jugular venous distention
C) Orthopnea
D) Paroxysmal nocturnal dyspnea
Answer B: — Peripheral edema and jugular venous distention
Rationale: Right ventricular failure causes systemic venous congestion, leading to peripheral edema and
JVD. ---
5. How does a myocardial infarction cause tissue damage?
A) Ischemia from coronary artery occlusion leads to necrosis of cardiac myocytes
B) Increased cardiac contractility causes hypertrophy
C) Decreased systemic vascular resistance causes hypoperfusion
D) Valvular stenosis causes backflow
Answer A: — Ischemia from coronary artery occlusion leads to necrosis of cardiac myocytes
Rationale: The extent of damage depends on the duration of ischemia and collateral circulation. ---
6. What is the primary cause of myocardial infarction?
A) Coronary artery spasm
B) Atherosclerotic plaque rupture with thrombosis
C) Myocardial hypertrophy
D) Valvular heart disease
Answer B: — Atherosclerotic plaque rupture with thrombosis
,Rationale: Most myocardial infarctions result from rupture of an unstable atherosclerotic plaque, leading to
platelet aggregation and thrombus formation. ---
7. Describe the difference between systolic and diastolic heart failure.
A) Systolic failure = reduced ejection fraction; diastolic failure = preserved ejection fraction but impaired
ventricular filling
B) Systolic failure = preserved ejection fraction; diastolic failure = reduced ejection fraction
C) Systolic failure = right-sided; diastolic failure = left-sided
D) Systolic failure = acute; diastolic failure = chronic
Answer A: — Systolic failure = reduced ejection fraction; diastolic failure = preserved ejection
fraction but impaired ventricular filling
Rationale: Systolic failure results from weakened contraction; diastolic from stiff ventricles. ---
8. What pathophysiologic change occurs in hypertension?
A) Persistent elevation of arterial pressure due to increased vascular resistance or cardiac output
B) Decreased systemic vascular resistance
C) Increased vascular compliance
D) Decreased afterload
Answer A: — Persistent elevation of arterial pressure due to increased vascular resistance or cardiac
output
Rationale: Chronic hypertension leads to end-organ damage if untreated. ---
9. A patient with hypertension has been non-adherent with medications. What vascular changes are
most likely occurring?
A) Decreased peripheral resistance
B) Arterial wall thickening and narrowing
C) Increased vascular compliance
D) Decreased afterload
Answer B: — Arterial wall thickening and narrowing
Rationale: Chronic hypertension causes smooth muscle hypertrophy and intimal thickening, leading to
increased peripheral resistance and narrowing of arterial lumens. ---
, 10. Which compensatory mechanism occurs FIRST in response to decreased cardiac output?
A) Activation of the renin-angiotensin-aldosterone system
B) Sympathetic nervous system activation
C) Release of atrial natriuretic peptide
D) Ventricular hypertrophy
Answer B: — Sympathetic nervous system activation
Rationale: The SNS is activated immediately, causing increased heart rate and vasoconstriction to maintain
perfusion to vital organs. ---
11. What is the mechanism behind aneurysm formation?
A) Weakening of vessel wall due to hypertension, atherosclerosis, or connective tissue disorders
B) Acute inflammation of the vessel wall
C) Increased vascular compliance
D) Decreased systemic vascular resistance
Answer A: — Weakening of vessel wall due to hypertension, atherosclerosis, or connective tissue
disorders
Rationale: This leads to dilation and risk of rupture. ---
12. What is the pathophysiology of infective endocarditis?
A) Infection of the endocardial surface, often the heart valves, leading to vegetations
B) Inflammation of the pericardium
C) Ischemia of the myocardium
D) Valvular stenosis
Answer A: — Infection of the endocardial surface, often the heart valves, leading to vegetations
Rationale: Vegetations can embolize and cause systemic infection. ---
13. How does shock lead to cellular injury?
A) Reduced perfusion causes hypoxia, anaerobic metabolism, lactic acidosis, and cell death
B) Increased perfusion causes oxidative stress
C) Increased cardiac output causes hypertension
D) Decreased vascular resistance causes hyperperfusion
Answer A: — Reduced perfusion causes hypoxia, anaerobic metabolism, lactic acidosis, and cell death
Rationale: Shock can be cardiogenic, hypovolemic, distributive, or obstructive. ---
2026/2027
Section 1: Cardiovascular Disorders (Questions 1–35)
1. What is the primary pathophysiologic mechanism in atherosclerosis?
A) Accumulation of lipid-laden macrophages in arterial walls forming plaques
B) Acute inflammation of the pericardium
C) Decreased systemic vascular resistance
D) Valvular stenosis
Answer A: — Accumulation of lipid-laden macrophages in arterial walls forming plaques
Rationale: Atherosclerosis involves endothelial injury, inflammation, and cholesterol deposition, leading to
plaque formation, vessel narrowing, and reduced blood flow. ---
2. What distinguishes stable angina from unstable angina?
A) Stable angina occurs at rest; unstable angina occurs with exertion
B) Stable angina occurs predictably with exertion and is relieved by rest; unstable angina occurs at rest and
is unpredictable
C) Stable angina is caused by coronary spasm; unstable angina is caused by anemia
D) Stable angina indicates infarction; unstable angina indicates ischemia
Answer B: — Stable angina occurs predictably with exertion and is relieved by rest; unstable angina
occurs at rest and is unpredictable
Rationale: Unstable angina indicates plaque rupture or thrombosis and may precede myocardial infarction. -
--
,3. What is the main consequence of left-sided heart failure?
A) Peripheral edema and jugular venous distention
B) Pulmonary congestion leading to dyspnea, orthopnea, and pulmonary edema
C) Hepatomegaly and splenomegaly
D) Ascites and peripheral edema
Answer B: — Pulmonary congestion leading to dyspnea, orthopnea, and pulmonary edema
Rationale: Left ventricular dysfunction increases pulmonary venous pressure, causing pulmonary
congestion. ---
4. What is a common sign of right-sided heart failure?
A) Pulmonary crackles
B) Peripheral edema and jugular venous distention
C) Orthopnea
D) Paroxysmal nocturnal dyspnea
Answer B: — Peripheral edema and jugular venous distention
Rationale: Right ventricular failure causes systemic venous congestion, leading to peripheral edema and
JVD. ---
5. How does a myocardial infarction cause tissue damage?
A) Ischemia from coronary artery occlusion leads to necrosis of cardiac myocytes
B) Increased cardiac contractility causes hypertrophy
C) Decreased systemic vascular resistance causes hypoperfusion
D) Valvular stenosis causes backflow
Answer A: — Ischemia from coronary artery occlusion leads to necrosis of cardiac myocytes
Rationale: The extent of damage depends on the duration of ischemia and collateral circulation. ---
6. What is the primary cause of myocardial infarction?
A) Coronary artery spasm
B) Atherosclerotic plaque rupture with thrombosis
C) Myocardial hypertrophy
D) Valvular heart disease
Answer B: — Atherosclerotic plaque rupture with thrombosis
,Rationale: Most myocardial infarctions result from rupture of an unstable atherosclerotic plaque, leading to
platelet aggregation and thrombus formation. ---
7. Describe the difference between systolic and diastolic heart failure.
A) Systolic failure = reduced ejection fraction; diastolic failure = preserved ejection fraction but impaired
ventricular filling
B) Systolic failure = preserved ejection fraction; diastolic failure = reduced ejection fraction
C) Systolic failure = right-sided; diastolic failure = left-sided
D) Systolic failure = acute; diastolic failure = chronic
Answer A: — Systolic failure = reduced ejection fraction; diastolic failure = preserved ejection
fraction but impaired ventricular filling
Rationale: Systolic failure results from weakened contraction; diastolic from stiff ventricles. ---
8. What pathophysiologic change occurs in hypertension?
A) Persistent elevation of arterial pressure due to increased vascular resistance or cardiac output
B) Decreased systemic vascular resistance
C) Increased vascular compliance
D) Decreased afterload
Answer A: — Persistent elevation of arterial pressure due to increased vascular resistance or cardiac
output
Rationale: Chronic hypertension leads to end-organ damage if untreated. ---
9. A patient with hypertension has been non-adherent with medications. What vascular changes are
most likely occurring?
A) Decreased peripheral resistance
B) Arterial wall thickening and narrowing
C) Increased vascular compliance
D) Decreased afterload
Answer B: — Arterial wall thickening and narrowing
Rationale: Chronic hypertension causes smooth muscle hypertrophy and intimal thickening, leading to
increased peripheral resistance and narrowing of arterial lumens. ---
, 10. Which compensatory mechanism occurs FIRST in response to decreased cardiac output?
A) Activation of the renin-angiotensin-aldosterone system
B) Sympathetic nervous system activation
C) Release of atrial natriuretic peptide
D) Ventricular hypertrophy
Answer B: — Sympathetic nervous system activation
Rationale: The SNS is activated immediately, causing increased heart rate and vasoconstriction to maintain
perfusion to vital organs. ---
11. What is the mechanism behind aneurysm formation?
A) Weakening of vessel wall due to hypertension, atherosclerosis, or connective tissue disorders
B) Acute inflammation of the vessel wall
C) Increased vascular compliance
D) Decreased systemic vascular resistance
Answer A: — Weakening of vessel wall due to hypertension, atherosclerosis, or connective tissue
disorders
Rationale: This leads to dilation and risk of rupture. ---
12. What is the pathophysiology of infective endocarditis?
A) Infection of the endocardial surface, often the heart valves, leading to vegetations
B) Inflammation of the pericardium
C) Ischemia of the myocardium
D) Valvular stenosis
Answer A: — Infection of the endocardial surface, often the heart valves, leading to vegetations
Rationale: Vegetations can embolize and cause systemic infection. ---
13. How does shock lead to cellular injury?
A) Reduced perfusion causes hypoxia, anaerobic metabolism, lactic acidosis, and cell death
B) Increased perfusion causes oxidative stress
C) Increased cardiac output causes hypertension
D) Decreased vascular resistance causes hyperperfusion
Answer A: — Reduced perfusion causes hypoxia, anaerobic metabolism, lactic acidosis, and cell death
Rationale: Shock can be cardiogenic, hypovolemic, distributive, or obstructive. ---
