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NSG 5140 Advanced Pathophysiology Midterm
Exam Review 2 Graded A+ | South College
Questions And Correct Answers (Verified
Answers) Plus Rationales 2026 Q&A | Instant
Download PDF
1. Which of the following best describes the pathophysiological mechanism
underlying primary hypertension?
A) Decreased systemic vascular resistance
B) Increased cardiac output with normal peripheral resistance
C) Increased systemic vascular resistance with normal or increased cardiac output
D) Decreased blood volume
C) Increased systemic vascular resistance with normal or increased cardiac
output
Rationale: Primary (essential) hypertension is characterized by increased systemic
vascular resistance due to arteriolar vasoconstriction, often accompanied by
normal or increased cardiac output. This results from complex interactions
between genetic, environmental, and neurohormonal factors including renin-
angiotensin-aldosterone system activation and sympathetic nervous system
overactivity.
2. What is the primary pathophysiological mechanism of left-sided heart
failure?
A) Right ventricular hypertrophy
B) Left ventricular failure leading to increased pulmonary capillary pressure
C) Right ventricular failure causing systemic congestion
D) Decreased left ventricular afterload
B) Left ventricular failure leading to increased pulmonary capillary pressure
pg. 1
,2
Rationale: Left heart failure causes blood to back up into the pulmonary
circulation, increasing hydrostatic pressure in pulmonary capillaries. This leads to
pulmonary congestion, edema, and impaired gas exchange. The elevated
pulmonary pressures eventually can lead to right-sided heart failure (cor
pulmonale).
3. Which laboratory finding is characteristic of acute myocardial infarction?
A) Decreased troponin I
B) Elevated creatine kinase-MB (CK-MB)
C) Decreased myoglobin
D) Elevated B-type natriuretic peptide (BNP) only
B) Elevated creatine kinase-MB (CK-MB)
Rationale: CK-MB is a cardiac-specific enzyme that rises within 3-4 hours of
myocardial infarction, peaking at 12-24 hours, and returning to normal within 48-
72 hours. Troponin I and T are more cardiac-specific and remain elevated longer,
making them preferred biomarkers. BNP elevation indicates heart failure, not
acute MI.
4. The pathophysiology of atherosclerotic plaque formation involves all of the
following EXCEPT:
A) Endothelial injury
B) Lipid accumulation in the intima
C) Smooth muscle cell proliferation
D) Decreased platelet aggregation
D) Decreased platelet aggregation
Rationale: Atherosclerosis involves endothelial injury, LDL oxidation, monocyte
adhesion and migration, foam cell formation, smooth muscle cell proliferation, and
platelet aggregation. Platelet aggregation is actually increased due to exposed
collagen and tissue factor. Decreased platelet aggregation would be protective
against atherosclerosis.
pg. 2
,3
5. Which of the following best describes the mechanism of action of digoxin?
A) Increases sodium-potassium ATPase activity
B) Inhibits sodium-potassium ATPase, increasing intracellular calcium
C) Blocks beta-adrenergic receptors
D) Decreases myocardial contractility
B) Inhibits sodium-potassium ATPase, increasing intracellular calcium
Rationale: Digoxin inhibits the sodium-potassium ATPase pump, leading to
increased intracellular sodium. This reduces the sodium-calcium exchanger
activity, increasing intracellular calcium. Higher calcium levels enhance
myocardial contractility (positive inotropic effect).
6. What is the primary pathophysiological mechanism of cardiogenic shock?
A) Decreased systemic vascular resistance
B) Pump failure resulting in inadequate tissue perfusion
C) Hypovolemia
D) Septic vasodilation
B) Pump failure resulting in inadequate tissue perfusion
Rationale: Cardiogenic shock results from the heart's inability to pump sufficient
blood to meet tissue demands. This is most commonly due to extensive myocardial
infarction, severe heart failure, or arrhythmias. The resultant decreased cardiac
output leads to tissue hypoxia, anaerobic metabolism, and lactic acidosis.
7. Which electrocardiogram (ECG) finding is most characteristic of
pericarditis?
A) ST-segment elevation with reciprocal depression
B) Diffuse ST-segment elevation
C) Q waves in multiple leads
D) Prolonged QT interval
B) Diffuse ST-segment elevation
Rationale: Pericarditis typically presents with diffuse ST-segment elevation in
multiple leads (concave upward) without reciprocal changes, unlike myocardial
pg. 3
, 4
infarction which shows ST elevation in leads corresponding to the affected area
with reciprocal depression. PR-segment depression is also commonly seen in
pericarditis.
8. The pathophysiological mechanism of cardiac tamponade involves:
A) Decreased pericardial pressure
B) Compression of the heart due to fluid accumulation in the pericardial space
C) Increased cardiac output
D) Decreased central venous pressure
B) Compression of the heart due to fluid accumulation in the pericardial
space
Rationale: Cardiac tamponade occurs when fluid accumulates in the pericardial
space, increasing intrapericardial pressure and compressing the heart. This limits
ventricular filling (diastolic dysfunction), leading to decreased stroke volume,
cardiac output, and pulsus paradoxus. Central venous pressure increases, and
jugular venous distention is observed.
9. Which of the following describes the pathophysiology of infective
endocarditis?
A) Inflammation of the myocardium
B) Infection and inflammation of the endocardial surface of the heart
C) Inflammation of the pericardial sac
D) Degenerative changes in cardiac valves
B) Infection and inflammation of the endocardial surface of the heart
Rationale: Infective endocarditis is a microbial infection of the endocardial
surface, most commonly affecting heart valves. Vegetations composed of fibrin,
platelets, and microorganisms form on the valve surface. These vegetations can
embolize, cause valvular dysfunction, and lead to systemic complications.
10. What is the primary mechanism of varicose vein formation?
pg. 4
NSG 5140 Advanced Pathophysiology Midterm
Exam Review 2 Graded A+ | South College
Questions And Correct Answers (Verified
Answers) Plus Rationales 2026 Q&A | Instant
Download PDF
1. Which of the following best describes the pathophysiological mechanism
underlying primary hypertension?
A) Decreased systemic vascular resistance
B) Increased cardiac output with normal peripheral resistance
C) Increased systemic vascular resistance with normal or increased cardiac output
D) Decreased blood volume
C) Increased systemic vascular resistance with normal or increased cardiac
output
Rationale: Primary (essential) hypertension is characterized by increased systemic
vascular resistance due to arteriolar vasoconstriction, often accompanied by
normal or increased cardiac output. This results from complex interactions
between genetic, environmental, and neurohormonal factors including renin-
angiotensin-aldosterone system activation and sympathetic nervous system
overactivity.
2. What is the primary pathophysiological mechanism of left-sided heart
failure?
A) Right ventricular hypertrophy
B) Left ventricular failure leading to increased pulmonary capillary pressure
C) Right ventricular failure causing systemic congestion
D) Decreased left ventricular afterload
B) Left ventricular failure leading to increased pulmonary capillary pressure
pg. 1
,2
Rationale: Left heart failure causes blood to back up into the pulmonary
circulation, increasing hydrostatic pressure in pulmonary capillaries. This leads to
pulmonary congestion, edema, and impaired gas exchange. The elevated
pulmonary pressures eventually can lead to right-sided heart failure (cor
pulmonale).
3. Which laboratory finding is characteristic of acute myocardial infarction?
A) Decreased troponin I
B) Elevated creatine kinase-MB (CK-MB)
C) Decreased myoglobin
D) Elevated B-type natriuretic peptide (BNP) only
B) Elevated creatine kinase-MB (CK-MB)
Rationale: CK-MB is a cardiac-specific enzyme that rises within 3-4 hours of
myocardial infarction, peaking at 12-24 hours, and returning to normal within 48-
72 hours. Troponin I and T are more cardiac-specific and remain elevated longer,
making them preferred biomarkers. BNP elevation indicates heart failure, not
acute MI.
4. The pathophysiology of atherosclerotic plaque formation involves all of the
following EXCEPT:
A) Endothelial injury
B) Lipid accumulation in the intima
C) Smooth muscle cell proliferation
D) Decreased platelet aggregation
D) Decreased platelet aggregation
Rationale: Atherosclerosis involves endothelial injury, LDL oxidation, monocyte
adhesion and migration, foam cell formation, smooth muscle cell proliferation, and
platelet aggregation. Platelet aggregation is actually increased due to exposed
collagen and tissue factor. Decreased platelet aggregation would be protective
against atherosclerosis.
pg. 2
,3
5. Which of the following best describes the mechanism of action of digoxin?
A) Increases sodium-potassium ATPase activity
B) Inhibits sodium-potassium ATPase, increasing intracellular calcium
C) Blocks beta-adrenergic receptors
D) Decreases myocardial contractility
B) Inhibits sodium-potassium ATPase, increasing intracellular calcium
Rationale: Digoxin inhibits the sodium-potassium ATPase pump, leading to
increased intracellular sodium. This reduces the sodium-calcium exchanger
activity, increasing intracellular calcium. Higher calcium levels enhance
myocardial contractility (positive inotropic effect).
6. What is the primary pathophysiological mechanism of cardiogenic shock?
A) Decreased systemic vascular resistance
B) Pump failure resulting in inadequate tissue perfusion
C) Hypovolemia
D) Septic vasodilation
B) Pump failure resulting in inadequate tissue perfusion
Rationale: Cardiogenic shock results from the heart's inability to pump sufficient
blood to meet tissue demands. This is most commonly due to extensive myocardial
infarction, severe heart failure, or arrhythmias. The resultant decreased cardiac
output leads to tissue hypoxia, anaerobic metabolism, and lactic acidosis.
7. Which electrocardiogram (ECG) finding is most characteristic of
pericarditis?
A) ST-segment elevation with reciprocal depression
B) Diffuse ST-segment elevation
C) Q waves in multiple leads
D) Prolonged QT interval
B) Diffuse ST-segment elevation
Rationale: Pericarditis typically presents with diffuse ST-segment elevation in
multiple leads (concave upward) without reciprocal changes, unlike myocardial
pg. 3
, 4
infarction which shows ST elevation in leads corresponding to the affected area
with reciprocal depression. PR-segment depression is also commonly seen in
pericarditis.
8. The pathophysiological mechanism of cardiac tamponade involves:
A) Decreased pericardial pressure
B) Compression of the heart due to fluid accumulation in the pericardial space
C) Increased cardiac output
D) Decreased central venous pressure
B) Compression of the heart due to fluid accumulation in the pericardial
space
Rationale: Cardiac tamponade occurs when fluid accumulates in the pericardial
space, increasing intrapericardial pressure and compressing the heart. This limits
ventricular filling (diastolic dysfunction), leading to decreased stroke volume,
cardiac output, and pulsus paradoxus. Central venous pressure increases, and
jugular venous distention is observed.
9. Which of the following describes the pathophysiology of infective
endocarditis?
A) Inflammation of the myocardium
B) Infection and inflammation of the endocardial surface of the heart
C) Inflammation of the pericardial sac
D) Degenerative changes in cardiac valves
B) Infection and inflammation of the endocardial surface of the heart
Rationale: Infective endocarditis is a microbial infection of the endocardial
surface, most commonly affecting heart valves. Vegetations composed of fibrin,
platelets, and microorganisms form on the valve surface. These vegetations can
embolize, cause valvular dysfunction, and lead to systemic complications.
10. What is the primary mechanism of varicose vein formation?
pg. 4
