NR 507 Week 5: Cardiovascular, Respiratory, and Renal
Pathophysiology 2026 Chamberlain
1. Which compensatory mechanism is primarily responsible for the long-term
increase in blood volume in heart failure?
A. Sympathetic nervous system activation
B. Renin-angiotensin-aldosterone system (RAAS)
C. Release of Atrial Natriuretic Peptide (ANP)
D. Peripheral vasoconstriction
Answer: B
Rationale: The RAAS is activated due to decreased renal perfusion in heart failure, leading
to sodium and water retention, which increases blood volume.
2. In left-sided heart failure, why does pulmonary edema occur?
A. Increased systemic vascular resistance
B. Decreased oncotic pressure in the capillaries
C. Right ventricular hypertrophy
D. Increased hydrostatic pressure in the pulmonary capillaries
Answer: D
Rationale: Left ventricular failure leads to a backup of blood into the left atrium and
pulmonary veins, increasing pulmonary capillary hydrostatic pressure and forcing fluid
into the alveoli.
,3. Which clinical manifestation is most characteristic of right-sided heart failure?
A. Crackles in the lungs
B. Peripheral edema
C. Orthopnea
D. Paroxysmal nocturnal dyspnea
Answer: B
Rationale: Right-sided heart failure causes blood to back up into the systemic circulation,
leading to jugular venous distention, hepatomegaly, and peripheral edema.
4. Which valvular disorder is characterized by a loud S1 and a mid-diastolic
rumble at the apex?
A. Aortic stenosis
B. Mitral regurgitation
C. Aortic regurgitation
D. Mitral stenosis
Answer: D
Rationale: Mitral stenosis involves narrowing of the mitral valve, which obstructs flow
from the left atrium to the left ventricle, producing a diastolic murmur.
5. Which process is considered the ‘hallmark’ of the pathogenesis of
atherosclerosis?
A. Endothelial injury and inflammation
B. Smooth muscle cell proliferation
C. Vasodilation of the media
D. Decreased LDL oxidation
Answer: A
Rationale: Atherosclerosis begins with endothelial injury, which triggers an inflammatory
response and the accumulation of lipid-laden macrophages (foam cells).
, 6. A patient presents with chest pain that occurs at rest and has increased in
frequency and duration. This is classified as:
A. Stable angina
B. Prinzmetal angina
C. Silent ischemia
D. Unstable angina
Answer: D
Rationale: Unstable angina is chest pain that is unpredictable, occurs at rest, or is
increasing in severity, indicating a high risk for myocardial infarction.
7. ST-segment elevation on an ECG typically indicates which of the following?
A. Subendocardial ischemia
B. Old myocardial scar tissue
C. Transmural myocardial infarction
D. Hypokalemia
Answer: C
Rationale: ST-elevation (STEMI) indicates transmural injury to the heart muscle, meaning
the full thickness of the wall is affected.
8. What is the primary physiological effect of Brain Natriuretic Peptide (BNP)?
A. Vasodilation and diuresis
B. Sodium and water retention
C. Vasoconstriction
D. Increased heart rate
Answer: A
Rationale: BNP is released in response to ventricular stretch and works to decrease
preload and afterload through vasodilation and promoting sodium/water excretion.
Pathophysiology 2026 Chamberlain
1. Which compensatory mechanism is primarily responsible for the long-term
increase in blood volume in heart failure?
A. Sympathetic nervous system activation
B. Renin-angiotensin-aldosterone system (RAAS)
C. Release of Atrial Natriuretic Peptide (ANP)
D. Peripheral vasoconstriction
Answer: B
Rationale: The RAAS is activated due to decreased renal perfusion in heart failure, leading
to sodium and water retention, which increases blood volume.
2. In left-sided heart failure, why does pulmonary edema occur?
A. Increased systemic vascular resistance
B. Decreased oncotic pressure in the capillaries
C. Right ventricular hypertrophy
D. Increased hydrostatic pressure in the pulmonary capillaries
Answer: D
Rationale: Left ventricular failure leads to a backup of blood into the left atrium and
pulmonary veins, increasing pulmonary capillary hydrostatic pressure and forcing fluid
into the alveoli.
,3. Which clinical manifestation is most characteristic of right-sided heart failure?
A. Crackles in the lungs
B. Peripheral edema
C. Orthopnea
D. Paroxysmal nocturnal dyspnea
Answer: B
Rationale: Right-sided heart failure causes blood to back up into the systemic circulation,
leading to jugular venous distention, hepatomegaly, and peripheral edema.
4. Which valvular disorder is characterized by a loud S1 and a mid-diastolic
rumble at the apex?
A. Aortic stenosis
B. Mitral regurgitation
C. Aortic regurgitation
D. Mitral stenosis
Answer: D
Rationale: Mitral stenosis involves narrowing of the mitral valve, which obstructs flow
from the left atrium to the left ventricle, producing a diastolic murmur.
5. Which process is considered the ‘hallmark’ of the pathogenesis of
atherosclerosis?
A. Endothelial injury and inflammation
B. Smooth muscle cell proliferation
C. Vasodilation of the media
D. Decreased LDL oxidation
Answer: A
Rationale: Atherosclerosis begins with endothelial injury, which triggers an inflammatory
response and the accumulation of lipid-laden macrophages (foam cells).
, 6. A patient presents with chest pain that occurs at rest and has increased in
frequency and duration. This is classified as:
A. Stable angina
B. Prinzmetal angina
C. Silent ischemia
D. Unstable angina
Answer: D
Rationale: Unstable angina is chest pain that is unpredictable, occurs at rest, or is
increasing in severity, indicating a high risk for myocardial infarction.
7. ST-segment elevation on an ECG typically indicates which of the following?
A. Subendocardial ischemia
B. Old myocardial scar tissue
C. Transmural myocardial infarction
D. Hypokalemia
Answer: C
Rationale: ST-elevation (STEMI) indicates transmural injury to the heart muscle, meaning
the full thickness of the wall is affected.
8. What is the primary physiological effect of Brain Natriuretic Peptide (BNP)?
A. Vasodilation and diuresis
B. Sodium and water retention
C. Vasoconstriction
D. Increased heart rate
Answer: A
Rationale: BNP is released in response to ventricular stretch and works to decrease
preload and afterload through vasodilation and promoting sodium/water excretion.
