Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Ch. 1: Anatomical Overview — Heart chambers and
circulation
Question Stem: A 68-year-old man with sudden-onset
shortness of breath has jugular venous distention, lung crackles,
and an S3 gallop. Which aspect of cardiac anatomy best
explains why left ventricular dysfunction produces pulmonary
edema?
A. Right ventricle pumps into high-resistance pulmonary
arteries leading to increased pulmonary capillary pressure
,B. Left ventricle pumps into systemic circulation; failure
increases left atrial pressure transmitted to pulmonary veins
C. Right atrium receives systemic venous return causing
backpressure into lungs when overloaded
D. The foramen ovale closes after birth, preventing right-to-left
shunting that would relieve pulmonary congestion
Correct Answer: B
Rationale — Correct: Left ventricular failure raises left
ventricular end-diastolic pressure; that pressure is transmitted
back into the left atrium and pulmonary veins, increasing
pulmonary capillary hydrostatic pressure and causing
pulmonary edema. (Anatomical continuity from LV → LA →
pulmonary veins explains pulmonary congestion.)
Rationale — Incorrect:
A. Right ventricle physiology relates to pulmonary, but
increased pulmonary vascular resistance does not explain LV-
failure–driven pulmonary edema.
C. Right atrial/systemic venous backpressure causes systemic
edema, not pulmonary edema from LV failure.
D. The foramen ovale closure is irrelevant to LV failure
producing pulmonary venous hypertension.
Teaching Point: LV failure raises pulmonary venous pressure,
causing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Anatomical Overview — Heart
chambers and circulation
,2
Reference: Ch. 1: Heart Failure — Pathophysiology and
compensatory mechanisms
Question Stem: A patient with chronic systolic heart failure has
cool extremities, low urine output, and rising BUN/creatinine
despite diuretics. Which compensatory mechanism is most
responsible for reduced renal perfusion in heart failure?
A. Increased natriuretic peptide release causing vasodilation
B. Activation of the renin–angiotensin–aldosterone system
(RAAS) causing vasoconstriction and sodium retention
C. Increased pulmonary venous pressure causing renal
vasodilation
D. Sympathetic withdrawal decreasing renal vascular tone
Correct Answer: B
Rationale — Correct: Reduced cardiac output triggers RAAS
activation; angiotensin II causes systemic vasoconstriction and
aldosterone-mediated sodium/water retention, reducing renal
perfusion and worsening congestion and renal function.
Rationale — Incorrect:
A. Natriuretic peptides oppose RAAS and promote natriuresis;
they would increase renal blood flow, not reduce it.
C. Pulmonary venous pressure affects lungs; it does not directly
vasodilate renal vessels.
D. Sympathetic withdrawal would increase renal perfusion, not
, decrease it; in HF there is sympathetic activation, not
withdrawal.
Teaching Point: In HF, RAAS activation preserves perfusion but
worsens congestion and renal hypoperfusion.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Compensatory
mechanisms
3
Reference: Ch. 1: Left Heart Failure — Clinical signs and
patterns
Question Stem: A 74-year-old woman with chronic
hypertension now complains of exertional dyspnea and
orthopnea. On exam: bibasilar crackles, displaced point of
maximal impulse (PMI), and inspiratory rales. Which clinical
finding most specifically differentiates left-sided from right-
sided heart failure?
A. Peripheral pitting edema
B. Hepatomegaly and jugular venous distention
C. Pulmonary rales and orthopnea
D. Ascites
Correct Answer: C
Rationale — Correct: Pulmonary rales and orthopnea are
manifestations of elevated left-sided filling pressures and
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1
Reference: Ch. 1: Anatomical Overview — Heart chambers and
circulation
Question Stem: A 68-year-old man with sudden-onset
shortness of breath has jugular venous distention, lung crackles,
and an S3 gallop. Which aspect of cardiac anatomy best
explains why left ventricular dysfunction produces pulmonary
edema?
A. Right ventricle pumps into high-resistance pulmonary
arteries leading to increased pulmonary capillary pressure
,B. Left ventricle pumps into systemic circulation; failure
increases left atrial pressure transmitted to pulmonary veins
C. Right atrium receives systemic venous return causing
backpressure into lungs when overloaded
D. The foramen ovale closes after birth, preventing right-to-left
shunting that would relieve pulmonary congestion
Correct Answer: B
Rationale — Correct: Left ventricular failure raises left
ventricular end-diastolic pressure; that pressure is transmitted
back into the left atrium and pulmonary veins, increasing
pulmonary capillary hydrostatic pressure and causing
pulmonary edema. (Anatomical continuity from LV → LA →
pulmonary veins explains pulmonary congestion.)
Rationale — Incorrect:
A. Right ventricle physiology relates to pulmonary, but
increased pulmonary vascular resistance does not explain LV-
failure–driven pulmonary edema.
C. Right atrial/systemic venous backpressure causes systemic
edema, not pulmonary edema from LV failure.
D. The foramen ovale closure is irrelevant to LV failure
producing pulmonary venous hypertension.
Teaching Point: LV failure raises pulmonary venous pressure,
causing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Anatomical Overview — Heart
chambers and circulation
,2
Reference: Ch. 1: Heart Failure — Pathophysiology and
compensatory mechanisms
Question Stem: A patient with chronic systolic heart failure has
cool extremities, low urine output, and rising BUN/creatinine
despite diuretics. Which compensatory mechanism is most
responsible for reduced renal perfusion in heart failure?
A. Increased natriuretic peptide release causing vasodilation
B. Activation of the renin–angiotensin–aldosterone system
(RAAS) causing vasoconstriction and sodium retention
C. Increased pulmonary venous pressure causing renal
vasodilation
D. Sympathetic withdrawal decreasing renal vascular tone
Correct Answer: B
Rationale — Correct: Reduced cardiac output triggers RAAS
activation; angiotensin II causes systemic vasoconstriction and
aldosterone-mediated sodium/water retention, reducing renal
perfusion and worsening congestion and renal function.
Rationale — Incorrect:
A. Natriuretic peptides oppose RAAS and promote natriuresis;
they would increase renal blood flow, not reduce it.
C. Pulmonary venous pressure affects lungs; it does not directly
vasodilate renal vessels.
D. Sympathetic withdrawal would increase renal perfusion, not
, decrease it; in HF there is sympathetic activation, not
withdrawal.
Teaching Point: In HF, RAAS activation preserves perfusion but
worsens congestion and renal hypoperfusion.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure — Compensatory
mechanisms
3
Reference: Ch. 1: Left Heart Failure — Clinical signs and
patterns
Question Stem: A 74-year-old woman with chronic
hypertension now complains of exertional dyspnea and
orthopnea. On exam: bibasilar crackles, displaced point of
maximal impulse (PMI), and inspiratory rales. Which clinical
finding most specifically differentiates left-sided from right-
sided heart failure?
A. Peripheral pitting edema
B. Hepatomegaly and jugular venous distention
C. Pulmonary rales and orthopnea
D. Ascites
Correct Answer: C
Rationale — Correct: Pulmonary rales and orthopnea are
manifestations of elevated left-sided filling pressures and
