Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1.
Reference: Ch. 1: Anatomical Overview — Four chambers and
valve anatomy
Question Stem: A 72-year-old man is admitted after sudden
onset dyspnea, bibasilar crackles, and orthopnea. Chest x-ray
shows pulmonary edema. Which structural finding most directly
explains increased pulmonary capillary hydrostatic pressure
causing his symptoms?
Options:
A. Right ventricular dilation with tricuspid regurgitation
B. Left ventricular systolic dysfunction with elevated left
ventricular end-diastolic volume
,C. Atrial septal defect with left-to-right shunt
D. Pulmonic stenosis increasing right atrial pressure
Correct Answer: B
Rationales:
• Correct (B): Elevated left ventricular end-diastolic volume
(in systolic dysfunction) increases left atrial and pulmonary
venous pressures, raising pulmonary capillary hydrostatic
pressure and causing pulmonary edema. This links
chamber pathology to hydrostatic pulmonary edema.
• A: Right ventricular dilation and tricuspid regurgitation
primarily cause systemic venous congestion, not
pulmonary edema.
• C: ASD with left-to-right shunt increases pulmonary blood
flow chronically but typically causes volume overload
rather than acute pulmonary capillary hydrostatic pressure
spike.
• D: Pulmonic stenosis raises right-sided pressures and
causes systemic venous signs, not left-sided pulmonary
edema.
Teaching Point: Left ventricular failure raises pulmonary
capillary hydrostatic pressure causing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Anatomical Overview & Heart
Failure
,2.
Reference: Ch. 1: Heart Failure — Preload, Afterload, and
Treatment of Heart Failure
Question Stem: A patient with chronic hypertension and heart
failure has elevated afterload. Which medication class will most
directly reduce afterload and thereby decrease left ventricular
wall stress?
Options:
A. Loop diuretics (e.g., furosemide)
B. ACE inhibitors (e.g., lisinopril)
C. Cardiac glycosides (e.g., digoxin)
D. Beta-blockers (e.g., metoprolol)
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors reduce systemic vascular
resistance (arterial vasodilation), lowering afterload and LV
wall stress — a primary mechanism for improving forward
output in systolic heart failure.
• A: Loop diuretics reduce preload via volume removal but
do not directly lower systemic vascular resistance
(afterload).
• C: Digoxin increases inotropy and can modestly reduce
symptoms but has minimal direct effect on afterload.
, • D: Beta-blockers reduce heart rate and myocardial oxygen
demand and provide long-term remodeling benefits, but
they do not acutely lower afterload like vasodilators.
Teaching Point: Vasodilators (ACE inhibitors) reduce afterload
and left ventricular wall stress.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3.
Reference: Ch. 1: Left vs. Right Heart Failure — Symptoms and
Signs of Heart Failure
Question Stem: A patient with chronic left-sided heart failure
develops new peripheral pitting edema and hepatomegaly.
Which pathophysiologic change best explains these new
findings?
Options:
A. Isolated left ventricular systolic dysfunction causing
pulmonary venous congestion
B. Development of right ventricular failure with systemic venous
congestion
C. Increased pulmonary capillary permeability from alveolar
inflammation
D. Renal failure causing hypoalbuminemia and third-spacing
Correct Answer: B
Rationales:
Simple: Color Edition
3rd Edition
Author(s)Aaron Berkowitz MD PhD
TEST BANK
1.
Reference: Ch. 1: Anatomical Overview — Four chambers and
valve anatomy
Question Stem: A 72-year-old man is admitted after sudden
onset dyspnea, bibasilar crackles, and orthopnea. Chest x-ray
shows pulmonary edema. Which structural finding most directly
explains increased pulmonary capillary hydrostatic pressure
causing his symptoms?
Options:
A. Right ventricular dilation with tricuspid regurgitation
B. Left ventricular systolic dysfunction with elevated left
ventricular end-diastolic volume
,C. Atrial septal defect with left-to-right shunt
D. Pulmonic stenosis increasing right atrial pressure
Correct Answer: B
Rationales:
• Correct (B): Elevated left ventricular end-diastolic volume
(in systolic dysfunction) increases left atrial and pulmonary
venous pressures, raising pulmonary capillary hydrostatic
pressure and causing pulmonary edema. This links
chamber pathology to hydrostatic pulmonary edema.
• A: Right ventricular dilation and tricuspid regurgitation
primarily cause systemic venous congestion, not
pulmonary edema.
• C: ASD with left-to-right shunt increases pulmonary blood
flow chronically but typically causes volume overload
rather than acute pulmonary capillary hydrostatic pressure
spike.
• D: Pulmonic stenosis raises right-sided pressures and
causes systemic venous signs, not left-sided pulmonary
edema.
Teaching Point: Left ventricular failure raises pulmonary
capillary hydrostatic pressure causing pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Anatomical Overview & Heart
Failure
,2.
Reference: Ch. 1: Heart Failure — Preload, Afterload, and
Treatment of Heart Failure
Question Stem: A patient with chronic hypertension and heart
failure has elevated afterload. Which medication class will most
directly reduce afterload and thereby decrease left ventricular
wall stress?
Options:
A. Loop diuretics (e.g., furosemide)
B. ACE inhibitors (e.g., lisinopril)
C. Cardiac glycosides (e.g., digoxin)
D. Beta-blockers (e.g., metoprolol)
Correct Answer: B
Rationales:
• Correct (B): ACE inhibitors reduce systemic vascular
resistance (arterial vasodilation), lowering afterload and LV
wall stress — a primary mechanism for improving forward
output in systolic heart failure.
• A: Loop diuretics reduce preload via volume removal but
do not directly lower systemic vascular resistance
(afterload).
• C: Digoxin increases inotropy and can modestly reduce
symptoms but has minimal direct effect on afterload.
, • D: Beta-blockers reduce heart rate and myocardial oxygen
demand and provide long-term remodeling benefits, but
they do not acutely lower afterload like vasodilators.
Teaching Point: Vasodilators (ACE inhibitors) reduce afterload
and left ventricular wall stress.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure
3.
Reference: Ch. 1: Left vs. Right Heart Failure — Symptoms and
Signs of Heart Failure
Question Stem: A patient with chronic left-sided heart failure
develops new peripheral pitting edema and hepatomegaly.
Which pathophysiologic change best explains these new
findings?
Options:
A. Isolated left ventricular systolic dysfunction causing
pulmonary venous congestion
B. Development of right ventricular failure with systemic venous
congestion
C. Increased pulmonary capillary permeability from alveolar
inflammation
D. Renal failure causing hypoalbuminemia and third-spacing
Correct Answer: B
Rationales:
