Clinical Pathophysiology Test Bank (3rd Ed | Berkowitz) – NCLEX & HESI Pathophysiology Review with Verified Answers & Rationales

Clinical Pathophysiology Made Ridiculously
Simple: Color Edition
3rd Edition


Author(s)Aaron Berkowitz MD PhD



TEST BANK




Reference: Berkowitz, 2023, Ch. 1: Heart Failure – Left vs. Right
Heart Failure
Question stem: A 68-year-old man with a history of long-
standing hypertension presents with exertional dyspnea,
orthopnea, and bibasilar crackles. His ejection fraction is
reduced on echocardiography. Which physiologic change best
explains his pulmonary symptoms?
A. Increased right ventricular afterload causing systemic venous
congestion

,B. Elevated left ventricular end-diastolic pressure increasing
pulmonary capillary hydrostatic pressure
C. Decreased preload to the left ventricle reducing pulmonary
blood flow
D. Increased pulmonary vascular resistance due to pulmonary
embolism
Correct answer: B
Rationale (correct): In left-sided systolic heart failure, reduced
LV contractility elevates LV end-diastolic pressure which
transmits backward to pulmonary capillaries, raising hydrostatic
pressure and causing pulmonary edema and crackles.
Incorrect A: Right ventricular afterload affects systemic venous
pressure, not pulmonary congestion.
Incorrect C: Decreased LV preload would reduce pulmonary
congestion, not cause it.
Incorrect D: Pulmonary embolism raises pulmonary resistance
but presents differently (sudden dyspnea, pleuritic pain).
Teaching point: Left-sided failure raises pulmonary capillary
hydrostatic pressure → pulmonary edema.
Citation: Berkowitz, 2023, Ch. 1: Heart Failure


2
Reference: Berkowitz, 2023, Ch. 1: Preload, Afterload, and
Treatment of Heart Failure

,Question stem: A patient with acute decompensated heart
failure is given IV nitroprusside. Which immediate
hemodynamic effect explains symptom improvement?
A. Increased preload through venoconstriction
B. Reduced afterload via arteriolar vasodilation
C. Direct increase in myocardial contractility
D. Increased heart rate by sympathetic stimulation
Correct answer: B
Rationale (correct): Nitroprusside is a potent arterial
vasodilator that lowers systemic vascular resistance (afterload),
decreasing LV workload and improving forward cardiac output
and pulmonary congestion.
Incorrect A: Nitroprusside causes venodilation, not
venoconstriction, decreasing preload.
Incorrect C: It does not directly increase contractility.
Incorrect D: Reflex tachycardia can occur but is not the primary
therapeutic mechanism.
Teaching point: Reducing afterload improves forward flow and
relieves congestion in systolic failure.
Citation: Berkowitz, 2023, Ch. 1: Preload, Afterload, Treatment


3
Reference: Berkowitz, 2023, Ch. 1: Right Heart Failure & The
Kidneys in Heart Failure

, Question stem: A patient with chronic right-sided heart failure
develops progressive peripheral edema and ascites. Which
renal response best contributes to this fluid accumulation?
A. Suppression of renin release leading to natriuresis
B. Activation of RAAS with sodium and water retention
C. Increased glomerular filtration rate causing volume loss
D. Decreased antidiuretic hormone (ADH) secretion producing
diuresis
Correct answer: B
Rationale (correct): In heart failure, reduced effective arterial
blood volume activates the RAAS, promoting sodium and water
retention and worsening edema.
Incorrect A: RAAS is activated, not suppressed, in low effective
perfusion.
Incorrect C: GFR typically falls in heart failure, promoting
retention.
Incorrect D: ADH is often increased, not decreased, promoting
free water retention.
Teaching point: Heart failure triggers RAAS activation → sodium
and water retention, exacerbating edema.
Citation: Berkowitz, 2023, Ch. 1: The Kidneys in Heart Failure


4