GOULD'S PATHOPHYSIOLOGY FOR THE
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — Concept and Scope:
Etiology → Pathogenesis → Manifestations
Stem
A 58-year-old patient presents with progressive dyspnea and
lower-extremity edema. The clinician documents long-standing
poorly controlled hypertension. Which pathophysiologic
sequence best explains how chronic elevated afterload
produces these clinical manifestations? (Apply mechanism →
organ response → clinical effect.)
,Options
A. Chronic increased afterload → cardiomyocyte hyperplasia →
increased myocardial contractility → reduced edema
B. Chronic increased afterload → concentric left ventricular
hypertrophy → reduced ventricular compliance and eventual
systolic dysfunction → pulmonary congestion and peripheral
edema
C. Chronic increased afterload → diffuse myocardial necrosis →
immediate drop in cardiac output → isolated peripheral edema
D. Chronic increased afterload → valvular degeneration → right-
sided heart failure → pulmonary congestion
Correct answer
B
Rationales
• Correct (B): Chronic increased afterload (hypertension)
causes pressure overload leading to concentric
hypertrophy (increased cardiomyocyte size) with thicker
ventricular wall and reduced compliance. Over time this
adaptive hypertrophy may decompensate, impairing
systolic and diastolic function and producing pulmonary
congestion and peripheral edema. This description links
etiology → cellular/organ adaptation → manifestations
consistent with Gould.
• Incorrect (A): Myocardial cells enlarge (hypertrophy) but
not by hyperplasia; hyperplasia of cardiomyocytes does
not occur postnatally. Also hypertrophy initially preserves
, or increases contractility, but long-term maladaptation
causes dysfunction.
• Incorrect (C): Chronic afterload causes adaptive
hypertrophy rather than diffuse necrosis; necrosis is not
the immediate mechanism in pressure overload.
• Incorrect (D): Afterload-induced hypertrophy primarily
affects the left ventricle; valvular degeneration and
isolated right-sided failure are not the expected sequence.
Teaching point
Pressure overload → concentric hypertrophy → reduced
compliance → failure manifestations.
Citation (APA)
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
2
Reference
Ch. 1 — Introduction to Pathophysiology — Terminology:
Etiology categories (idiopathic, iatrogenic, nosocomial)
Stem
A patient develops neutropenia after receiving chemotherapy
and subsequently acquires Pseudomonas bloodstream infection
while hospitalized. Which etiologic labels best apply to (1) the
neutropenia and (2) the bloodstream infection?
, Options
A. (1) Idiopathic; (2) Iatrogenic
B. (1) Iatrogenic; (2) Nosocomial
C. (1) Nosocomial; (2) Idiopathic
D. (1) Iatrogenic; (2) Idiopathic
Correct answer
B
Rationales
• Correct (B): Neutropenia caused by chemotherapy is an
unintended adverse effect of medical treatment —
iatrogenic. A bloodstream infection acquired during a
hospital stay is nosocomial (hospital-acquired). This
matches the textbook classifications of etiology.
• Incorrect (A): Chemotherapy-induced neutropenia is not
idiopathic.
• Incorrect (C): Neutropenia in this context is treatment-
related (iatrogenic), not acquired in hospital; the infection
is nosocomial, not idiopathic.
• Incorrect (D): The bloodstream infection being idiopathic is
incorrect; its timing in hospital indicates nosocomial.
Teaching point
Iatrogenic = caused by medical treatment; nosocomial =
hospital-acquired infection.
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — Concept and Scope:
Etiology → Pathogenesis → Manifestations
Stem
A 58-year-old patient presents with progressive dyspnea and
lower-extremity edema. The clinician documents long-standing
poorly controlled hypertension. Which pathophysiologic
sequence best explains how chronic elevated afterload
produces these clinical manifestations? (Apply mechanism →
organ response → clinical effect.)
,Options
A. Chronic increased afterload → cardiomyocyte hyperplasia →
increased myocardial contractility → reduced edema
B. Chronic increased afterload → concentric left ventricular
hypertrophy → reduced ventricular compliance and eventual
systolic dysfunction → pulmonary congestion and peripheral
edema
C. Chronic increased afterload → diffuse myocardial necrosis →
immediate drop in cardiac output → isolated peripheral edema
D. Chronic increased afterload → valvular degeneration → right-
sided heart failure → pulmonary congestion
Correct answer
B
Rationales
• Correct (B): Chronic increased afterload (hypertension)
causes pressure overload leading to concentric
hypertrophy (increased cardiomyocyte size) with thicker
ventricular wall and reduced compliance. Over time this
adaptive hypertrophy may decompensate, impairing
systolic and diastolic function and producing pulmonary
congestion and peripheral edema. This description links
etiology → cellular/organ adaptation → manifestations
consistent with Gould.
• Incorrect (A): Myocardial cells enlarge (hypertrophy) but
not by hyperplasia; hyperplasia of cardiomyocytes does
not occur postnatally. Also hypertrophy initially preserves
, or increases contractility, but long-term maladaptation
causes dysfunction.
• Incorrect (C): Chronic afterload causes adaptive
hypertrophy rather than diffuse necrosis; necrosis is not
the immediate mechanism in pressure overload.
• Incorrect (D): Afterload-induced hypertrophy primarily
affects the left ventricle; valvular degeneration and
isolated right-sided failure are not the expected sequence.
Teaching point
Pressure overload → concentric hypertrophy → reduced
compliance → failure manifestations.
Citation (APA)
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
2
Reference
Ch. 1 — Introduction to Pathophysiology — Terminology:
Etiology categories (idiopathic, iatrogenic, nosocomial)
Stem
A patient develops neutropenia after receiving chemotherapy
and subsequently acquires Pseudomonas bloodstream infection
while hospitalized. Which etiologic labels best apply to (1) the
neutropenia and (2) the bloodstream infection?
, Options
A. (1) Idiopathic; (2) Iatrogenic
B. (1) Iatrogenic; (2) Nosocomial
C. (1) Nosocomial; (2) Idiopathic
D. (1) Iatrogenic; (2) Idiopathic
Correct answer
B
Rationales
• Correct (B): Neutropenia caused by chemotherapy is an
unintended adverse effect of medical treatment —
iatrogenic. A bloodstream infection acquired during a
hospital stay is nosocomial (hospital-acquired). This
matches the textbook classifications of etiology.
• Incorrect (A): Chemotherapy-induced neutropenia is not
idiopathic.
• Incorrect (C): Neutropenia in this context is treatment-
related (iatrogenic), not acquired in hospital; the infection
is nosocomial, not idiopathic.
• Incorrect (D): The bloodstream infection being idiopathic is
incorrect; its timing in hospital indicates nosocomial.
Teaching point
Iatrogenic = caused by medical treatment; nosocomial =
hospital-acquired infection.
