PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction
Question Stem
A 68-year-old man presents with progressive dyspnea and
bilateral lower-extremity edema. Chest x-ray shows
cardiomegaly and pulmonary vascular congestion. Which
pathophysiologic concept best explains the patient’s clinical
manifestations?
Options
A. Homeostatic set-point elevation
B. Failure of compensatory mechanisms leading to
decompensation
,C. Increased cellular proliferation due to neoplastic
transformation
D. Acute inflammatory response causing vascular permeability
Correct Answer
B
Rationales
Correct (B): Heart failure reflects failure of compensatory
mechanisms (e.g., neurohormonal activation, hypertrophy) that
initially maintain function but eventually decompensate,
producing pulmonary congestion and edema. Mechanisms
described in introductory pathophysiology explain progressive
organ dysfunction.
A: “Set-point elevation” describes regulated shifts (e.g., fever)
not the progressive pump failure seen in cardiomyopathy.
C: Neoplastic proliferation produces mass/tissue invasion, not
the circulatory congestion and edema pattern.
D: Acute inflammation increases vascular permeability locally;
generalized pulmonary vascular congestion with cardiomegaly is
circulatory, not primarily inflammatory.
Teaching Point
Compensatory mechanisms can maintain function short-term
but cause decompensation when exhausted.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
,2
Reference
Ch. 1 — Introduction
Question Stem
A nursing student must explain the difference between etiology
and pathogenesis to a classmate using the example of peptic
ulcer disease from H. pylori infection. Which statement best
distinguishes the two?
Options
A. Etiology is the mechanism of tissue injury; pathogenesis
names the causative agent.
B. Etiology names the causative agent; pathogenesis describes
the sequence of cellular and molecular events leading to
disease.
C. Etiology describes clinical manifestations; pathogenesis
describes disease prevalence.
D. Etiology and pathogenesis are interchangeable terms.
Correct Answer
B
Rationales
Correct (B): Etiology identifies the cause (H. pylori);
pathogenesis explains how bacterial colonization, mucosal
inflammation, and acid damage lead to ulcer formation — the
sequence of events.
, A: This reverses the definitions. Mechanism of injury is part of
pathogenesis, not etiology.
C: Etiology/pathogenesis are not about clinical manifestations
vs prevalence.
D: They are distinct concepts used differently in
pathophysiology.
Teaching Point
Etiology = cause; pathogenesis = steps from cause to tissue
injury.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
A 55-year-old woman with long-standing hypertension develops
concentric left ventricular hypertrophy. Which cellular
adaptation best describes this change and what is its likely
physiologic trigger?
Options
A. Hyperplasia due to increased functional demand
B. Hypertrophy due to increased workload from pressure
overload
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1
Reference
Ch. 1 — Introduction
Question Stem
A 68-year-old man presents with progressive dyspnea and
bilateral lower-extremity edema. Chest x-ray shows
cardiomegaly and pulmonary vascular congestion. Which
pathophysiologic concept best explains the patient’s clinical
manifestations?
Options
A. Homeostatic set-point elevation
B. Failure of compensatory mechanisms leading to
decompensation
,C. Increased cellular proliferation due to neoplastic
transformation
D. Acute inflammatory response causing vascular permeability
Correct Answer
B
Rationales
Correct (B): Heart failure reflects failure of compensatory
mechanisms (e.g., neurohormonal activation, hypertrophy) that
initially maintain function but eventually decompensate,
producing pulmonary congestion and edema. Mechanisms
described in introductory pathophysiology explain progressive
organ dysfunction.
A: “Set-point elevation” describes regulated shifts (e.g., fever)
not the progressive pump failure seen in cardiomyopathy.
C: Neoplastic proliferation produces mass/tissue invasion, not
the circulatory congestion and edema pattern.
D: Acute inflammation increases vascular permeability locally;
generalized pulmonary vascular congestion with cardiomegaly is
circulatory, not primarily inflammatory.
Teaching Point
Compensatory mechanisms can maintain function short-term
but cause decompensation when exhausted.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
,2
Reference
Ch. 1 — Introduction
Question Stem
A nursing student must explain the difference between etiology
and pathogenesis to a classmate using the example of peptic
ulcer disease from H. pylori infection. Which statement best
distinguishes the two?
Options
A. Etiology is the mechanism of tissue injury; pathogenesis
names the causative agent.
B. Etiology names the causative agent; pathogenesis describes
the sequence of cellular and molecular events leading to
disease.
C. Etiology describes clinical manifestations; pathogenesis
describes disease prevalence.
D. Etiology and pathogenesis are interchangeable terms.
Correct Answer
B
Rationales
Correct (B): Etiology identifies the cause (H. pylori);
pathogenesis explains how bacterial colonization, mucosal
inflammation, and acid damage lead to ulcer formation — the
sequence of events.
, A: This reverses the definitions. Mechanism of injury is part of
pathogenesis, not etiology.
C: Etiology/pathogenesis are not about clinical manifestations
vs prevalence.
D: They are distinct concepts used differently in
pathophysiology.
Teaching Point
Etiology = cause; pathogenesis = steps from cause to tissue
injury.
Citation (Simplified APA)
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3
Reference
Ch. 1 — Introduction
Question Stem
A 55-year-old woman with long-standing hypertension develops
concentric left ventricular hypertrophy. Which cellular
adaptation best describes this change and what is its likely
physiologic trigger?
Options
A. Hyperplasia due to increased functional demand
B. Hypertrophy due to increased workload from pressure
overload
