PATHOPHYSIOLOGY OF DISEASE: AN
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANKS
Q1
Reference
Ch. 1 — Introduction — Concepts of Homeostasis and Disease
Stem
A 58-year-old man with long-standing hypertension develops
progressive exertional dyspnea and orthopnea.
Echocardiography shows concentric left ventricular hypertrophy
with preserved ejection fraction. Which pathophysiologic
principle best explains the heart’s initial adaptation to chronic
pressure overload and its later transition to symptomatic heart
failure?
,A. Hyperplasia driven by increased cardiomyocyte mitosis
B. Hypertrophy via increased sarcomere addition and altered
gene expression
C. Metaplasia of myocardium to fibroblastic tissue as an
adaptive change
D. Apoptosis-mediated loss of myocytes leading to chamber
dilation
Correct answer
B
Rationale — Correct (B)
Pressure overload induces cardiomyocyte hypertrophy by
adding sarcomeres in parallel and activating fetal gene
programs; this increases wall thickness to normalize wall stress.
Over time maladaptive remodeling, altered calcium handling,
and energy mismatch contribute to symptomatic heart failure.
This mechanism is described in the text’s introduction linking
homeostatic compensation to later decompensation.
Rationales — Incorrect
A. Cardiomyocyte hyperplasia is minimal in adult human hearts;
mitotic proliferation is not the primary adaptive response.
C. Metaplasia refers to replacement of one differentiated cell
type by another (e.g., epithelial), not myocardial adaptation to
pressure.
D. While apoptosis contributes to progression, the initial
compensation is hypertrophy, not primary apoptosis causing
dilation.
,Teaching point
Pressure overload → cardiomyocyte hypertrophy (sarcomere
addition); chronic stress → maladaptive remodeling.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
Q2
Reference
Ch. 1 — Introduction — Reversible vs Irreversible Cell Injury
Stem
A 42-year-old woman presents after a near-drowning episode.
Serum lactate is markedly elevated, and she has transient
hypoxemia. Liver biopsy 24 hours later shows cell swelling and
clumping of nuclear chromatin without loss of nuclei. Which
statement best matches the pathophysiologic distinction
illustrated?
A. Clumping of chromatin indicates irreversible injury and
imminent necrosis.
B. Cell swelling and chromatin clumping are features of
reversible injury due to ATP depletion.
C. Nuclear dissolution is required to classify injury as reversible.
D. Presence of clumped chromatin indicates apoptosis rather
than reversible injury.
, Correct answer
B
Rationale — Correct (B)
Reversible injury from acute hypoxic/ischemic insults commonly
produces ATP depletion leading to failure of ion pumps, cell
swelling, and nuclear chromatin clumping—changes that can be
reversible if perfusion and ATP are restored. The introduction
emphasizes morphological correlates distinguishing reversible
from irreversible injury.
Rationales — Incorrect
A. Chromatin clumping alone is not definitive for irreversible
injury; nuclear fragmentation or dissolution indicates
irreversibility.
C. Nuclear dissolution (karyolysis) is a marker of irreversible
necrosis, but its absence does not prove irreversible damage.
D. Apoptosis shows nuclear fragmentation and cell shrinkage
with apoptotic bodies, not simple chromatin clumping.
Teaching point
ATP depletion → ion pump failure → swelling and chromatin
clumping (potentially reversible).
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
Q3
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANKS
Q1
Reference
Ch. 1 — Introduction — Concepts of Homeostasis and Disease
Stem
A 58-year-old man with long-standing hypertension develops
progressive exertional dyspnea and orthopnea.
Echocardiography shows concentric left ventricular hypertrophy
with preserved ejection fraction. Which pathophysiologic
principle best explains the heart’s initial adaptation to chronic
pressure overload and its later transition to symptomatic heart
failure?
,A. Hyperplasia driven by increased cardiomyocyte mitosis
B. Hypertrophy via increased sarcomere addition and altered
gene expression
C. Metaplasia of myocardium to fibroblastic tissue as an
adaptive change
D. Apoptosis-mediated loss of myocytes leading to chamber
dilation
Correct answer
B
Rationale — Correct (B)
Pressure overload induces cardiomyocyte hypertrophy by
adding sarcomeres in parallel and activating fetal gene
programs; this increases wall thickness to normalize wall stress.
Over time maladaptive remodeling, altered calcium handling,
and energy mismatch contribute to symptomatic heart failure.
This mechanism is described in the text’s introduction linking
homeostatic compensation to later decompensation.
Rationales — Incorrect
A. Cardiomyocyte hyperplasia is minimal in adult human hearts;
mitotic proliferation is not the primary adaptive response.
C. Metaplasia refers to replacement of one differentiated cell
type by another (e.g., epithelial), not myocardial adaptation to
pressure.
D. While apoptosis contributes to progression, the initial
compensation is hypertrophy, not primary apoptosis causing
dilation.
,Teaching point
Pressure overload → cardiomyocyte hypertrophy (sarcomere
addition); chronic stress → maladaptive remodeling.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
Q2
Reference
Ch. 1 — Introduction — Reversible vs Irreversible Cell Injury
Stem
A 42-year-old woman presents after a near-drowning episode.
Serum lactate is markedly elevated, and she has transient
hypoxemia. Liver biopsy 24 hours later shows cell swelling and
clumping of nuclear chromatin without loss of nuclei. Which
statement best matches the pathophysiologic distinction
illustrated?
A. Clumping of chromatin indicates irreversible injury and
imminent necrosis.
B. Cell swelling and chromatin clumping are features of
reversible injury due to ATP depletion.
C. Nuclear dissolution is required to classify injury as reversible.
D. Presence of clumped chromatin indicates apoptosis rather
than reversible injury.
, Correct answer
B
Rationale — Correct (B)
Reversible injury from acute hypoxic/ischemic insults commonly
produces ATP depletion leading to failure of ion pumps, cell
swelling, and nuclear chromatin clumping—changes that can be
reversible if perfusion and ATP are restored. The introduction
emphasizes morphological correlates distinguishing reversible
from irreversible injury.
Rationales — Incorrect
A. Chromatin clumping alone is not definitive for irreversible
injury; nuclear fragmentation or dissolution indicates
irreversibility.
C. Nuclear dissolution (karyolysis) is a marker of irreversible
necrosis, but its absence does not prove irreversible damage.
D. Apoptosis shows nuclear fragmentation and cell shrinkage
with apoptotic bodies, not simple chromatin clumping.
Teaching point
ATP depletion → ion pump failure → swelling and chromatin
clumping (potentially reversible).
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
Q3
