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 — Cellular Adaptation: Hypertrophy vs
Hyperplasia
Stem
A 62-year-old man with long-standing hypertension presents
with exertional dyspnea. Echocardiography shows concentric
left ventricular wall thickening without chamber dilation. Biopsy
reveals increased cardiomyocyte size with no increase in cell
number. Which mechanistic process best explains the
ventricular change?
,A. Hyperplasia due to increased cardiomyocyte proliferation
driven by local growth factors
B. Hypertrophy via increased synthesis of contractile proteins in
response to sustained pressure overload
C. Metaplasia with replacement of myocardium by fibrous
tissue from chronic stress
D. Atrophy caused by chronic ischemia and reduced workload of
ventricular myocytes
Correct answer
B
Rationale — Correct (B)
Concentric left ventricular thickening in chronic pressure
overload reflects hypertrophy: individual cardiomyocytes
increase in size by adding sarcomeres (increased synthesis of
contractile proteins) rather than increasing cell number. This
adaptation is driven by mechanical stress–activated signaling
pathways (e.g., mechanotransduction and growth factor
signaling) described in Chapter 1. Hypertrophy improves wall
stress initially but may progress to maladaptive heart failure.
Rationale — Incorrect
A. Hyperplasia implies increased cell number; adult
cardiomyocytes are terminally differentiated and do not
proliferate appreciably, so hyperplasia is not the mechanism.
C. Metaplasia is change in cell phenotype (e.g., epithelial) —
myocardium replacing with fibrous tissue is fibrosis/scar, not
metaplasia.
,D. Atrophy denotes decreased cell size and function from
reduced workload or trophic signals; here cells are larger, not
atrophic.
Teaching point
Hypertrophy increases cell size (sarcomeres) in nonproliferative
tissues under sustained mechanical load.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2)
Reference
Ch. 1 — Introduction — Reversible vs Irreversible Cell Injury
Stem
A patient suffers prolonged limb ischemia. Early biopsy (hours)
shows cell swelling, blebbing, and loss of microvilli; later biopsy
(days) shows dense eosinophilic cytoplasm, nuclear pyknosis,
and loss of nuclei. Which sequence of pathophysiologic events
is most consistent with this progression?
A. Initial irreversible mitochondrial rupture leading immediately
to nuclear fragmentation
B. Early ATP depletion causing Na⁺/K⁺ pump failure and
swelling; sustained injury causing membrane rupture and
nuclear condensation (irreversible injury)
C. Primary lysosomal enzyme activation causing reversible cell
, swelling followed by apoptotic chromatin condensation
D. Early oxidative DNA damage producing immediate apoptosis,
with swelling representing late-stage apoptosis
Correct answer
B
Rationale — Correct (B)
Reversible injury is characterized by ATP depletion → failure of
Na⁺/K⁺ ATPase → intracellular Na⁺ and water influx → cell
swelling and membrane blebbing. Prolonged ischemia causes
irreversible injury: loss of membrane integrity, mitochondrial
dysfunction, and nuclear changes (pyknosis, karyorrhexis,
karyolysis). Chapter 1 describes ATP depletion and membrane
damage as pivotal to this transition.
Rationale — Incorrect
A. Mitochondrial rupture is a late event; it does not account for
initial reversible swelling.
C. Lysosomal enzyme leakage contributes to irreversible
necrosis, not reversible swelling; apoptosis has distinct nuclear
morphology.
D. Apoptosis is typically energy-requiring and shows cell
shrinkage rather than early swelling.
Teaching point
ATP depletion → pump failure → reversible swelling; persistent
insult → membrane loss and irreversible necrosis.
INTRODUCTION TO CLINICAL MEDICINE
8TH EDITION
AUTHOR(S)GARY D. HAMMER; STEPHEN J.
MCPHEE
TEST BANK
1)
Reference
Ch. 1 — Introduction — Cellular Adaptation: Hypertrophy vs
Hyperplasia
Stem
A 62-year-old man with long-standing hypertension presents
with exertional dyspnea. Echocardiography shows concentric
left ventricular wall thickening without chamber dilation. Biopsy
reveals increased cardiomyocyte size with no increase in cell
number. Which mechanistic process best explains the
ventricular change?
,A. Hyperplasia due to increased cardiomyocyte proliferation
driven by local growth factors
B. Hypertrophy via increased synthesis of contractile proteins in
response to sustained pressure overload
C. Metaplasia with replacement of myocardium by fibrous
tissue from chronic stress
D. Atrophy caused by chronic ischemia and reduced workload of
ventricular myocytes
Correct answer
B
Rationale — Correct (B)
Concentric left ventricular thickening in chronic pressure
overload reflects hypertrophy: individual cardiomyocytes
increase in size by adding sarcomeres (increased synthesis of
contractile proteins) rather than increasing cell number. This
adaptation is driven by mechanical stress–activated signaling
pathways (e.g., mechanotransduction and growth factor
signaling) described in Chapter 1. Hypertrophy improves wall
stress initially but may progress to maladaptive heart failure.
Rationale — Incorrect
A. Hyperplasia implies increased cell number; adult
cardiomyocytes are terminally differentiated and do not
proliferate appreciably, so hyperplasia is not the mechanism.
C. Metaplasia is change in cell phenotype (e.g., epithelial) —
myocardium replacing with fibrous tissue is fibrosis/scar, not
metaplasia.
,D. Atrophy denotes decreased cell size and function from
reduced workload or trophic signals; here cells are larger, not
atrophic.
Teaching point
Hypertrophy increases cell size (sarcomeres) in nonproliferative
tissues under sustained mechanical load.
Citation
Hammer, G. D., & McPhee, S. J. (2025). Pathophysiology of
Disease (8th ed.). Chapter 1.
2)
Reference
Ch. 1 — Introduction — Reversible vs Irreversible Cell Injury
Stem
A patient suffers prolonged limb ischemia. Early biopsy (hours)
shows cell swelling, blebbing, and loss of microvilli; later biopsy
(days) shows dense eosinophilic cytoplasm, nuclear pyknosis,
and loss of nuclei. Which sequence of pathophysiologic events
is most consistent with this progression?
A. Initial irreversible mitochondrial rupture leading immediately
to nuclear fragmentation
B. Early ATP depletion causing Na⁺/K⁺ pump failure and
swelling; sustained injury causing membrane rupture and
nuclear condensation (irreversible injury)
C. Primary lysosomal enzyme activation causing reversible cell
, swelling followed by apoptotic chromatin condensation
D. Early oxidative DNA damage producing immediate apoptosis,
with swelling representing late-stage apoptosis
Correct answer
B
Rationale — Correct (B)
Reversible injury is characterized by ATP depletion → failure of
Na⁺/K⁺ ATPase → intracellular Na⁺ and water influx → cell
swelling and membrane blebbing. Prolonged ischemia causes
irreversible injury: loss of membrane integrity, mitochondrial
dysfunction, and nuclear changes (pyknosis, karyorrhexis,
karyolysis). Chapter 1 describes ATP depletion and membrane
damage as pivotal to this transition.
Rationale — Incorrect
A. Mitochondrial rupture is a late event; it does not account for
initial reversible swelling.
C. Lysosomal enzyme leakage contributes to irreversible
necrosis, not reversible swelling; apoptosis has distinct nuclear
morphology.
D. Apoptosis is typically energy-requiring and shows cell
shrinkage rather than early swelling.
Teaching point
ATP depletion → pump failure → reversible swelling; persistent
insult → membrane loss and irreversible necrosis.
