Pathophysiology of Disease: An Introduction to
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
Ch. 1 — Introduction
1. Reference
Ch. 1 — Introduction
Question Stem
A 62-year-old patient develops progressive muscle weakness
after prolonged exposure to a new myotoxic medication. Which
cellular adaptation best explains reversible reduction in cell size
that decreases metabolic demand while preserving function?
Options
A. Dysplasia
B. Atrophy
,C. Hypertrophy
D. Metaplasia
Correct Answer
B
Rationales
Correct: Atrophy is a decrease in cell size and metabolic activity
that conserves resources and can be reversible when the
stimulus is removed. This explains reduced muscle mass with
decreased workload or toxic insult.
A: Dysplasia is disordered growth and differentiation, usually
pre-neoplastic, not simply size reduction.
C: Hypertrophy is increased cell size due to increased functional
demand, the opposite of atrophy.
D: Metaplasia is a reversible change in cell type (differentiation),
not a reduction in cell size.
Teaching Point
Atrophy reduces cell size and metabolic demand; often
reversible if the stimulus is removed.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
2. Reference
Ch. 1 — Introduction
,Question Stem
A patient’s failing heart increases ventricular wall thickness in
response to chronic pressure overload. Which molecular
mechanism most directly drives cardiomyocyte hypertrophy?
Options
A. Increased proteasomal degradation of contractile proteins
B. Activation of growth-related gene transcription via MAPK and
calcineurin pathways
C. Replacement of myocytes by fibroblasts and collagen
deposition
D. Loss of satellite cell-mediated regeneration
Correct Answer
B
Rationales
Correct: Hypertrophy is driven by intracellular signaling (e.g.,
MAPK, calcineurin/NFAT) that upregulates growth-promoting
genes and protein synthesis.
A: Increased proteasomal degradation leads to atrophy, not
hypertrophy.
C: Fibrosis and collagen deposition are features of remodeling,
not the primary mechanism of hypertrophy.
D: Loss of regenerative satellite cells impairs repair but does not
explain hypertrophic growth signaling.
Teaching Point
Hypertrophy involves growth-signaling pathways (MAPK,
calcineurin) that increase protein synthesis.
, Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3. Reference
Ch. 1 — Introduction
Question Stem
During ischemia, cells shift to anaerobic glycolysis. Which
immediate biochemical change most directly results in reduced
ATP-dependent ion pump activity and subsequent cellular
swelling?
Options
A. Increased NADH oxidation in mitochondria
B. Intracellular accumulation of lactate and decreased pH
C. Rapid depletion of intracellular ATP impairing Na⁺/K⁺-ATPase
D. Increased synthesis of mitochondrial respiratory complexes
Correct Answer
C
Rationales
Correct: ATP depletion compromises Na⁺/K⁺-ATPase, leading to
intracellular Na⁺ accumulation, water influx, and cellular
swelling.
A: Increased NADH oxidation would imply restored respiration;
ischemia increases NADH due to impaired oxidative
phosphorylation.
Clinical Medicine
8th Edition
Author(s)Gary D. Hammer; Stephen J. McPhee
TEST BANK
Ch. 1 — Introduction
1. Reference
Ch. 1 — Introduction
Question Stem
A 62-year-old patient develops progressive muscle weakness
after prolonged exposure to a new myotoxic medication. Which
cellular adaptation best explains reversible reduction in cell size
that decreases metabolic demand while preserving function?
Options
A. Dysplasia
B. Atrophy
,C. Hypertrophy
D. Metaplasia
Correct Answer
B
Rationales
Correct: Atrophy is a decrease in cell size and metabolic activity
that conserves resources and can be reversible when the
stimulus is removed. This explains reduced muscle mass with
decreased workload or toxic insult.
A: Dysplasia is disordered growth and differentiation, usually
pre-neoplastic, not simply size reduction.
C: Hypertrophy is increased cell size due to increased functional
demand, the opposite of atrophy.
D: Metaplasia is a reversible change in cell type (differentiation),
not a reduction in cell size.
Teaching Point
Atrophy reduces cell size and metabolic demand; often
reversible if the stimulus is removed.
Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
2. Reference
Ch. 1 — Introduction
,Question Stem
A patient’s failing heart increases ventricular wall thickness in
response to chronic pressure overload. Which molecular
mechanism most directly drives cardiomyocyte hypertrophy?
Options
A. Increased proteasomal degradation of contractile proteins
B. Activation of growth-related gene transcription via MAPK and
calcineurin pathways
C. Replacement of myocytes by fibroblasts and collagen
deposition
D. Loss of satellite cell-mediated regeneration
Correct Answer
B
Rationales
Correct: Hypertrophy is driven by intracellular signaling (e.g.,
MAPK, calcineurin/NFAT) that upregulates growth-promoting
genes and protein synthesis.
A: Increased proteasomal degradation leads to atrophy, not
hypertrophy.
C: Fibrosis and collagen deposition are features of remodeling,
not the primary mechanism of hypertrophy.
D: Loss of regenerative satellite cells impairs repair but does not
explain hypertrophic growth signaling.
Teaching Point
Hypertrophy involves growth-signaling pathways (MAPK,
calcineurin) that increase protein synthesis.
, Citation
Hammer & McPhee (2021). Pathophysiology of Disease (8th
Ed.). Ch. 1.
3. Reference
Ch. 1 — Introduction
Question Stem
During ischemia, cells shift to anaerobic glycolysis. Which
immediate biochemical change most directly results in reduced
ATP-dependent ion pump activity and subsequent cellular
swelling?
Options
A. Increased NADH oxidation in mitochondria
B. Intracellular accumulation of lactate and decreased pH
C. Rapid depletion of intracellular ATP impairing Na⁺/K⁺-ATPase
D. Increased synthesis of mitochondrial respiratory complexes
Correct Answer
C
Rationales
Correct: ATP depletion compromises Na⁺/K⁺-ATPase, leading to
intracellular Na⁺ accumulation, water influx, and cellular
swelling.
A: Increased NADH oxidation would imply restored respiration;
ischemia increases NADH due to impaired oxidative
phosphorylation.
