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 — Cellular adaptation:
atrophy
Stem (2–4 sentences)
A 72-year-old man with long-standing unilateral limb
immobilization after a femur fracture demonstrates visibly
decreased muscle bulk and reduced strength in the affected leg
after 8 weeks. Laboratory markers are within normal limits.
Which cellular mechanism best explains the decreased muscle
mass in the immobilized limb?
,Options
A. Increased protein synthesis due to persistent satellite cell
activation
B. Reduced cellular workload leading to decreased protein
synthesis and increased ubiquitin–proteasome activity
C. Persistent inflammation causing extensive necrosis of
myocytes
D. Metaplastic transformation of muscle cells into fibroblasts
Correct answer
B
Rationale — Correct (3–4 sentences)
Disuse atrophy results from reduced mechanical load that
downregulates protein synthesis and upregulates proteolytic
pathways (ubiquitin–proteasome), causing loss of contractile
proteins and decreased muscle fiber size. Satellite cell activation
and hypertrophy would increase mass (A is incorrect). Necrosis
from persistent inflammation would show elevated markers and
tissue damage not typical of uncomplicated disuse (C is
incorrect). Metaplasia (D) is a change in cell type, not the
reduction in size seen with atrophy.
Rationales — Incorrect
A. Increased protein synthesis and satellite cell activation
produce hypertrophy, not the atrophy observed.
C. Necrosis produces cell rupture and inflammatory markers;
immobilization atrophy is a regulated, non-necrotic process.
D. Metaplasia refers to replacement of one differentiated cell
,type with another, which does not account for selective muscle
thinning.
Teaching point (≤20 words)
Disuse atrophy: decreased workload → reduced protein
synthesis + increased proteolysis (ubiquitin–proteasome).
Citation
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 — Cellular adaptation:
hypertrophy
Stem (2–4 sentences)
A patient with well-controlled hypertension develops concentric
left ventricular hypertrophy over several months.
Echocardiography shows thicker ventricular walls but normal
chamber size. What is the predominant cellular adaptation and
intracellular mechanism responsible for the increased
myocardial wall thickness?
Options
A. Increased myocyte cell number via hyperplasia mediated by
growth factors
B. Cardiac myocyte hypertrophy mediated by increased
synthesis of contractile proteins and MAP kinase signaling
, C. Metaplastic replacement of cardiomyocytes with skeletal
muscle cells
D. Ischemic necrosis with fibroblast proliferation and scar
formation
Correct answer
B
Rationale — Correct (3–4 sentences)
Pressure overload causes myocardial cells (terminally
differentiated) to enlarge (hypertrophy) through increased
synthesis of actin and myosin and activation of growth-signaling
pathways (e.g., MAP kinase). Hyperplasia (A) does not occur in
adult cardiac muscle because myocytes are nonproliferative.
Metaplasia (C) and ischemic necrosis with scar (D) are not
mechanisms of adaptive concentric hypertrophy.
Rationales — Incorrect
A. Hyperplasia implies increased cell number, which is atypical
for adult cardiomyocytes.
C. Metaplasia involves cell-type switching, not increased
contractile protein synthesis.
D. Ischemic necrosis causes cell death and fibrosis, producing
dysfunction rather than organized hypertrophy.
Teaching point (≤20 words)
Pressure overload → cardiomyocyte hypertrophy via increased
contractile protein synthesis and growth signaling (MAPK).
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — Cellular adaptation:
atrophy
Stem (2–4 sentences)
A 72-year-old man with long-standing unilateral limb
immobilization after a femur fracture demonstrates visibly
decreased muscle bulk and reduced strength in the affected leg
after 8 weeks. Laboratory markers are within normal limits.
Which cellular mechanism best explains the decreased muscle
mass in the immobilized limb?
,Options
A. Increased protein synthesis due to persistent satellite cell
activation
B. Reduced cellular workload leading to decreased protein
synthesis and increased ubiquitin–proteasome activity
C. Persistent inflammation causing extensive necrosis of
myocytes
D. Metaplastic transformation of muscle cells into fibroblasts
Correct answer
B
Rationale — Correct (3–4 sentences)
Disuse atrophy results from reduced mechanical load that
downregulates protein synthesis and upregulates proteolytic
pathways (ubiquitin–proteasome), causing loss of contractile
proteins and decreased muscle fiber size. Satellite cell activation
and hypertrophy would increase mass (A is incorrect). Necrosis
from persistent inflammation would show elevated markers and
tissue damage not typical of uncomplicated disuse (C is
incorrect). Metaplasia (D) is a change in cell type, not the
reduction in size seen with atrophy.
Rationales — Incorrect
A. Increased protein synthesis and satellite cell activation
produce hypertrophy, not the atrophy observed.
C. Necrosis produces cell rupture and inflammatory markers;
immobilization atrophy is a regulated, non-necrotic process.
D. Metaplasia refers to replacement of one differentiated cell
,type with another, which does not account for selective muscle
thinning.
Teaching point (≤20 words)
Disuse atrophy: decreased workload → reduced protein
synthesis + increased proteolysis (ubiquitin–proteasome).
Citation
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 — Cellular adaptation:
hypertrophy
Stem (2–4 sentences)
A patient with well-controlled hypertension develops concentric
left ventricular hypertrophy over several months.
Echocardiography shows thicker ventricular walls but normal
chamber size. What is the predominant cellular adaptation and
intracellular mechanism responsible for the increased
myocardial wall thickness?
Options
A. Increased myocyte cell number via hyperplasia mediated by
growth factors
B. Cardiac myocyte hypertrophy mediated by increased
synthesis of contractile proteins and MAP kinase signaling
, C. Metaplastic replacement of cardiomyocytes with skeletal
muscle cells
D. Ischemic necrosis with fibroblast proliferation and scar
formation
Correct answer
B
Rationale — Correct (3–4 sentences)
Pressure overload causes myocardial cells (terminally
differentiated) to enlarge (hypertrophy) through increased
synthesis of actin and myosin and activation of growth-signaling
pathways (e.g., MAP kinase). Hyperplasia (A) does not occur in
adult cardiac muscle because myocytes are nonproliferative.
Metaplasia (C) and ischemic necrosis with scar (D) are not
mechanisms of adaptive concentric hypertrophy.
Rationales — Incorrect
A. Hyperplasia implies increased cell number, which is atypical
for adult cardiomyocytes.
C. Metaplasia involves cell-type switching, not increased
contractile protein synthesis.
D. Ischemic necrosis causes cell death and fibrosis, producing
dysfunction rather than organized hypertrophy.
Teaching point (≤20 words)
Pressure overload → cardiomyocyte hypertrophy via increased
contractile protein synthesis and growth signaling (MAPK).
