HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — Definition & Scope
Stem
A 58-year-old patient develops fatigue and mild pallor after
several months of a chronic inflammatory condition. The
instructor asks students to explain how chronic disease can
cause decreased tissue function without an acute injury. Which
pathophysiologic principle best links a prolonged stressor to
decreased cellular function in affected tissues?
Options
A. Persistent stress produces irreversible membrane rupture
,leading to necrosis.
B. Chronic stress triggers adaptive cellular atrophy and
decreased functional demand.
C. Long-term inflammation causes hyperplasia that always
increases tissue function.
D. Repeated stress causes immediate mitochondrial
proliferation and enhanced ATP production.
Correct Answer
B
Rationale — Correct (3–4 sentences)
Chronic stressors commonly induce adaptive responses such as
atrophy, where cells reduce size and organelles to lower
metabolic demand. Atrophy preserves viability but decreases
functional capacity, explaining fatigue and pallor without acute
cell death. This mechanism reflects pathophysiologic adaptation
linking prolonged insult → reduced cellular activity.
Rationale — Incorrect
A. Irreversible membrane rupture and necrosis describe acute,
severe injury, not the slow functional decline of chronic stress.
C. Hyperplasia can occur with chronic stimulation but does not
universally increase function and is tissue-specific; it is not the
best general link to decreased function.
D. Mitochondrial proliferation with enhanced ATP occurs with
increased demand (e.g., hypertrophy), not as a typical
immediate response to repetitive stress causing dysfunction.
,Teaching Point (≤20 words)
Chronic stress → adaptive atrophy reduces metabolism and
function without immediate necrosis.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
2
Reference
Ch. 1 — Cellular Adaptation — Hypertrophy vs. Hyperplasia
Stem
A nursing student must distinguish mechanisms producing
increased organ size. A patient’s skeletal muscle enlarges after
resistance training. Which cellular change most plausibly
explains this enlargement?
Options
A. Hyperplasia via increased cell number due to satellite cell
proliferation alone.
B. Hypertrophy through increased synthesis of contractile
proteins in existing myocytes.
C. Metaplasia with conversion of muscle cells into adipocytes to
store energy.
D. Dysplasia from disordered growth and pleomorphism of
muscle fibers.
, Correct Answer
B
Rationale — Correct (3–4 sentences)
Skeletal muscle enlarges primarily by hypertrophy: existing
myocytes increase synthesis of contractile proteins and
organelles to meet greater workload. Satellite cell contribution
can support hypertrophy but the defining mechanism is
increased cell size and protein content. This links increased
functional demand to cellular structural change.
Rationale — Incorrect
A. Hyperplasia is rare in mature skeletal muscle; increased cell
number is not the primary mechanism for exercise-induced
muscle growth.
C. Metaplasia refers to reversible change from one
differentiated cell type to another, not to muscle converting
into fat.
D. Dysplasia is disordered growth often pre-neoplastic and does
not describe physiologic muscle enlargement.
Teaching Point (≤20 words)
Hypertrophy: increased cell size and protein synthesis in
response to greater functional demand.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.