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 — What Is
Pathophysiology and Why Study It?
Stem
A 58-year-old patient has progressive shortness of breath after
an episode of uncontrolled hypertension. You are asked to
explain how sustained increased workload leads to a change in
myocardial tissue. Which cellular adaptation most directly
accounts for increased myocardial work and preserves
contractile function initially?
,Options
A. Cardiac myocyte hyperplasia with increased cell number
B. Cardiac myocyte hypertrophy with increased cell size and
protein synthesis
C. Cardiac myocyte metaplasia with replacement by fibroblasts
D. Cardiac myocyte atrophy with loss of sarcomeres
Correct Answer
B
Rationale — Correct
Hypertrophy is the adaptive increase in cell size and contractile
proteins in response to increased workload; cardiac myocytes
(post-mitotic cells) enlarge via increased protein synthesis and
gene reprogramming, which initially preserves contractile
function. This mechanism is described as a typical adaptation to
chronic pressure overload.
Rationale — Incorrect
A. Mature cardiac myocytes have limited proliferative capacity;
hyperplasia is not the primary response to pressure overload.
C. Metaplasia is a change in cell type often due to chronic
irritation; replacement by fibroblasts would impair contractility
rather than preserve it.
D. Atrophy is loss of cell mass and would reduce contractile
function, the opposite adaptive response to increased
workload.
,Teaching Point
Hypertrophy increases cell size and contractile proteins to meet
chronic increased workload.
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 — Introduction to
Cellular Changes
Stem
A patient is exposed to a chemical that impairs mitochondrial
oxidative phosphorylation. Within minutes, which intracellular
event will most directly cause loss of ionic homeostasis and
cellular swelling?
Options
A. Activation of caspases leading to apoptosis
B. Decreased ATP production causing Na⁺/K⁺-ATPase failure and
Na⁺ influx
C. Increased protein synthesis causing endoplasmic reticulum
dilation
D. Enhanced autophagy removing damaged organelles
Correct Answer
B
, Rationale — Correct
Mitochondrial oxidative phosphorylation impairment reduces
ATP production; Na⁺/K⁺-ATPase function is ATP-dependent, so
pump failure causes intracellular Na⁺ accumulation, water
influx, and cell swelling — an early, reversible injury.
Rationale — Incorrect
A. Caspase activation is characteristic of apoptosis, a
programmed death pathway usually following specific signaling
rather than immediate ATP depletion.
C. Increased protein synthesis does not occur when ATP is
depleted; ER dilation can result from protein-folding stress but
is not the immediate cause of ionic loss with mitochondrial
failure.
D. Autophagy is a protective mechanism but does not acutely
reverse ionic imbalances caused by ATP loss.
Teaching Point
ATP depletion → Na⁺/K⁺ pump failure → Na⁺ accumulation →
cellular swelling.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3
HEALTH PROFESSIONS
7TH EDITION
• AUTHOR(S)KARIN C. VANMETER;
ROBERT J. HUBERT
TEST BANK
1
Reference
Ch. 1 — Introduction to Pathophysiology — What Is
Pathophysiology and Why Study It?
Stem
A 58-year-old patient has progressive shortness of breath after
an episode of uncontrolled hypertension. You are asked to
explain how sustained increased workload leads to a change in
myocardial tissue. Which cellular adaptation most directly
accounts for increased myocardial work and preserves
contractile function initially?
,Options
A. Cardiac myocyte hyperplasia with increased cell number
B. Cardiac myocyte hypertrophy with increased cell size and
protein synthesis
C. Cardiac myocyte metaplasia with replacement by fibroblasts
D. Cardiac myocyte atrophy with loss of sarcomeres
Correct Answer
B
Rationale — Correct
Hypertrophy is the adaptive increase in cell size and contractile
proteins in response to increased workload; cardiac myocytes
(post-mitotic cells) enlarge via increased protein synthesis and
gene reprogramming, which initially preserves contractile
function. This mechanism is described as a typical adaptation to
chronic pressure overload.
Rationale — Incorrect
A. Mature cardiac myocytes have limited proliferative capacity;
hyperplasia is not the primary response to pressure overload.
C. Metaplasia is a change in cell type often due to chronic
irritation; replacement by fibroblasts would impair contractility
rather than preserve it.
D. Atrophy is loss of cell mass and would reduce contractile
function, the opposite adaptive response to increased
workload.
,Teaching Point
Hypertrophy increases cell size and contractile proteins to meet
chronic increased workload.
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 — Introduction to
Cellular Changes
Stem
A patient is exposed to a chemical that impairs mitochondrial
oxidative phosphorylation. Within minutes, which intracellular
event will most directly cause loss of ionic homeostasis and
cellular swelling?
Options
A. Activation of caspases leading to apoptosis
B. Decreased ATP production causing Na⁺/K⁺-ATPase failure and
Na⁺ influx
C. Increased protein synthesis causing endoplasmic reticulum
dilation
D. Enhanced autophagy removing damaged organelles
Correct Answer
B
, Rationale — Correct
Mitochondrial oxidative phosphorylation impairment reduces
ATP production; Na⁺/K⁺-ATPase function is ATP-dependent, so
pump failure causes intracellular Na⁺ accumulation, water
influx, and cell swelling — an early, reversible injury.
Rationale — Incorrect
A. Caspase activation is characteristic of apoptosis, a
programmed death pathway usually following specific signaling
rather than immediate ATP depletion.
C. Increased protein synthesis does not occur when ATP is
depleted; ER dilation can result from protein-folding stress but
is not the immediate cause of ionic loss with mitochondrial
failure.
D. Autophagy is a protective mechanism but does not acutely
reverse ionic imbalances caused by ATP loss.
Teaching Point
ATP depletion → Na⁺/K⁺ pump failure → Na⁺ accumulation →
cellular swelling.
Citation
VanMeter, K. C., & Hubert, R. J. (2024). Gould’s Pathophysiology
for the Health Professions (7th ed.). Ch. 1.
3
