ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Ch. 1 — Cellular Injury — Ischemic Cell Injury
Stem: A 68-year-old man with longstanding peripheral arterial
disease reports sudden onset of severe, constant pain in his left
calf after gardening. The limb is pale, cool, and has decreased
distal pulses. Which pathophysiologic process best explains the
rapid ATP depletion and ionic pump failure in the ischemic
myocytes?
A. Uncoupling of oxidative phosphorylation due to
mitochondrial membrane damage
B. Excessive activation of lysosomal hydrolases leading to
,proteolysis
C. Overproduction of reactive oxygen species from reperfusion
injury
D. ATP depletion from impaired oxygen-dependent
mitochondrial ATP synthesis
Correct answer: D
Rationale — Correct (D):
Ischemia impairs oxygen delivery, halting oxidative
phosphorylation in mitochondria and causing rapid ATP
depletion. ATP-dependent Na⁺/K⁺-ATPase and Ca²⁺ pumps fail,
leading to ionic imbalances, cellular swelling, and injury
consistent with acute ischemic myocyte damage.
Rationale — Incorrect:
A. Uncoupling of oxidative phosphorylation is usually due to
toxin-mediated mitochondrial membrane damage (e.g.,
cyanide) and is not the primary immediate mechanism in
ischemia alone.
B. Lysosomal hydrolase activation occurs later after membrane
damage and is not the initiating event for ATP loss.
C. ROS overproduction is characteristic of reperfusion injury
after blood flow restoration, not the initial ischemic ATP
depletion.
Teaching point: ATP loss from halted oxidative phosphorylation
causes early ionic pump failure and cell swelling.
Citation: Ch. 1.
,Question 2
Reference: Ch. 1 — Cellular Adaptation — Hypertrophy vs.
Hyperplasia
Stem: A 52-year-old woman with chronic hypertension has
concentric left ventricular hypertrophy on echocardiogram and
reports exertional dyspnea. Pathologic examination shows
enlarged cardiac myocytes without increased cellular number.
Which stimulus and cellular response pair best describes this
adaptation?
A. Increased workload → hypertrophy via growth factor–
mediated gene transcription and increased sarcomeres
B. Hormonal excess → hyperplasia via stem cell proliferation
and increased cell number
C. Chronic inflammation → metaplasia via reprogramming of
stem cells
D. Reduced workload → atrophy via ubiquitin–proteasome
protein degradation
Correct answer: A
Rationale — Correct (A):
Chronic pressure overload (hypertension) increases myocardial
workload, triggering hypertrophy. Growth factor and
mechanical stress signaling (e.g., MAPK, calcineurin) increase
gene transcription for sarcomeric proteins, enlarging myocytes
without cell proliferation.
, Rationale — Incorrect:
B. Hormonal excess can cause hyperplasia in responsive tissues
(e.g., endometrium), but cardiac myocytes primarily
hypertrophy, not hyperplasia.
C. Metaplasia is replacement of one differentiated cell type by
another (e.g., Barrett esophagus), not the response seen in
cardiac pressure overload.
D. Reduced workload causes atrophy, but the patient
demonstrates hypertrophy, not atrophy.
Teaching point: Hypertrophy increases cell size via gene/protein
synthesis in response to increased mechanical load.
Citation: Ch. 1.
Question 3
Reference: Ch. 1 — Reversible vs. Irreversible Injury —
Membrane Integrity
Stem: A 35-year-old patient presents after acetaminophen
overdose. Early labs show elevated serum alanine
aminotransferase (ALT) and aspartate aminotransferase (AST).
Which process most directly causes the rise in these
intracellular enzymes in the bloodstream?
A. Increased synthesis of ALT/AST in hepatocytes in response to
toxin
B. Loss of plasma membrane integrity permitting cytosolic
enzyme leakage
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Ch. 1 — Cellular Injury — Ischemic Cell Injury
Stem: A 68-year-old man with longstanding peripheral arterial
disease reports sudden onset of severe, constant pain in his left
calf after gardening. The limb is pale, cool, and has decreased
distal pulses. Which pathophysiologic process best explains the
rapid ATP depletion and ionic pump failure in the ischemic
myocytes?
A. Uncoupling of oxidative phosphorylation due to
mitochondrial membrane damage
B. Excessive activation of lysosomal hydrolases leading to
,proteolysis
C. Overproduction of reactive oxygen species from reperfusion
injury
D. ATP depletion from impaired oxygen-dependent
mitochondrial ATP synthesis
Correct answer: D
Rationale — Correct (D):
Ischemia impairs oxygen delivery, halting oxidative
phosphorylation in mitochondria and causing rapid ATP
depletion. ATP-dependent Na⁺/K⁺-ATPase and Ca²⁺ pumps fail,
leading to ionic imbalances, cellular swelling, and injury
consistent with acute ischemic myocyte damage.
Rationale — Incorrect:
A. Uncoupling of oxidative phosphorylation is usually due to
toxin-mediated mitochondrial membrane damage (e.g.,
cyanide) and is not the primary immediate mechanism in
ischemia alone.
B. Lysosomal hydrolase activation occurs later after membrane
damage and is not the initiating event for ATP loss.
C. ROS overproduction is characteristic of reperfusion injury
after blood flow restoration, not the initial ischemic ATP
depletion.
Teaching point: ATP loss from halted oxidative phosphorylation
causes early ionic pump failure and cell swelling.
Citation: Ch. 1.
,Question 2
Reference: Ch. 1 — Cellular Adaptation — Hypertrophy vs.
Hyperplasia
Stem: A 52-year-old woman with chronic hypertension has
concentric left ventricular hypertrophy on echocardiogram and
reports exertional dyspnea. Pathologic examination shows
enlarged cardiac myocytes without increased cellular number.
Which stimulus and cellular response pair best describes this
adaptation?
A. Increased workload → hypertrophy via growth factor–
mediated gene transcription and increased sarcomeres
B. Hormonal excess → hyperplasia via stem cell proliferation
and increased cell number
C. Chronic inflammation → metaplasia via reprogramming of
stem cells
D. Reduced workload → atrophy via ubiquitin–proteasome
protein degradation
Correct answer: A
Rationale — Correct (A):
Chronic pressure overload (hypertension) increases myocardial
workload, triggering hypertrophy. Growth factor and
mechanical stress signaling (e.g., MAPK, calcineurin) increase
gene transcription for sarcomeric proteins, enlarging myocytes
without cell proliferation.
, Rationale — Incorrect:
B. Hormonal excess can cause hyperplasia in responsive tissues
(e.g., endometrium), but cardiac myocytes primarily
hypertrophy, not hyperplasia.
C. Metaplasia is replacement of one differentiated cell type by
another (e.g., Barrett esophagus), not the response seen in
cardiac pressure overload.
D. Reduced workload causes atrophy, but the patient
demonstrates hypertrophy, not atrophy.
Teaching point: Hypertrophy increases cell size via gene/protein
synthesis in response to increased mechanical load.
Citation: Ch. 1.
Question 3
Reference: Ch. 1 — Reversible vs. Irreversible Injury —
Membrane Integrity
Stem: A 35-year-old patient presents after acetaminophen
overdose. Early labs show elevated serum alanine
aminotransferase (ALT) and aspartate aminotransferase (AST).
Which process most directly causes the rise in these
intracellular enzymes in the bloodstream?
A. Increased synthesis of ALT/AST in hepatocytes in response to
toxin
B. Loss of plasma membrane integrity permitting cytosolic
enzyme leakage
