ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Ch. — Cellular Adaptation and Injury — Reversible
vs. Irreversible Cell Injury (Pathophysiology)
Stem: A 68-year-old man with poorly controlled type 2 diabetes
presents with a non-healing plantar ulcer. Tissue biopsy shows
patchy cell swelling, membrane blebbing, and mitochondrial
vacuolization without nuclear fragmentation. Which
pathophysiologic process best explains these findings?
A. Apoptosis due to programmed cell death
B. Reversible cell injury from hypoxia and metabolic stress
C. Coagulative necrosis from ischemic infarction
D. Autophagic cell death from prolonged starvation
,Correct answer: B
Rationale — Correct (B): The described features—cell swelling,
membrane blebbing, and mitochondrial changes without
nuclear fragmentation—are classic for reversible cell injury from
hypoxia/metabolic stress. Energy depletion impairs ion pumps,
causing sodium and water influx and organelle changes; if stress
is removed, cells may recover.
Rationale — Incorrect:
A. Apoptosis shows cell shrinkage, chromatin condensation and
apoptotic bodies, not swelling.
C. Coagulative necrosis includes preserved tissue architecture
with nuclear loss and denaturation; biopsy would show nuclear
changes.
D. Autophagy involves lysosomal digestion with
autophagosomes and is not characterized mainly by swelling
and blebbing.
Teaching point: Reversible injury → cell swelling, membrane
blebs, mitochondrial changes; nuclear integrity preserved.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Cellular Adaptation and Injury.
2
Reference: Ch. — Mechanisms of Cell Injury — Ischemia-
Reperfusion Injury (Oxidative Stress)
Stem: A 55-year-old woman undergoes thrombolysis for acute
,myocardial infarction. Shortly after reperfusion she develops
sudden worsening of myocardial dysfunction attributed to
oxidative damage. Which mechanism most likely mediates her
reperfusion injury?
A. Increased intracellular ATP production causing
hypercontracture
B. Burst of reactive oxygen species (ROS) causing lipid
peroxidation and membrane damage
C. Activation of apoptosis via intrinsic mitochondrial
cytochrome c release only during ischemia
D. Immediate restoration of ion pump function preventing
calcium overload
Correct answer: B
Rationale — Correct (B): Reperfusion triggers a burst of ROS
from mitochondria and activated neutrophils, causing lipid
peroxidation, membrane injury, and further mitochondrial
dysfunction. This oxidative stress is a primary mediator of
reperfusion injury.
Rationale — Incorrect:
A. ATP production rises but hypercontracture relates to calcium
overload and contractile protein damage rather than ATP
excess.
C. Apoptosis may be activated, but reperfusion ROS-driven
necrotic mechanisms and mitochondrial permeability transition
are central.
, D. Ion pumps are slow to recover; calcium overload often
worsens after reperfusion.
Teaching point: Reperfusion often worsens injury via ROS-
mediated membrane and mitochondrial damage.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Mechanisms of Cell Injury.
3
Reference: Ch. — Hypoxia and Cellular Metabolism — ATP
Depletion Effects
Stem: A hypotensive, hypoxic patient has cool, clammy skin and
altered mental status. At the cellular level, lack of ATP is most
directly responsible for which early pathophysiologic event?
A. Activation of caspases causing programmed cell death
B. Increased protein synthesis leading to hypertrophy
C. Failure of Na⁺/K⁺ ATPase pump causing intracellular sodium
and water accumulation
D. Lysosomal membrane stabilization preventing autolysis
Correct answer: C
Rationale — Correct (C): ATP depletion impairs the Na⁺/K⁺
ATPase, leading to sodium influx, water follows osmotically,
causing cellular swelling — an early, reversible change in
hypoxic injury.
Rationale — Incorrect:
A. Caspase activation relates to apoptosis, which can be ATP-
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Ch. — Cellular Adaptation and Injury — Reversible
vs. Irreversible Cell Injury (Pathophysiology)
Stem: A 68-year-old man with poorly controlled type 2 diabetes
presents with a non-healing plantar ulcer. Tissue biopsy shows
patchy cell swelling, membrane blebbing, and mitochondrial
vacuolization without nuclear fragmentation. Which
pathophysiologic process best explains these findings?
A. Apoptosis due to programmed cell death
B. Reversible cell injury from hypoxia and metabolic stress
C. Coagulative necrosis from ischemic infarction
D. Autophagic cell death from prolonged starvation
,Correct answer: B
Rationale — Correct (B): The described features—cell swelling,
membrane blebbing, and mitochondrial changes without
nuclear fragmentation—are classic for reversible cell injury from
hypoxia/metabolic stress. Energy depletion impairs ion pumps,
causing sodium and water influx and organelle changes; if stress
is removed, cells may recover.
Rationale — Incorrect:
A. Apoptosis shows cell shrinkage, chromatin condensation and
apoptotic bodies, not swelling.
C. Coagulative necrosis includes preserved tissue architecture
with nuclear loss and denaturation; biopsy would show nuclear
changes.
D. Autophagy involves lysosomal digestion with
autophagosomes and is not characterized mainly by swelling
and blebbing.
Teaching point: Reversible injury → cell swelling, membrane
blebs, mitochondrial changes; nuclear integrity preserved.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Cellular Adaptation and Injury.
2
Reference: Ch. — Mechanisms of Cell Injury — Ischemia-
Reperfusion Injury (Oxidative Stress)
Stem: A 55-year-old woman undergoes thrombolysis for acute
,myocardial infarction. Shortly after reperfusion she develops
sudden worsening of myocardial dysfunction attributed to
oxidative damage. Which mechanism most likely mediates her
reperfusion injury?
A. Increased intracellular ATP production causing
hypercontracture
B. Burst of reactive oxygen species (ROS) causing lipid
peroxidation and membrane damage
C. Activation of apoptosis via intrinsic mitochondrial
cytochrome c release only during ischemia
D. Immediate restoration of ion pump function preventing
calcium overload
Correct answer: B
Rationale — Correct (B): Reperfusion triggers a burst of ROS
from mitochondria and activated neutrophils, causing lipid
peroxidation, membrane injury, and further mitochondrial
dysfunction. This oxidative stress is a primary mediator of
reperfusion injury.
Rationale — Incorrect:
A. ATP production rises but hypercontracture relates to calcium
overload and contractile protein damage rather than ATP
excess.
C. Apoptosis may be activated, but reperfusion ROS-driven
necrotic mechanisms and mitochondrial permeability transition
are central.
, D. Ion pumps are slow to recover; calcium overload often
worsens after reperfusion.
Teaching point: Reperfusion often worsens injury via ROS-
mediated membrane and mitochondrial damage.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Ch. Mechanisms of Cell Injury.
3
Reference: Ch. — Hypoxia and Cellular Metabolism — ATP
Depletion Effects
Stem: A hypotensive, hypoxic patient has cool, clammy skin and
altered mental status. At the cellular level, lack of ATP is most
directly responsible for which early pathophysiologic event?
A. Activation of caspases causing programmed cell death
B. Increased protein synthesis leading to hypertrophy
C. Failure of Na⁺/K⁺ ATPase pump causing intracellular sodium
and water accumulation
D. Lysosomal membrane stabilization preventing autolysis
Correct answer: C
Rationale — Correct (C): ATP depletion impairs the Na⁺/K⁺
ATPase, leading to sodium influx, water follows osmotically,
causing cellular swelling — an early, reversible change in
hypoxic injury.
Rationale — Incorrect:
A. Caspase activation relates to apoptosis, which can be ATP-
