ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Part I — Central Concepts — Cellular Hypoxic Injury
/ ATP Depletion
Clinical stem: A 62-year-old man arrives with crushing chest
pain 2 hours after onset. ECG shows ST-segment elevations
and serum troponin is increasing. Within minutes of sustained
ischemia, the nurse expects which primary cellular change
explaining early cellular swelling?
Options:
A. Activation of caspase pathways producing controlled cell
shrinkage.
B. Loss of mitochondrial membrane potential causing
cytochrome-c release.
C. Failure of plasma membrane Na⁺/K⁺ ATPase due to ATP
,depletion. (Correct)
D. Increased lysosomal enzyme release leading to digestion of
cell contents.
Correct answer: C
Rationale — Correct (C): Ischemia causes rapid ATP depletion;
the Na⁺/K⁺ ATPase fails, intracellular Na⁺ accumulates, water
follows osmotically, and cells swell. This explains early
reversible cellular swelling in acute hypoxic injury.
Rationale — Incorrect:
A. Caspase activation mediates apoptosis (programmed cell
death, shrinkage), not early ischemic swelling.
B. Mitochondrial membrane dysfunction (and cytochrome-c
release) is downstream and more associated with
commitment to apoptosis, not immediate swelling.
D. Lysosomal rupture and autodigestion contribute to necrosis
later; early swelling is primarily ion pump failure.
Teaching point: ATP depletion → Na⁺/K⁺ pump failure →
intracellular Na⁺ and water accumulation — early hypoxic
swelling.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
2
Reference: Part I — Central Concepts — Ischemia-Reperfusion
& Oxidative Injury
Clinical stem: A 48-year-old woman underwent thrombolysis
,for acute limb ischemia. Shortly after reperfusion, her affected
limb becomes markedly edematous, with worsening pain and
rising CK. Which pathophysiologic process best explains
worsening tissue injury after reperfusion?
Options:
A. Activation of apoptosis via caspase-9 only.
B. Massive reactive oxygen species (ROS) generation causing
lipid peroxidation and membrane damage. (Correct)
C. Primary immune complex deposition in vessel walls.
D. Selective loss of lysosomal membranes causing protease
inactivation.
Correct answer: B
Rationale — Correct (B): Reintroduction of oxygen into
ischemic tissue rapidly generates ROS (superoxide, hydroxyl
radical) that peroxidize membrane lipids and damage proteins
and DNA — a hallmark of reperfusion injury.
Rationale — Incorrect:
A. Apoptosis may occur, but reperfusion injury is dominated
by ROS and inflammatory cell activation rather than isolated
caspase-9 activation.
C. Immune complex vasculitis is not the mechanism of acute
reperfusion damage.
D. Lysosomal membrane rupture releases hydrolases, not
inactivation; but this is not the central reperfusion
mechanism.
Teaching point: Reperfusion → ROS and inflammatory
mediator surge → additional membrane/protein/DNA
, damage.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
3
Reference: Part I — Central Concepts — Apoptosis
(Programmed Cell Death)
Clinical stem: A 55-year-old woman receives radiation therapy
for localized breast cancer. One month later, biopsy of
irradiated tissue shows cells with condensed chromatin and
membrane-bound apoptotic bodies. Which mechanism best
describes these findings?
Options:
A. Uncontrolled cell lysis with inflammation from necrosis.
B. ATP-dependent activation of caspases leading to orderly
nuclear fragmentation. (Correct)
C. Lysosomal rupture causing random digestion of cellular
structures.
D. Massive mitochondrial swelling causing immediate plasma
membrane rupture.
Correct answer: B
Rationale — Correct (B): Radiation induces DNA damage
triggering intrinsic apoptosis: mitochondria and caspases
orchestrate energy-dependent chromatin condensation and
formation of apoptotic bodies without provoking
inflammation.
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Part I — Central Concepts — Cellular Hypoxic Injury
/ ATP Depletion
Clinical stem: A 62-year-old man arrives with crushing chest
pain 2 hours after onset. ECG shows ST-segment elevations
and serum troponin is increasing. Within minutes of sustained
ischemia, the nurse expects which primary cellular change
explaining early cellular swelling?
Options:
A. Activation of caspase pathways producing controlled cell
shrinkage.
B. Loss of mitochondrial membrane potential causing
cytochrome-c release.
C. Failure of plasma membrane Na⁺/K⁺ ATPase due to ATP
,depletion. (Correct)
D. Increased lysosomal enzyme release leading to digestion of
cell contents.
Correct answer: C
Rationale — Correct (C): Ischemia causes rapid ATP depletion;
the Na⁺/K⁺ ATPase fails, intracellular Na⁺ accumulates, water
follows osmotically, and cells swell. This explains early
reversible cellular swelling in acute hypoxic injury.
Rationale — Incorrect:
A. Caspase activation mediates apoptosis (programmed cell
death, shrinkage), not early ischemic swelling.
B. Mitochondrial membrane dysfunction (and cytochrome-c
release) is downstream and more associated with
commitment to apoptosis, not immediate swelling.
D. Lysosomal rupture and autodigestion contribute to necrosis
later; early swelling is primarily ion pump failure.
Teaching point: ATP depletion → Na⁺/K⁺ pump failure →
intracellular Na⁺ and water accumulation — early hypoxic
swelling.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
2
Reference: Part I — Central Concepts — Ischemia-Reperfusion
& Oxidative Injury
Clinical stem: A 48-year-old woman underwent thrombolysis
,for acute limb ischemia. Shortly after reperfusion, her affected
limb becomes markedly edematous, with worsening pain and
rising CK. Which pathophysiologic process best explains
worsening tissue injury after reperfusion?
Options:
A. Activation of apoptosis via caspase-9 only.
B. Massive reactive oxygen species (ROS) generation causing
lipid peroxidation and membrane damage. (Correct)
C. Primary immune complex deposition in vessel walls.
D. Selective loss of lysosomal membranes causing protease
inactivation.
Correct answer: B
Rationale — Correct (B): Reintroduction of oxygen into
ischemic tissue rapidly generates ROS (superoxide, hydroxyl
radical) that peroxidize membrane lipids and damage proteins
and DNA — a hallmark of reperfusion injury.
Rationale — Incorrect:
A. Apoptosis may occur, but reperfusion injury is dominated
by ROS and inflammatory cell activation rather than isolated
caspase-9 activation.
C. Immune complex vasculitis is not the mechanism of acute
reperfusion damage.
D. Lysosomal membrane rupture releases hydrolases, not
inactivation; but this is not the central reperfusion
mechanism.
Teaching point: Reperfusion → ROS and inflammatory
mediator surge → additional membrane/protein/DNA
, damage.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
3
Reference: Part I — Central Concepts — Apoptosis
(Programmed Cell Death)
Clinical stem: A 55-year-old woman receives radiation therapy
for localized breast cancer. One month later, biopsy of
irradiated tissue shows cells with condensed chromatin and
membrane-bound apoptotic bodies. Which mechanism best
describes these findings?
Options:
A. Uncontrolled cell lysis with inflammation from necrosis.
B. ATP-dependent activation of caspases leading to orderly
nuclear fragmentation. (Correct)
C. Lysosomal rupture causing random digestion of cellular
structures.
D. Massive mitochondrial swelling causing immediate plasma
membrane rupture.
Correct answer: B
Rationale — Correct (B): Radiation induces DNA damage
triggering intrinsic apoptosis: mitochondria and caspases
orchestrate energy-dependent chromatin condensation and
formation of apoptotic bodies without provoking
inflammation.
