ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Part I — Cells, Homeostasis, and Disease — Cell Injury: Ischemia
and Hypoxic Injury Pathophysiology
Stem
A 68-year-old man with long-standing peripheral arterial
disease presents with sudden worsening of rest pain in his left
foot after he sat on a cold porch for several hours. The foot is
pale, cool, and painful; capillary refill is prolonged. Which
pathophysiologic process most likely explains the acute cellular
injury in the affected tissues?
,Options
A. Reperfusion-mediated oxidative stress causing mitochondrial
permeability transition
B. Chronic hypoxia causing adaptive cellular hypertrophy
C. Acute ischemia causing ATP depletion and failure of the
Na⁺/K⁺ ATPase
D. Autoimmune lymphocytic infiltration causing apoptosis of
endothelial cells
Correct answer
C
Rationale — Correct (C)
Acute ischemia rapidly depletes ATP, impairing the Na⁺/K⁺
ATPase, which leads to cellular sodium and water influx, cell
swelling, and loss of membrane integrity. These immediate
energy failure mechanisms explain the pale, cool, poorly
perfused tissue and acute pain. ATP depletion is the central
early event in ischemic cell injury.
Rationale — Incorrect
A. Reperfusion oxidative stress is important when blood flow is
restored, not the primary mechanism during ongoing acute
ischemia.
B. Chronic hypoxia may cause adaptive changes, not the sudden
ischemic decompensation described.
D. Autoimmune lymphocytic infiltration with apoptosis is a
slower, immune-mediated process and would present
differently.
,Teaching point
ATP depletion → Na⁺/K⁺ pump failure → cellular swelling is the
hallmark of acute ischemic injury.
Citation
Stewart, J. Anatomical Chart Company Atlas of Pathophysiology.
Part I.
2.
Reference
Part I — Cells, Homeostasis, and Disease — Free Radical &
Oxidative Injury
Stem
A 52-year-old woman undergoing thrombolytic therapy for
acute myocardial infarction develops sudden worsening of
myocardial function immediately after reperfusion. Which
mechanism best explains reperfusion-associated cellular
damage?
Options
A. Calcium-dependent protease activation due to prolonged
hypoxia only
B. Rapid generation of reactive oxygen species (ROS) and
oxidative damage to membranes
C. Granulomatous inflammation triggered by neutrophil
apoptosis
, D. Progressive telomere shortening leading to cellular
senescence
Correct answer
B
Rationale — Correct (B)
Reperfusion abruptly restores oxygen, producing reactive
oxygen species that damage lipids, proteins, and DNA.
Neutrophil activation and mitochondrial ROS generation cause
membrane lipid peroxidation and further mitochondrial injury,
explaining acute deterioration after reperfusion.
Rationale — Incorrect
A. Calcium activation occurs but is compounded by ROS during
reperfusion; ROS is the key reperfusion mediator.
C. Granulomatous inflammation is not typical of immediate
reperfusion injury.
D. Telomere shortening is a chronic aging mechanism, not acute
reperfusion injury.
Teaching point
Reperfusion injury: sudden ROS surge → lipid peroxidation and
mitochondrial damage.
Citation
Stewart, J. Anatomical Chart Company Atlas of Pathophysiology.
Part I.
3.
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Part I — Cells, Homeostasis, and Disease — Cell Injury: Ischemia
and Hypoxic Injury Pathophysiology
Stem
A 68-year-old man with long-standing peripheral arterial
disease presents with sudden worsening of rest pain in his left
foot after he sat on a cold porch for several hours. The foot is
pale, cool, and painful; capillary refill is prolonged. Which
pathophysiologic process most likely explains the acute cellular
injury in the affected tissues?
,Options
A. Reperfusion-mediated oxidative stress causing mitochondrial
permeability transition
B. Chronic hypoxia causing adaptive cellular hypertrophy
C. Acute ischemia causing ATP depletion and failure of the
Na⁺/K⁺ ATPase
D. Autoimmune lymphocytic infiltration causing apoptosis of
endothelial cells
Correct answer
C
Rationale — Correct (C)
Acute ischemia rapidly depletes ATP, impairing the Na⁺/K⁺
ATPase, which leads to cellular sodium and water influx, cell
swelling, and loss of membrane integrity. These immediate
energy failure mechanisms explain the pale, cool, poorly
perfused tissue and acute pain. ATP depletion is the central
early event in ischemic cell injury.
Rationale — Incorrect
A. Reperfusion oxidative stress is important when blood flow is
restored, not the primary mechanism during ongoing acute
ischemia.
B. Chronic hypoxia may cause adaptive changes, not the sudden
ischemic decompensation described.
D. Autoimmune lymphocytic infiltration with apoptosis is a
slower, immune-mediated process and would present
differently.
,Teaching point
ATP depletion → Na⁺/K⁺ pump failure → cellular swelling is the
hallmark of acute ischemic injury.
Citation
Stewart, J. Anatomical Chart Company Atlas of Pathophysiology.
Part I.
2.
Reference
Part I — Cells, Homeostasis, and Disease — Free Radical &
Oxidative Injury
Stem
A 52-year-old woman undergoing thrombolytic therapy for
acute myocardial infarction develops sudden worsening of
myocardial function immediately after reperfusion. Which
mechanism best explains reperfusion-associated cellular
damage?
Options
A. Calcium-dependent protease activation due to prolonged
hypoxia only
B. Rapid generation of reactive oxygen species (ROS) and
oxidative damage to membranes
C. Granulomatous inflammation triggered by neutrophil
apoptosis
, D. Progressive telomere shortening leading to cellular
senescence
Correct answer
B
Rationale — Correct (B)
Reperfusion abruptly restores oxygen, producing reactive
oxygen species that damage lipids, proteins, and DNA.
Neutrophil activation and mitochondrial ROS generation cause
membrane lipid peroxidation and further mitochondrial injury,
explaining acute deterioration after reperfusion.
Rationale — Incorrect
A. Calcium activation occurs but is compounded by ROS during
reperfusion; ROS is the key reperfusion mediator.
C. Granulomatous inflammation is not typical of immediate
reperfusion injury.
D. Telomere shortening is a chronic aging mechanism, not acute
reperfusion injury.
Teaching point
Reperfusion injury: sudden ROS surge → lipid peroxidation and
mitochondrial damage.
Citation
Stewart, J. Anatomical Chart Company Atlas of Pathophysiology.
Part I.
3.
