ANATOMICAL CHART COMPANY ATLAS
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Part I — Cellular Energy Failure and Ion Pump
Dysfunction
Stem: A 67-year-old man with prolonged hypotension after a
myocardial infarction becomes confused and oliguric. His labs
show rising serum potassium and metabolic acidosis. Which
pathophysiologic process best explains the acute cellular
changes causing these findings?
A. Increased Na⁺/K⁺-ATPase activity leading to intracellular K⁺
accumulation
,B. ATP depletion causing failure of membrane ion pumps and
cell swelling
C. Enhanced mitochondrial oxidative phosphorylation
increasing intracellular Ca²⁺
D. Upregulation of aquaporin channels causing intracellular
dehydration
Correct answer: B
Rationale — Correct: ATP depletion after ischemia impairs
Na⁺/K⁺-ATPase, causing Na⁺ and water influx, cell swelling, and
membrane dysfunction. Loss of pump function also causes K⁺ to
leak extracellularly, contributing to hyperkalemia and metabolic
disturbances. These mechanisms match hypotension →
ischemia → ATP failure.
Rationale — Incorrect A: Increased Na⁺/K⁺-ATPase activity
would maintain ionic gradients; it does not occur with ATP
depletion.
Rationale — Incorrect C: Oxidative phosphorylation is reduced
(not enhanced) during ischemia; intracellular Ca²⁺ rises
secondary to pump failure, not increased ATP production.
Rationale — Incorrect D: Aquaporin upregulation is not the
primary event in acute ischemic cell swelling.
Teaching point: ATP loss → ion pump failure → cell swelling and
membrane dysfunction.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
,Q2
Reference: Part I — Reperfusion Injury and Free Radical
Damage
Stem: After successful thrombolysis for acute limb ischemia, a
patient develops sudden worsening of tissue edema and a
transient rise in creatine kinase. Which mechanism most likely
produced this reperfusion-related deterioration?
A. Restoration of ATP halting protease activation
B. Sudden ROS generation causing lipid peroxidation and
membrane damage
C. Rapid endothelial proliferation stabilizing microvasculature
D. Increased anaerobic glycolysis producing excess lactate
Correct answer: B
Rationale — Correct: Reperfusion introduces oxygen to
ischemic tissue, generating reactive oxygen species (ROS) that
cause lipid peroxidation, membrane disruption, and enzyme
activation — worsening cellular injury and edema. CK rise aligns
with muscle cell membrane damage.
Rationale — Incorrect A: Restoration of ATP is gradual and does
not immediately halt protease activation; reperfusion initially
exacerbates damage.
Rationale — Incorrect C: Endothelial proliferation is a chronic
repair process, not an acute reperfusion effect.
Rationale — Incorrect D: Anaerobic glycolysis predominates in
ischemia, but reperfusion supplies oxygen; lactate alone does
not explain acute ROS-mediated damage.
, Teaching point: Reperfusion → ROS → lipid peroxidation →
worsened cell membrane injury.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
Q3
Reference: Part I — Calcium-Mediated Cellular Injury
Stem: A patient with severe hypoxia develops rising intracellular
calcium within cardiomyocytes. Which downstream effect best
explains progressive cell injury from calcium overload?
A. Activation of membrane-stabilizing kinases that prevent
apoptosis
B. Calcium-triggered activation of phospholipases, proteases,
and endonucleases
C. Increased mitochondrial ATP production that protects cells
D. Inhibition of lysosomal enzymes leading to reduced
autophagy
Correct answer: B
Rationale — Correct: Elevated intracellular Ca²⁺ activates
phospholipases (damaging membranes), proteases (degrading
cytoskeleton), and endonucleases (fragmenting DNA),
promoting necrosis or apoptosis. This cascade is central to
hypoxic cell injury.
Rationale — Incorrect A: Kinase activation in this context does
not stabilize membranes; calcium activates destructive
OF PATHOPHYSIOLOGY
4TH EDITION
• AUTHOR(S)JULIE STEWART
TEST BANK
Reference: Part I — Cellular Energy Failure and Ion Pump
Dysfunction
Stem: A 67-year-old man with prolonged hypotension after a
myocardial infarction becomes confused and oliguric. His labs
show rising serum potassium and metabolic acidosis. Which
pathophysiologic process best explains the acute cellular
changes causing these findings?
A. Increased Na⁺/K⁺-ATPase activity leading to intracellular K⁺
accumulation
,B. ATP depletion causing failure of membrane ion pumps and
cell swelling
C. Enhanced mitochondrial oxidative phosphorylation
increasing intracellular Ca²⁺
D. Upregulation of aquaporin channels causing intracellular
dehydration
Correct answer: B
Rationale — Correct: ATP depletion after ischemia impairs
Na⁺/K⁺-ATPase, causing Na⁺ and water influx, cell swelling, and
membrane dysfunction. Loss of pump function also causes K⁺ to
leak extracellularly, contributing to hyperkalemia and metabolic
disturbances. These mechanisms match hypotension →
ischemia → ATP failure.
Rationale — Incorrect A: Increased Na⁺/K⁺-ATPase activity
would maintain ionic gradients; it does not occur with ATP
depletion.
Rationale — Incorrect C: Oxidative phosphorylation is reduced
(not enhanced) during ischemia; intracellular Ca²⁺ rises
secondary to pump failure, not increased ATP production.
Rationale — Incorrect D: Aquaporin upregulation is not the
primary event in acute ischemic cell swelling.
Teaching point: ATP loss → ion pump failure → cell swelling and
membrane dysfunction.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
,Q2
Reference: Part I — Reperfusion Injury and Free Radical
Damage
Stem: After successful thrombolysis for acute limb ischemia, a
patient develops sudden worsening of tissue edema and a
transient rise in creatine kinase. Which mechanism most likely
produced this reperfusion-related deterioration?
A. Restoration of ATP halting protease activation
B. Sudden ROS generation causing lipid peroxidation and
membrane damage
C. Rapid endothelial proliferation stabilizing microvasculature
D. Increased anaerobic glycolysis producing excess lactate
Correct answer: B
Rationale — Correct: Reperfusion introduces oxygen to
ischemic tissue, generating reactive oxygen species (ROS) that
cause lipid peroxidation, membrane disruption, and enzyme
activation — worsening cellular injury and edema. CK rise aligns
with muscle cell membrane damage.
Rationale — Incorrect A: Restoration of ATP is gradual and does
not immediately halt protease activation; reperfusion initially
exacerbates damage.
Rationale — Incorrect C: Endothelial proliferation is a chronic
repair process, not an acute reperfusion effect.
Rationale — Incorrect D: Anaerobic glycolysis predominates in
ischemia, but reperfusion supplies oxygen; lactate alone does
not explain acute ROS-mediated damage.
, Teaching point: Reperfusion → ROS → lipid peroxidation →
worsened cell membrane injury.
Citation: Stewart, J. (4th ed.). Anatomical Chart Company Atlas
of Pathophysiology. Part I.
Q3
Reference: Part I — Calcium-Mediated Cellular Injury
Stem: A patient with severe hypoxia develops rising intracellular
calcium within cardiomyocytes. Which downstream effect best
explains progressive cell injury from calcium overload?
A. Activation of membrane-stabilizing kinases that prevent
apoptosis
B. Calcium-triggered activation of phospholipases, proteases,
and endonucleases
C. Increased mitochondrial ATP production that protects cells
D. Inhibition of lysosomal enzymes leading to reduced
autophagy
Correct answer: B
Rationale — Correct: Elevated intracellular Ca²⁺ activates
phospholipases (damaging membranes), proteases (degrading
cytoskeleton), and endonucleases (fragmenting DNA),
promoting necrosis or apoptosis. This cascade is central to
hypoxic cell injury.
Rationale — Incorrect A: Kinase activation in this context does
not stabilize membranes; calcium activates destructive
