McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher exposes cultured hepatocytes to a toxin that
selectively disrupts rough endoplasmic reticulum function.
Several hours later, the cells demonstrate impaired plasma
protein synthesis and intracellular accumulation of misfolded
peptides. Which mechanism most directly explains the resulting
cellular injury?
,A. Failure of oxidative phosphorylation with ATP depletion
B. Impaired post-translational protein folding triggering
unfolded protein response
C. Excessive lysosomal hydrolysis of structural proteins
D. Loss of mitochondrial calcium buffering capacity
Correct Answer: B
Rationale:
• Clinical Clue: Rough endoplasmic reticulum dysfunction
with accumulation of abnormal proteins points toward
protein-folding stress.
• Mechanism: The rough ER synthesizes and folds secretory
and membrane proteins. Misfolded proteins activate the
unfolded protein response, leading to cellular stress and
apoptosis if unresolved.
• Why the Correct Answer Is Right: Protein accumulation
and impaired secretion are hallmark consequences of ER
stress.
• Why the Other Options Are Wrong:
o A: ATP depletion is primarily mitochondrial.
o C: Lysosomal injury causes autophagy-related
degradation rather than protein synthesis failure.
o D: Mitochondrial calcium buffering is unrelated to
rough ER protein processing.
, • Exam Trap: Confusing ribosomal protein synthesis with
mitochondrial energy production.
• High-Yield Clinical Correlation: ER stress contributes to
neurodegenerative disorders and diabetes mellitus.
• Memory Anchor: “Rough ER = protein folding factory.”
Q2. A patient with chronic granulomatous disease has recurrent
bacterial and fungal infections despite normal neutrophil
counts. The defective cellular process most likely involves
failure of which organelle-dependent mechanism?
A. Peroxisomal β-oxidation
B. Golgi-mediated glycosylation
C. Lysosomal oxidative killing after phagosome fusion
D. Nuclear transcription factor activation
Correct Answer: C
Rationale:
• Clinical Clue: Chronic granulomatous disease involves
impaired intracellular pathogen killing.
• Mechanism: Neutrophils normally generate reactive
oxygen species within phagolysosomes after lysosomal
fusion.
• Why the Correct Answer Is Right: Defective respiratory
burst prevents effective lysosomal microbial destruction.
, • Why the Other Options Are Wrong:
o A: Peroxisomes metabolize fatty acids.
o B: Golgi glycosylation defects cause trafficking
abnormalities rather than recurrent catalase-positive
infections.
o D: Nuclear transcription defects are nonspecific here.
• Exam Trap: Associating all oxidative reactions with
mitochondria rather than phagolysosomes.
• High-Yield Clinical Correlation: CGD classically presents
with catalase-positive infections and granuloma formation.
• Memory Anchor: “Phagolysosome failure = persistent
infections.”
Q3. During severe ischemia, myocardial cells rapidly lose
membrane ion gradients and begin to swell. Which
pathophysiologic change best accounts for this early reversible
injury?
A. Irreversible fragmentation of nuclear DNA
B. ATP depletion causing Na+/K+ pump failure
C. Activation of caspase-mediated apoptosis
D. Excess extracellular calcium chelation
Correct Answer: B
Rationale:
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher exposes cultured hepatocytes to a toxin that
selectively disrupts rough endoplasmic reticulum function.
Several hours later, the cells demonstrate impaired plasma
protein synthesis and intracellular accumulation of misfolded
peptides. Which mechanism most directly explains the resulting
cellular injury?
,A. Failure of oxidative phosphorylation with ATP depletion
B. Impaired post-translational protein folding triggering
unfolded protein response
C. Excessive lysosomal hydrolysis of structural proteins
D. Loss of mitochondrial calcium buffering capacity
Correct Answer: B
Rationale:
• Clinical Clue: Rough endoplasmic reticulum dysfunction
with accumulation of abnormal proteins points toward
protein-folding stress.
• Mechanism: The rough ER synthesizes and folds secretory
and membrane proteins. Misfolded proteins activate the
unfolded protein response, leading to cellular stress and
apoptosis if unresolved.
• Why the Correct Answer Is Right: Protein accumulation
and impaired secretion are hallmark consequences of ER
stress.
• Why the Other Options Are Wrong:
o A: ATP depletion is primarily mitochondrial.
o C: Lysosomal injury causes autophagy-related
degradation rather than protein synthesis failure.
o D: Mitochondrial calcium buffering is unrelated to
rough ER protein processing.
, • Exam Trap: Confusing ribosomal protein synthesis with
mitochondrial energy production.
• High-Yield Clinical Correlation: ER stress contributes to
neurodegenerative disorders and diabetes mellitus.
• Memory Anchor: “Rough ER = protein folding factory.”
Q2. A patient with chronic granulomatous disease has recurrent
bacterial and fungal infections despite normal neutrophil
counts. The defective cellular process most likely involves
failure of which organelle-dependent mechanism?
A. Peroxisomal β-oxidation
B. Golgi-mediated glycosylation
C. Lysosomal oxidative killing after phagosome fusion
D. Nuclear transcription factor activation
Correct Answer: C
Rationale:
• Clinical Clue: Chronic granulomatous disease involves
impaired intracellular pathogen killing.
• Mechanism: Neutrophils normally generate reactive
oxygen species within phagolysosomes after lysosomal
fusion.
• Why the Correct Answer Is Right: Defective respiratory
burst prevents effective lysosomal microbial destruction.
, • Why the Other Options Are Wrong:
o A: Peroxisomes metabolize fatty acids.
o B: Golgi glycosylation defects cause trafficking
abnormalities rather than recurrent catalase-positive
infections.
o D: Nuclear transcription defects are nonspecific here.
• Exam Trap: Associating all oxidative reactions with
mitochondria rather than phagolysosomes.
• High-Yield Clinical Correlation: CGD classically presents
with catalase-positive infections and granuloma formation.
• Memory Anchor: “Phagolysosome failure = persistent
infections.”
Q3. During severe ischemia, myocardial cells rapidly lose
membrane ion gradients and begin to swell. Which
pathophysiologic change best accounts for this early reversible
injury?
A. Irreversible fragmentation of nuclear DNA
B. ATP depletion causing Na+/K+ pump failure
C. Activation of caspase-mediated apoptosis
D. Excess extracellular calcium chelation
Correct Answer: B
Rationale:
