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 hepatocytes to a toxin that
selectively disrupts rough endoplasmic reticulum function.
Several hours later, the cells demonstrate reduced plasma
, protein synthesis and intracellular accumulation of
unfolded proteins. Which mechanism most directly
explains the cellular injury?
A. Failure of oxidative phosphorylation leading to ATP
depletion
B. Impaired post-translational folding and transport of
secretory proteins
C. Loss of lysosomal hydrolase activation within acidic
vesicles
D. Increased cholesterol incorporation into the plasma
membrane
Correct Answer: B
Rationale:
• Clinical Clue: Hepatocytes with impaired plasma protein
production point toward rough endoplasmic reticulum
dysfunction.
• Mechanism: The rough ER synthesizes, folds, and
transports proteins destined for secretion or membrane
insertion.
• Why the Correct Answer Is Right: Disruption of rough ER
function causes accumulation of misfolded proteins and
impaired export of secretory proteins such as albumin.
• Why the Other Options Are Wrong:
, o A: ATP depletion is primarily linked to mitochondrial
injury.
o C: Lysosomal enzyme activation occurs in lysosomes
and Golgi-associated pathways.
o D: Cholesterol content affects membrane fluidity but
not protein synthesis directly.
• Exam Trap: Confusing rough ER dysfunction with Golgi or
mitochondrial injury.
• High-Yield Clinical Correlation: Unfolded protein
accumulation contributes to ER stress responses seen in
metabolic and neurodegenerative disorders.
• Memory Anchor: “Rough ER = ribosomes + protein
production.”
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 intracellular organelle
function?
A. Golgi-mediated protein glycosylation
B. Peroxisomal β-oxidation
C. Lysosomal destruction of phagocytosed organisms
D. Mitochondrial calcium buffering
Correct Answer: C
, Rationale:
• Clinical Clue: Chronic granulomatous disease involves
defective microbial killing by phagocytes.
• Mechanism: Lysosomes fuse with phagosomes to form
phagolysosomes, where oxidative and enzymatic
destruction occurs.
• Why the Correct Answer Is Right: Impaired intracellular
killing results from defective lysosomal-associated
respiratory burst activity.
• Why the Other Options Are Wrong:
o A: Glycosylation defects affect protein processing, not
phagocyte killing.
o B: Peroxisomal disorders impair lipid metabolism.
o D: Mitochondrial calcium buffering does not explain
recurrent catalase-positive infections.
• Exam Trap: Assuming normal neutrophil numbers imply
normal neutrophil function.
• High-Yield Clinical Correlation: Defective NADPH oxidase
activity prevents generation of reactive oxygen species
within phagolysosomes.
• Memory Anchor: “Lysosomes digest what phagocytes
ingest.”
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher exposes hepatocytes to a toxin that
selectively disrupts rough endoplasmic reticulum function.
Several hours later, the cells demonstrate reduced plasma
, protein synthesis and intracellular accumulation of
unfolded proteins. Which mechanism most directly
explains the cellular injury?
A. Failure of oxidative phosphorylation leading to ATP
depletion
B. Impaired post-translational folding and transport of
secretory proteins
C. Loss of lysosomal hydrolase activation within acidic
vesicles
D. Increased cholesterol incorporation into the plasma
membrane
Correct Answer: B
Rationale:
• Clinical Clue: Hepatocytes with impaired plasma protein
production point toward rough endoplasmic reticulum
dysfunction.
• Mechanism: The rough ER synthesizes, folds, and
transports proteins destined for secretion or membrane
insertion.
• Why the Correct Answer Is Right: Disruption of rough ER
function causes accumulation of misfolded proteins and
impaired export of secretory proteins such as albumin.
• Why the Other Options Are Wrong:
, o A: ATP depletion is primarily linked to mitochondrial
injury.
o C: Lysosomal enzyme activation occurs in lysosomes
and Golgi-associated pathways.
o D: Cholesterol content affects membrane fluidity but
not protein synthesis directly.
• Exam Trap: Confusing rough ER dysfunction with Golgi or
mitochondrial injury.
• High-Yield Clinical Correlation: Unfolded protein
accumulation contributes to ER stress responses seen in
metabolic and neurodegenerative disorders.
• Memory Anchor: “Rough ER = ribosomes + protein
production.”
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 intracellular organelle
function?
A. Golgi-mediated protein glycosylation
B. Peroxisomal β-oxidation
C. Lysosomal destruction of phagocytosed organisms
D. Mitochondrial calcium buffering
Correct Answer: C
, Rationale:
• Clinical Clue: Chronic granulomatous disease involves
defective microbial killing by phagocytes.
• Mechanism: Lysosomes fuse with phagosomes to form
phagolysosomes, where oxidative and enzymatic
destruction occurs.
• Why the Correct Answer Is Right: Impaired intracellular
killing results from defective lysosomal-associated
respiratory burst activity.
• Why the Other Options Are Wrong:
o A: Glycosylation defects affect protein processing, not
phagocyte killing.
o B: Peroxisomal disorders impair lipid metabolism.
o D: Mitochondrial calcium buffering does not explain
recurrent catalase-positive infections.
• Exam Trap: Assuming normal neutrophil numbers imply
normal neutrophil function.
• High-Yield Clinical Correlation: Defective NADPH oxidase
activity prevents generation of reactive oxygen species
within phagolysosomes.
• Memory Anchor: “Lysosomes digest what phagocytes
ingest.”
