McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher studying inherited metabolic disease
identifies a mutation that prevents ribosomal detachment
from the rough endoplasmic reticulum after protein
, synthesis. The affected cells demonstrate progressive
accumulation of unfolded secretory proteins and eventual
apoptosis. Which mechanism most directly explains the
cellular injury observed in this disorder?
A. Failure of lysosomal acidification leading to impaired
autophagy
B. Persistent activation of the unfolded protein response
within the endoplasmic reticulum
C. Increased peroxisomal beta-oxidation causing oxidative
membrane injury
D. Loss of mitochondrial fission resulting in ATP depletion
Correct Answer: B
Rationale:
• Clinical Clue: Accumulation of unfolded secretory proteins
within rough ER points toward ER stress.
• Mechanism: Persistent protein misfolding activates the
unfolded protein response (UPR), which initially attempts
adaptive correction but eventually triggers apoptosis.
• Why the Correct Answer Is Right: The rough ER is
responsible for synthesis and folding of secreted and
membrane proteins. Inability to process proteins
appropriately induces prolonged UPR activation and
cellular death.
• Why the Other Options Are Wrong:
, o A: Lysosomal dysfunction affects degradation rather
than ER protein folding.
o C: Peroxisomal beta-oxidation is unrelated to
ribosomal attachment.
o D: Mitochondrial fission abnormalities impair energy
regulation but do not specifically explain unfolded
secretory protein accumulation.
• Exam Trap: Confusing ER stress with lysosomal storage
pathology.
• High-Yield Clinical Correlation: ER stress contributes to
neurodegeneration, diabetes mellitus, and alpha-1
antitrypsin deficiency.
• Memory Anchor: “Misfolded proteins overload the rough
ER.”
Q2. A patient with severe hypoxemia develops cellular
swelling in hepatocytes shortly after circulatory collapse.
Electron microscopy demonstrates membrane blebbing
and dilated endoplasmic reticulum without nuclear
fragmentation. Which pathophysiologic change best
accounts for these findings?
A. Failure of ATP-dependent sodium-potassium transport
B. Excessive activation of caspase-mediated apoptosis
, C. Irreversible phospholipid membrane digestion
D. Rapid calcium sequestration into mitochondria
Correct Answer: A
Rationale:
• Clinical Clue: Cellular swelling after hypoxia indicates early
reversible injury.
• Mechanism: ATP depletion disables sodium-potassium
ATPase activity, allowing intracellular sodium and water
accumulation.
• Why the Correct Answer Is Right: Loss of membrane ion
homeostasis produces hydropic swelling and ER dilation
before irreversible necrosis develops.
• Why the Other Options Are Wrong:
o B: Apoptosis typically causes cell shrinkage, not
swelling.
o C: Irreversible membrane digestion implies late
necrotic injury.
o D: Calcium overload worsens injury but does not
directly explain osmotic swelling.
• Exam Trap: Equating all hypoxic injury with immediate
necrosis.
• High-Yield Clinical Correlation: Early ischemic injury is
often reversible if perfusion is restored rapidly.
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A researcher studying inherited metabolic disease
identifies a mutation that prevents ribosomal detachment
from the rough endoplasmic reticulum after protein
, synthesis. The affected cells demonstrate progressive
accumulation of unfolded secretory proteins and eventual
apoptosis. Which mechanism most directly explains the
cellular injury observed in this disorder?
A. Failure of lysosomal acidification leading to impaired
autophagy
B. Persistent activation of the unfolded protein response
within the endoplasmic reticulum
C. Increased peroxisomal beta-oxidation causing oxidative
membrane injury
D. Loss of mitochondrial fission resulting in ATP depletion
Correct Answer: B
Rationale:
• Clinical Clue: Accumulation of unfolded secretory proteins
within rough ER points toward ER stress.
• Mechanism: Persistent protein misfolding activates the
unfolded protein response (UPR), which initially attempts
adaptive correction but eventually triggers apoptosis.
• Why the Correct Answer Is Right: The rough ER is
responsible for synthesis and folding of secreted and
membrane proteins. Inability to process proteins
appropriately induces prolonged UPR activation and
cellular death.
• Why the Other Options Are Wrong:
, o A: Lysosomal dysfunction affects degradation rather
than ER protein folding.
o C: Peroxisomal beta-oxidation is unrelated to
ribosomal attachment.
o D: Mitochondrial fission abnormalities impair energy
regulation but do not specifically explain unfolded
secretory protein accumulation.
• Exam Trap: Confusing ER stress with lysosomal storage
pathology.
• High-Yield Clinical Correlation: ER stress contributes to
neurodegeneration, diabetes mellitus, and alpha-1
antitrypsin deficiency.
• Memory Anchor: “Misfolded proteins overload the rough
ER.”
Q2. A patient with severe hypoxemia develops cellular
swelling in hepatocytes shortly after circulatory collapse.
Electron microscopy demonstrates membrane blebbing
and dilated endoplasmic reticulum without nuclear
fragmentation. Which pathophysiologic change best
accounts for these findings?
A. Failure of ATP-dependent sodium-potassium transport
B. Excessive activation of caspase-mediated apoptosis
, C. Irreversible phospholipid membrane digestion
D. Rapid calcium sequestration into mitochondria
Correct Answer: A
Rationale:
• Clinical Clue: Cellular swelling after hypoxia indicates early
reversible injury.
• Mechanism: ATP depletion disables sodium-potassium
ATPase activity, allowing intracellular sodium and water
accumulation.
• Why the Correct Answer Is Right: Loss of membrane ion
homeostasis produces hydropic swelling and ER dilation
before irreversible necrosis develops.
• Why the Other Options Are Wrong:
o B: Apoptosis typically causes cell shrinkage, not
swelling.
o C: Irreversible membrane digestion implies late
necrotic injury.
o D: Calcium overload worsens injury but does not
directly explain osmotic swelling.
• Exam Trap: Equating all hypoxic injury with immediate
necrosis.
• High-Yield Clinical Correlation: Early ischemic injury is
often reversible if perfusion is restored rapidly.
