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
, reduced plasma protein secretion and intracellular
accumulation of misfolded peptides. The finding most
directly reflects impairment of which cellular process?
A. Oxidative phosphorylation
B. Post-translational protein synthesis and folding
C. Lysosomal degradation of glycogen
D. Cholesterol esterification within peroxisomes
Correct Answer: B
Rationale:
• Clinical Clue: Reduced secreted proteins with intracellular
peptide accumulation indicates defective protein
processing.
• Mechanism: The rough endoplasmic reticulum (RER)
synthesizes membrane-bound and secreted proteins and
initiates folding and quality control.
• Why the Correct Answer Is Right: Dysfunction of the RER
impairs synthesis and processing of export proteins,
leading to retention of abnormal peptides.
• Why the Other Options Are Wrong:
o A. Oxidative phosphorylation occurs in mitochondria.
o C. Lysosomal degradation involves hydrolytic enzymes
in lysosomes.
o D. Peroxisomes participate in fatty acid oxidation, not
protein folding.
,• Exam Trap: Confusing smooth ER with rough ER; smooth
ER is more involved in lipid synthesis and detoxification.
• High-Yield Clinical Correlation: Persistent ER stress
contributes to neurodegenerative disease and diabetes
mellitus.
• Memory Anchor: “Rough ER = ribosomes = released
proteins.”
Q2. A mutation causes failure of cadherin-mediated
junction formation between epithelial cells. Which
pathophysiologic consequence is most likely to occur?
A. Loss of intracellular ATP production
B. Increased paracellular permeability and impaired tissue
integrity
C. Failure of lysosomal acidification
D. Persistent activation of sodium-potassium ATPase
Correct Answer: B
Rationale:
• Clinical Clue: Cadherins are central adhesion molecules in
epithelial integrity.
• Mechanism: Cadherins mediate calcium-dependent cell-
to-cell adhesion through adherens junctions and
desmosomes.
, • Why the Correct Answer Is Right: Defective cadherin
interactions weaken tissue cohesion and increase
permeability between adjacent cells.
• Why the Other Options Are Wrong:
o A. ATP production is primarily mitochondrial.
o C. Lysosomal acidification depends on proton pumps.
o D. Sodium-potassium ATPase is unrelated to cadherin
signaling.
• Exam Trap: Confusing cell adhesion proteins with
membrane transport proteins.
• High-Yield Clinical Correlation: Loss of E-cadherin function
is associated with tumor invasion and metastasis.
• Memory Anchor: “Cadherins connect cells together.”
Q3. A patient with severe hypoxia develops cellular
swelling and reduced membrane potential. Which
mechanism best accounts for the earliest reversible
cellular injury?
A. Excessive lysosomal rupture
B. Depletion of ATP with failure of sodium-potassium
transport
C. Increased DNA transcription
D. Irreversible mitochondrial calcification
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
, reduced plasma protein secretion and intracellular
accumulation of misfolded peptides. The finding most
directly reflects impairment of which cellular process?
A. Oxidative phosphorylation
B. Post-translational protein synthesis and folding
C. Lysosomal degradation of glycogen
D. Cholesterol esterification within peroxisomes
Correct Answer: B
Rationale:
• Clinical Clue: Reduced secreted proteins with intracellular
peptide accumulation indicates defective protein
processing.
• Mechanism: The rough endoplasmic reticulum (RER)
synthesizes membrane-bound and secreted proteins and
initiates folding and quality control.
• Why the Correct Answer Is Right: Dysfunction of the RER
impairs synthesis and processing of export proteins,
leading to retention of abnormal peptides.
• Why the Other Options Are Wrong:
o A. Oxidative phosphorylation occurs in mitochondria.
o C. Lysosomal degradation involves hydrolytic enzymes
in lysosomes.
o D. Peroxisomes participate in fatty acid oxidation, not
protein folding.
,• Exam Trap: Confusing smooth ER with rough ER; smooth
ER is more involved in lipid synthesis and detoxification.
• High-Yield Clinical Correlation: Persistent ER stress
contributes to neurodegenerative disease and diabetes
mellitus.
• Memory Anchor: “Rough ER = ribosomes = released
proteins.”
Q2. A mutation causes failure of cadherin-mediated
junction formation between epithelial cells. Which
pathophysiologic consequence is most likely to occur?
A. Loss of intracellular ATP production
B. Increased paracellular permeability and impaired tissue
integrity
C. Failure of lysosomal acidification
D. Persistent activation of sodium-potassium ATPase
Correct Answer: B
Rationale:
• Clinical Clue: Cadherins are central adhesion molecules in
epithelial integrity.
• Mechanism: Cadherins mediate calcium-dependent cell-
to-cell adhesion through adherens junctions and
desmosomes.
, • Why the Correct Answer Is Right: Defective cadherin
interactions weaken tissue cohesion and increase
permeability between adjacent cells.
• Why the Other Options Are Wrong:
o A. ATP production is primarily mitochondrial.
o C. Lysosomal acidification depends on proton pumps.
o D. Sodium-potassium ATPase is unrelated to cadherin
signaling.
• Exam Trap: Confusing cell adhesion proteins with
membrane transport proteins.
• High-Yield Clinical Correlation: Loss of E-cadherin function
is associated with tumor invasion and metastasis.
• Memory Anchor: “Cadherins connect cells together.”
Q3. A patient with severe hypoxia develops cellular
swelling and reduced membrane potential. Which
mechanism best accounts for the earliest reversible
cellular injury?
A. Excessive lysosomal rupture
B. Depletion of ATP with failure of sodium-potassium
transport
C. Increased DNA transcription
D. Irreversible mitochondrial calcification
