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.
The affected cells subsequently demonstrate reduced
plasma protein synthesis and intracellular accumulation of
misfolded peptides. Which additional finding most directly
explains the progression toward cellular injury?
, A. Impaired oxidative phosphorylation within
mitochondria
B. Failure of Golgi-mediated lysosomal enzyme activation
C. Activation of the unfolded protein response within the
endoplasmic reticulum
D. Increased passive diffusion across the plasma
membrane
E. Excessive glycogen deposition in the cytosol
Correct Answer: C
Rationale:
• Clinical Clue: Accumulation of misfolded proteins after
rough ER injury suggests ER stress.
• Mechanism: Misfolded proteins trigger the unfolded
protein response (UPR), which attempts restoration but
can induce apoptosis if persistent.
• Why the Correct Answer Is Right: ER stress activates
adaptive signaling pathways that suppress translation and
increase chaperone activity.
• Why the Other Options Are Wrong:
o A: Mitochondrial dysfunction causes ATP depletion
but does not directly explain protein-folding stress.
o B: Lysosomal enzyme activation occurs in the Golgi
but is secondary here.
o D: Passive diffusion changes are nonspecific.
, o E: Glycogen accumulation is unrelated to ER protein
folding failure.
• Exam Trap: Confusing generalized cell injury with ER-
specific stress signaling.
• High-Yield Clinical Correlation: Persistent UPR activation
contributes to neurodegenerative disease and diabetes
mellitus.
• Memory Anchor: “Misfolded proteins activate the ER
alarm system.”
Q2. A child with recurrent bacterial infections is found to
have defective neutrophil migration through vascular
endothelium. Laboratory evaluation reveals impaired
leukocyte adhesion despite normal neutrophil counts.
Dysfunction of which cellular structure best accounts for
this presentation?
A. Gap junctions
B. Desmosomes
C. Tight junctions
D. Integrins
E. Microtubules
Correct Answer: D
Rationale:
, • Clinical Clue: Failure of leukocyte adhesion and migration
suggests defective integrin-mediated attachment.
• Mechanism: Integrins mediate cell-extracellular matrix
interactions and leukocyte adhesion to endothelial
surfaces.
• Why the Correct Answer Is Right: Leukocyte adhesion
deficiency commonly involves defective integrin
expression or activation.
• Why the Other Options Are Wrong:
o A: Gap junctions allow intercellular communication.
o B: Desmosomes provide mechanical anchoring
between epithelial cells.
o C: Tight junctions regulate paracellular permeability.
o E: Microtubules assist intracellular transport but are
not primary adhesion molecules.
• Exam Trap: Choosing structural junctions instead of
adhesion receptors.
• High-Yield Clinical Correlation: Leukocyte adhesion
deficiency presents with delayed umbilical cord separation
and absent pus formation.
• Memory Anchor: “Integrins help immune cells grip before
they migrate.”
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.
The affected cells subsequently demonstrate reduced
plasma protein synthesis and intracellular accumulation of
misfolded peptides. Which additional finding most directly
explains the progression toward cellular injury?
, A. Impaired oxidative phosphorylation within
mitochondria
B. Failure of Golgi-mediated lysosomal enzyme activation
C. Activation of the unfolded protein response within the
endoplasmic reticulum
D. Increased passive diffusion across the plasma
membrane
E. Excessive glycogen deposition in the cytosol
Correct Answer: C
Rationale:
• Clinical Clue: Accumulation of misfolded proteins after
rough ER injury suggests ER stress.
• Mechanism: Misfolded proteins trigger the unfolded
protein response (UPR), which attempts restoration but
can induce apoptosis if persistent.
• Why the Correct Answer Is Right: ER stress activates
adaptive signaling pathways that suppress translation and
increase chaperone activity.
• Why the Other Options Are Wrong:
o A: Mitochondrial dysfunction causes ATP depletion
but does not directly explain protein-folding stress.
o B: Lysosomal enzyme activation occurs in the Golgi
but is secondary here.
o D: Passive diffusion changes are nonspecific.
, o E: Glycogen accumulation is unrelated to ER protein
folding failure.
• Exam Trap: Confusing generalized cell injury with ER-
specific stress signaling.
• High-Yield Clinical Correlation: Persistent UPR activation
contributes to neurodegenerative disease and diabetes
mellitus.
• Memory Anchor: “Misfolded proteins activate the ER
alarm system.”
Q2. A child with recurrent bacterial infections is found to
have defective neutrophil migration through vascular
endothelium. Laboratory evaluation reveals impaired
leukocyte adhesion despite normal neutrophil counts.
Dysfunction of which cellular structure best accounts for
this presentation?
A. Gap junctions
B. Desmosomes
C. Tight junctions
D. Integrins
E. Microtubules
Correct Answer: D
Rationale:
, • Clinical Clue: Failure of leukocyte adhesion and migration
suggests defective integrin-mediated attachment.
• Mechanism: Integrins mediate cell-extracellular matrix
interactions and leukocyte adhesion to endothelial
surfaces.
• Why the Correct Answer Is Right: Leukocyte adhesion
deficiency commonly involves defective integrin
expression or activation.
• Why the Other Options Are Wrong:
o A: Gap junctions allow intercellular communication.
o B: Desmosomes provide mechanical anchoring
between epithelial cells.
o C: Tight junctions regulate paracellular permeability.
o E: Microtubules assist intracellular transport but are
not primary adhesion molecules.
• Exam Trap: Choosing structural junctions instead of
adhesion receptors.
• High-Yield Clinical Correlation: Leukocyte adhesion
deficiency presents with delayed umbilical cord separation
and absent pus formation.
• Memory Anchor: “Integrins help immune cells grip before
they migrate.”
