McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A 6-year-old child is diagnosed with recurrent severe
bacterial infections caused by impaired neutrophil
chemotaxis. Genetic analysis identifies a mutation
, affecting actin filament polymerization within leukocytes.
The defective cellular component most directly explains
failure of which process?
A. ATP synthesis within mitochondria
B. Maintenance of osmotic gradients across the plasma
membrane
C. Directed cellular movement toward inflammatory
mediators
D. Ribosomal assembly of lysosomal enzymes
Correct Answer: C
Rationale:
• Clinical Clue: Recurrent infections with impaired
chemotaxis indicate defective cytoskeletal function in
immune cells.
• Mechanism: Actin microfilaments are essential for cell
motility, pseudopod formation, and directed migration.
• Why the Correct Answer Is Right: Leukocyte chemotaxis
depends on rapid actin remodeling to permit movement
toward cytokine gradients.
• Why the Other Options Are Wrong:
o A: ATP synthesis is primarily mitochondrial.
o B: Osmotic gradients are maintained mainly by
membrane ion pumps.
, o D: Ribosomal assembly occurs independently of actin
polymerization.
• Exam Trap: Confusing cytoskeletal defects with
mitochondrial energy disorders.
• High-Yield Clinical Correlation: Disorders affecting actin
dynamics impair wound healing, phagocytosis, and
immune migration.
• Memory Anchor: “Actin allows action.”
Q2. A patient with chronic alcohol use develops
hepatocellular injury characterized by accumulation of
misfolded proteins within the cytoplasm. Cellular
adaptation initially increases synthesis of organelles
responsible for protein processing and detoxification.
Which organelle is most likely increased in abundance?
A. Rough endoplasmic reticulum
B. Lysosome
C. Peroxisome
D. Golgi apparatus
Correct Answer: A
Rationale:
• Clinical Clue: Misfolded protein accumulation and
detoxification demand increased protein-processing
capacity.
, • Mechanism: Rough endoplasmic reticulum (RER)
synthesizes membrane-bound and secreted proteins and
participates in quality control.
• Why the Correct Answer Is Right: Hepatocytes adapt to
increased metabolic stress through RER hypertrophy.
• Why the Other Options Are Wrong:
o B: Lysosomes degrade cellular debris but do not
synthesize proteins.
o C: Peroxisomes handle fatty acid oxidation and
peroxide metabolism.
o D: Golgi apparatus modifies and packages proteins
after synthesis.
• Exam Trap: Selecting Golgi because it “handles proteins.”
• High-Yield Clinical Correlation: Chronic toxin exposure can
induce organelle hypertrophy as a cellular adaptation.
• Memory Anchor: “Rough ER = ribosome-rich protein
factory.”
Q3. A researcher exposes cultured cells to a toxin that
selectively disrupts sodium-potassium ATPase activity.
Which immediate cellular change is most likely to occur?
A. Hyperpolarization due to potassium retention
B. Cellular swelling from osmotic water influx
The Biologic Basis for Disease in Adults
and Children
9th Edition
Author(s)Julia Rogers
TEST BANK
Q1. A 6-year-old child is diagnosed with recurrent severe
bacterial infections caused by impaired neutrophil
chemotaxis. Genetic analysis identifies a mutation
, affecting actin filament polymerization within leukocytes.
The defective cellular component most directly explains
failure of which process?
A. ATP synthesis within mitochondria
B. Maintenance of osmotic gradients across the plasma
membrane
C. Directed cellular movement toward inflammatory
mediators
D. Ribosomal assembly of lysosomal enzymes
Correct Answer: C
Rationale:
• Clinical Clue: Recurrent infections with impaired
chemotaxis indicate defective cytoskeletal function in
immune cells.
• Mechanism: Actin microfilaments are essential for cell
motility, pseudopod formation, and directed migration.
• Why the Correct Answer Is Right: Leukocyte chemotaxis
depends on rapid actin remodeling to permit movement
toward cytokine gradients.
• Why the Other Options Are Wrong:
o A: ATP synthesis is primarily mitochondrial.
o B: Osmotic gradients are maintained mainly by
membrane ion pumps.
, o D: Ribosomal assembly occurs independently of actin
polymerization.
• Exam Trap: Confusing cytoskeletal defects with
mitochondrial energy disorders.
• High-Yield Clinical Correlation: Disorders affecting actin
dynamics impair wound healing, phagocytosis, and
immune migration.
• Memory Anchor: “Actin allows action.”
Q2. A patient with chronic alcohol use develops
hepatocellular injury characterized by accumulation of
misfolded proteins within the cytoplasm. Cellular
adaptation initially increases synthesis of organelles
responsible for protein processing and detoxification.
Which organelle is most likely increased in abundance?
A. Rough endoplasmic reticulum
B. Lysosome
C. Peroxisome
D. Golgi apparatus
Correct Answer: A
Rationale:
• Clinical Clue: Misfolded protein accumulation and
detoxification demand increased protein-processing
capacity.
, • Mechanism: Rough endoplasmic reticulum (RER)
synthesizes membrane-bound and secreted proteins and
participates in quality control.
• Why the Correct Answer Is Right: Hepatocytes adapt to
increased metabolic stress through RER hypertrophy.
• Why the Other Options Are Wrong:
o B: Lysosomes degrade cellular debris but do not
synthesize proteins.
o C: Peroxisomes handle fatty acid oxidation and
peroxide metabolism.
o D: Golgi apparatus modifies and packages proteins
after synthesis.
• Exam Trap: Selecting Golgi because it “handles proteins.”
• High-Yield Clinical Correlation: Chronic toxin exposure can
induce organelle hypertrophy as a cellular adaptation.
• Memory Anchor: “Rough ER = ribosome-rich protein
factory.”
Q3. A researcher exposes cultured cells to a toxin that
selectively disrupts sodium-potassium ATPase activity.
Which immediate cellular change is most likely to occur?
A. Hyperpolarization due to potassium retention
B. Cellular swelling from osmotic water influx
