Understanding Pathophysiology
8th Edition
Author(s)Sue E. Huether
TEST BANK
Q1. A 42-year-old man develops progressive proximal muscle
weakness after several months of treatment with a medication
that disrupts mitochondrial protein synthesis. Muscle biopsy
demonstrates swollen mitochondria with disrupted cristae and
accumulation of intracellular lipid droplets. The patient’s
weakness is most directly explained by failure of which cellular
process?
A. Oxidative phosphorylation leading to ATP depletion
B. Lysosomal degradation of intracellular proteins
,C. Peroxisomal β-oxidation of long-chain fatty acids
D. Nuclear transcription of structural proteins
E. Ribosomal assembly of cytoskeletal microfilaments
Correct Answer: A
Rationale:
Clinical Clue:
Mitochondrial structural injury with lipid accumulation and
muscle weakness indicates impaired aerobic energy
production.
Mechanism:
Mitochondria generate ATP through oxidative phosphorylation.
Failure of the electron transport chain reduces ATP-dependent
cellular functions.
Why the Correct Answer Is Right:
Skeletal muscle is highly dependent on aerobic metabolism.
ATP depletion impairs actin-myosin cycling and membrane ion
pumps, producing weakness and myocyte dysfunction.
Why the Other Options Are Wrong:
B. Lysosomal dysfunction causes substrate accumulation
disorders rather than primary ATP failure.
C. Peroxisomal metabolism contributes to lipid handling but is
not the primary ATP source in muscle.
D. Nuclear transcription impairment would affect protein
synthesis globally but does not explain mitochondrial swelling.
,E. Ribosomal assembly defects would impair protein production
rather than directly causing energy failure.
Exam Trap (common misconception tested):
Confusing mitochondrial dysfunction with generalized protein
synthesis defects.
High-Yield Clinical Correlation:
Mitochondrial injury commonly affects tissues with high energy
demands such as muscle, myocardium, and neurons.
Q2. A researcher exposes cultured hepatocytes to a toxin that
causes failure of the sodium-potassium ATPase pump. Within
minutes, the cells become swollen with cytoplasmic
vacuolization. Which pathophysiologic change best accounts for
these findings?
A. Increased intracellular calcium causing apoptosis
B. Osmotic influx of water secondary to sodium accumulation
C. Increased extracellular potassium causing membrane rupture
D. Activation of lysosomal hydrolases from Golgi disruption
E. Excessive glucose influx causing glycogen deposition
Correct Answer: B
Rationale:
Clinical Clue:
Rapid cellular swelling after ATPase failure indicates disturbed
osmotic regulation.
, Mechanism:
The sodium-potassium pump maintains electrochemical
gradients. Pump failure leads to intracellular sodium
accumulation, followed by passive water entry.
Why the Correct Answer Is Right:
Loss of membrane ion homeostasis causes hydropic swelling,
an early reversible manifestation of cell injury.
Why the Other Options Are Wrong:
A. Calcium influx contributes to later irreversible injury rather
than immediate swelling.
C. Extracellular potassium elevation is not the primary osmotic
driver.
D. Lysosomal enzyme release occurs in severe irreversible
injury.
E. Glycogen accumulation does not produce acute hydropic
change.
Exam Trap (common misconception tested):
Mistaking early reversible injury for apoptotic or necrotic injury.
High-Yield Clinical Correlation:
Cell swelling is among the earliest morphologic manifestations
of ATP depletion.
Q3. A 6-year-old child has recurrent bacterial infections and
poor wound healing. Genetic testing reveals defective integrin
synthesis. Which cellular function is most directly impaired?
8th Edition
Author(s)Sue E. Huether
TEST BANK
Q1. A 42-year-old man develops progressive proximal muscle
weakness after several months of treatment with a medication
that disrupts mitochondrial protein synthesis. Muscle biopsy
demonstrates swollen mitochondria with disrupted cristae and
accumulation of intracellular lipid droplets. The patient’s
weakness is most directly explained by failure of which cellular
process?
A. Oxidative phosphorylation leading to ATP depletion
B. Lysosomal degradation of intracellular proteins
,C. Peroxisomal β-oxidation of long-chain fatty acids
D. Nuclear transcription of structural proteins
E. Ribosomal assembly of cytoskeletal microfilaments
Correct Answer: A
Rationale:
Clinical Clue:
Mitochondrial structural injury with lipid accumulation and
muscle weakness indicates impaired aerobic energy
production.
Mechanism:
Mitochondria generate ATP through oxidative phosphorylation.
Failure of the electron transport chain reduces ATP-dependent
cellular functions.
Why the Correct Answer Is Right:
Skeletal muscle is highly dependent on aerobic metabolism.
ATP depletion impairs actin-myosin cycling and membrane ion
pumps, producing weakness and myocyte dysfunction.
Why the Other Options Are Wrong:
B. Lysosomal dysfunction causes substrate accumulation
disorders rather than primary ATP failure.
C. Peroxisomal metabolism contributes to lipid handling but is
not the primary ATP source in muscle.
D. Nuclear transcription impairment would affect protein
synthesis globally but does not explain mitochondrial swelling.
,E. Ribosomal assembly defects would impair protein production
rather than directly causing energy failure.
Exam Trap (common misconception tested):
Confusing mitochondrial dysfunction with generalized protein
synthesis defects.
High-Yield Clinical Correlation:
Mitochondrial injury commonly affects tissues with high energy
demands such as muscle, myocardium, and neurons.
Q2. A researcher exposes cultured hepatocytes to a toxin that
causes failure of the sodium-potassium ATPase pump. Within
minutes, the cells become swollen with cytoplasmic
vacuolization. Which pathophysiologic change best accounts for
these findings?
A. Increased intracellular calcium causing apoptosis
B. Osmotic influx of water secondary to sodium accumulation
C. Increased extracellular potassium causing membrane rupture
D. Activation of lysosomal hydrolases from Golgi disruption
E. Excessive glucose influx causing glycogen deposition
Correct Answer: B
Rationale:
Clinical Clue:
Rapid cellular swelling after ATPase failure indicates disturbed
osmotic regulation.
, Mechanism:
The sodium-potassium pump maintains electrochemical
gradients. Pump failure leads to intracellular sodium
accumulation, followed by passive water entry.
Why the Correct Answer Is Right:
Loss of membrane ion homeostasis causes hydropic swelling,
an early reversible manifestation of cell injury.
Why the Other Options Are Wrong:
A. Calcium influx contributes to later irreversible injury rather
than immediate swelling.
C. Extracellular potassium elevation is not the primary osmotic
driver.
D. Lysosomal enzyme release occurs in severe irreversible
injury.
E. Glycogen accumulation does not produce acute hydropic
change.
Exam Trap (common misconception tested):
Mistaking early reversible injury for apoptotic or necrotic injury.
High-Yield Clinical Correlation:
Cell swelling is among the earliest morphologic manifestations
of ATP depletion.
Q3. A 6-year-old child has recurrent bacterial infections and
poor wound healing. Genetic testing reveals defective integrin
synthesis. Which cellular function is most directly impaired?
