, NURS 5315: ADVANCED PATHOPHYSIOLOGY
Comprehensive Graduate Examination & Clinical Decision-Making Key
50 Multiple-Choice Questions with Comprehensive Evidence-Based Rationales
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, PART I: EXAMINATION QUESTIONS
1. A 58-year-old male with a history of severe peripheral vascular disease undergoes muscle biopsy of the
gastrocnemius. The pathology report indicates significant atrophy of skeletal muscle fibers. Which cellular
mechanism is primarily responsible for this adaptive response?
A. Hypertrophy secondary to mechanical stretch and increased protein synthesis
B. Activation of the ubiquitin-proteasome pathway and increased autophagy
C. Dysplasia resulting from altered transcription factor expression
D. Apoptosis induced by mitochondrial cytochrome c release
2. During hypoxia-reperfusion injury, cellular damage is paradoxically exacerbated following the restoration
of blood supply. Which intracellular event is pivotal in driving this secondary ischemic injury phase?
A. Rapid restoration of intracellular potassium and decreased cytosolic sodium
B. Generation of reactive oxygen species (ROS) and opening of the mitochondrial permeability transition pore
(MPTP)
C. Inhibition of xanthine oxidase and depletion of neutrophil chemokines
D. Upregulation of anti-apoptotic Bcl-2 proteins in response to oxygen
3. A 4-year-old child presents with frequent lung infections and pancreatic exocrine insufficiency. Genetic
testing confirms Cystic Fibrosis with a homozygous delta-F508 mutation. How does this specific mutation
affect the CFTR protein functionally at the cellular level?
A. It causes misfolding of CFTR, leading to endoplasmic reticulum retention and degradation prior to reaching
the cell membrane.
B. It creates a premature stop codon resulting in complete absence of mRNA transcription.
C. It allows full expression on the plasma membrane but completely blocks ATP binding to the nucleotide-
binding domain.
D. It enhances CFTR degradation specifically at the basolateral membrane via hyperphosphorylation.
4. Irreversible cell injury differs fundamentally from reversible cell injury. Which ultrastructural change
serves as a definitive marker that cell death has become inevitable?
A. Cellular swelling and bleb formation on the plasma membrane
B. Severe swelling of mitochondria with amorphous dense bodies and rupture of lysosomes
C. Ribosomal detachment from the rough endoplasmic reticulum
D. Dilatation of the Golgi apparatus with lipid accumulation
5. A 42-year-old female undergoes a cervical biopsy that displays dysplasia (cervical intraepithelial neoplasia
- CIN II). Which statement best characterizes dysplasia in contrast to neoplasia?
A. Dysplasia represents an irreversible malignant conversion of stem cells.
B. Dysplasia involves disordered cell growth with loss of architectural orientation, but it remains potentially
reversible if the inciting stimulus is removed.
C. Dysplasia is characterized exclusively by cellular enlargement without alterations in nuclear-to-cytoplasmic
ratio.
D. Dysplasia reflects compensatory proliferation resulting from tissue ischemia.
Comprehensive Graduate Examination & Clinical Decision-Making Key
50 Multiple-Choice Questions with Comprehensive Evidence-Based Rationales
―――――――――――――――――――――――――――――――――――――――――――――――――
――――――
, PART I: EXAMINATION QUESTIONS
1. A 58-year-old male with a history of severe peripheral vascular disease undergoes muscle biopsy of the
gastrocnemius. The pathology report indicates significant atrophy of skeletal muscle fibers. Which cellular
mechanism is primarily responsible for this adaptive response?
A. Hypertrophy secondary to mechanical stretch and increased protein synthesis
B. Activation of the ubiquitin-proteasome pathway and increased autophagy
C. Dysplasia resulting from altered transcription factor expression
D. Apoptosis induced by mitochondrial cytochrome c release
2. During hypoxia-reperfusion injury, cellular damage is paradoxically exacerbated following the restoration
of blood supply. Which intracellular event is pivotal in driving this secondary ischemic injury phase?
A. Rapid restoration of intracellular potassium and decreased cytosolic sodium
B. Generation of reactive oxygen species (ROS) and opening of the mitochondrial permeability transition pore
(MPTP)
C. Inhibition of xanthine oxidase and depletion of neutrophil chemokines
D. Upregulation of anti-apoptotic Bcl-2 proteins in response to oxygen
3. A 4-year-old child presents with frequent lung infections and pancreatic exocrine insufficiency. Genetic
testing confirms Cystic Fibrosis with a homozygous delta-F508 mutation. How does this specific mutation
affect the CFTR protein functionally at the cellular level?
A. It causes misfolding of CFTR, leading to endoplasmic reticulum retention and degradation prior to reaching
the cell membrane.
B. It creates a premature stop codon resulting in complete absence of mRNA transcription.
C. It allows full expression on the plasma membrane but completely blocks ATP binding to the nucleotide-
binding domain.
D. It enhances CFTR degradation specifically at the basolateral membrane via hyperphosphorylation.
4. Irreversible cell injury differs fundamentally from reversible cell injury. Which ultrastructural change
serves as a definitive marker that cell death has become inevitable?
A. Cellular swelling and bleb formation on the plasma membrane
B. Severe swelling of mitochondria with amorphous dense bodies and rupture of lysosomes
C. Ribosomal detachment from the rough endoplasmic reticulum
D. Dilatation of the Golgi apparatus with lipid accumulation
5. A 42-year-old female undergoes a cervical biopsy that displays dysplasia (cervical intraepithelial neoplasia
- CIN II). Which statement best characterizes dysplasia in contrast to neoplasia?
A. Dysplasia represents an irreversible malignant conversion of stem cells.
B. Dysplasia involves disordered cell growth with loss of architectural orientation, but it remains potentially
reversible if the inciting stimulus is removed.
C. Dysplasia is characterized exclusively by cellular enlargement without alterations in nuclear-to-cytoplasmic
ratio.
D. Dysplasia reflects compensatory proliferation resulting from tissue ischemia.
