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Grand Canyon University NUR 631
NUR631 Actual Exam Questions and
Answers with Rationales 2026/2027 |
Advanced Physiology & Pathophysiology
Midterm | Pass Guarantee
Q001: A 28-year-old male presents with persistent fatigue and is found to have a
missense mutation in the β-globin gene leading to HbS. Which intracellular change
initiates the polymerisation of deoxy-HbS and subsequent red-cell sickling?
Options:
A. Decreased 2,3-BPG causing left-shift of O₂-dissociation curve
B. Increased intracellular Ca²⁺ activating scramblase
C. Deoxygenation exposing hydrophobic valine in β₆ position allowing β-sheet
polymerisation - CORRECT
D. Oxidation of spectrin causing membrane loss
ANSWER: C
Q002: A child with cystic fibrosis has a 3-bp deletion (ΔF508) in CFTR. Which
pathophysiologic consequence of misfolded-CFTR dominates early respiratory
disease?
Options:
A. Decreased ciliary beat frequency due to lack of ATP
B. Reduced airway-surface liquid depth and impaired mucociliary clearance -
CORRECT
C. Over-expression of ENaC leading to chloride secretion
D. Excessive mucin glycosylation causing plug formation
ANSWER: B
, 2
Q003: In Duchenne muscular dystrophy, loss of dystrophin leads to which
sequence of membrane events?
Options:
A. ↑Ca²⁺ influx → calpain activation → sarcomere protein degradation -
CORRECT
B. ↑Na⁺ influx → cell swelling → lysis
C. ↓K⁺ efflux → hyper-polarisation → apoptosis
D. ↑Cl⁻ efflux → depolarisation → contracture
ANSWER: A
Q004: A tumour suppressor gene undergoes two-hit Knudson-type inactivation.
Which intracellular signalling cascade is most commonly lost when p53 function is
abolished?
Options:
A. PI3K-Akt-mTOR pathway
B. G₁-S checkpoint via p21 transcription - CORRECT
C. MAPK-Erk proliferation signal
D. Wnt-β-catenin degradation complex
ANSWER: B
Q005: A 45-year-old female with BRCA1 mutation develops triple-negative breast
cancer. Which DNA-repair mechanism is primarily defective in her tumour cells?
Options:
A. Base-excision repair
B. Nucleotide-excision repair
C. Homologous recombination - CORRECT
D. Mismatch repair
ANSWER: C
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Q006: Chronic myeloid leukaemia cells express BCR-ABL fusion protein. Which
pathophysiologic change explains the anti-apoptotic effect?
Options:
A. Decreased Jak-STAT signalling
B. Constitutive phosphorylation of Crkl → activation of Ras → Bcl-xL up-
regulation - CORRECT
C. Inhibition of NF-κB transcription
D. Dephosphorylation of BAD
ANSWER: B
Q007: A patient with hereditary spherocytosis has a defect in ankyrin. Which
membrane abnormality produces haemolysis?
Options:
A. Increased membrane fluidity causing vesiculation
B. Loss of vertical protein interactions → lipid bilayer uncoupling → spherocyte
formation - CORRECT
C. Increased horizontal interactions → elliptocyte formation
D. Defective band-3 clustering → acanthocyte formation
ANSWER: B
Q008: In familial hypercholesterolaemia, defective LDL-receptors lead to which
endothelial dysfunction?
Options:
A. ↓NO synthesis due to lack of substrate arginine
B. ↑Oxidised LDL → ↓eNOS phosphorylation → ↓NO bioavailability -
CORRECT
C. ↓Endothelin-1 clearance → vasodilatation
D. ↑Prostacyclin synthesis → platelet aggregation
Grand Canyon University NUR 631
NUR631 Actual Exam Questions and
Answers with Rationales 2026/2027 |
Advanced Physiology & Pathophysiology
Midterm | Pass Guarantee
Q001: A 28-year-old male presents with persistent fatigue and is found to have a
missense mutation in the β-globin gene leading to HbS. Which intracellular change
initiates the polymerisation of deoxy-HbS and subsequent red-cell sickling?
Options:
A. Decreased 2,3-BPG causing left-shift of O₂-dissociation curve
B. Increased intracellular Ca²⁺ activating scramblase
C. Deoxygenation exposing hydrophobic valine in β₆ position allowing β-sheet
polymerisation - CORRECT
D. Oxidation of spectrin causing membrane loss
ANSWER: C
Q002: A child with cystic fibrosis has a 3-bp deletion (ΔF508) in CFTR. Which
pathophysiologic consequence of misfolded-CFTR dominates early respiratory
disease?
Options:
A. Decreased ciliary beat frequency due to lack of ATP
B. Reduced airway-surface liquid depth and impaired mucociliary clearance -
CORRECT
C. Over-expression of ENaC leading to chloride secretion
D. Excessive mucin glycosylation causing plug formation
ANSWER: B
, 2
Q003: In Duchenne muscular dystrophy, loss of dystrophin leads to which
sequence of membrane events?
Options:
A. ↑Ca²⁺ influx → calpain activation → sarcomere protein degradation -
CORRECT
B. ↑Na⁺ influx → cell swelling → lysis
C. ↓K⁺ efflux → hyper-polarisation → apoptosis
D. ↑Cl⁻ efflux → depolarisation → contracture
ANSWER: A
Q004: A tumour suppressor gene undergoes two-hit Knudson-type inactivation.
Which intracellular signalling cascade is most commonly lost when p53 function is
abolished?
Options:
A. PI3K-Akt-mTOR pathway
B. G₁-S checkpoint via p21 transcription - CORRECT
C. MAPK-Erk proliferation signal
D. Wnt-β-catenin degradation complex
ANSWER: B
Q005: A 45-year-old female with BRCA1 mutation develops triple-negative breast
cancer. Which DNA-repair mechanism is primarily defective in her tumour cells?
Options:
A. Base-excision repair
B. Nucleotide-excision repair
C. Homologous recombination - CORRECT
D. Mismatch repair
ANSWER: C
, 3
Q006: Chronic myeloid leukaemia cells express BCR-ABL fusion protein. Which
pathophysiologic change explains the anti-apoptotic effect?
Options:
A. Decreased Jak-STAT signalling
B. Constitutive phosphorylation of Crkl → activation of Ras → Bcl-xL up-
regulation - CORRECT
C. Inhibition of NF-κB transcription
D. Dephosphorylation of BAD
ANSWER: B
Q007: A patient with hereditary spherocytosis has a defect in ankyrin. Which
membrane abnormality produces haemolysis?
Options:
A. Increased membrane fluidity causing vesiculation
B. Loss of vertical protein interactions → lipid bilayer uncoupling → spherocyte
formation - CORRECT
C. Increased horizontal interactions → elliptocyte formation
D. Defective band-3 clustering → acanthocyte formation
ANSWER: B
Q008: In familial hypercholesterolaemia, defective LDL-receptors lead to which
endothelial dysfunction?
Options:
A. ↓NO synthesis due to lack of substrate arginine
B. ↑Oxidised LDL → ↓eNOS phosphorylation → ↓NO bioavailability -
CORRECT
C. ↓Endothelin-1 clearance → vasodilatation
D. ↑Prostacyclin synthesis → platelet aggregation
