NR 507 / NR507 Advanced Pathophysiology Midterm Exam | ACTUAL
EXAM | Questions & Verified Answers | Latest Update –
Chamberlain University
1.
A 45-year-old male presents with muscle cramps and weakness. Laboratory results reveal a
serum sodium of 128 mEq/L, potassium of 3.2 mEq/L, and calcium of 7.5 mg/dL. Which
pathophysiological mechanism best explains the hypokalemia-induced muscle dysfunction?
A. Decreased resting membrane potential leading to hyperpolarization and reduced excitability
B. Increased sodium–calcium exchanger activity causing intracellular calcium overload
C. Inhibition of Na⁺/K⁺-ATPase leading to membrane depolarization and sustained contraction
D. Reduced insulin-mediated glucose uptake into skeletal muscle
Correct Answer: C. Inhibition of Na⁺/K⁺-ATPase leading to membrane depolarization and
sustained contraction
Rationale: Hypokalemia decreases the activity of Na⁺/K⁺-ATPase, reducing potassium influx and
causing relative sodium influx; the ensuing depolarization inactivates voltage-gated sodium
channels and produces flaccid paralysis. Option A incorrectly suggests
hyperpolarization—hypokalemia initially hyperpolarizes but ultimately depolarizes when
extreme. Option B describes a mechanism seen in digitalis toxicity, not simple hypokalemia.
Option D is unrelated to hypokalemic myopathy.
, 2.
Which cellular adaptation is most characteristic of myocardial cells subjected to chronic pressure
overload?
A. Atrophy
B. Hyperplasia
C. Hypertrophy
D. Metaplasia
Correct Answer: C. Hypertrophy
Rationale: Pressure overload (e.g., systemic hypertension, aortic stenosis) increases ventricular
wall tension; terminally differentiated cardiomyocytes respond by enlarging (hypertrophy) to
reduce wall stress via the Laplace law. Atrophy (A) denotes decrease in cell size, not a response
to overload. Hyperplasia (B) is largely absent in adult human myocardium. Metaplasia (D) is a
change in cell type and does not occur in this context.
3.
A 6-year-old boy with cystic fibrosis has recurrent Pseudomonas aeruginosa pulmonary
infections. Which pathophysiological defect underlies his susceptibility?
A. Absent ciliary dynein arms preventing mucociliary clearance
,B. Decreased chloride secretion and increased sodium absorption producing thick, viscous
mucus
C. Defective neutrophil NADPH oxidase
D. Insufficient surfactant production
Correct Answer: B. Decreased chloride secretion and increased sodium absorption producing
thick, viscous mucus
Rationale: CFTR dysfunction in cystic fibrosis causes defective chloride secretion and excessive
epithelial sodium reabsorption, dehydrating airway surface liquid; resultant mucus stasis
obstructs airways and impairs bacterial clearance. Option A describes primary ciliary dyskinesia.
Option C describes chronic granulomatous disease. Option D is characteristic of neonatal
respiratory distress syndrome.
4.
A patient with diabetic ketoacidosis presents with Kussmaul respirations. Which acid–base
compensatory response is responsible for this clinical sign?
A. Renal generation of bicarbonate
B. Hyperventilation to reduce PaCO₂ and raise pH
C. Hypoventilation to retain CO₂
D. Intracellular buffering via phosphate ions
, Correct Answer: B. Hyperventilation to reduce PaCO₂ and raise pH
Rationale: Kussmaul respirations represent respiratory compensation for metabolic
acidosis—central chemoreceptors sense ↓pH and stimulate hyperventilation to blow off CO₂,
lowering carbonic acid and raising pH. Renal bicarbonate generation (A) takes hours to days.
Hypoventilation (C) would worsen acidosis. Intracellular buffering (D) occurs but does not
produce Kussmaul respirations.
5.
Which epigenetic modification most directly leads to transcriptional silencing of a
tumor-suppressor gene?
A. Histone H3 acetylation
B. CpG island demethylation
C. Histone deacetylation and CpG island methylation
D. Histone phosphorylation at serine 10
Correct Answer: C. Histone deacetylation and CpG island methylation
Rationale: DNA methyltransferases add methyl groups to CpG dinucleotides;
methyl-CpG-binding proteins recruit histone deacetylases, removing acetyl groups and
tightening chromatin, thereby blocking transcription. Acetylation (A) and demethylation (B)
generally activate transcription. Histone phosphorylation (D) is linked to DNA damage
signaling, not silencing.
EXAM | Questions & Verified Answers | Latest Update –
Chamberlain University
1.
A 45-year-old male presents with muscle cramps and weakness. Laboratory results reveal a
serum sodium of 128 mEq/L, potassium of 3.2 mEq/L, and calcium of 7.5 mg/dL. Which
pathophysiological mechanism best explains the hypokalemia-induced muscle dysfunction?
A. Decreased resting membrane potential leading to hyperpolarization and reduced excitability
B. Increased sodium–calcium exchanger activity causing intracellular calcium overload
C. Inhibition of Na⁺/K⁺-ATPase leading to membrane depolarization and sustained contraction
D. Reduced insulin-mediated glucose uptake into skeletal muscle
Correct Answer: C. Inhibition of Na⁺/K⁺-ATPase leading to membrane depolarization and
sustained contraction
Rationale: Hypokalemia decreases the activity of Na⁺/K⁺-ATPase, reducing potassium influx and
causing relative sodium influx; the ensuing depolarization inactivates voltage-gated sodium
channels and produces flaccid paralysis. Option A incorrectly suggests
hyperpolarization—hypokalemia initially hyperpolarizes but ultimately depolarizes when
extreme. Option B describes a mechanism seen in digitalis toxicity, not simple hypokalemia.
Option D is unrelated to hypokalemic myopathy.
, 2.
Which cellular adaptation is most characteristic of myocardial cells subjected to chronic pressure
overload?
A. Atrophy
B. Hyperplasia
C. Hypertrophy
D. Metaplasia
Correct Answer: C. Hypertrophy
Rationale: Pressure overload (e.g., systemic hypertension, aortic stenosis) increases ventricular
wall tension; terminally differentiated cardiomyocytes respond by enlarging (hypertrophy) to
reduce wall stress via the Laplace law. Atrophy (A) denotes decrease in cell size, not a response
to overload. Hyperplasia (B) is largely absent in adult human myocardium. Metaplasia (D) is a
change in cell type and does not occur in this context.
3.
A 6-year-old boy with cystic fibrosis has recurrent Pseudomonas aeruginosa pulmonary
infections. Which pathophysiological defect underlies his susceptibility?
A. Absent ciliary dynein arms preventing mucociliary clearance
,B. Decreased chloride secretion and increased sodium absorption producing thick, viscous
mucus
C. Defective neutrophil NADPH oxidase
D. Insufficient surfactant production
Correct Answer: B. Decreased chloride secretion and increased sodium absorption producing
thick, viscous mucus
Rationale: CFTR dysfunction in cystic fibrosis causes defective chloride secretion and excessive
epithelial sodium reabsorption, dehydrating airway surface liquid; resultant mucus stasis
obstructs airways and impairs bacterial clearance. Option A describes primary ciliary dyskinesia.
Option C describes chronic granulomatous disease. Option D is characteristic of neonatal
respiratory distress syndrome.
4.
A patient with diabetic ketoacidosis presents with Kussmaul respirations. Which acid–base
compensatory response is responsible for this clinical sign?
A. Renal generation of bicarbonate
B. Hyperventilation to reduce PaCO₂ and raise pH
C. Hypoventilation to retain CO₂
D. Intracellular buffering via phosphate ions
, Correct Answer: B. Hyperventilation to reduce PaCO₂ and raise pH
Rationale: Kussmaul respirations represent respiratory compensation for metabolic
acidosis—central chemoreceptors sense ↓pH and stimulate hyperventilation to blow off CO₂,
lowering carbonic acid and raising pH. Renal bicarbonate generation (A) takes hours to days.
Hypoventilation (C) would worsen acidosis. Intracellular buffering (D) occurs but does not
produce Kussmaul respirations.
5.
Which epigenetic modification most directly leads to transcriptional silencing of a
tumor-suppressor gene?
A. Histone H3 acetylation
B. CpG island demethylation
C. Histone deacetylation and CpG island methylation
D. Histone phosphorylation at serine 10
Correct Answer: C. Histone deacetylation and CpG island methylation
Rationale: DNA methyltransferases add methyl groups to CpG dinucleotides;
methyl-CpG-binding proteins recruit histone deacetylases, removing acetyl groups and
tightening chromatin, thereby blocking transcription. Acetylation (A) and demethylation (B)
generally activate transcription. Histone phosphorylation (D) is linked to DNA damage
signaling, not silencing.
