NR-507 Week 8 Final Exam
1. A 45-year-old male with a history of chronic alcohol use presents with jaundice, ascites, and
confusion. Laboratory studies show elevated ammonia levels. Which of the following best describes
the primary pathophysiologic mechanism contributing to his confusion?
A. Hepatic conversion of ammonia to urea is impaired due to hepatocellular damage, leading to increased
systemic ammonia that crosses the blood-brain barrier and impairs neurotransmitter function.
B. Increased portosystemic shunting bypasses the liver, allowing dietary protein to enter the systemic circulation
and directly cause cerebral edema.
C. Chronic alcohol exposure causes direct neuronal toxicity and downregulation of GABA receptors, leading to
increased excitotoxicity.
D. Ascites causes increased intra-abdominal pressure, reducing cerebral perfusion pressure and leading to
ischemic encephalopathy.
Answer: A
Rationale: Hepatic encephalopathy primarily results from the liver's failure to detoxify ammonia (and
other toxins) due to hepatocellular dysfunction and portosystemic shunting. Ammonia crosses the
blood-brain barrier, leading to astrocyte swelling and altered neurotransmission. Options B, C, and D
describe secondary or incorrect mechanisms.
2. A researcher is investigating a novel mutation in the CFTR gene that results in a protein that is
trafficked to the cell membrane but exhibits reduced chloride conductance. Which class of CFTR
mutation best describes this finding?
A. Class I (defective protein production)
B. Class II (defective protein processing)
C. Class III (defective regulation/gating)
D. Class IV (defective conductance)
Answer: D
Rationale: Class IV CFTR mutations result in a protein that reaches the cell surface but has reduced
chloride ion flow due to altered pore function. Class I involves no protein synthesis, Class II involves
defective processing and trafficking, and Class III involves impaired ATP-dependent gating.
3. A patient with a history of hypertension and type 2 diabetes presents with sudden onset of severe
chest pain radiating to the back. Blood pressure is 210/120 mm Hg in the right arm and 110/70 mm
Hg in the left arm. Which of the following pathophysiologic processes is most likely responsible?
A. Atherosclerotic plaque rupture in the left anterior descending coronary artery
B. Intimal tear in the ascending aorta with propagation into the aortic arch
C. Embolism from a left atrial myxoma lodging in the brachiocephalic artery
D. Spontaneous coronary artery dissection involving the left main coronary artery
Answer: B
Rationale: The presentation suggests aortic dissection, where an intimal tear allows blood to track within
the media, often extending into branch vessels. The blood pressure difference between arms is classic for
Page 1
,involvement of the aortic arch. Coronary artery disease (A) would not cause such a differential, and
embolic (C) or dissection (D) scenarios are less consistent with the sudden severe back pain and pulse
deficit.
4. In a patient with chronic kidney disease stage 4, which of the following laboratory findings is
most consistent with the development of renal osteodystrophy due to secondary
hyperparathyroidism?
A. Hypercalcemia, hypophosphatemia, elevated 1,25-dihydroxyvitamin D
B. Hypocalcemia, hyperphosphatemia, low 1,25-dihydroxyvitamin D
C. Hypercalcemia, hyperphosphatemia, elevated 25-hydroxyvitamin D
D. Hypocalcemia, hypophosphatemia, low 25-hydroxyvitamin D
Answer: B
Rationale: In CKD, reduced renal mass decreases phosphate excretion and 1-alpha-hydroxylase activity,
leading to hyperphosphatemia, hypocalcemia, and low 1,25-dihydroxyvitamin D. These stimulate PTH
secretion (secondary hyperparathyroidism), which drives bone turnover. Options A, C, and D do not
match the typical pattern of CKD-mineral bone disorder.
5. Which of the following best explains the development of pulmonary edema in a patient with
acute mitral regurgitation following a myocardial infarction?
A. Increased left ventricular end-diastolic pressure due to volume overload from the regurgitant jet
B. Decreased left atrial compliance due to ischemia, causing back pressure into pulmonary veins
C. Rupture of chordae tendineae leading to acute volume overload of the left atrium with rapid transmission of
high pressure to pulmonary circulation
D. Increased pulmonary artery resistance due to reflex vasoconstriction from left atrial stretch
Answer: C
Rationale: Acute mitral regurgitation (e.g., from papillary muscle rupture) causes sudden volume
overload into a normal-sized left atrium, resulting in a rapid rise in left atrial pressure that is directly
transmitted to the pulmonary veins, causing pulmonary edema. Option A describes chronic volume
overload, B is less specific, and D is a secondary effect.
6. A 60-year-old male with a 30-pack-year smoking history presents with weight loss, cough, and a
lung mass on CT. Biopsy shows small cell lung cancer. Which paraneoplastic syndrome is most
commonly associated with this histology?
A. Hypercalcemia due to PTHrP secretion
B. Syndrome of inappropriate antidiuretic hormone (SIADH)
C. Cushing syndrome due to ectopic ACTH
D. Lambert-Eaton myasthenic syndrome (LEMS)
Answer: B
Rationale: SCLC is neuroendocrine in origin and frequently secretes ADH, leading to SIADH
(hyponatremia). While ectopic ACTH (C) and LEMS (D) also occur, SIADH is the most common.
Hypercalcemia (A) is more typical of squamous cell carcinoma. The question asks for 'most commonly
associated,' making SIADH the correct answer.
Page 2
,7. A 55-year-old female with a history of rheumatoid arthritis on chronic prednisone presents with
acute onset of severe mid-epigastric pain radiating to the back. Serum lipase is 1200 U/L. Which of
the following is the most likely contributing pathophysiologic mechanism?
A. Autoantibodies against pancreatic acinar cells leading to autoimmune pancreatitis
B. Hypertriglyceridemia from corticosteroid-induced insulin resistance
C. Increased viscosity of pancreatic secretions due to corticosteroid use
D. Microvascular thrombosis from rheumatoid vasculitis
Answer: B
Rationale: Corticosteroids can induce hypertriglyceridemia, which is a known cause of acute
pancreatitis. While corticosteroids themselves are not directly toxic to the pancreas, the metabolic
effects (insulin resistance, dyslipidemia) increase risk. Autoimmune pancreatitis (A) is less associated
with RA, and options C and D are not well-supported mechanisms.
8. A 70-year-old male with a history of atrial fibrillation not on anticoagulation presents with acute
onset of aphasia and right-sided weakness. MRI shows an ischemic stroke in the left middle
cerebral artery territory. Which of the following best describes the expected histopathologic
changes in the ischemic core 24 hours after onset?
A. Neuronal shrinkage, eosinophilic cytoplasm, and pyknotic nuclei (red neurons)
B. Liquefactive necrosis with macrophage infiltration and cystic spaces
C. Gemistocytic astrocytes and Rosenthal fibers
D. Microglial nodules and neuronophagia
Answer: A
Rationale: Red neurons are characteristic of acute ischemic stroke within 12-24 hours, showing
shrinkage, eosinophilia, and nuclear pyknosis. Liquefactive necrosis (B) occurs after several days to
weeks. Gemistocytic astrocytes (C) are seen in chronic reactive gliosis, and microglial nodules (D) are
typical of viral encephalitis.
9. A 50-year-old female with a history of recurrent urinary tract infections presents with flank pain
and fever. CT shows a 2-cm staghorn calculus in the renal pelvis. Urine culture grows Proteus
mirabilis. Which of the following best describes the pathogenesis of this stone?
A. Increased urinary calcium excretion due to hyperparathyroidism
B. Urease-producing bacteria leading to alkaline urine and struvite stone formation
C. Defect in renal tubular transport of cystine
D. Decreased urinary citrate due to metabolic acidosis
Answer: B
Rationale: Proteus mirabilis produces urease, which hydrolyzes urea to ammonia, increasing urinary pH
and promoting precipitation of magnesium ammonium phosphate (struvite) stones. Staghorn calculi are
classic for infection-related stones. Option A describes calcium stones, C describes cystine stones, and D
describes calcium oxalate stones.
Page 3
, 10. A 65-year-old male with a history of hypertension and hyperlipidemia presents with an acute
anterior ST-elevation myocardial infarction. Which of the following best explains the underlying
mechanism of plaque rupture in his coronary artery?
A. Erosion of the endothelial layer due to high shear stress, exposing the basement membrane
B. Rupture of a thin fibrous cap over a large lipid core with macrophage infiltration
C. Intraplaque hemorrhage from vasa vasorum rupture
D. Calcific nodule protruding into the lumen causing turbulent flow
Answer: B
Rationale: The most common mechanism for acute coronary syndrome is rupture of a thin-cap
fibroatheroma, where a large lipid core and inflammatory cells (macrophages) weaken the fibrous cap.
Erosion (A) is more common in younger patients and smokers, intraplaque hemorrhage (C) can
contribute but is not the primary mechanism, and calcific nodules (D) are less frequent.
11. In the context of chronic kidney disease-mineral and bone disorder (CKD-MBD), which of the
following pathophysiological mechanisms best explains the development of vascular calcification in
patients with advanced CKD?
A. Increased fibroblast growth factor 23 (FGF23) leading to reduced renal phosphate excretion
B. Decreased klotho expression causing endothelial dysfunction and accelerated atherosclerosis
C. Elevated calcium-phosphate product promoting transformation of vascular smooth muscle cells to
osteoblast-like cells
D. Secondary hyperparathyroidism with excessive bone resorption releasing calcium into the bloodstream
Answer: C
Rationale: Vascular calcification in CKD-MBD is primarily driven by an elevated calcium-phosphate
product, which induces phenotypic transformation of vascular smooth muscle cells into osteoblast-like
cells that deposit bone matrix. While FGF23 and klotho are involved, the direct mechanism is the
transformation due to supersaturation. Secondary hyperparathyroidism contributes but is not the direct
cause of vascular calcification.
12. A patient with decompensated heart failure is started on intravenous nitroprusside. Which of
the following best describes the mechanism by which nitroprusside reduces preload and afterload?
A. Direct activation of guanylyl cyclase in vascular smooth muscle, increasing cGMP
B. Inhibition of phosphodiesterase-5, preventing cGMP breakdown
C. Blockade of calcium channels in vascular smooth muscle, reducing intracellular calcium
D. Release of nitric oxide that activates soluble guanylyl cyclase, increasing cGMP
Answer: D
Rationale: Nitroprusside is a nitric oxide donor; nitric oxide activates soluble guanylyl cyclase in
vascular smooth muscle, increasing cGMP and causing vasodilation. Direct activation (A) is inaccurate;
it is mediated by NO. PDE-5 inhibition (B) is the mechanism of sildenafil. Calcium channel blockade (C)
is not the primary action of nitroprusside.
Page 4
1. A 45-year-old male with a history of chronic alcohol use presents with jaundice, ascites, and
confusion. Laboratory studies show elevated ammonia levels. Which of the following best describes
the primary pathophysiologic mechanism contributing to his confusion?
A. Hepatic conversion of ammonia to urea is impaired due to hepatocellular damage, leading to increased
systemic ammonia that crosses the blood-brain barrier and impairs neurotransmitter function.
B. Increased portosystemic shunting bypasses the liver, allowing dietary protein to enter the systemic circulation
and directly cause cerebral edema.
C. Chronic alcohol exposure causes direct neuronal toxicity and downregulation of GABA receptors, leading to
increased excitotoxicity.
D. Ascites causes increased intra-abdominal pressure, reducing cerebral perfusion pressure and leading to
ischemic encephalopathy.
Answer: A
Rationale: Hepatic encephalopathy primarily results from the liver's failure to detoxify ammonia (and
other toxins) due to hepatocellular dysfunction and portosystemic shunting. Ammonia crosses the
blood-brain barrier, leading to astrocyte swelling and altered neurotransmission. Options B, C, and D
describe secondary or incorrect mechanisms.
2. A researcher is investigating a novel mutation in the CFTR gene that results in a protein that is
trafficked to the cell membrane but exhibits reduced chloride conductance. Which class of CFTR
mutation best describes this finding?
A. Class I (defective protein production)
B. Class II (defective protein processing)
C. Class III (defective regulation/gating)
D. Class IV (defective conductance)
Answer: D
Rationale: Class IV CFTR mutations result in a protein that reaches the cell surface but has reduced
chloride ion flow due to altered pore function. Class I involves no protein synthesis, Class II involves
defective processing and trafficking, and Class III involves impaired ATP-dependent gating.
3. A patient with a history of hypertension and type 2 diabetes presents with sudden onset of severe
chest pain radiating to the back. Blood pressure is 210/120 mm Hg in the right arm and 110/70 mm
Hg in the left arm. Which of the following pathophysiologic processes is most likely responsible?
A. Atherosclerotic plaque rupture in the left anterior descending coronary artery
B. Intimal tear in the ascending aorta with propagation into the aortic arch
C. Embolism from a left atrial myxoma lodging in the brachiocephalic artery
D. Spontaneous coronary artery dissection involving the left main coronary artery
Answer: B
Rationale: The presentation suggests aortic dissection, where an intimal tear allows blood to track within
the media, often extending into branch vessels. The blood pressure difference between arms is classic for
Page 1
,involvement of the aortic arch. Coronary artery disease (A) would not cause such a differential, and
embolic (C) or dissection (D) scenarios are less consistent with the sudden severe back pain and pulse
deficit.
4. In a patient with chronic kidney disease stage 4, which of the following laboratory findings is
most consistent with the development of renal osteodystrophy due to secondary
hyperparathyroidism?
A. Hypercalcemia, hypophosphatemia, elevated 1,25-dihydroxyvitamin D
B. Hypocalcemia, hyperphosphatemia, low 1,25-dihydroxyvitamin D
C. Hypercalcemia, hyperphosphatemia, elevated 25-hydroxyvitamin D
D. Hypocalcemia, hypophosphatemia, low 25-hydroxyvitamin D
Answer: B
Rationale: In CKD, reduced renal mass decreases phosphate excretion and 1-alpha-hydroxylase activity,
leading to hyperphosphatemia, hypocalcemia, and low 1,25-dihydroxyvitamin D. These stimulate PTH
secretion (secondary hyperparathyroidism), which drives bone turnover. Options A, C, and D do not
match the typical pattern of CKD-mineral bone disorder.
5. Which of the following best explains the development of pulmonary edema in a patient with
acute mitral regurgitation following a myocardial infarction?
A. Increased left ventricular end-diastolic pressure due to volume overload from the regurgitant jet
B. Decreased left atrial compliance due to ischemia, causing back pressure into pulmonary veins
C. Rupture of chordae tendineae leading to acute volume overload of the left atrium with rapid transmission of
high pressure to pulmonary circulation
D. Increased pulmonary artery resistance due to reflex vasoconstriction from left atrial stretch
Answer: C
Rationale: Acute mitral regurgitation (e.g., from papillary muscle rupture) causes sudden volume
overload into a normal-sized left atrium, resulting in a rapid rise in left atrial pressure that is directly
transmitted to the pulmonary veins, causing pulmonary edema. Option A describes chronic volume
overload, B is less specific, and D is a secondary effect.
6. A 60-year-old male with a 30-pack-year smoking history presents with weight loss, cough, and a
lung mass on CT. Biopsy shows small cell lung cancer. Which paraneoplastic syndrome is most
commonly associated with this histology?
A. Hypercalcemia due to PTHrP secretion
B. Syndrome of inappropriate antidiuretic hormone (SIADH)
C. Cushing syndrome due to ectopic ACTH
D. Lambert-Eaton myasthenic syndrome (LEMS)
Answer: B
Rationale: SCLC is neuroendocrine in origin and frequently secretes ADH, leading to SIADH
(hyponatremia). While ectopic ACTH (C) and LEMS (D) also occur, SIADH is the most common.
Hypercalcemia (A) is more typical of squamous cell carcinoma. The question asks for 'most commonly
associated,' making SIADH the correct answer.
Page 2
,7. A 55-year-old female with a history of rheumatoid arthritis on chronic prednisone presents with
acute onset of severe mid-epigastric pain radiating to the back. Serum lipase is 1200 U/L. Which of
the following is the most likely contributing pathophysiologic mechanism?
A. Autoantibodies against pancreatic acinar cells leading to autoimmune pancreatitis
B. Hypertriglyceridemia from corticosteroid-induced insulin resistance
C. Increased viscosity of pancreatic secretions due to corticosteroid use
D. Microvascular thrombosis from rheumatoid vasculitis
Answer: B
Rationale: Corticosteroids can induce hypertriglyceridemia, which is a known cause of acute
pancreatitis. While corticosteroids themselves are not directly toxic to the pancreas, the metabolic
effects (insulin resistance, dyslipidemia) increase risk. Autoimmune pancreatitis (A) is less associated
with RA, and options C and D are not well-supported mechanisms.
8. A 70-year-old male with a history of atrial fibrillation not on anticoagulation presents with acute
onset of aphasia and right-sided weakness. MRI shows an ischemic stroke in the left middle
cerebral artery territory. Which of the following best describes the expected histopathologic
changes in the ischemic core 24 hours after onset?
A. Neuronal shrinkage, eosinophilic cytoplasm, and pyknotic nuclei (red neurons)
B. Liquefactive necrosis with macrophage infiltration and cystic spaces
C. Gemistocytic astrocytes and Rosenthal fibers
D. Microglial nodules and neuronophagia
Answer: A
Rationale: Red neurons are characteristic of acute ischemic stroke within 12-24 hours, showing
shrinkage, eosinophilia, and nuclear pyknosis. Liquefactive necrosis (B) occurs after several days to
weeks. Gemistocytic astrocytes (C) are seen in chronic reactive gliosis, and microglial nodules (D) are
typical of viral encephalitis.
9. A 50-year-old female with a history of recurrent urinary tract infections presents with flank pain
and fever. CT shows a 2-cm staghorn calculus in the renal pelvis. Urine culture grows Proteus
mirabilis. Which of the following best describes the pathogenesis of this stone?
A. Increased urinary calcium excretion due to hyperparathyroidism
B. Urease-producing bacteria leading to alkaline urine and struvite stone formation
C. Defect in renal tubular transport of cystine
D. Decreased urinary citrate due to metabolic acidosis
Answer: B
Rationale: Proteus mirabilis produces urease, which hydrolyzes urea to ammonia, increasing urinary pH
and promoting precipitation of magnesium ammonium phosphate (struvite) stones. Staghorn calculi are
classic for infection-related stones. Option A describes calcium stones, C describes cystine stones, and D
describes calcium oxalate stones.
Page 3
, 10. A 65-year-old male with a history of hypertension and hyperlipidemia presents with an acute
anterior ST-elevation myocardial infarction. Which of the following best explains the underlying
mechanism of plaque rupture in his coronary artery?
A. Erosion of the endothelial layer due to high shear stress, exposing the basement membrane
B. Rupture of a thin fibrous cap over a large lipid core with macrophage infiltration
C. Intraplaque hemorrhage from vasa vasorum rupture
D. Calcific nodule protruding into the lumen causing turbulent flow
Answer: B
Rationale: The most common mechanism for acute coronary syndrome is rupture of a thin-cap
fibroatheroma, where a large lipid core and inflammatory cells (macrophages) weaken the fibrous cap.
Erosion (A) is more common in younger patients and smokers, intraplaque hemorrhage (C) can
contribute but is not the primary mechanism, and calcific nodules (D) are less frequent.
11. In the context of chronic kidney disease-mineral and bone disorder (CKD-MBD), which of the
following pathophysiological mechanisms best explains the development of vascular calcification in
patients with advanced CKD?
A. Increased fibroblast growth factor 23 (FGF23) leading to reduced renal phosphate excretion
B. Decreased klotho expression causing endothelial dysfunction and accelerated atherosclerosis
C. Elevated calcium-phosphate product promoting transformation of vascular smooth muscle cells to
osteoblast-like cells
D. Secondary hyperparathyroidism with excessive bone resorption releasing calcium into the bloodstream
Answer: C
Rationale: Vascular calcification in CKD-MBD is primarily driven by an elevated calcium-phosphate
product, which induces phenotypic transformation of vascular smooth muscle cells into osteoblast-like
cells that deposit bone matrix. While FGF23 and klotho are involved, the direct mechanism is the
transformation due to supersaturation. Secondary hyperparathyroidism contributes but is not the direct
cause of vascular calcification.
12. A patient with decompensated heart failure is started on intravenous nitroprusside. Which of
the following best describes the mechanism by which nitroprusside reduces preload and afterload?
A. Direct activation of guanylyl cyclase in vascular smooth muscle, increasing cGMP
B. Inhibition of phosphodiesterase-5, preventing cGMP breakdown
C. Blockade of calcium channels in vascular smooth muscle, reducing intracellular calcium
D. Release of nitric oxide that activates soluble guanylyl cyclase, increasing cGMP
Answer: D
Rationale: Nitroprusside is a nitric oxide donor; nitric oxide activates soluble guanylyl cyclase in
vascular smooth muscle, increasing cGMP and causing vasodilation. Direct activation (A) is inaccurate;
it is mediated by NO. PDE-5 inhibition (B) is the mechanism of sildenafil. Calcium channel blockade (C)
is not the primary action of nitroprusside.
Page 4
