Premium
PDF
PDF
Download Download
EXAMS
&As|LATEST UPDATE|ALREADY GRADED A+ | Questions & Answers
(Verified Answers) With Rationales ( Update)
This Document Contains:
GRAND CANYON NUR 634 FINAL EXAM 2025 Exam
Questions & Answers (Verified Answers) With Rationales
100% Guaranteed Pass
Complete A+ Guide
GRAND CANYON NUR 634 FINAL EXAM 2025 &As|LATEST
UPDATE|ALREADY GRADED A+ - 2026/2027 Update
Page 1
,Question 1
A patient with a history of chronic obstructive pulmonary disease (COPD) and type 2 diabetes
mellitus presents with acute dyspnea, wheezing, and a productive cough with purulent sputum.
Arterial blood gas (ABG) results show pH 7.31, PaCO2 55 mm Hg, PaO2 60 mm Hg, HCO3- 26
mEq/L. Spirometry reveals FEV1/FVC < 0.70 and FEV1 40% predicted. Which of the following
pathophysiological mechanisms most likely underlies the acute exacerbation?
A) Decreased alveolar ventilation due to diaphragmatic fatigue and increased airway resistance
B) Increased pulmonary capillary permeability leading to noncardiogenic pulmonary edema
C) Mucus hypersecretion and bronchospasm causing ventilation-perfusion mismatch and hypercapnia
D) Right ventricular failure resulting in decreased cardiac output and systemic congestion
Answer: C) Mucus hypersecretion and bronchospasm causing ventilation-perfusion mismatch and
hypercapnia
Explanation: In acute exacerbation of COPD, mucus hypersecretion and bronchospasm worsen V/Q
mismatch, leading to hypercapnia and hypoxemia. Option A describes chronic
respiratory failure but not the acute trigger. Option B is more typical of acute respiratory
distress syndrome. Option D is a late complication (cor pulmonale) but not the
immediate mechanism of exacerbation.
Question 2
A patient with heart failure with reduced ejection fraction (HFrEF) is on a regimen of lisinopril,
carvedilol, furosemide, and spironolactone. The patient develops hyperkalemia (serum K+ 6.2
mEq/L) and acute kidney injury (serum creatinine 3.0 mg/dL from baseline 1.2 mg/dL). Which of
the following medication adjustments is most appropriate while managing the hyperkalemia?
A) Discontinue spironolactone and lisinopril; continue carvedilol and furosemide
B) Discontinue furosemide and lisinopril; continue carvedilol and spironolactone
C) Discontinue carvedilol and spironolactone; continue lisinopril and furosemide
D) Discontinue all four medications and initiate hydralazine and isosorbide dinitrate
Answer: A) Discontinue spironolactone and lisinopril; continue carvedilol and furosemide
Explanation: Hyperkalemia in this setting is likely due to the combination of an ACE inhibitor
(lisinopril) and a potassium-sparing diuretic (spironolactone). Both should be held
temporarily. Carvedilol (beta-blocker) and furosemide (loop diuretic) can be continued.
Option B is incorrect because furosemide helps lower potassium. Option C would
discontinue carvedilol, which is beneficial in HFrEF. Option D is not first-line for acute
management.
Page 2
,Question 3
A patient with a history of recurrent calcium oxalate nephrolithiasis is found to have a 24-hour
urine collection showing low urine volume (<800 mL), hypercalciuria (350 mg/day), hyperoxaluria
(60 mg/day), and hypocitraturia (150 mg/day). Which of the following dietary and pharmacologic
interventions is most likely to reduce stone recurrence?
A) Increase dietary calcium intake and prescribe potassium citrate
B) Restrict dietary calcium and prescribe thiazide diuretics
C) Increase dietary oxalate-rich foods and prescribe allopurinol
D) Restrict dietary sodium and prescribe vitamin B6 supplementation
Answer: A) Increase dietary calcium intake and prescribe potassium citrate
Explanation: Low urine volume and hypocitraturia promote stone formation. Increasing dietary
calcium binds oxalate in the gut, reducing oxalate absorption and urinary oxalate.
Potassium citrate increases urinary citrate, inhibiting stone formation. Option B
(calcium restriction) can paradoxically increase oxalate absorption and stone risk.
Option C (increased oxalate) worsens hyperoxaluria. Option D (vitamin B6) is for
primary hyperoxaluria, not typical.
Question 4
A patient with cirrhosis and ascites develops acute confusion, asterixis, and a flapping tremor.
Laboratory studies show serum ammonia 120 ¼mol/L, normal electrolytes, and elevated liver
enzymes. Which of the following pathophysiological changes is the primary driver of this patient's
neurological symptoms?
A) Impaired urea cycle function leading to accumulation of glutamine in astrocytes and cerebral edema
B) Decreased hepatic clearance of gamma-aminobutyric acid (GABA) resulting in increased
GABAergic tone
C) Portosystemic shunting causing direct entry of benzodiazepine-like compounds into systemic
circulation
D) Increased production of false neurotransmitters such as octopamine that displace dopamine in the
basal ganglia
Answer: A) Impaired urea cycle function leading to accumulation of glutamine in astrocytes and
cerebral edema
Explanation: In hepatic encephalopathy, ammonia is not converted to urea due to liver failure.
Ammonia is metabolized by astrocytes to glutamine, causing osmotic swelling and
cerebral edema. Option B (GABA) is a contributing factor but not primary. Option C
(benzodiazepine-like compounds) is a secondary mechanism. Option D (false
neurotransmitters) is an older theory, not the primary driver.
Page 3
, Question 5
A patient with a history of recurrent venous thromboembolism (VTE) on warfarin therapy is
found to have an INR of 1.8 (therapeutic range 2.0-3.0). The patient is scheduled for elective
surgery in 2 days. Which of the following management strategies is most appropriate?
A) Administer oral vitamin K 2.5 mg and recheck INR the morning of surgery; if INR >1.5, give fresh
frozen plasma
B) Hold warfarin for 2 days and administer low molecular weight heparin (LMWH) bridging therapy
C) Continue warfarin at current dose and proceed with surgery as planned
D) Administer intravenous vitamin K 10 mg and transfuse prothrombin complex concentrate
Answer: B) Hold warfarin for 2 days and administer low molecular weight heparin (LMWH)
bridging therapy
Explanation: For patients with high thrombotic risk (recurrent VTE) undergoing surgery, bridging
with LMWH is recommended when INR is subtherapeutic. Option A (low-dose vitamin
K) is for over-anticoagulation, not for bridging. Option C (continue warfarin) risks
bleeding if INR >1.5 for surgery. Option D (high-dose vitamin K and PCC) is for
life-threatening bleeding, not preoperative preparation.
Question 6
A patient with type 2 diabetes mellitus and stage 3 chronic kidney disease (eGFR 45 mL/min/1.73
m2) is currently on metformin 1000 mg twice daily. The patient develops lactic acidosis after a
bout of gastroenteritis with vomiting and diarrhea. Which of the following mechanisms best
explains the increased risk of lactic acidosis in this scenario?
A) Metformin inhibits gluconeogenesis, leading to accumulation of lactate due to decreased hepatic
clearance
B) Dehydration and acute kidney injury reduce metformin clearance, leading to drug accumulation and
inhibition of mitochondrial complex I
C) Gastroenteritis causes lactic acidosis independently, and metformin has no role in the pathogenesis
D) Metformin increases peripheral glucose uptake, shifting metabolism toward anaerobic glycolysis
and lactate production
Answer: B) Dehydration and acute kidney injury reduce metformin clearance, leading to drug
accumulation and inhibition of mitochondrial complex I
Explanation: Metformin is renally cleared; acute kidney injury from dehydration decreases clearance,
leading to high drug levels. Metformin inhibits mitochondrial complex I, impairing
oxidative phosphorylation and promoting lactate production. Option A is incorrect
because metformin does not decrease hepatic lactate clearance. Option C is false
because metformin is a known risk factor. Option D misrepresents metformin's
mechanism.
Page 4
Download Download
EXAMS
&As|LATEST UPDATE|ALREADY GRADED A+ | Questions & Answers
(Verified Answers) With Rationales ( Update)
This Document Contains:
GRAND CANYON NUR 634 FINAL EXAM 2025 Exam
Questions & Answers (Verified Answers) With Rationales
100% Guaranteed Pass
Complete A+ Guide
GRAND CANYON NUR 634 FINAL EXAM 2025 &As|LATEST
UPDATE|ALREADY GRADED A+ - 2026/2027 Update
Page 1
,Question 1
A patient with a history of chronic obstructive pulmonary disease (COPD) and type 2 diabetes
mellitus presents with acute dyspnea, wheezing, and a productive cough with purulent sputum.
Arterial blood gas (ABG) results show pH 7.31, PaCO2 55 mm Hg, PaO2 60 mm Hg, HCO3- 26
mEq/L. Spirometry reveals FEV1/FVC < 0.70 and FEV1 40% predicted. Which of the following
pathophysiological mechanisms most likely underlies the acute exacerbation?
A) Decreased alveolar ventilation due to diaphragmatic fatigue and increased airway resistance
B) Increased pulmonary capillary permeability leading to noncardiogenic pulmonary edema
C) Mucus hypersecretion and bronchospasm causing ventilation-perfusion mismatch and hypercapnia
D) Right ventricular failure resulting in decreased cardiac output and systemic congestion
Answer: C) Mucus hypersecretion and bronchospasm causing ventilation-perfusion mismatch and
hypercapnia
Explanation: In acute exacerbation of COPD, mucus hypersecretion and bronchospasm worsen V/Q
mismatch, leading to hypercapnia and hypoxemia. Option A describes chronic
respiratory failure but not the acute trigger. Option B is more typical of acute respiratory
distress syndrome. Option D is a late complication (cor pulmonale) but not the
immediate mechanism of exacerbation.
Question 2
A patient with heart failure with reduced ejection fraction (HFrEF) is on a regimen of lisinopril,
carvedilol, furosemide, and spironolactone. The patient develops hyperkalemia (serum K+ 6.2
mEq/L) and acute kidney injury (serum creatinine 3.0 mg/dL from baseline 1.2 mg/dL). Which of
the following medication adjustments is most appropriate while managing the hyperkalemia?
A) Discontinue spironolactone and lisinopril; continue carvedilol and furosemide
B) Discontinue furosemide and lisinopril; continue carvedilol and spironolactone
C) Discontinue carvedilol and spironolactone; continue lisinopril and furosemide
D) Discontinue all four medications and initiate hydralazine and isosorbide dinitrate
Answer: A) Discontinue spironolactone and lisinopril; continue carvedilol and furosemide
Explanation: Hyperkalemia in this setting is likely due to the combination of an ACE inhibitor
(lisinopril) and a potassium-sparing diuretic (spironolactone). Both should be held
temporarily. Carvedilol (beta-blocker) and furosemide (loop diuretic) can be continued.
Option B is incorrect because furosemide helps lower potassium. Option C would
discontinue carvedilol, which is beneficial in HFrEF. Option D is not first-line for acute
management.
Page 2
,Question 3
A patient with a history of recurrent calcium oxalate nephrolithiasis is found to have a 24-hour
urine collection showing low urine volume (<800 mL), hypercalciuria (350 mg/day), hyperoxaluria
(60 mg/day), and hypocitraturia (150 mg/day). Which of the following dietary and pharmacologic
interventions is most likely to reduce stone recurrence?
A) Increase dietary calcium intake and prescribe potassium citrate
B) Restrict dietary calcium and prescribe thiazide diuretics
C) Increase dietary oxalate-rich foods and prescribe allopurinol
D) Restrict dietary sodium and prescribe vitamin B6 supplementation
Answer: A) Increase dietary calcium intake and prescribe potassium citrate
Explanation: Low urine volume and hypocitraturia promote stone formation. Increasing dietary
calcium binds oxalate in the gut, reducing oxalate absorption and urinary oxalate.
Potassium citrate increases urinary citrate, inhibiting stone formation. Option B
(calcium restriction) can paradoxically increase oxalate absorption and stone risk.
Option C (increased oxalate) worsens hyperoxaluria. Option D (vitamin B6) is for
primary hyperoxaluria, not typical.
Question 4
A patient with cirrhosis and ascites develops acute confusion, asterixis, and a flapping tremor.
Laboratory studies show serum ammonia 120 ¼mol/L, normal electrolytes, and elevated liver
enzymes. Which of the following pathophysiological changes is the primary driver of this patient's
neurological symptoms?
A) Impaired urea cycle function leading to accumulation of glutamine in astrocytes and cerebral edema
B) Decreased hepatic clearance of gamma-aminobutyric acid (GABA) resulting in increased
GABAergic tone
C) Portosystemic shunting causing direct entry of benzodiazepine-like compounds into systemic
circulation
D) Increased production of false neurotransmitters such as octopamine that displace dopamine in the
basal ganglia
Answer: A) Impaired urea cycle function leading to accumulation of glutamine in astrocytes and
cerebral edema
Explanation: In hepatic encephalopathy, ammonia is not converted to urea due to liver failure.
Ammonia is metabolized by astrocytes to glutamine, causing osmotic swelling and
cerebral edema. Option B (GABA) is a contributing factor but not primary. Option C
(benzodiazepine-like compounds) is a secondary mechanism. Option D (false
neurotransmitters) is an older theory, not the primary driver.
Page 3
, Question 5
A patient with a history of recurrent venous thromboembolism (VTE) on warfarin therapy is
found to have an INR of 1.8 (therapeutic range 2.0-3.0). The patient is scheduled for elective
surgery in 2 days. Which of the following management strategies is most appropriate?
A) Administer oral vitamin K 2.5 mg and recheck INR the morning of surgery; if INR >1.5, give fresh
frozen plasma
B) Hold warfarin for 2 days and administer low molecular weight heparin (LMWH) bridging therapy
C) Continue warfarin at current dose and proceed with surgery as planned
D) Administer intravenous vitamin K 10 mg and transfuse prothrombin complex concentrate
Answer: B) Hold warfarin for 2 days and administer low molecular weight heparin (LMWH)
bridging therapy
Explanation: For patients with high thrombotic risk (recurrent VTE) undergoing surgery, bridging
with LMWH is recommended when INR is subtherapeutic. Option A (low-dose vitamin
K) is for over-anticoagulation, not for bridging. Option C (continue warfarin) risks
bleeding if INR >1.5 for surgery. Option D (high-dose vitamin K and PCC) is for
life-threatening bleeding, not preoperative preparation.
Question 6
A patient with type 2 diabetes mellitus and stage 3 chronic kidney disease (eGFR 45 mL/min/1.73
m2) is currently on metformin 1000 mg twice daily. The patient develops lactic acidosis after a
bout of gastroenteritis with vomiting and diarrhea. Which of the following mechanisms best
explains the increased risk of lactic acidosis in this scenario?
A) Metformin inhibits gluconeogenesis, leading to accumulation of lactate due to decreased hepatic
clearance
B) Dehydration and acute kidney injury reduce metformin clearance, leading to drug accumulation and
inhibition of mitochondrial complex I
C) Gastroenteritis causes lactic acidosis independently, and metformin has no role in the pathogenesis
D) Metformin increases peripheral glucose uptake, shifting metabolism toward anaerobic glycolysis
and lactate production
Answer: B) Dehydration and acute kidney injury reduce metformin clearance, leading to drug
accumulation and inhibition of mitochondrial complex I
Explanation: Metformin is renally cleared; acute kidney injury from dehydration decreases clearance,
leading to high drug levels. Metformin inhibits mitochondrial complex I, impairing
oxidative phosphorylation and promoting lactate production. Option A is incorrect
because metformin does not decrease hepatic lactate clearance. Option C is false
because metformin is a known risk factor. Option D misrepresents metformin's
mechanism.
Page 4
