NR 565 FINAL EXAM REVIEW | WEEKS 5-8 | COMPLETE
Q&A GUIDE | 2026-2027 - 100 Questions and Answers Already
Graded A+ Premium Exam Tested And Verified
Subject Area Advanced Pharmacology
Description This exam covers advanced pharmacotherapeutic concepts from weeks 5-8 of NR
565, including cardiovascular, endocrine, respiratory, and gastrointestinal
pharmacotherapy, with emphasis on evidence-based prescribing, monitoring, and
patient education. It is designed to assess clinical decision-making and application
of pharmacokinetic and pharmacodynamic principles at the doctoral level.
Expected Grade A+
Total Questions 100
Duration 3 hours
Learning Outcomes 1. Evaluate and select appropriate pharmacotherapy for common chronic
conditions
2. Analyze drug interactions and adverse effects in complex patient scenarios
3. Apply pharmacokinetic principles to adjust dosing in special populations
4. Interpret clinical guidelines to optimize medication regimens
Accreditation Accredited by the Accreditation Commission for Education in Nursing (ACEN)
and consistent with AACN Essentials of Doctoral Education for Advanced
Nursing Practice.
Page 1
,1. A patient with type 2 diabetes and stage 3 chronic kidney disease (eGFR 45
mL/min/1.73m²) is currently on metformin 1000 mg BID. Which of the following
adjustments is most appropriate?
A. Continue current dose, monitor renal function every 3 months
B. Reduce metformin to 500 mg BID and monitor renal function
C. Discontinue metformin and start insulin therapy
D. Discontinue metformin and start a sulfonylurea
Answer: B. Reduce metformin to 500 mg BID and monitor renal function
Metformin is contraindicated when eGFR <30, but dose reduction is recommended
when eGFR is 30-45. Reducing to 500 mg BID aligns with guidelines. Continuing
current dose risks lactic acidosis. Switching to insulin or sulfonylurea is not first-line
without trial of dose reduction.
2. Which of the following anticoagulant reversal strategies is correct for a patient
with mechanical mitral valve on warfarin who develops a life-threatening
intracranial hemorrhage?
A. Administer vitamin K 10 mg IV and fresh frozen plasma (FFP)
B. Administer prothrombin complex concentrate (PCC) and vitamin K 10 mg IV
C. Administer recombinant factor VIIa alone
D. Administer protamine sulfate and vitamin K 10 mg IV
Answer: B. Administer prothrombin complex concentrate (PCC) and vitamin K 10
mg IV
For life-threatening bleeding on warfarin, PCC provides rapid reversal of INR.
Vitamin K is added to sustain reversal. FFP is slower and less effective. Factor VIIa is
not standard. Protamine reverses heparin, not warfarin.
Page 2
,3. A patient with heart failure with reduced ejection fraction (HFrEF) on lisinopril,
metoprolol succinate, and furosemide develops hyperkalemia (K+ 5.8 mEq/L).
Which medication is most likely contributing?
A. Lisinopril
B. Metoprolol succinate
C. Furosemide
D. All of the above
Answer: A. Lisinopril
ACE inhibitors like lisinopril reduce aldosterone, leading to potassium retention.
Metoprolol does not cause hyperkalemia; beta-blockers may shift potassium but not
significantly. Furosemide causes hypokalemia. Therefore, lisinopril is the most likely
cause.
4. A patient with asthma is prescribed a long-acting beta-agonist (LABA) and an
inhaled corticosteroid (ICS) in a single inhaler. Which statement best explains the
rationale for this combination?
A. LABA potentiates the anti-inflammatory effects of ICS at the receptor level
B. ICS reduces the risk of LABA-induced bronchospasm
C. The combination improves adherence by reducing inhaler burden
D. LABA and ICS have synergistic effects on airway remodeling
Answer: A. LABA potentiates the anti-inflammatory effects of ICS at the receptor
level
LABA and ICS have complementary mechanisms: LABA relaxes bronchial smooth
muscle, while ICS reduces inflammation. Additionally, LABA primes the glucocorticoid
receptor, enhancing anti-inflammatory gene transcription. This synergy improves
asthma control beyond monotherapy. While adherence is improved, the primary
rationale is pharmacodynamic synergy.
Page 3
, 5. Which of the following best describes the mechanism of action of GLP-1 receptor
agonists in the treatment of type 2 diabetes?
A. Stimulate insulin secretion only when glucose is elevated, slow gastric emptying, and
promote satiety
B. Inhibit DPP-4 enzyme, prolonging endogenous GLP-1 activity
C. Bind to pancreatic beta-cell receptors to increase insulin synthesis independently of
glucose
D. Block glucagon receptors in the liver, reducing gluconeogenesis
Answer: A. Stimulate insulin secretion only when glucose is elevated, slow gastric
emptying, and promote satiety
GLP-1 receptor agonists mimic endogenous GLP-1, which enhances glucose-dependent
insulin secretion, suppresses glucagon, slows gastric emptying, and increases satiety.
Option B describes DPP-4 inhibitors. Option C is incorrect because insulin secretion is
glucose-dependent. Option D is not the primary mechanism.
6. A patient on chronic omeprazole therapy for GERD develops hypomagnesemia.
Which of the following is the most plausible explanation?
A. Omeprazole chelates magnesium in the gut, preventing absorption
B. Omeprazole inhibits active transport of magnesium in the distal small intestine
C. Omeprazole reduces gastric acid, which is necessary for magnesium dissolution
D. Omeprazole increases renal excretion of magnesium
Answer: B. Omeprazole inhibits active transport of magnesium in the distal small
intestine
PPIs like omeprazole inhibit H+/K+-ATPase in parietal cells, but also inhibit active
transport of magnesium via TRPM6/7 channels in the intestine, leading to reduced
absorption. Chelation is not the mechanism. Gastric acid is not required for magnesium
dissolution. Renal excretion is not increased.
Page 4
Q&A GUIDE | 2026-2027 - 100 Questions and Answers Already
Graded A+ Premium Exam Tested And Verified
Subject Area Advanced Pharmacology
Description This exam covers advanced pharmacotherapeutic concepts from weeks 5-8 of NR
565, including cardiovascular, endocrine, respiratory, and gastrointestinal
pharmacotherapy, with emphasis on evidence-based prescribing, monitoring, and
patient education. It is designed to assess clinical decision-making and application
of pharmacokinetic and pharmacodynamic principles at the doctoral level.
Expected Grade A+
Total Questions 100
Duration 3 hours
Learning Outcomes 1. Evaluate and select appropriate pharmacotherapy for common chronic
conditions
2. Analyze drug interactions and adverse effects in complex patient scenarios
3. Apply pharmacokinetic principles to adjust dosing in special populations
4. Interpret clinical guidelines to optimize medication regimens
Accreditation Accredited by the Accreditation Commission for Education in Nursing (ACEN)
and consistent with AACN Essentials of Doctoral Education for Advanced
Nursing Practice.
Page 1
,1. A patient with type 2 diabetes and stage 3 chronic kidney disease (eGFR 45
mL/min/1.73m²) is currently on metformin 1000 mg BID. Which of the following
adjustments is most appropriate?
A. Continue current dose, monitor renal function every 3 months
B. Reduce metformin to 500 mg BID and monitor renal function
C. Discontinue metformin and start insulin therapy
D. Discontinue metformin and start a sulfonylurea
Answer: B. Reduce metformin to 500 mg BID and monitor renal function
Metformin is contraindicated when eGFR <30, but dose reduction is recommended
when eGFR is 30-45. Reducing to 500 mg BID aligns with guidelines. Continuing
current dose risks lactic acidosis. Switching to insulin or sulfonylurea is not first-line
without trial of dose reduction.
2. Which of the following anticoagulant reversal strategies is correct for a patient
with mechanical mitral valve on warfarin who develops a life-threatening
intracranial hemorrhage?
A. Administer vitamin K 10 mg IV and fresh frozen plasma (FFP)
B. Administer prothrombin complex concentrate (PCC) and vitamin K 10 mg IV
C. Administer recombinant factor VIIa alone
D. Administer protamine sulfate and vitamin K 10 mg IV
Answer: B. Administer prothrombin complex concentrate (PCC) and vitamin K 10
mg IV
For life-threatening bleeding on warfarin, PCC provides rapid reversal of INR.
Vitamin K is added to sustain reversal. FFP is slower and less effective. Factor VIIa is
not standard. Protamine reverses heparin, not warfarin.
Page 2
,3. A patient with heart failure with reduced ejection fraction (HFrEF) on lisinopril,
metoprolol succinate, and furosemide develops hyperkalemia (K+ 5.8 mEq/L).
Which medication is most likely contributing?
A. Lisinopril
B. Metoprolol succinate
C. Furosemide
D. All of the above
Answer: A. Lisinopril
ACE inhibitors like lisinopril reduce aldosterone, leading to potassium retention.
Metoprolol does not cause hyperkalemia; beta-blockers may shift potassium but not
significantly. Furosemide causes hypokalemia. Therefore, lisinopril is the most likely
cause.
4. A patient with asthma is prescribed a long-acting beta-agonist (LABA) and an
inhaled corticosteroid (ICS) in a single inhaler. Which statement best explains the
rationale for this combination?
A. LABA potentiates the anti-inflammatory effects of ICS at the receptor level
B. ICS reduces the risk of LABA-induced bronchospasm
C. The combination improves adherence by reducing inhaler burden
D. LABA and ICS have synergistic effects on airway remodeling
Answer: A. LABA potentiates the anti-inflammatory effects of ICS at the receptor
level
LABA and ICS have complementary mechanisms: LABA relaxes bronchial smooth
muscle, while ICS reduces inflammation. Additionally, LABA primes the glucocorticoid
receptor, enhancing anti-inflammatory gene transcription. This synergy improves
asthma control beyond monotherapy. While adherence is improved, the primary
rationale is pharmacodynamic synergy.
Page 3
, 5. Which of the following best describes the mechanism of action of GLP-1 receptor
agonists in the treatment of type 2 diabetes?
A. Stimulate insulin secretion only when glucose is elevated, slow gastric emptying, and
promote satiety
B. Inhibit DPP-4 enzyme, prolonging endogenous GLP-1 activity
C. Bind to pancreatic beta-cell receptors to increase insulin synthesis independently of
glucose
D. Block glucagon receptors in the liver, reducing gluconeogenesis
Answer: A. Stimulate insulin secretion only when glucose is elevated, slow gastric
emptying, and promote satiety
GLP-1 receptor agonists mimic endogenous GLP-1, which enhances glucose-dependent
insulin secretion, suppresses glucagon, slows gastric emptying, and increases satiety.
Option B describes DPP-4 inhibitors. Option C is incorrect because insulin secretion is
glucose-dependent. Option D is not the primary mechanism.
6. A patient on chronic omeprazole therapy for GERD develops hypomagnesemia.
Which of the following is the most plausible explanation?
A. Omeprazole chelates magnesium in the gut, preventing absorption
B. Omeprazole inhibits active transport of magnesium in the distal small intestine
C. Omeprazole reduces gastric acid, which is necessary for magnesium dissolution
D. Omeprazole increases renal excretion of magnesium
Answer: B. Omeprazole inhibits active transport of magnesium in the distal small
intestine
PPIs like omeprazole inhibit H+/K+-ATPase in parietal cells, but also inhibit active
transport of magnesium via TRPM6/7 channels in the intestine, leading to reduced
absorption. Chelation is not the mechanism. Gastric acid is not required for magnesium
dissolution. Renal excretion is not increased.
Page 4
