1
NURS 676 Advanced Pharmacology Midterm
Actual Exam 2026/2027: Questions And
Answers for Nurse Practitioner Success –
Pass Guaranteed - A+ Graded
Section 1: Pharmacokinetics and Pharmacodynamics (10 Questions)
Q1: A 65-year-old patient with chronic kidney disease (eGFR 30 mL/min/1.73m²) is prescribed
metformin for type 2 diabetes. According to current pharmacokinetic principles and FDA
guidelines, what is the appropriate recommendation?
A. Continue metformin at full dose since it's renally cleared but safe
B. Reduce the dose by 50% and monitor renal function closely
C. Discontinue metformin immediately due to eGFR <45 mL/min/1.73m²
D. Avoid metformin due to increased risk of lactic acidosis; consider alternative agents
[CORRECT]
Rationale: Metformin is contraindicated in patients with eGFR <30 mL/min/1.73m² due to the
risk of lactic acidosis. While the FDA has relaxed restrictions for eGFR 30-45 (use with caution,
monitor frequently), at eGFR 30, the risks outweigh benefits. Alternative agents such as SGLT2
inhibitors (if eGFR permits) or GLP-1 receptor agonists are preferred. The 2024-2025 ADA
guidelines emphasize agents with cardiovascular benefits in this high-risk population .
Q2: A patient on warfarin (INR 2.5, therapeutic) is started on amiodarone for atrial fibrillation.
What is the primary pharmacokinetic mechanism for the expected drug interaction?
A. Amiodarone inhibits CYP3A4, decreasing warfarin metabolism
B. Amiodarone inhibits CYP2C9 and CYP1A2, decreasing warfarin metabolism [CORRECT]
C. Amiodarone induces CYP2C9, increasing warfarin metabolism
D. Amiodarone displaces warfarin from plasma proteins
Rationale: Amiodarone is a potent inhibitor of multiple CYP450 enzymes including CYP2C9
and CYP1A2, which are primary metabolic pathways for S-warfarin (the more potent
enantiomer). This inhibition decreases warfarin clearance, leading to increased INR and bleeding
risk. The interaction requires a 30-50% reduction in warfarin dose and frequent INR monitoring.
CYP3A4 inhibition (A) is not the primary mechanism for warfarin interaction.
,2
Q3: A patient with depression is prescribed fluoxetine. The nurse practitioner notes the patient is
also taking tamoxifen for breast cancer. What is the primary concern with this combination?
A. Increased risk of serotonin syndrome
B. Fluoxetine inhibits CYP2D6, preventing conversion of tamoxifen to its active metabolite
endoxifen [CORRECT]
C. Decreased fluoxetine absorption due to tamoxifen
D. Increased tamoxifen metabolism reducing its efficacy
Rationale: Tamoxifen is a prodrug that requires CYP2D6-mediated metabolism to its active
metabolite endoxifen. Fluoxetine is a potent CYP2D6 inhibitor that can reduce endoxifen levels
by 50-70%, potentially compromising tamoxifen's efficacy in preventing breast cancer
recurrence. Alternative antidepressants with minimal CYP2D6 inhibition (e.g., citalopram,
escitalopram) should be considered.
Q4: A patient receiving digoxin for heart failure develops nausea, vomiting, and visual
disturbances (yellow-green halos). The serum digoxin level is 3.2 ng/mL (therapeutic 0.5-0.9
ng/mL). The patient is also taking furosemide 80 mg daily. What is the primary mechanism
contributing to this toxicity?
A. Furosemide increases digoxin absorption
B. Hypokalemia from furosemide increases digoxin binding to Na/K-ATPase [CORRECT]
C. Furosemide inhibits renal digoxin clearance
D. Digoxin displaces furosemide from protein binding sites
Rationale: Furosemide-induced hypokalemia is a major risk factor for digoxin toxicity.
Potassium and digoxin compete for binding to the Na/K-ATPase pump. When potassium levels
are low, digoxin binding increases, enhancing its pharmacodynamic effects and toxicity. The
therapeutic digoxin range has been revised downward to 0.5-0.9 ng/mL for heart failure
(previously 0.8-2.0 ng/mL). Treatment includes holding digoxin, correcting hypokalemia, and
administering digoxin-specific Fab antibodies (Digibind) for severe toxicity.
Q5: A patient with a history of codeine inefficacy for post-operative pain is found to be a
CYP2D6 poor metabolizer. What is the pharmacogenomic implication?
A. Codeine is converted to morphine by CYP2D6; poor metabolizers have inadequate analgesia
[CORRECT]
B. Codeine is inactivated by CYP2D6; poor metabolizers have increased toxicity
C. CYP2D6 metabolizes morphine to codeine; poor metabolizers need higher codeine doses
, 3
D. CYP2D6 is not involved in codeine metabolism
Rationale: Codeine is a prodrug that requires CYP2D6-mediated O-demethylation to its active
metabolite morphine (responsible for analgesia). Poor metabolizers (5-10% of Caucasians, 1-2%
of Asians) cannot effectively convert codeine to morphine, resulting in inadequate pain relief.
Conversely, ultra-rapid metabolizers (1-2% of Caucasians, up to 30% of North Africans) rapidly
convert codeine to morphine, risking toxicity. Alternative analgesics not dependent on CYP2D6
(e.g., morphine, oxycodone) should be used.
Q6: A patient with hypertension is prescribed lisinopril. The NP explains that the drug's efficacy
is partially dependent on the patient's genetic profile regarding which enzyme?
A. CYP3A4
B. ACE (angiotensin-converting enzyme) polymorphisms [CORRECT]
C. CYP2C19
D. Dopamine receptors
Rationale: ACE insertion/deletion (I/D) polymorphisms affect ACE inhibitor response. The D
allele is associated with higher ACE activity and potentially greater blood pressure reduction
with ACE inhibitors, though clinical significance varies. Pharmacogenomic testing for ACE
inhibitors is not yet standard practice but represents an emerging area of personalized medicine
in cardiovascular pharmacotherapy.
Q7: A loading dose of phenytoin is administered to a patient with status epilepticus. The loading
dose is calculated based on which pharmacokinetic parameter?
A. Clearance
B. Volume of distribution [CORRECT]
C. Half-life
D. Bioavailability
Rationale: Loading doses are calculated using the volume of distribution (Vd) to rapidly achieve
therapeutic concentrations: Loading Dose = (Vd × Target Concentration) / Bioavailability.
Phenytoin has a Vd of approximately 0.7 L/kg. Maintenance doses are based on clearance.
Phenytoin exhibits saturable (zero-order) metabolism at therapeutic concentrations, making
pharmacokinetics nonlinear and requiring careful monitoring.
Q8: A patient with atrial fibrillation is started on dronedarone. Which pharmacokinetic
consideration is essential for safe prescribing?
A. Dronedarone requires therapeutic drug monitoring due to narrow therapeutic index
NURS 676 Advanced Pharmacology Midterm
Actual Exam 2026/2027: Questions And
Answers for Nurse Practitioner Success –
Pass Guaranteed - A+ Graded
Section 1: Pharmacokinetics and Pharmacodynamics (10 Questions)
Q1: A 65-year-old patient with chronic kidney disease (eGFR 30 mL/min/1.73m²) is prescribed
metformin for type 2 diabetes. According to current pharmacokinetic principles and FDA
guidelines, what is the appropriate recommendation?
A. Continue metformin at full dose since it's renally cleared but safe
B. Reduce the dose by 50% and monitor renal function closely
C. Discontinue metformin immediately due to eGFR <45 mL/min/1.73m²
D. Avoid metformin due to increased risk of lactic acidosis; consider alternative agents
[CORRECT]
Rationale: Metformin is contraindicated in patients with eGFR <30 mL/min/1.73m² due to the
risk of lactic acidosis. While the FDA has relaxed restrictions for eGFR 30-45 (use with caution,
monitor frequently), at eGFR 30, the risks outweigh benefits. Alternative agents such as SGLT2
inhibitors (if eGFR permits) or GLP-1 receptor agonists are preferred. The 2024-2025 ADA
guidelines emphasize agents with cardiovascular benefits in this high-risk population .
Q2: A patient on warfarin (INR 2.5, therapeutic) is started on amiodarone for atrial fibrillation.
What is the primary pharmacokinetic mechanism for the expected drug interaction?
A. Amiodarone inhibits CYP3A4, decreasing warfarin metabolism
B. Amiodarone inhibits CYP2C9 and CYP1A2, decreasing warfarin metabolism [CORRECT]
C. Amiodarone induces CYP2C9, increasing warfarin metabolism
D. Amiodarone displaces warfarin from plasma proteins
Rationale: Amiodarone is a potent inhibitor of multiple CYP450 enzymes including CYP2C9
and CYP1A2, which are primary metabolic pathways for S-warfarin (the more potent
enantiomer). This inhibition decreases warfarin clearance, leading to increased INR and bleeding
risk. The interaction requires a 30-50% reduction in warfarin dose and frequent INR monitoring.
CYP3A4 inhibition (A) is not the primary mechanism for warfarin interaction.
,2
Q3: A patient with depression is prescribed fluoxetine. The nurse practitioner notes the patient is
also taking tamoxifen for breast cancer. What is the primary concern with this combination?
A. Increased risk of serotonin syndrome
B. Fluoxetine inhibits CYP2D6, preventing conversion of tamoxifen to its active metabolite
endoxifen [CORRECT]
C. Decreased fluoxetine absorption due to tamoxifen
D. Increased tamoxifen metabolism reducing its efficacy
Rationale: Tamoxifen is a prodrug that requires CYP2D6-mediated metabolism to its active
metabolite endoxifen. Fluoxetine is a potent CYP2D6 inhibitor that can reduce endoxifen levels
by 50-70%, potentially compromising tamoxifen's efficacy in preventing breast cancer
recurrence. Alternative antidepressants with minimal CYP2D6 inhibition (e.g., citalopram,
escitalopram) should be considered.
Q4: A patient receiving digoxin for heart failure develops nausea, vomiting, and visual
disturbances (yellow-green halos). The serum digoxin level is 3.2 ng/mL (therapeutic 0.5-0.9
ng/mL). The patient is also taking furosemide 80 mg daily. What is the primary mechanism
contributing to this toxicity?
A. Furosemide increases digoxin absorption
B. Hypokalemia from furosemide increases digoxin binding to Na/K-ATPase [CORRECT]
C. Furosemide inhibits renal digoxin clearance
D. Digoxin displaces furosemide from protein binding sites
Rationale: Furosemide-induced hypokalemia is a major risk factor for digoxin toxicity.
Potassium and digoxin compete for binding to the Na/K-ATPase pump. When potassium levels
are low, digoxin binding increases, enhancing its pharmacodynamic effects and toxicity. The
therapeutic digoxin range has been revised downward to 0.5-0.9 ng/mL for heart failure
(previously 0.8-2.0 ng/mL). Treatment includes holding digoxin, correcting hypokalemia, and
administering digoxin-specific Fab antibodies (Digibind) for severe toxicity.
Q5: A patient with a history of codeine inefficacy for post-operative pain is found to be a
CYP2D6 poor metabolizer. What is the pharmacogenomic implication?
A. Codeine is converted to morphine by CYP2D6; poor metabolizers have inadequate analgesia
[CORRECT]
B. Codeine is inactivated by CYP2D6; poor metabolizers have increased toxicity
C. CYP2D6 metabolizes morphine to codeine; poor metabolizers need higher codeine doses
, 3
D. CYP2D6 is not involved in codeine metabolism
Rationale: Codeine is a prodrug that requires CYP2D6-mediated O-demethylation to its active
metabolite morphine (responsible for analgesia). Poor metabolizers (5-10% of Caucasians, 1-2%
of Asians) cannot effectively convert codeine to morphine, resulting in inadequate pain relief.
Conversely, ultra-rapid metabolizers (1-2% of Caucasians, up to 30% of North Africans) rapidly
convert codeine to morphine, risking toxicity. Alternative analgesics not dependent on CYP2D6
(e.g., morphine, oxycodone) should be used.
Q6: A patient with hypertension is prescribed lisinopril. The NP explains that the drug's efficacy
is partially dependent on the patient's genetic profile regarding which enzyme?
A. CYP3A4
B. ACE (angiotensin-converting enzyme) polymorphisms [CORRECT]
C. CYP2C19
D. Dopamine receptors
Rationale: ACE insertion/deletion (I/D) polymorphisms affect ACE inhibitor response. The D
allele is associated with higher ACE activity and potentially greater blood pressure reduction
with ACE inhibitors, though clinical significance varies. Pharmacogenomic testing for ACE
inhibitors is not yet standard practice but represents an emerging area of personalized medicine
in cardiovascular pharmacotherapy.
Q7: A loading dose of phenytoin is administered to a patient with status epilepticus. The loading
dose is calculated based on which pharmacokinetic parameter?
A. Clearance
B. Volume of distribution [CORRECT]
C. Half-life
D. Bioavailability
Rationale: Loading doses are calculated using the volume of distribution (Vd) to rapidly achieve
therapeutic concentrations: Loading Dose = (Vd × Target Concentration) / Bioavailability.
Phenytoin has a Vd of approximately 0.7 L/kg. Maintenance doses are based on clearance.
Phenytoin exhibits saturable (zero-order) metabolism at therapeutic concentrations, making
pharmacokinetics nonlinear and requiring careful monitoring.
Q8: A patient with atrial fibrillation is started on dronedarone. Which pharmacokinetic
consideration is essential for safe prescribing?
A. Dronedarone requires therapeutic drug monitoring due to narrow therapeutic index
