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NURS 5334 EXAM 2 2026/2027 | Advanced Pharmacology
Review | UTA | Verified Q&A | Pass Guaranteed - A+
Graded
Section 1: Pharmacokinetics, Pharmacodynamics, &
Pharmacogenomics (Questions 1–12)
Q1: A 68-year-old male with atrial fibrillation is prescribed warfarin 5 mg daily.
Pharmacogenomic testing reveals he is a CYP2C9 *3/*3 poor metabolizer and
VKORC1 -1639G>A variant carrier. Based on these results, what is the most
appropriate initial prescribing action?
A. Prescribe the standard 5 mg daily dose and monitor INR at 4 weeks.
B. Reduce the initial dose to 2–3 mg daily and monitor INR within 3–5 days.
[CORRECT]
C. Switch to dabigatran 150 mg BID to avoid pharmacogenomic variability.
D. Prescribe warfarin 7.5 mg daily because poor metabolizers require higher doses.
Correct Answer: B
Rationale: CYP2C9 poor metabolizers and VKORC1 variant carriers have significantly
reduced warfarin clearance and increased sensitivity, requiring 30–50% dose
reductions with early INR monitoring. Option A delays necessary monitoring; C is
unnecessary if warfarin is indicated and manageable; D is physiologically opposite to
the correct approach. [Competency: Pharmacogenomics & Precision Prescribing]
Q2: A 45-year-old female with major depressive disorder is started on fluoxetine 20
mg daily. She is a known CYP2D6 poor metabolizer. Which of the following
represents the primary clinical concern in this patient?
A. Fluoxetine will be ineffective due to lack of conversion to active metabolite.
B. Fluoxetine plasma concentrations will be elevated, increasing risk of QT
prolongation and serotonin syndrome. [CORRECT]
,2
C. She will require doubling the fluoxetine dose to achieve therapeutic effect.
D. CYP2D6 poor metabolizer status has no clinical significance for fluoxetine therapy.
Correct Answer: B
Rationale: Fluoxetine is a CYP2D6 substrate; poor metabolizers accumulate parent
drug and active metabolite norfluoxetine, increasing adverse effect risk. Option A
confuses prodrugs with active drugs; C is dangerous and opposite to correct
management; D contradicts FDA pharmacogenomic guidance. [Competency:
Pharmacogenomics & Drug Metabolism]
Q3: A patient on chronic phenytoin therapy for seizure disorder presents with
nystagmus, ataxia, and confusion. Serum phenytoin level is 32 mcg/mL (therapeutic:
10–20 mcg/mL). The patient is also taking cimetidine 400 mg BID for GERD. Which
pharmacokinetic interaction best explains this clinical presentation?
A. Cimetidine inhibits CYP3A4, reducing phenytoin hepatic clearance.
B. Cimetidine inhibits CYP2C9 and CYP2C19, decreasing phenytoin metabolism.
[CORRECT]
C. Cimetidine induces CYP1A2, increasing phenytoin protein binding.
D. Cimetidine displaces phenytoin from albumin, increasing free fraction only.
Correct Answer: B
Rationale: Cimetidine is a non-selective CYP inhibitor affecting CYP2C9/2C19, the
primary enzymes metabolizing phenytoin. Option A incorrectly identifies CYP3A4; C
is wrong because cimetidine inhibits, not induces; D describes a minor interaction
insufficient to cause levels of 32 mcg/mL. [Competency: Cytochrome P450 Drug
Interactions]
Q4: A 78-year-old female with heart failure and eGFR 28 mL/min/1.73m² is
prescribed digoxin 0.25 mg daily for atrial fibrillation with rapid ventricular response.
After 5 days, she develops nausea, vomiting, and visual disturbances. Digoxin level is
3.2 ng/mL (therapeutic: 0.5–0.9 ng/mL). What is the most appropriate adjustment?
A. Continue 0.25 mg daily and add metoclopramide for nausea.
B. Reduce to 0.125 mg every 48 hours and recheck level in 7–10 days. [CORRECT]
,3
C. Switch to digitoxin, which is not renally cleared.
D. Increase dose to 0.375 mg daily because toxicity indicates underdosing.
Correct Answer: B
Rationale: Digoxin is 60–80% renally eliminated; eGFR <30 requires 50% dose
reduction or extended dosing intervals. Option A ignores life-threatening toxicity; C
is inappropriate—digitoxin is not available in the US and has a very long half-life; D is
lethal. [Competency: Renal Dosing & Pharmacokinetic Alterations]
Q5: A 55-year-old male with newly diagnosed HIV is prescribed abacavir as part of
initial antiretroviral therapy. Prior to initiation, which pharmacogenomic test is
mandatory per FDA labeling?
A. CYP2B6 genotyping for efavirenz co-administration
B. HLA-B*57:01 screening for hypersensitivity reaction risk [CORRECT]
C. CYP3A5 genotyping for abacavir metabolism
D. TPMT genotyping for myelosuppression risk
Correct Answer: B
Rationale: The FDA mandates HLA-B*57:01 screening before abacavir initiation due
to risk of fatal hypersensitivity reactions in carriers. Options A, C, and D are irrelevant
to abacavir—TPMT testing is for thiopurines, not antiretrovirals. [Competency:
Pharmacogenomics & Safety Screening]
Q6: A 62-year-old male with a history of ulcerative colitis requires azathioprine 100
mg daily. TPMT genotyping reveals intermediate metabolizer status. What is the
recommended prescribing approach?
A. Prescribe standard 100 mg daily with routine CBC monitoring.
B. Reduce initial dose by 30–50% and monitor CBC every 2 weeks. [CORRECT]
C. Avoid azathioprine entirely and select infliximab monotherapy.
D. Double the dose because intermediate metabolizers require more drug.
Correct Answer: B
Rationale: TPMT intermediate metabolizers have reduced thiopurine clearance,
increasing myelosuppression risk; CPIC guidelines recommend 30–50% dose
, 4
reduction with enhanced monitoring. Option A risks severe bone marrow
suppression; C is unnecessarily restrictive; D is dangerous. [Competency:
Pharmacogenomics & Dose Individualization]
Q7: A 42-year-old female with bipolar disorder is prescribed lithium carbonate 600
mg BID. Her baseline creatinine is 0.9 mg/dL and eGFR is >90. After 3 months, her
creatinine rises to 1.4 mg/dL (eGFR 52). Which pharmacokinetic principle best
explains the need for lithium dose adjustment?
A. Lithium undergoes extensive hepatic metabolism via CYP2D6.
B. Lithium is entirely renally eliminated without hepatic metabolism; reduced GFR
decreases clearance. [CORRECT]
C. Lithium is highly protein-bound and displaced by renal impairment.
D. Lithium induces its own metabolism, requiring dose escalation over time.
Correct Answer: B
Rationale: Lithium is filtered at the glomerulus without metabolism; renal function
directly determines clearance. Option A is incorrect—lithium is not a CYP substrate; C
is wrong—lithium is not protein-bound; D describes autoinduction, which does not
occur with lithium. [Competency: Pharmacokinetics in Renal Impairment]
Q8: A 34-year-old female weighing 58 kg presents with community-acquired
pneumonia. The APRN plans to prescribe gentamicin 2 mg/kg IV q8h. The patient's
serum creatinine is 1.1 mg/dL and eGFR is 68 mL/min. Using the Cockcroft-Gault
equation, what is the calculated creatinine clearance, and how should the dose be
adjusted?
A. CrCl 58 mL/min; no dose adjustment needed, administer 116 mg q8h.
B. CrCl 58 mL/min; extend interval to q12h or reduce dose by 25%. [CORRECT]
C. CrCl 72 mL/min; administer standard dose of 116 mg q8h.
D. CrCl 45 mL/min; reduce dose by 50% and obtain peak/trough levels.
Correct Answer: B
Rationale: Cockcroft-Gault for females: [(140–34) × 58 × 0.85] / (1.1 × 72) ≈ 58
mL/min. Aminoglycosides require dose reduction or interval extension when CrCl
NURS 5334 EXAM 2 2026/2027 | Advanced Pharmacology
Review | UTA | Verified Q&A | Pass Guaranteed - A+
Graded
Section 1: Pharmacokinetics, Pharmacodynamics, &
Pharmacogenomics (Questions 1–12)
Q1: A 68-year-old male with atrial fibrillation is prescribed warfarin 5 mg daily.
Pharmacogenomic testing reveals he is a CYP2C9 *3/*3 poor metabolizer and
VKORC1 -1639G>A variant carrier. Based on these results, what is the most
appropriate initial prescribing action?
A. Prescribe the standard 5 mg daily dose and monitor INR at 4 weeks.
B. Reduce the initial dose to 2–3 mg daily and monitor INR within 3–5 days.
[CORRECT]
C. Switch to dabigatran 150 mg BID to avoid pharmacogenomic variability.
D. Prescribe warfarin 7.5 mg daily because poor metabolizers require higher doses.
Correct Answer: B
Rationale: CYP2C9 poor metabolizers and VKORC1 variant carriers have significantly
reduced warfarin clearance and increased sensitivity, requiring 30–50% dose
reductions with early INR monitoring. Option A delays necessary monitoring; C is
unnecessary if warfarin is indicated and manageable; D is physiologically opposite to
the correct approach. [Competency: Pharmacogenomics & Precision Prescribing]
Q2: A 45-year-old female with major depressive disorder is started on fluoxetine 20
mg daily. She is a known CYP2D6 poor metabolizer. Which of the following
represents the primary clinical concern in this patient?
A. Fluoxetine will be ineffective due to lack of conversion to active metabolite.
B. Fluoxetine plasma concentrations will be elevated, increasing risk of QT
prolongation and serotonin syndrome. [CORRECT]
,2
C. She will require doubling the fluoxetine dose to achieve therapeutic effect.
D. CYP2D6 poor metabolizer status has no clinical significance for fluoxetine therapy.
Correct Answer: B
Rationale: Fluoxetine is a CYP2D6 substrate; poor metabolizers accumulate parent
drug and active metabolite norfluoxetine, increasing adverse effect risk. Option A
confuses prodrugs with active drugs; C is dangerous and opposite to correct
management; D contradicts FDA pharmacogenomic guidance. [Competency:
Pharmacogenomics & Drug Metabolism]
Q3: A patient on chronic phenytoin therapy for seizure disorder presents with
nystagmus, ataxia, and confusion. Serum phenytoin level is 32 mcg/mL (therapeutic:
10–20 mcg/mL). The patient is also taking cimetidine 400 mg BID for GERD. Which
pharmacokinetic interaction best explains this clinical presentation?
A. Cimetidine inhibits CYP3A4, reducing phenytoin hepatic clearance.
B. Cimetidine inhibits CYP2C9 and CYP2C19, decreasing phenytoin metabolism.
[CORRECT]
C. Cimetidine induces CYP1A2, increasing phenytoin protein binding.
D. Cimetidine displaces phenytoin from albumin, increasing free fraction only.
Correct Answer: B
Rationale: Cimetidine is a non-selective CYP inhibitor affecting CYP2C9/2C19, the
primary enzymes metabolizing phenytoin. Option A incorrectly identifies CYP3A4; C
is wrong because cimetidine inhibits, not induces; D describes a minor interaction
insufficient to cause levels of 32 mcg/mL. [Competency: Cytochrome P450 Drug
Interactions]
Q4: A 78-year-old female with heart failure and eGFR 28 mL/min/1.73m² is
prescribed digoxin 0.25 mg daily for atrial fibrillation with rapid ventricular response.
After 5 days, she develops nausea, vomiting, and visual disturbances. Digoxin level is
3.2 ng/mL (therapeutic: 0.5–0.9 ng/mL). What is the most appropriate adjustment?
A. Continue 0.25 mg daily and add metoclopramide for nausea.
B. Reduce to 0.125 mg every 48 hours and recheck level in 7–10 days. [CORRECT]
,3
C. Switch to digitoxin, which is not renally cleared.
D. Increase dose to 0.375 mg daily because toxicity indicates underdosing.
Correct Answer: B
Rationale: Digoxin is 60–80% renally eliminated; eGFR <30 requires 50% dose
reduction or extended dosing intervals. Option A ignores life-threatening toxicity; C
is inappropriate—digitoxin is not available in the US and has a very long half-life; D is
lethal. [Competency: Renal Dosing & Pharmacokinetic Alterations]
Q5: A 55-year-old male with newly diagnosed HIV is prescribed abacavir as part of
initial antiretroviral therapy. Prior to initiation, which pharmacogenomic test is
mandatory per FDA labeling?
A. CYP2B6 genotyping for efavirenz co-administration
B. HLA-B*57:01 screening for hypersensitivity reaction risk [CORRECT]
C. CYP3A5 genotyping for abacavir metabolism
D. TPMT genotyping for myelosuppression risk
Correct Answer: B
Rationale: The FDA mandates HLA-B*57:01 screening before abacavir initiation due
to risk of fatal hypersensitivity reactions in carriers. Options A, C, and D are irrelevant
to abacavir—TPMT testing is for thiopurines, not antiretrovirals. [Competency:
Pharmacogenomics & Safety Screening]
Q6: A 62-year-old male with a history of ulcerative colitis requires azathioprine 100
mg daily. TPMT genotyping reveals intermediate metabolizer status. What is the
recommended prescribing approach?
A. Prescribe standard 100 mg daily with routine CBC monitoring.
B. Reduce initial dose by 30–50% and monitor CBC every 2 weeks. [CORRECT]
C. Avoid azathioprine entirely and select infliximab monotherapy.
D. Double the dose because intermediate metabolizers require more drug.
Correct Answer: B
Rationale: TPMT intermediate metabolizers have reduced thiopurine clearance,
increasing myelosuppression risk; CPIC guidelines recommend 30–50% dose
, 4
reduction with enhanced monitoring. Option A risks severe bone marrow
suppression; C is unnecessarily restrictive; D is dangerous. [Competency:
Pharmacogenomics & Dose Individualization]
Q7: A 42-year-old female with bipolar disorder is prescribed lithium carbonate 600
mg BID. Her baseline creatinine is 0.9 mg/dL and eGFR is >90. After 3 months, her
creatinine rises to 1.4 mg/dL (eGFR 52). Which pharmacokinetic principle best
explains the need for lithium dose adjustment?
A. Lithium undergoes extensive hepatic metabolism via CYP2D6.
B. Lithium is entirely renally eliminated without hepatic metabolism; reduced GFR
decreases clearance. [CORRECT]
C. Lithium is highly protein-bound and displaced by renal impairment.
D. Lithium induces its own metabolism, requiring dose escalation over time.
Correct Answer: B
Rationale: Lithium is filtered at the glomerulus without metabolism; renal function
directly determines clearance. Option A is incorrect—lithium is not a CYP substrate; C
is wrong—lithium is not protein-bound; D describes autoinduction, which does not
occur with lithium. [Competency: Pharmacokinetics in Renal Impairment]
Q8: A 34-year-old female weighing 58 kg presents with community-acquired
pneumonia. The APRN plans to prescribe gentamicin 2 mg/kg IV q8h. The patient's
serum creatinine is 1.1 mg/dL and eGFR is 68 mL/min. Using the Cockcroft-Gault
equation, what is the calculated creatinine clearance, and how should the dose be
adjusted?
A. CrCl 58 mL/min; no dose adjustment needed, administer 116 mg q8h.
B. CrCl 58 mL/min; extend interval to q12h or reduce dose by 25%. [CORRECT]
C. CrCl 72 mL/min; administer standard dose of 116 mg q8h.
D. CrCl 45 mL/min; reduce dose by 50% and obtain peak/trough levels.
Correct Answer: B
Rationale: Cockcroft-Gault for females: [(140–34) × 58 × 0.85] / (1.1 × 72) ≈ 58
mL/min. Aminoglycosides require dose reduction or interval extension when CrCl
