NSG 533 EXAM 3 - WILKES ADVANCED
PHARMACOLOGY (2026-2027) ACTUAL
QUESTIONS AND ANSWERS
219 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NSG 533 EXAM 3 - WILKES ADVANCED PHARMACOLOGY (2026-2027) ACTUAL QUESTIONS AND
ANSWERS. It contains 219 carefully selected questions that reflect the most current exam content and testing
strategies. Each question is accompanied by a correct answer and a detailed rationale that explains the
underlying pathophysiology, pharmacology, or clinical reasoning.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions
Review Summary 219 Questions
Foundations - Application - NSG 533 3 Wilkes Advanced Pharmacology 2026-2027 Actual AND Advanced
Pharmacology Graduate
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
NSG 533 3 Wilkes Advanced 1-37 Appropriate, Mechanism, Requires, Disorder, Parameter
Pharmacology 2026-2027
Actual AND Advanced
Pharmacology Graduate
Explains 38-74 Requires, Prescribed, Chronic, Heart, Started
Mechanism 75-111 Therapy, Likely, Requires, Started, Explains
Develops 112-148 Explains, Requires, Warfarin, Medication, Failure
Appropriate 149-185 Explains, Develops, Diabetes, Requires, Severe
Effect 186-219 Requires, Agent, Likely, Prescribed, Mechanism
TOTAL 219 All questions include answers and detailed rationales
,Section A - NSG 533 3 Wilkes Advanced Pharmacology
2026-2027 Actual AND Advanced Pharmacology Graduate
Q1.
A patient with type 2 diabetes and chronic kidney disease (eGFR 30 mL/min) has
persistent hyperglycemia despite metformin and insulin glargine. Which agent's
pharmacology requires dose adjustment or avoidance in this setting?
A. Empagliflozin B. Sitagliptin
C. Liraglutide D. Insulin lispro
Correct: A - Empagliflozin
Rationale:Empagliflozin, an SGLT2 inhibitor, is generally not recommended when eGFR is
below 45 mL/min due to reduced efficacy and potential acute kidney injury risk. Sitagliptin
requires dose adjustment but is not contraindicated. Liraglutide and insulin lispro can be used
with renal impairment, though insulin may require dose titration.
Q2.
A patient on warfarin for atrial fibrillation is started on amiodarone for ventricular
arrhythmias. What is the most appropriate management strategy to prevent bleeding?
A. Discontinue warfarin and switch to B. Reduce warfarin dose by 30-50% and
dabigatran monitor INR closely
C. Increase warfarin dose to maintain D. Add aspirin for additional antiplatelet
therapeutic INR effect
Correct: B - Reduce warfarin dose by 30-50% and monitor INR closely
Rationale:Amiodarone inhibits CYP2C9, CYP3A4, and P-glycoprotein, increasing warfarin
levels and INR. The standard approach is to reduce warfarin dose by 30-50% and monitor
INR frequently. Switching to dabigatran may be an option but is not the immediate
management; increasing dose would worsen bleeding risk; aspirin adds unnecessary risk.
Q3.
A patient with major depressive disorder has failed two SSRIs and one SNRI. Which
pharmacogenomic finding would most likely guide the selection of a different
antidepressant?
A. CYP2D6 poor metabolizer phenotype B. CYP2C19 ultrarapid metabolizer
phenotype
C. HTR2A receptor polymorphism D. SLC6A4 promoter polymorphism
Page 3
, Section A - NSG 533 3 Wilkes Advanced Pharmacology 2026-2027 Actual AND Advanced Pharmacology Graduate
Correct: B - CYP2C19 ultrarapid metabolizer phenotype
Rationale:CYP2C19 ultrarapid metabolizers may have reduced exposure to SSRIs like
sertraline and citalopram, explaining treatment failure. CYP2D6 poor metabolizer status
affects drugs like fluoxetine and paroxetine but is less likely to cause failure. HTR2A and
SLC6A4 variants are associated with response but not directly with metabolism-based failure.
Q4.
Which drug-drug interaction is correctly paired with its mechanism and clinical
consequence?
A. Sildenafil + nitroglycerin - synergistic B. Warfarin + acetaminophen - displacement
hypotension via PDE5 inhibition and NO from protein binding leading to increased
donation INR
C. Clarithromycin + simvastatin - CYP3A4 D. Lithium + NSAIDs - reduced renal lithium
inhibition increasing myopathy risk clearance causing toxicity
Correct: C - Clarithromycin + simvastatin - CYP3A4 inhibition increasing myopathy risk
Rationale:Clarithromycin inhibits CYP3A4, increasing simvastatin levels and
myopathy/rhabdomyolysis risk. Sildenafil and nitroglycerin cause severe hypotension via
additive cGMP/NO effects, but not via PDE5 inhibition synergism. Acetaminophen-warfarin
interaction is not primarily protein displacement. Lithium-NSAID interaction reduces renal
lithium clearance, but the question asks for correct pairing; C is correct.
Q5.
A patient with opioid use disorder is stabilized on buprenorphine/naloxone. Which
statement best describes the pharmacological rationale for the naloxone component?
A. Naloxone potentiates buprenorphine's B. Naloxone precipitates withdrawal if the
analgesic effect drug is injected
C. Naloxone reduces buprenorphine's abuse D. Naloxone prolongs buprenorphine's
liability by blocking mu receptors half-life
Correct: B - Naloxone precipitates withdrawal if the drug is injected
Rationale:Naloxone has poor oral bioavailability but is absorbed if the combination is
injected, precipitating withdrawal. This deters diversion. Naloxone does not potentiate
buprenorphine, block mu receptors (buprenorphine does), or prolong half-life.
Q6.
A patient with heart failure with reduced ejection fraction (HFrEF) is tolerating
sacubitril/valsartan. Which laboratory parameter requires periodic monitoring due to the
drug's mechanism?
Page 4
PHARMACOLOGY (2026-2027) ACTUAL
QUESTIONS AND ANSWERS
219 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NSG 533 EXAM 3 - WILKES ADVANCED PHARMACOLOGY (2026-2027) ACTUAL QUESTIONS AND
ANSWERS. It contains 219 carefully selected questions that reflect the most current exam content and testing
strategies. Each question is accompanied by a correct answer and a detailed rationale that explains the
underlying pathophysiology, pharmacology, or clinical reasoning.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions
Review Summary 219 Questions
Foundations - Application - NSG 533 3 Wilkes Advanced Pharmacology 2026-2027 Actual AND Advanced
Pharmacology Graduate
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
NSG 533 3 Wilkes Advanced 1-37 Appropriate, Mechanism, Requires, Disorder, Parameter
Pharmacology 2026-2027
Actual AND Advanced
Pharmacology Graduate
Explains 38-74 Requires, Prescribed, Chronic, Heart, Started
Mechanism 75-111 Therapy, Likely, Requires, Started, Explains
Develops 112-148 Explains, Requires, Warfarin, Medication, Failure
Appropriate 149-185 Explains, Develops, Diabetes, Requires, Severe
Effect 186-219 Requires, Agent, Likely, Prescribed, Mechanism
TOTAL 219 All questions include answers and detailed rationales
,Section A - NSG 533 3 Wilkes Advanced Pharmacology
2026-2027 Actual AND Advanced Pharmacology Graduate
Q1.
A patient with type 2 diabetes and chronic kidney disease (eGFR 30 mL/min) has
persistent hyperglycemia despite metformin and insulin glargine. Which agent's
pharmacology requires dose adjustment or avoidance in this setting?
A. Empagliflozin B. Sitagliptin
C. Liraglutide D. Insulin lispro
Correct: A - Empagliflozin
Rationale:Empagliflozin, an SGLT2 inhibitor, is generally not recommended when eGFR is
below 45 mL/min due to reduced efficacy and potential acute kidney injury risk. Sitagliptin
requires dose adjustment but is not contraindicated. Liraglutide and insulin lispro can be used
with renal impairment, though insulin may require dose titration.
Q2.
A patient on warfarin for atrial fibrillation is started on amiodarone for ventricular
arrhythmias. What is the most appropriate management strategy to prevent bleeding?
A. Discontinue warfarin and switch to B. Reduce warfarin dose by 30-50% and
dabigatran monitor INR closely
C. Increase warfarin dose to maintain D. Add aspirin for additional antiplatelet
therapeutic INR effect
Correct: B - Reduce warfarin dose by 30-50% and monitor INR closely
Rationale:Amiodarone inhibits CYP2C9, CYP3A4, and P-glycoprotein, increasing warfarin
levels and INR. The standard approach is to reduce warfarin dose by 30-50% and monitor
INR frequently. Switching to dabigatran may be an option but is not the immediate
management; increasing dose would worsen bleeding risk; aspirin adds unnecessary risk.
Q3.
A patient with major depressive disorder has failed two SSRIs and one SNRI. Which
pharmacogenomic finding would most likely guide the selection of a different
antidepressant?
A. CYP2D6 poor metabolizer phenotype B. CYP2C19 ultrarapid metabolizer
phenotype
C. HTR2A receptor polymorphism D. SLC6A4 promoter polymorphism
Page 3
, Section A - NSG 533 3 Wilkes Advanced Pharmacology 2026-2027 Actual AND Advanced Pharmacology Graduate
Correct: B - CYP2C19 ultrarapid metabolizer phenotype
Rationale:CYP2C19 ultrarapid metabolizers may have reduced exposure to SSRIs like
sertraline and citalopram, explaining treatment failure. CYP2D6 poor metabolizer status
affects drugs like fluoxetine and paroxetine but is less likely to cause failure. HTR2A and
SLC6A4 variants are associated with response but not directly with metabolism-based failure.
Q4.
Which drug-drug interaction is correctly paired with its mechanism and clinical
consequence?
A. Sildenafil + nitroglycerin - synergistic B. Warfarin + acetaminophen - displacement
hypotension via PDE5 inhibition and NO from protein binding leading to increased
donation INR
C. Clarithromycin + simvastatin - CYP3A4 D. Lithium + NSAIDs - reduced renal lithium
inhibition increasing myopathy risk clearance causing toxicity
Correct: C - Clarithromycin + simvastatin - CYP3A4 inhibition increasing myopathy risk
Rationale:Clarithromycin inhibits CYP3A4, increasing simvastatin levels and
myopathy/rhabdomyolysis risk. Sildenafil and nitroglycerin cause severe hypotension via
additive cGMP/NO effects, but not via PDE5 inhibition synergism. Acetaminophen-warfarin
interaction is not primarily protein displacement. Lithium-NSAID interaction reduces renal
lithium clearance, but the question asks for correct pairing; C is correct.
Q5.
A patient with opioid use disorder is stabilized on buprenorphine/naloxone. Which
statement best describes the pharmacological rationale for the naloxone component?
A. Naloxone potentiates buprenorphine's B. Naloxone precipitates withdrawal if the
analgesic effect drug is injected
C. Naloxone reduces buprenorphine's abuse D. Naloxone prolongs buprenorphine's
liability by blocking mu receptors half-life
Correct: B - Naloxone precipitates withdrawal if the drug is injected
Rationale:Naloxone has poor oral bioavailability but is absorbed if the combination is
injected, precipitating withdrawal. This deters diversion. Naloxone does not potentiate
buprenorphine, block mu receptors (buprenorphine does), or prolong half-life.
Q6.
A patient with heart failure with reduced ejection fraction (HFrEF) is tolerating
sacubitril/valsartan. Which laboratory parameter requires periodic monitoring due to the
drug's mechanism?
Page 4
