NSG 533 Exam 3 Study Guide (2026/2027)
Advanced Pharmacology | Wilkes University
Comprehensive Questions & Verified Answers
Cardiovascular Pharmacotherapeutics | Endocrine Pharmacology | Respiratory Pharmacology | Neurologic Pharmacology
70 Pharmacology Questions with Verified Answers
April 2026
,Table of Contents
Introduction
Section 1: Antihypertensives (Q1-Q4)
Section 2: Antiarrhythmics (Q5-Q8)
Section 3: Anticoagulants (Q9-Q12)
Section 4: Heart Failure Drugs (Q13-Q16)
Section 5: Antilipemics (Q17-Q20)
Section 6: Diabetes Agents (Q21-Q26)
Section 7: Thyroid and Adrenal Drugs (Q27-Q32)
Section 8: Osteoporosis Drugs (Q33-Q35)
Section 9: Asthma Agents (Q36-Q40)
Section 10: COPD Agents (Q41-Q44)
Section 11: Antihistamines and Decongestants (Q45-Q49)
Section 12: Cough, Leukotriene Modifiers, and Mast Cell Stabilizers (Q50-Q52)
Section 13: Antiepileptics (Q53-Q58)
Section 14: Parkinson's Disease Drugs (Q59-Q63)
Section 15: Migraine Therapies (Q64-Q67)
Section 16: Other Neurologic Agents (Q68-Q70)
Answer Key
Page 2
, Introduction
This structured NSG 533 Exam 3 Study Guide for Wilkes University 2026/2027 provides a comprehensive set of
exam-style questions with correct answers and rationales. It emphasizes advanced pharmacological principles required for
clinical decision-making, including drug mechanisms of action, therapeutic indications, adverse effect management, drug
interactions, monitoring parameters, and evidence-based prescribing for patients with cardiovascular, endocrine,
respiratory, and neurologic conditions. Each question targets graduate-level pharmacological understanding essential for
advanced practice nursing prescriptive authority.
Feature Details
Total Questions 70 Advanced Pharmacology Questions
Format Multiple Choice (A-D) with Detailed Rationales
Sections 16 Pharmacology Sub-Domains
Focus MOA, therapeutic indications, adverse effects, drug interactions, monitoring
All correct answers appear in bold and cyan blue. Each rationale explains the drug's mechanism of action, the primary
therapeutic indication, critical adverse effects to monitor, key drug interactions, essential monitoring parameters (e.g., INR,
blood glucose, renal function, electrolytes), and why alternative options are incorrect, contraindicated, or therapeutically
inappropriate.
Section 1: Antihypertensives
Q1. A 58-year-old patient with type 2 diabetes mellitus and hypertension is started on lisinopril. Which mechanism best
explains the renal protective benefit of ACE inhibitors in this population?
A) Direct dilation of the afferent arteriole, increasing glomerular filtration rate
B) Stimulation of bradykinin production, improving renal blood flow
C) Inhibition of aldosterone secretion, causing natriuresis and volume depletion
D) Preferential dilation of the efferent arteriole, reducing intraglomerular pressure
Rationale:
ACE inhibitors preferentially dilate the efferent arteriole by decreasing angiotensin II production, which reduces intraglomerular pressure
and slows the progression of diabetic nephropathy. This effect is independent of blood pressure reduction. Option A is incorrect because
ACE inhibitors do not directly dilate the afferent arteriole; NSAIDs do the opposite by constriction. Option C describes a secondary effect
but is not the primary mechanism of renal protection. Option B is incorrect because while bradykinin accumulation contributes to the
cough side effect, it is not the primary mechanism of renal protection.
Q2. A 72-year-old woman with hypertension and bilateral renal artery stenosis begins taking losartan. Two weeks later, her
serum creatinine rises from 1.0 mg/dL to 2.8 mg/dL. What is the most likely mechanism for this acute kidney injury?
A) Losartan-induced interstitial nephritis due to hypersensitivity reaction
B) Excessive reduction in angiotensin II causing loss of efferent arteriolar tone in a kidney dependent on angiotensin II for
filtration
C) Direct tubular toxicity from losartan metabolites accumulating in the renal cortex
D) Volume depletion from losartan's natriuretic effect without adequate oral fluid intake
Rationale:
In bilateral renal artery stenosis, glomerular filtration is critically dependent on angiotensin II-mediated efferent arteriolar constriction to
maintain intraglomerular pressure. ARBs like losartan block this compensatory mechanism, leading to a precipitous drop in GFR and
acute kidney injury. Option A is incorrect because interstitial nephritis is not a characteristic adverse effect of ARBs. Option C is incorrect
as losartan is not directly tubulotoxic. Option D describes a contributing factor but is not the primary pathophysiologic mechanism.
Page 3
Advanced Pharmacology | Wilkes University
Comprehensive Questions & Verified Answers
Cardiovascular Pharmacotherapeutics | Endocrine Pharmacology | Respiratory Pharmacology | Neurologic Pharmacology
70 Pharmacology Questions with Verified Answers
April 2026
,Table of Contents
Introduction
Section 1: Antihypertensives (Q1-Q4)
Section 2: Antiarrhythmics (Q5-Q8)
Section 3: Anticoagulants (Q9-Q12)
Section 4: Heart Failure Drugs (Q13-Q16)
Section 5: Antilipemics (Q17-Q20)
Section 6: Diabetes Agents (Q21-Q26)
Section 7: Thyroid and Adrenal Drugs (Q27-Q32)
Section 8: Osteoporosis Drugs (Q33-Q35)
Section 9: Asthma Agents (Q36-Q40)
Section 10: COPD Agents (Q41-Q44)
Section 11: Antihistamines and Decongestants (Q45-Q49)
Section 12: Cough, Leukotriene Modifiers, and Mast Cell Stabilizers (Q50-Q52)
Section 13: Antiepileptics (Q53-Q58)
Section 14: Parkinson's Disease Drugs (Q59-Q63)
Section 15: Migraine Therapies (Q64-Q67)
Section 16: Other Neurologic Agents (Q68-Q70)
Answer Key
Page 2
, Introduction
This structured NSG 533 Exam 3 Study Guide for Wilkes University 2026/2027 provides a comprehensive set of
exam-style questions with correct answers and rationales. It emphasizes advanced pharmacological principles required for
clinical decision-making, including drug mechanisms of action, therapeutic indications, adverse effect management, drug
interactions, monitoring parameters, and evidence-based prescribing for patients with cardiovascular, endocrine,
respiratory, and neurologic conditions. Each question targets graduate-level pharmacological understanding essential for
advanced practice nursing prescriptive authority.
Feature Details
Total Questions 70 Advanced Pharmacology Questions
Format Multiple Choice (A-D) with Detailed Rationales
Sections 16 Pharmacology Sub-Domains
Focus MOA, therapeutic indications, adverse effects, drug interactions, monitoring
All correct answers appear in bold and cyan blue. Each rationale explains the drug's mechanism of action, the primary
therapeutic indication, critical adverse effects to monitor, key drug interactions, essential monitoring parameters (e.g., INR,
blood glucose, renal function, electrolytes), and why alternative options are incorrect, contraindicated, or therapeutically
inappropriate.
Section 1: Antihypertensives
Q1. A 58-year-old patient with type 2 diabetes mellitus and hypertension is started on lisinopril. Which mechanism best
explains the renal protective benefit of ACE inhibitors in this population?
A) Direct dilation of the afferent arteriole, increasing glomerular filtration rate
B) Stimulation of bradykinin production, improving renal blood flow
C) Inhibition of aldosterone secretion, causing natriuresis and volume depletion
D) Preferential dilation of the efferent arteriole, reducing intraglomerular pressure
Rationale:
ACE inhibitors preferentially dilate the efferent arteriole by decreasing angiotensin II production, which reduces intraglomerular pressure
and slows the progression of diabetic nephropathy. This effect is independent of blood pressure reduction. Option A is incorrect because
ACE inhibitors do not directly dilate the afferent arteriole; NSAIDs do the opposite by constriction. Option C describes a secondary effect
but is not the primary mechanism of renal protection. Option B is incorrect because while bradykinin accumulation contributes to the
cough side effect, it is not the primary mechanism of renal protection.
Q2. A 72-year-old woman with hypertension and bilateral renal artery stenosis begins taking losartan. Two weeks later, her
serum creatinine rises from 1.0 mg/dL to 2.8 mg/dL. What is the most likely mechanism for this acute kidney injury?
A) Losartan-induced interstitial nephritis due to hypersensitivity reaction
B) Excessive reduction in angiotensin II causing loss of efferent arteriolar tone in a kidney dependent on angiotensin II for
filtration
C) Direct tubular toxicity from losartan metabolites accumulating in the renal cortex
D) Volume depletion from losartan's natriuretic effect without adequate oral fluid intake
Rationale:
In bilateral renal artery stenosis, glomerular filtration is critically dependent on angiotensin II-mediated efferent arteriolar constriction to
maintain intraglomerular pressure. ARBs like losartan block this compensatory mechanism, leading to a precipitous drop in GFR and
acute kidney injury. Option A is incorrect because interstitial nephritis is not a characteristic adverse effect of ARBs. Option C is incorrect
as losartan is not directly tubulotoxic. Option D describes a contributing factor but is not the primary pathophysiologic mechanism.
Page 3
