NURS 5334 Advanced Pharmacology Practice Test |
2026/2027 Edition | 250 Verified Questions
NURS 5334 Exam 2 Latest Practice Test 2026-2027 QUESTIONS AND ANSWERS ALREADY
GRADED A+. 100% Verified Solutions | Updated Per Latest Guidelines | Graded A+
This comprehensive practice test for NURS 5334 Advanced Pharmacology Exam 2 features 250
meticulously verified questions with detailed correct answers and rationales. Designed to reflect the
latest 2026/2027 curriculum at the University of Texas at Arlington (UTA), this resource covers
pharmacokinetics, pharmacodynamics, drug classifications, and clinical applications. Each question is
accompanied by evidence-based explanations to reinforce learning and ensure exam readiness. Ideal
for students seeking to master advanced pharmacology concepts and achieve top scores.
Key Features:
Pharmacokinetics and Pharmacodynamics
Autonomic Nervous System Drugs
Cardiovascular Pharmacology
Central Nervous System Agents
Antimicrobial Therapy
Endocrine and Respiratory Pharmacology
Updates for 2026:
- Updated to reflect 2026/2027 UTA NURS 5334 curriculum changes
- Incorporated latest FDA-approved drug indications and warnings
- Enhanced rationales with current clinical practice guidelines
- Added new questions on emerging pharmacotherapies
- Revised distractors to improve critical thinking assessment
Abstract:
This advanced pharmacology practice test is meticulously curated for NURS 5334 Exam 2 at the University of
Texas at Arlington, encompassing 250 verified questions that align with the 2026/2027 academic year. The content
spans essential topics including pharmacokinetic principles, autonomic and cardiovascular pharmacology, central
nervous system agents, antimicrobial therapy, and endocrine/respiratory drugs. Each question is paired with a
correct answer and a detailed rationale that explains the underlying mechanism, clinical application, and evidence
base. The test emphasizes higher-order thinking by incorporating clinical scenarios and drug interactions,
preparing students for both the exam and real-world prescribing. Updated to reflect the latest guidelines from the
FDA and professional organizations, this resource ensures that learners engage with current, accurate
information. The structured format allows for systematic review, with questions organized by content area and
difficulty, facilitating targeted study. By mastering these questions, students will solidify their understanding of
pharmacotherapeutic principles and improve their ability to make safe, effective prescribing decisions.
Keywords:
Advanced Pharmacology, NURS 5334, Exam 2, Practice Test, Pharmacokinetics, Pharmacodynamics, Drug
Classifications, Clinical Pharmacology
Answer Format:
Each question includes the correct answer in bold, followed by a detailed rationale explaining the pharmacological
basis, clinical relevance, and why incorrect options are wrong. Distractors are analyzed to clarify common
misconceptions, and rationales cite current guidelines and primary literature where applicable.
Compliance Checklist:
Page 1
, Aligned with 2026/2027 UTA NURS 5334 syllabus
Questions verified by subject matter experts
Rationales updated per latest FDA and clinical guidelines
Includes both knowledge recall and application-level questions
Covers all major drug classes tested on Exam 2
Designed to simulate actual exam format and difficulty
Content Area Overview:
Content Area Questions Key Topics Weight
Pharmacokinetics and 1-40 Absorption, Distribution, Metabolism, 16%
Pharmacodynamics Excretion, Receptor Theory, Dose-Response
Autonomic Nervous System 41-80 Cholinergics, Anticholinergics, Adrenergics, 16%
Drugs Adrenergic Blockers
Cardiovascular Pharmacology 81-130 Antihypertensives, Antiarrhythmics, 20%
Antianginals, Heart Failure Drugs,
Anticoagulants
Central Nervous System Agents 131-170 Anxiolytics, Antidepressants, 16%
Antipsychotics, Antiepileptics, Opioids
Antimicrobial Therapy 171-210 Antibacterials, Antivirals, Antifungals, 16%
Antiparasitics, Resistance Mechanisms
Endocrine and Respiratory 211-250 Insulin, Oral Hypoglycemics, 16%
Pharmacology Corticosteroids, Thyroid Drugs,
Bronchodilators
Page 2
,Q1. A patient with atrial fibrillation is receiving warfarin. The international normalized ratio (INR) is 4.2,
and the patient has no signs of bleeding. Which of the following is the most appropriate management
strategy?
A. Administer vitamin K 10 mg intravenously and hold warfarin for one dose.
B. Hold warfarin, monitor INR daily, and resume at a lower dose when INR is therapeutic.
C. Administer fresh frozen plasma (FFP) 2 units and continue warfarin at the same dose.
D. Administer prothrombin complex concentrate (PCC) and discontinue warfarin permanently.
Correct Answer: B. Hold warfarin, monitor INR daily, and resume at a lower dose when INR is therapeutic.
Rationale: An INR of 4.2 without bleeding indicates a supratherapeutic but non-critical level. According to CHEST
guidelines, holding warfarin and monitoring INR is appropriate; vitamin K is reserved for INR >4.5 with bleeding
risk or >10. FFP and PCC are for major bleeding. Permanent discontinuation is not indicated.
Why Wrong:
A - Vitamin K is indicated for INR >4.5 with bleeding risk or >10; this INR does not meet criteria for
reversal.
C - FFP is indicated for active bleeding, not for asymptomatic elevation; continuing warfarin would worsen
INR.
D - PCC is for life-threatening bleeding; permanent discontinuation is not necessary as warfarin can be
resumed at lower dose.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 34
Q2. Which of the following best explains the mechanism by which metformin reduces hepatic glucose
production?
A. Activation of AMP-activated protein kinase (AMPK) in hepatocytes.
B. Inhibition of alpha-glucosidase in the small intestine.
C. Stimulation of insulin secretion from pancreatic beta cells.
D. Blockade of sodium-glucose cotransporter 2 (SGLT2) in renal tubules.
Correct Answer: A. Activation of AMP-activated protein kinase (AMPK) in hepatocytes.
Rationale: Metformin primarily activates AMPK in the liver, which reduces gluconeogenesis and fatty acid
synthesis, thereby decreasing hepatic glucose output. It does not stimulate insulin secretion (sulfonylureas do),
inhibit alpha-glucosidase (acarbose), or block SGLT2 (empagliflozin).
Why Wrong:
B - Alpha-glucosidase inhibitors delay carbohydrate absorption, not hepatic glucose production.
C - Metformin does not stimulate insulin secretion; that is the mechanism of sulfonylureas.
D - SGLT2 inhibitors increase urinary glucose excretion, not reduce hepatic production.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 48
Q3. A patient with type 2 diabetes and chronic kidney disease (eGFR 35 mL/min/1.73m²) is being started on
an SGLT2 inhibitor. Which of the following is the most important consideration regarding this therapy?
A. SGLT2 inhibitors are contraindicated when eGFR is below 45 mL/min/1.73m².
B. The dose must be reduced by 50% for patients with eGFR below 60 mL/min/1.73m².
C. SGLT2 inhibitors are not recommended for glycemic control when eGFR is below 45, but may be continued
for cardiorenal benefits.
D. SGLT2 inhibitors require therapeutic drug monitoring to avoid accumulation.
Correct Answer: C. SGLT2 inhibitors are not recommended for glycemic control when eGFR is below 45,
but may be continued for cardiorenal benefits.
Rationale: Current guidelines (ADA, KDIGO) state that SGLT2 inhibitors lose glycemic efficacy at eGFR <45, but
they still provide cardiovascular and renal protective benefits, so they may be continued. They are not
contraindicated, dose reduction is not standard, and therapeutic drug monitoring is not required.
Page 3
, Why Wrong:
A - SGLT2 inhibitors are not contraindicated; they can be used with caution for renal protection.
B - No dose adjustment is needed for renal impairment; efficacy diminishes but safety profile remains.
D - Therapeutic drug monitoring is not indicated for SGLT2 inhibitors; they have a wide safety margin.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 48; ADA Standards of Care 2026
Q4. A patient with major depressive disorder has not responded to adequate trials of two different SSRIs and
one SNRI. Which of the following augmentation strategies is most supported by evidence for
treatment-resistant depression?
A. Adding a second-generation antipsychotic such as aripiprazole.
B. Switching to a monoamine oxidase inhibitor (MAOI) as monotherapy.
C. Adding a benzodiazepine to enhance antidepressant effect.
D. Adding omega-3 fatty acids at a dose of 2 g/day.
Correct Answer: A. Adding a second-generation antipsychotic such as aripiprazole.
Rationale: Augmentation with atypical antipsychotics (e.g., aripiprazole, quetiapine) is a first-line strategy for
treatment-resistant depression, supported by multiple RCTs and STAR*D. MAOIs are reserved for later lines due to
safety concerns. Benzodiazepines do not treat depression, and omega-3s have modest evidence at best.
Why Wrong:
B - MAOIs are effective but require dietary restrictions and have serious interactions; they are not first-line
augmentation.
C - Benzodiazepines may worsen depression and are not antidepressant; they are used for anxiety.
D - Omega-3 fatty acids have inconsistent evidence and are not considered a standard augmentation strategy.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 16; APA Practice Guidelines 2025
Q5. A patient with acute heart failure is receiving intravenous furosemide. Which of the following laboratory
findings is most consistent with the development of furosemide-induced ototoxicity?
A. Serum potassium 3.0 mEq/L
B. Serum creatinine 2.5 mg/dL
C. Serum sodium 128 mEq/L
D. Serum albumin 2.0 g/dL
Correct Answer: B. Serum creatinine 2.5 mg/dL
Rationale: Furosemide ototoxicity is dose-dependent and more common in patients with renal impairment (elevated
creatinine). Hypokalemia, hyponatremia, and hypoalbuminemia are associated with furosemide use but are not
direct risk factors for ototoxicity. Renal dysfunction reduces drug clearance, increasing risk.
Why Wrong:
A - Hypokalemia is a common adverse effect but not a risk factor for ototoxicity.
C - Hyponatremia is not associated with furosemide ototoxicity.
D - Hypoalbuminemia may affect protein binding but is not a primary risk factor for ototoxicity.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 43
Q6. A patient with hypertension is started on lisinopril. After two weeks, the patient develops a dry cough.
Which of the following mechanisms best explains this adverse effect?
A. Accumulation of bradykinin due to inhibition of angiotensin-converting enzyme.
B. Direct irritation of bronchial mucosa by the drug.
C. Increased prostaglandin synthesis in the lungs.
D. Beta-receptor blockade leading to bronchoconstriction.
Correct Answer: A. Accumulation of bradykinin due to inhibition of angiotensin-converting enzyme.
Rationale: ACE inhibitors block the degradation of bradykinin, leading to its accumulation in the lungs, which
stimulates cough receptors. This is not due to direct irritation, prostaglandins, or beta-blockade. The cough is a
Page 4
2026/2027 Edition | 250 Verified Questions
NURS 5334 Exam 2 Latest Practice Test 2026-2027 QUESTIONS AND ANSWERS ALREADY
GRADED A+. 100% Verified Solutions | Updated Per Latest Guidelines | Graded A+
This comprehensive practice test for NURS 5334 Advanced Pharmacology Exam 2 features 250
meticulously verified questions with detailed correct answers and rationales. Designed to reflect the
latest 2026/2027 curriculum at the University of Texas at Arlington (UTA), this resource covers
pharmacokinetics, pharmacodynamics, drug classifications, and clinical applications. Each question is
accompanied by evidence-based explanations to reinforce learning and ensure exam readiness. Ideal
for students seeking to master advanced pharmacology concepts and achieve top scores.
Key Features:
Pharmacokinetics and Pharmacodynamics
Autonomic Nervous System Drugs
Cardiovascular Pharmacology
Central Nervous System Agents
Antimicrobial Therapy
Endocrine and Respiratory Pharmacology
Updates for 2026:
- Updated to reflect 2026/2027 UTA NURS 5334 curriculum changes
- Incorporated latest FDA-approved drug indications and warnings
- Enhanced rationales with current clinical practice guidelines
- Added new questions on emerging pharmacotherapies
- Revised distractors to improve critical thinking assessment
Abstract:
This advanced pharmacology practice test is meticulously curated for NURS 5334 Exam 2 at the University of
Texas at Arlington, encompassing 250 verified questions that align with the 2026/2027 academic year. The content
spans essential topics including pharmacokinetic principles, autonomic and cardiovascular pharmacology, central
nervous system agents, antimicrobial therapy, and endocrine/respiratory drugs. Each question is paired with a
correct answer and a detailed rationale that explains the underlying mechanism, clinical application, and evidence
base. The test emphasizes higher-order thinking by incorporating clinical scenarios and drug interactions,
preparing students for both the exam and real-world prescribing. Updated to reflect the latest guidelines from the
FDA and professional organizations, this resource ensures that learners engage with current, accurate
information. The structured format allows for systematic review, with questions organized by content area and
difficulty, facilitating targeted study. By mastering these questions, students will solidify their understanding of
pharmacotherapeutic principles and improve their ability to make safe, effective prescribing decisions.
Keywords:
Advanced Pharmacology, NURS 5334, Exam 2, Practice Test, Pharmacokinetics, Pharmacodynamics, Drug
Classifications, Clinical Pharmacology
Answer Format:
Each question includes the correct answer in bold, followed by a detailed rationale explaining the pharmacological
basis, clinical relevance, and why incorrect options are wrong. Distractors are analyzed to clarify common
misconceptions, and rationales cite current guidelines and primary literature where applicable.
Compliance Checklist:
Page 1
, Aligned with 2026/2027 UTA NURS 5334 syllabus
Questions verified by subject matter experts
Rationales updated per latest FDA and clinical guidelines
Includes both knowledge recall and application-level questions
Covers all major drug classes tested on Exam 2
Designed to simulate actual exam format and difficulty
Content Area Overview:
Content Area Questions Key Topics Weight
Pharmacokinetics and 1-40 Absorption, Distribution, Metabolism, 16%
Pharmacodynamics Excretion, Receptor Theory, Dose-Response
Autonomic Nervous System 41-80 Cholinergics, Anticholinergics, Adrenergics, 16%
Drugs Adrenergic Blockers
Cardiovascular Pharmacology 81-130 Antihypertensives, Antiarrhythmics, 20%
Antianginals, Heart Failure Drugs,
Anticoagulants
Central Nervous System Agents 131-170 Anxiolytics, Antidepressants, 16%
Antipsychotics, Antiepileptics, Opioids
Antimicrobial Therapy 171-210 Antibacterials, Antivirals, Antifungals, 16%
Antiparasitics, Resistance Mechanisms
Endocrine and Respiratory 211-250 Insulin, Oral Hypoglycemics, 16%
Pharmacology Corticosteroids, Thyroid Drugs,
Bronchodilators
Page 2
,Q1. A patient with atrial fibrillation is receiving warfarin. The international normalized ratio (INR) is 4.2,
and the patient has no signs of bleeding. Which of the following is the most appropriate management
strategy?
A. Administer vitamin K 10 mg intravenously and hold warfarin for one dose.
B. Hold warfarin, monitor INR daily, and resume at a lower dose when INR is therapeutic.
C. Administer fresh frozen plasma (FFP) 2 units and continue warfarin at the same dose.
D. Administer prothrombin complex concentrate (PCC) and discontinue warfarin permanently.
Correct Answer: B. Hold warfarin, monitor INR daily, and resume at a lower dose when INR is therapeutic.
Rationale: An INR of 4.2 without bleeding indicates a supratherapeutic but non-critical level. According to CHEST
guidelines, holding warfarin and monitoring INR is appropriate; vitamin K is reserved for INR >4.5 with bleeding
risk or >10. FFP and PCC are for major bleeding. Permanent discontinuation is not indicated.
Why Wrong:
A - Vitamin K is indicated for INR >4.5 with bleeding risk or >10; this INR does not meet criteria for
reversal.
C - FFP is indicated for active bleeding, not for asymptomatic elevation; continuing warfarin would worsen
INR.
D - PCC is for life-threatening bleeding; permanent discontinuation is not necessary as warfarin can be
resumed at lower dose.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 34
Q2. Which of the following best explains the mechanism by which metformin reduces hepatic glucose
production?
A. Activation of AMP-activated protein kinase (AMPK) in hepatocytes.
B. Inhibition of alpha-glucosidase in the small intestine.
C. Stimulation of insulin secretion from pancreatic beta cells.
D. Blockade of sodium-glucose cotransporter 2 (SGLT2) in renal tubules.
Correct Answer: A. Activation of AMP-activated protein kinase (AMPK) in hepatocytes.
Rationale: Metformin primarily activates AMPK in the liver, which reduces gluconeogenesis and fatty acid
synthesis, thereby decreasing hepatic glucose output. It does not stimulate insulin secretion (sulfonylureas do),
inhibit alpha-glucosidase (acarbose), or block SGLT2 (empagliflozin).
Why Wrong:
B - Alpha-glucosidase inhibitors delay carbohydrate absorption, not hepatic glucose production.
C - Metformin does not stimulate insulin secretion; that is the mechanism of sulfonylureas.
D - SGLT2 inhibitors increase urinary glucose excretion, not reduce hepatic production.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 48
Q3. A patient with type 2 diabetes and chronic kidney disease (eGFR 35 mL/min/1.73m²) is being started on
an SGLT2 inhibitor. Which of the following is the most important consideration regarding this therapy?
A. SGLT2 inhibitors are contraindicated when eGFR is below 45 mL/min/1.73m².
B. The dose must be reduced by 50% for patients with eGFR below 60 mL/min/1.73m².
C. SGLT2 inhibitors are not recommended for glycemic control when eGFR is below 45, but may be continued
for cardiorenal benefits.
D. SGLT2 inhibitors require therapeutic drug monitoring to avoid accumulation.
Correct Answer: C. SGLT2 inhibitors are not recommended for glycemic control when eGFR is below 45,
but may be continued for cardiorenal benefits.
Rationale: Current guidelines (ADA, KDIGO) state that SGLT2 inhibitors lose glycemic efficacy at eGFR <45, but
they still provide cardiovascular and renal protective benefits, so they may be continued. They are not
contraindicated, dose reduction is not standard, and therapeutic drug monitoring is not required.
Page 3
, Why Wrong:
A - SGLT2 inhibitors are not contraindicated; they can be used with caution for renal protection.
B - No dose adjustment is needed for renal impairment; efficacy diminishes but safety profile remains.
D - Therapeutic drug monitoring is not indicated for SGLT2 inhibitors; they have a wide safety margin.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 48; ADA Standards of Care 2026
Q4. A patient with major depressive disorder has not responded to adequate trials of two different SSRIs and
one SNRI. Which of the following augmentation strategies is most supported by evidence for
treatment-resistant depression?
A. Adding a second-generation antipsychotic such as aripiprazole.
B. Switching to a monoamine oxidase inhibitor (MAOI) as monotherapy.
C. Adding a benzodiazepine to enhance antidepressant effect.
D. Adding omega-3 fatty acids at a dose of 2 g/day.
Correct Answer: A. Adding a second-generation antipsychotic such as aripiprazole.
Rationale: Augmentation with atypical antipsychotics (e.g., aripiprazole, quetiapine) is a first-line strategy for
treatment-resistant depression, supported by multiple RCTs and STAR*D. MAOIs are reserved for later lines due to
safety concerns. Benzodiazepines do not treat depression, and omega-3s have modest evidence at best.
Why Wrong:
B - MAOIs are effective but require dietary restrictions and have serious interactions; they are not first-line
augmentation.
C - Benzodiazepines may worsen depression and are not antidepressant; they are used for anxiety.
D - Omega-3 fatty acids have inconsistent evidence and are not considered a standard augmentation strategy.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 16; APA Practice Guidelines 2025
Q5. A patient with acute heart failure is receiving intravenous furosemide. Which of the following laboratory
findings is most consistent with the development of furosemide-induced ototoxicity?
A. Serum potassium 3.0 mEq/L
B. Serum creatinine 2.5 mg/dL
C. Serum sodium 128 mEq/L
D. Serum albumin 2.0 g/dL
Correct Answer: B. Serum creatinine 2.5 mg/dL
Rationale: Furosemide ototoxicity is dose-dependent and more common in patients with renal impairment (elevated
creatinine). Hypokalemia, hyponatremia, and hypoalbuminemia are associated with furosemide use but are not
direct risk factors for ototoxicity. Renal dysfunction reduces drug clearance, increasing risk.
Why Wrong:
A - Hypokalemia is a common adverse effect but not a risk factor for ototoxicity.
C - Hyponatremia is not associated with furosemide ototoxicity.
D - Hypoalbuminemia may affect protein binding but is not a primary risk factor for ototoxicity.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 43
Q6. A patient with hypertension is started on lisinopril. After two weeks, the patient develops a dry cough.
Which of the following mechanisms best explains this adverse effect?
A. Accumulation of bradykinin due to inhibition of angiotensin-converting enzyme.
B. Direct irritation of bronchial mucosa by the drug.
C. Increased prostaglandin synthesis in the lungs.
D. Beta-receptor blockade leading to bronchoconstriction.
Correct Answer: A. Accumulation of bradykinin due to inhibition of angiotensin-converting enzyme.
Rationale: ACE inhibitors block the degradation of bradykinin, leading to its accumulation in the lungs, which
stimulates cough receptors. This is not due to direct irritation, prostaglandins, or beta-blockade. The cough is a
Page 4
