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NSG 5240 Advanced Pharmacology Final Exam 2026/2027 | South College Study Guide, Practice Questions & Answers

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• Comprehensive NSG 5240 Advanced Pharmacology exam preparation resource designed for South College nursing students, featuring focused practice questions and answers to reinforce key pharmacology concepts and support effective final-exam review. • Covers important Advanced Pharmacology concepts, medication principles, therapeutic considerations, adverse effects, drug interactions, and clinical decision-making areas commonly emphasized in nursing coursework. • Includes practice-focused questions with answer guidance to help identify knowledge gaps, strengthen recall, and improve confidence before the NSG 5240 Final Exam. • Useful for structured review alongside course materials, lectures, and personal study notes, helping you organize preparation more efficiently. • Also relevant for students reviewing NSG 5140 Midterm and Final Exam concepts where pharmacology knowledge overlaps with advanced nursing coursework. • Convenient digital study resource designed for focused, flexible exam preparation and last-minute review.

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NSG 5240 Advanced Pharmacology Final
Exam 2026/2027 | South College Study
Guide, Practice Questions & Answers

NSG 5240 ADVANCED PHARMACOLOGY FINAL EXAM 2026/2027
South College Study Guide, Practice Questions & Answers



OVERVIEW:

• This comprehensive 200-question study guide is designed to reinforce and assess
your mastery of advanced pharmacology principles, drug mechanisms, and clinical
applications essential for nursing practice.

• Use this material to identify knowledge gaps across all major pharmacological
categories, practice time management under exam conditions, and build
confidence in applying pharmacological concepts to real-world patient care
scenarios.



QUESTION 1

A 65-year-old male with hypertension is prescribed lisinopril, an ACE inhibitor.
Which of the following best describes the primary mechanism of action of this
drug?

A) Blocking beta-adrenergic receptors to decrease heart rate and contractility

B) Inhibiting the conversion of angiotensin I to angiotensin II

C) Directly relaxing vascular smooth muscle

D) Increasing renal sodium excretion without affecting the renin-angiotensin
system

E) Blocking calcium influx into cardiac and vascular smooth muscle cells

CORRECT ANSWER: B) Inhibiting the conversion of angiotensin I to angiotensin
II

,Rationale: ACE inhibitors work by blocking the enzyme responsible for converting
angiotensin I to angiotensin II, a potent vasoconstrictor. This reduces systemic
vascular resistance, decreases aldosterone secretion, and ultimately lowers blood
pressure. Options A, C, and E describe mechanisms of other antihypertensive drug
classes. Option D is incorrect because ACE inhibitors do not directly increase
sodium excretion.



QUESTION 2

A patient on warfarin presents with an INR of 8.5 (therapeutic range 2-3).
Which vitamin is used to reverse warfarin toxicity?

A) Vitamin A

B) Vitamin B12

C) Vitamin C

D) Vitamin K

E) Vitamin E

CORRECT ANSWER: D) Vitamin K

Rationale: Vitamin K is a cofactor required for the synthesis of clotting factors II,
VII, IX, and X. Warfarin inhibits vitamin K-dependent carboxylation of these factors.
Administration of vitamin K (phytonadione) reverses warfarin's anticoagulant effect
by restoring clotting factor synthesis. Fresh frozen plasma or prothrombin complex
concentrate may be used for rapid reversal in emergency situations.



QUESTION 3

Which of the following antiarrhythmic drugs works primarily by blocking
sodium channels and is classified as a Class I agent?

A) Amiodarone

B) Verapamil

,C) Procainamide

D) Beta-blockers

E) Digoxin

CORRECT ANSWER: C) Procainamide

Rationale: Procainamide is a Class Ia antiarrhythmic that blocks sodium channels,
decreasing the rate of depolarization and conduction velocity. While amiodarone
also has Class I activity, it is primarily classified as a Class III agent. Verapamil is a
Class IV (calcium channel blocker), beta-blockers are Class II, and digoxin is Class IV
with unique properties.



QUESTION 4

A 45-year-old female with type 2 diabetes is started on metformin. Which of
the following best explains how metformin reduces blood glucose levels?

A) Stimulating insulin secretion from pancreatic beta cells

B) Decreasing hepatic glucose production and increasing peripheral glucose uptake

C) Inhibiting alpha-glucosidase enzymes in the small intestine

D) Blocking SGLT2 transporters in the renal tubules

E) Increasing GLP-1 receptor signaling

CORRECT ANSWER: B) Decreasing hepatic glucose production and increasing
peripheral glucose uptake

Rationale: Metformin reduces blood glucose primarily by inhibiting hepatic
gluconeogenesis and enhancing peripheral glucose utilization without stimulating
insulin secretion. This results in improved insulin sensitivity. Options A, C, D, and E
describe mechanisms of other antidiabetic drug classes.



QUESTION 5

, Which of the following is a major adverse effect of statins that requires
patient monitoring and can potentially lead to treatment discontinuation?

A) Hyperkalemia

B) Muscle myopathy and rhabdomyolysis

C) Hyponatremia

D) Acute kidney injury

E) Hypercalcemia

CORRECT ANSWER: B) Muscle myopathy and rhabdomyolysis

Rationale: Statins inhibit HMG-CoA reductase, which not only reduces cholesterol
synthesis but also depletes mevalonate-derived products essential for muscle
function. This can lead to statin-induced muscle myopathy, ranging from mild
myalgia to severe rhabdomyolysis with potential acute renal failure. Patients should
be counseled to report muscle pain or weakness immediately.



QUESTION 6

A patient receiving gentamicin, an aminoglycoside antibiotic, develops acute
kidney injury. Which of the following best explains this toxicity?

A) Direct hepatotoxicity

B) Nephrotoxicity due to accumulation in renal proximal tubule cells

C) Hypersensitivity reaction

D) Hypomagnesemia

E) Ototoxicity

CORRECT ANSWER: B) Nephrotoxicity due to accumulation in renal proximal
tubule cells

Rationale: Aminoglycosides are primarily eliminated by the kidneys and
accumulate in renal proximal tubule cells, causing dose-dependent nephrotoxicity.
Risk factors include prolonged therapy, high doses, volume depletion, concurrent

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