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NSG 533 Exam 1 Advanced Pharmacology Questions And Answers 2026/2027 Wilkes University

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This document helps you master the NSG 533 Exam 1 Advanced Pharmacology exam at Wilkes University via targeted Q&A with detailed rationales. It covers pharmacokinetics and pharmacodynamics, drug metabolism and CYP450 interactions, pharmacogenomics, adverse drug reactions, drug interactions, autonomic nervous system pharmacology, cardiovascular and renal pharmacology, CNS agents, endocrine and metabolic pharmacology, antimicrobial pharmacotherapy, and gastrointestinal pharmacology. Engineered to maximize retention and sharpen clinical understanding, this test pack simplifies complex content, saving preparation time and helping you secure an A on your Exam 1 Assessment.

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,NSG 533 Exam 1 Advanced Pharmacology Questions And Answers
2026/2027 Wilkes University

Q1. Proton pump inhibitors suppress gastric acid secretion through
which mechanism?

A) Competitive blockade of histamine H1 receptors

B) Irreversible inhibition of the gastric H+/K+-ATPase

C) Neutralization of existing gastric acid within the lumen

D) Stimulation of prostaglandin degradation

Correct Answer: B) Irreversible inhibition of the gastric H+/K+-ATPase

Rationale: Proton pump inhibitors irreversibly inhibit the hydrogen-
potassium ATPase in gastric parietal cells, blocking the final step of acid
secretion. This produces more potent and sustained acid suppression than
histamine H2-receptor antagonists.

Q2. A person taking omeprazole for gastroesophageal reflux asks
when to take the medication for maximum effect. Which instruction
is most appropriate?

A) Take it only after symptoms begin

B) Take it immediately after the evening meal

C) Take it simultaneously with an antacid after every meal

D) Take it before a meal, preferably before breakfast

Correct Answer: D) Take it before a meal, preferably before breakfast

Rationale: Proton pumps become active in response to food. Administering
a PPI approximately 30–60 minutes before a meal allows adequate drug
absorption before maximal pump activation, improving acid suppression.

Q3. Which pharmacologic property best explains why famotidine
reduces gastric acid production?

A) It blocks histamine H2 receptors on parietal cells

B) It forms a physical coating over the entire stomach

C) It irreversibly inhibits proton pumps

D) It inhibits muscarinic receptors throughout the gastrointestinal tract

, Correct Answer: A) It blocks histamine H2 receptors on parietal cells

Rationale: Histamine stimulates gastric acid secretion through H2 receptors
on parietal cells. Famotidine competitively blocks these receptors, reducing
basal and stimulated acid secretion.

Q4. Long-term or high-intensity proton pump inhibitor therapy
warrants periodic reassessment primarily because prolonged acid
suppression has been associated with which concern?

A) Severe hyperglycemia

B) Irreversible adrenal suppression

C) Increased susceptibility to selected enteric infections and nutrient
abnormalities

D) Persistent bronchoconstriction

Correct Answer: C) Increased susceptibility to selected enteric infections
and nutrient abnormalities

Rationale: Sustained gastric acid suppression can alter gastrointestinal
microbial defenses and affect absorption of nutrients such as magnesium or
vitamin B12 in susceptible individuals. Long-term therapy should therefore
have a continuing clinical indication.

Q5. Which medication is most appropriate for protecting the gastric
mucosa in a high-risk patient who must continue long-term NSAID
therapy?

A) Diphenhydramine

B) Loperamide

C) A proton pump inhibitor

D) Metoclopramide

Correct Answer: C) A proton pump inhibitor

Rationale: NSAIDs inhibit prostaglandin synthesis and weaken mucosal
protection. PPIs substantially reduce gastric acid exposure and decrease the
risk of NSAID-associated ulcer formation and complications in high-risk
patients.

Q6. Misoprostol prevents NSAID-associated gastric injury through
which pharmacologic action?

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