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NSG 533 Exam 2 Advanced Pharmacology Questions And Answers 2026/2027 Wilkes University

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This document helps you master the NSG 533 Exam 2 Advanced Pharmacology exam at Wilkes University via targeted Q&A with detailed rationales. It covers pharmacokinetics and pharmacodynamics; pharmacogenomics and CYP450 drug interactions; pain management including the WHO analgesic ladder and opioid side effects; cardiovascular pharmacology with antihypertensives, antiarrhythmics, and anticoagulants; endocrine therapies for diabetes, thyroid, and adrenal disorders; respiratory pharmacology including asthma and COPD management; and psychopharmacology with antidepressants and mood stabilizers. Engineered to maximize retention and sharpen clinical judgment, this test pack simplifies complex content, saving preparation time and helping you secure an A on your Exam 2 Assessment.

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,NSG 533 Exam 2 Advanced Pharmacology Questions And Answers
2026/2027 Wilkes University

Q1. Nonsteroidal anti-inflammatory drugs reduce inflammatory pain
primarily through which pharmacologic mechanism?

A) Activation of central mu-opioid receptors

B) Inhibition of cyclooxygenase and reduction of prostaglandin synthesis

C) Enhancement of GABA-mediated neuronal inhibition

D) Blockade of voltage-gated calcium channels

Correct Answer: B) Inhibition of cyclooxygenase and reduction of
prostaglandin synthesis

Rationale: NSAIDs inhibit cyclooxygenase enzymes responsible for
prostaglandin synthesis. Reduced prostaglandin production decreases
peripheral sensitization, inflammation, pain, and fever. The same mechanism
also contributes to gastrointestinal, renal, and cardiovascular adverse
effects.

Q2. Compared with a nonselective NSAID, a selective COX-2 inhibitor
generally provides which pharmacologic advantage?

A) Complete elimination of cardiovascular risk

B) Greater platelet inhibition

C) Less inhibition of protective gastric COX-1 activity

D) Complete absence of renal adverse effects

Correct Answer: C) Less inhibition of protective gastric COX-1 activity

Rationale: Selective COX-2 inhibitors preferentially suppress inflammatory
prostaglandin production while sparing more COX-1 activity in gastric mucosa
and platelets. This can reduce gastrointestinal ulceration relative to some
nonselective NSAIDs, although renal and cardiovascular risks remain
important.

Q3. Severe acetaminophen overdose produces hepatic injury
primarily after excessive formation of which toxic metabolite?

A) NAPQI

B) Prostaglandin E2

, C) Salicylate

D) Bradykinin

Correct Answer: A) NAPQI

Rationale: Most acetaminophen undergoes safe conjugation, but a small
fraction is converted to NAPQI. Overdose depletes glutathione, allowing
NAPQI to bind hepatocellular proteins and produce potentially severe hepatic
necrosis.

Q4. When opioid therapy is warranted for new acute pain, which
formulation is generally preferred when initiating treatment?

A) Extended-release morphine

B) Transdermal fentanyl

C) Long-acting oxycodone

D) Immediate-release opioid

Correct Answer: D) Immediate-release opioid

Rationale: Immediate-release formulations are preferred when initiating
opioids for acute pain because exposure can be more closely matched to the
expected short duration of severe pain. Extended-release and long-acting
products create prolonged exposure and greater risk in opioid-naive patients.

Q5. Concurrent use of an opioid and a benzodiazepine creates
particular concern for which complication?

A) Severe hypertension

B) Additive sedation and respiratory depression

C) Hyperthyroidism

D) Acute uric acid nephropathy

Correct Answer: B) Additive sedation and respiratory depression

Rationale: Both medication classes depress central nervous system activity.
When combined, sedation and ventilatory suppression can be amplified,
substantially increasing the risk of respiratory compromise, overdose, coma,
and death.

Q6. Naloxone reverses opioid-induced respiratory depression
principally by acting as what?

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