Non-steroidal anti-inflammatory drugs (NSAIDs) MCQs With Answer

Non-steroidal anti-inflammatory drugs (NSAIDs) MCQs With Answer

Non-steroidal anti-inflammatory drugs (NSAIDs) are a cornerstone of pharmacotherapy for pain, inflammation and fever. This concise, keyword-rich introduction covers NSAIDs’ pharmacology, mechanism of action as COX inhibitors, common agents (aspirin, ibuprofen, naproxen, diclofenac, celecoxib), therapeutic uses, adverse effects such as GI bleeding, renal toxicity and cardiovascular risk, and key drug interactions. B. Pharm students will benefit from focused coverage of COX-1 vs COX-2 selectivity, analgesic and antipyretic properties, prostaglandin synthesis inhibition, and clinical monitoring. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. Which enzyme is primarily inhibited by traditional NSAIDs to reduce prostaglandin synthesis?

  • Cyclooxygenase (COX)
  • Lipoxygenase (LOX)
  • Phospholipase A2
  • Monoamine oxidase

Correct Answer: Cyclooxygenase (COX)

Q2. Aspirin differs from most other NSAIDs because it:

  • Reversibly inhibits COX-2 only
  • Irreversibly acetylates COX enzymes
  • Is a selective LOX inhibitor
  • Does not affect platelet function

Correct Answer: Irreversibly acetylates COX enzymes

Q3. Which NSAID is a selective COX-2 inhibitor commonly used to reduce inflammation with lower GI risk?

  • Ibuprofen
  • Naproxen
  • Celecoxib
  • Aspirin

Correct Answer: Celecoxib

Q4. The major mechanism responsible for NSAID-induced renal toxicity is:

  • Direct tubular necrosis from free radicals
  • Inhibition of prostaglandin-mediated renal vasodilation
  • Activation of the renin-angiotensin system by LOX products
  • Immune complex deposition in glomeruli

Correct Answer: Inhibition of prostaglandin-mediated renal vasodilation

Q5. Which adverse effect is most characteristically associated with long-term NSAID use?

  • Hepatic cirrhosis
  • Gastrointestinal ulceration and bleeding
  • Paresthesia of extremities
  • Hypoglycemia

Correct Answer: Gastrointestinal ulceration and bleeding

Q6. Low-dose aspirin is used for cardioprotection because it:

  • Increases prostacyclin synthesis
  • Irreversibly inhibits platelet COX-1 and thromboxane A2 formation
  • Blocks ADP receptors on platelets
  • Promotes fibrinogen synthesis

Correct Answer: Irreversibly inhibits platelet COX-1 and thromboxane A2 formation

Q7. Which drug interaction is clinically significant with NSAIDs and increases the risk of bleeding?

  • NSAIDs with metformin
  • NSAIDs with warfarin
  • NSAIDs with omeprazole
  • NSAIDs with insulin

Correct Answer: NSAIDs with warfarin

Q8. Which NSAID is most associated with Reye’s syndrome risk in children and therefore contraindicated in viral infections?

  • Ibuprofen
  • Aspirin
  • Naproxen
  • Paracetamol (acetaminophen)

Correct Answer: Aspirin

Q9. An NSAID that has both analgesic and antipyretic effects but weak anti-inflammatory action is:

  • Diclofenac
  • Aspirin
  • Paracetamol (acetaminophen)
  • Indomethacin

Correct Answer: Paracetamol (acetaminophen)

Q10. Which NSAID is often used to close a patent ductus arteriosus (PDA) in neonates?

  • Ibuprofen
  • Aspirin
  • Naproxen
  • Celecoxib

Correct Answer: Ibuprofen

Q11. COX-2 selective inhibitors increase the risk of cardiovascular events primarily because:

  • They reduce prostacyclin (PGI2) without affecting thromboxane A2
  • They increase nitric oxide synthesis
  • They cause platelet aggregation by COX-1 activation
  • They inhibit angiotensin converting enzyme

Correct Answer: They reduce prostacyclin (PGI2) without affecting thromboxane A2

Q12. Which NSAID is commonly associated with causing hepatotoxicity and therefore requires monitoring of liver enzymes?

  • Diclofenac
  • Ibuprofen
  • Aspirin
  • Celecoxib

Correct Answer: Diclofenac

Q13. Which pharmacokinetic property commonly affects NSAID dosing and duration of action?

  • Volume of distribution in cerebrospinal fluid
  • Plasma protein binding
  • Ability to cross the blood-brain barrier via active transport only
  • Excretion unchanged in bile exclusively

Correct Answer: Plasma protein binding

Q14. NSAID-induced inhibition of prostaglandin E2 (PGE2) in the stomach leads to:

  • Increased gastric mucus and bicarbonate secretion
  • Decreased gastric acid secretion
  • Reduced gastric mucosal defense and increased ulcer risk
  • Stimulation of gastric epithelial cell proliferation

Correct Answer: Reduced gastric mucosal defense and increased ulcer risk

Q15. Which NSAID is known for its strong central analgesic effect and is used in gout flares due to potent anti-inflammatory action?

  • Indomethacin
  • Paracetamol
  • Aspirin
  • Naproxen

Correct Answer: Indomethacin

Q16. A patient on chronic NSAID therapy develops hypertension and edema. The most likely mechanism is:

  • NSAID-induced increase in aldosterone production
  • NSAID inhibition of renal prostaglandins causing sodium and water retention
  • Direct myocardial sodium channel blockade
  • Peripheral vasodilation from COX-2 inhibition

Correct Answer: NSAID inhibition of renal prostaglandins causing sodium and water retention

Q17. Which statement about non-acetylated salicylates compared to aspirin is true?

  • They irreversibly inhibit platelet COX-1
  • They have less antiplatelet effect and are better tolerated gastrically
  • They are more potent antipyretics than aspirin
  • They selectively inhibit COX-2

Correct Answer: They have less antiplatelet effect and are better tolerated gastrically

Q18. Which laboratory parameter should be monitored in patients on long-term NSAID therapy who are at risk of renal impairment?

  • Serum creatinine and electrolytes
  • Serum amylase
  • Fasting blood glucose
  • Serum bilirubin only

Correct Answer: Serum creatinine and electrolytes

Q19. Which NSAID classically causes closure of the ductus arteriosus by inhibiting prostaglandin synthesis?

  • Selective COX-2 inhibitors
  • Acetaminophen
  • Aspirin and other non-selective NSAIDs
  • Leukotriene inhibitors

Correct Answer: Aspirin and other non-selective NSAIDs

Q20. NSAID hypersensitivity presenting with bronchospasm, nasal polyps and aspirin sensitivity is known as:

  • Serotonin syndrome
  • Aspirin-exacerbated respiratory disease (AERD)
  • Anaphylactic shock
  • Stevens-Johnson syndrome

Correct Answer: Aspirin-exacerbated respiratory disease (AERD)

Q21. Combining NSAIDs with which antihypertensive class may reduce antihypertensive efficacy?

  • Beta-blockers
  • ACE inhibitors and ARBs
  • Calcium channel blockers
  • Direct renin inhibitors

Correct Answer: ACE inhibitors and ARBs

Q22. Which mechanism explains NSAID interference with the cardioprotective effect of low-dose aspirin?

  • NSAIDs enhance aspirin acetylation of COX-1
  • Some NSAIDs reversibly block platelet COX-1 binding site, preventing aspirin access
  • NSAIDs deplete vitamin K
  • NSAIDs increase thromboxane A2 synthesis

Correct Answer: Some NSAIDs reversibly block platelet COX-1 binding site, preventing aspirin access

Q23. Which NSAID is most appropriate for a patient requiring frequent dosing with minimal GI risk due to short half-life?

  • Naproxen (long half-life)
  • Ibuprofen (shorter half-life, reversible COX inhibition)
  • Celecoxib (long half-life, COX-2 selective)
  • Piroxicam (very long half-life)

Correct Answer: Ibuprofen (shorter half-life, reversible COX inhibition)

Q24. Which laboratory effect is commonly seen with aspirin overdose (salicylate toxicity)?

  • Metabolic alkalosis followed by respiratory acidosis
  • Mixed respiratory alkalosis and metabolic acidosis
  • Isolated metabolic acidosis only
  • Hypokalemic metabolic alkalosis

Correct Answer: Mixed respiratory alkalosis and metabolic acidosis

Q25. Enterohepatic recirculation can prolong the effect of some NSAIDs. Which property favors enterohepatic cycling?

  • High renal clearance as unchanged drug
  • Phase II glucuronidation with biliary excretion
  • Exclusive metabolism by CYP3A4 to polar metabolites
  • Very low plasma protein binding

Correct Answer: Phase II glucuronidation with biliary excretion

Q26. Which NSAID is contraindicated in the third trimester of pregnancy due to risk of premature closure of the fetal ductus arteriosus?

  • Paracetamol
  • Naproxen
  • Ibuprofen
  • Both Naproxen and Ibuprofen

Correct Answer: Both Naproxen and Ibuprofen

Q27. Inhibition of which prostaglandin is most directly responsible for the antipyretic effect of NSAIDs?

  • Thromboxane A2
  • Prostaglandin E2 (PGE2)
  • Prostacyclin (PGI2)
  • Leukotriene B4

Correct Answer: Prostaglandin E2 (PGE2)

Q28. Which NSAID is commonly used topically to reduce localized musculoskeletal pain with lower systemic exposure?

  • Topical diclofenac
  • Oral indomethacin
  • Intravenous ketorolac only
  • Systemic aspirin powder

Correct Answer: Topical diclofenac

Q29. Which statement about drug–drug interaction between NSAIDs and methotrexate is correct?

  • NSAIDs increase methotrexate renal clearance
  • NSAIDs decrease methotrexate toxicity by inducing hepatic enzymes
  • NSAIDs can reduce renal excretion of methotrexate and increase toxicity
  • There is no interaction; both are safe together

Correct Answer: NSAIDs can reduce renal excretion of methotrexate and increase toxicity

Q30. For B.Pharm students, which monitoring parameter is most important when initiating a COX-2 inhibitor in a patient with cardiovascular risk factors?

  • Serum glucose levels monthly
  • Blood pressure and signs of edema
  • Blindness screening monthly
  • Routine ECG weekly

Correct Answer: Blood pressure and signs of edema

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