Anti-inflammatory agents – Sulindac MCQs With Answer
Sulindac is a widely studied nonsteroidal anti-inflammatory drug (NSAID) and prodrug used in analgesia and inflammatory disorders. This introduction covers sulindac’s mechanism of action as a COX inhibitor, hepatic activation to the active sulfide metabolite, pharmacokinetics (absorption, protein binding, enterohepatic recycling), clinical uses in rheumatoid and osteo-arthritis, common adverse effects (GI, renal, hypersensitivity), drug interactions (warfarin, ACE inhibitors, diuretics), and monitoring considerations important for B.Pharm students. These focused points help build a solid pharmacology foundation for exam preparation and clinical practice. Now let’s test your knowledge with 50 MCQs on this topic.
Q1. Which statement best describes sulindac’s status as a drug?
- Sulindac is an active NSAID that directly inhibits COX enzymes without metabolic conversion
- Sulindac is a prodrug that is converted in the liver to an active sulfide metabolite
- Sulindac is a selective COX-2 inhibitor structurally related to celecoxib
- Sulindac is an opioid analgesic used for severe pain
Correct Answer: Sulindac is a prodrug that is converted in the liver to an active sulfide metabolite
Q2. The primary pharmacodynamic action of sulindac sulfide is:
- Stimulation of prostaglandin synthesis
- Irreversible inhibition of acetylcholinesterase
- Reversible inhibition of cyclooxygenase (COX) enzymes reducing prostaglandin synthesis
- Blockade of TNF-alpha receptors
Correct Answer: Reversible inhibition of cyclooxygenase (COX) enzymes reducing prostaglandin synthesis
Q3. Which metabolite of sulindac is pharmacologically active?
- Sulindac sulfone
- Sulindac sulfide
- Parent sulindac only
- Sulindac glucuronide
Correct Answer: Sulindac sulfide
Q4. Sulindac’s reduced gastrointestinal toxicity compared with some NSAIDs is partly due to:
- It being highly selective for COX-2 only
- Its prodrug nature with hepatic activation and enterohepatic cycling which lowers gastric mucosal exposure
- Its inability to inhibit prostaglandin synthesis
- Its administration only by intravenous route
Correct Answer: Its prodrug nature with hepatic activation and enterohepatic cycling which lowers gastric mucosal exposure
Q5. Which clinical indication is sulindac commonly used for?
- Bacterial infections
- Rheumatoid arthritis and osteoarthritis
- Type 1 diabetes mellitus
- Parkinson’s disease
Correct Answer: Rheumatoid arthritis and osteoarthritis
Q6. The main adverse effect of sulindac that requires monitoring is:
- Hypoglycemia
- Gastrointestinal bleeding and ulceration
- Hearing loss
- Hyperthyroidism
Correct Answer: Gastrointestinal bleeding and ulceration
Q7. Sulindac interacts with warfarin primarily by:
- Enhancing warfarin metabolism leading to reduced INR
- Displacing warfarin from plasma proteins and inhibiting platelet function, increasing bleeding risk
- Acting as a vitamin K analog
- Increasing warfarin renal excretion
Correct Answer: Displacing warfarin from plasma proteins and inhibiting platelet function, increasing bleeding risk
Q8. Sulindac is contraindicated or used with caution in which condition?
- Osteoporosis
- Pregnancy, especially in the third trimester
- Seasonal allergic rhinitis
- Myopia
Correct Answer: Pregnancy, especially in the third trimester
Q9. The mechanism by which NSAIDs like sulindac can cause renal impairment involves:
- Direct destruction of glomerular basement membrane by sulindac
- Reduced prostaglandin-mediated renal blood flow leading to decreased glomerular filtration
- Activation of renin-angiotensin system independent of prostaglandins
- Inhibition of renal sodium channels directly
Correct Answer: Reduced prostaglandin-mediated renal blood flow leading to decreased glomerular filtration
Q10. Which statement about sulindac pharmacokinetics is correct?
- Sulindac is primarily excreted unchanged in urine
- Sulindac undergoes hepatic reduction to an active sulfide and oxidative conversion to a sulfone
- Sulindac has no enterohepatic recirculation
- Sulindac is administered as an inhaled spray for systemic action
Correct Answer: Sulindac undergoes hepatic reduction to an active sulfide and oxidative conversion to a sulfone
Q11. Which laboratory parameter should be monitored during long-term sulindac therapy?
- Serum amylase only
- Renal function (serum creatinine) and liver enzymes
- Serum insulin
- Pulmonary function tests
Correct Answer: Renal function (serum creatinine) and liver enzymes
Q12. Sulindac’s analgesic effect is primarily due to:
- Central opioid receptor agonism
- Inhibition of prostaglandin synthesis which reduces peripheral sensitization of nociceptors
- Blocking sodium channels in neurons
- Increasing serotonin levels in synapses
Correct Answer: Inhibition of prostaglandin synthesis which reduces peripheral sensitization of nociceptors
Q13. Which enzyme family is directly inhibited by sulindac sulfide?
- Cyclooxygenases (COX-1 and COX-2)
- CYP3A4 exclusively
- Monoamine oxidase
- DNA polymerase
Correct Answer: Cyclooxygenases (COX-1 and COX-2)
Q14. Enterohepatic recycling of sulindac contributes to:
- Decreased drug half-life
- Prolonged duration of action and possible prolonged exposure of GI mucosa
- Exclusive renal excretion
- Immediate drug inactivation
Correct Answer: Prolonged duration of action and possible prolonged exposure of GI mucosa
Q15. Which of the following is a common dose form for sulindac?
- Intravenous infusion only
- Oral tablets
- Transdermal patch
- Nasal spray
Correct Answer: Oral tablets
Q16. Sulindac’s chemical class is best described as:
- A sulfonylurea antidiabetic
- An indene acetic acid derivative (sulfinyl indene acetic acid)
- A benzodiazepine
- A macrolide antibiotic
Correct Answer: An indene acetic acid derivative (sulfinyl indene acetic acid)
Q17. A major advantage of sulindac over some other NSAIDs is:
- Complete absence of adverse effects
- Prodrug feature that may reduce direct gastric mucosal irritation
- Absolute selectivity for COX-1 leading to less bleeding
- It increases platelet aggregation
Correct Answer: Prodrug feature that may reduce direct gastric mucosal irritation
Q18. Sulindac sulfide’s inhibition of COX reduces formation of which mediator?
- Adenosine triphosphate (ATP)
- Prostaglandins
- Corticosteroids
- Insulin
Correct Answer: Prostaglandins
Q19. Which of the following adverse reactions is associated with sulindac and should prompt discontinuation?
- Mild headache lasting an hour
- Skin rash or signs of hypersensitivity such as Stevens-Johnson syndrome
- Temporary mild dry mouth
- Transient increase in appetite
Correct Answer: Skin rash or signs of hypersensitivity such as Stevens-Johnson syndrome
Q20. Sulindac may reduce the antihypertensive effect of which drug class?
- Beta blockers only
- ACE inhibitors and diuretics due to reduced prostaglandin-mediated renal effects
- Calcium channel blockers by CYP induction
- Statins by direct receptor blockade
Correct Answer: ACE inhibitors and diuretics due to reduced prostaglandin-mediated renal effects
Q21. In patients with a history of peptic ulcer disease, sulindac should be:
- Prescribed at high doses without precautions
- Used with caution; consider gastroprotection (PPI) or alternative therapy
- Used topically to avoid GI effects
- Combined with another NSAID for synergistic effect
Correct Answer: Used with caution; consider gastroprotection (PPI) or alternative therapy
Q22. Which metabolic pathway is important for activation of sulindac?
- Reduction of the sulfoxide to sulfide in the liver
- Hydrolysis by peptidases in plasma
- Oxidative deamination in kidneys
- Direct phosphorylation by kinases
Correct Answer: Reduction of the sulfoxide to sulfide in the liver
Q23. Sulindac sulfone is generally considered:
- The most active COX inhibitor metabolite
- An inactive or less active oxidative metabolite
- A neurotransmitter analog
- A pro-coagulant compound
Correct Answer: An inactive or less active oxidative metabolite
Q24. The risk of cardiovascular events with NSAIDs like sulindac is thought to arise from:
- Enhanced prostacyclin (PGI2) production only
- An imbalance between thromboxane A2 and prostacyclin leading to prothrombotic state
- Direct myocardial necrosis unrelated to COX
- Activation of beta-adrenergic receptors
Correct Answer: An imbalance between thromboxane A2 and prostacyclin leading to prothrombotic state
Q25. Which patient factor may prolong sulindac action and requires dose adjustment?
- Young age with hypermetabolism
- Severe hepatic impairment affecting reduction and clearance
- Recent vaccination
- High dietary fiber intake
Correct Answer: Severe hepatic impairment affecting reduction and clearance
Q26. Which monitoring sign could indicate sulindac-induced renal dysfunction?
- Decreased serum creatinine
- Increased serum creatinine and reduced urine output
- Increased hair growth
- Improved hearing
Correct Answer: Increased serum creatinine and reduced urine output
Q27. For B.Pharm students, the mechanism-based classification of sulindac is:
- Nonsteroidal anti-inflammatory drug (NSAID) with COX inhibition
- Anti-epileptic sodium channel blocker
- Benzodiazepine receptor agonist
- ACE inhibitor
Correct Answer: Nonsteroidal anti-inflammatory drug (NSAID) with COX inhibition
Q28. Which statement about sulindac and platelet function is correct?
- Sulindac irreversibly inhibits platelet aggregation like aspirin
- Sulindac can impair platelet aggregation reversibly, increasing bleeding risk
- Sulindac enhances platelet aggregation
- Sulindac has no effect on platelets
Correct Answer: Sulindac can impair platelet aggregation reversibly, increasing bleeding risk
Q29. Which co-administration increases risk of GI bleeding with sulindac?
- Proton pump inhibitors
- Low-dose aspirin or other NSAIDs
- Folic acid supplements
- Topical emollients
Correct Answer: Low-dose aspirin or other NSAIDs
Q30. Sulindac’s bioactivation requires which organ primarily?
- Kidney
- Liver
- Lungs
- Spleen
Correct Answer: Liver
Q31. Which adverse effect is more likely with sulindac compared to paracetamol?
- Hepatotoxicity and gastric ulceration
- Severe hypoglycemia
- Bronchospasm only seen with paracetamol
- Neuromuscular blockade
Correct Answer: Hepatotoxicity and gastric ulceration
Q32. Sulindac’s absorption after oral administration is generally described as:
- Poor and unpredictable with zero bioavailability
- Well absorbed from the gastrointestinal tract with good oral bioavailability
- Only absorbed when given intravenously
- Only absorbed via the transdermal route
Correct Answer: Well absorbed from the gastrointestinal tract with good oral bioavailability
Q33. Which patient history should raise caution before prescribing sulindac?
- History of controlled seasonal allergies only
- History of peptic ulcer disease and bleeding disorders
- Previous appendectomy decades ago
- History of mild myopia
Correct Answer: History of peptic ulcer disease and bleeding disorders
Q34. Which statement about sulindac and asthma is relevant?
- NSAIDs like sulindac can precipitate bronchospasm in aspirin-sensitive asthmatics
- Sulindac is the preferred NSAID in aspirin-exacerbated respiratory disease
- Sulindac cures asthma by anti-inflammatory action
- Sulindac has no respiratory effects
Correct Answer: NSAIDs like sulindac can precipitate bronchospasm in aspirin-sensitive asthmatics
Q35. Which metabolic product of sulindac is associated with lower COX inhibition?
- Sulindac sulfide (active)
- Sulindac sulfone (less active/inactive)
- Sulindac phosphate (nonexistent)
- Acetyl-sulindac (irrelevant)
Correct Answer: Sulindac sulfone (less active/inactive)
Q36. Which drug interaction is important to counsel about when starting sulindac?
- Concurrent use with metformin increases glucose levels
- Concurrent use with anticoagulants increases bleeding risk
- Concurrent use with vitamin C potentiates sulindac analgesia
- Concurrent use with topical steroids causes systemic steroid levels to fall
Correct Answer: Concurrent use with anticoagulants increases bleeding risk
Q37. Sulindac’s effect on prostaglandins in the gastric mucosa leads to:
- Increased mucous and bicarbonate secretion
- Decreased protective prostaglandins causing mucosal vulnerability
- Enhanced mucosal blood flow exclusively
- Immediate mucosal regeneration
Correct Answer: Decreased protective prostaglandins causing mucosal vulnerability
Q38. In pharmacology exams, sulindac is often contrasted with which NSAID due to differing COX selectivity?
- Acetaminophen (paracetamol)
- Aspirin or celecoxib to discuss COX-1 vs COX-2 selectivity
- Insulin
- Amoxicillin
Correct Answer: Aspirin or celecoxib to discuss COX-1 vs COX-2 selectivity
Q39. Which population requires dose adjustment or close monitoring when using sulindac?
- Patients with severe hepatic impairment and the elderly
- Healthy young adults with no comorbidities
- Patients with nearsightedness only
- Those taking daily multivitamins
Correct Answer: Patients with severe hepatic impairment and the elderly
Q40. Which test would be useful before starting chronic sulindac therapy?
- Baseline liver function tests and renal function tests
- Baseline audiometry
- Visual field testing
- Skin biopsy
Correct Answer: Baseline liver function tests and renal function tests
Q41. Sulindac’s analgesic dosing strategy for acute pain commonly emphasizes:
- Single lifetime dose only
- Using the lowest effective dose for the shortest duration to limit adverse effects
- High-dose continuous therapy regardless of response
- Using it only in combination with opioids
Correct Answer: Using the lowest effective dose for the shortest duration to limit adverse effects
Q42. Which structural feature differentiates sulindac from classical arylpropionic acids like ibuprofen?
- Sulindac contains a sulfoxide group in an indene acetic acid framework
- Sulindac is a peptide
- Sulindac is a steroidal molecule
- Sulindac is identical in structure to ibuprofen
Correct Answer: Sulindac contains a sulfoxide group in an indene acetic acid framework
Q43. Which adverse effect profile is most likely less pronounced with sulindac because it is a prodrug?
- Hepatic enzyme elevations
- Direct topical gastric mucosal irritation compared with non-prodrug NSAIDs
- Systemic renal effects
- CNS sedation
Correct Answer: Direct topical gastric mucosal irritation compared with non-prodrug NSAIDs
Q44. Sulindac’s active sulfide form is regenerated from the sulfoxide by which type of reaction?
- Oxidation
- Reduction
- Hydrolysis
- Photolysis
Correct Answer: Reduction
Q45. Which adverse hematologic effect can occur with sulindac use?
- Agranulocytosis and aplastic anemia in rare cases
- Polycythemia vera as a common effect
- Immediate erythropoietin surge
- Guaranteed thrombocytosis
Correct Answer: Agranulocytosis and aplastic anemia in rare cases
Q46. Which counselling point is appropriate for a patient starting sulindac?
- Take on an empty stomach always to improve absorption
- Report any signs of GI bleeding, rash, or reduced urine output; take with food to reduce GI upset
- Stop other antihypertensives immediately
- Increase alcohol intake to enhance efficacy
Correct Answer: Report any signs of GI bleeding, rash, or reduced urine output; take with food to reduce GI upset
Q47. Which assay type could be used to measure sulindac or metabolites in plasma for pharmacokinetic studies?
- High-performance liquid chromatography (HPLC) with UV or mass spectrometric detection
- Urine dipstick only
- Potentiometric glucose test
- Visual color matching
Correct Answer: High-performance liquid chromatography (HPLC) with UV or mass spectrometric detection
Q48. Sulindac may be preferred in some patients over other NSAIDs because:
- It has no effect on renal prostaglandins
- Its prodrug properties may reduce direct gastric irritation and it has an active systemic metabolite
- It is completely free of drug interactions
- It causes immediate platelet activation
Correct Answer: Its prodrug properties may reduce direct gastric irritation and it has an active systemic metabolite
Q49. Which descriptor best summarizes sulindac’s COX selectivity?
- Highly COX-2 selective like celecoxib
- Nonselective COX inhibitor with activity against both COX-1 and COX-2 after activation
- No interaction with COX enzymes
- Exclusive COX-3 inhibitor
Correct Answer: Nonselective COX inhibitor with activity against both COX-1 and COX-2 after activation
Q50. For an exam question on drug interactions, combining sulindac with which drug requires caution due to increased lithium levels?
- Metformin
- Thiazide diuretics and NSAIDs can increase lithium levels; caution is needed
- Propranolol lowers lithium levels
- Vitamin D prevents lithium interaction
Correct Answer: Thiazide diuretics and NSAIDs can increase lithium levels; caution is needed

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.
Mail- Sachin@pharmacyfreak.com