Paper I
2024 March (Supplementary) (2019 Scheme) · 100 marks · 180 min

Question

A 65-year-old lady presented with pain in both knees more on the left side. The pain is worsened by walking or standing for some time. X-Ray of knee shows narrowing of joint space, mild effusion and osteophytic projections. A diagnosis of Osteoarthritis of knee is made. She gave past history of ischemic heart disease a year back which was treated by angioplasty and a stent was placed. (

  • (a) Classify Non-steroidal Anti-Inflammatory Drugs (NSAIDs). ( 4 mark(s)
  • (b) Which NSAID will be suitable for reliving knee pain. Justify. ( 2 mark(s)
  • (c) Which NSAID is to be avoided. Why. ( 2 mark(s)
  • (d) Describe the mechanism of action, uses and adverse effects of Aspirin. 7 mark(s)
Q115 marksEssays

Answer

a) Classification of NSAIDs

ClassExamples
Non-selective COX inhibitorsIbuprofen, Naproxen, Diclofenac
Preferential COX-2 inhibitorsNimesulide, Meloxicam
Selective COX-2 inhibitorsCelecoxib, Etoricoxib
SalicylatesAspirin

b) NSAID suitable for this patient, with justification Naproxen — among non-selective NSAIDs, naproxen has the most favourable cardiovascular safety profile in large comparative trials, making it the preferred choice in a patient with a recent coronary stent and established ischemic heart disease, where minimizing added thrombotic risk is a priority alongside pain relief.

c) NSAID to avoid, and why Selective COX-2 inhibitors (e.g. Celecoxib, and also Diclofenac among non-selective agents) should be avoided — COX-2 inhibition suppresses vascular endothelial prostacyclin (an antiplatelet, vasodilator mediator) without the offsetting COX-1/thromboxane suppression that non-selective NSAIDs provide, shifting the hemostatic balance toward thrombosis — a specifically dangerous property in a patient with a recent stent and established coronary disease.

d) Aspirin — mechanism, uses, adverse effects Mechanism: irreversibly acetylates and inhibits cyclooxygenase (COX-1 and COX-2), blocking prostaglandin and thromboxane A2 synthesis. At low doses, predominantly and durably suppresses platelet thromboxane A2 (antiplatelet effect, since platelets cannot resynthesize COX); at higher doses, gives analgesic, antipyretic, and anti-inflammatory effects.

Uses: analgesia, antipyresis, anti-inflammatory use (high dose), antiplatelet prophylaxis (low dose) — particularly relevant to this patient, who would already be on low-dose aspirin post-stenting as part of dual antiplatelet therapy.

Adverse effects: GI irritation/peptic ulceration, increased bleeding risk, hypersensitivity/bronchospasm in aspirin-sensitive asthmatics, Reye’s syndrome (children with viral illness), salicylism/toxicity in overdose.

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