SN6 SHORT NOTE 5M ★ High-yield

Describe NSAID-induced peptic ulceration and its prevention.

Pharmacology · 2nd Professional — Para-Clinical

Mechanism of Nsaid-induced Mucosal Injury

NSAID inhibits COX-1 in the gastric mucosa → Loss of PGE2 and PGI2 → Reduced mucus and bicarbonate secretion, reduced mucosal blood flow, reduced epithelial restitution → Plus a direct topical irritant effect of the acidic drug, which becomes trapped in mucosal cells (ion trapping) → Erosions → ulceration → bleeding or perforation

The systemic effect matters more than the local one, which is why parenteral, rectal and enteric-coated preparations still cause ulcers — a point patients and prescribers frequently get wrong
Ulcers are often silent until they bleed or perforate, particularly in the elderly and in those on steroids, because the analgesic masks the pain

Risk Factors

Category	Factors
Patient	Age over 65; previous ulcer or gastrointestinal bleeding (the strongest single predictor); helicobacter pylori infection; serious comorbidity
Drug	High dose; long duration; more than one NSAID; the particular agent (piroxicam and ketorolac are among the worst; ibuprofen at low dose the least)
Concurrent drugs	Corticosteroids, anticoagulants, antiplatelets, SSRIs (which impair platelet serotonin) — each multiplies the risk
Lifestyle	Smoking, alcohol

CLINICAL PEARL

Low-dose aspirin is an NSAID for this purpose, and is the one most often forgotten. A patient on 75 mg of aspirin for the heart, an SSRI for mood and an occasional diclofenac for back pain is on three drugs that increase bleeding, none of which they would describe as strong medicine. Risk assessment means reviewing the whole list, not the NSAID alone.

Prevention

Strategy	Comment
Avoid the NSAID	Paracetamol, topical NSAIDs, physiotherapy, weight loss and exercise are genuinely effective for many musculoskeletal problems
Lowest dose, shortest duration	And review rather than repeat prescriptions indefinitely
Proton pump inhibitor	The standard co-prescription; effective, cheap and well tolerated
Misoprostol	Proven to reduce ulcer complications, but diarrhoea and abortifacient action limit its use
H2 blockers	Less effective than a proton pump inhibitor; standard doses do not prevent gastric ulcers
Selective COX-2 inhibitor	Halves gastric risk but adds cardiovascular risk; and the benefit is lost if the patient also takes aspirin
Test and treat H. Pylori	Before starting long-term NSAID therapy in a patient with a history of ulcer

Management of an Established NSAID Ulcer

Stop the NSAID if at all possible — the single most effective measure
Full-dose proton pump inhibitor for 4 to 8 weeks
Test for and eradicate H. Pylori
If the NSAID cannot be stopped, continue the proton pump inhibitor indefinitely and use the least toxic agent at the lowest dose
Endoscopy for alarm features — bleeding, anaemia, weight loss, vomiting, dysphagia, or age over 50 with new symptoms

Applied Aspects

Ask every patient with dyspepsia or anaemia about over-the-counter painkillers; in India these are bought freely and are rarely volunteered as "medicines"
Check haemoglobin in anyone on long-term NSAIDs, since chronic occult blood loss is common and silent
Never prescribe two NSAIDs together — the risk is additive and the benefit is not; this includes forgetting that the patient is already on aspirin
Consider topical NSAIDs for localised joint pain; systemic absorption is a small fraction of oral dosing with much lower gastric risk
Irrational fixed-dose combinations of two NSAIDs, or an NSAID with other agents, remain a problem in India and many have been banned

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