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Therapeutic strategies – the relief of symptoms and the maintenance of function; the slowing
or arrest of the tissue-damaging process
NSAIDS
- Suppress the signs and symptoms of inflammation including pain; also exerts
antipyretic effects
- All but one of the NSAIDs are weak organic acids as given; the exception, nabumetone,
is a ketone prodrug that is metabolized to the acidic active drug
- All NSAIDs can be found in the synovial fluid after repeated dosing
- NSAIDs anti-inflammatory activity is mediated chiefly through inhibition of
prostaglandin biosynthesis.
- Aspirin irreversibly acetylates and blocks platelet COX, while the non-COX-selective
NSAIDs are reversible inhibitors
- Selective COX-2 inhibitors do not affect platelet function at their usual doses; increases
the incidence of edema, hypertension, and possibly,myocardial infarction (Celecoxib &
Meloxicam)
- NSAIDs decrease the sensitivity of vessels to bradykinin and histamine, affect
lymphokine production from T lymphocytes, and reverse vasodilation of inflammation
- All newer NSAIDs are analgesic, anti-inflammatory, and antipyretic and all (except
selective COX2 inhibitors) inhibit platelet aggregation
- Reduce the incidence of colon cancer when taken chronically
- Aspirin – now rarely used as an anti-inflammatory medication, used for its antiplatelet
effect
- Irreversibly inhibits platelet COX so that aspirin’s antiplatelet effect lasts 8-10 dyas.