1. NSAIDs function by inhibiting COX and therefore leading to less prostaglandin synthesis.
    • Aspirin irreversibly inhibits COX.
    • Non-COX selective NSAIDs reversibly inhibit COX.
    • Selective COX-2 NSAIDs will not have anti-platelet function.
  2. Comparative effects as follows:
    • COX-2 drugs have less GI effects, but increased oedema and HTN.
    • NSAIDs overall will decrease the sensitivity of blood vessels to bradykinin and histamine, affect lymphokine production from T-cells and reverse vasodilation associated with inflammation.
      1. All NSAIDs will have analgesic/anti-pyretic and anti-inflammatory effects.
    • All NSAIDs (except the COX-2 specific ones) have anti-platelet activity.
    • Some NSAIDs (including aspirin) are thought to reduce colon cancer risk.
    • With respect to GI effects:
      1. Ibuprofen thought to have the least GIT effects.
      2. Piroxicam has 9x the GIT effects.
      3. Aspirin has double the GIT effects.
      4. Indomethacin may cause pancreatitis.
  1. PO. Some may be given IV or IM.
    • Importantly, food does not lower its bioavailability.
  1. All are weak acids and therefore absorbed well in the GIT.
  2. They are all highly protein bound (>98% to albumin).
  3. They are all found in high concentration in synovial fluids.
  1. Hepatic, by CYP systems and phase 2 reactions.
  1. Renal
Special precautions  
  1. Lithium – may increase lithium levels secondary to reducing renal blood flow.
  2. Increased risk of bleeding with other anticoagulants.
Adverse events
  1. Toxic effects
    • Mainly GIT (gastritis, nausea/vomiting, ulcers and bleeding)
    • Renal – AKI (probably secondary to altered renal blood flow due to reduced prostaglandin synthesis)
    • Hepatic – abnormal LFTs and rarely, hepatic failure.
    • CNS – tinnitus, dizziness and headaches.
  1. Good supportive care


Withdrawal syndrome  
Special notes