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  • NSAIDs

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    razoraz
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    NSAIDs have three main therapeutic effects: anti-inflammatory, analgesic, and antipyretic effects. They work by modifying the inflammatory reaction and reducing certain types of pain and fever. Common side effects include gastric irritation, effects on renal function, prolonged bleeding, and increased risk of heart attack. NSAIDs inhibit the COX enzymes, with varying degrees of inhibition of COX-1 and COX-2. They produce antipyretic effects by inhibiting prostaglandin production in the hypothalamus. Analgesic effects occur both peripherally and centrally in the spinal cord by decreasing sensitization to pain. Anti-inflammatory effects are achieved by decreasing prostaglandins that cause vasodilation and edema

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    NSAIDs have three main therapeutic effects: anti-inflammatory, analgesic, and antipyretic effects. They work by modifying the inflammatory reaction and reducing certain types of pain and fever. Common side effects include gastric irritation, effects on renal function, prolonged bleeding, and increased risk of heart attack. NSAIDs inhibit the COX enzymes, with varying degrees of inhibition of COX-1 and COX-2. They produce antipyretic effects by inhibiting prostaglandin production in the hypothalamus. Analgesic effects occur both peripherally and centrally in the spinal cord by decreasing sensitization to pain. Anti-inflammatory effects are achieved by decreasing prostaglandins that cause vasodilation and edema

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    83 views2 pages

    NSAIDs

    Uploaded by

    razoraz
    NSAIDs have three main therapeutic effects: anti-inflammatory, analgesic, and antipyretic effects. They work by modifying the inflammatory reaction and reducing certain types of pain and fever. Common side effects include gastric irritation, effects on renal function, prolonged bleeding, and increased risk of heart attack. NSAIDs inhibit the COX enzymes, with varying degrees of inhibition of COX-1 and COX-2. They produce antipyretic effects by inhibiting prostaglandin production in the hypothalamus. Analgesic effects occur both peripherally and centrally in the spinal cord by decreasing sensitization to pain. Anti-inflammatory effects are achieved by decreasing prostaglandins that cause vasodilation and edema

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    Attribution Non-Commercial (BY-NC)
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    NSAIDS Main therapeutic effects: an anti-inflammatory effect: modification of the inflammatory reaction an analgesic effect: reduction of certain types

    pes of (especially inflammatory) pain an antipyretic effect: lowering of body temperature when this is raised in disease (i.e. fever)

    Side effects: gastric irritation, which may range from simple discomfort to ulcer formation an effect on renal blood flow in compromised kidney tends to prolong bleeding through inhibition of platelet function may also all-but especially COX-2 selective drugs-increase the likelihood of thrombotic events such as myocardial infarction by inhibiting prostaglandin (PG) I2 synthesis

    COX-1, COX-2: closely related, catalyse the same reaction, BUT COX-1 - constitutive enzyme expressed in most tissues, including blood platelets, 'housekeeping' role, involved in tissue homeostasis, and is responsible for production of prostaglandins COX-2 - induced in inflammatory cells when activated (important primary inflammatory cytokines: IL-1 and TNF-)

    NSAIDs and COX: NSAIDS inhibit both enzymes, but vary in degree in inhibition.

    NSAIDs Anti-pyretic effects: Fever disturbance to hypothalamic thermostat NSAIDs reset the thermostat. inhibition of prostaglandin production in the hypothalamus in inflammatory reaction > bacterial endotoxins cause release of IL-1 (a pyrogen) from macrophage -> E-type prostaglandin elevate temperature set point

    NSAIDs Analgesic effects: first, peripherally, they decrease production of the prostaglandins that sensitise nociceptors to inflammatory mediators such as bradykinin and are therefore effective in arthritis, bursitis etc. ability to relieve headache - abrogation of the vasodilator effect of prostaglandins on cerebral vasculature second, central action, in spinal cord -> inflammatory lesions increase prostaglandin release within the cord, causing facilitation of transmission from afferent pain fibres to relay neurons in the dorsal horn

    NSAIDs Anti-inflammatory effects:

    decrease in prostaglandin E2 and prostacyclin reduces vasodilatation and, indirectly, oedema

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