Anti inflammatory drugs flashcards


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Anti inflammatory drugs flashcards

  2. 2. NSAIDS  Salicyclates  Aspirin  Mesalamine  Sodium-salicyclate  Propionic Acid Derivatives  Ibuprofen  Ketoprofen  Naproxen  Acetic Acid Derivatives  Diclofenac  Ketorolac  Oxicams  Piroxicam  Meloxicam  Indole Derivatives  Indomethacin  Selective COX-2 Inhibitors  Celecoxib
  3. 3. Analgesic-Antipyretic Drugs Anti-Inflammatory Steroids  Acetaminophen  Beclomethasone  Betamethasone  Budesonide  Cortisone  Dexamethasone  Hydrocortisone  Prednisone  Triamcinolone
  4. 4. NSAIDS  MoA: reversible, competitive inhibition of COX  Irreversible inactivation by Aspirin  Most block COX-1 and -2  Celecoxib is COX-2 inhibitor  Inhibit synthesis of PGs but NOT leukotrienes  Indomethacin is extremely potent  Reduce elevated temperature due to PGE1 & PGE2  Analgesic and antipyretic effects do not undergo tolerance  Toxicity: Acute renal failure & Nephrotic syndrome
  5. 5. Agents Effect NSAID Block Effect PGE2, PGI2, PGD2 Enhance early stages of inflammation Anti-inflammatory PGE2, PGI2 Pain receptors in peripherals Peripheral analgesic effect PGE1, PGE2 Increase body temp set Antipyretic point
  6. 6. SALICYCLATES  RS: moderate/high doses stimulate; toxic dose     depresses US: high doses cause inhibition of uric acid reabsorption, decrease GFR  hypovolemia  acute renal failure; chronic doses can cause renal lesions Hematopoietic: low/moderate = decreased platelet aggregation (decrease TXA2, increase PGI2); high dose = sideropenia (iron deficiency) Uses: general analgesic, Ulcerative colitis and Crohns’ disease (mesalamine & olsalazine), Thromboemolic disease prophylaxis Toxicity: 1% hypersensitivity, 15% adverse effects (heartburn, nausea, fecal blood loss, gastric bleeding, tinnitus, deafness, vertigo), toxicity in pregnancy, Reye’s syndrome in children, Analgesic nephropathy
  7. 7. Non-Salicyclate NSAIDS  All effects similar to salicyclates  Greatest analgesic agent efficacy: Ketorolac  Greatest anti-inflammatory: Indomethacin, Piroxicam, Diclofenac  MoA: COX-1 inhibition: indomethacin, piroxicam  COX-2 inhibition: celecoxib, meloxicam  COX-1 and 2 inhibitors: ibuprofen, naproxen, diclofenac
  8. 8. Non-Salicyclate NSAIDS  Propionic Acid Derivatives  MoA: reversible competitive inhibition of COX  Acetic Acid Derivates  MoA: reversible competitive inhibition of COX and decrease in oxygen radicals  Diclofenac: ankylosing spondylitis, eye inflammation, chronic tx of Rheumatoid Arthritis  Ketorolac: analgesic agent, 60% excreted by kidneys  renal damage  Oxicams  MoA: piroxicam is potent reversible COX-1 inhibition; meloxicam for COX-2  Piroxicam has 100% oral bio and ~50 hr half life
  9. 9. Indomethacin  Powerful COX-1 inhibitor  Also inhibits:  PLA2  PMN cell migration  T-Cell and B-Cell proliferation  Everything else is same as other NSAIDS  Can’t be used as antipyretic or analgesic agent due to toxicity  Uses: Barter’s syndrome, PDA, nephrogenic diabetes insipidus
  10. 10. Analgesic-Antipyretic Drugs  Acetaminophen  95% biotransformed in liver  Small amount toxic metabolite formed  NAPQI  hepatotoxicity  Potent COX inhibitor in CNS; weak in inflamed tissues
  11. 11. Anti-Inflammatory Steroids  Glucocorticoids  MoA:  Alters #, distribution, function of peripheral      macrophages; decreases leukocytes, macros, cyto, etc Inhibition of PG and LT synthesis Decrease postcapillary permeability Inhibits effects of complement system Strong inhibitors of cellular immunity Weak inhibitors of humoral immunity  Diagnostic use:  Dexamethasone suppression test used for differential diagnosis of Cushing’s Syndrome
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