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Nonsteroidal Anti-inflammatoryAka: Non-Steroidal Antiinflammatory, Non-Opioid Analgesics, NSAID

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  1. See Also
    1. Acetaminophen
    2. Pediatric Analgesics
    3. Narcotic Analgesics
  2. Mechanism
    1. Blocks Cyclooxygenase (COX)
    2. COX Enzyme converts arachidonic acid to PGG2
    3. COX1 Enzyme
      1. Location
        1. Gastric mucosa and intestinal mucosa
        2. Platelets
        3. Renal
        4. Vascular endothelium
      2. Inhibition Effects
        1. Predisposes to gastric or intestinal ulcers
        2. Predisposes to bleeding (anti-platelet adhesion)
        3. No anti-inflammatory effect
        4. Renal effects
          1. Fluid retention
          2. Decreased Glomerular Filtration Rate (GFR)
    4. COX2 Enzyme
      1. Location
        1. Brain
        2. Renal (ascending tubule, macula densa)
        3. Adenoma (colon)
        4. Cytokine-induced (inflammation related)
      2. Inhibition Effects
        1. Anti-inflammatory action
        2. Analgesic action
        3. Predisposes to renal injury in hypovolemia
        4. Decreased malignant potential of Colonic Polyps
        5. May have benefit in Alzheimer's Disease
  3. Adverse Effects
    1. NSAID Gastrointestinal Adverse Effects
    2. NSAID Renal Adverse Effects
    3. Bleeding risk
      1. Reversible inhibition of platelet aggregation
      2. Associated with standard NSAIDs (esp. Naprosyn)
      3. COX2 Inhibitors have minimal effect on bleeding
    4. Headache
    5. CNS effects (essp. Indomethacin)
    6. Interferes with Aspirin anti-platelet effects
      1. Avoid NSAIDs in patients with vascular disease
      2. Diclofenac may least effect platelet activity
      3. Take Aspirin 2 hours before or 8 hours post-Ibuprofen
      4. Take Aspirin 36 hours after last Naproxen
      5. Steinhubl (2005) Am College Card 45:1302
  4. Monitoring: Protocol for NSAID use in elderly
    1. Labs: Obtain at baseline and q3-12 months
      1. Complete Blood Count (CBC)
      2. Creatinine
      3. Liver Function Tests
    2. Review of Systems for NSAID adverse effects
      1. Nausea or Vomiting
      2. Dark stools or bloody stools
      3. Dyspepsia
      4. Cognitive changes
    3. References
      1. Lipsky (2000) J Rheumatol 27:1338
  5. Preparations: Non-Narcotic alternatives to NSAIDs
    1. Acetaminophen (Tylenol)
    2. Non-acetylated Salicylate
    3. Low dose Prednisone (Rheumatoid Arthritis)
    4. Single joint local Corticosteroid Injection
  6. Preparations: COX2 Selective NSAID
    1. Celecoxib (Celebrex) 200 mg PO qd-bid
    2. Rofecoxib (Vioxx) 25-50 mg PO qd
  7. Preparations: Acetic acids
    1. Partially COX2 selective (less GI adverse effects)
      1. Etodolac (Lodine) 200-400 mg PO bid-tid
        1. Etodolac 400 mg superior to Aspirin 650 mg
      2. Etodolac XL (Lodine XL) 400-1200 mg qd
      3. Nabumetone (Relafen) 1000 mg PO qd-bid
    2. Indoles
      1. Indomethacin 25-50 mg PO/PR tid
      2. Sulindac (Clinoril) 150-200 mg PO bid
      3. Tolmetin sodium (Tolectin) 200-600 mg PO tid
    3. Pyrrolo-pyrroles: Parenteral NSAID
      1. Ketorolac tromethamine (Toradol)
  8. Preparations: Salicylates
    1. Acetylsalicylic acid (Aspirin) 500-1000 mg q4-6 hours
    2. Trisalicylate (Trilisate) 1000-1500 mg q8-12 hours
    3. Diflunisal (Dolobid) 500 mg q8-12 hours
      1. Superior and longer acting than Aspirin 650 mg
      2. Superior and longer acting than Acetaminophen 650 mg
    4. Salsalate (Disalcid)
    5. Sodium Salicylate (Uracil 5)
    6. Sodium thiosalicylate (Tusal)
  9. Preparations: Propionic Acids
    1. Ibuprofen (Motrin)
      1. Ibuprofen 400 mg comparable to Tylenol #3
    2. Naproxen (Naprosyn) 500 mg q12 hours
      1. Naproxen 500 mg superior to Aspirin 650
    3. Naproxen Sodium (Anaprox) 550 mg q12 hours
      1. Naproxen Sodium 550 mg superior to Aspirin 650
    4. Flurbiprofen (Ansaid) 200-300 mg/day divided bid-qid
    5. Fenoprofen (Nalfon) 200 mg q4-6 hours
      1. Similar to Aspirin
      2. Avoid in renal insufficiency
    6. Ketoprofen (Orudis) 25-75 mg q6-8 hours
      1. Ketoprofen 25 mg comparable to Ibuprofen 400 mg
      2. Ketoprofen 50 mg more potent than Tylenol #3
    7. Oxaprozin (Daypro) 1200 mg qd
  10. Preparations: Oxicams
    1. General
      1. Long half life (once a day dosing)
    2. Isoxicam (Maxicam)
    3. Piroxicam (Feldene) 20 mg qd
  11. Preparations: Fenamate
    1. Meclofenamate (Meclomen) 50-100 mg PO q4-6 hours
      1. Comparable to Aspirin
    2. Diclofenac (Voltaren, Arthrotec)
      1. Oral:
        1. Diclofenac 50 mg PO q8 hours (Comparable to Aspirin)
        2. Arthrotec (50 mg Diclofenac with 200 mcg Misoprostel)
      2. Topical
        1. Diclofenac Gel
        2. Flector Patch (applied to most painful area every 12 hours)
  12. References
    1. Wolfe (1999) N Engl J Med 340:1888
    2. (2000) Med Lett Drugs Ther 42(1085):73
    3. (2000) Tarascon Pocket Pharmacopoeia

Anti-Inflammatory Agents, Non-Steroidal (C0003211)

Definition (MSH)Anti-inflammatory agents that are not steroids. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They are used primarily in the treatment of chronic arthritic conditions and certain soft tissue disorders associated with pain and inflammation. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. Certain NSAIDs also may inhibit lipoxygenase enzymes or TYPE C PHOSPHOLIPASES or may modulate T-cell function. (AMA Drug Evaluations Annual, 1994, p 1814-5)
Definition (NCI)A group of drugs that decrease fever, swelling, pain, and redness.
Definition (CSP)agents that counteract or suppress inflammation and are not steroids; most have in addition analgesic, antipyretic, and platelet-inhibitory actions; they act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins: inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects.
Definition (NCI)Anti-inflammatory agents that are not steroids. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They are used primarily in the treatment of chronic arthritic conditions and certain soft tissue disorders associated with pain and inflammation. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. Certain NSAIDs also may inhibit lipoxygenase enzymes or phospholipase C or may modulate T-cell function. (MeSH)
ConceptsPharmacologic Substance (T121)
EnglishAIANS, ANTI INFLAMM AGENTS NONSTEROIDAL, ANTIINFLAMM AGENTS NON STEROIDAL, ANTIINFLAMMATORY AGENTS NONSTEROIDAL, NON STEROIDAL ANTI INFLAMM AGENTS, Non Steroidal Anti Inflammatory Agents, Nonsteroidal Anti Inflammatory Agents, nonsteroidal antiinflammatory agent, Nonsteroidal Antiinflammatory Agents, Nonsteroidal Antiinflammatory Drug, NSAIA, NSAID, NSAIDs
Spanishagente antiinflamatorio no esteroide, agente antinflamatorio no esteroide, AINE, antiinflamatorio no esteroide, antinflamatorio no esteroide, droga antinflamatoria no esteroide
CreditsDerived from the NIH UMLS (Unified Medical Language System)



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