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Non Steroidal Anti Inflammatory Drugs, Nonopioid Analgesics

Non Steroidal Anti Inflammatory Drugs, Nonopioid Analgesics. By S.Bohlooli, PhD. The immune reponse. May lead to Cure More injury Eicosanoids Kinins Neuroptides Histamine Cytokines Free radicals. Therapeutic strategies. Relief of Pain

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Non Steroidal Anti Inflammatory Drugs, Nonopioid Analgesics

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  1. Non Steroidal Anti Inflammatory Drugs, Nonopioid Analgesics By S.Bohlooli, PhD

  2. The immune reponse • May lead to • Cure • More injury • Eicosanoids • Kinins • Neuroptides • Histamine • Cytokines • Free radicals

  3. Therapeutic strategies • Relief of Pain • Slowing or arresting the tissue damaging process • Drugs • NSAIDs • Glucocoticoids • Slow acting antirheumatic drugs: • Disease modifying antirheumatic drugs

  4. Non steroidal anti inflammatory drugs Chemistry & Pharmacokinetics Pharmacodynamics

  5. Chemistry

  6. Chemistry

  7. Pharmacokinetics

  8. Pharmacokinetics

  9. Pharmacodynamics • Inhibition of synthesis of prostaglandines • Inhibition of cyclooxygenase isoforms • Inhibition of chemotaxis • Down regulation of interleukin-1 • Decreased production of free radicals • Interface with calcium mediated intracellular events

  10. Pharmacodynamics

  11. Aspirin • Pharmcokinetics • Mechanism of action • Anti-inflammatory effects • Nonselective inhibitor of COX • Non-acetylated salicylate may work as oxygen scavenger • Analgesic effect • Antipyretic effect • Inhibition of COX in CNS • Inhibition of IL-1production • Antiplatelet effecys

  12. Clinical use • Mild to moderate pain • With opioids for cancer pain • High dose for: • Rheumatic fever • Rheumatic arthritis and other joint conditions • Decreased incidence of • Transient ischemic attacks • Coronary artery thrombosis • Colon cancer • May valuable in treating preeclampsia-eclampsia

  13. Adverse effect • Gastrointestinal upset • Gastric and duodenal ulcers • Hepatotoxicity • Bleeding • Asthma • Rashes • Renal toxicity • Upper gastrointestinal bleeding • Salicylism ( vomiting, tinnitus, vertigo)

  14. Cox-2 selective inhibitors • Developed in attempt to inhibit the synthesis of PGs in the site of inflammation • Many of them are sulfonamide derivatives • Some evidence suggests higher cardiovascular thrombotic event • Cox-2 is constitutively active within kidney so renal toxicity is documented for this group of drugs • Documented edema and hypertension

  15. Cox-2 selective inhibitors • Celecoxib • Etoricoxib: with highest ratio of selectivity • Meloxicam • Refecoxib • Valdecoxib

  16. Diclofenac Diflunisal Etodolac Fenoprofen Flurbiprofen Ibuprofen indomethacin Tenoxicam Tiaprofen tolmetin Ketoprofen Ketorolac Mefenamic acid Nabumetone Naproxen Oxaprozin Phenylbutazone Piroxicam Sulindac carpofen Non selective COX inhibitors lipooxygenase TNF- Nitric Oxide Phospholipase A2 Phosolipase A, C Neutophil migration T & B cell prolifration

  17. Clinical Pharmacology of the NSAIDs • Equally efficacious with few exceptions • Different on the basis of • Toxicity • Cost-effectiveness • There is no best NSAIDs for all patients

  18. Good Luck

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