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Comprehensive Guide to NSAIDs in Pain Management

Learn about non-steroidal anti-inflammatory drugs (NSAIDs) and their role in managing pain, inflammation, and immune response modulation. Explore the chemistry, pharmacokinetics, and pharmacodynamics of NSAIDs like aspirin, Cox-2 inhibitors, and more. Understand their clinical uses, adverse effects, and therapeutic strategies.

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Comprehensive Guide to NSAIDs in Pain Management

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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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