Chapter 24 Lecture - Anti-Inflamatory Importance

Chp 24 Antiinflamatory Inflammatory response to injury / infection; affected body parts burns red, hot, swollen, + painful -Prostaglandins play key roles in inflammatory response; produced by enzyme cox (cyclooxygenase). -COX1 -COX2 Produces prostaglandins Prostaglandins inflammation (fever, pain) Inflammation (fever, pain) Maintain gastric mucosa, -TXA2 (Platelet aggregation) Traditional NSAIDs block COX1+2; disrupting of GI mucosa →↑ R/F bleeding ulcers (Aspirin, ibuprofen, naproxen, diclofenac, Ketorolac) irreversibly inhibits platelets for days. Warfarin 2-3 days- -Selective COX2 inhibitors (Celecoxib): inflammation + pain, ↓er risk 4 GI side effects. Traditional (nonselective) NSAIDs: Aspirin, ibuprofen MOA: inhibits COX1+COX2 →↓ prostaglandins ↓ inflammation Uses: analgesic, antipyretic, inhibit plate aggregation; aspirin-anti-platelet SE/ADR: GI bleed, mal absorption / failure, TBP = CV complications, tinnitus, Reye's syndrome in children, thrombocytopenia Interactions: Other NSAIDs↓ 4Gs Garlic, ginger, ginkgo biloba, green tea. (↑ bleeding) is Caution: Best not to take 2 days before or 10m/2nd day of menstrual cycle due to ↑ bleeding. Contraindications: Renal failure, HTN Do not give to children ≤ 12 b/c Reye's syndrome: associated w/ use of aspirin during febrile illness (the flu, chicken pox, VRI) Etiology-unknown, linked to brain swelling + liver damage Sxs: vomiting, lethargy, delirium, personality A's + seizures. pg 208 COX2 Selective NSAID Celecoxib 2 MOA: Selectively inhibits COX2, fewer GI side effects. 3 Uses: Arthritis, acute pain, dysmenorrhea 4 ADR's: increased a ↑ RIE serious adverse or events (MI, CVA, new onset HTN; GI wounds (fewer than regular NSAIDs), hepatitis, acute kidney injury 5. Contraindications hx of heart disease 6. Interactions: ACE inhibitors, anti-coagulants, SSRIs, lithium, Ginkgo biloba ↑ R/F bleeding. Chp 24 gout one 2 accum latter of Uric Acid crystals into joints other body tismes → inflammation Patho UA under secretion by kidneys Overprodution of UA Exogenous (1 pinna dint) -Male predominant, great the (1st Attnek) Gout ty Allopurinol preferred urate (VA) rowering ding MOA: ↓ production of VA Use: Cont proveration tx of anmanic gout. 4.SE/ADR -Hepatotoxicity Hypersensitivity reactions Stoveni sonnson Syndrome (severe vash) -GI N/V Renal Renal failure CNS Drowsiness Caution & dose or withdrawal dag 4 renal impairment Monitoring: LFTS, renal function (PVN, crestinina) periodi ontley mtaractions: Thiazide/loop dinerties, rearfarin (allopurinol anticoagulant effects.)