Pharma W2 Part II: Anti-inflammatory & Antigout Drugs PDF

Inhibition of the leukotriene,...

Inhibition of the leukotriene, prostaglandin pathways or both pro inflammation leukotrienes and prostaglandins inducing vasodilation mediate inflammation by enhancing vascular bring big WBC into cell MOA permeability housekeeping, maintains GI mucosa COX1 Good one :) block COX enzyme, "non selective also, maintains renal reducing it's ability to NSAIDs" (aka they blood flow and GFR NSAIDs also called cause: inflammation, attack both COX1 & pain and fever COX2) contribute to COX2 inflammation enzyme inflammation, pain and fever GI intolerance Intro Bleeding Ranges from heartburn →mucosal lesions (ulcerations) → severe GI bleeding Adverse effects Labs Cr, GFR.. Kidney impairment depends partly on prostaglandins as they are vasodilators - may precipitate AKI all d/t COX1 inhibition protective response contraindications allergy, risk for bleeding, pregnancy Inflammation vascular dilation, this process is mediated pain, fever, loss of leukotrienes and permeability, blood by endogenous d/t function, redness and symptoms prostaglandins flow, exudation of fluids thrombi, including fatal MI and stroke except aspirin compounds swelling increase risk of adverse to site Warning events one is about making too Pharma W2 Part II: adults at greater risk much, and the other is either under or by leads to hyperuricemia hyperuricemia = about getting rid of too overproduction Anti-inflammatory little Nursing implications better taken with food, pt education inappropriate uric acid & Antigout Drugs Hyperuricemia → Crystal Formation → Painful Inflammation uric acid crystals are metabolism deposited in tissues and Anti-inflammatory joints = inflammatory response NSAIDs (most Antipyretic commonly prescribed prevents uric acid main uses allopurinol (Zyloprim®) drug classes) production Analgesia GOUT Inhibits the Platelet inhibition reabsorption of uric (aspirin) probenecid (Benuryl) acid = ↑ the excretion of antithrombotic effect uric acid MOA first line of tx, inhibits plt aggregation ↓ inflammatory (analgesia & anti- NSAIDs response of crystals in oldest inflammatory) joint tissue "salicylism" - if chronic narrow therapeutic ↑ HR, tinnitus, hearing can happen at lower index 1. Salicylates Aspirin Toxicity loss, dimension vision.. doses too colchicine unclear MOA contraindicated in children specially with viral leads to neurological deficits Reye's Syndrome illness (ej. influenza) - give them Tylenol instead (encephalitis) and liver damage nurse should be handled with caution (gloves and mask) because similar to narcotics (opioids) d/t its it is teratogenic analgesic use inhibits prostaglandin synthesis (creation) 2.Acetic acid derivatives ketorolac (Toradol) x short term use (up to a wk) x mod - severe acute pain adverse effects kidney impair, edema, GI pain, dyspepsia and nausea newer, costly, by prescription 3.COX-2 inhibitors Developed to decrease GI adverse effects of NSAIDs, as they attack both COX 1 & COX2 5 categories these inhibitors only attack COX2, so we only have baby adverse effects first and only COX2 inhibitor celecoxib (Celebrex) not to use in pt with sulfa allergy x mild - mod: OA, RA and gouty arthritis 4.Enolic acid derivatives piroxicam ex. most common drugs meloxicam (Mobic) nabumetone better tolerance to GI adverse effects antipyteric and anelgesic both COX1 and COX2 MOA inhibition 5.Propionic acid derivatives ibuprofen (Motrin, Advil) most common drugs somewhat better adverse effects and less drug interactions naproxen 2nd most used