Anti-inflammatory drugs
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- Lillian Copeland
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1 Anti-inflammatory drugs 1
2 Inflammatory process 1. stimulus (cut) 2. Initial local vasoconstriction( blood loss) 3. vasodilation, local immune/inflammatory reaction (heat, redness) 4. swelling and pain 5. damage repair, inflammatory response gradually subsides 6. healing 2
3 Inflammatory process calor dolor rubor tumor 3
4 Inflammation - presentation 4
5 Prostaglandins in inflammation COX unrelated to leukotriene production 5
6 COX-1 vs. COX-2 6
7 Anti-inflammatory drug classes classical NSAIDs COX-2 inhibitors leukotriene modifiers corticosteroids (Olga ) 7
8 Classical NSAIDs inhibition of COX enzymes decreased PG synthesis suppression of inflammatory processes 8
9 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) 9
10 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) resultant effect varies per action site anti-inflammatory effect: peripheral target sites inhibition of PG-mediated inflammatory cascade inflammatory process PG release inflammation: pain, swelling, heat, redness 10
11 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) resultant effect varies per action site antipyretic effect: central thermoregulation infection, inflammation, hypersensitivity elevated by pyrogens reset by aspirin inhibition of PGE2 synthesis and release 11
12 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) resultant effect varies per site analgesic effect: peripheral sites inflammatory process PG release histamine, bradykinin, other mediators 12 sensitization of sensory nerve endings
13 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) undesired effects: platelets irreversible aggregation inhibition bleeding complications 13
14 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) place in therapy diminishing use as antipyretic/analgesic (safety) other salicylates used for several inflammatory states (such as rheumatoid arthritis, inflammatory bowel disease) local use vs. cutaneous inflammation (methyl salicylate) 14
15 Classical NSAIDs Other NSAIDs propionic acid derivatives: - ibuprofen (Nurofen, Advil, Adex,Artofen ) - naproxen (Narocin, Naxyn, Point ) acetic acid derivatives: - indomethacin (Indomed, Indocin, Indovis ) - diclofenac (Voltaren, Abitren ) 15
16 Classical NSAIDs Other NSAIDs oxicams: - piroxicam (Brexin, Feldene Gel ) - norloxicam (Xefo ) naphthylalkylanone: nabumetone (Relifex, Nabuco ) pyranocarboxylic acid: etodolac (Etopan ) nimesulide (Mesulid ) 16
17 Classical NSAIDs Other NSAIDs mechanism: similar to that of aspirin - reversible binding to COX - differing COX-1/COX-2 selectivity 17
18 aspirin Classical NSAIDs Other NSAIDs simple vs. time-dependent competition irreversible binding COX competitive binding ibuprofen naproxen piroxicam simple competitors tight binding, slow self-dissociation arachidonic acid 18 time-dependent competitors diclofenac indomethacin
19 Classical NSAIDs Other NSAIDs potent anti-inflammatory effect effective antipyretics relatively mild analgesic effect 19
20 Classical NSAIDs GI toxicity presentation minor endoscopic lesions frequency 65% symptomatic 3-6mo 1% ulcer, bleeding, perforation 1yr 2-4% probably safer: nabumetone, etodolac, oxicams 20
21 Classical NSAIDs GI toxicity local effect (acidity) GI TOXICITY systemic effect (COX inhibition) nabumetone (non-acidic prodrug) increased COX-2 selectivity 21
22 Classical NSAIDs T 1/2 NSAID specific ADEs effect of effect of short ibuprofen indomethacin aseptic meningitis GI/CNS effects dig, warf, Li, Li diuretics furosemide anti-htns intermediate diclofenac etodolac naproxen LFTs --- pulmonary infiltrates warf, dig, Li, hypogly dig, Li warf, Li, ACEIs diuretics diuretics --- long nabumatone piroxiacm warf, Li diuretics diuretics 22 dig - digoxin; warf - warfarin; Li - lithium; hypogly hypoglycemics; PK PD
23 Classical NSAIDs Choosing an NSAID indication clinical data (evidence-based) ADEs/DDIs patient factors cost trial and error similar properties - varying effects 23
24 Cyclooxygenase pathway 24
25 COX-1 vs. COX-2 25
26 COX-2 selectivity 26
27 Selective COX-2 inhibitors celecoxib (Celebra, Celcox ) etoricoxib (Arcoxia ) rofecoxib (Vioxx ) valdecoxib (Bextra ) 27
28 COX-2 selectivity is relative some NSAIDs are more COX-2 selective than COX-2 selective inhibitors 28
29 Selective COX-2 inhibitors etoricoxib oral administration, good absorption heaptic CYP metabolism mostly-renal clearance T 1/2 ~ 22hr (once-daily) minor GI ADEs, dizziness, peripheral edema, BP DDIs - lithium, theophylline levels - warfarin effect - anti-htn effect of diuretics, ACEIs 29
30 Selective COX-2 inhibitors similar efficacy to that of NSAIDs main advantage: decreased GI toxicity other ADEs: generally similar to NSAIDs no anti-platelet effect CV risk: small BP increase, edema, renal effects caution if combined with aspirin (CHD/CVA prevention) 30
31 Selective COX-2 inhibitors some COX-2 selective inhibitors withdrawn: - rofecoxib (cardivascular/renal toxicity in long-term use) - valdecoxib (cardivascular/renal toxicity in short-term use, severe skin reactions) [ - nimesulide (hepatotoxicity) ] 31
32 Selective COX-2 inhibitors some COX-2 selective inhibitors withdrawn: an over-simplification COX-2 NSAIDs COX-1 complex, dynamic inter-relations incomplete mechanistic data limited long-term clinical data 32
33 Prostaglandins in inflammation choosing an anti-inflammatory 33
34 Pharmacotherapy anti-inflammatory drugs DRUGS FOR EXAM aspirin naproxen etoricoxib 34
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