Inflammatory Drugs Flashcards
Mechanism of acetaminophen
reversibly inhibits cyclooxygenase, mostly in CNS, inactivated peripherally
Use of acetaminophen
antipyretic, analgesic, NOT anti-inflammatory
use instead of aspirin in CHILDREN
Toxicity of acetaminophen
Hepatic necrosis due to overdose
NAPQI is toxic metabolite that depletes glutathione stores
Antidote to acetaminophen overdose
N-acetylcysteine which regenerates the glutathione stores
Mechanism of aspirin
irreversibly inhibits cyclooxygenase (1 and 2) via acetylation
decreases synthesis of TXA2 (increase bleeding time) and prostaglandins
increased bleeding time but NO effect on PT or PTT
Toxicity of aspirin
gastric ulceration, tinnitus (CN VIII)
chronic use: acute renal failure, interstitial nephritis, GI bleeding
cause respiratory alkalosis early, transitions to mixed metabolic acidosis-respiratory alkalosis
Toxicity of aspirin in CHILDREN
REYE syndrome in children treated with aspirin for viral infection
Mechanism of celecoxib
reversibly inhibits COX-2 found in inflammatory cells, vascular endothelium
Use of celecoxib
analgesic and anti-inflammatory
rheumatoid arthritis, osteoarthritis
Benefit of COX2 specific versus non-selective
spares COX1 thus:
- able to maintain gastric mucosa
- platelet function intact
Toxicity of celecoxib
increased risk of thrombosis, sulfa allergy
Name the NSAIDs
ibuprofen, naproxen, indomethacin, ketorolac, diclofenac
Mechanism of NSAIDs
reversibly inhibits cyclooxygenase (1 and 2)
blocks prostaglandin synthesis
Use of NSAIDs
antipyretic, anti-inflammatory, analgesic
Specific use of indomethacin
to close the PDA