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NSAIDs Pharmacology Lecture Notes Tissue Injury & Inflammatory Response Initial vasoconstriction occurs immediately after injury to minimize blood loss (temporary reaction) Chemical mediators released: histamines, kinins, and prostaglandins - crucial for inflammatory response Vasodilation follows - blood vessels widen, increasing blood flow to injured area Classic inflammatory symptoms: redness (erythema), swelling (edema), pain from nerve stimulation, fever/heat NSAIDs Classification & Examples Propionic derivatives: ibuprofen, naproxen Phenomates: mefenamic acid Available OTC: salicylates, propionic acid derivatives Prescription required: COX2 inhibitors, acetic acid derivatives, oxicams, phenomates Mechanism of Action COX enzymes: cyclooxygenase (COX1 & COX2) convert arachidonic acid to prostaglandins COX1: Always active, protects stomach lining, helps platelet aggregation COX2: Activated only during tissue injury, causes inflammation and pain NSAIDs inhibit COX enzymes, preventing prostaglandin production (prostaglandin inhibitors) Primary Effects Antipyretic: reduces fever Analgesic: pain relief Anticoagulant: prevents blood clots (especially aspirin) Specific Drug Categories Salicylates (aspirin): pain, inflammation, fever, anticoagulant effects Propionic acid derivatives: mild to moderate pain (1-6 on pain scale), inflammation, fever Acetic acid derivatives: more effective for inflammation but significant GI side effects COX2 inhibitors: second generation NSAIDs with better safety profile, target COX2 specifically Oxicams: long-term use for osteoarthritis/rheumatoid arthritis, longer half-life (once daily) Phenomates: especially effective for menstrual pain Major Side Effects Gastrointestinal Dyspepsia: heartburn, indigestion, abdominal pain, nausea Long-term risks: stomach lining damage, GI bleeding, perforation (holes in stomach/intestines) Bleeding signs to monitor: dark tarry stools, bleeding gums, petechiae, ecchymosis, purpura Higher risk patients: older adults, smokers, alcohol users, pre-existing ulcers Prevention: proton pump inhibitors or H2 receptor antagonists to reduce stomach acid Kidney Effects Impaired function: reduced urine output, fluid retention, weight gain, edema Monitor: BUN and creatinine levels for kidney function Mechanism: NSAIDs reduce blood flow to kidneys, worsening function and increasing kidney disease risk Cardiovascular Risk Non-aspirin NSAIDs increase heart attack and stroke risk Prescribe at smallest effective dose Special Considerations Menstrual Pain (Dysmenorrhea) Avoid aspirin for painful menstruation with heavy bleeding Use acetaminophen 2 days before and during first 2 days of menstrual period Aspirin-Specific Risks Salicylism/Aspirin toxicity: early symptoms from overdose, can progress to electrolyte imbalances, coma, respiratory depression Serum salicylate levels: >30 mg/dL mild toxicity, >50 mg/dL severe toxicity Treatment: activated charcoal, possible hemodialysis Reye's syndrome: rare but serious condition causing liver/brain swelling in children/adolescents recovering from viral infections (flu, chickenpox) Reye's syndrome symptoms: persistent vomiting, lethargy, confusion → irritability, aggression, disorientation, seizures, loss of consciousness Avoid aspirin in children/adolescents with viral infections Drug Interactions & Precautions Glucocorticoids: amplify stomach bleeding risk Alcohol: increases stomach bleeding - limit/avoid consumption Other NSAIDs: can negate heart protective effects of aspirin - space dosing apart Herbal supplements: garlic and ginseng enhance bleeding risk High-risk populations: older adults, smokers, certain health conditions (H7

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