Prostaglandin synthesis, inhibition NSAIDs

TABLE 36.2 Adverse Effects of NSAIDs - Relationship to Prostaglandin Synthesis inhibition and Cyclooxygenase Isoforms... 

Aspirin, non-acetylated salicylates, and other NSAIDs have analgesic, antipyretic, and anti-inflammatory actions. These agents inhibit cyclooxygenase (COX-1 and COX-2) enzymes, thereby preventing prostaglandin synthesis, which results in reduced nociceptor sensitization and an increased pain threshold. NSAIDs are the preferred agents for mild to moderate pain in situations that are mediated by prostaglandins (e.g., rheumatoid... 

Unfortunately, frequent exposure to NSAIDS may also cause two detrimental effects. These agents inhibit the activity of cyclo-oxygenase, an important enzyme in synthesis of gastroprotec-tive prostaglandins. More importantly, NSAIDS may cause breaks... 

NSAIDs act primarily by inhibiting prostaglandin synthesis, which is only a small portion of the inflammatory cascade. They possess both analgesic and antiinflammatory properties and reduce stiffness but do not slow disease progression or prevent bony erosions or joint deformity. They should seldom be used as monotherapy for RA instead, they should be viewed as adjuncts to DMARD treatment. Common NSAID dosage regimens are shown in Table 4-4. 

NSAIDs appear to prevent neurogenically mediated inflammation in the trigeminovascular system by inhibiting prostaglandin synthesis. 

Hypersensitivity to salicylates or nonsteroidal anti-inflammatory drugs (NSAIDs). Use extreme caution in patients with history of adverse reactions to salicylates. Cross-sensitivity may exist between aspirin and other NSAIDs that inhibit prostaglandin synthesis, and aspirin, and tartrazine. Aspirin cross-sensitivity does not appear to occur with sodium salicylate, salicylamide, or choline salicylate. Aspirin hypersensitivity is more prevalent in those with asthma, nasal polyposis, chronic urticaria. 

III.a.4.3. Changes in renal blood flow. Blood flow through the kidney is partially controlled by the production of renal vasodilatory prostaglandins. If the synthesis of these prostaglandins is inhibited (e.g. by indomethacin), the renal excretion of lithium is reduced with a subsequent rise in serum levels. The mechanism underlying this interaction is not entirely clear, as serum lithium levels are unaffected by some potent prostaglandin synthetase inhibitors (e.g. aspirin). If an NSAID is prescribed for a patient taking lithium the serum levels should be closely monitored. 

Mecfianism of Action-. A nonsteroidal anti-inflammatory drug (NSAID) that inhibits prostaglandin synthesis by inhibiting cyclooxygenase 1 and cyclooxygenase 2. Therapeutic Effect Produces anti-inflammatory effect. 

Mechanism of Action An NSAID that inhibits cyclooxygenase-2, the enzyme responsible for prostaglandin synthesis. Mechanism of action in treating familial adenomatous polyposis is unknown. Therapeutic Effect Reduces inflammation and relieves pain. 

Mecfianism of Action An NSAID that produces analgesic and anti-inflammatory effects by inhibiting prostaglandin synthesis. Therapeutic Effect Reduces the inflammatory response and intensity of pain. 

Mechanism of Action An NSAID that inhibits prostaglandin synthesis. Also produces vasodilation by acting centrally on the heat-regulating center of the hypothalamus. Therapeutic Effect Produces analgesic and anti-inflammatory effects and decreases... 

Mecfianism of Action An NSAID that inhibits prostaglandin synthesis, reducing the inflammatory response and the intensity of pain stimuli reaching the sensory nerve endings. Therapeutic Effect Produces analgesic and anti-inflammatory effects. Pharmacokinetics Rapidly and completely absorbed from the G1 tract. Food delays absorption of salsalate. Protein binding Fligh (to albumin). Metabolized in the liver. Excreted in urine. Removed by hemodialysis. Half-life 1 hr. 

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