This document classifies NSAIDs based on their selectivity for inhibiting COX-1 and COX-2 enzymes. It discusses their anti-inflammatory, analgesic, and antipyretic effects which are due to inhibiting prostaglandin production. Adverse effects include gastrointestinal, renal, platelet, and central nervous system issues. Drug interactions can increase risks of bleeding, toxicity, and altered effects when NSAIDs are taken with other drugs like anticoagulants, corticosteroids, and some antibiotics.
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NSAIDs
This document classifies NSAIDs based on their selectivity for inhibiting COX-1 and COX-2 enzymes. It discusses their anti-inflammatory, analgesic, and antipyretic effects which are due to inhibiting prostaglandin production. Adverse effects include gastrointestinal, renal, platelet, and central nervous system issues. Drug interactions can increase risks of bleeding, toxicity, and altered effects when NSAIDs are taken with other drugs like anticoagulants, corticosteroids, and some antibiotics.
This effect of NSAIDs is due to the inhibition of the enzyme COX, which converts arachidonic acid to prostaglandins, TXA2 and prostacyclin. Acetylsalicylic acid irreversibly inactivates COX-1 and COX-2 by acetylation of a specific serine resideu. Other NSAIDs reversibly inhibit COX-1 and COX-2 Additional anti-inflammatory mechanism may include: - interference with the potentiative action of other mediators of inflammation – bradykinin, histamine, serotonin - modulation of T-cell function - stabilization of lysosomal membranes - inhibition of chemotaxis
ANALGESIC EFFECT OF NSAIDs
This effect of NSAIDs is thought to be related to the peripheral inhibition of prostaglandin production, but it may also be due to the inhibition of pain stimuli at a subcortical site. NDAIDs prevent the potentiating action of prostaglandins on endogenous mediators of peripheral nerve stimulation ( e.g. bradykinin )
ANTIPYRETIC EFFECT OF NSAIDs
This effect is believed to be related to inhibition of the interleukin-1 and interleukin-6 induced production of prostaglandins in the hypothalmus and the „ resetting „ of the termoregulatory system, leading to vasodilation and increased heat loss CLINICAL USES O NSAIDs 1) analgesia 2) inflammation 3) antipyresis 4) antiplateled effect 5) cancer preventive agents ADVERSE EFFECTS OF NSAIDs 1) gastrointestinal effects: abdominal pain, gastric and duodenal ulcer, diarrhea, pancreatis gastrointestinal hemorrhage, hepatotoxicity 2) renal effects - disturbances of renal function with water and sodium retention 3) inhibition of platelet aggregation 4) central symptoms: headache, decreased hearing, tinnitus, dizziness, confusion, dpression 5) allergic reactions: asthma, rashes, photosensitivity
PHARMACODYNAMIC INTERACTION NSAIDs WITH OTHER DRUGS
NSAIDs + hypotensive drugs ( β-blockers, ACE-inhhibitors, diuretics ) = ↓ hypotensive effect NSAIDs + ehanol = ↑risk of bleeding from gastrointestinal tract NSAIDs + ticlopidine or clopidogrel = ↑risk of bleeding NSAIDs + lithium = ↑lithium toxicity NSAIDs + cylosporine or ACE-inhibitors or takrolimus= ↑nephrotoxicity of drugs NSAIDs + fluoroquinolons = ↑ toxic action of fluoroquinolons on CNS NSAIDs +oral antidiabetic drugs =↑ risk of hypoglycemia NSAIDs + cumarines = ↑risk of bleeding from gastrointestinal tract
PHARMACOKINETIC INTERACTION NSAIDs WITH OTHER DRUGS
NSAIDs + oral antidiabetic drugs = ↑ risk of hypoglycemia NSAIDs + cumarines =↑risk of bleeding NSAIDs + corticosteroids = ↑risk gastropathy and bleeding from gastrointestinal tract NSAIDs + aminogycosides = ↑ ototoxicity and nephrotoxicity of aminogycosides NSAIDs + fenytoine or valproinic acid = ↑action of fenytoine or valproinic acid NSAIDs + metotrexat or digoxin = ↑action and ↑ toxicity metotrexat or digoxin NSAIDs + tricycles antidepressive drugs neuroleptics or antiarrhytmic drugs or selective serotonin reuptake inhibitors ( SSRI ) = ↑ action of drugs