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Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDSSelectivityInflammatory responseMolecules involvednonselective proyotype : Ibuprofen propionic acid derivatives : naproxen, fenoprofen, ketoprofen, flurbiprofenAcetic acid derivatives : diclofenac, ketorolac, indomethacin, etodolac, sulindac, piroxicam, meloxicam, nabumetone, tolmetin, mefenamic acid, meclofenamate, flufenamic acidCyclooxygenase COX2 selective prototype : Celecoxib others : rofecoxib, valdecoxib, etoricoxib Transient local vasodilation and increased capillary permeabilityInfiltration of leukocytes and phagocytic cellsTissue degeneration and fibrosisHistamine Bradykinin & 5hydroxytryptamine (serotonin, 5HT)LeukotrienesProstanoids✓ One of the first identified mediators of the inflammatory process✓ Are useful only for the treatment of vascular events in the early transient phase of inflammationAmeliorate only certain types of inflammatory response✓ Exert pro-inflammatory actions✓ LT-receptor antagonists (montelukast and zafirlukast) approved for treatment of asthmaBiosynthesis is significantly increased in inflamed tissue includes the prostaglandins, leukotrienes, and prostacyclin; these are the products of cyclooxygenase cleavage of arachidonic acidEicosanoid SynthesisCOXCOX1COX2 Constitutive enzyme: its levels remain relatively constant, and it is distributed widely throughout the body COX-1 is thus believed to play a maintenance or protective role, responsible for production of cytoprotective mucus in the stomach and for platelet aggregation (clotting) Inducible enzyme: its levels and activity can increase rapidly and significantly in response to a stimulus The main stimuli for COX-2 induction are inflammatory mediators, and thus COX-2 is typically associated with inflammationTXA2 activates platelets: COX-1 is primarily responsible for generating TXA2PGI2 inhibits platelet activation.: COX-2 is responsible for generating PGI2PAIN & FEVERAspirin & NSAIDSPAIN 1. Bradykinin2. H+3. Neurotransmitters such as serotonin and ATP4. Neutrophins (nerve growth factor)5. LTs6. PGs7. Cytokines appear to liberate PGs and some of the other mediatorsMAIN COMPONENTSFEVERThe hypothalamus regulates the set point at which body temperature is maintainedenhance formation of cytokines such as IL-1, IL-6, TNF-, and interferons, which act as endogenous pyrogenselevated in fever, reflecting an infection, or resulting from tissue damage, inflammation, graft rejection, or malignancyCytokines increase the synthesis of PGE2/ Increase CAMP/ Triggers hypothalamus to elevate body temperatureNSAIDs suppress this response by inhibiting PGE2 synthesis production of superoxide radicalsapoptosisthe expression of adhesion molecules NO synthase proinflammatory cytokineso Modify lymphocyte activityo Alter cellular membrane functionsReversible competitive inhibitors of COXCovaIently Irreversible inhibits COX
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author Rita Hanna
This is a mind map of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). NSAIDs block the production of certain body chemicals that cause inflammation. NSAIDs are good at treating pain caused by slow tissue damage, such as arthritis pain. NSAIDs also work well in fighting back pain, menstrual cramps, and headaches.
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