NSAIDs
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Created by:
Rachnanjali on February 15, 2012
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28 terms
Terms | Definitions |
|---|---|
 Describe the biosynthetic pathway for production of PGs, TXA2, and LTs | Arachidonic acid found in PM is released after signaling from inflammatory mediators with phosholipidases. It is then acted on by various enzymes to form the different chemical mediators |
| COX 1/2 | Produce PGH2 from AA this is then converted by isomerases/thromboxane syntheses into prostaglandin, prostacyclin, or thromboxane |
| 5-lipooxygenase | Produces LTA4 from AA which is then converted to LTB4 in nphils. This compound can then be used by mast cells bphils and ephils to make LT |
| COX1 is expressed | constitively |
| COX2 is expressed | as needed |
| COX1 is found | ubquitously |
| COX2 is found | in inflamed or activated tissues |
| COX1 is responsible for | housekeeping/aggregation |
| COX2 is responsible for | Specialized functions/anti aggregation |
| COX 1 is induced by | nothing it is always on |
| COX2 is induced by | cytokines, shear stress, growth factors |
| COX1 is inhibited by | Aspirin/t-NSAIDs |
| COX2 is inhibited by | Aspirin/t-NSAIDs/Celecoxib |
| Vascular smooth muscle constricts and dilates in response to | PG12/PGE2/TXA2 |
| Platelets aggregate/don't aggregate in response to | TXA2/PG12 |
| GI tract decreases pepcid and acid secretions and increases mucous and muscle contractions in response to | PGE2,12,PGF2 |
| Kidney cells increase blood flow and diuresis in response to | PGE2/PG12 |
| Uterus increases contraction in response to | PGE2/PGF2 |
| Inflammatory cells enhance edema, leukocyte infiltration and pain through bradykinin in response to | PGE2 PGI2 |
| Describe the effects of leukotrienes on inflammatory cell function/pulmonary/vascular smooth muscle | LTB4=Increased neutrophil chemotaxis, aggregation, transmigration through endothelium LTC4/LTD4/LTE4 promote increased vascular permeability, bronchoconstriction, vasoconstriction |
| Describe the functional interaction of prostacyclin and TXA2 with relation to effects on vascular smooth muscle/platelets | PG12 promotes vasodilation and inhibits aggregation TXA2 promotes vasoconstriction and platelet aggregation |
| TXA2 is produced by | COX1 in platelets |
| PG12 is produced by | COX2 in endothelial cells |
| Aspirin | irreversible inhibition of of COX1/2, analgesic anti-inflammatory,antithrombotic,antipyretic GI effects, increased BT rare hypersensitivity |
| Acetaminophen | inhibits COX in CNS, analgesic and antipyretic, reversible increase in hepatic enzymes, dizziness and disorientation at higher doses, CNS depression at very high doses safe in pregnancy |
| NSAIDs | reversible inhibition of COX 1 and 2 analgesic, antypyretic, anti-inflammatory GI upset, n/v, renal failure, gastric irritation, safer than aspirin |
| COX2 inhibitors | reversible inhibitors of COX 2 analgesia, antipyretic, anti-inflammatory less ulcers than NSAIDs, renal side effects, prothrombotic |
| How come low does aspirin (not high dose) can exert an antithrombotic/cardiprotective effect. | Low dose aspirin selectively irreversibly inhibits COX 1 causing inhibtion of platelet TXA2 synthesis/aggregation. This is due to the fact that at low doses the majority of the drug is pre systemic (out of the tissues) and there is a greater effect on circulating platelets than on the COX 2 found in endothelial tissues. Moreover, platelets cannot synthesize new COX 1 while COX 2 recovery in the endothelial cells is faster. This is important because inhibition of COX 2 could actually lead to thrombotic events (inhibiting something that has anti-aggregatory effects) |
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