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24 Cards in this Set

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NSAIDs Mx of action?
To inhibit the cyclo oxyegnase step to prevent the biosynthesis of prostaglandins
Mechanisim of PGI2 and TXA2
Prostacyclin reduces platelet aggregation while Thrombaxane induces platelet aggregation
what is arachodonic acid
important precursor for alot of acids incld the formartion of prostaglandins and the lipo oxygenase pathway
Whats is the biggest producer of PG?
Neutrophils, macrophages and monocytes, responsible for the inflammatory response (PGe2)
Whats fx of and PGI2 (ip) PGD2 (DP ) receptors
Vasodilation and platelet aggr
fx of PGF2alpha (FP) receptor
Bronchoconstriction and uterine SM contraction, induction of labour
fx PGE2 of ep1, ep2, ep3 receptors respectively
-Brochial and GI sm contractions,
-Broncho and vasodilation,
-dec gastric acid sec inc in gastric mucousa and uterine sm cont
Name the carboxylic acid NSAIds
ASA, acetic acid (indomethacin) , propanoic acid (ib and naproxen) and fenamic acid
Mx of action of asprin
acetylates serine group in active site and blocks access to arachadonic acid
metabolism of salicytes
low dose , 1st order kinetics (conjugation to glycine)
toxic dose , 0 order kinetics (hepatic enzyme saturation)
T 1/2 OF peroxicam? and naproxen
50 hrs can be given once a day(possible)
14hr, 20x more potent than ASA and is better tolerated
cox 1 sitereceptors found in ?
and cox 2
kidney, stomach, intestine and platelet
- inflammatory response ( macrophages and synivocytes)
Nsaid bind cox 1 and cox 2 at which site
Arg 120, non selective binding
how does NSAIDs property affect pain
Lowered threshold of nociceptors (pain receptor) providing an hyperalgesia like effect
which PGs play a role in pain and fever
PGE2 (pain), PGE2, IL2 and TNF (fever)
how does Nsaid mediate anti pyresis
by inhibition if pg syntethsis in the hypothalmus, this is accompanied by vasodilation ie heat dissipitation
How does Nsaid induce renal failure and acute hypertension
By inhibitng PG which is vasodilators(pge2, i2, d2) and inhib AA which switches to LOX pathway inducing luekotrines ( which are vasoconstrictors) this acts at the renal and systemic levels. which could lead to both renal failure and acute hypertension.
Affects of PG in Na at thick acscending limb?
and cortical collecting tubule?
1) PG inibit K from leaving and thus Na levels dec
2) and PG inhibits entry of Na into urine and being excreted

therfore NSAIDs by inhib pg causes Na to be retained and inc its levels therby inc BP and causing hypertension
y does asprin induce astham and urticaria (hives)
Bcoz it inhbits PGE2 which cause bronchodilation and induces leukotrines which induces bronchocontricton which results in spasms , similar etiology in skin as well

cox 2 inhib are better tolerated
Coxibs (cox 2 inhib) why do they cause strokes?
cause of imbalance in PGI2 which is only inhib by cox2 and TXA2 by cox 1, so by inhib pgi2 u are counter acting the effects of platelet agg reduction without inhib its formation. leads to clot formation.
role of cox 2 in tumorigensesis
By inhib NFKappaB, u inhib pge2(prod in large quantities y tumore cells) production and thus cancer cell features eg,
-loss of e cadherin
- anchorage indep growth
-loss of contact inhib
- inc proliferation

can then undergo angiogensis which is drug resistance and mutation
cox 2 inhib
can lead to cancer cells apoptosis
contraindications for NSAIDS
- renal isufficiency
- heamophilia
- peptic ulcer /not recommended in preg
-asrpin hypersensitivity
- asthma
contraindications for NSAIDS
- renal isufficiency
- heamophilia
- peptic ulcer /not recommended in preg
-asrpin hypersensitivity
- asthma