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ANTI-INFLAMMATORY DRUGS (Mechanism of action (later events suppress as…
ANTI-INFLAMMATORY DRUGS
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Mechanism of action
later events suppress as well: cell proliferation, macrophage and fibroblasts activity, angiogenesis
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suppress early events of inflammation: vasodilatation, edema, leukocyte infiltration and leukocyte activation
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then etiher bind to substrate or inhibit activity of PLA2 to reduce production of arachidonic acid and PAF
Unwanted effects
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iatrogenic Cushing's
high BP, abdominal obesity with thin arms and legs, reddish stretch marks, round red face, fat lump between the shoulders, weak bones, acne and fragile skin
elevated corticosol levels exert negative feedback on CRH in the hypothalamus- decrease amount of ACTH released from anterior pituitary
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GLUCOCORTICOID RECEPTOR
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in absence of hormone, GR resides in cytosol complex with hsp90, hsp700 and protein FKBP52
endogenous cortisol diffuses through cell membrane into cytoplasm to bind to GR- release of hsp protein
Transactivation
direct mechanism:homodimerization of receptor, translocation via active transport into nucleus and binding to specfici DNA elements activating gene transcription
Transrepression
in absence of activated, other factors (NF-kB or AP-1) are able to transactivate target genes
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Nongenomic effects=independet of transcription effect-are only due to direct binding of activated GR to other proteins
Glucocorticoids effects
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decreased fibroblast activation, matrix deposition
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NSAIDs
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ASPIRIN
side effects: tinnitus, uricosuri,hypersensitivity
overdose leads to pyrexia, uncoupled oxidative metabolism, respiratory and metabolic acidosis
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