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Old 12-04-2011
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Poison How do these antidotes work?

1. why do we use aminocaproic acid as antidote for tPA, streptokinase toxicity?
2. why do we use beta-blocker as antidote for theophylline toxicity?
3. why do we use glucagon as a antidote for beta blocker toxicity
4. protamine for heparin toxicity?
please explain, the mode of action how they act as an antidote ASAP
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Old 12-04-2011
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Protamine sulphate is an antidote for heparin due to the property of chemical antagonism. It binds to heparin and makes in unavailable for action.


In beta blocker overdose,there is inhibition of beta2 receptors with resultant negative ionotropic and chronotropic activity.....glucagon thru its receptors which are G protein linked to adenlyl cyclase(Gs type) leads to positive ionotropic and chronotropic action.
this is what i remem.......
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Old 12-04-2011
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In theophylline overdose, there is antagonism of adenosine receptors. Adenosine thru its Gi coulped receptors(decrease in cAMP) causes reduced SA and AV nodal activity. So in theophylline overdose we can expect a condition that predisposes to arrythmias via increased nodal activity. Beta blockers thru beta1 antagonism causes reduced SA $ AV nodal activity so it reverses the effects of theophylline. hence used in theophylline overdose. hope its clear
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Old 12-04-2011
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tPA and streptokinase increase the degradation of fibrin thru activation of plasminogen to plasmin..hence fibrinolytics. Tranexaemic acid and amino caproic acid are antifibrinolytics- they bind to plasminogen and prevent its binding to fibrin, hence they prevent the action of plasminogen(plasmin) and arrest the lysis of clot & bleeding.
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Thumbs Up thanx for your co-operation

appreciate for your co-operative attitude ,thnx dude
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Old 12-04-2011
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Quote:
Originally Posted by CHAKRAM View Post
appreciate for your co-operative attitude ,thnx dude
welcome even we revise our topics by responding to the questions.
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