anticoagulant and antiplatelet drug
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- inhibitors of clotting factor synthesis:
- warfarin (coumadin)
- pradaxa-some significant advantage to
- inhibitors of thrombin:
aspirin, clopidogrel (plavix), dipyridamole
Thrombolytic drugs (fibrinolytic drugs)
activate the fibrinolytic pathway and lyse clots
Direct-acting anticoagulants (at low concentration and high concentration)
- At low concentrations, heparin binds to and accelerates antithrombin III (a serine protease inhibitor) activity 1000 fold, which in turn:
- - permanantly inactivates factor Xa.
- At high concentration:
- - the heparin-antithrombin III complex binds to and inactivates thrombin itself, inhibiting its proteolytic
Heparin: route of administer
parenterally e.g IV, deep ssubcutanecous, fat depot
Heparin should never be administer IM. Why?
bc of ms hematoma
Indirect-acting anticoagulants - mechanism of action
- Vitamin K serves as a cofactor in the g-carboxylation of glutamic acid residues of clotting factors II, VII, IX, and X.
- Vitamine K is oxidized in the carboxylation process and must be reduced enzymatically to regain cofactor activity.
-The coumarin-indanediones inhibit the reduction.
the most toxic effect of indirect-acting anticoagulants
indirect-acting anticoagulant - drug interaction
Antimicrobial agents: sensitivity to the coumarin-indanedione drugs may be increased.
Barbiturates: increase metabolism of coumarin (need to inc dosage)
NSAIA: sensitize patients to oral anticoagulants.
General therapeutic uses - anticoagulant
Aspirin - MofA
- Inhibition of TXA2 synthesis, resulting in
- decreased ADP release and aggregation.
Dipyridamole - MofA (platelet inhibitor)
Vasodilation and increase blood flow.
- Inhibition of phosphodiesterase, resulting
- in increased cAMP and reduced platelet aggregation.
plavix - MofA (platelet inhibitor)
blocks binding of ADP to its receptor on platelets, thereby inhibiting platelet aggregation
Fibrinolysis - plasmin
plasmin lyses the fibrin, and degrades factors V and VIII, inhibiting further clotting.
Fibrinolysis- Plasminogen activators
- Tissue-type plasminogen activator (t-PA):
- t-PA, a serine protease, adheres to fibrin molecule and absorbs plasminogen and then cleaves the plasminogen to liberate plasmin.
Urokinase: activating circulating plasminogen to plasmin
Fibrinolysis - streptokinase
It is an exotoxin from certain b- hemolytic strepococci. It binds noncovalently to plasminogen and confers plasmin-like proteolytic activity.
Fibrinolysis - anistreplase
a combination of streptokinase with an acylated plasminogen, which becomes deacylated in plasma. Deacylated form is the same as streptokinase-plasminogen complex.
Clinical use of plasminogen activators
Acute myocardial infarction
Life-threatening pulmonary embolism
Deep venous thrombosis
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