anticoagulant and antiplatelet drug

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  1. Anticoagulants
    • inhibitors of clotting factor synthesis:     
    •      warfarin (coumadin)
    •      pradaxa-some significant advantage to
    • coumadin

    • inhibitors of thrombin:
    •          heparin
  2. Antiplatelet drugs
    aspirin, clopidogrel (plavix), dipyridamole
  3. Thrombolytic drugs (fibrinolytic drugs)
    activate the fibrinolytic pathway and lyse clots
  4. 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

    • action on fibrinogen.
  5. Heparin: route of administer
    parenterally e.g IV, deep ssubcutanecous, fat depot
  6. Heparin should never be administer IM. Why?
    bc of ms hematoma
  7. Heparin antagonist
    protamine sulfate
  8. 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.
  9. the most toxic effect of indirect-acting anticoagulants
  10. 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.
  11. General therapeutic uses - anticoagulant
    Atrial fibrillation

    Myocardial infarction

    Cerebrovascular thrombosis

    Pulmonary  embolism

    atherosclerotic plaques

    Renal dialysis
  12. Aspirin - MofA
    • Inhibition of TXA2 synthesis, resulting in    
    • decreased ADP release and aggregation.
  13. Dipyridamole - MofA (platelet inhibitor)
    Vasodilation and increase blood flow.

    • Inhibition of phosphodiesterase, resulting
    • in increased cAMP and reduced platelet aggregation.
  14. plavix - MofA (platelet inhibitor)
    blocks binding of ADP to its receptor on platelets, thereby inhibiting platelet aggregation
  15. Fibrinolysis - plasmin
    plasmin lyses the fibrin, and degrades factors V and VIII, inhibiting further clotting.
  16. 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
  17. Fibrinolysis - streptokinase
    It is an exotoxin from certain b- hemolytic strepococci. It binds noncovalently to plasminogen and confers plasmin-like proteolytic activity.
  18. Fibrinolysis - anistreplase
    a combination of streptokinase with an acylated plasminogen, which becomes deacylated in plasma. Deacylated form is the same as streptokinase-plasminogen complex.
  19. Clinical use of plasminogen activators
    Acute myocardial infarction

    Life-threatening pulmonary embolism

    Deep venous thrombosis
Card Set:
anticoagulant and antiplatelet drug
2013-07-26 17:54:00

antithrombotic drug
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