Therapeutics of Cardiovascular Diseases <ul><li>Thrombosis and Haemostasis </li></ul><ul><li>2008 </li></ul><ul><li>Dr. Ge...
<ul><li>Management of disorders of haemostasis   (Coagulation DF) </li></ul><ul><li>Vitamin K </li></ul><ul><li>Mechanism ...
Platelets  (resting to activation) <ul><li>Shape change </li></ul><ul><li>Aggregation </li></ul>
TX A 2 -R GP IIb/IIIa PDE
<ul><li>Antiplatelet agents </li></ul><ul><li>Aspirin </li></ul><ul><li>Mechanism of action: Aspirin blocks the synthesis ...
 
<ul><li>Fibrinolysis </li></ul><ul><li>The fibrinolytic or thrombolytic system functions to dissolve a clot once repair of...
 
<ul><li>Fibrinolytic agents </li></ul><ul><li>Streptokinase </li></ul><ul><li>Mechanism of action: Streptokinase forms a c...
 
<ul><li>Thank You for Your Attention! </li></ul>
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Thrombosis Class05[2]

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Thrombosis Class05[2]

  1. 1. Therapeutics of Cardiovascular Diseases <ul><li>Thrombosis and Haemostasis </li></ul><ul><li>2008 </li></ul><ul><li>Dr. George Hsiao </li></ul>
  2. 2. <ul><li>Management of disorders of haemostasis   (Coagulation DF) </li></ul><ul><li>Vitamin K </li></ul><ul><li>Mechanism of action: Vitamin K is needed for the post-transcriptional  -carboxylation of glutamic acid residues of prothrombin (factor II) and clotting factors VII, IX, and X by the liver. Vitamin K is also necessary for normal calcification of bone. </li></ul><ul><li>Protamine </li></ul><ul><li>Mechanism of action: Protamine is a strongly basic protein, which forms an inactive complex with heparin , and as such is used in patients in whom heparin treatment has resulted in haemorrhage. </li></ul><ul><li>Clotting factors </li></ul><ul><li>Deficient clotting factors can be replaced by the administration of fresh plasma. Factor VIII and IX are available as freeze-dried concentrates. </li></ul><ul><li>Mechanism of action: All clotting factors are necessary for normal blood coagulation. </li></ul>
  3. 3. Platelets (resting to activation) <ul><li>Shape change </li></ul><ul><li>Aggregation </li></ul>
  4. 4. TX A 2 -R GP IIb/IIIa PDE
  5. 5. <ul><li>Antiplatelet agents </li></ul><ul><li>Aspirin </li></ul><ul><li>Mechanism of action: Aspirin blocks the synthesis of thromboxane A 2 from arachidonic acid in platelets, by acetylating and thus inhibiting the enzyme cyclooxygenase. Thromboxane A 2 stimulates phospholipase C, thus increasing calcium levels and causing platelet aggregation. </li></ul><ul><li>Dipyridamole </li></ul><ul><li>Mechanism of action: Dipyridamole causes inhibition of the phosphodiesterase enzyme that hydrolysis cAMP (cGMP). Increased cAMP (cGMP) levels result in decreased calcium levels and inhibition of platelet aggregation. </li></ul><ul><li>Glycoprotein IIb/IIIa inhibitors </li></ul><ul><li>Abciximab is the main drug currently in this class. </li></ul><ul><li>Mechanism of action: Abciximab is an antibody fragment directed towards the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor of platelets. Binding and inactivation of the GPIIb/IIIa receptor prevents platelet aggregation. </li></ul>
  6. 7. <ul><li>Fibrinolysis </li></ul><ul><li>The fibrinolytic or thrombolytic system functions to dissolve a clot once repair of the vessel is under way. Plasmin digests fibrin. It is formed from plasminogen through the action of plasminogen activators, the best example of which is tissue plasminogen activator (t-PA ). </li></ul>
  7. 9. <ul><li>Fibrinolytic agents </li></ul><ul><li>Streptokinase </li></ul><ul><li>Mechanism of action: Streptokinase forms a complex with, and activates, plasminogen into plasmin, a fibrinolytic enzyme. </li></ul><ul><li>Tissue-type plasminogen activators </li></ul><ul><li>Alteplase and reteplase are examples of t-PAs. </li></ul><ul><li>Mechanism of action: t-PAs are tissue-type plasminogen activators. </li></ul>
  8. 11. <ul><li>Thank You for Your Attention! </li></ul>
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