1. TRAUMA DUE TO TREATMENT Prof.S.Ramaswamy’s unit,M1 Dr.Sangeetha.C.Joseph
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10. 1.7 2.1 3.64 4.65 INR 21 21.2 22.4 21.3 aPTT Control-21 12.1 18.2 38.4 40.7 PT Control-11 DAY 8 DAY 6 DAY 3 DAY 1 INV
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18. INITIATION OF BLOOD COAGULATION Extrinsic Pathway Tissue trauma Leakage of Tissue Factor X Xa Prothrombin activator Ca +2 , factor VII Ca +2 Prothrombin Thrombin (factor II) Ca +2 Intrinsic Pathway Blood trauma/ contact with collagen Activation of factor XII, IX, VIII X Xa Ca +2 Prothrombin activator Prothrombin Thrombin (factor II) Activation of certain factors (VII, II, X and protein C and S) is essential for coagulation. This activation requires vit K (reduced form)
20. Warfarin Mechanism of Action Warfarin Synthesis of Non Functional Coagulation Factors Antagonism of Vitamin K Vitamin K VII IX X II
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22. PLASMA HALF-LIVES OF VITAMIN K-DEPENDENT PROTEINS Peak anticoagulant effect may be delayed by 72 to 96 hours 36h Factor X 24h Factor IX 6h Factor VII 72h Factor II
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29. INTERNATIONAL NORMALISED RATIO (INR) INR = [PT pt ] ISI [PT Ref ] PT pt – prothrombin time of patient PT Ref – prothrombin time of normal pooled sample ISI – International Sensitivity Index
44. May begin concomitantly with Heparin Therapy Heparin should be continued for a minimum of four days Time to peak antithrombotic effect of Warfarin therapy is delayed 96 hours (despite INR) When INR reaches desired therapeutic range, discontinue heparin ( after a minimum of four days ) Conversion from Heparin to Warfarin
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48. THE OVERALL ANTICOAGULATION QUALITY IS SIGNIFICANTLY BETTER WITH WARFARIN AS COMPARED TO ACENOCOUMAROL 72% 67% 64% 66% 68% 70% 72% % Responders Warfarin Acenocoumarol Thrombosis And Haemostasis 1994; 71(2): 188-191
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Notes de l'éditeur
The four Vitamin K dependent clotting factors are synthesized in the liver.
Warfarin acts as an anticoagulant by blocking the ability of Vitamin K to carboxylate the Vitamin K dependent clotting factors, thereby reducing their coagulant activity.
The signs of warfarin overdosage are listed on this slide. Hemorrhagic complications from warfarin therapy are more likely to occur with excessive degrees of anticoagulation, but even with an INR in the therapeutic range, bleeding can occur. Because of the likelihood of finding an underlying lesion in an individual who has gastrointestinal bleeding or significant genito-urinary bleeding in the face of therapeutic levels of anticoagulation, one is advised to consider and evaluate for underlying abnormalities predisposing to the bleeding. The return on such evaluations in the face of an excessive degree of anticoagulation diminishes, and one must use judgement whether or not to pursue an evaluation.
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