CLOTTING AND ANTICOAGULANTS

Blood thinners or Anticoagulants are medicines that prevent blood clots from forming in the bloodstream. This reduces the risk of medical problems that are caused by blood clots such as heart attacks, strokes, thrombosis and embolism.

 Before understanding the mode of action of warfarin, we’ll explore the clotting phases first.
           Let’s Go! 
            

           There are 4 phases of blood clotting which  are;
  • Vascular phase: After initial injury a brief period of arteriolar vasoconstriction occurs. As a result of reflex neurogenic mechanisms. It is augmented by the local secretion of factors such as endothelin. The effect is transient.
  • Platelet phase: Blood vessel wall, endothelial cells, prevent platelet adhesion and aggregation. platelet contain receptors for fibrinogen and von-Will brand factor. After vessel injury platelets adhere and aggregate and release permeability increasing factors, VPF. It loose their membrane and form a viscous plug.
  • Coagulation Phase: it has 2 major pathways, intrinsic pathways and extrinsic pathways. Both converge at a common point.
  • Fibrinolysis: enhances degradation of clots..    .                                                                                                                                                                                                                                              
 In response of clotting, anticoagulants are administrated via different routes. Parenteral Anti- coagulant are heparins either unfractionated heparins or enoxaparin, dalteperin ,reviperin and danaparoid .Oral anti-coagulants are warfarin, dicumarol  and phenindione. New oral anticoagulants are dabigatran and apixaban
            In this BlogSpot we’ll discuss more common  warfarin’s mode of action.

WARFARIN: WISCONSIN ALUMNI RESEARCH FOUNDATION COUMARIN

Warfarin-Pharmacokinetics:

  • Rapidly and completely absorbed
  • 100% bioavailability
  • Highly plasma protein bound (99%)
  • Crosses the placenta
  • Appears in milk
  • Variable but slow clearance
  • Biotransformation by liver by oxidation and glucuronidation. Its stops the synthesis of clotting factors VII, IX, X, and II.
  • Half-life is 40 hours.

Adverse Effects:

  • Bleeding: most common and serious adverse effect can be epistaxis, hematuria, and GIT bleeding, internal hemorrhages.
  • Cutaneous Necrosis: This is due to decreased activity of protein C.
  • Infarction: Infarction of breasts, fatty tissues, intestines and extremities due to venous thrombosis caused by again decreased activity of protein C.

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