Anticoagulants are medications that work by interfering with the function of clotting factors in the coagulation cascade, preventing the formation of thrombi, or blood clots. These medications are used to prevent or treat thromboembolic events, such as deep vein thrombosis, pulmonary embolism, ischemic stroke, transient ischemic attack, coronary artery disease or myocardial infarction.
They're also used in clients with coagulation disorders, including antiphospholipid syndrome and disseminated intravascular coagulation; as well as in clients who underwent coronary angioplasty or cardiac valve replacement; and during surgical procedures like cardiopulmonary bypass, percutaneous coronary intervention, extracorporeal membrane oxygenation, and in clients undergoing dialysis.
One of the most important anticoagulants is warfarin, which is given orally, and works as a vitamin K antagonist.
Normally, vitamin K is used by the liver as a cofactor for the synthesis and activation of the clotting factors II, VII, IX, and X, as well as the anticoagulant proteins C and S. During this process, the active form of vitamin K, called vitamin K hydroquinone, is converted into vitamin K epoxide, which is then recycled back into vitamin K hydroquinone by another enzyme called epoxide reductase.
Warfarin antagonizes the function of vitamin K by inhibiting the epoxide reductase enzyme and preventing vitamin K hydroquinone from getting recycled. As a result, there’s no synthesis and activation of the clotting factors II, VII, IX, and X, but also the anticoagulant proteins C and S. Out of all the vitamin K-dependent proteins, protein C has the shortest half-life so it is the first to be depleted in clients taking warfarin. This results in an initial period of hypercoagulation before the anticoagulant effect kicks in. To prevent this, bridging anticoagulation with LMWH is usually prescribed for a short period while starting warfarin therapy.