![]() Regular monitoring of the PT / INR required (as vitamin K antagonists affect the extrinsic coagulation pathway).Indirect/ delayed reversal by increasing production of coagulation factors (e.g., with vitamin K substitution).Direct reversal by replacement (e.g., with prothrombin complex concentrate, FFP ).Mutations and polymorphisms in gene VKORC1 alter the effect of vitamin K antagonists.Inhibit hepatic vitamin K epoxide reductase → ↓ hepatic synthesis (recycling) of the active, reduced form of vitamin K → ↓ γ- carboxylation of glutamate residues on coagulation factors II, VII, IX, and X as well as protein C and protein S.Overview of commonly used oral anticoagulants For all substances, it is important to consider the dose-dependent risk of bleeding, especially when combining different substances that affect hemostasis (e.g., aspirin, clopidogrel, ticagrelor). Because of their comparatively short half-life and fewer interactions, NOACs are easier to control and administer than warfarin and do not require regular monitoring to ensure their efficacy and safety. ![]() NOACs act selectively via inhibition of thrombin ( dabigatran) or factor Xa ( rivaroxaban, apixaban, edoxaban). ![]() Vitamin K antagonists are also metabolized by C-P450 ( CYP) enzymes and therefore interact with a broad range of foods and drugs. This effect can last for several days, which complicates exact dosing and makes regular monitoring necessary. Vitamin K antagonists inhibit the enzyme vitamin K epoxide reductase, thereby blocking hepatic synthesis of the active, reduced form of vitamin K (needed for carboxylation of coagulation factors II, VII, IX, and X, protein C, protein S). Non- vitamin K antagonist oral anticoagulants ( NOACs) like dabigatran and rivaroxaban have also gained popularity in recent years. The most common oral anticoagulatory agents are vitamin K antagonists such as warfarin and phenprocoumon. Anticoagulants are used for treating and preventing embolic events.
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