Clinical meaning
Anticoagulants prevent pathological clot formation by interfering with the coagulation cascade. They do NOT dissolve existing clots -- they prevent NEW clots from forming and existing clots from EXTENDING. The coagulation cascade has two pathways (intrinsic and extrinsic) that converge at Factor Xa, leading to thrombin (Factor IIa) generation and ultimately fibrin clot formation. HEPARIN (unfractionated heparin, UFH) works by binding to antithrombin III (AT-III), dramatically accelerating AT-III's ability to inactivate thrombin (IIa), Factor Xa, and other clotting factors. UFH requires IV or subcutaneous administration because it is a large molecule that cannot be absorbed orally. LOW MOLECULAR WEIGHT HEPARINS (enoxaparin/Lovenox, dalteparin/Fragmin) are smaller heparin fragments that primarily inhibit Factor Xa with more predictable pharmacokinetics, allowing fixed-dose subcutaneous administration without routine monitoring. WARFARIN (Coumadin) works by inhibiting vitamin K-dependent synthesis of clotting factors II, VII, IX, and X in the liver. It takes 3-5 days to achieve full anticoagulation because existing clotting factors must be depleted (Factor VII has the shortest half-life at 6 hours, but Factor II has a 60-hour half-life). This is why heparin is used as a BRIDGE during warfarin initiation. DIRECT ORAL ANTICOAGULANTS (DOACs): rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa) directly inhibit Factor Xa; dabigatran (Pradaxa) directly inhibits thrombin. DOACs have predictable pharmacokinetics and do NOT require routine monitoring.