Coagulability

Coagulability is the tendency of blood to clot, based on interactions among circulating coagulation factors, platelets, and vascular endothelium. In physiological terms, hemostasis proceeds in two linked phases: primary hemostasis forming a platelet plug, and secondary hemostasis creating a stable fibrin clot through the coagulation cascade. Coagulability is tightly regulated by procoagulant and anticoagulant forces, including natural anticoagulants such as antithrombin, protein C, and protein S, and by fibrinolysis, which dissolves clots via plasmin.

Variations in coagulability can be inherited or acquired. Inherited hypercoagulable states include factor V Leiden, prothrombin G20210A, and deficiencies of antithrombin, protein C, or protein S. Acquired conditions that increase coagulability include pregnancy, estrogen therapy, cancer, obesity, immobilization, surgery, and inflammation. Hypocoagulability arises from platelet disorders (thrombocytopenia), coagulation factor deficiencies (hemophilia A or B), vitamin K deficiency, liver disease, and certain medications; disseminated intravascular coagulation reflects simultaneous activation and consumption of coagulation factors.

Assessment of coagulability typically involves platelet count and coagulation tests such as prothrombin time (PT) with the international normalized ratio (INR) and activated partial thromboplastin time (aPTT). Specialized tests, including thrombin generation assays, may assess overall thrombotic tendency. Clinical implications range from thrombotic events (venous thromboembolism, arterial thrombosis) to bleeding risks, guiding strategies such as anticoagulation, antiplatelet therapy, or reversal of coagulopathy.