The pathogenesis of<unk>  is multi-factorial. It is characterized by hypercoagulability, which by itself or in synergy with endothelial injury or stasis (Virchow's Triad) can predispose to clot formation. Multiple genetic mutations and predisposing conditions have been associated with the increased risk of thrombosis due to abnormalities in the coagulation cascade. The most common genes involved in the pathogenesis of acquired<unk> s are Factor V Leiden and prothrombin gene mutations.
Thrombophilia pathophysiology
Antiphospholipid syndrome risk factors
Thrombocytopenia pathophysiology
Deep vein thrombosis pathophysiology
Portal vein thrombosis pathophysiology
Thrombosis pathophysiology
Polycythemia pathophysiology
Essential thrombocytosis pathophysiology