Thrombosis

Thrombosis is the formation of a blood clot within a blood vessel or the heart. The clot can obstruct blood flow and damage downstream tissue.

Virchow's triad: A model identifying abnormal blood flow, vessel-wall injury, and hypercoagulability as interacting causes of thrombosis. These three conditions organize the main pathways that lead to thrombus formation.
Deep vein thrombosis: A blood clot in a deep vein, usually in the leg or pelvis. It is a common venous form of thrombosis and a source of pulmonary emboli.
Anticoagulant: A drug that reduces blood clot formation by interfering with coagulation. Anticoagulants are used to prevent thrombus extension and new clot formation.
Hemostasis: The normal process that stops bleeding through vessel constriction, platelet activity, and coagulation. Hemostasis is a regulated response to injury; thrombosis is clot formation within the circulation.
Factor V Leiden: An inherited variant of the F5 gene that makes coagulation factor V resistant to activated protein C. It is a common inherited predisposition to venous thrombosis.
Coagulation: The cascade of reactions that generates fibrin and stabilizes a blood clot. Coagulation supplies the fibrin framework that can stabilize a thrombus.
Pulmonary embolism: Blockage of a pulmonary artery, usually by material that traveled from a deep vein. A venous thrombus can detach and obstruct blood flow in the lungs.
Antiplatelet drug: A medicine that reduces platelet activation or aggregation. Antiplatelet therapy is especially important for preventing arterial thrombotic events.
Embolism: An obstruction caused by material that travels through the bloodstream and lodges in a vessel. Thrombosis forms a clot in place; an embolus travels before causing an obstruction.
Antiphospholipid syndrome: An autoimmune disorder associated with arterial or venous thrombosis and pregnancy complications. It demonstrates how acquired autoimmunity can increase clotting risk.

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