Thrombophillia is an inherited or acquired disease condition that is characterised patient is predisposed to develop intravascular thrombosis. The pathogenesis of thrombus can be understood by a model proposed by Virchow and popularly its known as Virchow triad. According to this model the ultimate cause of thrombosis due to different aetiologies are by three mechanisms:
Abnormal Blood Flow
Hyperviscosity of blood are major determinants of arterial thrombosis. Causes of hyperviscosity includes acute leukemias, polycythemia vera, cryoglobulinemia and plasma cell dyscrasias such as multiple myeloma and waldenstrom macroglobulinemia. Venous thrombi on the other hand develop in low shear stress and the major determinant in this case is the presence of stasis of blood. Classical example of this mechanism is the DVT that occur in patients who are drive for long time or those who are bed ridden owing to trauma or head injury.
Endothelial injury leads to exposure of highly thrombogenic molecules that leads to activation of coagulation and ultimately the formation of intravascular thrombus. The thrombosis usually starts with platelet adhesion to abnormal endothelial surface or collagen present in sub endothelium. The adhered platelets get activated and they release their granule contents. The effect of these granules is the release of ADP, ATP, calcium and serotonin which leads to recruitment of more platelets and their activation. Finally there is formation of a platelet plug. This platelet plug provides a phospholipids rich surface where the activation of coagulation takes place and thrombus is formed.
Hypercoagulable state: These are inherited or acquired causes that lead to abnormalities of platelets, coagulation proteins or fibrinolytic factors causing development of thrombi.
Last modified: 12/02/2018