Changes

===Mechanism of Toxicity===

===Mechanism of Toxicity===

Normally, haemostastis is maintained by three key events.

Normally, haemostastis is maintained by three key events⁴. Firstly, platelets are activated, adhere to endothelial connective tissue and aggregate to form a platelet plug. Next, substances are released that trigger coagulation and vasoconstriction. Finally, once the vessel constricts soluble fibrinogen is polymerised to fibrin which reinforces the platelet plug.

 

The first phase is comprised of the platelet adhesion reaction in which activated platelets become sticky, attach to exposed endothelial connective tissue elements and build by aggregation to form a platelet plug. In the second phase, the so-called platelet release reaction, vasoactive and coagulation-triggering substances are released. The damaged vessel retracts, and the third phase, the coagulation mechanism by which soluble fibrinogen is converted to insoluble polymerized fibrin, is triggered.

This discussion addresses only those components of the coagulation mechanism (active in the second to third phases) whose concentration in plasma is influenced by vitamin K and only those compounds which act as vitamin K antagonists.

This discussion addresses only those components of the coagulation mechanism (active in the second to third phases) whose concentration in plasma is influenced by vitamin K and only those compounds which act as vitamin K antagonists.