6,502
edits
Changes
Jump to navigation
Jump to search
→Description
Primary haemostasis alone will only be temporarily beneficial unless the platelet plug is reinforced by fibrin assembled by the clotting cascade (secondary haemostsis). Secondary haemostasis is dependent on the interactions of a number of proteins (clotting factors) within the intrinsic, extrinsic and common pathways of the cascade. The clotting factors aer synthesisde in the liver. The factors circulate in the plasma in an inactive from. Fatos I, VII, IX and X are dependent upon vitamin K to become active.
Primary haemostasis alone will only be temporarily beneficial unless the platelet plug is reinforced by fibrin assembled by the clotting cascade (secondary haemostsis). Secondary haemostasis is dependent on the interactions of a number of proteins (clotting factors) within the intrinsic, extrinsic and common pathways of the cascade. The clotting factors aer synthesisde in the liver. The factors circulate in the plasma in an inactive from. Fatos I, VII, IX and X are dependent upon vitamin K to become active.
Fibrinolysis, the process of plasmin-induced fibrin breakdown, prevents uncontrolled widespread clotting and is comprised of a number of mechanisms. The two most important naturally occuring antigcoagulant proteins are antithrombin III (ATIII) and Proteoin C. When complexed with heparin sulphate, ATIII inactivates thrombin and can also inactivate factors IX and X. Firbrin degratation products (FDP) are the end products of fribrinoloysis.
Normally, haemostastis is maintained by three key events<sup>3</sup>. 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, fibrinogen is polymerised to fibrin which reinforces the platelet plug. Some components of the coagulation and fibrin formation stages are dependent on vitamin K, and it is these which are influenced by anticoagulant rodenticide activity.
Normally, haemostastis is maintained by three key events<sup>3</sup>. 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, fibrinogen is polymerised to fibrin which reinforces the platelet plug. Some components of the coagulation and fibrin formation stages are dependent on vitamin K, and it is these which are influenced by anticoagulant rodenticide activity.