Changes

[[Image:LH_Platelet_Histology.jpg|thumb|right|<center><p>'''Platelets'''</p>^{©RVC 2008}</center>]]

[[Image:LH_Platelet_Histology.jpg|thumb|right|<center><p>'''Platelets'''</p>^{©RVC 2008}</center>]]

Normally, [[Normal Mechanisms of Haemostatic Control|haemostastis]] is maintained by three key events:   

Normally, [[Normal Mechanisms of Haemostatic Control|haemostastis]] is maintained by three key events:   

*Primary haemostasis involves platelets and the blood vessels themselves and is triggered by injury to a vessel - platelets become activated, adhere to endothelial connective tissue and aggregate with other platelets. A fragile plug is formed which helps to stem haemorrhage from the vessel. Substances released from platelets during primary haemostasis include vasoactive compounds to induce vasoconstriction and other mediators that cause continued platelet activation and aggregation, as well as contraction of the platelet plug. Primary haemostasis ceases once defects in the vessels are sealed and bleeding stops.

*'''Primary haemostasis''' involves platelets and the blood vessels themselves and is triggered by injury to a vessel - platelets become activated, adhere to endothelial connective tissue and aggregate with other platelets. A fragile plug is formed which helps to stem haemorrhage from the vessel. Substances released from platelets during primary haemostasis include vasoactive compounds to induce vasoconstriction and other mediators that cause continued platelet activation and aggregation, as well as contraction of the platelet plug. Primary haemostasis ceases once defects in the vessels are sealed and bleeding stops.

*Secondary haemostasis, proteinaceous clotting factors interact in a cascade to produce fibrin to reinforce the clot. Two arms of the cascade are activated simultaneously to achieve coagulation: the intrinsic and extrinsic pathways. The intrinsic pathway is activated by contact with collagen due to vessel injury and involves the clotting factors XII, XI, IX and VIII. The extrinsic pathway is triggered by tissue injury and is effected via factor VII. These pathways progress independently before converging at the common pathway, which involves the factors X, V, II and I and ultimately results in the formation of fibrin from fibrinogen. Factors II, VII, IX and X are dependent upon vitamin K to become active.

*'''Secondary haemostasis''' occurs when proteinaceous clotting factors interact in a cascade to produce fibrin to reinforce the clot. Two arms of the cascade are activated simultaneously to achieve coagulation: the intrinsic and extrinsic pathways. The intrinsic pathway is activated by contact with collagen due to vessel injury and involves the clotting factors XII, XI, IX and VIII. The extrinsic pathway is triggered by tissue injury and is effected via factor VII. These pathways progress independently before converging at the common pathway, which involves the factors X, V, II and I and ultimately results in the formation of fibrin from fibrinogen. Factors II, VII, IX and X are dependent upon vitamin K to become active.

*Fibrinolysis is the final stage of restoring haemostasis - it prevents uncontrolled, widespread clot formation and breaks down the fibrin within blood clots.  The two most important anticoagulants involved in fibrinolysis are antithrombin III (ATIII) and Protein C. The end products of fibinolysis are fibrin degratation products (FDPs).

*'''Fibrinolysis''' is the final stage of restoring haemostasis - it prevents uncontrolled, widespread clot formation and breaks down the fibrin within blood clots.  The two most important anticoagulants involved in fibrinolysis are antithrombin III (ATIII) and Protein C. The end products of fibinolysis are fibrin degratation products (FDPs).