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Normally, haemostastis is maintained by three key events. The first stage, primary haemostasis, involves platelets and the blood vessels themselves. It is triggered by injury to a vessel, and platelets become activated, adhere to endothelial connective tissue and aggregate with other platelets. A fragile plug is thus formed which helps to stem haemorrhage from the vessel. Substances are released from platelets during primary haemostasis. Vasoactive compounds give vasoconstriction, and other mediators 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.
Normally, haemostastis is maintained by three key events. The first stage, primary haemostasis, involves platelets and the blood vessels themselves. It is triggered by injury to a vessel, and platelets become activated, adhere to endothelial connective tissue and aggregate with other platelets. A fragile plug is thus formed which helps to stem haemorrhage from the vessel. Substances are released from platelets during primary haemostasis. Vasoactive compounds give vasoconstriction, and other mediators 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.
The platelet plug formed by primary haemostasis is fragile and must be reinforced in order to provide longer-term benefit. In 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 I, VII, IX and X are dependent upon vitamin K to become active.
The platelet plug formed by primary haemostasis is fragile and must be reinforced in order to provide longer-term benefit. In 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 I, VII, IX and X are dependent upon vitamin K to become active.
The end product of haemostasis is a solid clot composed of fused platelest enclosed in a mesh of fibrin strands. Excessive clot formation is prevented by the fibrinolytic system, which acts to breakdown fibrin within blood clots.
The end product of haemostasis is a solid clot of fused platelets enclosed in a mesh of fibrin strands. It is important that uncontrolled, widespread clot formation is prevented, and so a fibrinolytic system exists to breakdown 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).
==Tests Evaluating Primary Haemostasis==
==Tests Evaluating Primary Haemostasis==