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Normal Mechanisms of Haemostatic Control (view source)
Revision as of 09:20, 29 September 2010
, 09:20, 29 September 2010→Platelet factors
==Platelet factors==
==Platelet factors==
Platelet responses are critical in maintaining haemostasis. When platelets are activated, the haemostatic plug is formed. Regulation by thrombosthenin gives clot organisation and fibrin formation; the clot continues to organise and contract over the 3-5 days following formation.
==Platelet Release==
A series of events activates platelets to allow them to form the haemostatic plug:
===Adhesion===
The first stage in platelet activation is an increase in the adhesiveness of platelets which may be initiated by several scenarios:
*The release of ADP from damaged endothelial cells.
*Platelet contact with collagen or basement membrane.
*Platelet contact with some denatured proteins and antibody-antigen complexes.
A friable and leaking plug is formed within 1 minute by this adhesion stage.
===Agglutination===
More ADP is released, bringing and linking more platelets into the clot.
===Aggregation===
This is also known as viscous metamorphosis - platelets aggregate to form a tightly packed mosaic which results in compaction of the plug. This gives a good temporary seal to the injured vessel in about 5-30 minutes.
===Disruption===
Further aggregation of platelets is stimulated by prostaglandin endoperoxide (PGG2) release. Platelet breakdown produces phospholipids (platelet factors 3 and 4).
Platelet factors catalyse the conversion of soluble fibrinogen to insoluble fibrin resulting in a progessive infiltration of the initial thrombocyte plug by strands of fibrin, leading to the formation of a composite plug. The fibrin also polymerises, causing coagulation of the blood and clot formation.
Platelet factors catalyse the conversion of soluble fibrinogen to insoluble fibrin resulting in a progessive infiltration of the initial thrombocyte plug by strands of fibrin, leading to the formation of a composite plug. The fibrin also polymerises, causing coagulation of the blood and clot formation.