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Normal Mechanisms of Haemostatic Control (view source)
Revision as of 16:18, 15 October 2013
, 16:18, 15 October 2013no edit summary
==Introduction==
==Introduction==
Haemostasis is the normal spontaneous arrest of bleeding from ruptured blood vessels. Normal haemostasis depends on a combination of events: the vascular response, which occurs mainly at capillary and small blood vessel level, the platelet (or thrombocyte) response, which also occurs in capillaries and small vessels, and the blood coagulation response which takes place in the arteries and veins.
Haemostasis is the normal spontaneous arrest of bleeding from ruptured blood vessels. Normal haemostasis depends on a combination of events: the vascular response, which occurs mainly at capillary and small blood vessel level, the platelet (or [[Thrombocytes|thrombocyte]]) response, which also occurs in capillaries and small vessels, and the blood coagulation response which takes place in the arteries and veins.
Heamostasis is also conventionally classified into:
*'''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''' 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).
==Vascular Responses==
==Vascular Responses==
==Coagulation physiology==
==Coagulation physiology==
[[Image:2000px-Coagulation full svg.png|right|thumb|300px|<p>'''Coagulation Cascade''' Source: Wikimedia Commons. Author: Joe D (2007)</p>]]
The process of blood coagulation is a cascade system involving a series of conversions of proenzymes to active forms. The amount and speed of conversion increases at each level. The major trigger for the system is contact activation.
The process of blood coagulation is a cascade system involving a series of conversions of proenzymes to active forms. The amount and speed of conversion increases at each level. The major trigger for the system is contact activation.
==Platelet Responses==
==Platelet Responses==
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 responses are critical in maintaining haemostasis. When platelets are activated, the haemostatic plug is formed. Regulation by the contractile platelet protein thrombosthenin gives clot organisation and fibrin formation; the clot continues to organise and contract over the 3-5 days following formation. Thrombosthenin is present in platelet granules and in the platelet membrane.
A series of events activates platelets to allow them to form the haemostatic plug:
A series of events activates platelets to allow them to form the haemostatic plug:
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.
After the clot has formed, the platelets actively contract; the contractile protein is thrombosthenin. The fibrin strands shorten, increasing the strength of the clot and bringing the blood vessel walls closer together. The clot is progressively broken down by [[Haemostasis - Pathology#Fibrinolysis|fibrinolysis]] and infiltration by new fibroblasts and capillaries occurs.
After the clot has formed, the platelets actively contract; the contractile protein is thrombosthenin. The fibrin strands shorten, increasing the strength of the clot and bringing the blood vessel walls closer together. The clot is progressively broken down by fibrinolysis and infiltration by new fibroblasts and capillaries occurs.
[[Granulation Tissue|Granulation tissue]] is formed within 3 days, and permanent repair, either functional or non-functional, occurs in around 1 week.
[[Granulation Tissue|Granulation tissue]] is formed within 3 days, and permanent repair, either functional or non-functional, occurs in around 1 week.
==Regulation of Coagulation==
==Regulation of Coagulation==
The blood coagulation process is beneficial, as it is designed to minimise blood loss, however, if the mechanism is prematurely or inadvertently triggered or fibrin deposition becomes excessive, the blood vessels may become obstructed. There is an inhibition system to guard against the cascade being inappropriately triggered, and a mechanism to remove clots once their purpose has been achieved - ([[Haemostasis - Pathology#Fibrinolysis|fibrinolysis]]). Normally there is a dynamic equilibrium between clotting and fibrinolysis so that the vascular system is guarded from the two principal hazards - [[Haemorrhage - Pathology|haemorrhage]] and excessive clotting.
The blood coagulation process is beneficial, as it is designed to minimise blood loss, however, if the mechanism is prematurely or inadvertently triggered or fibrin deposition becomes excessive, the blood vessels may become obstructed. There is an inhibition system to guard against the cascade being inappropriately triggered, and a mechanism to remove clots once their purpose has been achieved - fibrinolysis. Normally there is a dynamic equilibrium between clotting and fibrinolysis so that the vascular system is guarded from the two principal hazards - [[Haemorrhage|haemorrhage]] and excessive clotting.
===Natural Inhibitors===
===Natural Inhibitors===
*Inactive kininogen (a 2-globulin fraction of plasma) is activated by plasmin and kallikreins which increases vascular permeability and leucocyte migration and may give rise to the pain sensation.
*Inactive kininogen (a 2-globulin fraction of plasma) is activated by plasmin and kallikreins which increases vascular permeability and leucocyte migration and may give rise to the pain sensation.
===The Complement System===
===The Complement System===
[[Complement|The complement system]] is another cascade system where inactive precursors in plasma are triggered by:
The [[Complement|complement system]] is another cascade system where inactive precursors in plasma are triggered by:
* Bacterial enzymes
* Bacterial enzymes
* Antigen-antibody complexes
* Antigen-antibody complexes
[[Category:Haemostasis|A]]
[[Category:Haemostasis and Bleeding Disorders]]
[[Category:Cardiology Section]]