Haemostatic Mechanism (Clotting Mechanism)

Blood  Clotting: Factors, Mechanism

 

Hemostasis mechanism of preventing blood loss

• One drawback of a circulatory system such as ours, in which the liquid blood is under high pressure, is that serious bleeding can take place after even a slight injury.
• To prevent the possibility of uncontrolled bleeding, we have a three-part hemostatic mechanism consisting of:
  • The constriction of blood vessels
  • The clumping together (aggregation) of platelets
  • Blood clotting
• Overall, hemostasis is a specific type of homeostasis that prevents blood loss.

1. Vasoconstrictive phase:

• Normally, when a tissue is damaged and blood escapes from a blood vessel, the vessel wall constricts in order to narrow the opening of the vessel and slow the flow of blood.
• This vasoconstriction is due to contraction of the smooth muscle of the vessel wall as a direct result of the injury and the release of vasoconstrictor chemicals from platelets.
• Proper vasoconstriction is also enhanced by pain reflexes, producing constriction in proportion to the extent of the injury.
• Constriction of capillaries, which donot have muscular layers, is due to the vascular compression caused by the pressure of lost blood that accumulates in surrounding tissues.
• Injured blood vessels may continue to constrict for 20 min or more.

2. Platelet phase:

• The next event in hemostasis is the escape from blood vessels of platelets, which swell and adhere to the collagen in adjacent connective tissues.
• This attachment stimulates vasoconstriction.
• By now, the platelets have become very sticky, so that as more and more of them move into the injured are they stick together.
• In about a minute they can clog a small opening in the vessel with a platelet plug.
• The process is called platelet aggregation.
• It is important partly because it successfully stops hundreds of small hemorrhages every day and partly because it triggers the blood-clotting mechanism.

3. Coagulation phase: Basic mechanism of blood clotting

• If the blood vessel damage is so extensive that the platelet plug cannot stop the bleeding, the complicated process of blood clotting- the coagulation phase- begins.
• The basic clotting mechanism involves the following events:
• Supported by a plasma globulin called antihemophilic factor (AHF), blood platelets disintegrate and release the enzyme thromboplastinogenase and platelet factor 3.
• Thromboplastinogenase combines with AHF to convert the plasma globulin thromboplastinogen into the enzyme thromboplastin.
• Thromboplastin combines with calcium ions to convert the inactive plasma protein prothrombin into the active enzyme thrombin.
• Thrombin acts as a catalyst to convert the soluble plasma protein fibrinogen (‘giving birth to fibrin’) into the insoluble, stringy plasma protein fibrin.
• The fibrin threads entangle the blood cells and create a clot.
• The basic process may be summarized as follows:
  • Thromboplastinogen —–Thromboplastinogenase+ antihemophilic factor——-> Thromboplastin
  • Prothrombin ——-Thromboplastin+ calcium ions-——-> Thrombin
  • Fibrinogen ——thrombin————> Fibrin

List of Blood clotting factors:

Coagulation factors number and name	Description and origin	Function
Plasma coagulation factors:
factor I: Fibrinogen	Plasma protein synthesized in liver.	Precursor of fibrin, converted to fibrin in final stage of clotting. Serum is plasma minus fibrinogen.
factor II: Prothrombin	Plasma protein synthesized in liver. Synthesis requires vitamin K.	Precursor of thrombin, the enzyme that converts fibrinogen into fibrin.
factor III: Thromboplastin	Complex lipoprotein formed from disintegrating platelets or tissues.	Combines with calcium to convert prothrombin into active thrombin.
factor IV: Calcium ions	Inorganic ion in plasma, acquired from bones and diet.	Essential for formation of thrombin and for all stages of clotting
factor V: Proaccelerin, labile factor, or accelerator globulin	Plasma protein synthesized in liver.	Necessary for extrinsic and intrinsic pathways
factor VI	No longer thought to be a separate entity, possibly the same as factor V.
factor VII: Serum prothrombin conversion accelerator (SPCA), stable factor or proconvertin	Plasma protein synthesized in liver. Synthesis requires vitamin K.	Necessary for first phase of extrinsic pathway.
facor VIII: Antihemophilic factor (AHF), antihemophilic factor A, or antihemolytic globulin (AHG)	Plasma protein synthesized in liver and other tissues.	Necessary for first phase of intrinsic pathway. Deficiency causes hemophilia A, genetic disorder
factor IX: Plasma thromboplastin component (PTC), Christmas factor, or antihemophilic factor B	Plasma protein synthesized in liver. Synthesis requires vitamin K.	Necessary for first phase of intrinsic pathway. Deficiency causes hemophilia B.
factor X: Stuart-Prower factor or Stuart factor	Plasma protein synthesized in liver. Synthesis requires vitamin K.	Necessary for early phases of extrinsic and intrinsic pathways.
factor XI: Plasma thromboplastin antecendent (PTA) or antihemophilic factor C	Plasma protein synthesized in liver.	Necessary for first phase of intrinsic pathway. Deficiency causes hemophilia C.
factor XII: Hageman factor or glass factor	Plasma protein, source unknown.	Necessary for first phase of intrinsic pathway, activates plasmin, activated by contact with glass, probably involved with clotting outside body.
factor XIII: Fibrin-stabilizing factor (FSF) or Larki-Lorand factor	Protein present in plasma and platelets, source unknown.	Necessary for final phase of clotting.

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