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Intrinsic pathway of blood clotting.

Posted by Mumtaz khan Thursday, 10 November 2011

         The intrinsic pathway of blood clotting is more complex than extrinsic and it occurs more slowly. It is so named because its activators are in direct contact with blood.In other words,the activators are in direct contact with blood.In other words the activators are within or intrinsic to blood.If the endothelial cells become damaged,blood can come in contact with the exposed collagen.In addition the trauma to the endothelial cells causes damage to the blood platelets resulting in the release of phospholipids by the platelets contact with collagen activates c.f  XII.Activated c.f XII further activates c.f.XII Activation of c.f XI in presence of co-factor Calcium ions activates c.f IX.activation of c.f IX under the influence of co-factor Calcium ions,c.f VIII and phospholipids of platelets will activate c.f X. Activation of c.f X in combination with c.f V again under the influence of co-factor Calcium results in formation of Prothombinase.This takes several minutes.As a result completion of stage I in intrinsic pathway is of longer duration as compared to that in Extrinsic pathway.
Stage 2 and stage 3 are similar as described for Extrinsic pathway.
The last step involved which is common to both the pathways is conversion of loose fibrin threads into more stabilizing and strengthened fibrin threads is done by activated c.f XIII. C.f. XIII is activated by thrombin,then at the end the clot becomes sturdy whereby blood corpuscles have been trapped in the meshwork of stabilized fibrin in threads and what oozes out is watery straw coloured fluid serum which is plasma protein and other coagulation factor.

Once a clot is formed it plugs the ruptured area of blood vessel and prevents bleeding hemorrhage. Clot retraction or syneresis is consolidation or tightening of the fibrin clot. The fibrin threads attached to the damaged surface of blood vessel gradually contract.As the clot retracts it pulls the edges of damaged blood vessels closer and thus the risk of hemorrhage is further decreased and during this retraction some serum escapes betweeen the fibrin threads.
At times clotting mechanism starts at site which may spread beyond the area of damaged blood vessels.This is because thrombin has 2 positive feedback effects,whereby it may directly activate c.f V or result in release of phospholipids from the activated platelets from activated platelets.The combined effect of these resulting in synthesis of prothrombinase which in turn accelarates more and more synthesis of thrombin.If this remains unchecked a clot would continue to get larger and larger.Normally,however fibrin has the ability to inactivate much of the thrombin formed and this helps to stop the spread of thrombin into blood :Thus limiting the spread of the blood clot beyond the site of damage.


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