37 - Coagulation Factors part 3 of 7

KYJ37- Series part 3- Coagulation.

Summarising Coagulation : the solidification of liquid blood into
A solid gel is called Coagulation. It starts with either an injury to a vessel wall , or blood coming into contact with a negatively charged surface eg Bacteria, tissue injuries.

In the first two episodes we looked at the extrinsic pathway (vessel wall injury) and simplified the steps and coagulation factors (F):
F3 activates F7
F7 activates F10
F10 activates F2 (prothrombin into Thrombin)

Easy to remember if we say this simple math equation.
3+7=10 (2 Easy). A euphemism for the steps.

The activation of F10 was described as the beginning of the what is called the "Common Pathway", so named because both the extrinsic and intrinsic coagulation paths lead to the activation of F10 (Factor X).

So let's kick of from the Thrombin (factor IIa) the activated form of a Factor II.

Thrombin is a protein enzyme which is pivotal in the clotting cascade. Thrombin (FIIa) converts a plasma protein called Fibrinogen (Factor I) into the end product of coagulation, Fibrin (Factor Ia).

Fibrin are fine strands of fibres or strands which bond together in plasma to form a mesh like net.

This mesh wraps itself around and through platelets that aggregate at the site of the injured blood vessel.  They sort of weave the platelet clot into a tight stable clump called a Fibrin Clot.  The net like mesh further traps blood cells and more platelets together causing solidification of the blood.

Ultimately, all coagulation pathways lead to this final process of a Fibrinogen being converted (activated) into Fibrin.

Look at any scab or clot and what you are looking at is blood cells, platelets, and solidified plasma (Fibrin).

The whole process started with the exposure of blood to Tissue a Factor (FIII) and it finished with Factor I activated.

In our next edition, we will look at Factor 12 and the initiation of the Contact Pathway (Intrinsic) ,