35- Coagulation series 1 of 7

KYJ Series Part1-Coagulation factors.

I've posted before about the differences between clotting and coagulation.  In summary, clotting is the clumping of platelets and coagulation is the solidification of fluid blood into a solid jelly.

The subject of this mini- series of  posts is Coagulation, and specifically the different proteins that cause it to happen.

There are 14 factors involved in the complex cascade that we know of as coagulation. Most of them have funky names that honour people in history who had a deficiency or a discovery of one or more factors, or some complicated chemical name. But all coag factors have a Roman numeral name , and it is these that I will refer to most.

Most nurses will remember the old intrinsic and extrinsic coagulation pathways, from 1st or 2nd year of their studies. This old theory has since been replaced by a similar "contact  activation vs common coagulation pathways"

This series will tackle this as simply as possible.

Start off with the following basics:

A blood vessel is lined by dynamic cells (endothelium) that produce many substances that repel platelets, constrict vessels, and inhibit solidification of blood.

If damaged, the underlying collagen surface of the vessel is exposed, and attracts platelets to stick to the injured vessel wall.  This exposed collagen also initiates the first steps of the coagulation cascade.

Here we start.
Damaged endothelium, allows platelets to stick because a substance in the collagen called Tissue factor (factor III) attracts platelets and his starts the cascade.
 Enter another substance secreted by endothelium.  Endothelium makes and stores von Willebrand factor (vWF). Von Willebrand factor is secreted from the endothelial cell both into the plasma and also under the endothelial layer into the subendothelial matrix. It is a large protein that acts like glue sticking platelets to one another and to the subendothelial matrix at an injury site.

The other major function of vWF is to act as a carrier protein for factor VIII (antihaemophilic factor).  More on this factor in another post.

So vonWillebrand Factor (vWF) allows platelets to stick to their mates- this is called platelet aggregation and when this happens, the platelet undergoes activation and the result is a fragile and unstable clot.

The unstable clot is called a Primary platelet plug, because it aims to plug the hole in the vessel wall at the site of endothelial injury.

To stabilise and strengthen the clot, plasma is activated to form strands of insoluble fibrin, which wraps around the clot like a mesh, and traps more platelets, and blood cells floating past.

The activation of plasma takes place by the release of the tissue factor (factor III) and vWF now joining with a plasma protein called proconvertin (factor VII).

This chemical cocktail activates Factor VII into VIIa .  The little "a" means activated.

This is the contact activation or (extrinsic) pathway under way.

In our next part we will
Look at the role of activated factor VII (FVIIa), and the solidification of plasma.

Summary:
Vessel injury exposes FIII to platelets and plasma.
Platelets respond by using vWF to stick together.
Plasma responds by activating FVII.

It does get exciting from here on in.