Blood Clotting-A Dual Process

In the past week I have been busy reading more sources and trying to piece together exactly what goes on in the process from when you get an injury to when your blood forms a clot. I made a mistake when I did the initial research on this topic; I didn't take into account all the processes that create a clot.

Initially, I was under the impression that there was a chemical response that activated the platelets to form a platelet clot. I thought this platelet clot was a blood clot and fibrinogen was the activator and the molecule that formed the web like structure of the clot holding the platelets together. But that is only half the story.

On the other side you have the extrinsic pathway. This is what makes the fibrinogen into the insoluble fibers that form the clot. The extrinsic pathway is a series of activations where the produce of one reaction is the catalyst for the next activation. The steps in this activation pathway are knows as factors. The final factor is thrombin. Thrombin has a dual purpose in blood clotting. First, it is a negative feedback loop that causes the intrinsic pathway to repeat itself. It also is the activator for fibrinogen to form in fibrin monomers which in turn are activated to form into insoluble fibrin polymers, which trap blood cells into forming the red clot.

Both the red clot and the white clot combine to form a blood clot. Each process does half of the clotting.

My original question of : What would happen if you did something to the platelet receptor alphaIIbBeta3 still stands. You cant form a blood clot without both parts of the clotting process in check. The platelet white clot is the first to attach to the vascular injury and without it, the red clot cant do anything.

I can still focus on the platelet receptors, but it was important to understand the whole clotting process before I start. One does not exist without the other.