The blood clotting process prevents massive bleeding that could cause death if left unchecked.

Note the clot formed by a mesh of fibrin threads

Blood clotting is an extremely important process for our health, as it prevents excessive blood loss from bleeding. When any type of injury occurs that generates blood extravasation, clotting immediately begins, which is based on physical and chemical changes in the blood, with the involvement of several factors.

Clotting occurs thanks to a series of reactions that take place between proteins called clotting factors . Usually these factors are represented by Roman numerals, and the activated form is indicated by a letter “a” that appears right after the numeral.

According to the classic model of blood clotting proposed in 1964, initially platelets release an enzyme called thromboplastin at the injured site. This, in turn, together with calcium ions, transforms the enzyme prothrombin into thrombin, which is a proteolytic enzyme that transforms fibrinogen into fibrin monomers by removing some peptides. These monomers polymerize and form fibrin strands. Finally, a network is formed from these wires, where blood cells, platelets and plasma are trapped, constituting the clot.

Thrombin is not normally present in the bloodstream and must be formed by changes in prothrombin, an inactive precursor. This is thanks to the action of a thrombin converting principle. The production of this principle occurs through the intrinsic or extrinsic path, which converge to a common path. The first pathway occurs when blood flow velocity is low, leading to the activation of enzymes within the blood, which triggers clotting and thrombus formation. In the extrinsic pathway, in turn, an interaction of blood elements with those outside the intravascular space is required. In both the extrinsic and intrinsic pathways, calcium ions are involved and acting as cofactors, allowing the reactions to take place.

After approximately one hour, the clot begins to retract, probably due to contraction of the platelet pseudopods. There begins the release of the so-called serum, which has a similar constitution to blood plasma, but does not have some clotting factors.

Currently, another model of blood clotting has been proposed and is based on the activation of the clotting process on different cell surfaces. According to the current model, which replaces the traditional “cascade” hypothesis, we can divide the process into four overlapping steps: initiation, amplification, propagation, and termination. In the initiation phase, vascular endothelium and blood cells are disturbed and FVIIa interacts with TF, a transmembrane protein. In the amplification phase, thrombin activates platelets, cofactors V and VIII, and factor XI on the platelet surface. In propagation, thrombin production and plug formation occurs at the site of injury. At completion, in turn, clot limitation occurs to prevent vessel occlusion.

It is important to note that some substances are directly linked to the delay in blood clotting. Among them, we can mention sodium citrate, potassium oxalate and heparin . The latter is widely used in the prevention of thrombotic diseases by inhibiting the action of some clotting factors.

Acquired or hereditary diseases can also cause clotting problems, causing both bleeding and thrombosis. Hemophilia , for example, is a serious hereditary problem that causes difficulty in clot formation and the occurrence of prolonged or spontaneous bleeding due to an abnormal synthesis of a clotting factor.

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