The hemostasis It is a set of physiological processes that aims to stop bleeding when a blood vessel injury occurs. This mechanism includes the formation of a plug or clot that stops the bleeding and then all the mechanisms for the repair of the damage..
The goal of hemostasis is to keep the cardiovascular system, which is a closed circulation system, intact. The hemostatic system, therefore, works like a plumber in a water pipe system, plugging leaks or leaks and then repairing them to restore the damaged structure..
As the hemostatic process is quite complex and involves the participation of many different physiological mechanisms, it has been divided into two processes in order to facilitate its study. Thus, we speak of primary hemostasis and secondary hemostasis..
Primary hemostasis deals with the initial study of the hemostatic process, that is, the formation of the platelet plug. Secondary hemostasis takes care of the coagulation process itself.
Two thousand years ago, the Greek philosopher Plato described that "the blood when it left the body formed fibers." Plato was the first to use the term "Fibrin”Referring to blood.
This description was later accepted by many other philosophers, but it was not until the late 1800s and early 1900s that platelets were discovered and the first model of the clotting mechanism was made..
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When damage occurs to a blood vessel, three processes are activated sequentially. First, local vasoconstriction occurs, that is, the smooth muscle of the vascular wall contracts, reducing the diameter of the vessel to reduce blood loss.
Sometimes, when the vessels are very small, the constriction is so effective that it occludes the lumen of the tube and by itself stops the bleeding..
Injury to the vascular endothelium promotes adhesion of platelets to the injury site, and this platelet adhesion promotes the aggregation of more platelets that either end up occluding the site of injury or, in small vessels, can obstruct the vessel and stop blood flow in the vessel. affected vessel.
This process is self-limited, so that the platelet plug does not spread throughout the vessel, and constitutes the second process.
The blood clot is then formed by the sequential activation of a series of enzymes of the coagulation system that are circulating in the blood in their inactive form. These processes stop bleeding, but circulation must be restored (third process).
Therefore, once the initial objective has been achieved, which is to prevent leakage, the vessel walls are repaired and now the formed clot is smoothed or destroyed (fibrinolysis) and the blood flows normally again through the entire and perfectly reconstituted vessel..
This entire complex hemostatic process is rigorously regulated, so that its effects are limited to the injured area and damage can be quickly contained. Alterations in the physiological balance or regulation of hemostasis give rise to pathological states that present with thrombosis or bleeding.
Primary hemostasis refers to all the processes that allow the platelet plug to form. This involves platelet adhesion, activation, secretion, and aggregation..
Platelets are small nucleusless cell fragments 1 to 4 microns in diameter. These are formed by the fractionation of cells produced by the bone marrow that are called megakaryocytes. Platelets have a half-life of 8 to 12 days and are very active structures.
In the hemostasis process, the first thing that occurs is a vasoconstriction due to contraction of the smooth muscle of the vascular wall in the area of injury. This contraction is produced by direct mechanical effect of the element that injured the vessel and / or by activation of the perivascular nerve fibers.
When a blood vessel is injured, the collagen located just below the endothelium is exposed and platelets adhere to it and become activated. When activated, attached platelets release adenosine diphosphate (ADP) and thromboxane Atwo. These substances in turn induce the adhesion and activation of more platelets.
Adhesion and aggregation can continue until one of the small-caliber injured vessels is completely obstructed. Initially the platelet plug is loose, then during the next clotting process the fibrin strands will turn it into a rigid plug.
In areas adjacent to the vascular lesion, endothelial cells begin to secrete prostafilin, which is a substance with antiplatelet effects, that is, it prevents platelets from adhering.
The secretion of prostafilin by the vascular endothelium in the healthy areas peripheral to the lesion, it delimits the extension, along the vessel, of the platelet plug and confines it to the lesion area.
Activated platelets also secrete serotonin, a substance that is capable of enhancing vasoconstriction. In addition, they secrete thromboplastin, which is a substance that activates part of the coagulation cascade, as will be described later.
Other substances secreted by platelets are proteins called "fibrin stabilization factor" and a "growth factor". The growth factor induces the growth of endothelial cells, fibroblasts and smooth muscle cells of the injured vessel.
The final effect of the growth of the structures of the vascular wall induced by the growth factors released by the platelets is to initiate the repair of the vascular lesion..
Secondary hemostasis refers to the coagulation process itself. It is an enzymatic process that involves a cascade of reactions by which soluble fibrinogen is converted into fibrin, an insoluble substance that polymerizes and crosslinks to form a stable clot..
In extensive vascular lesions, the clot begins to appear about 15 to 20 seconds after the injury. On the other hand, in minor injuries this appears 1 to 2 minutes later.
Three types of substances are responsible for starting this enzymatic cascade.
1- Activating substances from the injured vascular wall.
2- Substances produced by platelets.
3- Blood proteins that adhere to the injured vascular wall.
More than 50 substances related to blood clotting processes have been found. These can be classified into those that promote clotting, which are called procoagulants, and those that inhibit clotting, which are called anticoagulants..
The balance between the activity of these two groups of substances will be responsible for whether or not the blood clots. Normally anticoagulants predominate, except in the area where some trauma to a vessel occurs in which the activity of procoagulant substances will predominate.
The enzymatic activation cascade ends up activating a group of substances that are collectively called prothrombin activator. These prothrombin activators catalyze the transformation of prothrombin into thrombin, the latter acting as an enzyme that converts fibrinogen to fibrin..
Fibrin is a fibrous protein that polymerizes and forms a network in which it traps platelets, blood cells, and plasma. These fibrin fibers additionally adhere to the injured surface of the vessel. This is how the clot forms.
Once formed, the clot begins to retract and squeezes out all the serum that was inside. The squeezed liquid is serum and not plasma, as it does not contain coagulation factors or fibrinogen..
Platelets are essential for clot retraction to occur. These produce the stabilizing factor fibrin, which is a procoagulant substance. In addition, they contribute directly to the retraction process by activating their own contractile proteins (myosin)..
A plasma protein called plasminogen, also called profibrinolysin, is trapped in the clot along with other plasma proteins. Injured vascular tissues and endothelium release a potent plasminogen activator called tissue plasminogen activator (t-PA).
The release of t-PA is slow and is completed within a few days after the clot has formed and the bleeding has stopped. T-PA activates plasminogen and converts it to plasmin, a proteolytic enzyme that digests fibrin fibers and much of the clotting factors confined in the clot.
Thus, plasmin removes the clot once the vessel is repaired. If the clot was in a small vessel obstructing blood flow, the effect of plasmin rechannels the vessel and flow is restored. Thus concludes the hemostatic process.
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