The process of hemostasis is made up of different mechanisms, all with the same objective; to prevent excessive blood loss and promote healing, maintaining an equilibrium.
When the endothelium is ‘provoked,’ it reacts by activating a series of reactions (biochemical) that ensures a state of hemostatic balance. The initial reaction takes place when the vascular endothelium wall and platelets come in contact with one another.
The process further initiates certain collagen including types VI, III and I. Also activated in the initial response are laminins, microfibrils, von Willebrand Factor (vWF), fibronectin, and thrombospondin.
A common and important role that activated blood components perform is enabling platelet adhesion by initiating changes in the morphology of platelets.
Further discussed below are some significant clotting factors
1. Stuart factor
It functions in both intrinsic and extrinsic pathway, the first member of the thrombin pathway or final common pathway with the liver as its source.
It takes quite some combinations to activate the Stuart factor. The combinations that enable activation are calcium, proconvertin, Anti-hemoplytic factor, and the Christmas factor. The major role of the clotting factor is to change prothrombin to thrombin. It does this with the help of platelet phospholipids.
Although, both of their efforts are not enough to enable the conversion. Therefore, a catalyst is needed to speed up the reaction. That catalyst is Proaccelerin in the activated state.
The pathway of Proconvertin is extrinsic which also comes from the liver. Stable factor and Serum Prothrombin Conversion Accelerator (SPCA) are other names used to refer to the clotting factor.
After being activated by thromboplastin, it in turn activates the Stuart factor. It plays a role in the conversion of prothrombin to thrombin with its involvement in the activation of the Stuart factor which combines with other factors to enable the conversion.
3. Calcium Ions
Calcium ions are a key player in the hemostatic process for there are several calcium-dependent activities that cannot take place in its absence.
The pathway is both extrinsic and intrinsic where the bone is a major source. Also, it originates from the gastrointestinal track out of ingested foods that have undergone digestion.
Gamma, beta, and alpha are the three polypeptide chains that constitute fibrinogen. Thrombin converts fibrinogen into fibrin which helps stop excessive blood loss by forming a mesh around the injured tissues.
Insoluble fibrin will be the end result when thrombin acts on soluble fibrinogen during the conversion process. Fibrinogen originates from the liver and it is both intrinsic and extrinsic.
People who suffer from mutations in fibrinogen are found to suffer from thromboembolism. It is an inherited disorder where mutations occur in certain varieties which include dysfunctional fibrinogen (hyperfibrinogenemia), total lack of fibrinogen (afibrinogenemia), and limited presence of fibrinogen (hypofibrinogenemia).
Prothrombin and thrombin are inseparable in function because the Stuart factor enzymatically cleaves prothrombin into thrombin. Prothrombin is a serine protease dependent on vitamin K. The pathway is both intrinsic and extrinsic and comes from the liver.
Actually, fibrin cannot be formed in the absence of prothrombin. This is due to the fact that in order for the fibrin to be formed, the conversion of prothrombin to thrombin must take place first. Afterwards, the formed thrombin finalizes the process by converting fibrinogen to fibrin.
Lack of prothrombin in severe and prolonged cases can be life-threatening. The reason in support of this concern is that individuals with deficiencies of prothrombin are exposed to a variety of diseases which include: Hypoprothrombinemia or dysprothrombinemia, hemorrhagic diathesis, and menorrhagia (suffered by women).
6. Anti-hemoplytic factor (AHF)
Intrinsic in pathway, the coagulation factor works with calcium and the Christmas factor to enable activation of Stuart factor. It is solely activated by thrombin that originates from platelets and endothelium lining of blood vessels.
Anti-hemophilic factor A and Antihemophilic globulin are some of several designations that refer to the same clotting factor.
Individuals with a deficiency of AHF are likely to suffer from Hemophilia A. The disorder is a recessive coagulation disease that is X-linked (genetic) which is also referred to as classical hemophilia. It is termed classical because it is the most common category of hemophilia. Its victims depict progressive, gradual development of the condition posing great threat to the life of the involved person.
The start of manifestation can develop as early as at a young age, and the condition can dictate the health of the individual throughout lifetime.
Classical hemophilia is characterized by traumatic and spontaneous bleeding.
It originates from the liver and follows an intrinsic pathway. Prekallikrein works together with Hageman factor and Kininogen to ensure activation of PTA (Plasma Thromboplastin Antecedent).
The active form of prekallikrein is called Kallikrein which is a serine protease. It is Kallikrein that enables production of brandykinin when it cleaves kininogen.
8. Hageman factor
Hageman factor becomes activated when it comes in direct contact with injured blood vessel walls. It is intrinsic and comes from the liver.
The activation of a degrader for blood clots (plasmin) and PTA are its functions. However, in order to activate PTA, it requires support from both kininogen and prekallikrein.
9. Christmas factor
Anti-hemophilic factor B and Plasma Thromboplastin Component (PTC) are other names for the Christmas factor. It comes from the liver and it is intrinsic in pathway.
In order for the clotting factor to be activated, calcium and PTA must be present.
The Christmas factor functions to activate another factor, the Stuart factor. It does the activation process with the help of calcium and Anti-hemoplytic factor.
A deficiency of the Christmas factor causes the Christmas disease (hemophilia B).
Involved in the intrinsic pathway, it is also originated from the liver. Kininogen performs its major role in the mechanism of hemostasis by activating PTA. It does this successfully having its activities combined with the Hageman factor and Prekallikrein.
There are basically two essential life processes that entirely rely on hemostasis: It’s importance in preventing excessive loss of blood in response to injury, as well as maintenance of blood fluidity within required physiological conditions.
When hemostasis ensures balance on both important functions, a state of equilibrium is achieved. But when the balance is disturbed as a result of vascular injury, a procoagulant response is activated. The activation of a response is generally referred to as pathological disturbance.
However, this does not guarantee that the procoagulant response only becomes activated when injury occurs because some individuals genetically inherit deficiencies in coagulant factors resulting to alterations of normal functioning.
To top it all, hemostasis is simply a mechanism of the body that concerns prevention of further blood loss where the clotting factors initiate collaborative mechanisms to help ensure that hemostatic balance is regained.
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