10 Significant Clotting Factors
The process of hemostasis is made up of a number of mechanisms, all with the same objective; to prevent excessive blood loss and initiate a quicker healing, thereby maintaining an equilibrium. A brief overview of the mechanism of hemostasis in case of a disturbance to the vascular endothelium is that, 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. This further initiates certain collagen types VI, III and I. Also activated in the initial response are laminins, microfibrils, von Willebrand Factor (vWF), fibronectin and thrombospondin. One common and important role that these activated components have is that they enable platelet adhesion by initiating changes in the morphology of platelets.
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Further discussed below are some significant clotting factors
1. Stuart factor
Stuart Power Factor is the other biological name that can be used to refer to the Stuart factor. It is both intrinsic and extrinsic. The liver is its source. It takes quite some combinations to activate the Stuart factor. The combinations that enable its activation are calcium, proconvertin, Anti-hemoplytic factor and the Christmas factor. Its major role is to change prothrombin to thrombin. It does this with the help of platelets phospholipids. Though, both of their efforts are not enough to enable the conversion and therefore, a catalyst is needed to speed up the reaction. That catalyst is Proaccerin in the activated state.
The pathway of Procovertin is extrinsic and it also comes from the liver. Stable factor and Serum Prothrombin Conversion Accelerator (SPCA) are the other names used to refer to clotting factor. After being activated by thromboplastin, it in turn activates the Stuart factor. That means that it plays a role in the conversion of prothrombin to thrombin for its involvement with Stuart factor activation that combines with other factors to enable the conversion.
3. Calcium Ions
Calcium ions is a key player in the hemostatic process because there are several calcium-dependent procedures that cannot take place in its absence. Its pathway is both extrinsic and intrinsic and the bone is its major source. Also, it originates from the gastrointestinal track from food undergoing digestion.
Gamma, beta and alpha are the three polypeptide chains that constitute fibrinogen. Thrombin converts fibrinogen into fibrin that help 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 said to suffer from thromboembolism. This is an inherited disorder and the mutations occur in certain varieties. They 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 onto thrombin. It is a serine protease that is dependent on vitamin K. Its 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. Then, the formed thrombin finalizes the process by converting fibrinogen to fibrin. Lack of prothrombin can be termed as a near-disaster concern. 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)
This factor works with calcium and Christmas factor to enable activation of Stuart factor. It is solely activated by thrombin that originates from platelets and endothelium lining of blood vessels. It is intrinsic in pathway. Anti-hemophilic factor A and globulin are its other designations. Individuals with the 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 a great threat to life. The stage of manifestation develops 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 that is a serine protease. It is Kallikrein that enables production of brandykinin when it cleaves kininogen.
8. Hageman factor
Hageman factor gets activated when it comes in direct contact with injured blood vessel walls. It is intrinsic and comes from the liver. Activation of a degrader of blood clots (plasmin) and PTA are its functions. Though, 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 Christmas factor. It comes from the liver and it is intrinsic in pathway. In order to be activated, calcium and PTA must be present. It also activates another factor, the Stuart factor. It does the activation process with the help of calcium and Anti-hemoplytic factor. Deficiency of Christmas factor causes the Christmas disease (hemophilia B).
Being intrinsic and having originated from the liver, Kininogen performs its major role in the hemostasis mechanism by activating PTA. It does this successfully when its functions are combined with Hageman factor and Prekallikrein.
There are two life processes that entirely rely on the mechanisms of hemostasis. The mechanism has the task of preventing a lot of blood loss due to injury, and maintaining the blood fluidity within required physiological conditions. When hemostasis ensures a balance in the two life processes, a state of equilibrium is achieved. But when the balance is disturbed as a result of vascular injury, a procoagulant response is activated. The activators of the response is what generally referred to as pathological disturbances. Though, it is not a guarantee that the procoagulant response gets activated only when injury occurs, some people genetically inherit deficiencies of coagulant factors. To top it all, hemostasis is simply a mechanism of the body with concerns in the prevention of further blood loss where the clotting factors are collaborative mechanisms that help ensure hemostasis balance is regained.
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