10 Facts About Hemostasis

hemostasis
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What is Hemostasis?

Before we proceed to learn more about some vital aspects, let us first define hemostasis in the simplest form.

Hemostasis Definition: It is the natural process that causes bleeding to stop.

1. Primary and secondary hemostasis

In this process in which the body naturally forms clots to stop blood loss, hemostasis is promoting maintenance of the state of equilibrium in blood fluidity as an initial stage of wound healing where blood changes from liquid to gel. This balance is called hemostatic balance.

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There are two primary mechanisms that are involved in the prevention of excessive blood loss following an injury and the maintenance of fluidity of the blood within physiologically suitable conditions that are dependent on hemostasis.

The mechanisms are primary and secondary hemostasis which are two phases in order for the hemostatic process to take place when initiating the healing of a vascular injury. After the primary hemostatic process, which has the purpose of minimizing excessive blood loss, comes secondary hemostasis that entails the coagulation cascade.

In the presence of blood vessel injury, the cells that are present in the injured region convey signals to initiate primary hemostasis. Procoagulant response is used to describe this initial response, while its activators (vascular injury or genetic trigger) are referred to as pathological disturbances.

2. Hemostasis entails a series of mechanisms

Both phases of hemostasis (primary and secondary) consist of various detailed mechanisms that ensure hemostatic balance is maintained or regained. These mechanisms are reactions that are biochemical in nature and rely on one another rather than performing own functions separately.

The mechanisms do not occur at the same time but may initiate simultaneously upon endothelial damage depending on the location and degree of injury. The approach is a series of reactions that are procedural biologically. Their performance is fascinating in nature in that one process either activates the next or combines with it to execute a certain function.

  • Primary Hemostasis sequence of events include platelet adhesion, platelet activation, and platelet plug formation.
  • Secondary Hemostasis sequence of events include initiation of thrombin generation, amplification of thrombin generation, propagation of thrombin generation, and fibrin formation.

3. Initial hemostasis in response to vascular injury

When blood platelets and the damaged vascular endothelium comes in contact with each other, a reaction takes place. This initial reaction activates collagens types VI, I and III, vWF (von Willebrand Factor, laminins, thrombospondin, microfibrils, and fibronectin.

The vWF in particular, enables the attachment of platelets on the surfaces of endothelial cells. Also, the vWF has the role of connecting collagen fibrils and glycoprotein complex. The primary objective of initial activation is compelling the platelets to change in morphology to enable platelet adhesion and consequently, bring a stop to the blood loss.

4. Formation of fibrin during the hemostasis

Platelet adhesion is not as simple as it may be depicted here because it also entails quite a series of mechanisms. For platelet adhesion to take place, fibrinogen must be converted to fibrin. It is fibrin that is directly obliged to close the wound by forming a network of fibers that cover the injured area.

When the actual healing process is completed, the fibrin is dissolved by proteolytic enzymes, produced in the plasma component of the blood. Fibrin is formed by having Fibrinogen become converted to Fibrin by Thrombin.

5. Implications on the mutations of fibrinogen

Some individuals genetically inherit a deficiency in coagulant factors. This places their hemostatic systems to trigger abnormal blood clotting in the body without the presence of an injury. The individual may suffer from various conditions related to the lack of coagulant factors.

A mutation in fibrinogen is a circumstance that may develop. Individuals with underlying mutations are likely to suffer from thromboembolism. The condition is genetically inherited and occurs in a variety of other linked conditions.

Hyperfibrinogenemia, hypofibrinogenemia, and afibrinogenemia are some of the associated conditions.

Hyperfibrinogenemia pertains to dysfunctional fibrinogen, hypofibrinogenemia refers to reduced levels of fibrinogen, and afibrinogenemia means fibrinogen deficiency.

Also, when an individual lacks some proteins of the GPIb-GPIX-GPV and vWF complex, the individual may suffer from bleeding disorders.

6. Extrinsic cascade with hemostasis

In the event that the tissue factor (TF), which is referred to as factor III, is exposed due to an injury, the extrinsic pathway is activated. It has a major role in enabling the rapid release of thrombin through what is called a thrombin burst. It is the TF that forms the thrombin burst.

The role of thrombin in the coagulation cascade cannot be ignored for it provides feedback on activation functions.

The extrinsic cascade process consists of activities such as FVII being in contact with TF after isolating itself from the circulation; formation of activated complex in injured tissue; TF-FVIIa activation of FX and FIX; thrombin activation of FVII; conversion of FXa to FX through activation; and prothrombinase complex formation.

Prothrombinase complex participates in thrombin creation by activating prothrombin to thrombin.

7. How to enhance hemostasis by controlling levels of thrombin

An uncontrolled level of thrombin in the blood signals adverse health conditions. Thrombin inhibitors and feedback mechanisms are two processes that have a primary role in regulating the activities of thrombin in the blood.

The Antithrombin III is an inhibitor that prevents the activities of kallikrein, plasmin, Xia, Xa,and XIIa in the blood.

On the other hand, feedback mechanisms are known to initiate equilibrium between inactive and active enzymes. For this reason, they regulate levels of Thrombin, which entails active Thrombin levels.

8. Consequences on hemostasis due to deficiency in AHF

The Anti-hemolytic factor (AHF) originates from the platelets and blood vessel endothelial linings. It is also known as globulin, and Antihemophilic factor A.

Hemophilia A, or classical Hemophilia is a disorder associated with the deficiency of AHF. It is a recessive X-linked, genetic coagulation disorder. Classical hemophilia is the most common type of hemophilia and manifests as early as the individual’s young years. Unexplained bruises and excessive bleeding are major characteristics of the disorder.

9. Role of prothrombin in hemostasis

Prothrombin depends on vitamin K for activation, and it is a serine protease. The protein plays a substantial role in the formation of fibrin because prothrombin is converted into thrombin, where thrombin converts fibrinogen to fibrin.

Deficiency of prothrombin may suggest certain underlying medical conditions like menorrhagia in women, hypoprothrombinemia, and hemorrhagic diathesis.

10. Coagulation cascade in hemostasis

The coagulation cascade incorporates intrinsic and extrinsic pathways in the stages of hemostasis. Factors XII, XI, IX, and VIII activates the intrinsic pathway whereas, factors III, and VII initiates the extrinsic pathway.

For the activation of intrinsic pathway to be successful, the clotting factors needed for its initiation must be exposed to subendothelial collagen. On the other hand, extrinsic pathway activation must involve calcium ions.

Both the intrinsic and extrinsic pathways merge to activate factor X and later culminates to the common pathway. The common pathway entails coagulation factors I, V, II, and XIII. This results to the formation of the fibrin clot.



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