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Lesson 8
Blood Coagulation


Coagulation of the blood is only one of the components in the larger function of stopping blood flow known as hemostasis. Hemostasis is a process in which there is a stoppage of blood flow from an injured blood vessel. It may be viewed as the combination of clotting and lysing mechanisms that maintain the integrity of the vascular system. There are two phases of hemostasis: Primary hemostasis, which is the formation of the platelet plug. Then there is secondary hemostasis, which is, the introduction of coagulation factors to form fibrin clot.

Platelets play a major role in the hemostatic process. Within 1 to 2 seconds after injury to a blood vessel, platelets come in contact with and adhere to the injured tissues (platelet adhesiveness). As a result, the platelets become swollen and extend pseudopodia. Serotonin (5-hydroxytryptamine), ADP, catecholamines, and platelet factor 4 (a glycoprotein with antiheparin activity) are released by the platelets. The ADP released by the platelets and also by the injured tissues causes the platelets to stick to one another (known as platelet aggregation; when platelets attach to non-platelet surfaces, this is called platelet adhesion). Platelets continue to aggregate until the site of injury is healed.

The vascular system also affects the hemostatic process through the function of vasoconstriction. The vascular mechanism involves the veins, arteries, and capillaries themselves. Their effectiveness depends on thickness of the vessel wall and its structure, contractibility, and retractibility. Bleeding into the tissues surrounding a wound increases perivascular pressure about small vessels, causing collapse and reduction of blood flow in larger vessels. Following the formation of a clot, clot retraction begins due to the action of actomyosin (thrombosthenin, the platelet contractile protein), which represents 15-20% of platelet protein.


Blood coagulation is the formation of a clot from liquid blood. When bleeding occurs, clotting is initiated by aggregation of platelets (see Figure 8-1). The platelets congeal to plug the site of the injury. The congealing (viscous metamorphosis) process is stimulated by contact with collagen (the supporting tissue surrounding blood vessels) or by the formation of thrombin. Hemostasis is not achieved without the simultaneous formation of fibrin. Platelet and plasma factors are activated, and by a complex process, a fibrin clot is formed. The arrest of bleeding is attained when a firm fibrin network seals the blood vessel wound with enough strength to withstand the impact of intravascular pressure.

Bleeding disorders such as hemorrhaging and thrombosis, occur in the following instances: injury to the vascular system, inadequate number of platelets and/or dysfunctional platelets, inadequate fibrin clotting mechanisms, and inadequate fibroblastic repair. The laboratory performs a variety of tests that assist the physician in his investigation of blood coagulation. Several of these tests measure the overall coagulation process. The bleeding disorders are due to one or several of the many factors involved in this process. In most instances, prolonged bleeding is due to a deficiency of one factor or another. However, in some instances it is due to therapeutic anticoagulants that are intentionally injected to interfere with the coagulation mechanism. In a few rare instances, prolonged bleeding is due to a natural or antigenically stimulated increase in circulating anticoagulants produced in the body.

Figure 8-1. Formation of unstable platelet plug.

The coagulation process is divided into two systems: the intrinsic pathway, which is the dominant pathway, all of the components are found in the circulating blood. The extrinsic pathway relies on thromboplastin, or tissue factor, (factor III), which is released from the damaged cells and tissues (see Figure 8-2). The distinction between the intrinsic and extrinsic pathways becomes blurred upon deeper analysis. As more and more information is gathered, it shows how each interacts with the other and feedback mechanisms work in combination. Examples of such is how activated factor XII, will trigger factor VII to its active form. Additional crossovers show with the activation of factor XI by activated factor VII.

Figure 8-2. Coagulation systems.

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