Circulatory System: Functions of blood-3

Subject: Anatomy and Physiology

Overview

Blood Clotting (Coagulation)

Blood coagulation, or clotting, is the final but most potent line of defense against bleeding. The process of coagulation turns blood from a liquid to a gel. When a vessel has been damaged, it is crucial for the blood to clot fast, but it is also crucial for the blood not to clot in the absence of vascular injury. With over 30 chemical interactions, it is the body's most complicated process.

Normally, the bloodstream contains several chemicals that are essential for clotting that are inactive. A few dormant enzymes, calcium ions, and other chemicals produced by platelets or injured tissues are among these elements. Procoagulants and anticoagulants are terms used to describe substances that influence clot formation.

Procoagulants and anticoagulants are kept in balance. The majority of procoagulants are liver-produced proteins. They are constantly present in inactive form in the plasma. The procoagulants (clotting factors) become active when there is an injury. When one factor in the clotting pathway is activated, it acts as an enzyme to activate the following one, and eventually a clot is formed.

Each clotting factor depends on the activation of the one before it during the series of reactions that cause blood clotting. The process of coagulation primarily involves three crucial events:

  • Two reaction pathways to coagulation called the extrinsic and intrinsic pathway work simultaneously to form a complex substance called prothrombin activator (prothrombinase). From this point on, the clotting mechanisms have a common pathway.
  • Prothrombin activator converts a plasma protein called prothrombin into thrombin.
  • Thrombin converts fibrinogen (a plasma protein) into fibrin mesh, which traps blood cells and seals the hole.

The Coagulation Pathways

The Extrinsic Pathway

Clotting factors generated by the injured blood vessels and perivascular tissue start the extrinsic route. Extrinsic describes the fact that these components enter the bloodstream from cells that are not located inside blood vessels. This route can produce a clot in about 15 seconds. A tissue thromboplastin is released by the perivascular tissue and broken blood arteries (factor III). Tissue thromboplastin activates factor VII in the presence of Ca2+, and factor VII in turn activates factor X when factor V is present. Factor X activation completed the extrinsic route. The main difference between the extrinsic and intrinsic routes is how they get to activated factor X.

The Intrinsic Pathway

The intrinsic pathway is so named because it uses only clotting factors found in the blood itself. Everything needed to initiate clotting is present in the plasma or platelets. Damage to the endothelium of the blood vessel initiates the intrinsic pathway. It takes 3 to 6 minutes for a clot to form by this pathway.

 If the endothelium of blood vessel becomes damaged, blood comes in contact with the collagen fiber lying around the endothelium of the blood vessels. Damaged platelets, at the same time release platelet phospholipids (PF3). Once the collagen fiber comes in contact, it then activates factor XIL Through a cascade of reactions, this leads to activated factors XI, IX, and VIII, in an or each serves as an enzyme that catalyzes the next step. Finally a factor X is activated through of reactions. This pathway also requires Ca2+ and PF3 in the activation factor X, which completes the intrinsic pathway.

The Common Pathway

The subsequent processes in both the intrinsic and extrinsic pathways, together referred to as the common route, occur once factor X is activated. In the second step, prothrombin activator is created by the combination of factors X, III, and V in the presence of Ca2+ and PF3. This enzyme transforms the inactive prothrombin (factor II) into the active enzyme thrombin.

In the third step, thrombin changes plasma protein factor 1 (soluble fibrinogen) into insoluble fibrin threads. Red blood cells and platelets are caught in a fibrin network of threads that forms a clot. Thrombin also activates factor XIII (fibrin stabilizing factor) in the presence of calcium ions, which crosslinks the free fibrin threads and binds them tightly together to create a stabilized clot.

 Once a clot begins to form, it launches a self-accelerating positive feedback process that seals off the damaged vessels more quickly.

Vitamin K and Coagulation of Blood

A fat-soluble vitamin, vitamin K may be found in green leafy vegetables. Bacteria found in the large intestine produce some of the vitamin K. In the liver, vitamin K serves as a cofactor for the production of prothrombin and the factors VII, IX, and X. Warfarin is one example of a coumarin group drug that is used as an anticoagulant and works by opposing vitamin K's activity. These medications cause a deficit in prothrombin and other clotting factors by inhibiting the activity of vitamin K in the liver. Blood cannot clot properly when certain clotting factors are absent.

Dissolution of the Clot

The procedure of breaking up a clot, known as fibrinolysis, is also triggered when one forms. The breakdown of the clot is required to restore normal blood flow through the blood arteries once the repair of the vascular lesion has advanced. Thus, the fibrinolysis procedure eliminates the unnecessary clot. A brief chain of processes with a positive feedback element leads to fibrinolysis. Plasminogen, an inert blood protein found in the clot, is activated by chemicals found in blood and bodily tissues. Plasminogen is subsequently transformed into the active enzyme plasmin, an enzyme that dissolves fibrin. Thrombin, activated factor XII, and tissue plasminogen activator are some of these substances. Most tissues' endothelial cells produce these chemicals, which are then excreted into the blood.

As the plasmin is formed, it dissolves the clot by digesting fibrin threads and inactivating substances such as fibrinogen, prothrombin and factor XII.

What Keeps Blood Fluid

 Several controls are required to prevent coagulation when it is not needed. These include the following:

  • Vascular Endothelium- The smooth vascular endothelium prevents the platelets adhesions and activation of factor XII.
  • Dilution- At normal rates of blood flow, the thrombin (formed in small amounts in plasma) is diluted so quickly that a clot has little chance to form. If flow decreases, however, enough thrombin can accumulate to cause clotting (mounts in plasma) eases, however, enough
  • Anticoagulants- Several natural anticoagulants are present in the plasma. Antithrombin secreted by liver, deactivates thrombin before it can act on fibrinogen. Heparin interferes with the formation of prothrombin activator, blocks the action of thrombin on fibrinogen, promotes the action of antithrombin. Another anticoagulant, activated protein c A inactivates the two major clotting factors not blocked by antithrombin, and enhances activity of plasminogen activators.
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