coagulation

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Related to Clotting cascade: plasminogen, INR

coagulation

 [ko-ag″u-la´shun]
1. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation or hotocoagulation.
2. in colloid chemistry, solidification of a sol into a gelatinous mass.
blood coagulation clotting.
diffuse intravascular coagulation (disseminated intravascular coagulation (DIC)) see disseminated intravascular coagulation.
coagulation factors factors essential to normal blood clotting, whose absence, diminution, or excess may lead to abnormality of the clotting. Twelve factors, commonly designated by Roman numerals, have been described (I–V and VII–XIII; VI is no longer considered to have a clotting function). (See table 6.)

Factor I is a high-molecular-weight plasma protein that is converted to fibrin through the action of thrombin; deficiency conditions are called afibrinogenemia and hypofibrinogenemia. Called also fibrinogen. Factor II is a glycoprotein present in the plasma that is converted into thrombin in the common pathway of coagulation; deficiency is called hypoprothrombinemia. Called also prothrombin. Factor III is involved in the extrinsic pathway of coagulation, activating factor X; called also tissue thromboplastin or factor.

Factor IV is calcium, required in many stages of blood clotting. Factor V is a heat- and storage-labile material, present in plasma and not in serum and is involved in the intrinsic and extrinsic pathways of coagulation, causing the cleavage of prothrombin to the active thrombin. Deficiency causes parahemophilia. Called also accelerator globulin or factor and proaccelerin. Factor VI is no longer considered in the scheme of hemostasis, and hence is assigned neither a name nor a function.

Factor VII is a heat- and storage-stable material, present in serum and in plasma and participating in the extrinsic pathway of coagulation, acting with factor III to activate factor X. Deficiency, either hereditary or acquired (vitamin k deficiency), leads to hemorrhagic tendency. Called also proconvertin and serum prothrombin conversion accelerator (SPCA). Factor VIII is a relatively storage-labile material that participates in the intrinsic pathway of coagulation, acting as a cofactor in the activation of factor X. Deficiency, an X-linked recessive trait, results in hemophilia a (classical hemophilia). Called also antihemophilic factor (AHF) and antihemophilic globulin (AHG). Factor IX is a relatively storage-stable substance involved in the intrinsic pathway of coagulation, acting to activate factor X. Deficiency of this factor results in a hemorrhagic syndrome called hemophilia b (or Christmas disease), which is similar to classical hemophilia A. It is treated with purified preparations of the factor, derived from human plasma or recombinant, or with factor IX complex. Called also plasma thromboplastin component (PTC) and antihemophilic factor B.

Factor X is a heat-labile material with some storage stability, which is involved in both intrinsic and extrinsic pathways of coagulation, uniting them to begin the common pathway. Once activated, it complexes with calcium, phospholipid, and activated factor V to form prothrombinase, which cleaves and activates prothrombin to thrombin. Called also Stuart or Stuart-Prower factor. Factor XI is a stable factor involved in the intrinsic pathway of coagulation, activating factor IX. Deficiency results in hemophilia c. Called also plasma thromboplastin antecedent (PTA) and antihemophilic factor C. Factor XII is a stable factor activated by contact with glass or other foreign substances, which initiates coagulation through the intrinsic pathway by activating factor XI; called also Hageman factor. Factor XIII is a factor that polymerizes fibrin monomers, enabling fibrin to form a firm blood clot. Deficiency causes a clinical hemorrhagic diathesis. Called also fibrin-stabilizing factor.

co·ag·u·la·tion

(kō'ag-yū-lā'shŭn),
1. Clotting; the process of changing from a liquid to a solid, said especially of blood (that is, blood coagulation). In vertebrates, blood coagulation is a result of cascade regulation from fibrin.
2. A clot or coagulum.
3. Transformation of a sol into a gel or semisolid mass, for example, the coagulation of the white of an egg by means of boiling. In any colloidal suspension, the disperse phase is greatly reduced via coagulation, thereby leading to a complete or partial separation of the coagulant; usually an irreversible phenomenon unless the basic nature of the substance is chemically altered.

coagulation

Hematology Clot formation Surgery The physical disruption of tissue to form an amorphous residuum, as in electrocoagulation and photocoagulation. See Coagulopathy, Interstitial laser coagulation.

co·ag·u·la·tion

(kō-ag'yū-lā'shŭn)
1. Clotting; the process by which a liquid, especially blood, changes from a liquid to a solid.
2. A clot or coagulum.
3. Transformation of a solution into a gel or semisolid mass.

coagulation

the separation or precipitation of suspended particles from a dispersed state.

Coagulation

The entire process of blood clotting.

co·ag·u·la·tion

(kō-ag'yū-lā'shŭn)
1. Clotting; the process of changing from a liquid to a solid, said especially of blood (i.e., blood coagulation).
2. A clot or coagulum.
References in periodicals archive ?
Does povidone-iodine 10% solution have chemical properties that hasten the clotting cascade?
suggested a correlation between garlic and warfarin, which resulted in over-anti-coagulation.[4,9] It is postulated that garlic has no effect on the clotting cascade, but may decrease the elimination of warfarin.
On the one hand, our understanding of the role of endothelial injury in the activation of the blood clotting cascade and the formation of acute thrombi is well elucidated and has been so for many decades.
Direct thrombin inhibitors inhibit the clotting cascade by binding to and blocking thrombin.
This is achieved through a complex series of chemical reactions termed the clotting cascade. The clotting cascade also stops the clot activation cycle and removes blood clots by fibrinolysis once no longer needed (Fischer 2007).
In the clotting cascade, vitamin K serves as a cofactor for the synthesis of various proteins (e.g., factors II, VII, IX, X, and others).
The activation of plasma FXIII (pFXIII) occurs in the final phase of the clotting cascade by the concerted action of thrombin and [Ca.sup.2+].
The activated platelets aggregate and stimulate the clotting cascade, resulting in a high risk for thrombosis (Kanaan & Al-Homsi, 2009).
Once the clots have done their job, the body sends APC to destroy Factor V and thus dampen the clotting cascade. But for people with the genetic defect, there's no brake on this process.
As a series of reactions, this multi-stepped process is often referred to as the clotting cascade. The process not only produces clots to stop bleeding but also begins a process called fibrinolysis, which will dissolve (lyse) a clot in order to re-establish flow in the vessel and facilitate the healing process.