coagulation

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Related to coagulation pathways: Extrinsic pathway, Clotting cascade

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.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

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.
Farlex Partner Medical Dictionary © Farlex 2012

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.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

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.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

coagulation

the separation or precipitation of suspended particles from a dispersed state.
Collins Dictionary of Biology, 3rd ed. © W. G. Hale, V. A. Saunders, J. P. Margham 2005

Coagulation

The entire process of blood clotting.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

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.
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
It is also well established that there is cross-talk between the coagulation pathways and inflammation in sepsis (Hack 2000; Levi and van der Poll 2005).
These changes provide biologically plausible mechanisms by which UFPs may promote thrombus formation, namely, activating the TF-mediated extrinsic coagulation pathway and inhibiting the anticoagulant effects of protein C through suppression of thrombomodulin (Nemerson 1988; Van der Meeren et al.
In the present study, we have shown that the combination of 20% mannitol and 3% HS does not affect the intrinsic coagulation pathway at doses used intraoperatively for anti-oedematous therapy according to data obtained from the InTEM analysis.
Exposure of the blood to tissue factor triggers the extrinsic coagulation pathway whose function is monitored by the PT through interaction of tissue factor with activated coagulation factor VII (FVII).
This fibrin clot forms via (1) the intrinsic coagulation pathway, when activated factor XII (FXIIa) binds to the exposed endothelial cells at the site of injury and (2) the extrinsic coagulation pathway, when small amounts of circulating FVIIa bind to tissue factor released from injured endothelial tissues.
The active protein in this fibrinolytic system is plasmin, which is produced as plasminogen and is activated by (1) kallikrein generated by the intrinsic coagulation pathway, (2) tissue plasminogen activator released from the injured endothelial cells, and (3) urokinase produced by kidney endothelial cells.
The level of TFPI, a specific inhibitor of the extrinsic coagulation pathway, in the blood of the rats in the SW group was elevated from 2 hours after seawater exposure and was 2.11-fold greater than that in the rats of the control group at 4 hours.