coagulation

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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

/co·ag·u·la·tion/ (ko-ag″u-la´shun)
1. formation of a clot.
2. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation.
3. in colloid chemistry, the solidification of a sol into a gelatinous mass.

blood coagulation  the sequential process by which the multiple coagulation factors of blood interact in the coagulation cascade, resulting in formation of an insoluble fibrin clot.
diffuse intravascular coagulation , disseminated intravascular coagulation (DIC) a bleeding disorder characterized by reduction in the elements involved in blood clotting due to their use in widespread clotting within the vessels. In the late stages, it is marked by profuse hemorrhaging.

coagulation

[kō·ag′yəlā′shən]
Etymology: L, coagulare, to curdle
1 the process of transforming a liquid into a solid, especially of the blood. See also blood clotting.
2 (in colloid chemistry) the transforming of the liquid dispersion medium into a gelatinous mass.
3 the hardening of tissue by some physical means, as by electrocoagulation or photocoagulation. coagulable, adj.

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.

blood coagulation

the process of clotting, which is one of the body's natural means of stopping bleeding (haemostasis), activated by damage to the vessel lining. Results from a complex cascade reaction, dependent on the presence of ionized calcium and involving many 'clotting factors', some always present in the blood and some released from damaged tissue and platelets. The endproduct is a mesh of fibrin in which blood cells are trapped to form a solid mass. See also anticoagulant.

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.

coagulation (kōag´ūlā´shən),

n causing a liquid to solidify; clotting.

coagulation

1. formation of a clot.
2. in surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation.

activated coagulation time (ACT)
a test of the intrinsic or common pathway of coagulation, using diatomaceous earth as an activating agent to hasten coagulation of whole blood, the time being measured. More sensitive than Lee-White or capillary tube tests. See also clotting time.
biterminal coagulation
see monopolar electrocoagulation.
coagulation cascade
the sequence of enzymatic reactions leading to the formation of a blood clot. Each is initiated by the preceding and, in turn, produces the enzyme that catalyzes the next with an amplification of the process as it progresses.
cerebrospinal coagulation
normal CSF does not coagulate. Inflammation of the meninges or contamination of the fluid by blood, possibly during collection, can cause coagulation in a sample.
coagulation defects
disseminated intravascular coagulation (DIC)
widespread formation of thromboses in the microcirculation, mainly within the capillaries. It is a secondary complication of a wide variety of disorders all of which activate in some way the intrinsic coagulation sequence. Paradoxically, the intravascular clotting ultimately produces hemorrhage because of rapid consumption of fibrinogen, platelets, prothrombin, and clotting factors V, VIII and X. Because of this pathology, DIC is sometimes called defibrination syndrome or consumption coagulopathy. Called also diffuse intravascular coagulation. Called also consumption coagulopathy, defibrination syndrome, defibrinogenation syndrome.
coagulation factors
see clotting factors. platelet factors also play a role in coagulation. They are designated by Arabic numerals from 1 to 4.
coagulation inhibitors
these systems prevent widescale intravascular coagulation as a result of minor injury. The important systems are c1-inactivator, antithrombin III, alpha1-antitrypsin, α2-macroglobulin, factor XIa inhibitor, lipoprotein factor Xa inhibitor.
coagulation necrosis
coagulation pathways
the coagulation cascade can follow alternative routes depending on the initiating factor. The extrinsic pathway is initiated by tissue thromboplastin (factor III) and involves calcium ions and factor VII. In the intrinsic pathway, factors XII, XI, IX and VIII are activated by exposure to subendothelial collagen or foreign surfaces. Both pathways lead to the activation of factor X and proceed along the common pathway, involving factors V, II, I and XIII, to the formation of a fibrin clot.
coagulation proteins
see clotting factors.
synovial coagulation
normal synovial fluid does not clot, but gels on standing (thixotropism). It contains no fibrinogen, nor any of the coagulation factors. Clotting is an indication of damage to the synovial membrane.
coagulation tests
are used to determine the integrity of the coagulation pathways, and platelet function. In general, the common tests for the intrinsic or common pathways are the activated partial thromboplastin time (APTT) and activated coagulation time (ACT). One-stage prothrombin time (OSPT) is usually used to evaluate the extrinsic or common pathways, and platelet count, clot retraction, bleeding time and activated coagulation time reflect platelet numbers and function.
coagulation time
see clotting time.
unipolar coagulation
see bipolar electrocoagulation.