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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.
see monopolar electrocoagulation.
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.
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.
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.
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.
see coagulative necrosis.
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.
see clotting factors.
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.
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.
see clotting time.
see bipolar electrocoagulation.