coagulation

(chemistry) A separation or precipitation from a dispersed state of suspensoid particles resulting from their growth; may result from prolonged heating, addition of an electrolyte, or from a condensation reaction between solute and solvent; an example is the setting of a gel.
(meteorology) agglomeration

For more information on coagulation, visit Britannica.com.

A process involving the denaturation of proteins, the loss of their native, soluble structure, so that they become insoluble; it may be effected by heat, strong acids and alkalis, metals, and other chemicals. Some proteins are coagulated by specific enzymic action; the action of chymosin in cheese making is to coagulate the proteins of milk.

The final stage in blood clotting is the precipitation of insoluble fibrin, formed from the soluble plasma protein fibrinogen. The enzyme responsible is prothrombin, which is normally inactive, but in response to injury is activated by a cascade of events. Vitamin K is required for the synthesis of prothrombin, and clotting requires calcium ions. See also blood plasma.

Definition: clotting
Antonyms: dissolution, dissolving, melting, opening, softening, thinning

Causing a liquid to solidify; clotting.

Precipitation of suspended particles from a dispersed state (e.g. the clotting of blood). Blood coagulation involves the interaction of a number of factors (coagulation factors) that lead to the conversion of soluble fibrinogen into insoluble fibrin fibres, and the formation of a solid mass called a blood clot.

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 c. 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 c. — see monopolar electrocoagulation.
• c. 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 c. — 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.
• c. defects — see coagulopathy.
• disseminated intravascular c. (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.
• c. factors — see clotting factors. platelet factors also play a role in coagulation. They are designated by Arabic numerals from 1 to 4.
• c. 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.
• c. necrosis — see coagulative necrosis.
• c. 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.
• c. proteins — see clotting factors.
• synovial c. — 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.
• c. 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.
• c. time — see clotting time.
• unipolar c. — see bipolar electrocoagulation.