Coagulation cascade

cascade

 [kas-kād´]

a series of steps or stages (as of a physiological process) that, once initiated, continues to the final step because each step is triggered by the preceding one, resulting in amplification of the signal, information, or effect at each stage. In electronics, the term is applied to multiple amplifiers. Examples in biochemistry include blood coagulation and the complement system.

coagulation cascade the series of steps beginning with activation of the intrinsic or extrinsic pathways of coagulation, or of one of the related alternative pathways, and proceeding through the common pathway of coagulation to the formation of the fibrin clot.

The coagulation cascade. This scheme emphasizes the understanding of 1, the importance of the tissue factor pathway in initiating clotting in vivo; 2, the interactions between pathways; and 3, the pivotal role of thrombin in sustaining the cascade by feedback activation of coagulation factors. HMWK = high-molecular-weight kininogen; PK = prekallikrein; PL = phospholipid; PT = prothrombin; TF = tissue factor; Th = thrombin. From Schafer, 1994.

coagulation cascade

the series of steps beginning with activation of the intrinsic or extrinsic pathways of coagulation and proceeding through the common pathway of coagulation to the formation of the fibrin clot. Each step involves activation of a proenzyme (zymogen), the activated form catalyzing activation of the following step. See also common pathway of coagulation, extrinsic pathway of coagulation, intrinsic pathway of coagulation.

Coagulation cascade

The sequence of biochemical activities, involving clotting factors, that stop bleeding by forming a clot.

Mentioned in: Fibrin Split Products, Partial Thromboplastin Time

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.

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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

see coagulopathy.

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

see coagulative 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.