Coagulation cascade


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Related to Coagulation cascade: Coagulation factors

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.

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.
References in periodicals archive ?
The role of the coagulation cascade in the continuum of sepsis and acute lung injury and acute respiratory distress syndrome.
These factors are primarily involved in the intrinsic pathway of the coagulation cascade (Figure 1).
Those tests are based on the old coagulation cascade model (intrinsic and extrinsic pathways); therefore, they do not offer any information about the interaction between platelets and coagulation factors (14) or about the stability of the thrombus, because these tests are concluded before the clot is stabilized by the action of FXIIIa.
Thrombocytopenia and heparin's effect on the coagulation cascade might have then allowed progression of hemorrhage and formation of the large lingual hematoma.
However, when presented with a patient who is suspected of having an infection of any source and who has the physiologic changes of systemic inflammation, activation of the coagulation cascade, impaired fibrinolysis, and altered microcirculation, the astute clinician can detect the ravages of severe sepsis by the development of organ system dysfunction.
In higher organisms, the coagulation cascade is activated to stop the loss of blood after vascular injury by forming a fibrin clot.
Thus, the coagulation cascade and the fibrinolytic systems are functionally separate.
This means that the immune system and coagulation cascade are left practically unaffected by blood/membrane contact.
It is necessary to understand the basics of the coagulation cascade in order to recognize the difference between the mechanism of action of unfractionated heparin and enoxaparin (see Figure 1).
Platelet effects, rather than interference with the coagulation cascade, are responsible for gingos anticoagulant activity, said Dr.
Two of the new proteins thwart clotting by binding to and inactivating factor Xa; the third protein stymies factor VIIa and "inhibits the initiation of the entire coagulation cascade," says Vlasuk.