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Blood coagulation, Thromboplastin

Thromboplastin is present in tissue juices and in platelets. In experimental studies on blood coagulation, thromboplastin is usually obtained by extracting it with saline from brain or lung. In the blood vessels, the thromboplastin that starts the coagulation process is generated by the disintegration of the blood platelets (which will be discussed in more detail later), but thromboplastin release coincides with the release of vasconstricting substances. [Pg.399]

Stefan Sinn MH. Blood coagulation thromboplastin time measurements on a nanoparticle coated quartz crystal microbalance biosensor in excellent agreement with standard clinical methods. J Biosens Bioelectron 2013 04 4-9. [Pg.226]

The extrinsic mechanism of blood coagulation begins when a blood vessel is ruptured and the surrounding tissues are damaged. The traumatized tissue releases a complex of substances referred to as tissue thromboplastin. The tissue thromboplastin further complexes with factor VII and Ca++ ions to activate factor X directly. [Pg.236]

Vitamin K activity is associated with several quinones, including phylloquinone (vitamin Kj), menadione (vitamin K3), and a variety of menaquinones (vitamin K2). These quinones promote the synthesis of proteins that are involved in the coagulation of blood. These proteins include prothrombin, factor VII (proconvertin), factor IX (plasma thromboplastin), and factor X (Stuart factor). A detailed discussion of blood coagulation is found in Chapter 22. The vitamin K quinones are obtained from three major sources. Vitamin K is present in vari-... [Pg.779]

Hepatic injury can also alter the synthesis of the blood coagulation cascade and prolong prothrombin and activated partial thromboplastin times. These effects on vitamin K dependent coagulation factors II (prothrombin), VII, IX, and X and protein C, protein S, and protein Z tend to affect the prothombin time (PT) more frequently than the activated partial thromboplastin time (APTT) however in some cases of hepatotoxicity, the APTT changes may be more marked than those for PT (Pritchard et al. 1987). [Pg.56]

The relatively high incidence of thromboembolic phenomena in women on the pill prompted an examination on the effects of the estrogenic and/or progesteronic components in the pill on the surface charge characteristics of the vascular system. Electrophoretic mobilities of erythrocytes and platelets and blood coagulation times were determined with samples of blood drawn from 33 women on the pill and 30 control subjects. The electrophoretic mobilities were reduced thrombin recalcification times were not affected but thrombin times and partial thromboplastin times were shortened. [Pg.474]

The coumarin anticoagulants are employed in therapy to depress blood coagulation and to prevent thrombosis in diseases of the coronary artery and in other conditions [419]. These compounds act only in vivo by blocking the synthesis of four proteins in the prothrombin complex (factors II = prothrombin, VII = proconvertin, IX = plasma thromboplastin component, and X = Stuart-Prower factor) necessary for the normal blood coagulation process. These proteins are... [Pg.124]

Thromboplastin formation is the most mysterious phase of blood coagulation. Compared to the formation of thrombin and fibrin, thromboplastin formation is slow and may therefore be critical in controlling diseases resulting from increased rates of blood coagulation. In his review, Pool [3] distinguishes between the formation of extrinsic and intrinsic thromboplastin activators (see Figs. 7-1 and 7-2). [Pg.400]

During blood coagulation, prothrombin is activated to yield thrombin. Tissue thromboplastin and calcium are required for the activation. The exact mechanism of activation is not known, and little information is available on the product of the activation—thrombin. [Pg.401]

The deficiencies in blood coagulation may involve one or more of the factors responsible for the process and can be classified as deficiencies in (1) the thromboplastin systems, (2) prothrombin formation, and (3) the conversion of fibrinogen to fibrin. [Pg.406]

THROMBOPLASTIN A substance that aids blood coagulation factors. [Pg.377]

Baseline complete blood count (CBC) and coagulation tests (activated partial thromboplastin time and International Normalized Ratio) should be obtained, as most patients will receive antithrombotic therapy, which increases the risk for bleeding. [Pg.87]

Prothrombin time (PT) A measure of coagulation representing the amount of time required to form a blood clot after the addition of thromboplastin to the blood sample PT is also known as Quick s test. [Pg.1575]


See other pages where Blood coagulation, Thromboplastin is mentioned: [Pg.418]    [Pg.235]    [Pg.36]    [Pg.93]    [Pg.352]    [Pg.120]    [Pg.136]    [Pg.186]    [Pg.256]    [Pg.8]    [Pg.1288]    [Pg.1592]    [Pg.857]    [Pg.118]    [Pg.1789]    [Pg.2157]    [Pg.549]    [Pg.863]    [Pg.199]    [Pg.616]    [Pg.616]    [Pg.616]    [Pg.616]    [Pg.616]    [Pg.1478]    [Pg.10]    [Pg.418]    [Pg.169]    [Pg.257]    [Pg.399]    [Pg.399]    [Pg.218]    [Pg.491]    [Pg.83]    [Pg.109]    [Pg.495]   


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Blood coagulation

Thromboplastin

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