Diferenzas entre revisións de «Factor X»

 
Na etapa 3 ou de xeración da trombina, o [[factor XI]]a activa o factor IX libre sobre a superficie de plaquetas activadas. O factor IXa activado co [[factor VIII]]a forma o [[tenase|complexo "tenase"]] (do inglés ''ten'', 'dez', xa que activa o factor X). Este complexo "tenase" activa máis factor X, o cal, á súa vez, forma novos complexos protrombinase co factor Va. O factor Xa é o principal compoñente do complexo protrombinase, que converte grandes cantidades de protrombina (a chamada "explosión de trombina"). Cada molécula do factor Xa pode serar mil moléculas de trombina. Esta grande explosión de trombina é a responsable da [[polimerización]] da [[fibrina]] para formar un [[trombo]].
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Inhibition of the synthesis or activity of Factor X is the mechanism of action for many anticoagulants in use today. Warfarin, a synthetic derivative of [[coumarin]], is the most widely used oral anticoagulant in the US. In some European countries, other coumarin derivatives ([[phenprocoumon]] and [[acenocoumarol]]) are used. These agents known as [[vitamin K antagonists]] (VKA), inhibit the vitamin K-dependent carboxylation of Factors II (prothrombin), VII, IX, X in the hepatocyte. This carboxylation after the translation is essential for the physiological activity.<ref>{{cite book |last=Golan |first=D. E. |year=2012 |title=Principles of Pharmacology The Pathophysiologic Basis of Drug Therapy |location=Philadelphia |publisher=Lippincott Williams & Wilkins |page=387 |isbn=978-1-4511-1805-6}}</ref>
 
A inhibición da síntese ou da actividade do factor X é o mecanismo de acción de moitos anticoagulantes que se usan hoxe. A warfarina, un derivado sintético da [[coumarina]], é o anticoagulante oral máis comunmente usado nos EUA, mentres que nos países europeos se usan outros derivados da coumarina, como o [[fenprocoumón]] e o [[acenocoumarol]]. Estes axentes coñecidos como [[antagonista da vitamina K|antagonistas da vitamina K]], inhiben a [`carboxilación]] dependente da [[vitamina K]] dos factores II (protrombina), VII, IX e X nos [[hepatocito]]s. Esta carboxilación despois da tradución é esencial para a actividade fisiolóxica.<ref>{{cite book |last=Golan |first=D. E. |year=2012 |title=Principles of Pharmacology The Pathophysiologic Basis of Drug Therapy |location=Philadelphia |publisher=Lippincott Williams & Wilkins |page=387 |isbn=978-1-4511-1805-6}}</ref>
Heparin (unfractionated heparin) and its derivatives [[low molecular weight heparin|low molecular weight heparin (LMWH)]] bind to a [[blood plasma|plasma]] cofactor, [[antithrombin|antithrombin (AT)]] to inactivate several coagulation factors IIa, Xa, XIa and XIIa. The affinity of unfractionated heparin and the various LMWHs for Factor Xa varies considerably. The efficacy of heparin-based anticoagulants increases as selectivity for Factor Xa increases. LMWH shows increased inactivation of Factor Xa compared to unfractionated heparin, and fondaparinux, an agent based on the critical pentasacharide sequence of heparin, shows more selectivity than LMWH. This inactivation of Factor Xa by heparins is termed "indirect" since it relies on the presence of AT and not a direct interaction with Factor Xa.
 
A heparina (heparina non fraccionada) e os seus derivados [[heparina de baixo peso molecular|heparinas de baixo peso molecular]] (LMWH) únense a un cofactor [[plasma sanguíneo|plasmático]], a [[antitrombina|antitrombina (AT)]] para inactivar varios factores de coagulación, o IIa, Xa, XIa e XIIa. A afinidade da heparina non fraccionada e as varias LMWH polo factor Xa varía considerablemente. A eficacia dos anticoagulantes baseados na heparina increméntase a medida que se incrementa a selectividade polo factor Xa. O LMWH mostra un aumento da inactivación do factor Xa comparado coa heparina no fraccionada, e o fondaparinux, un axente baseado na secuencia pentasacárida esencial da heparina, mostra máis selectividade que a LMWH. Esta inactivación do factor Xa polas heparinas denomínase "indirecta", xa que depende da presenza de antitrombina e no dunha interacción directa co factor Xa.
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Recently a new series of specific, direct acting inhibitors of Factor Xa has been developed. These include the drugs [[rivaroxaban]], [[apixaban]], [[betrixaban]], LY517717, [[darexaban]] (YM150), [[edoxaban]] and 813893. These agents have several theoretical advantages over current therapy. They may be given orally. They have rapid onset of action. And they may be more effective against Factor Xa in that they inhibit both free Factor Xa and Factor Xa in the prothrombinase complex.<ref name="ATVB">{{cite journal | vauthors = Turpie AG | title = Oral, direct factor Xa inhibitors in development for the prevention and treatment of thromboembolic diseases | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 27 | issue = 6 | pages = 1238–47 | date = June 2007 | pmid = 17379841 | doi = 10.1161/ATVBAHA.107.139402 }}</ref>
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