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2011, Número 1

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Residente 2011; 6 (1)


Conceptos generales sobre dímero-D, coagulación y patología trombótica

Tello-González A, Rubio-Jurado B, Íñiguez-Franco P, Rebolloso E, García CDE, Salazar-Páramo M, Nava A

Idioma: Español
Referencias bibliográficas: 43
Paginas: 51-58
Archivo PDF: 295.75 Kb.


RESUMEN

El dímero-D (DD) es el principal producto de la degradación de la fibrina por la plasmina y es generado en el paso final de la formación de trombos. Se forma por dos monómeros adyacentes unidos por un enlace de cadena cruzada y por medio de la acción secuencial de tres enzimas: trombina, Factor XIIIa y plasmina. La coagulación de la sangre está mediada por los componentes celulares y plasmáticos solubles de proteínas. En respuesta a una lesión vascular, las plaquetas circulantes se adhieren, agregan, y proporcionan los fosfolípidos de la superficie celular para el ensamblaje de complejos enzimáticos de la coagulación sanguínea. El mecanismo de activación de la coagulación es dado por la hemostasia; la primaria se inicia con la activación del endotelio y la secundaria corresponde a la activación de la cascada de la coagulación. Existen 3 causas que contribuyen a la trombosis: cambios en la pared del vaso, en la composición sanguínea, o en flujo sanguíneo (estasis). La trombosis es mediada por moléculas de adhesión endotelial (molécula de adhesión intracelular, molécula de adhesión vascular y E selectina), activación del complemento, activación de la proteína quinasa del mitogen P 38, y factor nuclear B. Las causas de los procesos trombóticos pueden ser hereditarias o adquiridas. La trombosis arterial es dominada por cambios en la pared del vaso (aterosclerosis). Mientras cambios en el flujo de sangre y de la composición de la sangre son factores dominantes de trombosis venosas.


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