Rashin aiki da coagulation wani bangare ne na cututtukan hanta kuma muhimmin abu ne a cikin mafi yawan hasashen sakamako. Canje-canje a cikin daidaiton hemostasis yana haifar da zubar jini, kuma matsalolin zubar jini koyaushe babbar matsala ce ta asibiti. Abubuwan da ke haifar da zubar jini za a iya raba su zuwa (1) hauhawar jini a cikin portal, wanda ba shi da alaƙa da tsarin hemostatic; (2) zubar jini a cikin mucosa ko rauni, sau da yawa tare da narkewar thrombus da wuri ko babban fibrinolysis, wanda ake kira hanzarta coagulation a cikin jijiyoyin jini da fibrinolysis a cikin cututtukan hanta Melt (AICF). Tsarin hyperfibrinolysis ba a bayyana ba, amma ya haɗa da canje-canje a cikin coagulation a cikin jijiyoyin jini da fibrinolysis. Ana ganin coagulation mara kyau a cikin thrombosis na portal vein (PVT) da thrombosis na mesenteric vein, da kuma thrombosis na venous depthrombosis (DVT). Waɗannan yanayin asibiti galibi suna buƙatar maganin hana coagulation ko rigakafi. Microthrombosis a cikin hanta wanda hypercoagulation ke haifarwa sau da yawa yana haifar da toshewar hanta.
An bayyana wasu muhimman canje-canje a cikin hanyar hemostasis, wasu suna zubar jini wasu kuma suna iya yin ɗigon jini (Hoto na 1). A cikin cirrhosis na hanta mai ɗorewa, tsarin zai sake daidaitawa saboda abubuwan da ba su da tsari, amma wannan daidaiton ba shi da ƙarfi kuma wasu abubuwa za su yi tasiri sosai, kamar matsayin yawan jini, kamuwa da cuta ta tsarin, da aikin koda. Thrombocytopenia na iya zama canjin da aka fi sani da cuta saboda hypersplenism da raguwar thrombopoietin (TPO). An kuma bayyana rashin aikin platelet, amma waɗannan canje-canjen hana ɗaukar jini an rage su sosai ta hanyar ƙaruwar von Willebrand factor (vWF) na endothelial. Hakazalika, raguwar abubuwan da ke haifar da procoagulant daga hanta, kamar factors V, VII, da X, yana haifar da tsawaita lokacin prothrombin, amma wannan yana raguwa sosai ta hanyar raguwar abubuwan da ke haifar da anticoagulant daga hanta (musamman furotin C). Bugu da ƙari, haɓakar endothelial-derived factor VIII da ƙarancin furotin C suna haifar da yanayin da ba shi da ƙarfi sosai. Waɗannan canje-canje, tare da raguwar jijiyoyin jini da lalacewar endothelial (Virchow's triad), sun haifar da ci gaban haɗin gwiwa na PVT da DVT lokaci-lokaci a cikin marasa lafiya da ke fama da cirrhosis na hanta. A takaice, hanyoyin hemostatic na cirrhosis na hanta sau da yawa ana sake daidaita su ta hanyar da ba ta da tabbas, kuma ci gaban cutar za a iya karkatar da shi ta kowace hanya.
Nassoshi: O'Leary JG, Greenberg CS, Patton HM, Caldwell SH.AGA Sabunta Aikin Asibiti: Haɗuwa a cikin Ciwon Ciki. Gastroenterology.2019,157(1):34-43.e1.doi:10.1053/j.gastro.2019.03.070.
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