In liver disease, prothrombin time is longer than usual. In addition, the amounts of both coagulation factors and anticoagulation factors are reduced because the liver cannot productively synthsize them as it did when healthy. Nonetheless, there are two exceptions in this falling tendency, that are, coagulation factor VIII and von Willebrand factor, a platelet adhesive protein. Both inversely rise in the setting of hepatic insufficiency, thanks to the drop of hepatic clearance and compensatory productions from other sites of the body. Fibrinolysis generally proceeds faster in the scenarios of acute liver failure as well as advanced stage of liver disease in contrast to chronic liver disease in which concentration of fibrinogen remains unchanged.