Coagulation abnormalities can develop as a result of decreased synthesis or activation of coagulation factors and anticoagulant proteins produced in the liver (ie, factors V, VII, IX, X, XI, XII, fibrinogen, prothrombin, antithrombin, protein C, plasminogen, α2-macroglobulin, and α1-antitrypsin). Decreased enteric absorption of fat-soluble vitamins can lead to vitamin K–responsive bleeding in animals with EHBDO or bile duct immunoinjury (feline sclerosing cholangitis), or in cats with HL. Cats with liver disease appear predisposed to vitamin K–responsive coagulopathies. Conventional coagulation assessments may not reflect impending coagulopathies that remain unsuspected after physical examination, analysis of urine or feces, or mucosal bleeding time test. Dogs with congenital or acquired portosystemic shunting usually develop low protein C activity (<70% activity) that seemingly reflects the severity of portosystemic shunting. Although coagulation factors may be significantly lower in some of these dogs than in age-matched control groups, symptomatic coagulopathy is rare.