Factor V Leiden mutation
Answer:A Nonalcoholic steatohepatitis
His elevated prothrombin time that corrects with normal plasma points to coagulation factor deficiency, and factors II, VII, IX, and X are synthesized in the liver and affect this “extrinsic” pathway. They are vitamin K dependent and are therefore affected by coumadin therapy.
His hepatic steatosis diminishes liver function. Hemophilia A results from loss of factor VIII function and affects just the partial thromboplastin time. Antiphospholipid syndrome has an inhibitory effect upon in vitro coagulation tests and does not correct with addition of normal plasma.
The factor V Leiden mutation leads to difficulty inactivating factor V by the action of protein C, thus causing thrombosis, not bleeding.
Gram negative sepsis releases lipopolysaccharide that activates coagulation on a wide scale, consuming coagulation factors and platelets, so both the prothrombin time and partial thromboplastin time are elevated while the platelet count is decreased, typical for disseminated intravascular coagulopathy. The lack of vonWillebrand factor leads to impaired platelet function.