Amino acids (except for the branched-chain amino acids leucine, isoleucine, and valine) are taken up by the liver via the portal circulation and are metabolized to urea. Severe liver damage disrupts normal amino acid metabolism and is reflected in elevated serum levels of non-branched-chain amino acids. Since urea cannot be produced, ammonia cannot be handled. Elevated levels of serum ammonia certainly playa large role in the development of hepatic encephalopathy in patients with liver failure and portal hypertension. Therefore, levels of ammonia and, in the case of alkylosis, ammonium ion rise at the expense of urea. Other mechanisms leading to increased blood ammonia levels include excessive amounts of intestinal nitrogen (e.g., resulting from bleeding); decreased intestinal motility allowing greater bacterial deamination of amino acids; depressed renal function leading to an increase in blood urea nitrogen and a greater opportunity for bacterial urease to convert this to ammonia; alkalosis, which will preferentially lead the NHt /NH3 equilibrium in favor of ammonia; and portal hypertension, which will allow ammonia from the gut to bypass hepatic detoxification.