serum ammonia

Introduction

ammonia is biosynthesised through normal amino acid metabolism and is important for normal animal acid/base balance but is toxic in high concentrations
ammonia load is increased with high protein intake or GIT bleeding
in fish and aquatic invertebrates, it is excreted directly into the water
in mammals, sharks, and amphibians, the liver converts ammonia to less toxic urea via the urea cycle and then excreted in urine
- liver failure may result in toxic levels of ammonia which contributes to the features of hepatic encephalopathy
in birds, reptiles, and terrestrial snails, metabolic ammonium is converted into uric acid, which is solid, and can therefore be excreted with minimal water loss
plants can use these excreted nitrogenous wastes to create new amino acids and proteins

see hepatic encephalopathy
toxic levels in mammals usually arise in those with liver impairment who then have:
- an illness which exacerbates the liver impairment, and/or,
- increased ammonia production load such as from high protein intake, GIT bleeding or a catabolic state causing protein breakdown such as hyperthermia, and sepsis / septicaemia
in addition, some ammonia is excreted in faeces and urine
- Thiazide diuretics impair ammonia excretion in urine
- lactulose may increase fecal excretion of ammonia by increasing fecal acidity through increased fermentation of the lactulose