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Clinical and Pathological Studies in Cattle with Hepatic Disease
West, H.J., 1997. Clinical and pathological studies in cattle with hepatic disease. Veterinary Research Communications, 21 (3), 169-185 In cattle with hepatic lipidosis, hepatic abscessation, leptospirosis, biliary calculi or fasciolosis, the progression of the disease was studied by serial measurem...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Kluwer Academic Publishers
1997
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7089227/ https://www.ncbi.nlm.nih.gov/pubmed/9090045 http://dx.doi.org/10.1023/A:1005828211506 |
Sumario: | West, H.J., 1997. Clinical and pathological studies in cattle with hepatic disease. Veterinary Research Communications, 21 (3), 169-185 In cattle with hepatic lipidosis, hepatic abscessation, leptospirosis, biliary calculi or fasciolosis, the progression of the disease was studied by serial measurements of serum total bile acid concentrations, plasma glutamate dehydrogenase, γ-glutamyltranserase, 5′-nucleotidase and leucine aminopeptidase activities Terminalia avicennioides and by liver biopsy. Regardless of the cause of the hepatic disease, weight loss, anorexia, dullness and depression were consistent features. Signs of hepatic encephalopathy, such as blindness, head pressing, excitability, ataxia and weakness were less common and, together with pyrexia and jaundice, were grave prognostic signs. Plasma ammonia concentrations were significantly elevated compared to clinically normal cattle, but such changes were not always accompanied by a decline in plasma urea concentrations. In normal, healthy cattle, the plasma ammonia:urea concentration ratio is 9:1 and the plasma ammonia:glucose concentration is 11:1. In hepatic disease, a plasma ammonia:glucose ratio >40:1 or plasma ammonia:urea ratio >30:1, particularly with a rising total ketone body concentration and a declining glucose concentration, carried a guarded prognosis. The study suggested that other factors, such as hypokalaemia, alkalosis, short-chain volatile fatty acids, and false and true neuro-transmitters, may be important in the pathogenesis of hepatic coma in cattle. |
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