ISSN 2398-2950      

Liver: failure

ffelis

Introduction

  • Cause: loss of 70% or more of functional hepatic mass due to chronic disease, or acute overwhelming insults, eg toxins, infection.
  • Signs: anorexia, depression, vomiting, diarrhea, jaundice, hepatic encephalopathy.
  • Diagnosis: histopathology, blood biochemistry and liver function tests; determination of inciting cause.
  • Treatment: supportive, eg fluid therapy; depends on cause.
  • Prognosis: depends on cause - liver has powerful regenerative capacity.

Pathogenesis

Etiology

Pathophysiology

  • Loss of hepatic function   →  
    • Impaired fat digestion and metabolism and increased mobilization from peripheral stores   →   hyperlipidemia.
    • Impaired carbohydrate metabolism   →   hypoglycemia or hyperglycemia.
    • Impaired protein synthesis   →   catabolism of body protein   →   increased ammonia levels and cachexia.
    • Loss of detoxifying capacity and development of arteriovenous shunts   →   hepatic encephalopathy.
    • Altered metabolism of hormones   →   disrupted circulating hormonal levels, eg insulin, glucagon, growth hormone, insulin-like growth factors, corticosteroids, catecholamines   →   polydipsia/polyuria (due to increased corticosteroids in liver failure), fluid retention.
    • Decreased synthesis of clotting proteins (plus vitamin K deficiency due to anorexia and fat maldigestion due to lack of bile acids)   →   coagulation disorders.
    • Loss of detoxifying capacity and development of arteriovenous shunts   →   hepatic encephalopathy.
  • Acute fulminating liver failure   →   release of tissue thromboplastins and other stimulators of coagulation   →   DIC.
  • Portal hypertension +/- concurrent hypoalbuminemia   →   ascites.
  • Jaundice develops as result of failure of the hepatocytes to remove unconjugated bilirubin from circulation.
  • In the normal animal this unconjugated bilirubin is conjugated with glucoronic acid which is excreted in the bile.
  • Accumulation of bilirubin in the tissue results in yellow discoloration.

Timecourse

  • Depends on underlying hepatic disease.

Diagnosis

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Treatment

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Further Reading

Publications

Refereed papers

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