Canis ISSN: 2398-2942

Liver: chronic disease - overview

Contributor(s): Nick Bexfield

Introduction

  • Includes: chronic active hepatitis, copper associated hepatitis, drug induced hepatitis, lobular dissecting hepatitis, idiopathic hepatitis.
  • Cause: malformation, toxicity, neoplasia, endocrinopathy, infection.
  • Signs: may present as acute hepatitis, or may be non-specific: lethargy, anorexia, vomiting. Signs of hepatic encephalopathy.
  • Diagnosis: biochemistry, hepatic function tests, ultrasonography, ultimately hepatic biopsy.
  • Treatment: elimination of cause if known, supportive and symptomatic measures.
  • Prognosis: depends on underlying cause.

Pathogenesis

Etiology

Pathophysiology

  • Cumulative hepatic insult → functional reserve capacity exceeded (>70% damage) → failure to perform diverse metabolic functions → clinical signs.
  • Increased resistance to blood flow through liver due to hepatocytes swelling → development of portal hypertension →ascites. Ascites may also develop due to hypoalbuminemia Hypoproteinemia.
  • Acquired shunting vessels may develop due to sustained portal hypertension.
  • Failure to detoxify ammonia from intestine due to reduced hepatic mass and presence of acquired shunting vessels → hepatic encephalopathy Hepatic encephalopathy.
  • Portal hypertension → gastrointestinal wall congestion and edema → gastrointestinal ulceration → hematemesis and melena.
  • Inadequate bile delivery to intestine → impairment of fat digestion → diarrhea.
  • Decreased production of clotting factors →bleeding tendency.
  • Inflammation of biliary system → partial obstruction to biliary flow →icterus.
  • Decreased production of urea in the urea cycle → reduced blood urea.
  • Decreased production of albumin →hypoalbuminemia.
  • Chronic liver disease may result in fibrosis. If the injury is severe and/or ongoing, the liver will respond by laying down fibrous tissue. This represents a final common pathway to a variety of insults to the liver.
  • When bridging fibrosis causes permanent distortion of the liver associated with regenerative nodules, it is termed cirrhosis Liver: cirrhosis.

Timecourse

  • >12 weeks of active illness.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Au A Y, Hasenwinkel J M, Frondoza C G (2013) Hepatoprotective effects of S-adenosylmethionine and silybin on canine hepatocytes in vitro. J Anim Physiol Anim Nutr (Berl) 97 (2), 331-41 PubMed.
  • Mandigers P J, van den Ingh T S, Spee B, Penning L C, Bode P, Rothuizen J (2004) Chronic hepatitis in Doberman pinschers. A review. Vet Q 26 (3), 98-106 PubMed.
  • Watson P J (2004) Chronic hepatitis in dogs: a review of current understanding of the aetiology, progression and treatment. Vet J 167 (3), 228-241 PubMed.
  • Center S A (1999) Chronic liver disease: current concepts of disease mechanisms. JSAP 40 (3), 106-114 PubMed.
  • Sevelius E (1995) Diagnosis and prognosis of chronic hepatitis and cirrhosis in dogs. JSAP 36 (12), 521-528 PubMed.
  • Andersson M, Sevelius E (1991) Breed, sex and age distribution in dogs with chronic liver disease: a demographic study. JSAP 32 (1), 1-5 VetMedResource.

Other sources of information

  • Watson P J (2005) Diseases of the liver. In: BSAVA Manual of Canine and Feline Gastroenterology. 2nd edn. Eds: E J Hall, J W Simpson & D A Williams. BSAVA Publications. pp 240-268.
  • Willard M D (2005) Inflammatory canine hepatic disorders. In:T extbook of Veterinary Internal Medicine. 6th edn. Eds: S J Ettinger & E C Feldman. W B Saunders, Philadelphia. pp 1442-1447.


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