Difference between revisions of "Liver Failure"

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==Liver Function==
 
==Liver Function==
  
* PROTEIN METABOLISM
+
===Protein Synthesis===
 
Protein synthesis, regulation of amino acids Ammonia synthesis and detoxification
 
Protein synthesis, regulation of amino acids Ammonia synthesis and detoxification
* CARBOHYDRATE METABOLISM
+
 
 +
===Carbohydrate Metabolism===
 
Blood glucose regulation Maintenance of glycogen reserve Regulation of intermediary carbohydrate metabolism
 
Blood glucose regulation Maintenance of glycogen reserve Regulation of intermediary carbohydrate metabolism
* LIPID METABOLISM
+
 
 +
===Lipid Metabolism===
 
Synthesis of cholesterol, phospholipids and lipoproteins; fatty acid oxidation Bile acid synthesis and regulation
 
Synthesis of cholesterol, phospholipids and lipoproteins; fatty acid oxidation Bile acid synthesis and regulation
* BIOTRANSFORMATION AND EXCRETION
+
 
 +
===Biotransformation and Excretion===
 
Bilirubin, ammonia, steroid hormones Drugs, copper, cholesterol
 
Bilirubin, ammonia, steroid hormones Drugs, copper, cholesterol
* IMMUNOLOGICAL FUNCTIONS
+
 
 +
===Immunological Functions===
 
Antigen trapping by Kupffer's cells Synthesis of complement, interleukin
 
Antigen trapping by Kupffer's cells Synthesis of complement, interleukin
* VITAMIN ACTIVATION, STORAGE AND ELIMINATION
+
 
* STORAGE OF MINERALS (IRON, COPPER, ZINC, MANGANESE)
+
===Vitamin Storage, Activation and Elimination===
* INACTIVATION OF ENDOCRINE HORMONE
+
 
 +
===Storage of Minerals===
 +
IRON, COPPER, ZINC, MANGANESe
 +
 
 +
===Inactivation of Endocrine Hormones===
  
 
==Clinical Signs==
 
==Clinical Signs==
Line 67: Line 75:
 
* Coagulation profile
 
* Coagulation profile
  
 +
plasma ammonia
 +
abdominocentesis
 +
 +
===Biopsy===
 +
 +
==Treatment==
 +
* Remove causative agent
 +
* Stop inflammation
 +
* Minimise fibrosis
 +
* Promote regeneration
 +
* Treat secondary complications such a ascites, secondary bacterial infection and hepatic encephalopathy.
 +
 +
==References==
 +
Rutgers, C (1996) '''Liver disease in dogs''' ''In Practice 1996 18: 433-44''
  
 +
Rutgers, C (1996) ''Feline liver disease''' ''In Practice 1998 20: 16-2''
  
 +
Dunn, j (1992) '''Assessment of liver damage and function''' ''In Practice 1992 14: 193-200''
  
[[Category:Liver - General Pathology]]
+
Bexfield, N & Watson, P (2006) '''Diagnosis of canine liver disease''' ''In Practice 2006 28: 444-45''
[[Category:To_Do_-_Clinical]]
 
[[Category:To Do - Siobhan Brade]]
 

Revision as of 18:42, 25 August 2011

Introduction

Liver failure results from inadequate liver function. It occurs even though the liver has a large functional reserve and a high regenerative capacity.

Causes

Low Liver Mass

With low liver mass the functional reserve is depleted

NB: liver enzyme levels in blood may not be markedly raised in chronic ongoing liver damage because there may be few liver cells remaining to leak enyzmes

Remodelling of the Vascular and Connective Components after Damage

This may lead to inadequate nutritional supply to the hepatocytes, thus reducing their function

Impaired Function of One Specific/Many of its Diverse Functions

1) Failure of detoxification

Aldosterone - a failure of its proper inactivation results in hypervolaemia since a feature of this hormone is to cause sodium and hence water rentention. This is a factor in the development of ascites

Oestrogen - a failure of its proper inactivation will result in an accumulation of this hormone with atrophy of the genitals and an enlargement of the breasts in the male

Plant Pigments - failure to detoxify will lead to their accumulation in the tissues and photosenistisation may result if they are photodynamic

2) Metabolic upset

  • The failing liver is unable to convert ammonia to urea, resulting in a rise in the level of blood ammonia
  • Lowered level of plasma albumin contributes to the development of ascites

Liver Function

Protein Synthesis

Protein synthesis, regulation of amino acids Ammonia synthesis and detoxification

Carbohydrate Metabolism

Blood glucose regulation Maintenance of glycogen reserve Regulation of intermediary carbohydrate metabolism

Lipid Metabolism

Synthesis of cholesterol, phospholipids and lipoproteins; fatty acid oxidation Bile acid synthesis and regulation

Biotransformation and Excretion

Bilirubin, ammonia, steroid hormones Drugs, copper, cholesterol

Immunological Functions

Antigen trapping by Kupffer's cells Synthesis of complement, interleukin

Vitamin Storage, Activation and Elimination

Storage of Minerals

IRON, COPPER, ZINC, MANGANESe

Inactivation of Endocrine Hormones

Clinical Signs

The animal may present with non specific signs such as weight loss, anorexia, vomiting, diarrhoea, lethargy and PU/PD. The may also present with syndromes specifically related to primary or secondary liver disease such as:

  • Hepatomegaly or fibrosis of the liver
  • Drug intolerance

Diagnosis

Laboratory Tests

  • Haematology, biochemistry, urinanalysis
  • Serum bile acid test pre- and post-prandial
  • Coagulation profile

plasma ammonia abdominocentesis

Biopsy

Treatment

  • Remove causative agent
  • Stop inflammation
  • Minimise fibrosis
  • Promote regeneration
  • Treat secondary complications such a ascites, secondary bacterial infection and hepatic encephalopathy.

References

Rutgers, C (1996) Liver disease in dogs In Practice 1996 18: 433-44

Rutgers, C (1996) Feline liver disease' In Practice 1998 20: 16-2

Dunn, j (1992) Assessment of liver damage and function In Practice 1992 14: 193-200

Bexfield, N & Watson, P (2006) Diagnosis of canine liver disease In Practice 2006 28: 444-45