Difference between revisions of "Liver Failure"
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==Liver Function== | ==Liver Function== | ||
− | + | ===Protein Synthesis=== | |
Protein synthesis, regulation of amino acids Ammonia synthesis and detoxification | Protein synthesis, regulation of amino acids Ammonia synthesis and detoxification | ||
− | + | ||
+ | ===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=== | ||
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=== | ||
Bilirubin, ammonia, steroid hormones Drugs, copper, cholesterol | Bilirubin, ammonia, steroid hormones Drugs, copper, cholesterol | ||
− | + | ||
+ | ===Immunological Functions=== | ||
Antigen trapping by Kupffer's cells Synthesis of complement, interleukin | 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== | ==Clinical Signs== | ||
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* 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'' | ||
− | + | Bexfield, N & Watson, P (2006) '''Diagnosis of canine liver disease''' ''In Practice 2006 28: 444-45'' | |
− | |||
− |
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:
- Bleeding Tendencies or coagulopathy
- Hypoalbuminaemia and ascites
- 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