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*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.
*Tilley, L. P. & Smith, F. W. K. (2007) '''Blackwell's Five-minute Veterinary Consult: Canine & Feline (Fourth Edition)''' ''Blackwell Publishing''
*Tilley, L. P. & Smith, F. W. K. (2007) '''Blackwell's Five-minute Veterinary Consult: Canine & Feline (Fourth Edition)''' ''Blackwell Publishing''
=From Pathology=
==Hepatic lipidosis - fatty liver syndrome==
*also known as lipid mobilisation syndrome
*any persistent abnormal accumulation of fat within [[Liver - Anatomy & Physiology|liver]] cells
*associated with
**dietary factors: obesity and starvation
**increased demand for energy: pregnancy, lactation, and starvation in physiological states
**''[[DM|Diabetes mellitus]]'', ketosis, and pregnancy toxaemia in pathological conditions
**abnormal hepatocytic function: prevents fatty acids from forming complexes with proteins to form low density lipoproteins for secretion into the blood
*enlarged [[Liver - Anatomy & Physiology|liver]] with round edges
*lightish yellow in colour
*cut surface is uniform and greasy to handle
The following are several important specific diseases in which fatty change is the main finding:
===associated with obesity===
Overfeeding will lead to the accumulation of fat in the [[Liver - Anatomy & Physiology|liver]]
This is a normal physiological function but if a sudden check in dietary intake is imposed it may tip such an animal into serious ill health
====Bovine====
*fat cow syndrome (extreme form of fatty liver)
*occurs in well-fed dairy cows a few days postpartum
*an excessive accumulation of liver fat without being able to export it from the [[Liver - Anatomy & Physiology|liver]] (during late dry period and early lactation)
*amount of fat deposited influenced by:
**Body Condition Score (how fat the cow is)
**Milk Yield (energy requirement)
**Appetite (low in fat cows)
*triggered by various conditions:
**abomasal displacement
**mastitis
**metritis
**retained [[Gestation -Placenta - Anatomy & Physiology|placenta]]
*can be fatal due to [[Liver - Anatomy & Physiology|liver]] failure (up to 25% has been reported)
=====Clinical=====
*cow is sick
*poor appetite
*excessive weight loss
*downer
*high incidence of post parturient disease
=====Gross=====
*fat infiltration of [[Liver - Anatomy & Physiology|liver]]
*enlarged
*rounded edges
*pale yellow colour
*friable
NB: will also get fat infiltration of [[Liver - Anatomy & Physiology|liver]] in cows which have not been eating for several days so interpret carefully
=====Prevention=====
*dry off cows at correct BCS (up to 3.5)
*do not adjust BCS during dry period
*do not starve fat dry cows
*maintain appetite over late dry and calving period to prevent excessive weight loss and fat mobilisation
*use transistion diet
====Feline====
*feline fatty [[Liver - Anatomy & Physiology|liver]] syndrome
*fairly similar and associated solely with obesity
*diagnosis on cytology/histopathology
*Survival rate is only 50-60%
*Pathophysiology:
**Incompletely understood
**Obese cats that lose 30-40% of body weight exhibit a similar syndrome to naturally occurring hepatic lipidosis
**But many causative factors for naturally occurring hepatic lipidosis:
***Peripheral lipolysis secondary to absolute or relative lack of insulin
***Protein-calories malnutrition
***Amino acid deficiencies – inability to synthesize apolipoproteins necessary to mobilize hepatic fat
***Deficiency of lipotrophic compounds
***Error of fatty acid oxidation
***Hepatic perioxosomal damage due to oxidative stress
*Cats with hepatic lipidosis have higher nonesterified fatty acids (NEFAs) compared to controls and those with cholangiohepatitis
**NEFAs are derived from lipolysis of fat stores and enter the [[Liver - Anatomy & Physiology|liver]]
**They are oxidized in the [[Liver - Anatomy & Physiology|liver]] for energy or converted to phospholipids or cholesterol or reesterified to triglycerides
**Limited increase in lipoprotein synthesis and secretion of triglycerides in VLDLs
**Capacity for increase in oxidation by mitochondria and ketone body synthesis is low
**Rate of fatty acid esterification to triglycerides is not limited so can lead to a marked increase in the accumulation of stored hepatic triglycerides
*Also all triglyceride accumulation in hepatocytes in these cats comes from mobilized peripheral adipose stores during nutritional stress
**high levels of triglyceride concentrations in the [[Liver - Anatomy & Physiology|liver]] will cause:
***severe periacinar necrosis
***jaundice
***hepatic encephalopathy
***high mortality rate
*Lipolysis – under control of hormone-sensitive lipase hydrolyses triglycerides to NEFAs and glycerol
**Insulin – inhibits it
*Catecholamines (eg: released in stress, etc – neural input), glucocorticoids, thyroxine, GH and glucagons all promote lipolysis
*Lower insulin levels in cats with hepatic lipidosis or cholangiohepatitis compared to controls; and lower glucogon:insulin ratio in diseased cats
**But as not lipidosis specific, not likely to be the main factor involved
*Higher serum triglycerides in lipidotic cats compared to controls
[[Equine Hyperlipidaemia]]
[[Ovine White Liver Disease]]
===associated with derangement of carbohydrate metabolism===
====[[Diabetes Mellitus]]====
====[[Ketosis]]====
===associated with anoxia and toxaemia===
====anoxia====
*passive congestion
*anaemias
====toxaemia====
*toxins absorbed from the gut interfere with many stages of triglyceride metabolism
[[Category:Liver_-_Degenerative_Pathology]][[Category:Cat]][[Category:Cattle]]