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