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| | ==[[Liver, Hydropic Degeneration]]== | | ==[[Liver, Hydropic Degeneration]]== |
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| | + | [[Hepatic Lipidosis]] |
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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 hyperlipidemia==== | | ====Equine hyperlipidemia==== |