Category:Liver - Degenerative Pathology

Liver, Hydropic Degeneration

Hepatic lipidosis - fatty liver syndrome

• also known as lipid mobilisation syndrome
• any persistent abnormal accumulation of fat within liver cells
• associated with
  • dietary factors: obesity and starvation
  • increased demand for energy: pregnancy, lactation, and starvation in physiological states
  • 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 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

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 (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 placenta
• can be fatal due to 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
• enlarged
• rounded edges
• pale yellow colour
• friable

NB: will also get fat infiltration of 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 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
  • They are oxidized in the 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 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 hyperlipidemia

• fat pony syndrome
• occurs exclusively in fat ponies especially fat Shetland ponies
• more susceptible if pregnant and lactating
• may be triggered by some reduction in feed intake
• Clinical signs
  • dullness
  • colic
  • anorexia
  • hepatic encephalopathy
  • mania (sometimes)

NB: similar to that in cats, as well as fatal (within a week)

Ovine White Liver Disease

• Australia and Europe
• young lambs on lush pasture
• clinical signs
  • ill thrift
  • anorexia
  • jaundice
  • photosensitisation
• treatment
  • responsive to Vitamin B12 and cobalt

associated with derangement of carbohydrate metabolism

Diabetes mellitus

• where there is insufficient insulin or a decrease in number of insulin receptors in cells
• seen mostly in dogs
• produces a markedly fatty liver due to release of fat from the fat stores for use as an energy source

Ketosis

• due to an excessive drain on carbohydrate stores because pregnant and lactating animals have a continuous demand for glucose
• ketosis results when fat metabolism which occurs in response to the increased energy demand is excessive
• ketone bodies accumulate in the blood and there is marked fatty change in the liver
• can occur in starvation but commonly seen in two conditions in livestock:

ketosis of cattle (acetonemia)

• occurs in high yielding dairy cows a few weeks postpartum
• due to excessive loss of glucose in the milk
• milk yield drops
• smell of ketones on the breath
• ketones excreted in the milk
• self-limiting condition

pregnancy toxaemia in sheep

• occurs in ewes in late pregnancy carrying twin lambs 'twin lamb disease'
• drain of carbohydrate stores is due to rapidly growing foetuses
• serious condition and highly fatal
• clinical signs (neurological)
  • apparent blindness
  • dullness
  • convulsions
  • coma
• sequelae
  • foetuses die
  • apparent recovery in ewe until toxaemia from the decomposing foetuses results in the ewe's death

associated with anoxia and toxaemia

anoxia

• passive congestion
• anaemias

toxaemia

• toxins absorbed from the gut interfere with many stages of triglyceride metabolism