Liver Diseases (TV4102, Lecture 37 Notes)

List the major functions of the liver

- Storage of micronutrients

- Carbohydrate, protein and lipid metabolism

- Detoxification and excretion

- Maintaining plasma osmolality

- Production of coagulation proteins

List clinical signs of liver dysfunction

- Failure to convert ammonia to urea produces nervous signs due to the toxic effects of ammonia on the brain

- Failure to excrete bile pigments (cholestasis) produces jaundice

- Failure to remove phytoporphyrin from chlorophyll of green plants will produce photosensitisation

- Failure of albumin production leads to hypoproteinaemic oedema

- Advanced damage can consume all clotting factors, resulting in haemorrhage

- Weight loss due to anorexia or failure of metabolic function

- Diarrhoea due to portal hypertension (passive venous congestion)

- Ascites due to portal hypertension

List reactions to liver dysfunction

- Inflammation, due to bacteria, spores or toxins

- Degeneration

- Fibrosis with chronic injuries

- Bile duct hyperplasia

List indicators of hepatocellular injury

SDH (sorbitol dehydrogenase)

- Liver specific

- Returns to normal within 4-5 days of the insult

GLDH (glutamate dehydrogenase)

- Liver specific

- Indicative of hepatic necrosis

AST (aspartate aminotransferase)

- Increases occur with both hepatocellular injury and muscle injury (not liver specific)

List indicators of cholestasis

ALP (alkaline phosphatase)

- Increased due to bile stasis

GGT (gamma glutamyl transferase)

- Indicator of cholestasis in cattle

Bilirubin

- Increases can be due to biliary stasis as a result of cholangitis or obstruction with calculi/parasites

List indicators of hepatic dysfunction

Glucose - hypoglycaemia may occur due to impaired hepatic gluconeogenesis.

Urea - decreases, while ammonia increases, may result in neurological signs.

Albumin - low.

Discuss bacterial liver disease

- GIT bacteria enter via portal blood supply

e.g. Clostridium haemolyticum, Cl. novyi or Salmonella spp.

- Bacteria may form liver abscesses

e.g. Fusobacterium necrophorum or Trueperella pyogenes

- Consider seeding from a navel infection

List clinical signs of liver abscess

- Feedlot cattle may have reduced feed efficiency

- Signs of toxaemia when an abscess ruptures into the peritoneal cavity

- Sudden death when abscess ruptures and empties into a major blood vessel

- Extension of abscess into posterior vena cava can result in multiple lung abscesses, hepatomegaly, diarrhoea and venous congestion

Discuss management of liver abscess

- Feedlot cattle prophylactically with in-feed antibiotics (including tylosin phosphate or virginiamycin)

- Prevent rumen acidosis by increasing the roughage component in the ration, using buffers and taking care with feed bunk management

Discuss rift valley fever

- Exotic

- Causes abortion in pregnant animals and high mortality in young animals

- Characterised by necrotic hepatitis and generalised haemorrhagic state

Discuss parasitic liver disease

- Fasciolosis (Fasciola hepatica) or Hydatid lesions (Echinococcosis)

- Lesions are sterile and degenerated, do not pose a health risk to humans

- Present with chronic wasting disease of calves and yearlings, may cause ill-thrift, anaemia and death

Discuss Fasciolosis

- Prepatent period = 8 weeks

- Perform faecal egg count +/- milk or serum ELISA

- PM with tracts of liver necrosis caused by migrating immature flukes and adult flukes visible in bile ducts

- Control intermediate host (snails)

- Administer triclabendazole (effective against all stages), monitor for resistance

Discuss acute hepatotoxicities

- May be associated with toxic plants, blue-green algae or acute bovine liver disease (emerging fungal or pasture toxin?)

Discuss lantana poisoning

- Contains lantadene A and B

- Cattle reared on country often avoid eating the plant, caution with hunger during dry conditions or slashing

- Present with inappetence, listlessness, constipation, and absence of rumen contractions, followed by photosensitisation with animals being agitated, kicking at their belly, frequent urination and mucous membrane extreme jaundice

- Oral treatment with activated charcoal 5 g/kg LW or bentonite 5 mg/kg, plus electrolytes

Describe pathophysiology of lantana poisoning

- Small amounts of toxin absorbed from the intestine cause liver damage, followed by rumen atony

- Lantadenes damage the canalicular membranes of the bile ducts to cause cholestasis

- As the animal starts to eat again more toxin is moved from the rumen to the small intestine, when absorbed they get another dose of toxin

Discuss steroidal saponins

- Contained in Panicum spp and Urochloa decumbens

- Metabolised in the rumen and liver, conjugated in hepatocytes with glucuronic acid

- Combine with calcium ions in the lumen of bile ductules to produce insoluble crystals

- Present with photosensitisation and jaundice

Discuss facial eczema

- Caused by a toxin produced by the spores of the saprophytic fungus Pithomyces chartarum

- Grows in dead litter of pasture under warm, moist conditions when humidity is close to 100% and minimum night temperatures are >12oC following light rain or irrigation

- Spores contain sporidesmin which is absorbed from the intestine and transported to the liver, where it causes severe damage via phytoporphyrin

- Present with irritation and reddening of lightly/non-pigmented skin, restless, seeking shade, licking, 3rd eyelid margins may appear burnt, coronitis or sloughing of non-pigmented skin

Classify facial ecaema with GGT serum concentrations

Discuss prevention of facial eczema

- Routine spore counts

- Avoid low grazing or pastures with increased litter

- Administering zinc compounds, reduce effects on the liver (avoid toxicity causing hypocalcaemia)

Discuss aflatoxins

- Toxins produced by moulds (e.g. Aspergillus) interfereing with blood clotting to cause acute or chronic liver necrosis

- Grow in damp, warm conditions on peanuts, peanut hay, mouldy bread, cotton-seed meal, sorghum and maize

- Present with blindness, circling, stumbling, aggression, photosensitisation, diarrhoea and tenesmus

Discuss chronic copper poisoning

- Slow accumulation of copper in the liver

- Overdosing with copper injections or supplements, using grain treated with copper-based fungicides

- Copper-loaded liver starts to self-destruct, releasing copper into the bloodstream, produceing acute haemolytic crisis

- Present with haemoglobinuria, jaundice and sudden death

- PM with gun metal black kidneys

Discuss pyrrolizidine alkaloid toxicitiy

- Chronic ingestion of weeds such as Senecio jacobaea (ragwort) and Crotalaria spp. (rattlepods)

- Pyrrolizidine metabolites inhibit mitosis causing replacement with fibrotic tissue

- Present with initial depression, anorexia, diarrhoea, tenesmus, ill-thrift, wasting and later nervous signs associated with hepato-encephalopathy

Discuss acute hepatotoxicities