Equine liver disease + hyperlipidaemia Flashcards
What is the function of the equine liver?
- Digestive and secretory (bile salts)
- Metabolic (CHO, protein, fat metabolism)
- Detoxification/excretory (first pass from GIT)
- Synthetic (clotting factors, proteins)
- Storage (vitamins, minerals)
What is jaundice?
Ddx for jaundice?
- Retention of bilirubin - unconjugated predominant in horses
- Ddx = Anorexia, Haemolysis, Liver failure
What are CS of liver disease - may not always be present?
- Jaundice
- Weight loss
- Depression / CNS signs (central blindness / head pressing, yawning)
- Skin lesions
- Haemorrhage
- Colic
- Oedema
- Diarrhoea
- Bilateral laryngeal paralysis
What skin lesions are seen in horses?
- Hepatic photosensitisation
- phylloerythrin accumulation - activated by UV light
- Ddx primary phtosensitisation = tetracyclines or st johns wort
- Ddx immune mediated vasculitis
- Ddx contact - clover
What are liver specific enzymes?
- GGT
- SDH
- GLDH
What are non liver specific enzymes?
- AST + muscle
- ALP + bone, intestine, kidney, placenta, leukocytes
- LDH-5 + muscle
What enzyme is most sensitive to liver disease?
- GGT - increases in all types of liver disease
What are some liver function tests?
- Bile Acids = biological detergent
– Absorption of lipids \ lipid soluble vitamins etc
– Excretion of cholesterol
– 90% of bile acids get reabsorbed in SI, returns via enterohepatic circulation
– Liver failure – decreased absorption - Bilirubin (total, conjugated and unconjugated)
– Unconjugated:
*Liver failure, haemolysis, anorexia, intestinal obstruction, Gilbert’s syndrome
*Associated with poorer outcome in one paper
– Conjugated:
*>25% of total bilirubin: hepatocellular failure
*>30% of total bilirubin: choleostasis - Ammonia
– RBCs produce NH3
– Measure within 15mins
– If not, separate plasma within 15 min
– Keep on ice / freeze
– Keep tube stoppered - Urea decreases - Lack of ammonia metabolism
- Globulins increase - Failure of Kupffer cells to remove intestinal antigens
- Triglycerides increase - Inadequate carbohydrate metabolism and gluconeogenesis
- Decrease synthesis of proteins - E.g. clotting factors, albumin
Where would you take biopsy?
RHS
* Shoulder + elbow – tuber coxae
* ICS 7ish – 15ish
* Ventral lung – costochondral junction
LHS
* ICS 6ish – 9ish
* Adjacent to spleen
-find on ultrasonography first
What is the pathogenesis of ragwort poisoning?
- Pyrrolizidine alkaloid toxicity
- Megalocytosis, fibrosis + persistent toxic effect
- more commonly ingested in hay
- Usually only showing signs prior to death >70% loss of liver function - weight loss, behavioural change, anorexia
How would you treat ragwort?
- Supportive tx = fluid therapy, electrolytes, glucose
- Drugs to reduce production of ammonia - metronidazole
What can a horse with Cholangiohepatitis or cholelithiasis present with?
- Fever - ascending infection
- Jaundice
- colic
How would you treat chronic active hepatitis?
- Corticosteroids (prednisolone) or immunosuppressive meds (azathioprine)
What can cause acute hepatitis?
- Theiler’s disease-associated virus
- Other viruses – parvovirus, hepacivirus
- Aflatoxins
- Liver fluke (Fasciola hepatica)
- Range from mild to severe CNS signs, jaundice and discoloured urine
How would you manage hepatic encephalopathy?
- Avoid sedation but if required – alpha -2 agonist, not diazepam
- Reduce production of neurotoxins
» Metronidazole – decrease ammonia producing bacteria
» Lactulose
-Poorly digested /absorbed carbohydrate
-Increases H+ production
-NH3 converted to NH4+ - Fluid balance, regulate glucose and sodium balance
How would you reduce inflammation + fibrosis?
- Prednisolone/dexamethasone
- Silymarin (milk thistle)
How would you manage a diet in a liver disease horse?
- Carbohydrate- based feed – maintain/gain weight
- Moderate quantities of high quality protein (branch chain amino acids, not aromatic)
– Legume, grass, wheat bran, maize - Fat soluble vitamin supplementation
What are risk factors of hyperlipaemia?
- Breed
- Obesity
- Females
- Age vs insulin sensitivity
- Underlying disease
- Transport, stress, lactation
- Starvation
What is the breakdown of hyperlipaemia?
- Breakdown of stored fat (HSL) - FA’s to liver - energy
- Liver poor ketogenic capability, energy production overwhelmed
– triglycerides accumulate in liver and in plasma - Ideally want to promote re-uptake in periphery by LPL - clear plasma
How does hyperlipaemia present?
- Non-specific: anorexia, lethargy, weakness
– progress to more severe CNS & other signs - Signs may be underlying disease, hyperlipaemia or secondary liver disease
- Need to be aware of at risk animals
How is hyperlipaemia diagnosed?
- Cloudy serum
- TG’s >5mmol/l = hyperlipaemia
- TG’s <5 (but >1.5) = hyperlipidaemia
What is Tx of hyperlipaemia?
- Treat underlying disease +parasites
- POSITIVE ENERGY BALANCE
- Correction of dehydration, electrolyte imbalances, acidosis
- Other symptomatic therapy
- Normalisation of lipid metabolism
- Poor prognosis