Equine liver disease + hyperlipidaemia Flashcards

1
Q

What is the function of the equine liver?

A
  • Digestive and secretory (bile salts)
  • Metabolic (CHO, protein, fat metabolism)
  • Detoxification/excretory (first pass from GIT)
  • Synthetic (clotting factors, proteins)
  • Storage (vitamins, minerals)
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2
Q

What is jaundice?
Ddx for jaundice?

A
  • Retention of bilirubin - unconjugated predominant in horses
  • Ddx = Anorexia, Haemolysis, Liver failure
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3
Q

What are CS of liver disease - may not always be present?

A
  • Jaundice
  • Weight loss
  • Depression / CNS signs (central blindness / head pressing, yawning)
  • Skin lesions
  • Haemorrhage
  • Colic
  • Oedema
  • Diarrhoea
  • Bilateral laryngeal paralysis
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4
Q

What skin lesions are seen in horses?

A
  • Hepatic photosensitisation
  • phylloerythrin accumulation - activated by UV light
  • Ddx primary phtosensitisation = tetracyclines or st johns wort
  • Ddx immune mediated vasculitis
  • Ddx contact - clover
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5
Q

What are liver specific enzymes?

A
  • GGT
  • SDH
  • GLDH
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6
Q

What are non liver specific enzymes?

A
  • AST + muscle
  • ALP + bone, intestine, kidney, placenta, leukocytes
  • LDH-5 + muscle
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7
Q

What enzyme is most sensitive to liver disease?

A
  • GGT - increases in all types of liver disease
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8
Q

What are some liver function tests?

A
  • 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
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9
Q

Where would you take biopsy?

A

RHS
* Shoulder + elbow – tuber coxae
* ICS 7ish – 15ish
* Ventral lung – costochondral junction
LHS
* ICS 6ish – 9ish
* Adjacent to spleen

-find on ultrasonography first

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10
Q

What is the pathogenesis of ragwort poisoning?

A
  • 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
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11
Q

How would you treat ragwort?

A
  • Supportive tx = fluid therapy, electrolytes, glucose
  • Drugs to reduce production of ammonia - metronidazole
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12
Q

What can a horse with Cholangiohepatitis or cholelithiasis present with?

A
  • Fever - ascending infection
  • Jaundice
  • colic
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13
Q

How would you treat chronic active hepatitis?

A
  • Corticosteroids (prednisolone) or immunosuppressive meds (azathioprine)
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14
Q

What can cause acute hepatitis?

A
  • 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
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15
Q

How would you manage hepatic encephalopathy?

A
  • 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
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16
Q

How would you reduce inflammation + fibrosis?

A
  • Prednisolone/dexamethasone
  • Silymarin (milk thistle)
17
Q

How would you manage a diet in a liver disease horse?

A
  • 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
18
Q

What are risk factors of hyperlipaemia?

A
  • Breed
  • Obesity
  • Females
  • Age vs insulin sensitivity
  • Underlying disease
  • Transport, stress, lactation
  • Starvation
19
Q

What is the breakdown of hyperlipaemia?

A
  • 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
20
Q

How does hyperlipaemia present?

A
  • 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
21
Q

How is hyperlipaemia diagnosed?

A
  • Cloudy serum
  • TG’s >5mmol/l = hyperlipaemia
  • TG’s <5 (but >1.5) = hyperlipidaemia
22
Q

What is Tx of hyperlipaemia?

A
  • Treat underlying disease +parasites
  • POSITIVE ENERGY BALANCE
  • Correction of dehydration, electrolyte imbalances, acidosis
  • Other symptomatic therapy
  • Normalisation of lipid metabolism
  • Poor prognosis