Equine liver disease and hyperlipaemia Flashcards
List the 5 functions 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)
Describe the approach to investigating liver disease in horses
- History and clinical examination
- Suspicion -> conformation of liver disease
- Determine aetiology
- Assess liver function
- Assess the severity of pathology and prognosis
How can you determine the aetiology of liver disease?
History
Testing in-contacts
Forage analysis
US
Biopsy
Serology/PCR
How can you assess liver function?
Blood analysis
Clinical signs
How can you assess the severity of pathology and prognosis in liver disease?
Liver biopsy
Blood analysis
Clinical signs
Describe the generalised clinical signs of liver disease
- Not consistent: may be none, some or all
- Focal, inflammatory and acute disease are more likely to show signs OR may be signs of liver failure
- Jaundice
- Weight loss
- Depression/CNS signs
- Skin lesions
What is the cause of jaundice?
Retention of bilirubin (unconjugated in horses)
List the 3 main differentials of jaundice
Anorexia (mild increase)
Haemolysis
Liver failure
Why does liver disease cause weight loss?
Failure of the liver to process nutrients -> negative energy balance
What depressive/CNS signs are seen in liver disease?
Quiet / dull
Yawning
May progress to:
- Somnolence (drowsiness or strong desire to fall asleep)
- Central blindness
- Head pressing
- Compulsive walking
- Sham chewing
Why are CNS signs seen in liver disease?
One of the liver functions is to remove toxic substances e.g. ammonia. If these aren’t removed then a horse can develop CNS signs
Describe the main skin lesion seen in liver disease
Hepatic photosensitisation
Describe the pathogenesis of hepatic photosensitisation
Toxins in the skin, haven’t been removed by the liver so they are activated by UV light -> photosensitisation
List the DDx of hepatic photosensitisation
- Tetracyclines
- St John’s Wort
- Immune mediated vasculitis
- Contact e.g. clover
List some other non-specific signs of liver disease
- Haemorrhage
- Colic
- Oedema
- Diarrhoea
- Bilateral laryngeal paralysis
- Anorexia/inappetence
Which liver enzymes are of biliary origin in the liver
GGT
ALP
Which liver enzymes are of hepatocellular origin in the liver
SDH
GLDH
AST
LDH
Which 3 liver enzymes are liver specific
GGT
SDH
GLDH
Which 3 liver enzymes are not liver specific
AST
ALP
LDH
What are the non-liver sources of AST, ALP and LDH
AST - muscle
ALP - bone, intestine, kidney, pancreas, leukocytes
LDH - muscle
Which liver enzyme is a sensitive indicator of liver disease?
GGT
Which liver enzyme is high in foals, pregnancy and GI disease?
ALP
What are liver enzymes used to assess?
Liver damage, not function
Increased GGT and ALP indicate what type of liver disease?
biliary – e.g. cholangiohepatitis
Increased AST, GLDH and LDH indicate what type of liver disease?
hepatocellular – e.g. serum hepatitis
How are bile acids used to assess the function of the liver?
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
How is unconjugated bilirubin used as a liver function test?
- Liver failure, haemolysis, anorexia, intestinal obstruction, Gilbert’s syndrome
- The liver isn’t conjugating bilirubin
- Not water soluble so wont be seen in urine
How is conjugated bilirubin used as a liver function test?
> 25% of total bilirubin: hepatocellular failure
30% of total bilirubin: choleostasis
- Water soluble: when increased can spill over into urine
- Bile duct is lost: conjugated bilirubin cant go into the intestine so it leaks out into systemic circulation
How is ammonia used to assess liver function?
RBCs produce NH3
Measure within 15mins
If not, separate plasma within 15 min
Keep on ice / freeze
Keep tube stoppered
How do the levels of urea change in liver disease?
Decrease
- lack of ammonia metabolism
How do the levels of globulins change in liver disease?
Increase
- failure of Kupffer cells to remove intestinal antigens
Why do the levels of triglycerides increase in liver disease?
Inadequate carbohydrate metabolism and gluconeogenesis
Describe the ultrasound landmarks on the LHS of the horse to find the liver
6th - 9th ICS
Adjacent to spleen
Describe the ultrasound landmarks on the RHS of the horse to find the liver
Shoulder + elbow - tuber coxae
7th - 15th ICS
Describe how how the anatomy appears on right sided US when assessing the liver
- Lung is bright white due to air
- Reverberation artefacts seen – bouncing of sound waves between the probe and a bright white surface i.e. lung – characteristic of gas
- Curve = right dorsal colon
- Can see vascular structures – hepatic arteries, veins and portal veins in the liver
Describe how how the anatomy appears on left sided US when assessing the liver
Always scan R and L lobes
Better for atrophied livers
Good for comparison to spleen
Biopsy possible under US guidance
Spleen is a lighter grey compared to the liver
List the potential complications of a liver biopsy
- Haemorrhage: do not perform if clinical coagulopathy
- Inappropriate sample e.g. focal lesions
- Negative culture (>50%)
- Infections: cover with antibiotics if septic hepatitis
- Pneumothorax: rare
Ragwort poisoning causes what kind of toxicity?
Pyrrolizidine alkaloid toxicity
Senecio jacobaea
How does a horse with liver disease due to ragwort poisoning present?
- Frequently may only see signs of liver failure just prior to death
- Liver has 70% reserve function
- Can be delayed disease over a year after exposure
- Early clinical signs are difficult to detect and non-specific
List some other clinical signs of ragwort poisoning
- Inspiratory dyspnoea: laryngeal paralysis
- Severe CNS signs - hepatic encephalopathy usually 10 depression, but occasionally maniacal
- Colic: gastric impaction
- Photosensitisation
- Haemorrhages e.g. epistaxis post tubing
- Icterus
How can ragwort poisoning be diagnosed?
History
Clinical presentation
Clinical pathology
Ultrasound
Biopsy
How can ragwort poisoning be treated?
- Should you? - Probably not if bile acids > 50umol/l
- Can try supportive - fluid therapy, electrolytes, glucose (if required)
- Reduce hepatic encephalopathy: moderate to low protein diet, high BCAA’s
What is the cause of cholangiohepatitis and cholelithiasis
Ascending bile duct infection from GIT
How does cholangiohepatitis and cholelithiasis present?
Fever
Jaundice
Colic
How is cholangiohepatitis and cholelithiasis diagnosed?
- Marked elevations in esp. GGT
- Biopsy may yield positive culture: neutrophilic inflammation
- Ultrasound can help ID changes
- Biopsy useful: histo (neutrophils) & culture
Therapy for chronic active hepatitis should include?
Corticosteroids
List some causes of acute hepatitis
Theiler’s disease-associated virus
Other viruses – parvovirus, hepacivirus
Aflatoxins
Liver fluke (Fasciola hepatica)
How should cases of hepatic encephalopathy be approached/treated?
- Avoid sedation but if required, alpha -2 agonist, not diazepam
- Reduce production of neurotoxins: metronidazole to reduce ammonia producing bacteria or lactulose
- Reduce inflammation and fibrosis: steroids
- Diet
Describe the diet for a patient with hepatic encephalopathy
- Carbohydrate- based feed – maintain/gain weight
- Moderate quantities of high quality protein (branch chain amino acids, not aromatic)
- Fat soluble vitamin supplementation (A D E K)
Define hyperlipaemia
Increased triglyceride conc of the blood
How does the serum appear in cases of hyperlipaemia?
Dense, white, cloudy serum
List the risk factors of hyperlipaemia
Breed
Obesity
Females
Age vs insulin sensitivity
Underlying disease
Transport, stress, lactation
Starvation
Describe the pathogenesis 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
- But LPL can’t keep up with HSL & liver
How do horses with hyperlipaemia present?
Non-specific: anorexia, lethargy, weakness
Progress to more severe CNS & other signs
Signs may be underlying disease, hyperlipemia or secondary liver disease
How is hyperlipaemia diagnosed?
Cloudy serum
TG’s > 5 mmol/l = hyperlipaemia
TG’s < 5 (but > 1.5) = hyperlipidaemia
How is hyperlipaemia treated?
- Treat underlying disease +parasites
- POSITIVE ENERGY BALANCE
- Correction of dehydration, electrolyte imbalances, acidosis
- Other symptomatic therapy
- Normalisation of lipid metabolism
Describe the prognosis of hyperlipaemia
Guarded to poor (mortality in > 50%)
Worse if female, other organ involvement, poor initial response, failure to eat
Get them out of the box especially if used to being out
