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Y4 EQ - Gastrointestinal tract > Equine liver disease and hyperlipaemia > Flashcards

Equine liver disease and hyperlipaemia Flashcards

1
Q

List the 5 functions 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

Describe the approach to investigating liver disease in horses

A
  • History and clinical examination
  • Suspicion -> conformation of liver disease
  • Determine aetiology
  • Assess liver function
  • Assess the severity of pathology and prognosis
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3
Q

How can you determine the aetiology of liver disease?

A

History
Testing in-contacts
Forage analysis
US
Biopsy
Serology/PCR

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4
Q

How can you assess liver function?

A

Blood analysis
Clinical signs

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5
Q

How can you assess the severity of pathology and prognosis in liver disease?

A

Liver biopsy
Blood analysis
Clinical signs

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6
Q

Describe the generalised clinical signs of liver disease

A
  • 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
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7
Q

What is the cause of jaundice?

A

Retention of bilirubin (unconjugated in horses)

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8
Q

List the 3 main differentials of jaundice

A

Anorexia (mild increase)
Haemolysis
Liver failure

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9
Q

Why does liver disease cause weight loss?

A

Failure of the liver to process nutrients -> negative energy balance

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10
Q

What depressive/CNS signs are seen in liver disease?

A

Quiet / dull
Yawning
May progress to:
- Somnolence (drowsiness or strong desire to fall asleep)
- Central blindness
- Head pressing
- Compulsive walking
- Sham chewing

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11
Q

Why are CNS signs seen in liver disease?

A

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

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12
Q

Describe the main skin lesion seen in liver disease

A

Hepatic photosensitisation

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13
Q

Describe the pathogenesis of hepatic photosensitisation

A

Toxins in the skin, haven’t been removed by the liver so they are activated by UV light -> photosensitisation

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14
Q

List the DDx of hepatic photosensitisation

A
  • Tetracyclines
  • St John’s Wort
  • Immune mediated vasculitis
  • Contact e.g. clover
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15
Q

List some other non-specific signs of liver disease

A
  • Haemorrhage
  • Colic
  • Oedema
  • Diarrhoea
  • Bilateral laryngeal paralysis
  • Anorexia/inappetence
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16
Q

Which liver enzymes are of biliary origin in the liver

A

GGT
ALP

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17
Q

Which liver enzymes are of hepatocellular origin in the liver

A

SDH
GLDH
AST
LDH

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18
Q

Which 3 liver enzymes are liver specific

A

GGT
SDH
GLDH

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19
Q

Which 3 liver enzymes are not liver specific

A

AST
ALP
LDH

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20
Q

What are the non-liver sources of AST, ALP and LDH

A

AST - muscle
ALP - bone, intestine, kidney, pancreas, leukocytes
LDH - muscle

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21
Q

Which liver enzyme is a sensitive indicator of liver disease?

A

GGT

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22
Q

Which liver enzyme is high in foals, pregnancy and GI disease?

A

ALP

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23
Q

What are liver enzymes used to assess?

A

Liver damage, not function

24
Q

Increased GGT and ALP indicate what type of liver disease?

A

biliary – e.g. cholangiohepatitis

25
Q

Increased AST, GLDH and LDH indicate what type of liver disease?

A

hepatocellular – e.g. serum hepatitis

26
Q

How are bile acids used to assess the function of the liver?

A

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

27
Q

How is unconjugated bilirubin used as a liver function test?

A
  • Liver failure, haemolysis, anorexia, intestinal obstruction, Gilbert’s syndrome
  • The liver isn’t conjugating bilirubin
  • Not water soluble so wont be seen in urine
28
Q

How is conjugated bilirubin used as a liver function test?

A

> 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

29
Q

How is ammonia used to assess liver function?

A

RBCs produce NH3
Measure within 15mins
If not, separate plasma within 15 min
Keep on ice / freeze
Keep tube stoppered

30
Q

How do the levels of urea change in liver disease?

A

Decrease
- lack of ammonia metabolism

31
Q

How do the levels of globulins change in liver disease?

A

Increase
- failure of Kupffer cells to remove intestinal antigens

32
Q

Why do the levels of triglycerides increase in liver disease?

A

Inadequate carbohydrate metabolism and gluconeogenesis

33
Q

Describe the ultrasound landmarks on the LHS of the horse to find the liver

A

6th - 9th ICS
Adjacent to spleen

34
Q

Describe the ultrasound landmarks on the RHS of the horse to find the liver

A

Shoulder + elbow - tuber coxae
7th - 15th ICS

35
Q

Describe how how the anatomy appears on right sided US when assessing the liver

A
  • 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
36
Q

Describe how how the anatomy appears on left sided US when assessing the liver

A

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

37
Q

List the potential complications of a liver biopsy

A
  • 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
38
Q

Ragwort poisoning causes what kind of toxicity?

A

Pyrrolizidine alkaloid toxicity
Senecio jacobaea

39
Q

How does a horse with liver disease due to ragwort poisoning present?

A
  • 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
40
Q

List some other clinical signs of ragwort poisoning

A
  • 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
41
Q

How can ragwort poisoning be diagnosed?

A

History
Clinical presentation
Clinical pathology
Ultrasound
Biopsy

42
Q

How can ragwort poisoning be treated?

A
  • 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
43
Q

What is the cause of cholangiohepatitis and cholelithiasis

A

Ascending bile duct infection from GIT

44
Q

How does cholangiohepatitis and cholelithiasis present?

A

Fever
Jaundice
Colic

45
Q

How is cholangiohepatitis and cholelithiasis diagnosed?

A
  • Marked elevations in esp. GGT
  • Biopsy may yield positive culture: neutrophilic inflammation
  • Ultrasound can help ID changes
  • Biopsy useful: histo (neutrophils) & culture
46
Q

Therapy for chronic active hepatitis should include?

A

Corticosteroids

47
Q

List some causes of acute hepatitis

A

Theiler’s disease-associated virus
Other viruses – parvovirus, hepacivirus
Aflatoxins
Liver fluke (Fasciola hepatica)

48
Q

How should cases of hepatic encephalopathy be approached/treated?

A
  • 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
49
Q

Describe the diet for a patient with hepatic encephalopathy

A
  • 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)
50
Q

Define hyperlipaemia

A

Increased triglyceride conc of the blood

51
Q

How does the serum appear in cases of hyperlipaemia?

A

Dense, white, cloudy serum

52
Q

List the risk factors of hyperlipaemia

A

Breed
Obesity
Females
Age vs insulin sensitivity
Underlying disease
Transport, stress, lactation
Starvation

53
Q

Describe the pathogenesis 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
  • But LPL can’t keep up with HSL & liver
54
Q

How do horses with hyperlipaemia present?

A

Non-specific: anorexia, lethargy, weakness
Progress to more severe CNS & other signs
Signs may be underlying disease, hyperlipemia or secondary liver disease

55
Q

How is hyperlipaemia diagnosed?

A

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

56
Q

How is hyperlipaemia treated?

A
  • Treat underlying disease +parasites
  • POSITIVE ENERGY BALANCE
  • Correction of dehydration, electrolyte imbalances, acidosis
  • Other symptomatic therapy
  • Normalisation of lipid metabolism
57
Q

Describe the prognosis of hyperlipaemia

A

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

Y4 EQ - Gastrointestinal tract (9 decks)

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