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Equine Final Year > Liver Disease In The Horse > Flashcards

Liver Disease In The Horse Flashcards

1
Q

What are the main functions of the hepatic system? (4)

A
  • Protein metabolism
  • Plasma proteins: Albumin, clotting, Acute phase proteins, transport proteins
  • Amino acid breakdown and ammonia excretion
  • Energy metabolism
  • Carbohydrate, lipid
  • Detoxification
  • Drug metabolism and bile excretion
  • Mononuclear phagocyte system
  • Kupfer cells
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2
Q

When are clinical signs seen with hepatic dysfunction?

A

When 80% is lost

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3
Q

Name clinical signs of hepatic dysfunction (6)

A

–Weight loss

–Anorexia

–Icterus

•Hyperbilirubinaemia

–Hepatic encephalopathy

–Colic

•Stretching of capsule due to acute hepatocellular swelling or biliary obstruction (cholelithiasis) causing colic

–Depression

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4
Q

Name 4 rare signs of hepatic dysfunction (6)

A
  • Photosensitization
  • Diarrhoea
  • Bilateral Laryngeal paralysis
  • Bleeding
  • Ascites
  • Dependant Oedema
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5
Q

NAme 4 very rare signs of hepatic dysfunction (7)

A
  • Steatorrhea
  • Tenesmus
  • Generalised seborrhea
  • Pruritus
  • Endotoxic shock
  • Polydipsia
  • Pigementuria
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6
Q

Define Steatorrhea

A

excessive fat in faeces – faeces have oily appearance and are foul smelling

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7
Q

What broad category of signs are seen with hepatic encepalopathy?
Name 3 of the clinical signs

A

Ceentral (cerebral) signs

  • Circling, Head Pressing
  • Ataxia
  • Yawning or behaviour change
  • Seizures (rare)
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8
Q

How can you manage hepatic encephalopathy

A

•Seizure control

–Sedation

–Barbiturates

–NOT DIAZEPAM

• Supportive management

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9
Q

What can cause central (cerebral) sigs with hepatic encephalothy?(6)

A

–Neurotoxins

•GI derived

–Decreased Breakdown (liver)

–Excess production (GI disease)

–Presence of false neurotransmission molecules

•Ammonia, GABA

–Increased BBB permeability

–Impaired CNS energy metabolism

–Altered BCAA:AAA ratio

–Increased Manganese

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10
Q

What is phylloerythrin and what happens if the liver does not function properly?

A

–A gut derived breakdown product of chlorophyll, which is usually metabolized by the liver. If the liver is not working this results in the production of free radicals activated by UV light = inflammation in the skin

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11
Q

What happens if Phylloerythrins is combined with liver disease?

Which skin is normally affected?

A

–UV light → oxidative cascade → inflammation and skin sloughing

–Mainly in unpigmented (white) skin as very efficient absorption UV light

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12
Q

What is an important differential Phylloerythrin?

A

St Johns Wort Toxicity

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13
Q

What causes the effects from St Johns Wort Toxicity?

A

–Hypercin

  • Absorbed by the body
  • Activated by exposure to sunlight.

–Photosensitivity

–Inflammation of unpigmented skin

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14
Q

What is the difference between Phylloerythrin and St Johns Wort?

A

St Johns Wort has normal hepatic function

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15
Q

A) How common are coagulopathies?

B) Which clotting proteins are synthesised by the liver? (5)

C) Which pathway is the first to show prolongation (Prothrombin Time) and why?

A

A) Rare

B) II, VII, IX, X and Protein C

C) Extrinsi - due to a short half life of Factor VII

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16
Q

How can we diagnoe hepatic disease? (5)

A
  • History
  • Non-specific clinical signs
  • Clinical examination findings
  • Liver function tests

–Bilirubin, ammonia, bile acids

•Conjugated vs normal bilirubin:CARE

–Dye clearance test

  • RARELY USED (if ever)
  • Liver enzyme activities

–SDH, GGT, GLDH, AST, ALP, LDH

–Ask for the specific isoenzyme

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17
Q

What can cause hyperbilirubinaemia with pre-hepatic? (2)

A

–Increased production

•Haemolysis –RBC broken down

–Increase unconjugated bilirubin

  • NB Foals: High bilirubin due to foetal Hb metabolism
  • There is more of it for the liver to keep up with conjugating it
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18
Q

What can cause hyperbilirubinaemia with intra-hepatic? (2)

A

–Impaired hepatic uptake

•Anorexia in horses

–Primarily unconjugated bilirubin

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19
Q

What can cause hyperbilirubinaemia with post-hepatic? (2)

A

–Impaired excretion

•Biliary obstruction (cholangitis, hepatitis, etc)

–Mainly conjugated bilirubin

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20
Q

Why may bile acids increase?

A
  • May increase with chronic starvation
  • (3 days)
  • Highly specific for liver disease / dysfunction

–Especially chronic disease

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21
Q

Why do you not need to pre and post prandial with a horse?

A

•just need a baseline.

–No gall bladder

–Eat 18 hour a day

–No surge in bile acid

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22
Q

What is the issue of using albumin for hepatic dysfunction?

A

–Rarely decreased in significant hepatic disease

  • Long half life (20 days)
  • Up to 3 weeks for detectable changes in hepatic failure
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23
Q

What is the issue of using ammonia for hepatic dysfunction?

A

–Requires citrated sample

  • Requires assay within 1 hour
  • Ideally a control from an animal on the same diet should be assessed

–No relation between the presence of hepatic encephalopathy and the amount of ammonia

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24
Q

What do high liver enzyme activities indicate?

A

Liver insult

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25
Q

Which areas can liver enzyme activity result from (2) How do you telll the difference?

A
  • Biliary system
  • Hepatocytes

= difference in half life

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26
Q

What do you use liver enzyme results in conjunction with?

A

With assays of the hepatic function

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27
Q

What tests can we use for hepatocellular damage? (2) What are the benefits of these?

A
  • Glutamate dehydrogenase (GLDH)
    • Short half life (14h)
    • Stable in serum (2d)
  • Sorbitol dehydrogenase (SDH)
    • Highly liver specific, very sensitive
    • Short half life (12h) unstable in serum – assay within 12 hours
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28
Q

What test can we use to test for Biliary damage (cholestasis)? What are the reasons of using this?

A
  • Gamma glutamyl transferase (GGT)
    • Pancreatic and renal production as well
    • Only into renal tubules
    • Long half life (3d)
    • Stable in serum (2d)
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29
Q

What tests can we use that are less specific for hepatocellular damage (2) Why are they less specific?

A
  • Lactate dehydrogenase5 (LDH 5)
    • Also produced by muscle and kidney
    • Only determined in specialist labs
  • Aspartate aminotransferase
    • Also produced by skeletal muscle
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30
Q

What less specific marker can we use for Biliary damage (cholestasis) and why is this?

A

Alkaline phosphatase

  • Also produced by bone (high in foals), intestine and kidney
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31
Q

Why do we do a liver biopsy?

A

•Identify underlying pathology

–Target therapy

–Formulate prognosis

  • Animals with abnormal liver function
  • Animals with structural pathology (ultrasound)
  • Animals with persistently increased serum enzyme activity
32
Q

What are the sites for percutaenous biopsies?

A

–12th-14th RIC – ultrasound guidance helpful

–5th – 8th LIC – ultrasound guidance standard

33
Q

Why do you need to take care with cirrhosis?

A

liver is smaller and definitely need U/S guidance!

34
Q

How can we prepare a pateit for a liver biopsy?

A

–± Determination of clotting function

–Sedation, local anaesthesia

35
Q

What is the importance of Haemoperitoneum on a liver biopsy?

A

Common but of little significance

36
Q

Where would you do the biopsy? Draw a skeleton

A
37
Q

Label this ultrasound

A
38
Q

What can be used to predict survival?

A

Liver histopathology

39
Q

What is the assumption with the liver biopdy scoring system?

A

The liver is uniformly affected when one area can be affected a lot more

40
Q

What can be seen in this liver biopsy?

A

Irreversible cytopathology

Necrosis

Megalocytosis

(Mild, moderate or severe)

41
Q

What can be seen in this liver biopsy?

A

Inflammation, hemosiderin

Numbers per portal tract

42
Q

What does this liver biopsy show?

A

Bile duct proliferation and fibrosis

43
Q

Name 2 focal hepatic injuries (3)

A

–Abscess, neoplasia, zonal hypoxic injury (anaemia, heart failure, toxicosis)

44
Q

Name an acute generalised injury (3)

A

–Infection – ascending cholagiohepatitis, necrosis, infection

45
Q

Name a chronic gneralised injury (3)

A

–Inflammation, hypoxia, antimitotic agents,

»Biliary hyperplasia and nodular regeneration

46
Q

What is in ragwort that makes it so bad for the liver?

A

Pyrrolizidine Alkaloids

47
Q

What are pyrrolizidine Alkaloids metabolised by and to?

A

•Metabolized by microsomal enzymes of the hepatocyte to pyrroles

48
Q

How does ragwort cause the liver damage?

A

–Pyrroles cross-link double stranded DNA preventing mitosis and resulting in megalocytes

•As cells die, replaced by fibrous tissue

49
Q

What is seen on histology with ragwort toxicity?

A

–Fibrosis, megalocytosis, bile duct proliferation

50
Q

What is the clinical presentation of ragwort toxcicity?

A

•Signs apparent one to six months after ingestion

–Cumulative

•Onset of signs often acute

–Weight loss

–Laryngeal paralysis

•Increased plasma activities of liver-derived enzymes

51
Q

What can be seen here?

A

Megalocytosis

Fibrosis

52
Q

What i the treatment and prognosis with ragwort toxcicity?

A
  • No specific antidote
  • Supportive therapy

–High protein, palatable diet

•Prognosis

–Serum bile acid > 50 umol/L or extensive fibrosis on histopathology associated with poor outcome

53
Q

What are the 3 causes of acute hepatitis? What is the issue with the way they present?

A

–Tyzzer’s Disease

–Infectious Necrotic Hepatitis

–Toxins = IRON

•Although all are rare they present the same

54
Q

Tyzzer’s disease:

A) What is the cause?

B) Who is affected?

C) What is seen on post morte diagnosis?

D) Outcome?

A

A) Clostridium piliforme (Bacillus piliformis) –Soil living organism - shed in adult horse faeces - acquired by coprophagia

B) Foals between 6 and 44 days old

C) Liver swollen, with 1 to 5mm white foci throughout parenchyma –Coagulative necrosis

D) Generally fatal

55
Q

Infectious Necrotic Hepatitis:

A) Cause?

B) How does it present?

C) Treatment?

D) Prognosis?

A

A) Clostridium novyi type B (“Black Disease”)

B) Progressive, acute –Clinical signs last 24 to 72 hours before death

C) Penicillin

D) No reported survivors

56
Q

What can iron injections cause? What is the prognosis?

A

–Acute fatal syndrome of neonatal foals

–Ferrous fumarate

–Syndrome worse if iron given before colostrum

–Encephalopathy, icterus, per acute death

–Some survivors - full recovery

57
Q

Name 4 toxins causing centrolobular necrosis (6)

A

–Arsenic (pesticide)

–Carbon tetrachloride (fumigant)

–Chlorinated hydrocarbons (insecticide)

–Monensin (ionophore) – NB cardiotoxic

–Phenol (wood preservative, disinfectant)

–Paraquat (herbicide)

58
Q

What causes Periportal changes?

A

Phophrous - fertiliser

59
Q

What is Cholangiohepatitis?

A

Inflammation of hepatocytes and biliary tree

60
Q

What are te causes of cholangiohepatitis? (7)

A
  • Primary
  • Secondary

–Choleliathiasis

–Duodenal inflammation

–Intestinal obstruction

–Neoplasia

–Parasitism

–Certain toxins

61
Q

Primary Cholangiohepatitis:

A) What clinical signs are seen? (6)

B) What enzymes are elevated?(2)

C) How is a diagnosis made?

A

A) often vague and include weight loss, depression, poor performance, anorexia, icterus and fever

B) Hepatocellular and billiary enzymes are elevated

C) Liver histopathology

–Evidence of hepatocellular necrosis, acute inflammation and fibrosis

  • Lymphocytic/plasmacytic inflammation – cause unknown but a similar condition in humans is autoimmune
  • Neutrophilic inflammation– cause believed to be bacterial infection from the GIT ascending up the bile duct
62
Q

Cholelithiasis:

A) What pathogenesis?

B) What is the compositon?

C) What signs are seen?

A

A)

–Nidus

–Ascending biliary inflammation or infection

B)

–Bilirubin

–Esters of bile acids and cholesterol

–Calcium phosphate

C)

  • Anorexia
  • Intermittent colic

–Icterus, pyrexia

63
Q

How can you manage liver disease?

A

•Horses that are anorexic or hypoglycemic

–Dextrose iv (NB 5% detrose is free water)

  • To reduce production of ammonia or enteric toxins
  • Diet
  • Small amounts of feeds more regularly
  • highly palatable, HIGH carbohydrate, LOW protein, containing branched chain amino acids but eating anything is better than nothing – small feeds
  • Good things – molassed sugar beet, corn, bran, grass hay, grass
  • Bad things – oats, alfalfa, fat
  • Supplement B vitamins and folic acid
  • Supplement ADEK
64
Q

What specific treatment do we have for liver disease? (4)

A

•Lactulose 80-120 ml po q 6hr

–Decreases ammonia absorption (hepatic encephalopathy)

•Metronidazole or Neomycin PO

–Decrease GI production of NH3

–Infection – if clostridia is involved

  • DMSO reduce cerberal oedema
  • No basis for flumazenil in the horse

–Inconsistent results in other species

65
Q

How can we treat Cholangiohepatitis?

A

–Neutrophils predominate on biopsy

–Antibiotics

–Plasma cells and lymphocytes predominate on biopsy

–Steroids – if there is evidence of an exaggerated inflammatory reponse

66
Q

How can you treat Cholelithiasis?

A

–Antibiotics for ascending infection

–TMP/Sulpha, Penicillin & Gentamicin

–Treat for 2 weeks after clinical signs resolve

•DMSO may help to dissolve to choliaths

67
Q

What are the Clinical signs of hyperlipaemia?

A

•Initial signs

–Anorexia

–Lethargy

–Weakness

•Signs of progression

–Reluctance to move, in coordination

–Dysphagia

–Head pressing, circling

–Recumbency, paddling of legs, nystagmus

–Convulsions

–Profound depression, coma

68
Q

What are the Risk factors for hyperlipaemia (7)

A
  • Obesity
  • Breed

–Shetland, Miniature horse,

–Ponies

–Donkey

•Gender

–Female

  • Pregnancy/lactation
  • Stress
  • Disease
  • Anorexia
  • Malnutrition
69
Q

Name 6 Diseases associated with hyperlipaemia (8)

A
  • Intestinal parasitism
  • Enteritis / Colitis
  • Gastric / Large colon impactions
  • Dysphagia
  • Lymphosarcoma
  • Equine Hyperadrenocorticism
  • Peritonitis
  • Metritis
70
Q

What i the Pathophysiology of hyperlipaemia in horses?

A

NEB => Uncontrolled break down of lipid stores

71
Q

Draw the physiology of equine hyperlipaemia?

A
72
Q

How do endotoxins affect the pathophysiology of equine hyperlipaemia?

A

Increases hepatic synthesis and secretions of VLDL from the liver

Inhibition of LPL activity at high endotoxin concentration (negative effect)

  • The enzyme which helps TAG into cells
73
Q

How does azotaemia affect hyperlipaemia?

A

Interference with LPL action

74
Q

How can you diagnose hyperlipaemia? What is the difference with hyperlipidaemia?

A
  • Measure plasma triglyceride concentration
  • >5mmol/L = hyperlipaemia
  • 1.5-5mmol/L = at risk

–Hyperlipidaemia

–Grey area – window of opportunity to get them back to normal

•Other common abnormalities

–GGT, ALP, SDH, Bile Acids and glucose

75
Q

How do you treat hyperlipaemia?

A
  • Investigate/treat underlying causes
  • Supportive therapy

–Fluid therapy

  • Address fluid/electrolyte deficits
  • 5% dextrose/glucose at 2ml/kg/hr

–Partial parenteral nutrition (glucose + AA)

  • Monitor glycaemia
  • ± insulin infusion
  • ??LMW Heparin but lipoprotein lipase already overexpressed

–The effect is limited

•Nutritional support

–Maintain energy balance

–Enteral nutrition

  • ‘Ready break’, Complan, Stud cubes etc
  • Small amounts frequently
  • or JUST GET THEM TO EAT!!!

–BCAA supplementation

  • Valine
  • Leucine
  • Isoleucine

Beet-pulp is high in carbs and is low in proteins but also has lots of these so might be just easy to include this to the diet

76
Q

What is the prognosis of hyperlipaemia?

A
  • POOR- published estimated mortality is 60-100% of affected ponies.
  • In animals that survive, triglycerides return to normal in 3 to 10 days
77
Q

How do you prevent hyperlipaemia?

A
  • Avoiding breeding or transporting grossly obese ponies
  • Controlled exercise and feed intake
  • Avoid drastic weight reduction

Equine Final Year (102 decks)

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