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Alimentary > Icterus in horses > Flashcards

Icterus in horses Flashcards

1
Q

What is the result of transamination?

A

a new amino acid and a new keto acid. Products can be oxidised for energy OR used in gluconeogenesis

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2
Q

Formula for urea =

A

ammonia+ammonia+carbon dioxide = urea (in liver)

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3
Q

What can happen to glucose-6-phosphate in the liver?

A

stored as glycogen
oxidised for form ATP
used in synthesis of FAs and cholesterol

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4
Q

Primary role of liver in lipid metabolism?

A

to esterify FAs (from diet or released from adipose tissue) into Tg for export into other tissues.

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5
Q

What happens to VLDLs?

A

taken up by adipose tissue or converted to intermediate or LDLs

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6
Q

Can the liver use free FAs for energy?

A

yes

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7
Q

What % of bile acids are reabsorbed by enterohepatic circulation?

A

95%

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8
Q

What is bilirubin the breakdown product of?

A

haemoglobin and myoglobin. Also produced in macrophages from biliverdin. Released into circulation bound to albumin as unconjugated bilirubin.

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9
Q

How does the liver detoxify substances? Examples of toxins?

A

via biotransformation, e.g.
ENDOGENOUS = ammonia, bilirubin, steroid hormones
EXOGENOUS = drugs, plant toxins, insecticides

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10
Q

What do Kuppfer cells do?

A

They are hepatic macrophages. They produce many inflammatory mediators (ILs, TNF), important role in filtering portal blood.

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11
Q

Clinical signs - hepatic dysfunction

A

variable
non-specific
depend on extent and duration of disease
usually, >80% liver function lost before signs

COMMON:
depression
anorexia
colic
HE
weight loss
icterus
LESS COMMON:
photosensitisation
diarrhoea
bilateral laryngeal paralysis 
haemorrhagic diathesis
ascites
dependent oedema
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12
Q

Why might you get colic with hepatic dysfunction?

A
  • acute hepatocellular swelling in acute hepatocellular disease
  • biliary obstruction in cholelithiasis
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13
Q

Pathogenesis of HE

A

Likely to be multi-factorial:

  • Reduce ammonia clearance
  • Imbalance bewteen AAA and BCAA (may increase production of false NT in the brain due to increased systemic AAA entering brain)
  • Other theories too
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14
Q

When/why might you see weight loss with heptic disease?

A

most likely with chronic liver disease

due to decreased intake, plus loss of normal hepatic metabolic activities

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15
Q

What is icterus caused by?

A

HYPERBILIRUBINAEMIA, either:

  1. increased bilirubin production
  2. impaired hepatic uptake or conjugation (most common)
  3. impaired excretion of bilirubin
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16
Q

What is indicated if conjugated bilirubin concentration is greater than 30% of total?

A

cholestaiss

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17
Q

What do erythema and oedema due to photosensitisation lead to?

A

pruritis, pain, vesicles, ulceration, necrosis, sloughing

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18
Q

Why might you get diarrhoea with liver dysfunction? 3

A

alterations in intestinal microflora
portal hypertension
deficiency of bile acids

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19
Q

Define heamorrhagic diathesis

A

predisposition to bleeding

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20
Q

Name diagnostic tests that are specific to liver disease - 3

A

Increased bile acids
Increased SDH
Increased gamma-glutamyl transferase

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21
Q

When are increased bile acids highest?

A

Highest in obstructive disease (increased, but not as much, with anorexia)

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22
Q

What does increased SDH indicate?

A

Acute liver disease (short half-life)

23
Q

What does increased AST suggest?

A

Could be a liver problem but could also be skeletal muscle (also from cardiac mm, RBCs, intestinal cells and kidney).

Long half life

24
Q

Sources contributing to increased ALP

A

Liver, bone, intestine, placenta, kidney, WBCs

25
Q

When is ALP normally increased?

A

normal foals
during pregnancy
by haemolysis
GIT disease

26
Q

What does increased gamma-glutamyl transferase suggest?

A

cholestasis (only other source of this is the kidney but this is excreted into urine, not blood)

27
Q

What might you see on a hepatic ultrasound?

A

size
changes in parenchyma
dilated bile ducts, choleliths

BUT can only image 20% liver

28
Q

Where would you take a liver biopsy?

A

RHS, 12-14th ICS on line between tuber coxae and point halfway between the point of the elbow and the shoulder (pre-biopsy evaluation of coagulation parameters recommended)

29
Q

Define bridging fibrosis

A

the presence of fibrosis that reaches from a portal area to another portal area (cirrhosis consists of extensive bridging fibrosis)

30
Q

How might you sedate an HE animal? 2

A

xylazine or detomidine

31
Q

Treatment - HE

A

liquid paraffin, magnesium sulfate (to reduce toxin absorption)
Mannitol (for cerebral oedema)
Oral neomycin (decreases bacterial population)
Oral lactulose (inhibit ammonia absorption)
Oral BCAA (no evidence)

32
Q

Dietary management - HE

A

High carbohydrate, limit protein (protein source to be rich in BCAA
Ensure malnutrition doesn’t occur
Recommended diet: beet pulp, cracked corn, molasses. Oat hay

33
Q

What anit-inflammatories might you give in HE? 3

A

Flunixin meglumine
DMSO (may dissolve intrabiliary sludge/small stones)
Pentoxifylline (reduces hepatic fibrosis in humans)

34
Q

Desribe megalocytes

A

large, flattened RBC corpuscle having no nucleus, twice diameter of ordinary red corpuscle, found in considerable numbers in the blood during profound anaemia

35
Q

Diagnosis - ragowort poisoning/ pyrrolizidine-alakaloid toxicity

A

PRESUMPTIVE - history, clinical(pathologic) signs of liver disease
DEFINITIVE - liver biopsy (megalocytosis, biliary hyperplasia, fibrosis)

36
Q

Prognosis - ragwort posioning

A

typically death in 10 day s of hepatic failure signs
bile acid conc >50micromol/l = grave prognosis
regeneration not possible if fibrosis and megalocytosis extensive –> poor prognosis

37
Q

Causes - acute hepatitis

A

Theiller’s disease
Bacterial - Tyzzer’s, Infectious Necrotic Hepatitis (C.novyi B)
Toxic
Viral - EHV in foals, EIA, EVA
Parasitic - migration of Parascarus equorum, Strongylus edentatus/equines/vulgaris

38
Q

Epidemiology - Theiller’s disease

A

outbreak or single case

often follows exposure to equine biologic product 4-10 weeks earlier

39
Q

Pathogenesis - Theiller’s disease

A

small liver

moderate to severe centrilobular to midzonal hepatocellular necrosis with haemorrhage

40
Q

Diagnosis - Theiller’s

A

History+ abrupt onset of signs, evidence of hepatic insufficiency
Biopsy can be supportive

41
Q

What age of horse is affected by C. piloformis B

A

Foals 7-42 days
May be found dead without clinical signs
Non-specific clinical signs

42
Q

Epidemiology - Tyzzer’s

A

Excreted in faeces of normal horses –> foals infected when they ingest it –> bacteria replicate (GIT) –> reach liver and heart (via blood and lymphatics) –> acute multifocal hepatitis and enteritis
Definitive diagnosis - PME and identify organism using silver stains

43
Q

Define cholelithiasis

A

stones in bile ducts

44
Q

Define choledocholithiasis

A

stones in common bile duct

most common cause of biliary obstruction in horses

45
Q

Define hepatoliathiasis

A

stones in intrahepatic bile ducts (variation of choleliathiasis)

46
Q

Causes of stone formation

A

uncertain
ascariasis
ascending biliary infection or inflammation
biliary stasis
changes in bile composition
presence of FB
bacteria (Salmonella, E. coli, Aeromonas)

47
Q

Diagnosis - stone formation

A

Increased liver enzyme activity (esp GGT, SDH, AST)
ultrasound (dilated bile ducts, cholelith evidence)
biopsy (histopathology + culture)

48
Q

Treatment - stones

A

Long term AMs (potentiated sulphonamides, enrofloxacin)
General supportive care
Surgery?
Variable prognosis (depends on fibrosis extent, number/location of choleliths, severity of clinical signs)

49
Q

Which breeds are predisposed to hyperlipaemia and hepatic lipidosis

A

Shetlands, Miniature horses, other pony and donkey breeds (especially if obese)
Increased risk - pregnancy, lactation or if a primary disease entity exists

50
Q

Clinical signs - hyperlipaemia and heptic lipidosis

A 
icterus
anorexia
weakness
severe depression
ataxia
muscle weakness
recumbency
diarrhoea
mild colic
fever 
odemea
If severe fatty infiltration, signs of hepatic failure may occur
51
Q

Diagnosis - hyperlipaemia and hepatic lipidosis - 3

A

Breed, clinical signs
Tg measure in serum
Liver biopsy (usually not necessary)

52
Q

Treatment - Hyperlipaemia and hepatic lipidosis

A

Treat hepatic disease (supportive)
Reverse the NEB
Eliminate stress/treat concurrent disease
Inhibit further fat mobilisation from adipose tissue
Increase Tg uptake by peripheral tissues (heparin increases activity of lipoprotein lipase but this is already maximised in hyperlipaemic ponies)

53
Q

Prognosis - hyperlipaemia and hepatic lipidosis

A

poor - mortality of 60-100%

54
Q

Prevention - hyperlipaemia and hepatic lipidosis - 3

A

avoid obesity and stress

monitor Tg levels in sick ponies (–>early attention to nutritional needs)

Alimentary (37 decks)

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