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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
When is ALP normally increased?
normal foals during pregnancy by haemolysis GIT disease
26
What does increased gamma-glutamyl transferase suggest?
cholestasis (only other source of this is the kidney but this is excreted into urine, not blood)
27
What might you see on a hepatic ultrasound?
size changes in parenchyma dilated bile ducts, choleliths BUT can only image 20% liver
28
Where would you take a liver biopsy?
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
Define bridging fibrosis
the presence of fibrosis that reaches from a portal area to another portal area (cirrhosis consists of extensive bridging fibrosis)
30
How might you sedate an HE animal? 2
xylazine or detomidine
31
Treatment - HE
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
Dietary management - HE
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
What anit-inflammatories might you give in HE? 3
Flunixin meglumine DMSO (may dissolve intrabiliary sludge/small stones) Pentoxifylline (reduces hepatic fibrosis in humans)
34
Desribe megalocytes
large, flattened RBC corpuscle having no nucleus, twice diameter of ordinary red corpuscle, found in considerable numbers in the blood during profound anaemia
35
Diagnosis - ragowort poisoning/ pyrrolizidine-alakaloid toxicity
PRESUMPTIVE - history, clinical(pathologic) signs of liver disease DEFINITIVE - liver biopsy (megalocytosis, biliary hyperplasia, fibrosis)
36
Prognosis - ragwort posioning
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
Causes - acute hepatitis
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
Epidemiology - Theiller's disease
outbreak or single case | often follows exposure to equine biologic product 4-10 weeks earlier
39
Pathogenesis - Theiller's disease
small liver | moderate to severe centrilobular to midzonal hepatocellular necrosis with haemorrhage
40
Diagnosis - Theiller's
History+ abrupt onset of signs, evidence of hepatic insufficiency Biopsy can be supportive
41
What age of horse is affected by C. piloformis B
Foals 7-42 days May be found dead without clinical signs Non-specific clinical signs
42
Epidemiology - Tyzzer's
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
Define cholelithiasis
stones in bile ducts
44
Define choledocholithiasis
stones in common bile duct | most common cause of biliary obstruction in horses
45
Define hepatoliathiasis
stones in intrahepatic bile ducts (variation of choleliathiasis)
46
Causes of stone formation
uncertain ascariasis ascending biliary infection or inflammation biliary stasis changes in bile composition presence of FB bacteria (Salmonella, E. coli, Aeromonas)
47
Diagnosis - stone formation
Increased liver enzyme activity (esp GGT, SDH, AST) ultrasound (dilated bile ducts, cholelith evidence) biopsy (histopathology + culture)
48
Treatment - stones
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
Which breeds are predisposed to hyperlipaemia and hepatic lipidosis
Shetlands, Miniature horses, other pony and donkey breeds (especially if obese) Increased risk - pregnancy, lactation or if a primary disease entity exists
50
Clinical signs - hyperlipaemia and heptic lipidosis
``` 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
Diagnosis - hyperlipaemia and hepatic lipidosis - 3
Breed, clinical signs Tg measure in serum Liver biopsy (usually not necessary)
52
Treatment - Hyperlipaemia and hepatic lipidosis
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
Prognosis - hyperlipaemia and hepatic lipidosis
poor - mortality of 60-100%
54
Prevention - hyperlipaemia and hepatic lipidosis - 3
avoid obesity and stress | monitor Tg levels in sick ponies (-->early attention to nutritional needs)

Alimentary (37 decks)

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