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Flashcards in Icterus in horses Deck (54):
1

What is the result of transamination?

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

2

Formula for urea =

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

3

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

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

4

Primary role of liver in lipid metabolism?

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

5

What happens to VLDLs?

taken up by adipose tissue or converted to intermediate or LDLs

6

Can the liver use free FAs for energy?

yes

7

What % of bile acids are reabsorbed by enterohepatic circulation?

95%

8

What is bilirubin the breakdown product of?

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

9

How does the liver detoxify substances? Examples of toxins?

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

10

What do Kuppfer cells do?

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

11

Clinical signs - hepatic dysfunction

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

12

Why might you get colic with hepatic dysfunction?

- acute hepatocellular swelling in acute hepatocellular disease
- biliary obstruction in cholelithiasis

13

Pathogenesis of HE

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

14

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

most likely with chronic liver disease
due to decreased intake, plus loss of normal hepatic metabolic activities

15

What is icterus caused by?

HYPERBILIRUBINAEMIA, either:
1. increased bilirubin production
2. impaired hepatic uptake or conjugation (most common)
3. impaired excretion of bilirubin

16

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

cholestaiss

17

What do erythema and oedema due to photosensitisation lead to?

pruritis, pain, vesicles, ulceration, necrosis, sloughing

18

Why might you get diarrhoea with liver dysfunction? 3

alterations in intestinal microflora
portal hypertension
deficiency of bile acids

19

Define heamorrhagic diathesis

predisposition to bleeding

20

Name diagnostic tests that are specific to liver disease - 3

Increased bile acids
Increased SDH
Increased gamma-glutamyl transferase

21

When are increased bile acids highest?

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

22

What does increased SDH indicate?

Acute liver disease (short half-life)

23

What does increased AST suggest?

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

Long half life

24

Sources contributing to increased ALP

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)