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Alimentary > Equine Icterus and Hepatic Encepalopahy > Flashcards

Equine Icterus and Hepatic Encepalopahy Flashcards

1
Q

What blood results are likely to be seen in pre-hepatic hyperbilibinamia? `

A
  • Primarily UNconjugated bilirubin (+- conjugated if > liver capacity)
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2
Q

What are the most common causes of haemolysis in horses?

A
  • NI (neonatal isoerythrolysis, an IMHA) due to incompatibility beween sire and dam blood type
  • Infections eg. EIA
  • Drugs eg. Penicillin
  • Toxins eg. oion
  • True autoimmune HA [rare]
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3
Q

What blood results may be seen with hepatic hyperbilirubinaemia?

A

Increased unconjugated aswell

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4
Q

What is the most common cause of hepatic icterus in horses?

A

> Anorexia for >2d (-> shortage of ligandin [release usually stimulated by eating] protein responsible for unconjugated bilirubin uptake into liver)
- Also any acute hepatocellular disease

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5
Q

Why are horses difficult when diagnosing icterus?

A

10-15% normal horses look mildly icteric

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6
Q

Is post-hepatic icterus common in horses?

A

No

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7
Q

Give 2 most common causes of post-hepatic icterus in horses

A
  • Cholangitis
  • Cholangiohepatitis
  • > impaired excretion of bilirubin
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8
Q

How is cholestasis defined diagnostically?

A

Conjugated bilirubin >30%bilirubin

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9
Q

How common are PSS in horses?

A

RARE

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10
Q

What are the firs 3 questions to ask yourself when presented with an icteric horse?

A
  • Anorexic? = do nothing, feed
  • Foal? = NI
  • Pale? = Heamolyic aneamia
  • > If none of these, most likely hepatic causes (liver disease)
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11
Q

Give 6 functions of the liver

A
  1. Bile excretion
  2. Protein metabolism
  3. Carb metabolism
  4. Lipid metabolism
  5. Detoxification
  6. Immune system (Kuppfer cells)
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12
Q

How do bile acid tests differ in horses?

A

No need for pre- and post- prandial as no gall bladder so bile excreted continuously

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13
Q

What does the impressive regeneration and reserve capacity of the liver mean clinically?

A
  • Likely to have dysfunctioned for several days prior to onset of clinical signs
  • BUT able to regenerate so hepatic disease is not always followed by hepatic failure
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14
Q

What are common clinical signs of liver dysfunction in horses? Less common signs?

A
  • Depression
  • Anorexia
  • Colic (mild, due to hepatocellular swelling and biliary obstruction)
  • Abnormal behaviour
  • Weight loss (chronic disease, v food intake, metabolic dysfunction)
  • Icterus
    Less common
    > Photosensitizatio
    > D+
    > Bilat laryngeal paralysis
    > Haemorhagic diathesis
    > Ascites
    > Dependent oedema
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15
Q

What is the general pathogenesis of hepatic encephalopathy?

A
  • v ammonia clearance and ^ aromatic AAs (cf. Branched chain AAs) -> false neurotransmitters and neurotoxicity
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16
Q

What causes photosensitisation?

A

Phylloerythrin - photodynamic agent formed by bacteria in gut - usually absorbed, conjugated and excreted by liver

  • liver dysfunction -> ^ phylloerythrin
  • exposure to UV -> cell membrane damage and necrosis
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17
Q

Give 4 diagnostics useful for working up liver disease

A
  • Clinical signs
  • Blood work
  • ultrasound
  • Biopsy
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18
Q

Which 3 blood parameters are most liver specific?

A
  • Bile acids
  • SDH
  • GGT (also excreted by kidney and mammary but never into blood stream except from liver)
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19
Q

What can be seen on hepatic ultrasonography?

A

> Only 20% of liver!!! Lung overlies

  • size (estimate)
  • changes in echogenicity
  • dilated bile ducts, abscesses, neoplasia
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20
Q

What are the general principles of treatment of hepatic disease?

A
  • Supportive, goal to maintain animal until liver regenerates
  • Correct acid/base balance and fluid deficit (due to v intake)
  • IV glucose if anorectic
  • ABs if suspect infection
  • Anti-inflammatories
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21
Q

What change suggests regeneration is unlikely?

A

Fibrosis

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22
Q

How can hepatic encephalopathy be treated?

A
  • Sedation CAREFUL! Horses unaware of suroundings
  • Manitol/hypertonic saline: cerebral oedema
  • Oral lactulose to limit ammonia abdorption long term
  • oral BCAAs (no evidence for this but does no harm)
  • Dietary modification
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23
Q

How may the diet be modified to minimise effects of hepatic encephalopathy?

A
  • ^ carbs, limited protein BUT DO NOT RESTRICT!! (horses v protein diet anyway so further restriction not helpful)
  • Recommended diet
    > Beet pulp
    > Cracked corn
    > Molasses
    > Sorghum, bran, milo (instead of beet pulp)
    > Oat/meadow hay (not Lucerne or alfalfa)
  • BUT if this is all horses will eat then let them
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24
Q

Give 4 anti-inflamatories commonly used for treatment of liver disease. Which are most commonly used?

A
  • NSAIDS (flunixin meglumine)
  • Corticosteroids (dexamethasone, prednisolone [care-> laminits])
    > DMSO (smelly, carcinogenic, free radical scavenger, used rarely)
    > Pentoxyfylline to limit fibrosis (used rarely)
25
Q

Is liver disease usually diagnosed as a specific pathology?

A 
No [liver has minimal ways to respond to insult and aetiological agent often not seen on biopsy]
 BUT 
- PA toxicity 
- Cholaniohepatitis 
May be diagnosed definitivel
26
Q

What is the technical name for ragwort poisoning?

A

Pyrrolizidine Alkaloid toxicity

27
Q

Is ragwort poisoning a long or short term effect? Pathogenesis?

A

Long term - ingested over 4-12 weeks [initially clinically silent]
> Pyrrolizidine alkaloids metabolised by liver to toxic pyrrole derivatives
> Anti-mitotic by crosslinking DNA in hepatocytes
> Megalocyte production, death and fibrosis

28
Q

How is ragwort ingestion supposedly minimised?

A

Ragwort control Act 2003

29
Q

What specific finding indicates pyrrolizidine poisoning?

A

Megalocytosis of hepatocytes on biopsy.

  • clinical signs often non-specific
  • history of ingestion may hint
30
Q

In which breeds is hyperlipaemia common?

A
  • Sheltlands, miniatures, ponies

- Obese animals

31
Q

When is hyperlipaemic disease seen?

A

Negatvie energy balance due to disease, stress, pregnancy, lactation etc.

32
Q

Which enzyme releases fatty acids from adipose tissue?

A

Hormone sensitive lipase

33
Q

Which enzyme encourgaes uptake of TG/VLDLs to the tissues?

A

Lipoproein lipase

34
Q

Why can hyperlipaemia result from a normal physiological process in NEB?

A

Excess FA delivery and TG production (ponies/miniatures v. good at this!!)

35
Q

What clinical signs are associated with hyperlipaemia?

A
  • lethargy
  • anorexia
  • weakness
  • icterus (liver doesn’t function as well when full of fat)
  • mild colic and D+
  • recumbency
    +- more severe liver disase signs
36
Q

How is hyperlipaemia diagnosed?

A

Bloods - measure TGs in serum by PCV
> also predisposition of breed, history and clinical sign
+- liver biopsy

37
Q

Which is more severe, hyperlipidaemia or hyperlipaemia?

A

Hyperlipaemia

38
Q

What is the treatment for hyperlipaemia?

A
  1. Reverse NEB (encourage to eat or force fed)
  2. Treat hepatic disease with supportive therapy
  3. Eliminate stress/treat concurrent 1* disease (?wean foal)
  4. Inhibit further fat mobilisation (restore + energy balance, give INSULIN to inhibit hormone sensitive lipase.
  5. ^ TG uptake by peripheral tissues - HEPARIN increases activity of lipoprotein lipase. Probably not that useful as likely to already be maximally active.
39
Q

What is the prognosis for hyperlipaemia?

A

Poor once severe clinical signs apparent but good if caught early - always suspect!
> monitor TG levels in sick ponies
> ensure adequate nutrition
> prevent obesity

40
Q

What is the treatment and prognosis for pyrrolizidine alkaloid toxicity?

A

No specific treatment

  • Poor prognosis
  • Death <10d after clinical signs of liver failure
  • Regneration NOT possible if fibrosis present and megalocytoisis extensive
41
Q

Give 5 causes of acute hepatitis

A
  1. Theiller’s disease
  2. Bacterial - Tyzzers disease
  3. Toxic
  4. Viral - EHV in foals, EIA, EVA adults
  5. Parasitic (migration of Parascarus Equorum, Strongylus edentatuseuinus/vulguris)
42
Q

What is the cause of theillers disease?

A

Unknown

> outbreaks or single cases

43
Q

What other names is Theillers disease known by?

A
  • Serum sickness
  • Acute necrotic hepatitis
  • Serum associated hepatitis
44
Q

What is the pathology associated with Theillers disease and how is it diagnosed?

A
  • Widespread hepatic necrosis
  • Small liver at PM
  • Dx: history, abrupt onset of clinical signs, hepatic insufficiency
45
Q

What is the treatment and prognosis of Theillers disease?

A

No specific treatment, prognosis poor if severe HE seen

46
Q

What is the common name for infectious hepatitis? Which organism is responsible?

A

> Tyzzers disease

> Clostridium piliformis

47
Q

What aged horses are seen with Tyzzers disease?

A

Only foals 7-42d

48
Q

What clinical signs are assocated with Tyzzers disease?

A

May be none - found dead

Otherwise non-specific, off suck, depression, recumbency

49
Q

What is the pathogenesis of Tyzzer’s disease?

A
  • Multifocal hepatitis and enteritis
50
Q

How may Tyzzer’s be definitively diagnosed?

A

Anti-mortem: Difficult

Post-mortem: ID microorganism

51
Q

How is Tyzzer’s treated? Prognosis?

A

ABs, supportive therapy

> Prognosis grave. Only 1 known report of successful treatment

52
Q

What is the pathogenesis of cholelithiasis/cholangiohepatitis?

A
  • cause for stone formation often unknown
    > parasites
    > ascending biliary tract infection/inflammation
    > biliary stasis
53
Q

Why is gallstones never diagnosed in horses?

A

They have no gallbladder - Instead BILE DUCT stones present

54
Q

What clinical signs are strongly indicative of cholelithiasis/cholangiohepatitis?

A

Fever + icterus + colic = strongly suggestive

55
Q

How may cholelithiasis be more definitively diagnosed?

A

> Enzymes (GGT, SDH, AST)
Ultrasound (dilated bile ducts, choleliths)
Biopsy (histopath for inflammation, culture for ascending infection)

56
Q

How is cholelithiasis treated?

A
  • Longterm antimicrobials (weeks/months)
  • Supportive care
  • DMSO?
  • Anti-inflams?
  • Others?
57
Q

What is the prognosis for cholelithiasis?

A
  • dependant on number and extent of choleliths, fibrosis, severity of clinical signs
58
Q

What are the 4 main diseases of the liver?

A

> Pyrrolizine alkaloid toxicity
Hyperlipaemia
Cholelithiasis
Unknown cause!

59
Q

What is prognosis of liver disease dependant upon?

A

Degree of fibrosis

Alimentary (30 decks)

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