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3. Equine > Equine Hepatic Diseases > Flashcards

Equine Hepatic Diseases Flashcards

1
Q

metabolic functions of the liver

A

– Gluconeogenesis
– Conversion of amino acids to glucose or glycogen
– Urea-cycle enzymes
> Conversion of ammonia to urea
– Phylloerythrin metabolism

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2
Q

how often does the equine liver renew itself

A

Liver undergoes constant repair.
– Renewed in horses every 50-70 days.

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3
Q

synthetic functions of the liver

A

– Albumin
- cholesterol
- glucose
- urea
– Clotting proteins
* Fibrinogen (Factor I)
* Prothrombin (Factor II)
* Factors VII, IX, X
- amino acids

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4
Q

Excretory functions of the liver
- horse gall bladder?

A

– Conjugation of bilirubin
– Production of bile
– NO gall bladder in the horse

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5
Q

liver detocification
- endogenous and exogenous compounds

A

– Endogenous compounds
* Endotoxins
* Bilirubin
* Ammonia
<><><>
– Exogenous compounds
* Drugs
* Planttoxins

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6
Q

how much liver functional capacity can be lost before liver failure

A
  • Liver failure occurs after loss of 75-80% of functional capacity
  • Tremendous functional reserve and regenerative capacity
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7
Q

Primary liver diseases we are concerned about in the horse:

A

– Serum-associated acute hepatitis
(Theiler’s disease)
– Chronic active hepatitis
– Pyrrolizidine alkaloid toxicosis
– Obstructive cholelithiasis (gallstones)
– Cholangio-hepatitis/cholangitis
– Tyzzer’s disease (foals 7-42 days)
– Toxic hepatopathies
– Hepatic neoplasia (RARE)
– Portosystemic vascular shunts (RARE)

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8
Q

secondary liver disease
- what are these?
- which are we worried about in the horse?

A
  • Affects liver as part of a more generalized
    disorder
  • Metabolic disorders
    <><><><>
  • Hyperlipemia (“fatty liver”)
    –Ponies, minis, donkeys, “cold” blooded horses
  • Hyperadrenocorticism (pituitary tumor PIPD)
  • Neoplastic metastases
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9
Q

Pyrrolizidine poisoning
- what plant?
- pathogenesis?

A
  • Tansy Ragwort (Senecio jacobaea)
    – contains at least six pyrrolizidine alkaloids (not toxic)
    – combined with liver enzymes after ingestion
    > they are converted to pyrroles > liver dysfunction
    – Antimitotic effect on DNA > hepatocytes cannot divide > die + replaced by fibrosis
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10
Q

Pyrrolizidine poisoning
- diagnosis and prognosis

A

– Liver biopsy
* Triad of fibrosis, bile duct proliferation, and megalocytes
<><><>
* Prognosis
– horses are most seriously affected followed by goats
– >600 alkaloids identified

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11
Q

cholelithiasis
- what is this, how common
- pathogenesis
- stone composition

A
  • Choledo-cholelithiasis (common bile duct) is the most common biliary obstruction in the horse (occurs more frequently in the horse than in other domestic animals)
    <><>
  • Pathogenesis
    – Unknown: ascending infection, parasites, foreign body etc)
    <><>
  • Composition of stones: mixed
    – Bilirubin, CaPO4, cholesterol esters, bile pigments, etc
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12
Q

cholelithiasis
- signalment
- risk factors
- clinical signs
- Dx labwork

A
  • Signalment: ADULTS, no breed or sex predilection
    <><>
  • Risk factors: enteric Gram – infection from SI
    <><>
  • Clinical Signs
    – Intermittent abdominal pain w pyrexia and icterus – Less commonly HE, photosensitization, weight loss
    <><>
  • Lab evaluation
    – Increased liver enzymes (GGT, ALP, bile acids)
    – Suspect cholestasis if direct is >30% of total bilirubin
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13
Q

what do we see on US in cholelithiasis

A

– Hepatomegaly and bile duct dilation
– Generally multiple choleliths seen

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14
Q

cholelithiasis Tx options, prognosis

A

– Medical:
* long term broad spectrum AB’s (enrofloxacin/ ceftiofur)
* Fluid therapy
* DMSO: helps dissolve Ca glucoronidate calculi??
* Bile salt therapy: contraindicated in horses
<><>
– Surgical: relief of obstruction
<><>
– Guarded prognosis

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15
Q

cholelithiasis monitoring

A

– Repeat US, sequential GGT/ALP

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16
Q

Tyzzers disease
- pathogen
- signalment
- risk factors

A
  • Etiology: Clostridium piliformis
  • Signalment: 7-40 days of age
  • Risk factors: parturition
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17
Q

Tyzzers disease pathophysiology
- transmission
- carriers
- contagiousness

A

– Fecal-oral route of transmission
– Carrier state may exist ????
– Not a highly contagious disease

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18
Q

Tyzzers disease clinical signs

A

– Often found dead w no history of signs
– Fever, depression and anorexia
– Icterus, hypoxia, coma, seizures etc

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19
Q

Tyzzers disease diagnosis

A

– Lab evaluation
> elevated enzymes, severe hypoglycemia
– Definitive only at post-mortem
– Organism difficult to identify in routine stains

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20
Q

Tyzzers disease Tx

A

– No reports of successful treatments (1 report)
– Antimicrobial therapy (pen, tetracyclines, erythromycin)

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21
Q

primary liver tumour in horses - how common?

A

rare

22
Q

Equine Hyperlipemia
- who is susceptible
- what is this?
- risk factors?

A

– Small, fat-obese, female Pony or Miniature Horse
– Metabolic disease
– Negative-energy balance
– Fatty infiltration of liver
– Hepatic failure
– Anorexia / Starvation
– Late-pregnancy / Lactation
– Parasitism
– Transportation

23
Q

Equine Hyperlipemia
- Dx

A
  • Equine Hyperlipemia
    – Opaque, fatty appearance to
    plasma
    –increased serum triglycerides > 500 mg/dL
    <><>
  • increased liver enzymes
    > SDH, GGT, AST
    <><>
  • Liver biopsy: fatty infiltration
24
Q

Causes of hepatitis
* Viral:

A

– Equine parvovirus-hepatitis (EqPV-H)
– Non-primate hepacivirus (NPHV)
– Equine genus Pegivirus
– Theiler’s Disease Associated Virus (TDAV)

25
Q

Theiler’s disease
- what is it?
- lesions/ severity

A

an acute hepatitis frequently occurring several weeks after administration of a biological substance of equine origin
<><>
- can lead to hepatic necrosis (4-18%) which can be fatal (2%), several weeks (4-24 weeks) after the vaccination
> ie. related to the vaccine protocol

26
Q

equine biologic products associated with Theiler’s disease, or other hepatic diseases

A
  • Tetanus antitoxin
  • Botulinum antitoxin
  • Antiserum against Streptoccocus equi
  • Pregnant mare’s serum
  • Equine plasma
  • Allogeneic stem cells
27
Q

Equine parvovirus-hepatitis
- prevalence
- transmission

A
  • Virus prevalence: 13% (serum PCR)
  • Sero-prevalence: 15%
    <><><><>
  • Transmission:
    – Iatrogenic through biologic products, otherwise unknown
    <>
    – Viral DNA in nasal secretions and feces at peak viremia
  • Transmission routes remains to be determined
28
Q

are clinical signs of liver disease pathognomonic?

A

no
– Signs secondary to failure of a specific liver function

29
Q

does icterus mean liver disease? is it always present with liver disease? where should we look?

A

– Icterus may be present in horses with diseases NOT directly involving liver (Fasting)
– Sclera: best mucous membrane to assess !!
– Examine in direct sunlight
– May NOT see icterus in chronic hepatic failure

30
Q

non-liver disease issue that can produce icterus in the horse?

A

– Anorexia and fasting can produce icterus in the horse

31
Q

Anorexia and fasting can produce icterus in the horse
- how?

A

– Failure of hepatic uptake of free bilirubin
– Failure of transport of free bilirubin

32
Q

If conjugated bilirubin >25% of total serum
bilirubin, indicates….
- conjugated bilirubin has an affinity for…
> consequence

A

– If conjugated bilirubin >25% of total serum bilirubin indicates biliary obstruction
– Conjugated bilirubin has a much greater affinity for connective tissue
– Greater degree of icterus in cholestatic liver disease

33
Q

Hepatic encephalopathy signs

A
  • Generalized muscle weakness
  • Truncal ataxia, weakness, dysphagia
  • Behavioural abnormalities
    – Yawning, head pressing, compulsive walking
    <><><><>
    – Severe depression:
  • head drooped
  • Sleepy
  • yawning (excessive)
    <><>
    – Defective vision:
  • sluggish PLR
  • sluggish menace
    <><>
    – Ataxia, incoordination, circling
    – Compulsive walking
    – Head pressing (terminal sign)
34
Q

liver disease physical findings, in general

A

– Anorexia, depression, dullness, weight loss
– Behavioural abnormalities
<><>
* Normal TPR
* Anorexia
* Depression/lethargy
* Weight loss (chronic)
* Icterus
– Hepatic encephalopathy signs
<><><><>
– ± Colic
– ± Photosensitization
* Dysfunctional liver NOT capable of metabolizing phylloerythrin (photodynamic agent)
– Constipation
* pass small, hard fecal balls

35
Q
  • Clinical Pathology: Serum enzymes in liver disease
  • where they are from
  • properties
A

– Gamma-glutamyl transpeptidase (GGT)
* bile duct and hepatic cellular damage (t/2 14-26 d)
<><>
– Glutamate dehydrogenase (GLDH)
* cytoplasmic (mitochondrial)
<><><><>
– Sorbitol dehydrogenase (SDH)
* cytoplasmic ( very short half life)
<><>
– Alkaline phosphatase (AP)
* High in foals (bone metabolism), associated with biliary S
<><>
– Aspartate aminotransferase (AST, GOT)
* Mostly in hepatocytes (t/22 h or more d in LA)

36
Q
  • Clin Path: Serum biochemistry
  • bile acids for liver disease
  • normal variation?
  • sensitive or no? other metrics?
A

– Elevated total serum bile acids (SBA) (0-6 normal)
* >20 μmol/L
<><><><>
– No significant diurnal variation
– No post-prandial rise in bile acids as horses do NOT have a gall bladder
<><><><>
– Sensitive indicator especially in chronic cases
* Total serum bilirubin/conjugated bilirubin increased

37
Q
  • Clin Path: Serum biochemistry
  • non-bile acids tests
A
  • increased blood ammonia (in HE)
    <><>
  • ± decreased serum [Urea]
    > NOT a consistent finding in hepatic failure
    <><>
    – ± Hypoglycemia
  • terminal event
    <><>
    – Hypoproteinemia/hypoalbuminemia
  • terminal event
  • Albumin t/2 3 weeks
38
Q

urinalysis results for liver disease

A

– ± Bilirubinuria
– ± Hemoglobinuria
– ± Urobilinogenuria

39
Q

Liver biopsy:
what should we do before performing a liver biopsy? what tests? what needle? how to get the right site?

A

– Perform blood coagulation tests before
* Prothrombin time (PT)
– Activated partial thromboplastin
time (APTT)
– “Tru-Cut” biopsy needle
– Site: via ultrasound guidance or percutaneous over right 12th intercostal space

40
Q

liver disease Ddx

A

– Other causes of progressive weight loss
– Other causes of acute neurologic dysfunction
* Rabies, EPM, WNV, EEE, WEE
– Other causes of icterus
– Other causes of colic

41
Q

Liver disease therapy, general goals

A

– Support liver functions
– Reduce hepatic workload
– Allow sufficient time for hepatic regeneration

42
Q

liver disease therapy - glucose considerations, reasoning

A
  • Maintain blood [glucose]:
    – Hypoglycemia occurs in liver failure
    – 50 g dextrose IV/hour for 48 hours
    – Decreases hepatic workload
    – Oral glucose by stomach tube
43
Q

liver disease therapy - water and electrolytes, reason

A

– Maintain hydration
– Preserve hepatic microcirculation
– Aid renal excretion of hepatotoxins

44
Q

what IV fluid therapy to give for liver disease

A

– Balanced Electrolyte Solution IV (LRS)
– ± Add KCl (20 mEq/L) to fluids
– Correct acid-base imbalances SLOWLY
– Avoid IV HCO3 unless severe acidosis

45
Q

Liver disease therapy - how do we combat hepatic encephalopathy?

A

Decrease absorption and production of
NH3 from gastrointestinal tract
– Lactulose
– Mineral oil
– Dioctyl sodium sulfosuccinate (DSS)
– Oral antibiotics (neomycin) ??
– Metronidazole

46
Q

exercise vs rest for liver disease

A
  • Stall rest:
  • Keep out of direct sunlight
  • Risk of photosensitization
47
Q

liver disease diet, vitamins

A

Diet:
* Low protein & readily digestible CHOs
* Attempting to decrease production of NH3 by gut bacteria
* Avoid legume hays (too high protein)
* Avoid wheat, soya beans, oats
* Feed diet high in BCAAs
> Sorghum grains, beet pulp (soaked)
<><><>
Vitamins:
– Vitamin B complex and K1 parenteral

48
Q

when would we give antibiotics for liver disease?

A

– Suppurative cholangitis/cholangiohepatitis

49
Q

how to control abnormal behaviour due to liver disease
- when to act?
- what to use?
- cautions?

A

– Sedation/anti-convulsants
– Only administer if having seizures
– Care: drugs are slowly metabolized
– Use LOW doses of sedatives/tranquilizers NOT diazepam

50
Q

Poor prognosis for liver disease with:

A
  • Chronic hepatic failure
  • Severe encephalopathy
  • Hemoglobinemia/hemoglobinuria
  • Pyrexia
51
Q

Prevention of liver disease - what can clients avoid?

A

– Limit use of equine anti-sera
– Avoid hay or pellets that may contain pyrrolizidine alkaloid-containing plants

3. Equine (17 decks)

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