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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?

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
Theiler's disease - what is it? - lesions/ severity
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
equine biologic products associated with Theiler's disease, or other hepatic diseases
* Tetanus antitoxin * Botulinum antitoxin * Antiserum against Streptoccocus equi * Pregnant mare's serum * Equine plasma * Allogeneic stem cells
27
Equine parvovirus-hepatitis - prevalence - transmission
* 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
are clinical signs of liver disease pathognomonic?
no – Signs secondary to failure of a specific liver function
29
does icterus mean liver disease? is it always present with liver disease? where should we look?
– 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
non-liver disease issue that can produce icterus in the horse?
– Anorexia and fasting can produce icterus in the horse
31
Anorexia and fasting can produce icterus in the horse - how?
– Failure of hepatic uptake of free bilirubin – Failure of transport of free bilirubin
32
If conjugated bilirubin >25% of total serum bilirubin, indicates.... - conjugated bilirubin has an affinity for... > consequence
– 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
Hepatic encephalopathy signs
* 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
liver disease physical findings, in general
– 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
* Clinical Pathology: Serum enzymes in liver disease - where they are from - properties
– 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
* Clin Path: Serum biochemistry - bile acids for liver disease - normal variation? - sensitive or no? other metrics?
– 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
* Clin Path: Serum biochemistry - non-bile acids tests
* 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
urinalysis results for liver disease
– ± Bilirubinuria – ± Hemoglobinuria – ± Urobilinogenuria
39
Liver biopsy: what should we do before performing a liver biopsy? what tests? what needle? how to get the right site?
– 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
liver disease Ddx
– 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
Liver disease therapy, general goals
– Support liver functions – Reduce hepatic workload – Allow sufficient time for hepatic regeneration
42
liver disease therapy - glucose considerations, reasoning
* 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
liver disease therapy - water and electrolytes, reason
– Maintain hydration – Preserve hepatic microcirculation – Aid renal excretion of hepatotoxins
44
what IV fluid therapy to give for liver disease
– Balanced Electrolyte Solution IV (LRS) – ± Add KCl (20 mEq/L) to fluids – Correct acid-base imbalances SLOWLY – Avoid IV HCO3 unless severe acidosis
45
Liver disease therapy - how do we combat hepatic encephalopathy?
Decrease absorption and production of NH3 from gastrointestinal tract – Lactulose – Mineral oil – Dioctyl sodium sulfosuccinate (DSS) – Oral antibiotics (neomycin) ?? – Metronidazole
46
exercise vs rest for liver disease
* Stall rest: * Keep out of direct sunlight * Risk of photosensitization
47
liver disease diet, vitamins
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
when would we give antibiotics for liver disease?
– Suppurative cholangitis/cholangiohepatitis
49
how to control abnormal behaviour due to liver disease - when to act? - what to use? - cautions?
– Sedation/anti-convulsants – Only administer if having seizures – Care: drugs are slowly metabolized – Use LOW doses of sedatives/tranquilizers NOT diazepam
50
Poor prognosis for liver disease with:
* Chronic hepatic failure * Severe encephalopathy * Hemoglobinemia/hemoglobinuria * Pyrexia
51
Prevention of liver disease - what can clients avoid?
– 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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