Liver Diseases of Horses (Hostnik) Flashcards

1
Q

Equine:
What empties into the duodenum at the major duodenal papilla, located on a slightly raised mucosal ridge?

A

Both the bile duct and pancreatic duct

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2
Q

Equine:
What opens at the minor duodenal papilla?

A

Accessory pancreatic duct

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3
Q

Equine Definition:
Is a complex clinical syndrome characterized by the abnormal mental status that accompanies severe hepatic insufficiency

A

Hepatic Encephalopathy (HE)

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4
Q

(T/F) Hepatic Encephalopathy generally is considered to be a potentially reversible metabolic encephalopathy

A

True

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5
Q

Acute Disease:
- Is a hepatotropic Single-stranded DNA virus capable of causing hepatitis in infected horses
- Has been found in consecutive horses with Theiler’s disease that received tetanus antitoxin or other equine-origin blood products

A

Equine parvovirus

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6
Q

Equine:
What was the first of the three new blood-borne viruses to be reported?

A

Nonprimate Hepacivirus
- is a flavivirus, uncommon in mules or donkeys

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7
Q

List the nutrient metabolism of liver functions:

A
  • Carbohydrates
  • Fat
  • Protein
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8
Q

What are common clinical findings of liver disease in a horse?

A
  • Depression
  • Anorexia
  • Colic
  • Weight loss
  • Icterus (important indicator)
  • Pigmenturia
  • Hepatic Encephalopathy (HE)
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9
Q
  • Caused by hyperbilirubinemia
  • 10-15% of horses normally have slightly yellow sclera
    - related to fasting
A

Ictures (jaundice)

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10
Q
  • Phylloerythin (derived from chlorophyll) is normally metabolized and excreted by the equine liver
  • In disease, increases in phylloerythrin in the blood react with UV light to cause damage and necrosis of unpigmented skin
    - the liver is not detoxifying that substance properly
A

Photosensitization

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11
Q
  • Augmented GABA activity in the brain (sleepy horses)
  • Altered expression of benzodiazepine receptors
  • Increased neurosteroids (not much is known)
  • False neurotransmitter accumulation
  • Inflammatory mediator expression
  • Increased BBB permeability and cerebral hypertension
    These are other mechanisms/pathogenesis that may be involved with …
A

Hepatic Encephalopathy

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12
Q

What are the main enzymes that we look for in lab testing in a clinical assessment of the liver in horses?

A
  • Asparte aminotransferase (AST)
    - Not specific to the liver (come from muscle, RBCs)
  • Sorbitol dehydrogenase (SDH)
    - Liver-specific in a horse
    - is the main one that we look at for hepatocellular leakage
    (both are hepatical leakage enzymes when the hepatocyte is damaged they leak out into the blood)
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13
Q

Clinical Assessment of the liver in horses
List the two enzymes that are liver-specific:

A
  • SDH
    • increases seen with ongoing injury
    • shorter half-life than AST (increase quicker, and decrease quicker)
  • GGT
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14
Q

Clinical Assessment of the liver in horses
What enzymes are biliary/cholestatic (hepatobiliary)?

A
  • Gamma-glutamyl transferase (GGT)
  • Alkaline phosphatase (ALP)
    - non-specific (also bone, intestinal, renal, mammary, placenta, leukocytes, corticosteroids)
    (are actually induced)
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15
Q

Equine Functional Tests:
- Indirect (unconjugated)
- Direct (conjugated)
- In horses with Anorexia of any cause, we see an increase in UNconjugated ___________ due to a decrease in the proteins required to import UNconjugated __________ into the liver

A

bilirubin (increase)

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16
Q

Equine Functional Tests:
- Per- and post-prandial measurement is not necessary since horses continuously secrete bile
- Horses DON’T have a gallbladder

A

Increase Bile Acids

17
Q

Equine Functional Tests Results: Liver Disease

A
  • Increased Bilirubin
  • Increased Bile Acids
  • Increased Ammonia
  • Decreased UREA (BUN)
  • Decreased Glucose
  • Coagulation testing (depends on what you are measuring)
18
Q

Bilirubin
- Hemolysis
- Fasting hyperbilirubinemia

A

Unconjugated (indirect)

19
Q

Bilirubin
- Cholestasis

A

Conjugated (direct)

20
Q

(T/F) Abdominal radiographs are useful to evaluate the liver in equids

A

False, Abdominal radiographs are NOT useful

21
Q
  • Chronic megalocytic Hepatopathy
  • Delayed onset, chronic, progressive liver failure due to ingestion of pyrrolizidine alkaloid-containing plants
  • Metabolized by the liver after ingestion into toxic pyrrole derivatives
    - Alkylate nucleic acids and protein, preventing cellular replication and protein synthesis
    - Causes hepatocytes to enlarge -> megalocytes
    - When megalocytes die, it causes fibrosis
A

Pyrrolizidine Alkaloid Toxicity

22
Q

Equine:
What do you see in a liver biopsy of a horse with pyrrolizidine alkaloid toxicity?

A
  • Megalocytosis
  • Biliary hyperplasia
  • Fibrosis
23
Q

NAVLE

  • Clostridium piliforme
    • Motile, pleomorphic, Gram-Negative, spore-forming, obligate intracellular bacterium
  • Acute necrotizing hepatitis in FOALS (3 weeks old - between 7 & 42 days)
  • Foals ingest contaminated soil or feces from the dam (relatively common in the enviroment - cases are sporadic)
  • Travels to the liver and heart via lymphatics and hematogenous spread
A

Tyzzer’s Disease

24
Q

What is the primary disease associated with Tyzzer’s Disease (highly fatal)?

A

Acute, multifocal hepatitis
(but also myocarditis and enteritis are seen)
-> will see grossly an enlarged, swollen lover with 1- to 5-mm white foci throughout (coagulative necrosis and inflammation)

25
Q
  • Serum hepatitis, serum sickness, acute hepatic necrosis
  • Now –> Viral hepatitis
  • Acute or subacute hepatitis with liver necrosis in Adult Horses
  • Association with the administration of equine-derived biological products (typically 4-10 weeks before the onset of hepatic failure)
    - Most common is Tetanus Antitoxin
A

Theiler’s Disease

26
Q
  • Likely caused by Equine Parvovirus-Hepatitis (EqPV-H) – acute hepatic necrosis and subclinical hepatitis
  • Equine Hepacivirus – mild, subclinical hepatitis
A

Theiler’s disease
- Treatment:
- Supportive care
- Prognosis is guarded with acute disease and hepatic failure