Hepatobiliary System, Pt. 4 Flashcards

1
Q

What is hepatitis, cholangitis, cholangiohepatitis, cholecystitis, and choledochitis?

A

HEPATITIS = inflammation of the liver parenchyma

CHOLANGITIS = inflammation of the bile ducts/ductules in the portal triad

CHOLANGIOHEPATITIS = inflammation of the bile ducts with extension into the liver parenchyma

CHOLECYSTITIS = inflammation of the gallbladder

CHOLEDOCHITIS = inflammation of the larger/common bile ducts

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2
Q

What is the most common cause of multifocal random (miliary) hepatitis? How does it present grossly?

A

infectious agents, like viruses, bacteria, and certain protozoa

multifocal random spots of necrosis and hemorrhage of the liver parenchyma

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3
Q

What are the herpesviruses affecting horses, canids, felines, bovines, and suids? What other system do they commonly affect other than the liver?

A
  • equine herpesvirus 1 - abortigenic
  • canid herpesvirus 1 - renal hemorrhage in puppies
  • feline herpesvirus 1 - rhinotracheitis
  • bovine herpesvirus 1 - infectious rhinotracheitis
  • suid herpesvirus 1 - pseudorabies

(all cause miliary hepatitis, commonly in young or aborted animals)

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4
Q

Equine herpesvirus-1:

A
  • foal multifocal hepatic necrosis
  • abortigenic virus
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5
Q

Equine herpesvirus hepatitis, histology:

A
  • loss of plate/chord pattern - hepatocytes separated
  • blood out of sinusoids
  • eosinophilic intranuclear viral inclusion bodies
  • hepatocellular necrosis
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6
Q

What causes canine infectious hepatitis? What is seen histologically? Why is it rare now?

A

canine adenovirus 1

centrilobular hepatocellular necrosis with intranuclear viral inclusion bodies in hepatocytes and endothelial cells

widespread use of effective vaccine that utilizes CAV-2 in a distemper combination

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7
Q

What is commonly seen in dogs that recover from canine infectious hepatitis?

A

first exposure (vaccine) or infection causes the animal to begin producing antibodies, and upon second exposure these antibodies will complex with antigens (virus) and deposit into the vessels of the eye —> corneal edema (blue eye disease)

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8
Q

Canine infectious hepatitis:

A
  • hepatic necrosis
  • hemorrhage (due to endothelial tropism) in the intestine
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9
Q

How does canine infectious hepatitis compare to herpesvirus hepatitis histologically?

A

not as eosinophilic intranuclear inclusion bodies as herpesvirus (still need PCR to confirm)

  • disassociated hepatocytes
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10
Q

What causes Theiler’s disease, or equine serum hepatitis? How does it present grossly?

A

infection by equine parvovirus-hepatitis

small, flaccid “dishrag” liver

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11
Q

What are the main 3 routes of infection of liver bacterial disease?

A
  1. portal vein
  2. umbilical vein in newborns (hepatic abscesses common)
  3. hepatic artery
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12
Q

How can bacterial infections in the biliary system affect the liver? How do parasites affect the liver? Other tissues?

A

ascending infection from gallbladder spreads to the liver

parasitic infection impairs the liver, making it susceptible to bacterial infections

hardware disease and ruminal acidosis allows bacteria access to the portal vein

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13
Q

What causes hepatic necrobacillosis? How does it present grossly?

A

Fusobacterium necrophorum

multifocal coagulative necrosis, commonly surrounded by red inflammation

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14
Q

What causes tuberculosis? How does this affect the liver?

A

Mycobacterium bovis

multifocal caseous granuloma formation

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15
Q

What are 4 common sequelae of hepatic abscesses?

A
  1. complete healing or encapsulation
  2. induce adhesions
  3. extend to hepatic vein leading to thrombophlebitis of the vena cava, endocarditis, and pulmonary abscesses/thrombi
  4. toxemia —> shock —> death
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16
Q

Omphalophlebitis, calf:

A
  • miliary abscesses in left lobe
  • infection from mother or non-sterile procedures
17
Q

What causes Tyzzer’s disease? What is the pathogenesis?

A

Clostridium piliforme (G-) infection in young and immunocompromised foals, calves, dogs, and cats

ingestion allows proliferation of the bacterium in the GIT, where it can reach portal circulation and the liver

18
Q

How does Tyzzer’s disease present grossly?

A

multifocal hepatic necrosis

  • Clostridium piliforme
19
Q

Tyzzer’s disease, histopathology:

A
  • intracytoplasmic filamentous bacteria
  • Warthrin-Starry stain
20
Q

How do parasites cause damage to the liver?

A

migrating larvae see liver parenchyma and/or bile ducts as final resting place and causes damage getting there

21
Q

What is the characteristic hepatic lesion of Ascaris suum?

A

fibrous scars (milk-spotted liver) deposited in the migration tracts of the ascarid larvae due to their migration throughout the tissue

  • pigs!
22
Q

What is Fascioloides magna? What characteristic lesion is seen in the liver parenchyma?

A

liver fluke of ruminants that lives in the hepatic parenchyma and causes extensive tissue damage by migrating throughout the liver

black excretory pigment within the migration tracts

23
Q

Fascioloides magna, ox:

A

destructive pigmented lesions

24
Q

How do tapeworms commonly affect the liver?

A

cysticercosis - formation of multifocal cysts containing larvae

25
Q

Cysticerus fasciolaris, cyst histology:

A
26
Q

What coccidia commonly causes hepatic disease in rabbits? How does it present grossly?

A

Eimeria stediae

cholangiohepatitis - linear tracts of enlarged bile ducts

27
Q

Eimeria stediae infection, rabbit, histology:

A

L = enlarged ducts

R = epithelial cells containing microgameocytes (green) and macrogameocytes (black) - different stages of the coccidia

28
Q

What species are commonly affected by histomoniasis? How does it affect the liver?

A

chickens, turkeys

multifocal necrotizing hepatitis with target-like lesions (black head disease)

29
Q

Chronic hepatitis is commonly idiopathic in dogs. What is a small subset of cases caused by? What is a common sequel?

A

copper accumulation (can be treated!)

hepatic necrosis with inflammation may lead to cirrhosis

30
Q

What breed has a genetic disposition to develop copper-associated hepatopathy? What other breed is predisposed?

A

Bedlington terrier - genetic mutation

Doberman Pinscher

31
Q

What is the cause of copper-associated hepatopathy in Bedlington terriers? What is the pathogenesis? How do these animals present?

A

mutation in the COMMD1 gene

copper accumulation —> acute hepatic necrosis —> release of copper into systemic circulation —> hemolytic crisus due to RBC toxicity —> anemia and icterus

progressive liver failure causes wasting, ascites, and signs of hepatic encephalopathy

32
Q

Hepatic copper, dog:

A
  • common in Bedlington terriers
  • rhodanine stain
  • treatable!
33
Q

What are 4 common ways of managing canine copper-associated hepatopathy?

A
  1. dietary copper restriction
  2. copper chelation with D-penicillamine
  3. zinc - interferes with copper uptake
  4. antioxidant treatment with S-adenosylmethionine (SAMe) and vitamin E
34
Q

What makes cats predisposed to triaditis? What 3 organs are included?

A

common bile duct fuses with the pancreatic duct fuses with the pancreatic duct before entering the major papilla

  1. cholangitis
  2. pancreatitis
  3. inflammatory bowel disease
35
Q

What are the 11 common (nonspecific) clinical signs associated with feline triaditis?

A
36
Q

Feline triaditis:

A
37
Q

What 3 additional tests can be used to diagnose feline triaditis?

A
  1. feline pancreatic lipase immunoreactivity (fPLI)
  2. serum cobalamine and folate concentrations for IBD and chronic pancreatitis
  3. ultrasonography can identify presence of multiorgan inflammatory disease
38
Q

What is the gold standard for diagnosing feline triaditis?

A

biopsy identifying liver, GI, and pancreatic inflammation