C13 Hepatobiliary Pathology II Flashcards

1
Q

Hepatitis definition
- pattern depends on what

A

Hepatitis: presence of inflammatory cells and/or infectious agents in the parenchyma, focal or diffuse
o Pattern of inflammation depends on the cause, but most infectious agents produce patchy lesions that don’t cause hepatic insufficiency

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2
Q

Acute hepatitis: usually a mix of

A

inflammation, apoptosis/necrosis, regeneration

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3
Q

Chronic hepatitis:
- consistent feature
- definition
- causes
- progression
- signs

A
  • Chronic hepatitis: fibrosis is a consistent feature
    o Chronic necroinflammatory disease lasting more than 6 months
    o Idiopathic most common but also bile obstruction, infection, toxins, etc
    o Does not progress to cirrhosis or severe fibrosis unless protracted damage
    o Nonspecific signs initially, then typical liver insufficiency
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4
Q

Chronic hepatitis in dogs
- how common
- causes
- stain, assessment

A

o Common
o Most cases idiopathic, but copper accumulation is a well known cause
o Copper regulated primarily via biliary excretion
o < 400 μg/g normal, > 1,800-2,000 μg/g pathogenic
o Can stain with rhodanine but biochemical assessment is more reliable

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5
Q

Chronic hepatitis in dogs: copper
- what mutation, breed
- presentation
- progression
- other breeds?

A

o COMMD1 mutation in Bedlington terrier: impaired copper excretion
o Autosomal recessive, presents with progressive liver failure
o Can develop hemolytic crisis if copper released into systemic circulation
o Other predisposed breeds (defects unknown): Labrador, Doberman, Westie, English and American cocker spaniel, Skye terrier, standard poodle, Dalmatian, English springer spaniel

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6
Q

Chronic hepatitis in other species
- copper possible in cats?
- causes

A

o Copper-associated hepatitis also reported in cats
o Usually associated with toxin ingestion in herbivores but the lesions are nonspecific, so it is difficult to determine a precise cause

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7
Q

Cholecystitis
- common?
- cause?
- predisposition
- type in calves and cause?

A

Cholecystitis: inflammation of the gallbladder (uncommon)
o Bacterial reflux via ducts or hematogenous
o Choleliths (stones) or parasites predispose
o Fibrinous cholecystitis in calves with salmonellosis

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8
Q

Cholangitis

A

inflammation of the biliary tree

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9
Q

Cholangiohepatitis
- cause?
- progression

A

Cholangiohepatitis: inflammation centred on the biliary tract and extending into the parenchyma (more common than cholangitis)
o Usually ascending bacterial infection from gut (bile stasis)
o Rarely descending infection (cattle with hepatic abscesses)
o Can rapidly cause death via septicaemia but chronic inflammation more common
o Chronic inflammation leads to fibrosis and biliary proliferation

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10
Q

Cholangitis in cats
- types:
> causes, presentations

A

Neutrophilic: common, part of ‘triaditis’ (inflammatory bowel disease,
pancreatitis, cholangitis) and with bile obstruction
o Ascending bacteria, mostly E. coli
o Neutrophils in the acute stage and later periportal hepatocellular necrosis
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Lymphocytic: slowly progressive, lymphoid infiltrates and portal fibrosis
o Believed to be immune-mediated

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11
Q

Cholelithiasis
- form where, from what
- effects?

A
  • Cholelithiasis: usually form in gallbladder, mix of cholesterol, bile pigment, salts
    o Rare in animals, usually asymptomatic but can block ducts
    o Large stones can cause pressure necrosis of mucosa
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12
Q

more common causes of biliary obstruction

A
  • Biliary obstruction is more commonly due to inflammation
    o Occasionally, ducts can be compressed by tumours, etc.
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13
Q

can we get jaundice from blockage of main bile duct? what about smaller ducts? why?

A
  • Blockage of the main bile duct leads to jaundice, but not blockage of smaller ducts (the rest of the liver compensates)
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14
Q

what happens if biliary tract ruptures

A
  • If the biliary tract ruptures, the omentum can’t block the hole and bile leaks
    o Even if sterile, severe irritation (bile peritonitis), can be rapidly fatal
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15
Q

viral causes of multifocal hepatic necrosis

A

adenoviruses, influenza, herpesvirus in neonates

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16
Q

viral causes of lymphohistiocytic hepatitis and apoptosis

A

porcine circovirus 2

17
Q

viral causes of granulomatous hepatitis in cats

A

o Granulomatous hepatitis: feline coronavirus (feline infectious peritonitis)

18
Q

do many viruses directly target the liver?

A

no

19
Q

Rabbit haemorrhagic disease (calicivirus)
- geography
- historic use
- symptoms
- prevention
- reportable?

A

o Endemic in UK, Europe; sporadic outbreaks in North America
o Deliberately used as pest control in Australia
o Sudden death with no signs or anorexia +/- hemorrhages, neurological signs
shortly before death, all have hepatic necrosis and inflammation
o Vaccine used in pets but not available here
o REPORTABLE DISEASE!

20
Q

Infectious canine hepatitis
- agent
- prevention
- presentation
- spread
- cells affected
- lesions, signs

A

Infectious canine hepatitis: canine adenovirus 1 (now rare due to vaccination)
o Often subclinical, if severe case vomiting, abdominal pain, +/- jaundice
o Oronasal spread, replicates in tonsils (may cause tonsillitis)
o Virus targets endothelium and hepatocytes: centrilobular necrosis
o Connective tissue is intact so liver can regenerate
o Lesions in other organs (hemorrhages) are related to endothelial damage
o Recovering cases have corneal edema (‘blue eye’) due to type III sensitivity

21
Q

Equine serum hepatitis
- linked to what pathogen
- sympotms
- usually seen when?
- symptoms
- liver appearance

A

Equine serum hepatitis: linked to Theiler’s disease- associated virus (flavivirus)
o Common cause of acute hepatic failure in horses
o Usually seen after passive immunization but some
outbreaks unrelated to this
o Long incubation period (42-60 days) but sudden
clinical onset, death in 6-24 hours
o Lethargy, jaundice, photosensitivity, mania,
blindness, ataxia, sudden death
o Small, flaccid liver due to loss of cells (‘dishrag liver’)

22
Q

clinical significance of bacterial hepatitis

A
  • Bacterial hepatitis is common but usually focal and not clinically significant
23
Q

will sustained bacteremia form liver lesions?

A
  • Almost every sustained or repeated bacteremia will form liver lesions
24
Q

bacteria that can cause inflammatory liver in all species

A

Salmonella, Mycobacteria

25
Q

Hepatic abscesses
- common in what animals
- sequel to what
- consequences

A

Hepatic abscesses: most common in feedlot cattle +/- sheep, single or multiple
o Often not found until slaughter, common sequel to rumenitis
o Variable possible consequences…
§ Can form adhesions
§ Can rupture into hepatic veins,
producing thrombosis and emboli
§ Really large emboli can be fatal
o May also contain fungi

26
Q

Hepatic necrobacillosis
- agent
- secondary to what
- appearance

A

Fusobacterium necrophorum
o Secondary to omphalitis or rumenitis, produces a leukotoxin
o Multifocal dry areas of coagulative necrosis surrounded by hemorrhage

27
Q

Leptospirosis
- disease presentation

A

systemic disease with acute jaundice, cholestasis, renal failure

28
Q

Infectious hepatitis (black disease)
- agent
- pathogenesis
- prevention

A

Cows, sheep
- vaccine
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Clostridium novyi type B
- spores in soil ingested, cross mucous membranes
> Live in Kupffer cells
> Flukes > Necrosis causes anaerobic conditions
> Spores activate, produce necrotizing toxins
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- Acute, fatal disease – unexpected deaths
- Congested SQ vessels (hence ‘black’)
- Rapid decomposition
- Abdominal fluid clots on exposure to air
- Yellow-white liver necrosis with red rim

29
Q

Bacillary haemoglobinuria
- species
- agent
- pathogenesis
- lesions, signs

A

Cows, sheep
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Clostridium haemolyticum
o Similar pathogenesis to black disease, mostly seen in areas with flukes
o Affects cattle and sheep, similar hepatic lesions to black disease (usually bigger)
o Intravascular hemolysis, anemia, hemoglobinuria
o Red-brown kidneys due to hemoglobin, port wine colour urine

30
Q

Clostridium piliforme
- disease, species
- lesions
- Dx
- foals presentation

A

Tyzzer’s disease of rodents, dogs, cats, foals, calves
o Focal hepatitis and necrosis (pale foci up to a few millimetres)
o Hard to culture, confirmed by finding organisms at the periphery of necrosis
o In foals, deaths between 1-4 weeks old, often found dead after short illness

31
Q

signs of migrating larvae in the liver

A

Migrating larvae cause physical damage (hemorrhage, necrosis, inflammation)
o Look for eosinophils
o Healing via fibrosis
o Sometimes trapped larvae form eosinophilic granulomas

32
Q

flukes in the liver have what characteristic trait

A

Several species of trematodes (flukes) specifically infect the liver
o Characteristic black pigment

33
Q

Fasciola hepatica
- possible consequences
- lesions

A

o Larvae migrate through liver, can
cause fatal anemia in heavy infection
o Don’t forget about black disease!
o Adults live in bile ducts, causing
dilation and fibrosis

34
Q

Dicrocoelium dendriticum
- what is it

A

o Similar to F. hepatica but milder
o Land snails and ants in life cycle

35
Q

Fascioloides magna
- natural host
- anatomic home
- effects in different animals

A

o Natural host is deer, lives in parenchyma and connects with bile ducts
o In cows, migrates briefly, no connection to bile ducts
o In sheep, never stops migrating – small burdens are deadly

36
Q

Eimeria stiedae
- species
- anatomic infection location and pattern

A

o Significant pathogen of (meat) rabbits, infects bile ducts (multifocal nonrandom)

37
Q

liver ‘abscess’ may be what parasite class?

A

o Tapeworm cysts (beware the ‘abscess’!)