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Y3 Liver and Pancreas pathology > Liver and Biliary System 3 > Flashcards

Liver and Biliary System 3 Flashcards

1
Q

Inflammation of the liver is termed?

A

Hepatitis

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2
Q

Describe the features of acute hepatitis

A
  • Degeneration / necrosis of hepatocytes
  • Leukocyte infiltration in: periportal connective tissue and/or within sinusoids [bacterial infections: neutrophils; viral infections: lymphocytes…]
  • Increased numbers of leukocytes in sinusoids
  • Activation of Kupffer cells
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3
Q

Cholestasis implies?

A

Impediment of bile flow

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4
Q

How does acute inflammation look histologically?

A
  • Inflammatory cells are smaller that hepatocytes, get more nuclei clustered together so it looks more basophilic
  • Pigments (bile associated with cholestasis)
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5
Q

Describe chronic hepatitis

A
  • Predominantly periportal infiltration by lymphocytes and plasma cells
  • Progressive periportal fibrosis -> bridging fibrosis
  • Hepatocyte apoptosis/necrosis and some evidence of regeneration
  • Necrosis leads to loss of architecture
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6
Q

How does repair of the liver occur in chronic inflammation?

A

Fibrosis

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7
Q

Chronic active hepatitis is important in which spp/breed?

A

Dogs - Doberman (e.g. Doberman hepatitis)

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8
Q

Describe chronic active hepatitis, including its causes

A
  • Activity: determined by quantity of inflammation and extent of hepatocellular death
  • Cause: unknown (idiopathic) in most canine cases, but some cases seen in association with leptospirosis, infectious canine hepatitis, aflatoxicosis, copper
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9
Q

What is the progression/end stage of chronic active hepatitis?

A

Cirrhosis

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10
Q

Define hydropic degeneration

A

Entry of fluid into hepatocytes

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11
Q

Define cholangitis / cholangiohepatitis

A

= inflammation originating from the biliary tree

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12
Q

Progressive chronic changes of cholangitis / cholangiohepatitis lead to?

A

Biliary cirrhosis

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13
Q

Feline cholangitis / cholangiohepatitis is often associated with which conditions?

A

Inflammatory bowel disease

Chronic pancreatitis

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14
Q

What are the clinical findings of Feline cholangitis / cholangiohepatitis?

A

Ascites
Jaundice
Polyphagia (excessive eating/appetite)
Weight loss

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15
Q

Describe the three characteristic histological lesions/stages of Feline cholangitis / cholangiohepatitis

A
  1. Suppurative cholangitis / cholangiohepatitis
  2. Lymphocytic and plasmacytic periportal infiltration, bile duct hyperplasia and periportal fibrosis
  3. Biliary cirrhosis (severe porto-portal fibrosis, bile duct hyperplasia, nodular hepatic hyperplasia)
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16
Q

Name 6 example causes of viral hepatitis

A

1) Infectious canine hepatitis [CAV-1]
2) Equine herpesvirus infection [EHV-1]
3) Canine herpesvirus infection [CaHV-1]
4) Rabbit haemorrhagic disease [calicivirus]
5) Feline calicivirus (FCV)
6) Feline infectious peritonitis [coronavirus]

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17
Q

What is the viral agent of infectious canine hepatitis?

A

Canine adenovirus type I

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18
Q

Describe the pathogenesis of infectious canine hepatitis throughout the body

A

Oronasal infection -> tonsils, regional lymph nodes, lymphatics, thoracic duct -> blood (viraemia) -> liver (hepatocytes, Kupffer cells), eye (corneal epithelium), kidney (glomerular endothelium), blood vessels (endothelium)

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19
Q

Compare high vs low titre infections of infectious canine hepatitis in how they affect the liver

A
  • High titre: acute (necrotising) hepatitis

* Low titre: chronic hepatitis, fibrosis, persistent infection

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20
Q

Describe the histology of a liver with infectious canine hepatitis

A
  • Sharply delineated hepatic necrosis (mainly peri-acinar), i.n. inclusion bodies
  • Centrilobular necrosis
  • Necrotic hepatocytes
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21
Q

Describe the gross and pathological features of canine infectious hepatitis

A
  • Liver: fibrin deposition, multifocal to coalescing haemorrhage due to damage to endothelium
  • Activation of clotting cascade
  • Exhaustion of clotting factors
  • Also seen in kidney cortex, lung and brain
  • Oedema of the gall bladder
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22
Q

Describe the pathogenesis of Equine herpes virus 1

A

Transplacental infection

• Uterus (endothelial cells), (peri)vasculitis, thrombi -> placental detachment -> late abortion (> 7th month)

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23
Q

Describe the lesions caused by equine herpes virus 1

A

Fetus: multifocal necrosis in:

• Liver, lungs, thymus, spleen (follicles), brain, adrenal glands

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24
Q

Describe the histology of a liver with equine herpes virus infection

A

Disseminated multifocal necrosis, inflammation and intranuclear inclusion bodies

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25
Q

Describe the pathogenesis and features of canine herpes virus infection

A
  • Intra-uterine infection/infection during birth/ingestion or inhalation as neonate
  • Death common in fetal infection or neonates infected by 1 week of age
  • Multifocal necrosis (i.n. inclusion bodies) with haemorrhage, DIC
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26
Q

Rabbit haemorrhagic disease is caused by which agent?

A

Calicivirus

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27
Q

Describe the pathogenesis of rabbit haemorrhagic disease

A
  • Faecal-oral infection (highly contagious; transmitted on fomites)
    • (per)acute disease with:
  • Massive necrosis of hepatocytes (the virus infects hepatocytes)
  • DIC (microthrombi e.g. in lung capillaries and renal glomeruli)
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28
Q

How does rabbit haemorrhagic disease present clinically?

A

Haemorrhage
Multi-organ failure
Death

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29
Q

What is the viral agent of feline infectious peritonitis?

A

Feline coronavirus

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30
Q

Describe the pathogenesis of feline infectious peritonitis

A
  • Oral infection -> infection of enterocytes -> monocyte-associated viraemia
  • Granulomatous (peri)phlebitis / serositis / hepatitis etc.
  • Viral hepatitis occurs in the course of systemic infection (i.e. viraemia)
31
Q

What are the two main affects of bacterial hepatitis on the liver?

A

Liver abscesses and granulomas

32
Q

Where are the route of entry to the liver for bacterial access

A
  • The portal vein
  • Umbilical veins in neonates
  • Hepatic artery (generalised bacteraemia)
  • Ascending infection via the bile duct / system
  • Parasitic migration
  • Direct extension of infection from an adjacent tissue
33
Q

Which agent causes necrobacillosis?

A

Fusobacterium necrophorum

34
Q

Necrobacillosis affects which spp?

A

Ruminants: rumenitis-liver abscess syndrome

35
Q

Hoe does rumenitis-liver abscess syndrome (necrobacillosis) occur?

A
  • Carbohydrate-rich diet
  • > ruminal acidosis
  • > defects in ruminal mucosa
  • > access of bacteria to blood vessels
  • > portal vein
  • > liver: multifocal necrosis, abscess formation
36
Q

Describe the features of rumenitis-liver abscess syndrome (necrobacillosis)

A
  • Coagulative necrosis > liquefies > abscess formation
  • Capsular surface: raised white/creamy nodules
  • Maybe incidental finding at abattoir (cattle), but will cause weight loss and decreased milk yield
37
Q

Multifocal nodules of a similar size indicate?

A

Haematogenous spread (via the blood)

38
Q

Which agent causes Tularaemia?

A

Francisella tularensis (ZOONOSIS)

39
Q

What acts as the reservoir/vector of Tularaemia?

40
Q

Describe the pathogenesis of Tularaemia

A
  • Inoculation site (skin lesions, tick bite, prey animals: intestine)
    • localised infection and regional lymphadenitis -> bacteraemia, dissemination
41
Q

Describe the pathological and gross appearance of Tularaemia

A
  • Ulceration of lymph nodes (or Peyer`s patches with enteric infection)
  • Necrotising lymphadenitis
  • Hepatitis
  • Splenitis
  • Multifocal hepatic and splenic necrosis
42
Q

What is the agent of Pseudotuberculosis?

A

Yersinia pseudotuberculosis (zoonosis)

43
Q

Describe the pathogenesis of pseudotuberculosis

A
  • Hares, rodents, ruminants, cats
  • Primarily enteric infection -> invasion of mucosa and Peyer’s patches -> microabscesses in intestinal wall and mesenteric lymph nodes
  • In immunosuppressed individuals: dissemination (liver, spleen kidneys)
  • Invasion of intestinal mucosa via M cells (overlying GALT) > bacteraemia (often in immunosuppressed animals)
44
Q

Describe the overall pathogenesis of Leptospirosis

A
  • Penetration of mucous membranes / abraded skin -> replication in blood -> kidneys, liver, spleen, brain, eyes, genital tract
    • Serum antibodies clear spirochaetes from organs, but: persistence in renal tubular epithelium can occur
45
Q

Describe the pathogenesis of Leptospirosis in dogs

A
  • Liver: dysfunction due to cell damage by leptospiral toxins (hepatocellular necrosis); development of chronic active hepatitis
  • Kidneys: tubular necrosis (esp. L. grippotyphosa, L. canicola)
  • Also: DIC, uveitis, abortion
46
Q

Describe the gross effects of Leptospirosis in the kidneys, liver and lungs of a dog

A
  • Kidneys: interstitial nephritis and tubular necrosis
  • Liver: mottled appearance due to haemorrhage and necrosis
  • Lung: multifocal haemorrhage (DIC)
47
Q

What are the consequences of periportal inflammation and necrosis due to Leptospirosis?

A
  • Intracanalicular bile plugs > jaundice

- Intravascular haemolysis > jaundice > centrolobular necrosis (hypoxia)

48
Q

How does leptospirosis cause jaundice?

A
  • Due to intravascular haemolysis (some serovars) AND/OR bile stasis (bile plugs)
  • Haemolysis leads to anaemia; centrolobular necrosis in liver secondary to ischaemia / hypoxia
49
Q

Describe the histological liver lesions in a dog with Leptospirosis

A 
• Loss of tight junctions between hepatocytes [loss of pressure between cells = hepatocyte dissociation]
- Signals regeneration of the liver
- Induction of mitosis
• Rounded cells
• Eosinophilic granular cytoplasm
• Dark shrunken basophilic nuclei
• Loss of cords/plates (dissociation)
• Multifocal haemorrhage, hepatocellular dissociation, mitoses and binucleated cells
50
Q

Name the agent that causes Tyzzer’s disease

A

Clostridium piliforme (zoonosis)

51
Q

Which species are affected by Tyzzer’s disease?

A
  • Laboratory rodents, guinea pigs, foals, dogs, cats

- Young or immunocompromised animals

52
Q

Describe the pathogenesis of Tyzzer’s disease

A

Contact with rodent (prey) faeces -> proliferation in intestinal epithelial cells (ulcerative, necrotising colitis and typhlitis) -> with immunosuppression (?): spread to liver -> necrosis

53
Q

How are different organs grossly affected by Tyzzer’s disease?

A

Colon - diffuse fibrino-necrotising colitis

Liver - disseminated multifocal necrosis

54
Q

Name 3 protozoal infections that cause parasitic hepatitis

A
  • Toxoplasmosis [Toxoplasma gondii]
  • Coccidiosis [Eimeria stiedai]
  • Leishmaniasis [Leishmania infantum]
55
Q

Describe the features of Toxoplasmosis

A
  • Zoonosis
  • Seen in numerous species
  • Hepatitis with generalised infection
  • Sheep, goat, swine: with uterine infection
  • Tachyzoites in hepatocytes -> multifocal necrosis
56
Q

Where does Coccidiosis replicate?

A

Bile duct epithelium -> induction of proliferation of the bile duct epithelium

57
Q

Describe the features of Leishmaniasis

A
  • Infection via biting insects
  • With generalised, chronic infection
  • Infection of macrophages -> replication -> rupture of cells, release -> infection of new cells (and biting flies)
58
Q

How does Leishmaniasis affect the liver?

A
  • Granulomatous hepatitis

- Swollen, rounded liver with texture abnormality

59
Q

Which spp cause metazoan infections of the liver?

A

Trematodes [liver flukes: Fasciola hepatica, Dicrocoelium dendriticum]

60
Q

Describe the process of acute fascioliasis

A
  • Due to larval migration (1 mm long flukes)
  • Migration pathways cause haemorrhage and necrosis with eosinophils and granulomatous inflammation
  • Granulomatous inflammation occurs with larval death (encystment of flukes which fail to reach the bile duct)
61
Q

What are the 3 outcomes of acute fascioliasis in the liver

A

1) Healing - granulation tissue followed by residual scarring resulting in a diffuse fibrosis
2) Black disease (Clostridium novyi) - Spores are latent in macrophages (liver), need anaerobic areas to proliferate!
3) Chronic fascioliasis

62
Q

Describe the histological appearance of acute fascioliasis

A

blood-filled tunnels Containing cellular debris, inflammatory cells (eosinophils) and larvae; the surrounding parenchyma undergoes coagulation necrosis.
Histiocytes and multinucleated giant cells remove debris

63
Q

Describe the gross clinical features in a liver with acute fascioliasis

A

Multifocal haemorrhage and granulomatous hepatitis

64
Q

What is the cause of chronic fascioliasis?

A

Mature flukes in bile ducts

65
Q

Describe the lesions of chronic fascioliasis

A

Chronic hyperplastic cholangitis, peribiliary fibrosis + calcification (mechanical irritation, bile stasis, excretions)
• Fibrosis +/- mineralisation
• Granulomatous inflammation

66
Q

What are the consequences of chronic fascioliasis?

A

Anaemia, hypoproteinaemia, chronic debilitation, death (sheep)

67
Q

Describe the histology of chronic fascioliasis

A

Chronic hyperplastic cholangitis and peribiliary fibrosis (result of traumatic activities of the adult flukes)

68
Q

Describe the pathophysiology of chronic fascioliasis

A
  • Haematophagic activities of the flukes plus the traumatic irritation of the spines cause a hyperplastic cholangitis resulting in haemorrhage leading to anaemia
  • Albumin loss from “leaky” intercellular junctions (protein-losing enteropathy) -> hypoproteinaemia with ascites and wasting
69
Q

Chronic cholangitis/fascioliasis has what appearance?

A

‘Pipe stream’

70
Q

Which 2 cestode spp affect the lungs?

A

Echinococcus

Cysticercus

71
Q

Describe the pathophysiology of cestodes

A
  • Egg > oncosphere migrates thorough intestinal mucosa > Blood > predilection site >larval stage >lymph > lung
  • Hydatid cyst = one of larval stages (metacestode)
  • Hydatid cyst: numerous brood capsules which bud off inner epithelium > fluid “hydatid sand”
  • Clinical signs are rare; often incidental finding at abattoir
72
Q

Name 2 nematodes that affect the liver

A

Ascaris suum

Toxocara canis

73
Q

What affect do Ascaris suum have on the liver?

A

“milk spot liver” (pig)
• Egg hatches in intestine > migrates to the liver (L2) > L3 > blood
• Milk spot = cloudy whitish spot <1cm diameter
• Fibrous repair

Y3 Liver and Pancreas pathology (4 decks)

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