Pathology of the Liver and Pancreas Flashcards

1
Q

What are the three hepatic zones?

A

Periportal (centroacinar) - around portal triads Midzonal Centrilobular (periacinar) - borders hepatic venules

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2
Q

What is the ‘limiting plate’?

A

This is the boundary between the portal tract and surrounding liver parenchyma.

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3
Q

How does the prognosis of portosystemic shunts that are congenital and acquired differ?

A

Congenital - usually one shunt so more easily surgically corrected Acquired - shunts are secondary to fibrosis and are multiple so harder to correct.

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4
Q

What might indicate the prescence of a portosystemic shunt on microscopy?

A

The lack of a portal vein prescence

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5
Q

What developmental/congenital disorders can affect the liver?

A

Congenital cysts Displacements (e.g. diaphragmatic hernia) Tension lipidosis (focal areas of subscapular fatty change) Capsular fibrosis Telangiectasis (focal areas of dilated tissue)

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6
Q

Describe when venous congestion of the liver might occur, the gross and microscopic appearance of an affected liver.

A

Secondary to heart failure Gross : enlarged and oozes blood from cut surface. ‘Nutmeg liver’ Micro: Engorged sinusoids, Congested periacinar areas with atrophied hepatocytes, fatty change of periportal areas

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7
Q

What are the common pigments that may be seen microscopically? Are they significant?

A

Melanin - incidental Haemosiderin - blood breakdown product but often incidental Bile - jaundice Lipofuscin (brown pigment) - incidental with ageing.

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8
Q

What can cause hydropic change? Is it reversible?

A

Hypoxia, mild toxin damage, metabolic stress It is reversible

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9
Q

In what disease goes glycogen accumulation occur?

A

Hypoadrenocorticism

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10
Q

What is the gross & micro apearance of a liver undergoing vacuolar hepatopathy?

A

Gross - Enlarged pale liver Micro - multifocal/diffuse swelling/vacuolation of hepatocytes

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11
Q

What things can cause lipidosis of the liver?

A

Diet (obesity and starvation) Increased energy demand (pregnancy, lactation) Disease (diabetes mellitus, ketosis, pregnancy toxaemia)

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12
Q

Why does lipidosis occur?

A

Hepatocytes malfunction and cant combine fatty acids with proteins to form LDL.

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13
Q

What does the following image depict? How does this disease occur?

A

Lysosomal storage disease. This is an inherited deficiency in lysosomal enzymes leading to storage of material inside macrophages that accumulate at multiple sites.

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14
Q

What does the gross appearance of an amyloidotic liver look like?

A

Liver enlarged and friable with a texture like candle wax.

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15
Q

How can necrosis of the liver occur?

A

Toxins

Infections

Nutritional deficiencies

Ischaemia

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16
Q

What are the different patterns of liver necrosis and what are they associated with?

A

Random - infectious

Zonal - Ischaemia/toxic

Massive - hepatosis dietetica

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17
Q

Describe the different patterns of fibrosis of the liver.

A

Periacinar fibrosis - Surrounds CV

Biliary fibrosis - around bile ducts also inflammation centred on portal triads

Post-necrotic scaring - following massive necrosis

Cirrhosis - years of cycles of fibrosis followed by regeneration

18
Q

What are the different types of inflammation of the liver?

A

Hepatitis - liver parenchyma

Cholangitis - bile ducts

Cholangiohepitits - both

19
Q

Describe what happens in acute hepatits, and the events that can happen if the animal survives.

A

Necrosis followed by inflammation. If survives then the following can happen:

  • Resolution by regeneration
  • Fibrosis and Scarring
  • Encapsulation and abscessation
  • Persistance of granulomatous disease
20
Q

What types of virus can cause hepetitis?

A

Adenoviruses (canine infectous hepetitis)

Herpesviruses (EHV)

Coronaviruses (FIP)

21
Q

Why is canine infectious hepetitis so infective?

A

It is shed in the urine long term

22
Q

Describe the lesions seen in neonates infected with herpes virus.

A

Multinodular white dots

Foci of necrosis with nuclear inclusion bodies

Necrosis can also occur in lungs, spleen, kidneys and adrenals

23
Q

What are the two forms of FIP?

A

Wet and Dry forms

24
Q

What routes of infection are there for bacterial hepatitis?

A

Direct extension from adjacent tissues

Haematogenous spread e.g. umbilical vein, portal vein from alimentary tract, hepatic artery

Abcessation - umbilical infecitons, rumenitis

25
Q

What pathology is associated with Fusobacterium necrophorum?

A

Multiple pale foci throughout the liver which may form abscesses.

Micro: Coagulative necrosis with peripheral bacteria

26
Q

What is the aetiology of ‘black disease’?

A

Clostridium novyi type B infection which often precipitates from fluke migration through the liver.

27
Q

Decribe gross and microscopic lesions associated with ‘black disease’

A

Subcut venous congestion

Fibrinous third space fluid

Pale foci of necrosis containing bacteria surrounded by a ring of haemmorrhage

28
Q

Describe pathology findings of Clostridium haemolyticum

A

Large necrotic focus in the liver with haemoglobin staining of kidneys

29
Q

What animals does Tyzzers disease infect? What is the causative organism?

A

Laboratory rodents, yound horses, immunosupressed cats/dogs.

Clostridium piliforme

30
Q

What stain is used in the following image and what organism does it visualise?

A

Clostridium piliforme. Silver stain. ‘Wheat Sheaf’ appearance

31
Q

What does this image depict?

A

A leptospire. This is heamosiderin staining due to the haemolytic aneamia caused by the organism. There is also hepatocyte dissociation causing cholestasis.

32
Q
A
33
Q

Describe the pathological changes associated with Salmonellosis.

A

Gross

Severe haemorrhagic inflammation of the ileum.

paratyphoid nodules in the liver - pale foci of necrosis

Micro:

Foci of necrosis

Mononuclear inflammatory cells

34
Q

Are parasites in the liver pathologic?

A

Most are indicental apart from fluke.

35
Q

What does the following image show?

A

Incidental fibrous tags formed following repair after parasites have left the liver.

36
Q

Describe acute and chronic liver intoxication.

A

Acute: widespread bodily haemorrhage as the liver consumes and fails to produce clotting factors.

Chronic: fibrosis and biliary hyperplasia. The liver continually is damaged and regenerates so chronic intoxication is often not noticed until it reaches a very late stage.

37
Q

What is cholecystitis? And what is a common reaction to this?

A

Inflammation of the gall bladder. Hyperplasia of the mucosa is common reaction to irritation of this area.

38
Q

How can biliary obstruction occur and what is the severity of a rupture?

A

Parasites, choleliths (rare). Obstruction from nearby inflammatory or neoplastic process.

Rupture is very severe as omentum can’t contain the leak and will lead to peritonitis.

39
Q

What does the following image depict?

A

a malignant neoplasia of the liver

40
Q

What microsopy findings indicate acute pancreatitis?

A

Haemorrhagic oedema and necrosis affecting pancreas and peripancreatic fat.

41
Q

Is nodular hyperplasia significant?

A

No

42
Q

What types of pancreatic neoplasia are rare/not rare?

A

Adenoma - rare

Carcinoma more common and often very agressive.