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Y3 Liver and Pancreas pathology > Liver and Biliary System 2 > Flashcards

Liver and Biliary System 2 Flashcards

1
Q

What type of necrosis is most common in the liver?

A

Coagulative

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2
Q

How does coagulative necrosis appear histologically?

A
  • Intact but dead hepatocytes

- Shrunken cells / intensely eosinophilic / altered nuclei

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3
Q

How is necrosis classified in the liver?

A

According to location e.g. focal, zonal or diffuse

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4
Q

Describe focal necrosis in the liver

A
  • Aggregates of necrotic hepatocytes; random

- With disseminated infections > haematogenous / septicaemia

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5
Q

Describe zonal necrosis of the liver

A
  • In particular part of lobule / acinus, but: in whole liver
  • Centrolobular / periacinar necrosis
  • Mid-zonal necrosis
  • Periportal necrosis
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6
Q

How would disseminated multifocal necrosis appear grossly?

A
  • White spots = necrosis
  • Red rings = blood / haemorrhage
  • EITHER disseminated or random or zonal (centrolobular is most common)
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7
Q

Describe the 3 zones in the liver

A
  • Periportal = zone 1, Surrounding triads
  • Mid-zonal = zone 2
  • Centrolobular = zone 3
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8
Q

Which zone of necrosis is the most common and why?

A

Centrobular / periacinar necrosis (zone 3)

  • Hepatocytes most at risk of hypoxia
  • Metabolically active (cytochrome P450)
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9
Q

Describe massive (diffuse) necrosis

A
  • Necrosis of entire lobe(s)

- With extensive zonal necrosis or circulatory disorder (infarction)

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10
Q

Describe the cause of massive (diffuse) necrosis in pigs and the associated diseases

A
  • Vitamin E / selenium deficiency = Hepatosis dietetica
  • Associated with oedema of gall bladder wall and “Mulberry heart disease” (multifocal myocardial haemorrhage and myofibre degeneration)
  • Necrosis of whole acini > no surviving parenchyma > can’t regenerate
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11
Q

What are the different outcomes of hepatic necrosis?

A

• Removal of dead hepatocytes
• Resolution by either:
- regeneration of hepatocytes
- or: replacement of parenchyma by fibrous scar tissue (due to destruction of reticular framework)

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12
Q

Describe the reticulin framework and explain how it effects the outcome of necrosis

A
  • Fibres that support cords of hepatic sinusoids
  • If this is retained then the liver has a huge capacity to regenerate and it will reform lobules
  • If this is lost the liver has to repair in other ways which can lead to chronic liver disease due to the laying down of fibrosis
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13
Q

What is the influencing factor on where fibrosis occurs at the site of necrosis?

A

Depends on the distribution of injury

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14
Q

What are the 4 different types of fibrosis?

A
  • Periportal/biliary fibrosis
  • Centrolobular/periacinar fibrosis
  • Diffuse/bridging fibrosis
  • Post-necrotic scarring (after massive necrosis)
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15
Q

Describe the 3 types of bridging fibrosis

A

Central-central: connects central veins (with chronic congestion)
Porto-portal: follows portal inflammation which extends to portal venules
Porto-central: after centrolobular necrosis

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16
Q

What is the outcome of bridging fibrosis?

A

Extensive fibrosis between hepatic cords
- Blue represents collagen – this prevents the exchange of oxygen and nutrients between the blood and hepatocytes which is impairing liver function

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17
Q

Describe hepatic cirrhosis and how it occurs

A

= end stage liver disease due to several causes

• Liver tries to repair itself but cant due to the ongoing fibrosis and degeneration -> hypoxia

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18
Q

What are the 3 characteristic features of hepatic cirrhosis?

A

DEGENERATION disruption of entire liver architecture
REGENERATION regenerative nodules of hepatocytes
REPAIR bridging fibrosis [central pathogenic process]

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19
Q

What are the two possible progressions of fibrosis in the liver?

A
  • Worsen to cirrhosis

- Be reversible

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20
Q

Describe the features of regenerative nodules that occur in cirrhosis

A
  • Composed of hepatocytes that look normal
  • Lack of lobular organisation [no cords, no central vein, no portal triad]
  • Often hydropic degeneration of hepatocytes
  • Surrounded by fibrous connective tissue
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21
Q

What process acts as a further attempt of regeneration in liver

A

Bile duct proliferation

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22
Q

Describe the further characteristics of cirrhosis as it progresses?

A
  • Parenchymal injury and fibrosis are diffuse throughout the whole organ
  • Balance between regeneration and constrictive scarring -> nodularity
  • Reorganisation of vascular structure [anastomoses] -> acquired extra-hepatic shunts
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23
Q

Describe the gross appearance of hepatic cirrhosis

A

Lots of nodular fibrosis, the liver between the nodules is paler and contracted due to fibrosis and scarring
Cut surface: pale areas of fibrosis with some prexisting tissue and new nodules

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24
Q

Describe the histological appearance of hepatic cirrhosis

A

Regenerative nodules with surrounding fibrosis. In-between there are the remains of the pre-existing hepatic parenchyma – shrunken and irregular

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25
Q

What are the causes of hepatic cirrhosis?

A
  • Majority of veterinary cases: idiopathic
  • Dogs: persistent CAV-1 or leptospira infection?
  • Parasitic cirrhosis
  • Post-necrotic
  • Cardiac
  • Pigments
  • Biliary
  • Toxins
26
Q

Which 3 conditions occur in sequelae to hepatic cirrhosis?

A
  • Jaundice
  • Ascites
  • Hepatoencephalic syndrome
27
Q

Describe jaundice and its causes

A
  • Due to high bilirubin levels in blood
  • Yellow tinge of all tissues [sclera, omentum, mesentery, fat, aorta…]
  • Seen only grossly [bilirubin is in solution] – not histo
  • Always diffuse!
28
Q

Describe the 3 types of jaundice

A 
Pre-hepatic = excessive haemolysis 
Hepatic = severe hepatic injury 
Post-hepatic = obstructed bile flow (cholestasis)
29
Q

Why does ascites occur in sequalae to hepatic cirrhosis?

A

Due to portal hypertension

30
Q

What is Hepatoencephalic syndrome?

A

Failure of liver to remove ammonia from the blood

31
Q

What are the products of the degradation of haemoglobin?

A
  • Haem
  • Biliverdin
  • Bilirubin
32
Q

What are the components of bile?

A
  • water
  • cholesterol
  • bile salts: Na and K salts of bile acids
  • bile pigments (bilirubin) from Hb molecule
33
Q

Describe pre-hepatic jaundice

A

Due to excessive haemolysis of erythrocytes in peripheral blood -> unconjugated bilirubin in blood

34
Q

What are the causes of pre-hepatic jaundice?

A
  • Infections: Leptospirosis, Equine infectious anaemia, Anthrax, etc
  • Massive internal haemorrhage [bilirubin from disintegrating erythrocytes]
  • Icterus neonatorum [bilirubin glucoronyl transferase still insufficient]
35
Q

Describe the causes of hepatic jaundice

A

Due to severe hepatic injury by:

a) toxic substances
b) infectious agents [e.g. leptospirosis]

36
Q

Describe the pathophysiology of hepatic jaundice

A
  • Either: damaged hepatocytes do not uptake bilirubin or perform conjugation -> unconjugated bilirubin in blood
  • or: severe hepatocyte swelling blocks outflow of bile from canaliculi -> conjugated bilirubin accumulates in liver and is reabsorbed into the blood
37
Q

Describe the pathophysiology of post-hepatic jaundice

A

Due to obstruction of normal bile flow -> conjugated bilirubin accumulates in the liver and is reabsorbed into the blood

38
Q

What are the causes of post-hepatic jaundice?

A
  • Obstruction of ducts [e.g. liver fluke…]
  • Fibrous tissue in cirrhosis
  • Cholangitis
  • Gall stones
  • Pressure on ducts [abscesses, granulomas, neoplasms]
  • Closure of excretory duct [duodenal papilla]
39
Q

The liver is responsible for the synthesis of which substances?

A
  • Glucose
  • Low density lipoproteins
  • Urea
  • Soluble plasma proteins
40
Q

Which 2 molecules are catabolised in the liver?

A
  • Lipids

- Ketone bodies

41
Q

Which substances is secreted/excreted by the liver?

A

Bile

42
Q

What are the other functions of the liver?

A
  • Detoxification

- Carbohydrate, lipid and protein metabolism

43
Q

Which conditions are associated with disturbances of liver functions?

A
  • Jaundice
  • Hypoalbuminemia: reduced synthesis and secretion of albumin -> ascites
  • Coagulopathy
  • Hyperammonaemia
  • Portal hypertension
44
Q

Why do coagulopathies occur when there are disturbances with liver function?

A

Reduced synthesis and secretion of clotting factors

45
Q

Describe the lesions seen with hepatic encephalopathy

A
  • Cerebral oedema (Status spongiosus)
  • Neuronal necrosis and swelling
  • Degeneration of astrocytes [Alzheimer type II cells]
46
Q

Which 2 conditions can be mistaken for neoplasia in the liver?

A

Nodular hyperplasia

Regenerative nodules

47
Q

Describe nodular hyperplasia

A
  • Not a neoplasm
  • Common in old dogs
  • Usually multiple, expanding, compressing adjacent tissue
  • Contain portal areas
48
Q

Describe regenerative nodules

A
  • Not a neoplasm
  • Common in old dogs
  • Multiple or numerous
  • Adjacent tissue usually fibrotic
  • Loss of lobular architecture
49
Q

Name the 5 hepatic primary neoplasms

A
  • Hepatocellular adenoma
  • Hepatocellular carcinoma
  • Bile duct adenoma
  • Bile duct carcinoma
  • Haemangiosarcoma
50
Q

Where do primary hepatic neoplasms arise from?

A

Hepatocytes and biliary epithelium

51
Q

Describe the features of a hepatocellular adenoma and its gross appearance

A
  • Usually single tan coloured, surrounding tissue looks normal
  • Sharply delineated
  • No portal areas / lobular structure
  • Compression of adjacent tissue without invasion
  • May become quite large
  • No metastasis
52
Q

How does a hepatocellular adenoma look histologically?

A

Hepatocytes with no lobular architecture, lack sinusoids, some areas of blood in between

53
Q

Describe the features of a hepatocellular carcinoma, including its 3 growth patterns

A
  • Compression and invasion of adjacent tissue
  • Metastasis [invasion of portal vessels]
  • Growth pattern:
    • Trabecular
    • Acinar
    • Solid
54
Q

Describe the gross appearance of a hepatocellular carcinoma

A

Less of a boundary between normal and abnormal, also multifocal lesions where it has spread within the organ (intra-organ metastasis).

55
Q

Describe the histological appearance of a hepatocellular carcinoma

A

Neoplastic cells (vary in size, large nuclei), also some non-neoplastic (smaller)

56
Q

Describe the features and gross appearance of a bile duct adenoma

A
  • Often cystic [cystadenoma]
  • Usually single
  • Sharply delineated
  • Compression of adjacent tissue
  • May become quite large
57
Q

Describe the features and gross appearance of a bile duct carcinoma

A
  • Commonly spreads along biliary tract
  • Metastasis [spread to hepatic serosa, via lymph nodes to lungs]
  • Often inducing desmoplasia
  • Neoplastic tissue and fibrous tissue – feel very firm
  • Sunken centre in the middle of the nodules
58
Q

Describe how the liver can act as different sites for a haemangiosarcoma

A

Liver as primary site

or: as site of metastases
or: as one of several sites with multicentric development

59
Q

Describe the 3 routes of metastasis to the liver

A

a) portal vein [from pancreas and intestine]
b) veins / arteries at sites of entry [any other neoplasms]
c) contact metastases [serosa; from malignant tumours in abdominal cavity]

60
Q

Which tumour type most commonly metastasises to the liver?

A

Lymphoma

61
Q

Describe the characteristic appearance of carcinomas in the liver

A

Carcinomas have a characteristic sunken centre in the middle of nodules due to necrosis

Y3 Liver and Pancreas pathology (4 decks)

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