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Pathology > Histopathology - Liver and Biliary disease > Flashcards

Histopathology - Liver and Biliary disease Flashcards

1
Q

blood supply of liver

A

dual

  • hepatic portal vein (carries some oxygenated blood)
  • hepatic artery
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2
Q

what is the advantage of the dual blood supply?

A

liver does not tend to get affected by ischaemic diseases

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3
Q

what are the cells of the liver?

A 
hepatocytes
bile ducts
blood vessels
endothelial cells (endothelium is discontinuous in liver)
kupffer cells (resident macrophages)
stellate cells
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4
Q

what do stellate cells do?

A
  • most people = store Vit A
  • when activated, they become myofibroblasts and lay down collagen
  • responsible for scarring in liver disease
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5
Q

in what direction does blood flow in the liver?

A

from portal tract to central vein

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6
Q

what do the cells in zone 3 contain?

A

more metabolically active enzymes

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7
Q

what is the limiting plate?

A

ring of collagen around portal triad

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8
Q

describe the endothelium in the liver?

A

endothelial cells in liver have no basement membrane
have spaces between them = fenestrated sinusoidal endothelium
kupffer cells found within sinusoids

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9
Q

where do stellate cells sit in the endothelium?

A

in space of Disse

space between endothelial cells and hepatocytes

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10
Q

what are the changes that happen to liver histology in liver injury?

A
  1. kupffer cells activated
  2. endothelial cells stick together (blood finds it hard to make it through)
  3. collagens are secreted into space of Disse
  4. hepatocytes lose microvilli
    = blood can’t diffuse into hepatocytes
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11
Q

what is the definition of cirrhosis?

A
  • whole liver is involved
  • fibrosis
  • nodules of regenerating hepatocytes
  • distortion of liver vascular architecture (intra and extra hepatic shunting of blood)
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12
Q

what is the normal blood flow through the liver?

A

normally blood comes from intestines
it is then filtered through liver
comes out via hepatic vein

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13
Q

what happens in extrahepatic shunting of blood?

A
  • blood can’t go through liver as fibrosed
  • blood never reaches liver
  • backlogs into sites of porto-systemic anastomosis
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14
Q

what happens in intrahepatic shunting of blood?

A
  • blood comes through liver but does not come into contact with hepatocytes
  • straight from intestines to portal vein
  • blood is unfiltered and toxic
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15
Q

what are the 2 ways cirrhosis can be classified?

A
  1. according to nodule size (micronodular, macronodular)

2. according to aetiology (alochol/insulin resistance, viral hepatitis)

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16
Q

what is micronodular associated with?

A

alcoholism

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17
Q

what is macronodular associated with?

A

viral infections

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18
Q

what are the complications of cirrhosis?

A
  • portal HTN = varices, splenomegaly
  • hepatic encephalopathy
  • liver cell cancer
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19
Q

what is the aetiology of acute hepatitis?

A
  • viruses (A+E Mostly)

- drugs

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20
Q

what is the histology in acute hepatitis?

A
  • spotty necrosis
  • lots of apoptosis
  • lymphocyte and macrophage damage hepatocytes
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21
Q

what is the aetiology of chronic hepatitis?

A
  • viral hepatitis
  • drugs
  • AI
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22
Q

what is the histology in chronic hepatitis?

A
  • severity of inflammation = GRADE (how bad does it look)

- severity of fibrosis = STAGE (how far has it spread)

23
Q

what are the different patterns of injury in hepatitis?

A
  • portal inflammation (inflammation limited to portal tracts)
  • interface hepatitis (T cell mediated destruction of hepatocytes, inflammation crosses limiting plate)
  • lobular inflammation
24
Q

how does fibrosis lead to intrahepatic shunting?

A

instead of going through hepatocytes, blood goes straight from portal tract to central vein
doesn’t get filtered

25
Q

what are the 3 histological patterns in ALD?

A
  • fatty liver
  • alcoholic hepatitis
  • cirrhosis
26
Q

what are the features of alcoholic hepatitis?

A
  • ballooning
  • mallory denk bodies (collapased cytoskeleton of hepatocytes)
  • apoptosis
  • pericellular fibrosis
27
Q

what is NAFLD caused by?

A

caused by insulin resistance associated with raised BMI and diabetes

28
Q

what does NAFLD look like histologically?

A
  • a lot like alcoholic liver disease

- distinguished based on history

29
Q

what is PBC characterised by?

A

bile duct loss associated with chronic inflammation (with granulomas)
CAUSED BY INFLAMMATION
more common in females

30
Q

what is the diagnostic test for PBC?

A

Anti-mitochondrial antibodies

31
Q

what is the histology in PBC?

A
  • bile duct surrounded by epithelioid macrophages

- suggests granulomatous destruction of bile ducts

32
Q

what is PSC characterised by?

A
  • periductal bile loss
  • CAUSED BY FIBROSIS
  • associated with UC and inc risk of cholangiocarcinoma
  • more common in men
33
Q

what is the diagnostic test in PSC?

A

bile duct imaging

ERCP shows beading of bile ducts

34
Q

what is haemochromatosis?

A

genetic (gene on chromosome 6)
increased in gut iron absorption
women present later (lower Fe levels)

35
Q

where does haemochromatosis cause damage?

A
  • iron deposits in hepatocytes = liver damage
  • iron deposits in heart = cardiomyopathy
  • iron deposits in testes = infertility
  • iron deposits in skin = bronzed skin
  • iron deposits in pancreas = diabetes
36
Q

how is haemosiderosis different?

A
  • iron overload
  • doesn’t cause cirrhosis
  • iron accumulates in macrophages which are capable of dealing with it
  • occurs due to lots of blood transfusions
37
Q

what is wilson’s disease?

A
  • accumulation of copper
  • due to failure of excretion of copper by hepatocytes into bile
  • defective genes from Chr 13
38
Q

where does copper accumulate and cause symptoms?

A
  • in liver and CNS (hepato-lenticular degeneration)
  • iris (Kayser-Fleischer rings)
  • lentiform nucleus of basal ganglia (movement disorders)
39
Q

how do you stain for copper?

A

Rhodanine stain

40
Q

how do you treat Wilson’s?

A

penicillamine (copper chelating agent)

41
Q

what is AI hepatitis?

A
  • more common in females
  • active form of chronic hepatitis
  • lots of plasma cells
  • more inflammation than in viral hepatitis
42
Q

antibodies and tx in AI hepatitis

A

Anti-smooth muscle actin antibodies

responds to steroids

43
Q

what us A1AT characterised by?

A

failure to secrete A1AT

44
Q

where is the deficiency of A1AT?

A

is in the blood

actually an excess in hepatocytes

45
Q

why is there an excess of A1AT in hepatocytes?

A

protein sequence is wrong
CANNOT fold properly and cannot exist in hepatocytes
A1AT forms globules with hepatocytes and damages them
= chronic hepatitis

46
Q

what stain can be used to stain for these globules?

A

periodic acid-schiff stain

47
Q

what else can a deficiency of A1AT lead to?

A

inc risk of emphysema

48
Q

what are the specific (to the liver) and general causes of granulomas

A

specific: PBC, drugs
general: TB, sarcoidosis

49
Q

what are the benign liver tumours?

A
  • liver cell adenoma
  • bile duct adenoma
  • haemangioma (most common tumour of liver overall)
50
Q

what are hepatic adenomas associated with?

A

COCP

51
Q

what is the most common cause of liver malignancy?

A

secondary tumours

52
Q

what are the different primary malignant tumours of the liver?

A
  • hepatocellular carcinoma
  • hepatoblastoma (primitive cell tumour, mostly children)
  • cholangiocarcinoma (ass w/ PSC, worm infections, cirrhosis)
  • haemangiosarcoma
53
Q

why is the liver such a common site for secondary tumours?

A
  • liver supplied by hepatic artery
  • this is branch of aorta
  • tumour cells in systemic circulation likely to get to liver
  • all blood from portal circulation goes to liver (tumours from stomach, bowel, pancreas)

Pathology (21 decks)

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