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review histopath > Histo: Liver > Flashcards

Histo: Liver Flashcards

1
Q

What is the average weight of a liver?

A

1500 g

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2
Q

Describe the blood supply to the liver.

A

Dual blood supply: hepatic artery and hepatic portal vein

NOTE: this means that the liver does not tend to get affected by ischaemia

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3
Q

List the main cell types of the liver.

A
  • Hepatocytes
  • Bile ducts (cholangiocytes)
  • Blood vessels
  • Endothelial cells
  • Kupffer cells
  • Stellate cells
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4
Q

How is the arrangement of endothelial cells in the liver different from other parts of the body?

A

The endothelial cells do not sit on a basement membrane and the endothelium is discontinuous (there are no tight junctions)

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5
Q

What is the role of stellate cells and what could happen to them when activated?

A
  • Storage of vitamin A
  • When activated, they become myofibroblasts that lay down collagen (this is responsible for scarring in liver disease)
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6
Q

outline the arrangement of structures within a normal liver.

A
  • There will be portal tracts consisting of a branch of the hepatic artery, a branch of the portal vein and a bile duct
  • Blood will flow from the portal tract to the central vein
  • There is a ring of collagen around the portal tract called the limiting plate
  • There are three zones of hepatocytes in between the portal tract and the central vein
  • Zone 3 is closest to the central vein and contains the most metabolically active enzymes
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7
Q

Describe the arrangement of hepatocytes, endothelial cells, stellate cells and Kupffer cells in a normal liver.

A
  • There are spaces in between endothelial cells and there is a gap in between the endothelial cells and the hepatocytes (space of Disse)
  • Stellate cells sit within the space of Disse
  • Kupffer cells are found within the sinusoids
  • Blood can easily get through the spaces in the endothelial cells in the space of Disse where they are exposed to hepatocytes
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8
Q

Describe how these arrangements change in liver disease.

A
  • Kupffer cells become activated (inflammatory response)
  • Endothelial cells stick together so blood finds it more difficult to get into the space of Disse
  • Stellate cells become activated and secrete basement membrane-type collagens into the space of Disse
  • Hepatocytes lose their microvilli
  • All these changes make it difficult for blood to be exposed to hepatocytes
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9
Q

What are the key features of cirrhosis?

A
  • The whole liver is involved
  • There is extensive fibrosis and nodules of regenerating hepatocytes
    *Distortion of liver vascular architecture: intra- and extra-hepatic shunting of blood
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10
Q

Name and describe the two types of shunting that occur in cirrhosis.

A
  • Extra-hepatic: blood never reaches the liver because it backlogs into sites of porto-systemic anastamosis
  • Intra-hepatic: blood goes through the liver but it does not come into contact with hepatocytes (so the blood is unfiltered)
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11
Q

How can cirrhosis be classified?

A
  • According to nodule size (old system): micro- or macronodular
  • According to aetiology: alcohol/insulin resistance or viral hepatitis
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12
Q

How do these two classications of cirrhosis overlap?

A

Alcoholic tends to be micronodular

Viral tends to be macronodular

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13
Q

List some complications of cirrhosis.

A
  • Portal hypertension
  • Hepatic encephalopathy
  • Hepatocellular carcinoma

NOTE: cirrhosis may be reversible

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14
Q

What causes acute hepatitis?

A
  • Hepatitis virus (A and E)
  • drugs
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15
Q

What is a common histological feature of all acute hepatitis?

A

Spotty necrosis

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16
Q

What are some causes of chronic hepatitis?

A
  • Viral hepatitis
  • Drugs
  • Autoimmune
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17
Q

How can the histology in chronic hepatitis be used to grade and stage the disease?

A
  • Severty of inflammation = grade (how bad does it look)
  • Severity of fibrosis = stage (how far has it spread)
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18
Q

What is interface hepatitis?

A
  • Aka piecemeal hepatitis
  • Inflammation crosses the limiting plate making it difficult to distinguish where the portal tract ends and the hepatocytes begin
19
Q

What are the three histological patterns of alcoholic liver disease?

A
  • Fatty liver
  • Alcoholic hepatitis
  • Cirrhosis

NOTE: these may co-exist (they are not distinc entities)

20
Q

List some histological features of alcoholic hepatitis.

A
  • Ballooning - cell swell and may contain pink depositis within cells (Mallory Denk bodies/Mallory hyaline)
  • Apoptosis
  • Pericellular fibrosis (chicken wire fibrosis)
21
Q

In which part of the liver do the histological features of alcoholic hepatitis tend to be seen and why?

A
  • Zone 3
  • Alcohol is not toxic, but acetaldehyde is toxic
  • Zone 3 cells contain the most alcohol dehydrogenase thereby producing the most acetaldehyde
  • Furthermore, by the time blood reaches zone 3 (after passing zones 1 and 2) it is relatively hypoxic making the cells in zone 3 even more vulnerable to damage
22
Q

Describe the histological appearance of non-alcoholic fatty liver disease.

A
  • Looks like alcoholic hepatitis

NOTE: caused by insulin resistance associated with a raised BMI and diabetes

23
Q

How is NAFLD distinguished from alcoholic lver disease?

A

Based on the history

AST:ALT ratio <2 in NAFLD

24
Q

What is primary biliary cholangitis?

A

Autoimmune conditions characterised by bile duct loss associated with chronic inflammation (with granulomas)

25
Q

What is the diagnostic test for PBC?

A
  • Anti-mitochondrial antibodies (AMA)
26
Q

What is the histological appearance of PBC?

A

Bile ducts surrounded by epithelioid macrophages, suggestive of chronic granulomatous destruction of bile ducts

27
Q

What is primary sclerosing cholangitis?

A
  • Autoimmune condition characterised by periductal bile duct fibrosis leading to loss of bile ducts

NOTE: in PBC, bile duct loss is aused by inflammation, whereas in PSC it is caused by fibrosis

NOTE: PSC is associated with ulcerative colitis and is associated with an increased risk of cholangiocarcinoma

28
Q

What is the diagnostic test for PSC?

A
  • Bile duct imaging
29
Q

What causes haemochromatosis and which gene is implicated?

A
  • Caused by increased gut iron absorption
  • HFe gene on chromosome 6

NOTE: women tend to present later because they have naturally lower iron levels

30
Q

What is haemosiderosis?

A

Type of iron overload characterised by the accumulation of iron in macrophages

Usually occurs as a result of receiving blood transfusions

31
Q

What is Wilson’s disease?

A

Characterised by an accumulation of copper due to the failure of excretion of copper by hepatocytes into the bile

Responsible gene (ATP7B) is found on Chr13

32
Q

How does Wilson’s disease lead to movement disorders?

A

Accumulation of copper in the lentiform nucleus of the basal ganglie leads to movement disorders

33
Q

How is the severity of disease in autoimmune disease different from viral hepatitis?

A
  • Autoimmune hepatitis is very active with lots of plasma cells
  • The degree of inflammation is usually worse than in viral hepatitis
34
Q

How is autoimmune hepatitis diagnosed?

A

Anti-smooth muscle antibodies (ASMA)

35
Q

How is autoimmune hepatitis treated?

A

Steroids (responds very well)

36
Q

Describe the levels of alpha-1 antitrypsin in the blood and liver in a patient with alpha-1 antitrypsin deficiency.

A
  • The mutation means that the protein cannot fold properly and cannot exit hepatocytes
  • This leads to the alpha-1 antitrypsin forming globules within hepatocytes which causes damage leading to chronic hepatitis
  • An inability to exit the liver leads to a deficiency of alpha-1 antitrypsin elsewhere in the body which leads to an increased risk of emphysema
37
Q

Why is the liver so susceptible to drug-related injury?

A

It is the main site of drug transformation

It is also where toxic drug metabolites are formed

38
Q

List some causes of hepatic granulomas.

A
  • Specific: PBC, drugs
  • General: TB, sarcoidosis
39
Q

List the main types of benign liver tumour. State which is most common.

A
  • Liver cell adenoma
  • Bile duct adenoma
  • Haemangioma (MOST COMMON)
40
Q

What is the most common type of malignant liver tumour?

A

Secondary tumours

41
Q

List some types of primary liver tumour.

A
  • Hepatocellular carcinoma
  • Hepatoblastoma
  • Cholangiocarcinoma
  • Haemangiosarcoma
42
Q

What are some risk factors for cholangiocarcinoma?

A
  • PSC
  • Liver fluke
  • Cirrhosis
  • Gallstones
43
Q

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

A
  • It is supplied by the hepatic artery so tumour cells from the systemic circulation could reach the liver
  • It is also supplied by the portal artery meaning that tumours from the stomach, bowels and pancreas will reach the liver before any other part of the body

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