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YEAR 5: 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 - liver macrophages
  • 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 sinusoids
  • 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

How are endothelial cells unique in the liver

why

A

endothelial cells are discontinuous

allows blood to come into contact with hepatocytes

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9
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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10
Q

What are the key features of cirrhosis?

A
  • The whole liver is involved
  • There is extensive fibrosis and nodules of regenerating hepatocytes
  • Shunting occurs - intra-hepatic and extra-hepatic shunts are created
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11
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 (varices - oesophageal, haemorrhoids, caput medsuae)
  • Intra-hepatic: blood goes through the liver but it does not come into contact with hepatocytes (so the blood is unfiltered)

this is the problem with cirrhosis

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12
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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13
Q

How do these two classications of cirrhosis overlap?

A

Alcoholic tends to be micronodular

Viral tends to be macronodular

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14
Q

List some complications of cirrhosis.

A
  • Portal hypertension –> hepatosplenomegaly
  • Hepatic encephalopathy
  • Hepatocellular carcinoma

NOTE: cirrhosis may be reversible

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15
Q

What causes acute hepatitis?

A
  • Hepatitis virus (A and E)
  • drugs

all heptatitis viruses can cause hepatitis

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16
Q

What is a common histological feature of all acute hepatitis?

A

Spotty necrosis

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17
Q

What are some causes of chronic hepatitis?

A
  • Viral hepatitis
  • Drugs
  • Autoimmune
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18
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)

Stage is more important than grade

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19
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

inflammation between portal tract + parenchyma –> leads to fibrosis

20
Q

how is grade assessed in liver cirrhosis

A
21
Q

how is stage assessed in liver cirrhosis

A

bridiging fibrosis - basis of intrahepatic shunting

22
Q

What are the three histological patterns of alcohol related liver disease?

A
  • Steatosis (Fatty liver)
  • Steatohepatitis (alcoholic related hepatitis)
  • Cirrhosis

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

23
Q

List some histological features of alcoholic hepatitis.

A
  • Ballooning of hepatocytes - cell swell and may contain pink depositis within cells (Mallory Denk bodies)
  • fat
  • Apoptosis
  • Pericellular fibrosis

Mostly in Zone 3

Acetoaldehyde causes collapse of filaments in cells

24
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
25
Q

Describe the histological appearance of metabolic dysfunction associated steatotic liver disease (MASLD)
(non-alcoholic fatty liver disease).

A
  • Looks like alcohol related hepatitis

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

Need to know the history to distinguish the cause

26
Q

How is MASLD distinguished from alcohol related liver disease?

A

Based on the history

AST:ALT ratio <2 in NAFLD

27
Q

What is primary biliary cholangitis?

A

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

28
Q

What is the diagnostic test for PBC?

A
  • Anti-mitochondrial antibodies (AMA)

usually IgM

29
Q

What is the histological appearance of PBC?

A

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

30
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 granulomatous 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

31
Q

What is the diagnostic test for PSC?

A
  • Bile duct imaging
32
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

Iron in hepatocytes

33
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

34
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

Copper in liver and CNS (hepatolenticular degeneration)

35
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

36
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
37
Q

How is autoimmune hepatitis diagnosed?

A

Anti-smooth muscle antibodies (ASMA)

38
Q

How is autoimmune hepatitis treated?

A

Steroids (responds very well)

39
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 + cirrhosis
  • An inability to exit the liver leads to a deficiency of alpha-1 antitrypsin elsewhere in the body which leads to pan-lobular emphysema
40
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

41
Q

List some causes of hepatic granulomas.

A
  • Specific: PBC, drugs
  • General: TB, sarcoidosis
42
Q

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

A
  • Liver cell adenoma
  • Bile duct adenoma
  • Haemangioma (MOST COMMON) - endothelial cells
43
Q

What is the most common type of malignant liver tumour?

A

Secondary tumours

44
Q

List some types of primary liver tumour.

A
  • Hepatocellular carcinoma
  • Hepatoblastoma (primitive cells)
  • Cholangiocarcinoma
  • Haemangiosarcoma
45
Q

What are some risk factors for cholangiocarcinoma?

A
  • PSC
  • Worm infections
  • Cirrhosis

can arise from intrahepatic or extrahepatic ducts (inc. gallbladder)

46
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 vein meaning that tumours from the stomach, bowels and pancreas will reach the liver before any other part of the body

YEAR 5: HISTOPATH (20 decks)

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