Liver Flashcards

1
Q
  1. 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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2
Q
  1. 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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3
Q
  1. 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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4
Q
  1. 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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5
Q
  1. 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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6
Q
  1. 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 into the space of Disse where they are exposed to hepatocytes

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7
Q

What happens to the structure of the liver when injured?

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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8
Q
  1. 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 anastomosis
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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9
Q

What is the association between aetiology and nodulartiy of cirrhosis

A

Alcoholic tends to be micronodular

Viral tends to be macronodular

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10
Q
  1. List some complications of cirrhosis.
A

Portal hypertension
Hepatic encephalopathy
Hepatocellular carcinoma

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11
Q
  1. What causes acute hepatitis?
A
Hepatitis virus (A and E)
Drugs
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12
Q
  1. What is a common histological feature of all acute hepatitis?
A

Spotty necrosis

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13
Q
  1. How can the histology in chronic hepatitis be used to grade and stage the disease?
A

Severity of inflammation = grade (how bad does it look)

Severity of fibrosis = stage (how far has it spread)

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14
Q
  1. 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

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15
Q
  1. List some histological features of alcohol hepatitis.
A

Ballooning – cell swell and may contain pink deposits within cells (Mallory Denk bodies/Mallory hyaline)
Apoptosis
Pericellular fibrosis

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16
Q
  1. What is primary biliary cholangitis?
A

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

17
Q
  1. What is the diagnostic test for PBC?
A

Anti-mitochondrial antibodies (AMA)

18
Q
  1. What is the histological appearance of PBC?
A

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

19
Q
  1. 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 caused 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

20
Q
  1. What is the diagnostic test for PSC?
A

Bile duct imaging

21
Q
  1. 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

22
Q
  1. 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

23
Q
  1. 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 chromosome 13
24
Q
  1. How is autoimmune hepatitis diagnosed?
A

Anti-smooth muscle antibodies (ASMA)

25
Q
  1. 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 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

26
Q
  1. List the main types of benign liver tumour. State which is most common.
A

Liver cell adenoma
Bile duct adenoma
Haemangioma (MOST COMMON)

27
Q
  1. List some types of primary liver tumour.
A

Hepatocellular carcinoma
Hepatoblastoma
Cholangiocarcinoma
Haemangiosarcoma