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YEAR 5: Histopathology - PK Edited > 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, and what are the zones

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

Describe how the cell 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 4 key features of cirrhosis?

A
  • The whole liver is involved
  • There is extensive fibrosis
  • nodules of regenerating hepatocytes
  • Shunting occurs (intra and extrahepatic)
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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

Does viral and alcoholic cirrhosis cause micro or macronodular cirrhosis?

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
  • Seen in chronic hepatitis
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19
Q

What are the three histological patterns of alcoholic liver disease?

A
  • Fatty liver - accumulation of fat droplets (steatosis), which is fully reversible if alcohol is avoided
  • Alcoholic hepatitis - seen acutely after a night of heavy drinking. Ranges from asymptomatic to fulminant liver failure
  • Cirrhosis - micronodular cirrhosis

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

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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
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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
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22
Q

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

A
  • Looks like alcoholic hepatitis - hepatocyte ballooning + mallory denk bodies

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

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23
Q

How is NAFLD distinguished from alcoholic liver disease?

A

Based on the history

AST:ALT ratio <2 in NAFLD but >2 in ALD

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24
Q

What is primary biliary cholangitis?

A

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

Intrahepatic! + slow development of cirrhosis over years

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25
Q

What is the diagnostic test for PBC?

A
  • Anti-mitochondrial antibodies (AMA) (>90% positive)
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26
Q

What is the histological appearance of PBC?

A

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

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27
Q

What is primary sclerosing cholangitis?

A
  • Autoimmune condition characterised by periductal bile duct fibrosis leading to loss of bile ducts, extrahepatic and intrahepatic

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

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28
Q

What is the diagnostic test for PSC?

A
  • Bile duct imaging by ERCP
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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 (as A1AT usually protects the lung from damage by e.g. smoke)
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 (in children)
  • Cholangiocarcinoma
  • Haemangiosarcoma
42
Q

What are some risk factors for cholangiocarcinoma?

A
  • PSC
  • Worm infections
  • Cirrhosis
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
44
Q

Most common cause of chronic liver disease in the west?

A

NAFLD / MAFLD

45
Q

most common benign lesion of the liver?

A

haemangioma

46
Q

what liver tumour is associated with OCP?

A

Hepatic adenoma

47
Q

what is the commonest carcinoma seen in the liver?

A

metastatic adenocarcinoma (from other places!)

48
Q

commonest primary malignant tumour of the liver?

A

HCC

49
Q

Describe zone 1, zone 2 and zone 3 of the liver?

A

Zone 1 - closest to portal triad. Periportal hepatocytes are affected first in viral hepatitis

Zone 2 - midzone

Zone 3 - closest to terminal central vein. Perivenular hepatocytes are the most metabolically active (thus most sensitive to metabolic toxins e.g. drugs and alcohol)

50
Q

What happens as a result of extrahepatic shunting?

A

Blood pools in portosystemic anastamoses (oesophageal varices, caput medusae, anorectal varices)

51
Q

AST:ALT ratio in alcoholic liver disease vs NAFLD

A

> 2 in ALD
<2 in NAFLD

52
Q

Major causes of cirrhosis? (+ genetic causes + drugs)

A

NAFLD
ALD
Hepatitis (BCD)

Autoimmune
PSC, PBC

Haemochromatosis
Wilson’s
A1AT
Galactosaemia (cannot convert galactose -> glucose so it builds up in liver)
Glycogen storage disease (cannot break down glycogen, so it builds up in the liver)

Drugs - methotrexate

53
Q

What score for prognosis in liver cirrhosis?

A

Modified child’s pugh score

54
Q

Macroscopic characteristics of the three liver pathologies in alcohol-related liver disease?

A

Hepatic steatosis/fatty liver - large, pale, yellow greasy liver

Alcoholic hepatitis - large fibrotic liver

Cirrhosis - looks cirrhotic

55
Q

What conditions make up NAFLD

A

Simple steatosis
NASH = steatosis + hepatitis. Can progress to cirrhosis

56
Q

What gene and antibodies are associated with autoimmune hepatitis?

A

HLA-DR3

Antinuclear antibody, anti-smooth muscle antibody
anti-LKM antibody (anti liver kidney microsomal antibody)

57
Q

What is seen on histology with autoimmune hep?

A

plasma cells

58
Q

Histology shows bile duct loss with granulomas - diagnosis?

A

Primary biliary cholangitis

59
Q

Blood tests for PBC?

A

raised ALP, raised cholesterol, raised IgM (as autoimmune)

60
Q

Treatment for PBC and PSC

A

ursodeoxycholic acid +/- liver transplant

61
Q

PSC vs PBC - in terms of male and female prevelence?

A

PBC - F>M
PSC - M>F

62
Q

What diseases is PSC associated with, and what antibody?

A

IBD - esp UC and increased risk of cholangiocarcinoma (PBC is not)
p-ANCA antibody

63
Q

What would USS show of PBC vs PSC?

A

PBC - no dilatation of bile ducts (as being closed)
PSC - dilatation of bile ducts

64
Q

histology of PSC?

A

onion skinning fibrosis

65
Q

inheritance pattern of haemochromatosis, wilson’s and A1AT?

A

haemo and wilsons - autosomal recessive
A1AT - autosomal dominant

66
Q

what stain for iron

A

Prussian blue

67
Q

what stain for copper

A

rhodanine stain

68
Q

what rings in eyes for wilson’s

A

kayser fleischer rings

69
Q

two benign tumours of the liver?

A

hepatic adenoma and haemangioma (most common)

70
Q

Ix for HCC?

A

AFP!!!!! (also raised in yolk sac tumours), USS

YEAR 5: Histopathology - PK Edited (29 decks)

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