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4 - Y5 a Path lectures 2021/22 > ** Histopath : Liver Pathology > Flashcards

** Histopath : Liver Pathology Flashcards

1
Q

What is the weight of the liver

A

• Weight: 1500 g

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2
Q

What is the liver’s blood supply

A
  • Hepatic portal vein
  • Hepatic artery
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3
Q

Does the liver tend to be affected by ischaemic diseases?

A

because of dual blood supply the liver does NOT tend to get affected by ischaemic diseases

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4
Q

Which cells are present in the liver?

A

• Hepatocytes
• Bile ducts (cholangiocytes)
• Blood vessels
• Endothelial cells
• Kupffer cells
• Resident macrophages
• Stellate cells

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5
Q

What is the function of the stellate cells in the liver?

A
  • In most people, these cells don’t do much other than store vitamin A
  • When activated, they become myofibroblasts and lay down collagen
  • They are responsible for most of the scarring in liver disease
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6
Q

Describe the structure of the endothelial cells in the liver

A
  • In the liver, the endothelial cells do NOT sit on a basement membrane
  • The endothelium is discontinuous - there are no tight junctions
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7
Q

What does this show?

A

liver

  • The portal tract is at the bottom left and the central vein is at the top right
  • The blood will flow from the portal tract to the central vein
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8
Q

What does the portal tract consist of?

A
  • : portal triad = hepatic artery (branch), portal vein (branch) and bile duct
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9
Q

How many zones are there in the liver?

A

THREE zones in the liver: 1, 2 and 3

  • The cells look the same but they are functionally very different
  • ‘They begin life in zone 1, grow up in zone 2 and retire in zone 3’
  • Therefore, cells in zone 3 have more metabolically active enzymes
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10
Q

Describe the normal structure of the liver

A
  • normal hepatocytes have microvilli
  • REMEMBER: endothelial cells in the liver have NO basement membrane and have spaces between them
  • Kupffer cells are found within the sinusoids
  • Stellate cells sit in the space between the endothelial cells and the hepatocytes, known as the space of Disse
  • Blood can easily get through the spaces between endothelial cells and come into contact with hepatocytes
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11
Q

What are the changes that happen to the liver’s microstructure during liver injury?

A
  • Changes in Liver Injury
    • Kupffer cells become activated (typical inflammatory response)
    • Endothelial cells stick together so blood finds it hard to make it through
    • IMPORTANT: in liver injury, basement membrane-type collagens are secreted into the space of Disse by activated stellate cells
    • Hepatocytes lose their microvilli
    • Because of all of these changes, blood finds it hard to diffuse into the hepatocytes
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12
Q

Define 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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13
Q

What is extra-hepatic shunting?

A

extra-hepatic shunting is referring to the shunting of blood to sites of porto-systemic anastomosis (e.g. gastro-oesophageal junction)

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14
Q

What is the difference between intra-hepatic and extra-hepatic shunting?

A
  • Normally, blood comes from the intestines, is filtered through the liver and comes out via the hepatic vein
  • Extrahepatic Shunting - the blood never reaches the liver because it backlogs into the sites of porto-systemic anastomosis
  • Intrahepatic Shunting - the blood comes through the liver but it does NOT come into contact with hepatocytes (so the blood is unfiltered and toxic)
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15
Q

How is cirrhosis classified?

A
  • According to NODULE SIZE (old method)
    • Micronodular
    • Macronodular
    • According to AETIOLOGY
      • Alcohol/insulin resistance
      • Viral hepatitis
  • There is some overlap between these two forms of classification:
    • Micronodular tends to be associated with alcoholism
    • Macronodular tends to be associated with viral infections
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16
Q

What are the complications of cirrhosis?

A
  • Complications of Cirrhosis
    • Portal hypertension
    • Hepatic encephalopathy
      • Liver cell cancer
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17
Q

Is cirrhosis reversible?

A

cirrhosis may be REVERSIBLE

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18
Q

What is the aetiology of acute hepatitis?

A
  • Viruses (mainly hepatitis A and E)
  • Drugs
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19
Q

What does this show?

A

Acute hepatitis

  • A common histological feature of all types of acute hepatitis (regardless of aetiology) is spotty necrosis
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20
Q

What is the aetiology of chronic hepatitis?

A
  • Viral hepatitis
  • Drugs
  • Autoimmune
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21
Q

How is chronic hepatitis classified?

A
  • Severity of inflammation = GRADE (‘how bad does it look’)
  • Severity of fibrosis = STAGE (‘how far has it spread’)
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22
Q

What does this show?

A

Interface Hepatitis

  • Used to be called ‘piecemeal hepatitis’
  • It is difficult to see where the portal tract ends and the hepatocytes begin because the inflammation crosses the limiting plate
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23
Q

What does this show? What is the blue structure?

A

normal portal tract

blue = collagen

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24
Q

What does this show?

A
  • there is a lot of fibrosis in between the portal tract and the central vein
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25
Q

What is a consequence of fibrosis between the portal tract and the central vein?

A
  • This fibrosis will lead to intrahepatic shunting - instead of going through the hepatocytes, blood will go straight from the portal tract to the central vein without being filtered
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26
Q

How does liver disease progress?

A
  • Liver disease will progress in a sequence
  • Patients will develop fibrosis, which gets progressively worse
  • Eventually they will get cirrhosis
  • Once you have cirrhosis, you could become decompensated and you might need a liver transplant
  • Cirrhosis is also a risk factor for HCC
  • NOTE: HCC is becoming increasingly common in non-cirrhotic livers
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27
Q

What are the 3 patterns of Alcoholic Liver Disease?

A
  • Fatty liver
  • Alcoholic hepatitis
  • Cirrhosis

NOTE: they may co-exist, they are not distinct entities

28
Q

Is fatty liver changes reversible?

A
  • anyone that drinks in excess will undergo some fatty change but this is reversible
29
Q

What does this show?

A

Alcoholic Hepatitis

  • Ballooning (with or without Mallory Denk bodies)
    • This is when the cells swell
    • Mallory Denk bodies are pink deposits found within the cells (sometimes referred to as ‘Mallory hyaline’)
  • Apoptosis
  • Pericellular fibrosis

These changes are mainly seen in ZONE 3, where we find the most metabolically active cells in the liver

30
Q

The cells in which zone are most vulnerable to changes seen in alcoholic hepatitis?

A

zone 3

  • alcohol is NOT toxic, acetaldehyde IS toxic - so, the cells that get damaged are the ones that contain the most alcohol dehydrogenase, thereby having the greatest capacity to produce acetaldehyde
    • Furthermore, by the time the blood has gone past zones 1 and 2 and reached zone 3, it is relatively hypoxic
    • This means that cells in zone 3 are particularly vulnerable to damage
31
Q

What type of hepatitis is found in NAFLD?

A
  • Non-alcoholic steatohepatitis is the hepatitis that results from NAFLD
32
Q

How do you distinguish between NAFLD and alcoholic liver disease histologically?

A
  • Histologically looks a lot like alcoholic liver disease
  • It is distinguished from alcoholic liver disease based on the history
33
Q

What is the cause of Non-Alcoholic Fatty Liver Disease (NAFLD)?

A
  • Caused by insulin resistance associated with raised BMI and diabetes
34
Q

What is Primary Biliary Cholangitis?

A
  • Characterised by bile duct loss associated with chronic inflammation (with granulomas)
  • More common in FEMALES
35
Q

What is the diagnostic test for What is Primary Biliary Cholangitis?

A
  • Diagnostic Test: anti-mitochondrial antibodies (AMA)
36
Q

What does this show?

A

Primary Biliary Cholangitis

  • The bile duct is surrounded by epithelioid macrophages, suggestive of granulomatous destruction of bile ducts
  • This is the diagnostic lesion for PBC
37
Q

What is Primary Sclerosing Cholangitis?

A
  • Characterised by periductal bile duct fibrosis leading to loss
  • More common in MALES
38
Q

What is the difference between primary biliary cholangitis and primary sclerosing cholangitis?

A

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

39
Q

Which conditions is Primary Sclerosing Cholangitis associated with?

A
  • Associated with ulcerative colitis
  • Associated with an increased risk of cholangiocarcinoma
40
Q

What is the diagnostic test for Primary Sclerosing Cholangitis?

A
  • Diagnostic Test: bile duct imaging
41
Q

What does this show?

A

Primary Sclerosing Cholangitis

42
Q

What is Haemochromatosis?

A
  • Genetically determined increased in gut iron absorption
  • As women tend to have lower iron levels than men, they tend to present with haemochromatosis LATER
43
Q

What is the genetics of haemachromatosis?

A
  • The implicated gene (HFe) is located on chromosome 6
44
Q

What are the complications of haemachromotosis?

A
  • Iron deposition in parenchymal cells leads to organ damage (e.g. iron deposits in the hepatocytes leading to liver damage)
  • It can deposit in the:
    • heart → cardiomyopathy
    • testes → infertility
    • pancreas → diabetes
45
Q

What is Haemosiderosis?

A
  • This is a type of iron overload
  • It is characterised by the accumulation of iron in macrophages
46
Q

What is the most common cause of haemosiderosis?

A
  • This usually occurs as a result of receiving blood transfusions
47
Q

What does this show?

A

Haemochromatosis

48
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
    *
49
Q

What are the Ix for ?wilson’s disease?

A
  • Assessed by biopsy or biochemistry
50
Q

What are the genetics behind Wilson’s disease?

A
  • Responsible genes are found on chromosome 13
51
Q

What are the complications of Wilson’s disease?

A
  • Copper accumulates in the
    • liver + CNS (sometimes referred to as hepato-lenticular degeneration)
    • iris (Kayser-Fleischer rings)
  • Accumulation in the lentiform nucleus of the basal ganglia leads to movement disorders
52
Q

What is Autoimmune Hepatitis?

A
  • This is a very active form of chronic hepatitis with lots of plasma cells
  • The degree of inflammation is often much worse than in viral hepatitis
  • More common in FEMALES
53
Q

Which antibodies are implicated in Autoimmune Hepatitis?

A
  • Antibodies: Anti-smooth muscle antibodies (ASMA)
54
Q

How is the diagnosis of autoimmune hepatitis confirmed?

A
  • Responds to STEROIDS (important to confirm the diagnosis)
55
Q

What is Alpha-1 Antitrypsin Deficiency?

A
  • Characterised by a failure to secrete alpha-1 antitrypsin from hepatocytes into the blood
56
Q

Summarise the pathophysiology of Alpha-1 Antitrypsin Deficiency

A
  • Alpha-1 antitrypsin is made in hepatocytes
  • Protein sequence is wrong so it CANNOT fold properly and cannot exit the hepatocytes
  • → alpha-1 antitrypsin forms globules within the hepatocytes which damages them and leads to chronic hepatitis
  • → deficiency of Alpha-1 antitrypsin in the blood
57
Q

What are the complications of Alpha-1 Antitrypsin Deficiency?

A
  • A deficiency of alpha-1 antitrypsin in the rest of the body leads to increased risk of emphysema
58
Q

What does a Drug-Related Liver Injury picture look like?

A
  • ANY type of liver disease can be caused by a drug (i.e. it could look like a hepatocellular problem or a cholestatic problem)
  • NOTE: because the liver is the main site of drug transformation, it is also the main site where toxic metabolites are formed
    • E.g. zone 3 is worst affected in paracetamol overdose because that is where the most NAPQI is formed
59
Q

What does this show?

A

Hepatic Granulomas

60
Q

What are the causes of hepatic granulomas?

A

Specific causes:

  • PBC
  • drugs

General causes:

  • TB
  • Sarcoidosis
61
Q

Name some benign liver tumours

A
  • Liver cell adenoma
  • Bile duct adenoma
  • Haemangioma (MOST COMMON)
62
Q

Name some malignant liver tumours

A
  • Secondary tumours (MOST COMMON)
  • Primary tumours
    • Hepatocellular carcinoma
    • Hepatoblastoma
    • Cholangiocarcinoma
    • Haemangiosarcoma
63
Q

What is hepatocellular carcinoma associated with?

A
  • Associated with cirrhosis in the West, and
  • associated with viral infections in developing countries
64
Q

What is cholangiocarcinoma associated with?

A
  • Associated with:
    • PSC
    • Worm infections
    • Cirrhosis
65
Q

Which structures can cholangiocarcinomas arise from?

A
  • Can arise from:
    • Intrahepatic ducts
    • Extrahepatic ducts (including gallbladder)

4 - Y5 a Path lectures 2021/22 (37 decks)

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