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YR5 Histopathology > Liver Pathology > Flashcards

Liver Pathology Flashcards

1
Q

Describe hepatocyte function in each zone

A
  1. “Born”
  2. “Grow up”
  3. Reach maturity, most metabolically active + eventually die
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2
Q

What occurs in zone 3 of the liver?

A

Hepatocytes metabolise xenobiotics to toxic substances
Thus most alcoholic liver damage occurs in zone 3

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3
Q

Describe the blood flow in the liver

A

Hepatic artery + portal vein bring blood to liver
Blood travels through sinusoids, O2 absorbed by hepatocytes along the way
pO2 much lower when blood reaches zone 3 where cells are most metabolically active - problem in alcoholics

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4
Q

What is shown by each arrow?

A

Blue: Portal triad
Yellow: Central vein

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5
Q

What is shown by each arrow?

A

Blue: Portal vein
Purple: Bile duct
Green: Hepatic artery

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6
Q

What is shown in this picture?

A

Yellow: Hepatocytes
Red: Bile duct canaliculi
red + white cells lining sinusoids

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7
Q

Describe the organisation of cells in a sinusoid

A

Hepatic sinusoid: blood flows through
Kupfer cells: resident macrophages in sinusoids
Discontinuous endothelial cells: allows blood plasma to enter space of disse
Stellate cells: in space of disse, store Vit A
Hepatocytes with microvillous border projecting into space of disse

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8
Q

Describe the cellular changes in a sinusoid due to liver injury (5)

A

Kupfer cells are activated
Stellate cells become myofibroblasts- contract + secrete collagen
Gaps between endothelial cells closed, firmly attached
Fibrillar collagen deposited in space of disse
Difficult for blood to reach hepatocytes + hepatocytes lose microvillous border

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9
Q

Which 4 features define cirrhosis?

A
  1. Whole liver involved
  2. Fibrosis
  3. Nodules of regenerating hepatocytes
  4. Distortion of liver vascular architecture: intra- + extra-hepatic shunting of blood (e.g. gastro-oesophageal)
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10
Q

What are the functional consequences of the vascular problems in cirrhosis?

A

No metabolic homeostasis
Hepatocytes themselves don’t receive nutrition they require

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11
Q

What is the consequence of the liver being unable to filter blood due to intra and extra hepatic shunts?

A

Unfiltered, toxic blood goes to heart + is delivered to the rest of the body

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12
Q

What is shown here?

A

Whole liver involved
Nodules

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13
Q

What is shown here?

A

Nodule surrounded by fibrous tissue

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14
Q

How is cirrhosis classified?

A

According to aetiology
1. Alcohol/ insulin resistance (usually micro nodular)
2. Viral hepatitis etc. (usually macro nodular)

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15
Q

Give 3 clinical complications of cirrhosis

A

Portal HTN
Hepatic encephalopathy
Liver cell cancer

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16
Q

What is shown here?

A

Large oesophageal varicie

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17
Q

What is shown here? What causes this?

A

Enlarged spleen
Back pressure of blood in portal circulation leads to passive enlargement of spleen
If palpable, likely portal HTN + probably cirrhotic

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18
Q

What can be seen here?

A

Cirrhotic liver with cancer visible

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19
Q

Until recently what was believed about cirrhosis?

A

That it was irreversible
It may be reversible if equilibrium is shifted as fibrosis is dynamic
Collagen is deposited + can be broken down

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20
Q

What are the most common causes of acute hepatitis?

A

Viruses: Hep A-E. A+E most common
Drugs: all drugs metabolised by liver. If PO, will reach gut 1st then transported to liver

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21
Q

What can be seen here? What is this pathogonomic of?

A

Spotty necrosis in Acute hepatitis
Damage to hepatocytes a/w lymphocytes
Damage focused in liver lobule

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22
Q

What are the most common causes of chronic hepatitis?

A

Viral hepatitis: B, C, D - D dependent on B
Drugs
AI: F>M, more prone to other AI

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23
Q

How are the histological findings in chronic hepatitis assessed?

A

Grade: severity of inflammation- how awful it looks down microscope
Stage: severity of fibrosis- how far along from normal to cirrhotic

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24
Q

What can be seen here?

A

Blue: inflammatory cells in portal tract
Red: limiting plate- interface between portal tract + hepatocytes

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25
What can be seen here?
Interface hepatitis aka piecemeal necrosis Limiting plate more difficult to see Inflammation crossing limiting plate Hepatocyte apoptosis drives fibrosis
26
What can be seen here?
Lobular inflammation
27
How does the histology differ in acute and chronic hepatitis?
Acute: most inflammation in lobules Chronic: most inflammation in or around portal tract
28
What can be seen here?
Fibrous tissue stretching from portal tract to central vein "Bridging fibrosis" allows intrahepatic shunting Blood enters portal tract, goes direct to central vein, bypasses hepatocytes
29
Once a patient has developed bridging fibrosis, what are they at increased risk of?
Cirrhosis Hepatocellular carcinoma Liver transplantation Death
30
What are the 3 patterns of alcoholic liver disease?
1. Fatty liver: metabolic change, reversible 2. Alcoholic hepatitis: inflammation 3. Cirrhosis
31
What is this and how does it differ from normal?
Fatty liver, yellow, greasy Normal: red, beefy colour
32
What is seen here?
Fatty change Each hepatocyte contains a large droplet of fat
33
Give 4 histological features of alcoholic hepatitis
Ballooning (+/- Mallory Denk bodies) Apoptosis Pericellular fibrosis Mainly seen in Zone 3
34
How does ballooning of hepatocytes occur?
In Z3, Alcohol converted by alcohol dehydrogenase to acetaldehyde Acetaldehyde is toxic: causes cross linking of intermediate filaments of liver Once cross linked + clumped, cells can't retain shape, can't transport fluids or proteins out well, so balloon Clumped cytoskeleton = Mallory Denk body
35
What is the diagnosis? What can be seen here?
Alcoholic hepatitis Big white droplets of fat Ballooned hepatocytes with dark pink clumps (Mallory Denk bodies) Neutrophils
36
What can be seen here?
Pericellular fibrosis (Orange arrow)
37
Describe this
Alcohol induced cirrhosis Pale yellow Micronodular
38
What can be seen here?
Fat in nodule Surrounded by fibrosis
39
Give 3 facts about non alcoholic fatty liver disease (inc. non alcoholic steatohepatitis)
Histologically looks like alcoholic liver disease Due to insulin resistance a/w high BMI + DM Tx: Mx of DM + weight loss
40
Give 5 facts about primary biliary cholangitis
F > M Middle aged Bile ducts are lost due to chronic inflammation (often granulomatous) Diagnostic test: detection of Anti-mitochondrial antibodies 50% have cirrhosis
41
Give 5 facts about primary sclerosis cholangitis
M > F Periductal bile duct fibrosis leads to obstruction + loss of intra + extra hepatic bile ducts a/w UC Increased risk of cholangiocarcinoma Diagnostic test: MRCP/ ERCP imaging
42
What is the diagnosis? What can be seen?
PSC Dense consecutive fibrosis "onion skin"
43
Give 4 facts about haemochromatosis
Genetically determined increased gut iron absorption (Chr 6) Parenchymal damage to organs secondary to iron deposition In liver: fibrosis - cirrhosis In skin: bronze pigmentation In pancreas: severe pancreatitis, islet damage + DM
44
What can be seen here? What is the diagnosis?
Iron in hepatocytes Haemocromatosis
45
What is haemosiderosis? What causes this?
Accumulation of iron in macrophages Results from multiple blood transfusion e.g. in sickle cell/ thalassemia
46
What is seen here? What is the diagnosis?
Iron in scattered cells (macrophages) No iron in hepatocytes Haemosiderosis
47
Give 3 facts about Wilsons disease
Accumulation of copper due to failure of excretion by hepatocytes into bile Deposits in CNS: lenticular degeneration- psych disturbances Deposits in cornea: kayser fleishcer rings on slit lamp
48
What can be seen here? What causes this?
Copper on rhodanine stain Wilsons disease
49
Give 4 facts about AI hepatitis
F > M Very active chronic hepatitis, auto antibodies from plasma cells in liver Anti-smooth muscle actin antibodies in serum Responds to steroids
50
Give 4 facts about alpha-1 antitrypsin deficiency
Failure to secrete alpha-1 antitrypsin Intra-cytoplasmic inclusions due to misfolded protein from excess alpha 1 antitrysin in hepatocytes Causes hepatitis + cirrhosis a/w emphysema
51
Why is alpha 1 antitrypsin deficiency associated with emphysema?
Alpha 1 antitrypsin usualy dampens inflammation Without this, inflammation in lung is prolonged, allowing more lung destruction
52
What can be seen here?
Globules of alpha 1 antitrypsin misfolded protein accumulating in hepatocytes
53
What can be seen here? Why?
Hepatocytes around portal tract are ok Hepatocytes in zone 2 + 3 are gone because this is where paracetamol is activated to NAPQI which is toxic
54
Give 2 general and 2 specific causes of hepatic granulomas
General: TB + Sarcoid Specific: PBC + drugs
55
What can be seen here? What pathology is this seen in?
Giant cell surrounded by activated macrophages Hepatic granuloma
56
Give 3 types of benign liver tumour
1. Liver cell adenoma 2. Bile duct adenoma 3. Haemangioma: endothelial
57
What is this?
Liver cell adenoma Sharply defined tumour, not invading local tissue
58
What malignant tumours can arise in the liver?
1. Secondary MORE COMMON: all blood from portal circulation goes via liver- mets from stomach, pancreas, small intestine, large intestine 2. Primary
59
What is seen here?
Secondary liver tumours Often multiple when secondary
60
What are the 4 primary malignant liver tumours?
1. Hepatocellular carcinoma- liver cell 2. Hepatoblastoma: more common in kids 3. Cholangiocarcinoma: bile ducts 4. Haemangiosarcoma: endothelial cells
61
What is liver cell cancer usually associated with, especially in the West? Where may this not be seen?
a/w Cirrhosis, often in elderly men In countries where Hep B more common may not be a/w cirrhosis as Hep B can be directly oncogenic
62
What can be seen here?
Hepatocellular carcinoma
63
Cholangiocarcinoma can be associated with which 3 conditions? From which bile ducts can it arise?
PSC Worm infections Cirrhosis Can arise from intra-hepatic + extra-hepatic ducts (inc. gall bladder)
64
What can be seen here?
Cholangiocarcinoma

YR5 Histopathology (27 decks)

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