Histopathology - Liver tutorial Flashcards

1
Q

Why does the liver rarely undergo ischaemia?

A

It has a dual blood supply (hepatic artery and portal vein)

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2
Q

Which zone of the liver is the portal tract in?

A

In zone 1 (has the best blood supply)

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3
Q

What is the importance of zone 3?

A

Contains the most metabolically active hepatocytes but most prone to ischaemia

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4
Q

What is special about the endothelial cels in the liver?

A

They do not sit on a basement membrane and are discontinuous (fenestrated)

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5
Q

Resident macrophages in liver?

A

Kuppfer cells

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6
Q

Function of stellate cells when normal and in liver damage

A

Normal: produce vitamin A

Liver damage: stellate cells become activated to myofibroblasts and lay down collagen

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7
Q

Which cells in the liver are responsible for liver scarring

A

Stellatecells

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8
Q

Liver injury changes

A

Hepatocytes lose microvilli
Kuppfer cells become activated
Stellate cells become activated to myofibroblasts
Deposition of scar tissue in space of disse by stellate cells
Loss of fernestration in endothelium

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9
Q

Definition of cirrhosis

A

Whole liver involved
Fibrosis
Nodules of regenerating hepatocytes
Distortion of liver vasculature: both intra and extrahepatic shunting of blood (due to bridging fibrosis)

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10
Q

What is cirrhosis classification based on?

A

Aetiological cause of cirrhosis

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11
Q

The patterns of nodular regeneration in alcoholic/ NAFLD hepatitis causing cirrhosis

A

MICRONODULAR reorganisation

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12
Q

The patterns of nodular regeneration in viral hepatitis causing cirrhosis?

A

MACRONODULAR reorganisation

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13
Q

Pathological finding in acute hepatitis

A

Spotty necrosis

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14
Q

Pathoological finding in chronic hepatitis

A

Interface hepatitis/piecemeal necrosis

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15
Q

Is cirrhosis reversible?

A

YES

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16
Q

Which hepatitis viruses can casue acute hepatiits?

A

A and E

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17
Q

3 main causes of chronic hepatitis

A

Viruses, drugs and autoimmune

18
Q

Grade and stage of chronic hepatitis

A
Grade = degree of inflammation
Stage = severity of fibrosis/scarring
19
Q

How is alcohol toxic to the liver?

A

Alcohol itself is not toxic but the metabolic product of acetaldehyde is

20
Q

Three histological patterns of alcoholic liver disease

A

Fatty change, alcoholic hepatitis and cirrhosis

21
Q

Features of alcoholic hepatitis

A

Ballooning (+/- mallory denk bodies), apoptosis, pericellular fibrosis

22
Q

Which zone is affected most in alcoholic hepatiits

A

Zone 3 as it has the highest concentration of aldehyde dehydrogenase as cells most metabolically active

23
Q

Histology of NAFLD

A

Identical to alcoholic liver disease

24
Q

Pathophysiology of PBC

A

Bile duct loss due to CHRONIC inflammation with GRANULOMAS

25
Histology of PBC
Bile ducts surrounded by epithelioid macrophages NO bile duct dilatation INTRAHEPATIC
26
Antibody in PBC
AMA
27
PSC
Periductal bile duct fibrosis WITHOUT inflammation
28
PSC associations
UC, Cholangiocarcinoma, pANCA
29
PSC histology
Intra AND extrahepatic
30
How is PSC diagnoised? Common findings?
Radiology On USS --> onion skinning, duct dilatation ERCP: Beads on a string
31
Haemochromatosis: which gene and which chromosome?
HFe, Chr6
32
What is haemosiderosis?
Iron deposition in MACROPHAGES
33
When do people get haemosiderosis?
Transfusion haemosiderosis
34
Wilson's disease mutation on which Chr?
Chr13
35
Stain for Wilson's
Rhodanine
36
Autoimmune hepatitis antibody
ASMA
37
Management of autoimmune hepatitis
Steroid responsive
38
Causes of hepatic granulomas
PBC, drugs, TB, sarcoid
39
Most common benign tumours of liver
Haemangiomas
40
Most common malignant liver tumour?
Secondary tumours
41
Other types of malignant liver cancers
HCC, cholangiocarcinoma, hepatoblastoma (children)