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
Q

Histology of PBC

A

Bile ducts surrounded by epithelioid macrophages
NO bile duct dilatation
INTRAHEPATIC

26
Q

Antibody in PBC

A

AMA

27
Q

PSC

A

Periductal bile duct fibrosis WITHOUT inflammation

28
Q

PSC associations

A

UC, Cholangiocarcinoma, pANCA

29
Q

PSC histology

A

Intra AND extrahepatic

30
Q

How is PSC diagnoised? Common findings?

A

Radiology
On USS –> onion skinning, duct dilatation
ERCP: Beads on a string

31
Q

Haemochromatosis: which gene and which chromosome?

A

HFe, Chr6

32
Q

What is haemosiderosis?

A

Iron deposition in MACROPHAGES

33
Q

When do people get haemosiderosis?

A

Transfusion haemosiderosis

34
Q

Wilson’s disease mutation on which Chr?

A

Chr13

35
Q

Stain for Wilson’s

A

Rhodanine

36
Q

Autoimmune hepatitis antibody

A

ASMA

37
Q

Management of autoimmune hepatitis

A

Steroid responsive

38
Q

Causes of hepatic granulomas

A

PBC, drugs, TB, sarcoid

39
Q

Most common benign tumours of liver

A

Haemangiomas

40
Q

Most common malignant liver tumour?

A

Secondary tumours

41
Q

Other types of malignant liver cancers

A

HCC, cholangiocarcinoma, hepatoblastoma (children)