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Clinical Pathology > 59 Hepatobiliary diseases > Flashcards

59 Hepatobiliary diseases Flashcards

1
Q

When is jaundice visible?

A

When bilirubin >40umol/l.

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2
Q

Simply describe the metabolism of bilirubin:

A

Unconjugated bilirubin is produced in RBC breakdown.
Conjugated in the liver and excreted in bile.
Some is reabsorbed by the gut - enters the enterohepatic circulation.

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3
Q

What is pre-hepatic jaundice?
2 causes:
Sign?

A

Too much bilirubin produced.
Haemolytic anaemia, Gilbert’s syndrome.
Yellow skin + sclera.

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4
Q

What is hepatic jaundice due to?
3 causes:
Signs:

A

Too few functioning hepatic cells.
Acute liver injury, chronic liver disease, inborn.
Jaundice + dark urine.

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5
Q

What is post-hepatic jaundice?
Causes:
Signs:

A

Bile duct obstruction.
Stone, stricture, tumour.
Jaundice, pale stools, dark urine.

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6
Q

Why do ALT + AST rise in hepatic injury?

What is seen in acute vs chronic?

A

Leak from damaged hepatocytes.

Very high= acute. Mildly high= chronic.

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7
Q

What produces a raised Alk Phos?

A

Leak from injured bile duct cells.

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8
Q

Which histological change is seen first in obstructive jaundice?

A

Bile in parenchyma.

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9
Q

What are the later histological changes in obstructive jaundice? (4)

A

Portal tract expansion.
Oedema.
Ductular reaction: proliferation + fibrosis.
Bile salt + copper accumulation.

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10
Q

How is jaundice investigated? (2)

A

Ultrasound to check for dilated ducts.

If none seen - liver biopsy.

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11
Q

What are most cases of non obstructive jaundice due to?

A

Acute hepatitis.

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12
Q

What is the clinical spectrum of acute hepatitis? (6)

A 
Asymptomatic
Malaise
Jaundice
Coagulopathy
Encephalopathy
Death
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13
Q

What are the causes of acute hepatitis? (4)

A

Viral.
Drugs (paracetamol).
Autoimmune.
Alcohol.

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14
Q

What histological changes are seen in acute hepatitis? (4)

A

Heapocyte disarray (apoptosis).
Inflammatory cells.
Confluent panacinar necrosis (all cells dead).
Bridging necrosis (cells die between vascular structures).

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15
Q

What are the causes of chronic hepatitis? (7)

A 
Viral.
Autoimmune.
Drugs.
Fatty liver disease.
Non-alcoholic fatty liver disease.
Alcohol.
Iron, copper, α1-antitrypsin.
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16
Q

What is a biopsy used for in chronic hepatitis?

A

Determine cause.

Assess stage.

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17
Q

Describe the four stages of chronic liver disease histology:

A

Normal.
Portal fibrosis.
Bridging fibrosis.
Cirrhosis.

18
Q

Who is Hep D seen in?
How is Hep E spread?
Name three causes of Hepatitis in immunocompromised:

A

Preinfected with Hep B.
Waterborne.
EBV, CMV, HSV.

19
Q 
Hep A:
Route:
Acute jaundice?
Progression to chronic?
Treatment?
Prophylaxis?
A 
Faecal-oral.
acute? Common.
progression? Never.
Rx? None.
Prophylaxis? Vaccine, Ig.
20
Q 
Hep B:
Route:
Acute jaundice?
Progression to chronic?
Treatment?
Prophylaxis?
A 
Parenteral.
jaundice? Common.
progression? 10% 
Rx? IFN + lamivudine.
Prophylaxis? Vaccine, Ig
21
Q 
Hep C:
Route:
Acute jaundice?
Progression to chronic?
Treatment?
Prophylaxis?
A 
Parenteral.
jaundice? Uncommon.
progression? >70% 
Rx? IFN + ribavirin.
Prophylaxis? None.
22
Q

What changes are seen in the liver with alcohol? (3).

Histological changes in FLD + NAFLD? (2)

A

Fatty change.
Alcoholic steatohepatitis.
Cirrhosis.

Ballooned hepatocyte with mallory body.
Pericellular fibrosis.

23
Q

What is non-alcoholic fatty liver disease associated with? (4)

A

Obesity.
Diabetes.
Hyperlipidaemia.
Drugs.

24
Q

Name a intrinsic and idiosyncratic hepatotoxic drug:

A

Paracetamol.

Amoxicillin.

25
What are the criteria for drug induced liver injury? (4)
Onset of abnormal LFTs 5-90 days after drug. 50% reduction after stopping, under 30/180 days. Alternative causes excluded. Increase in LFTs by 100% on re-challenge.
26
What pattern of cell death is seen in paracetamol hepatotoxicity?
Uniform zonal necrosis.
27
How does paracetamol toxicity occur?
Safe metabolism by glucuronyl transferase + sulphotransferase. Then... CYP2E1 converts drug to NAPQI. NAPQI levels higher than glutathione -> necrosis.
28
Why does alcohol exacerbate paracetamol toxicity?
Induces CYP2E1 enzymes.
29
How is paracetamol toxicity treated?
IV N-acetyl cysteine, which restores glutathione levels.
30
Define cirrhosis:
Diffuse hepatic process of fibrosis and conversion of normal liver architecture into structurally abnormal nodules (regenerating tissue surrounded by fibrosis).
31
What are the autoimmune causes of cirrhosis? (3)
Autoimmune hepatitis, Primary biliary cirrhosis Primary sclerosing cholangitis
32
What are the complications of cirrhosis?
Portal hypertension -> oesophageal varices. Liver cell failure -> oedema, bruising, muscle wasting, decreased detox, ascites. Jaundice + itching. Reticulo-endothelial cells -> infection.
33
Why does cirrhosis lead to ascites? (3)
Low albumin production. Portal hypertension. Aldosterone related fluid retention.
34
What is α1-antitrypsin deficiency? Histological stain? Sequelae? (2)
Abnormal enzyme can't be exported from cells. PAS +ve globules in hepatocytes. Accumulation -> cirrhosis. Lack in blood -> active neutrophil enzymes + emphysema.
35
What is haemochromatosis? Histological stain? Rx?
Inborn error of iron metabolism leads to deposition in organs. Perl's blue. Venesection.
36
What are the effects of haemochromatosis? (5)
``` Liver cirrhosis. Diabetes. Pigmented skin. Arthritis. Cardiomyopathy. ```
37
What is wilson's disease? Stain? Effects? (3) Rx?
Inborn error of copper metabolism. Rhodanine stain (brown). Cirrhosis, Kayser-Fleischer rings, ataxia. Chelation.
38
What are the physical signs of cirrhosis? (6)
``` Ascites Muscle wasting Bruising Gynaecomastia Spider naevi Caput medusa (varies from umbilicals) ```
39
What are the complications of portal hypertension? (3)
Splenomegaly – low platelets Oesophageal varices – haemorrhage Piles (perianal varices)
40
What causes pre-sinusoidal portal hypertension? (3)
Portal fibrosis. Sarcoid. Schistosomiasis.
41
What causes sinusoidal portal hypertension?
Cirrhosis.
42
What causes post sinusoidal portal hypertension?
Hepatic vein thrombosis | = Budd Chiari syndrome

Clinical Pathology (66 decks)

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