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Clinical Pathology > Diseases of the hepatobiliary system > Flashcards

Diseases of the hepatobiliary system Flashcards

1
Q

What is the commonest sign of liver disease?

A

Jaudice

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2
Q

When is jaundice visible?

A

When bilirubin >40umol/l

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3
Q

What is pre-hepatic jaundice?

A

Too much bilirubin produced

- Haemolytic anaemia

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4
Q

What is hepatic jaundice?

A

Too few functioning liver cells

  • Acute diffuse liver cell injury
  • End stage chronic liver disease
  • Inborn errors
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5
Q

What is post hepatic jaudice?

A

Bile duct obstruction

- stone, stricture, tumour – bile duct, pancreas

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6
Q

What kind of bile is in excess in pre-hepatic jaundice?

A

Unconjugated – bound to albumin, insoluble, not excreted

- patient notices yellow eyes/skin only

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7
Q

What kind of bile is in excess in hepatic jaundice?

A

Mainly conjugated,
Soluble
- patient notices yellow eyes and dark urine

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8
Q

What kind of bile is in excess in post-hepatic jaundice?

A

conjugated - soluble, excreted, but can’t get into gut

- patient notices yellow eyes, pale stool and dark urine

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9
Q

Which liver enzymes leak from hepatocytes?

A

ALT and AST

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10
Q

What does a mild increase of ALT/AST over a long time indicate?

A

Chronic liver disease

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11
Q

What do very high levels of ALT/AST indicate?

A

Severe acute liver disease.

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12
Q

What does Alk Phos leak from?

A

Bile duct

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13
Q

What does a high alk phos reading indicate?

A

Obstructive jaundice and chronic biliary disease.

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14
Q

What does raised conjugated bilirubin without extrahepatic duct obstruction indicate?

A

Disease of hepatocytes or intraheptic bile ducts.

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15
Q

Why might albumin be low?

A

Has long half life so levels may be low in chronic liver insufficiency.

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16
Q

How are clotting factors measured?

A

PT and INR

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17
Q

What is INR?

A

International normalised ratio - ratio of pt’s clotting time to normal control.

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18
Q

Why might PT/INR be prolonged?

A

Severe liver injury

Obstructive jaundice - can’t absorb fat soluble vitamins

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19
Q

What is the first histopathological sign of obstructive jaundice?

A

Bile in the liver parenchyma

- jaundice in the skin, patient is yellow

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20
Q

What are the other histopathological signs of obstructive jaundice?

A

Portal tract expansion

Oedema

Ductular reaction – proliferation of ductules around the edge

Bile salts and
- copper cant get out
- Accumulate in hepatocytes
(bile salts in skin – patient is itchy)

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21
Q

What is the first investigation in someone with jaundice?

A

USS to check for bile duct dilation.

If ducts not dilated biopsy performed.

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22
Q

What are most non-obstructive cases of jaundice due to?

A

Acute hepatitis

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23
Q

What is the clinical definition of hepatitis?

A

Liver enzymes raised, any cause

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24
Q

What is the histopathological defenition of hepatitis?

A

Inflammation seen on biopsy.

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25
Q

What does the clinical presentation of hepatitis depend on?

A

The amount of hepatocytes that are injured/killed and how well the remaining ones can regenerate.

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26
Q

What are the commonest causes of acute hepatitis in the UK?

A

Alcohol

Paracetamol toxicity

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27
Q

What are the other causes of acute hepatitis?

A

Viral
- A, B & E

Drug induced

Autoimmune

Seronegative (i.e. idiopathic)

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28
Q

What are the histopathological features of mild acute hepatitis?

A

Lobular disarray

Inflammatory cells

Hepatocytes vary in cells

Spotty necrosis

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29
Q

What are the histopathological features of severe acute hepatitis?

A

Confluent panacinar necrosis

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30
Q

What is bridging necrosis and where is it seen?

A

Confluent necrosis of adjacent hepatocytes in a ‘bridge’ between a portal tract and hepatic vein.

Seen in acute hepatitis of intermediate severity

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31
Q

What are the causes of chronic hepatitis?

A

Immunological injury - virus

  • autoimmune
  • drugs

Toxic/metabolic injury

  • fatty liver disease
  • alcohol, non-alcoholic fatty liver disease (NAFLD)
  • drugs

Genetic inborn errors

  • iron
  • copper
  • alpha1antitrypsin

Biliary disease

  • autoimmune
  • duct obstruction
  • drugs,

Vascular disease

  • clotting disorders
  • drugs
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32
Q

What is the pathology of chronic liver disease?

A

Injury to liver cells, inflammation, formation of scar tissue and regeneration of hepatocytes
- Non-specific features of injury

Specific pathological features depend on the cause of injury

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33
Q

How are biopsies used in liver diease?

A

To determine the cause of the damage
- specific features, if present

To assess the stage of disease

  • how much scarring,
  • spectrum from normal to cirrhosis
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34
Q

What are the stages of liver disease?

A

A normal
B portal fibrosis
C bridging fibrosis
D cirrhosis

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35
Q

What are the features of stage D?

A

and hepatocytes form nodules surrounded by fibrous tissue. Portal blood entering the liver can flow through vessels in the fibrous tissue, and not percolate through sinusoids. The cirrhotic liver therefore is inefficient in its metabolic function, even though it is or normal size or larger.

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36
Q

What are the characteristics of the Hep A virus?

A

Type - Picorna RNA

Route - Faeco-oral

Acute jaundice - common

Chronic hepatitis? - never

Chronic infection worldwide - none

Treatment - none

Prophylaxis - Vaccine Ig

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37
Q

What are the characteristics of the Hep B virus?

A

Type - Hepadna DNA

Route - parenteral

Acute jaundice - common

Chronic hepatitis? - 10% adults

Chronic infection worldwide - 350m

Treatment - IFN, lamivundine + new ones

Prophylaxis - Vaccine Ig

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38
Q

What are the characteristics of the Hep C virus?

A

Type - Flavivirus RNA

Route - parenteral

Acute jaundice - uncommon

Chronic hepatitis? - >70%

Chronic infection worldwide - 170m

Treatment - IFN, ribovarin + new ones

Prophylaxis - none

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39
Q

In which infection only would you see hepatitis d?

A

Only in people with Hep E

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40
Q

What is the epidemiology of Hep E?

A

Waterborne, increasingly recognised in UK in last few years, zoonosis, pigs

41
Q

Which viruses also cause hepatitis as part of systemic disease?

A

EBV

CMV

HSV

42
Q

What kind of hepatitis is caused by alcohol?

A

Alcoholic steatohepatitis

43
Q

What are the histopathological changes seen in alcoholic steahepatitis?

A

Fatty change

Ballooned hepatocytes with Mallory Bodies

Inflammatory cells

Fibrosis in portal tracts

44
Q

What is non-alcohol fatty liver disease (NAFLD)?

A

Same pathological spectrum as alcoholic liver disease

  • Steatosis
  • steatohepatitis
  • cirrhosis
  • HCC
45
Q

What is NAFLD associated with?

A

Metabolic syndrome

  • obesity
  • type 2 diabetes
  • hyperlipidaemia
  • also some drugs

Commonest cause of liver disease.

46
Q

What is the pathogenesis of NAFLD?

A

Insulin resistance results from excess of calorie intake over the body’s demands.

Fat is stored in the body in various compartments including the liver - this depends on genetic factors.

If stored in the liver, this is seen as fatty liver or steatosis.

Long term, as a result of continuing excess calories, plus other factors, some people with steatosis develop steatohepatitis.

This is liver cell injury, inflammation and fibrosis due to liver cell stress, when the liver cell mitochondria start to be injured by the oxidative stress of too much energy transfer.

This evolves slowly and is reversible in the early stages – but if continuous for years results in cirrhosis.

The cirrhosis is eventually ‘cryptogenic’ because the microscopic features of fatty liver disease eventually disappear as the liver is completely re-modelled.

47
Q

What is the classification of drug-induced liver injury?

A

Intrinsic

  • predictable
  • anyone taking this drug is likely to get liver damage
  • e.g. paracetamol overdose

Idiosyncratic

  • rare and unpredictable
  • metabolic
  • immunological
  • e.g. amoxicillin
48
Q

What ratio is used to determine to classify acute liver injury into hepatic, cholecystatic or mixed?

A

Ratio of ALT:Alk phos
(x upper limit of normal)

> 5 hepatocellular (hepatitic)

49
Q

What are the simplified standardised criteria for DILI?

A
  1. Onset of abnormal LFTs after intake of drug
    - ‘suggestive’ 5-90 days
    - ‘compatible’ 90 days
  2. Improvement (50% reduction) in LFTs after stopping drug
    - ‘Very suggestive’
50
Q

What are the hitopathological features of intrinsic hepatotoxicity seen in paracetamol overdose?

A

Uniform zonal necrosis

No inflammation

Hepatocytes around the portal tracts are spared and able to regenerate the liver back to normal if the toxicity is not too severe and the patient survives

51
Q

What is the toxic metabolite of paracetamol?

A

N-acetyl-p-benzoquinone-imine (NAPQI)

52
Q

What is given to reverse paracetamol overdose?

A

N-acetyl cystein - restores Glutathione

53
Q

What is the definition of cirrhosis?

A

Defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.

Liver cells still present, but portal vein blood bypasses the sinusoids so the liver cells cannot perform their functions.

Pressure inside the liver increases, portal hypertension

54
Q

What are the causes of cirrhosis?

A

Alcohol

Non-alcoholic steatohepatitis (metabolic syndrome)

Chronic viral hepatitis – B, C

Autoimmune liver disease

  • autoimmune hepatitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis

Metabolic

  • iron
  • copper
  • alpha 1 antitrypsin
55
Q

What does cirrhosis convert to liver into?

A

A mass of regenerating nodules wrapped by fibrous scar tissue.

56
Q

What are the complications of cirrhosis?

A

Structural changes, fibrosis

  • Portal hypertension – see below
  • Increased blood flow, stiff liver
  • Pressure rises in portal vein
  • Oesophageal varices

Liver cell failure

  • fewer hepatocytes +/- blood bypasses sinusoids
  • Synthetic - oedema, bruising, muscle wasting
  • Detoxifying – drugs, hormones, encephalopathy,
  • Ascites – low albumin, portal hypertension, hormone fluid retention (aldosterone)

Excretion

  • Bile - jaundice
  • Bile salts – itching

Reticulo-endothelial cells
- Vulnerable to infection

57
Q

What is alpha 1 antitrypsin?

A

Alpha 1 antitrypsin

  • protein made in the liver excreted into blood
  • functions to neutralise proteolytic enzymes, particularly from active polymorphs.
58
Q

What is alpha 1 antitrypsin deficiency?

A

This inborn error of metabolism results in abnormal structure of A1AT

  • folds wrongly and can’t be excreted from hepatocytes.
  • there are many types, the commonest is PiZZ

The accumulated A1AT forms globules of glycoprotein
- stain positive with PAS diastase stain.

This damages liver cells

  • may lead to fibrosis and cirrhosis
  • very variable, sometimes in childhood, sometimes in adulthood.
59
Q

What other disease does alpha 1 antitrypsin deficiency play a part in?

A

The low levels of A1AT in the serum make the patient susceptible to emphysema of the lung, especially if the patient also smokes.

60
Q

What is haemochromatosis?

A
  • Relatively common abnormality of the HFE gene, the C282Y is the usual severe genotype.
  • Leads to a failure of iron absorption regulation, and excess iron is stored in various organs – including liver, pancreas, skin, joints, heart.
  • Patients have high serum levels of transferrin, and high transferrin saturation.
  • Large amounts of iron in hepatocytes cause liver injury and eventually cirrhosis and high risk of hepatocellular carcinoma.
61
Q

What stain is used in liver biopsies to detect haemochromatosis?

A

Perl’s stain

62
Q

What is the treatment for haemochromatosis?

A

Frequent venesection

63
Q

What is Wilson disease?

A

Too little caeruloplasmin – the copper transport protein in the blood. Copper accumulates in

  • liver: cirrhosis
  • eyes: Kayser-Fleischer rings
  • brain: ataxia, etc

Patients have low serum copper, high urinary copper (24 hour urine collection) and high levels of copper in the liver tissue.

Some patients present with acute liver failure and haemolysis. This is life threatening and an indication for super-urgent liver transplantation.

64
Q

What stain is used in biopsy to test for copper?

A

Rhodanine stain

65
Q

What is the treatment for Wilson disease?

A

Chelation

66
Q

What are the systemic effects of liver failure?

A

Ascites

Muscle wasting

Bruising

Gynaecomastia

Spider naevi
- small clusters of dilated capillary vessels in the skin due to hormone imbalance

Caput medusa
- dilated veins radiating around the umbilicus in patients with severe portal hypertension, due to recanalisation of the embryonic vitelline vein to the umbilicus.

67
Q

What is portal hypertension?

A

Increased pressure of blood in the portal veins (

68
Q

What are the main causes of hypertension?

A

Pre-sinusoidal

Sinusoidal

Post-sinusoidal

69
Q

What are the complications of portal hypertension?

A

Splenomegaly
- low platelets

Oesophageal varices
- haemorrhage

Piles

  • perianal
  • varices
  • most aren’t due to portal hypertension

Part of cause of ascites

70
Q

What is pre-sinusoidal portal hypertension?

A

Due to disease of the portal vein or its intrahepatic branches. The liver cell function is well preserved and the patient has problems from oesophageal varices and splenomegaly but not ascites. Pre-hepatic causes can be treated by a shunt procedure to decompress the portal vein into the hepatic vein.

71
Q

What is sinusoidal portal hypertension?

A

Due to disease within the liver parenchyma. This is the commonest cause, a result of any of the causes of cirrhosis. Because there is also liver cell insufficiency, the patients also have ascites, (low albumin, disturbed metabolism of aldosterone, fluid regulating hormone) – and so risk developing liver failure if they have a shunt procedure.

72
Q

What is post-sinusoidal portal hypertension?

A

The blood can’t flow out of the liver due to obstruction at a level between the intrahepatic branches of the hepatic veins (usually drug induced injury) and the right atrium (e.g. constrictive pericarditis). Budd Chiari syndrome (rare) is thrombosis of the hepatic vein, and is nearly always associated with an pro-coagulant clotting disorder. This causes ascites and an enlarged liver (hepatomegaly). It can usually be successfully treated by stenting the veins and anticoagulation.

73
Q

What is a major risk factor for hepatocellular carcinoma (HCC)?

A

Cirrhosis

70% malignant tumours in cirrhotic patients

74
Q

What percentage of HCC is found in non-cirrhotic patients?

A

2%

75
Q

What is the epidemiology of HCC?

A

Male»female

Increasing incidence in West – obesity, alcohol.

Geographical variation ++ depending on prevalence of viral hepatitis

76
Q

What are the clinical features of HCC?

A
  • worsening liver function

- weight loss

77
Q

What surveillance is performed in patients with cirrhosis?

A

6 monthly ultrasound scan

78
Q

What protein might be used to detect HCC?

A

Alpha feto-protein in serum.

  • raised in 75% but only 50% non-cirrhotic patients
79
Q

What is the macroscopic appearance of HCC?

A

Expansile soft nodules, often green (bile)

80
Q

What is the distribution of HCC?

A

Involvement of

  • Portal vein 60%
  • Hepatic vein 20%
  • Bile duct 5%
81
Q

What is the histopathological appearance of HCC?

A

Cancer cells look a bit like hepatocytes,

May produce bile = diagnostic

Confirm with immunohistochemistry

82
Q

What is the prognosis of HCC?

A

Very poor (

83
Q

What are the treatment options for HCC?

A

Surgery - if non-cirrhotic or small, peripheral

Transplant
- 1 tumour

84
Q

What are the TNM stages for HCC?

A

pT1
- Solitary tumour without vascular invasion

pT2
- Solitary tumour with vascular invasion or multiple tumours , none more than 5cm in greatest dimension

pT3a
- Multiple tumours, any more than 5cm

pT3b
- Single or multiple tumours of any size involving a major branch of the portal vein or hepatic vein.

pT4
- Tumour(s) with direct invasion of adjacent organs other than the gall bladder or with perforation of visceral peritoneum

85
Q

What are the early stages of HCC?

A

pT1 and pT2

86
Q

Which cancer metastasises to the liver and forms a few large nodules?

A

Large bowel

87
Q

Which five cancers form multinodular/infitrative metastases?

A

Lung

Pancreas

Breast

Stomach

Melanoma

88
Q

What is ‘the other primary liver cancer’?

A

Cholangiocarcinoma

- adenocacinoma arising in the bile ducts

89
Q

What are the two types of cholangiocarcinoma?

A

Intrahepatic

  • From small intrahepatic ducts
  • Peripheral, mass forming, presents late
  • Risk factor – none or cirrhosis
Perihilar
- From large ducts, 
- Causes obstructive jaundice early
- Risk factor: bile duct disease
primary sclerosing cholangitis
Liver flukes
90
Q

How much bile is excreted bile the liver per day?

A

0.5-1 litre per day

91
Q

Where is bile concentrated?

A

The gall bladder

92
Q

What is bile composed of?

A

bile salts

phospholipids

cholesterol

bilirubin

calcium salts

mucin from peribiliary glands

93
Q

What are gallstones?

A

When constituents precipitate.

10-20% adults in UK.

94
Q

What are the risk factors for gallstones?

A

Cholesterol stones
- yellow, opalescent

Pigment stones
- small black – in haemolytic anaemia

Mixed stones (most common)

10% contain calcium - visible on plain Xray

95
Q

What are the complications of gallstones?

A

Inflammation of the gallbladder (cholecystitis)

Mucocele

Predisposition to carcinoma of the gallbladder

Obstruction of the biliary system resulting in biliary colic and jaundice

Infection of static bile, causing cholangitis and liver abscesses

Gallstone ileus due to intestinal obstruction by a gallstone that has entered the gut through a fistulous connection with the gallbladder

Pancreatitis.

96
Q

What are the indications for a cholecystectomy?

A

Pain

Gallstones

Pancreatitis

Gall bladder polyp (rarely)

97
Q

What are the features of acute cholecystitis?

A

Duct blocked by stone.

Initially sterile, later infected.

Large, swollen, congested, ulcerated.

Complications – empyema, rupture

98
Q

What are the features of chronic cholecystitis?

A

Usually gall stones

Small, fibrotic, stones,

Fibrosis, Rokitansky Aschoff sinuses

99
Q

What percentage of gall bladder cancers are discovered during routine cholecystectomies?

A

50%

Clinical Pathology (65 decks)

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