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Medicine Gastrointestinal > Liver Pathology > Flashcards

Liver Pathology Flashcards

1
Q

Pathogenesis of liver disease

A

Insult to hepatocytes → grading (degree of inflammation) → staging (degree of fibrosis) → cirrhosis

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2
Q

Causes of acute liver failure

A

Viruses, alcohol, drugs, bile duct obstruction

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3
Q

Outcomes of acute liver failure

A

Complete recovery, chronic liver disease, death

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4
Q

What is jaundice?

A

Yellowing of the skin due to bilirubin

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5
Q

Pre-hepatic jaundice:

  • Why does it occur?
  • Examples of causes
  • Is bilirubin conjugated or unconjugated?
A
  • When there is too much haem to break down
  • Haemolytic anaemia
  • Unconjugated bilirubin
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6
Q

Hepatic jaundice:

  • Why does it occur?
  • Examples of causes
  • Is bilirubin conjugated or unconjugated?
A
  • When liver cells are injured or dead
  • Pregnancy, acute liver failure, alcoholic hepatitis, cirrhosis, bile duct loss
  • Both unconjugated and conjugated bilirubin
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7
Q

Post-hepatic jaundice:

  • Why does it occur?
  • Examples of causes
  • Is bilirubin conjugated or unconjugated?
A
  • Bile cannot escape the bowel
  • Congenital biliary atresia, gallstones in common bile duct, strictures of common bile duct, tumours
  • Conjucated
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8
Q

What is liver cirrhosis defined by?

A

Bands of fibrosis separating regenerative nodules of hepatocytes

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9
Q

2 types of liver cirrhosis

A

Macronodular and micronodular

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10
Q

Causes of liver cirrhosis

A

Alcohol, gallstones, hepatitis B and C, iron overload, autoimmune liver disease

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11
Q

Complications of liver cirrhosis

A

Portal hypertension, ascites, liver failure

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12
Q

Clinical features of chronic liver disease

A

Oedema, ascites, haematemesis, gynaecomastia, spider naevi, purpura and bleeding, coma, infection

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13
Q

What causes oedema in chronic liver disease?

A

Hypoalbuminaemia

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14
Q

What causes ascites in chronic liver disease?

A

Hypoalbuminaemia, secondary hypoaldosteronism, portal hypertension

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15
Q

What causes haematemesis in chronic liver disease?

A

Ruptured oesophageal varices due to portal hypertension

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16
Q

What causes gynaecomastia in chronic liver disease?

A

Hyperoestrogenism

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17
Q

What causes spider naevi in chronic liver disease?

A

Hyperoestrogenism

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18
Q

What causes purpura and bleeding in chronic liver disease?

A

Reduced clotting factor synthesis

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19
Q

What causes coma in chronic liver disease?

A

Failure to eliminate toxic gut bacterial metabolites

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20
Q

What causes infection in chronic liver disease?

A

Reduced Kupffer cells and numbers

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21
Q

Pathogenesis of alcoholic liver disease

A

o Increased peripheral release of fatty acids and increased synthesis of fatty acids within liver cells
o Acetaldehyde, a product of alcohol metabolism, is probably responsible for liver cell injury, manifested by the formation of Mallory’s hyaline
o There is increased collagen synthesis by fibroblasts and by the perisinusoidal cells of Ito

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22
Q

Duration of liver disease and alcoholic liver disease:

  • 2-3 days
  • 4-6 weeks
  • Months-years
  • Years
A

2-3 days → fatty liver → reversible
4-6 weeks → hepatitis → reversible
Months-years → fibrosis → irreversible
Years → cirrhosis → irreversible

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23
Q

Weekend binge drinking:

  • Pathology in hepatocytes
  • Outcome
  • Differential diagnoses
A
  • Fat vacuoles in hepatocytes
  • Reversible outcome
  • NASH, pregnancy, drugs, nutritional, diabetes, hepatitis C
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24
Q

Heavy drinking for weeks to months:

  • Histological features
  • Outcome
A
  • Hepatocyte necrosis, neutrophils, mallory bodies, pericellular fibrosis
  • Reversible if drinking stops
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25
Q

Heavy drinking for months to years:

  • Histological features
  • Outcome
A
  • Collagen is laid down around cells, bands of fibrosis separating regenerative nodules
  • Irreversible
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26
Q

Outcomes for alcoholic liver disease

A

Cirrhosis, portal hypertension, varices, ascites, malnutrition, hepatocellular carcinoma

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27
Q

Non-alcoholic steatohepatitis:

  • Which patients does it occur in?
  • What can it lead to?
A
  • Non drinkers, diabetes, obesity, hyperlipidaemia

- Fibrosis and cirrhosis

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28
Q

Viruses that can cause:

  • Hepatitis A
  • Hepatitis B
  • Hepatitis C
  • Hepatitis D
A
  • Hepatitis A = Epstein Barr virus
  • Hepatitis B = yellow fever virus
  • Hepatitis C = herpes simplex virus
  • Hepatitis D = cytomegalovirus
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29
Q

Hepatitis A:

  • Spread
  • Incubation period
  • Is there a carrier state?
  • Outcome
A
  • Faecal-oral spread
  • Short incubation period
  • No carrier state
  • Mild illness with usually full recovery
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30
Q

Hepatitis B:

  • Spread
  • Incubation period
  • How does it cause liver disease?
  • Is there a carrier state?
  • Outcomes
A
  • Spread by blood, blood products, sexually, vertically
  • Long incubation period
  • Causes liver disease by antiviral immune response
  • Carriers exist
  • Death, chronic hepatitis, cirrhosis, hepatocellular carcinoma, asymptomatic
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31
Q

Hepatitis C:

  • Spread
  • Incubation period
  • Outcomes
A
  • Blood, blood products
  • Short incubation period
  • Chronic hepatitis, cirrhosis
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32
Q

Aetiology of chronic hepatitis

A

Hepatitis B, hepatitis C, primary biliary cirrhosis, autoimmune hepatitis, drug induced hepatitis, primary sclerosing cholangitis

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33
Q

Primary biliary cirrhosis:

  • What is it caused by?
  • More common in males or females?
  • Outcome
A
  • Autoimmune disease associated with autoantibodies to mitochondria
  • Females (90%)
  • Bile duct loss leads to cholestasis, liver injury, inflammation, fibrosis and cirrhosis
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34
Q

Autoimmune hepatitis:

  • More common in males or females?
  • Which cells are numerous?
  • What are autoantibodies to?
A
  • Females
  • Plasma cells are numerous
  • Autoantibodies to smooth muscle, nuclear or LKM, raised IgG
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35
Q

Primary sclerosing cholangitis:

  • What is it?
  • What can it lead to?
  • What disease is it associated with?
  • Which gender is it more common in?
  • What does histological staining show?
A
  • Chronic inflammatory process affecting intra- and extra-hepatic bile ducts
  • Leads to periductnal fibrosis, duct destruction, jaundice and fibrosis
  • Ulcerative colitis
  • Femakes
  • Periductnal onion-skinning fibrosis
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36
Q

Haemochromatosis:

  • What is it?
  • Primary causes
  • Secondary causes
A
  • Excess of iron in the liver
  • Genetic condition, increased absorption of iron
  • Iron overload from diet, transfusions, iron therapy
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37
Q

Is primary haemochromatosis autosomal dominant or recessive?

A

Recessive

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38
Q

Where in the liver does iron accumulate?

A

Hepatocytes

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39
Q

Which staining is used to confirm iron?

A

Perls staining

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40
Q

Wilson’s disease:

  • What is it?
  • Where does copper accumulate?
  • Signs
  • What can it cause?
A
  • Inherited autosomal recessive disorder of copper metabolism
  • Liver and brain
  • Kayser-Fleischer rings at corneal limbus and low serum caeruloplasmin
  • Chronic hepatitis and neurological deteriorateion
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41
Q

Alpha-1-antitrypsin deficiency:

  • What is it?
  • What does it cause?
A
  • Inherited autosomal recessive disorder of an enzyme inhibitor
  • Empyema, cirrhosis
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42
Q

Primary tumours of the liver

A

Hepatocellular adenoma, hepatocellular carcinoma

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43
Q

Where can liver cancer metastasise from?

A

Colon, pancreas, breast, lung, etc

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44
Q

Hepatocellular carcinoma:

  • What is it associated with?
  • How does it present?
A
  • HBV, HCV, cirrhosis

- Mass, pain, obstruction

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45
Q

What is acute liver disease?

A

The rapid development of hepatic dysfunction without prior liver disease

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46
Q

Functions of the liver

A
  • Protein metabolism
  • Carbohydrate metabolism
  • Lipid metabolism
  • Bile acid metabolism
  • Bilirubin metabolism
  • Hormone and drug metabolism
  • Immunological defence
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47
Q

Liver function tests

A

ALT/AST, Alk phos, GGT, bilirubin, albumin, prothrombin time

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48
Q

Duration of acute liver disease

A

<6 months duration

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49
Q

Acute liver failure

A

Causing encephalopathy and prolonged coagulation

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50
Q

Clinical features of acute liver disease

A

Jaundice, lethargy, nausea, anorexia, pain, itch, arthralgia, abnormal liver function tests

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51
Q

Causes of acute liver disease

A

Viral A, B, C, D, E, CMV, EBV, drugs, shock to liver, cholangitis, alcohol, malignancy, chronic liver disease, overuse of paracetamol, Budd Chiari, acute fatty liver or cholestasis of pregnancy

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52
Q

Investigations for acute liver disease

A

LFTs incl. albumin and bilirubin, prothrombin time, US, virology

53
Q

Treatment of acute liver disease

A

Rest (3-6 months), fluids, no alcohol, sodium bicarbonate bath for itch, cholestyramine for itch, ursodeoxycholic acid for itch, observation for fulminant hepatic failure

54
Q

Antibiotics that can cause liver injury

A

Co-amoxiclav, flucloxacillin, NSAID

55
Q

Fulminant hepatic failure:

- What is it?

A

Acute episodes of severe liver dysfunction (jaundice and encephalopathy) in a patient with a previously normal liver

56
Q

Causes of fulminant hepatic failure

A

Paracetamol, viral, drugs, HBV, mushrooms, malignancy, Wilson’s, Budd Chiari

57
Q

Clinical cause and complications of fulminant hepatic failure

A
  • Encephalopathy
  • Hypoglycaemia
  • Coagulopathy
  • Circulatory failure
  • Renal failure
  • Infection
58
Q

Treatment for fulminant hepatic failure

A

Supportive, inotropes and fluids, renal replacement, management of raised ICP, liver transplant

59
Q

What is chronic liver disease?

A

Liver disease of a duration > 6 months

60
Q

Pathology in chronic liver disease

A

Recurrent inflammation and repair with fibrosis of the liver and regeneration of hepatocytes

61
Q

Outcome of chronic liver disease

A

Progression to cirrhosis

62
Q

Causes of chronic liver disease

A

Alcohol, NAFLD, hepatitis C, primary biliary cholangitis, autoimmune hepatitis, hepatitis B, haemochromatosis, primary sclerosing cholangitis, Wilson’s disease, alpha-1 anti-trypsin, Budd Chiari, drugs

63
Q

How much of the population have non alcoholic fatty liver disease?

A

20-30%

64
Q

How much of the population with NAFLD have non-alcoholic steatohepatitis?

A

20-30%

65
Q

Spectrum of pathology in non-alcoholic steatohepatitis

A

Steatosis → steatohepatitis → steatohepatitis with fibrosis → cirrhosis

66
Q

Steatohepatitis:

  • What is it?
  • Describe inflammation
  • Describe hepatocyte degeneration
  • Describe fibrosis
A
  • Inflammation and concurrent fat accumulation of the liver
  • Usually mild, lobular and mixed mononuclear and neutrophilic infiltrate
  • Mallory bodies and ballooning
  • Initially pericellular fibrosis, later bridging
67
Q

Metabolic risk factors for non-alcoholic fatty liver disease

A

Type II diabetes, obesity, HDL cholesterol <40mg/dL in men and <50mg/dL in women, hypertension, triglycerides ≥150mg/dL

68
Q

Diagnosis of simple steatosis

A

Ultrasound

69
Q

Treatment for simple steatosis

A

Weight loss and exercise

70
Q

Diagnosis of non-alcoholic steatohepatitis

A

Liver biopsy

71
Q

Treatment for non-alcoholic steatohepatitis

A

Weight loss and exercise and other treatments are experimental

72
Q

Examples of autoimmune liver diseases

A

Primary biliary cholangitis, primary sclerosing cholangitis, autoimmune hepatitis

73
Q

Primary biliary cholangitis - which cell mediates it?

A

T-cell, CD4 cells reactive to M2 target

74
Q

Symptoms of primary biliary cholangitis

A

Itch without rash, fatigue, xanthelasma and xanthomas

75
Q

Diagnosis of primary biliary cholangitis

A

2 of 3:

  • Positive AMA (antimitochondrial antibodies)
  • Cholestatic LFTs (alkaline phosphate and gamma GT are elevated more than ALT)
  • Liver biopsy
76
Q

Treatment for primary biliary cholangitis

A

Urseo-deoxycholic acid (first line), obeticholic acid

77
Q

How does urseo-dexycholic acid work?

A

Causes increased flow of bile from the liver and washes toxic bile salts out

78
Q

Type I immunology in autoimmune hepatitis:

  • When does it present?
  • Which antibodies are associated?
  • Which antigen is associated?
A
  • Presents in adult, commonly affecting teenage girls and adults
  • ANA antibody, ASMA antibody
  • Soluble liver antigen
79
Q

Type II immunology in autoimmune hepatitis:

  • When does it present?
  • Which antibodies are associated?
A
  • Children and young adults

- Liver-kidney-microsomal-1 antibody, AMA may also be present

80
Q

Clinical presentation of autoimmune hepatitis

A

Jaundice, general fatigue, elevated AST and ALT, elevated PT, malaise, nausea, abdominal pain, anorexia

81
Q

Diagnosis of autoimmune hepatitis

A

Elevated AST and ALT, elevated IgG, rule out other causes, presence of autoimmune antibodies, liver biopsy

82
Q

Genetic predisposing factors to autoimmune hepatitis

A

HLA-DR3 (severe form), HLA-DR4

83
Q

Drugs associated with autoimmune hepatitis

A
  • Oxyphenisatin, Methyldopa, Nitrofurantoin, Diclofenac, Minocycline, Statins
84
Q

Combination therapy for treatment of autoimmune hepatitis

A

Prednisolone (30g daily then taper down to 15mg at week 4 then maintain on 5mg daily) + azothioprine (50-100mg daily)

85
Q

Primary sclerosing cholangitis:

  • What is it?
  • Clinical presentation
  • Diagnosis
  • Treatment
A
  • Autoimmune destructive disease of large and medium sized bile ducts
  • Recurrent cholangitis
  • Imaging of biliary tree
  • Maintain bile flow, monitor for cholangiocarcinoma and colorectal cancer
86
Q

Treatment for haemochromatosis

A

Venesection weekly or 2 weekly

87
Q

Clinical presentation of Wilson’s disease?

A

Chorea-athetoid movements, cirrhosis or sub-fulminant liver failure, Kaiser Fleischer rings

88
Q

Treatment for Wilson’s disease

A

Copper chelation drugs

89
Q

Clinical presentation of alpha-1 anti-trypsin deficiency

A

Lung emphysema (exacerbation by smoking), liver disposition of mutant protein, cell damage

90
Q

Treatment for alpha 1 anti-trypsin deficiency

A

Supportive management

91
Q

Where is the genetic mutation in alpha 1 anti-trypsin deficiency?

A

A1AT gene

92
Q

Budd Chiari:

  • What is it?
  • Clinical presentation
  • Diagnosis
  • Mangement
A
  • Thrombosis of the hepatic veins
  • Acute - jaundice, tender hepatomegaly, chronic - ascites
  • Ultrasound of hepatic veins
  • Recanilisation or TIPS
93
Q

Most common liver tumour

A

Haemangioma

94
Q

What is haemangioma?

A

Hypervascular tumour that is usually a single, small, well demarcated capsule

95
Q

Diagnosis of haemangioma

A

Ultrasound - echogenic spot, well demarcated
CT - venous enhancement from periphery to centre
MRI - high intensity area

96
Q

Focal nodal hyperplasia:

- What is it?

A

Benign nodule formation of normal liver tissue. Classically, but not always, central scar containing a large artery, radiating branches to the periphery

97
Q

Histology of focal nodal hyperplasia

A

Sinusoids, bile ductules and Kupffer cells

98
Q

Diagnosis of focal nodal hyperplasia

A

Ultrasound - nodule with varying echogenicity
CT - hypervascular mass with central scar
MRI - iso or hypo intense
FNA - normal hepatocytes and Kupffer cells with central core

99
Q

What is hepatic adenoma?

A

Benign neoplasm composed of normal hepatocytes, no portal tract, central veins or bile ducts

100
Q

What medication is hepatic adenoma associated with?

A

Contraceptive hormones and anabolic steroids

101
Q

Presentation of hepatic adenoma

A

Usually asymptomatic, RUQ pain, may present with rupture, haemorrhage or malignant transformation

102
Q

Where in the liver are hepatic adenomas most commonly found?

A

Right lobe

103
Q

Symptoms of hepatic adenoma

A

Pain, bleeding. Size related

104
Q

Diagnosis of hepatic adenoma

A

Ultrasound - filling defect
CT - diffuse arterial enhancement
MRI - hypo or hyper intense lesion
FNA may be needed

105
Q

Treatment for hepatic adenoma

A

Stop hormones, weight loss, for males: surgical excision, for females: imaging after 6 months - <5cm or reducing in size annual MRI, >5cm or increasing in size surgical excision

106
Q

Simple cyst

A

Liquid collection lined by epithelium

107
Q

What are symptoms of simple cyst related to?

A

Intracystic haemorrhage, infection, rupture, compression

108
Q

Hydatid cyst:

  • What is it caused from?
  • Management
A
  • Echinococcus granulosus

- Surgery, albendazole, percutaneous drainage

109
Q

Polycystic liver disease:

  • What is it?
  • What does it result in?
  • 3 types
A
  • Embryonic ductal plate malformation of the intrahepatic biliary tree
  • Results in numerous cysts throughout liver parenchyma
  • Von Meyenburg complexes, polycystic liver disease, autosomal dominant polycistic kidney disease
110
Q

Another name for Von Meyenburg complexes

A

Microhamartomas

111
Q

Symptoms of polycystic liver disease

A

Asymptomatic, abdominal pain, abdominal distension, atypical symptoms due to voluminous cysts resulting in compression of adjacent tissue or failure of the affected organ

112
Q

Management of polycystic liver disease

A

Care of symptoms, conservative treatment to halt cyst growth, somatostatin analogues, surgery in selective patient group with PCLD, ADPKD or liver failure

113
Q

Clinical features of liver abscess

A

High fever, leucocytosis, abdominal pain, complex liver lesion, history of abdominal or biliary infection or dental procedure

114
Q

Management of liver abscess

A

Broad spectrum antibiotics, aspiration/drainage percutaneously, echocardiogram, operation if no clinical improvement

115
Q

Hepatocellular carcinoma:

  • Risk factors
  • Clinical features
  • On examination
A
  • Cirrhosis of any cause (alcohol, hepatitis B/C, aflatoxin)
  • Weight loss and RUQ pain, asymptomatic, worsening of pre-existing chronic liver disease, acute liver failure
  • Signs of cirrhosis, hard enlarged RUQ mass, liver bruit (rare)
116
Q

Where can hepatocellular carcinoma metastasise to?

A

Rest of liver, portal vein, lymph nodes, lung, bone, brain

117
Q

What value of AFP is highly suggestive of hepatocellualr carcinoma?

A

> 100mg/L

118
Q

Diagnosis of hepatocellular carcinoma

A

Clinical presentation, elevated AFP, ultrasound, triphasic CT scan, MRI, biopsy

119
Q

What does prognosis with hepatocellular carcinoma depend on?

A

Tumour size, extrahepatic spread, underlying liver disease, patient performance status

120
Q

Best available treatment for hepatocellular carcinoma

A

Liver transplant

121
Q

When is liver transplant for hepatocellular carcinoma given?

A

Single tumour <5cm or less than 3 tumours less than 3cm each

122
Q

When is resection feasible for hepatocellular carcinoma?

A

Small tumours with preserved liver function. No jaundice or portal hypertension

123
Q

In which patients is local ablation given as treatment for hepatocellular carcinoma?

A

When resection is not feasible, patient with advanced liver cirrhosis

124
Q

Process of chemoembolisation in hepatocellular carcinoma

A

Transarterial chemoembolisation, chemotherapy is selectively injected into hepatic artery, then an embolic agent is injected

125
Q

Which patients can receive chemoembolisation as treatment for hepatocellualr carcinoma?

A

Those with early cirrhosis

126
Q

Systemic therapy for hepatocellular carcinoma:

  • Name of drug
  • What does it do?
A
  • Sorafenib

- Multikinase inhibitor of vascular endothelial gf receptor

127
Q

Fibro-lamellar carcinoma:

  • When does it present?
  • AFP
  • CT
  • Management
A
  • Young patients (5-35 years old)
  • Normal AFP
  • CT shows stellate star with radial septa showing persistent enhancement
  • Surgical resection or transplantation, transarterial chemoebolism if unresectable
128
Q

Diagnosis of metastases to the lvier

A

Imaging or fine needle aspiration

Medicine Gastrointestinal (24 decks)

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