Liver neoplasms and chronic liver disease Flashcards

1
Q

What are the common primary sites for metastatic tumour to the liver?

A
  • 90% of liver tumours are secondary metastases
  • The primary sites are commonly the:
    • Lung
    • Stomach
    • Colon
    • Breast
    • Uterus
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2
Q

List risk factors/causes for the development of primary hepatocellular carcinoma

A

Hepatocellular carcinoma is the most common malignant tumour worldwide - Common in China/sub-saharan africa although rare in west

  • Causes:
    • Chronic hepatitis
    • Cirrhosis
    • Metabolic liver diseases
    • Aspergillus alfatoxin
    • Parasites
    • Anabolic steroids
    • Greater risk in males
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3
Q

Define cirrhosis

Give its key characteristics

A

Cirrhosis of the liver is an irreversible consequence of chronic hepatic injury, and has 3 key characteristics:

  1. Destruction of liver cells
  2. Associated chronic inflammation, stimulating fibrosis
  3. Regeneration of hepatocytes to form nodules
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4
Q

Describe the pathology of cirrhosis of the liver

(What happens to cells in the liver?)

A
  • Fibrosis is due to growth factors released from inflammatory cells, Kupffer cells and hepatocytes
  • The inflammatory cells may be due to the disease process itself (hepatitis), or recruited in response to liver cell necrosis (chronic alcoholism)
  • Stellate cels are activated to form myofibroblasts and secrete collagen, and nodules form due to the natural capacity of heptocytes to divide and regenerate in response to damage, but these nodules lack normal vascular and bile drainage connections
  • Micronodular cirrhosis (nodules <3mm) occurs as a result of alcoholic liver damage or biliary tract disease
  • Macronodular cirrhosis (nodules >3mm) occurs due to previous hepatitis
  • Biliary cirrhosis is less common (fibrosis centred around intrahepatic bile ducts), and can be primary biliary cirrhosis or secondary (primary sclerosing cholangitis)
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5
Q

What are the common causes of cirrhosis of the liver?

A
  • Alcholic liver disease
  • Cryptogenic liver disease (no cause found on investigation)
  • Non-alcoholic fatty liver disease (NAFLD)
  • Chronic viral hepatitis
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6
Q

What initial investigations would you do for a patient with suspected cirrhosis?

A

History & abdominal examination

Bloods to determine severity of disease:

  • Liver function: albumin & INR are the best indicators
  • Liver damage: LFTs (ALT & AST enzymes)
  • Complications: U&Es/ABG (hepatorenal/hepatopulmonary syndrome)

Liver screen to determine type of disease:

  • Viral serology, serum antibodies/Immunogloblins, AFP, iron studies, serum copper, aplha1-antitrypsin level

Imaging to determine type of disease:

  • Ultrasound & duplex:
    • Liver can be shrunken or enlarged
    • Splenomegaly may be present
    • Portal system flow may be reversed
    • Can also show focal lesions or portal vein thrombosis
  • Endoscopy:
    • Detection and treatment of suspected varices, should be undertaken in anyone with suspected cirrhosis
  • CT/MRI if indicated

Further investigations: Ascitic tap (for MCS if infection suspected), Liver biopsy (to confirm severity and type of liver disease)

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7
Q

Describe the classic history of chronic liver disease?

A
  • Fatigue
  • Weight loss/anorexia
    • Due to early satiety with hepatomegaly
    • Patient often may notice central ‘weight gain’ of ascites
  • Jaundice
  • Leg swelling
    • Due to: Increased intra-abdominal pressure & low oncotic pressure
  • Bleeding/bruising
    • Due to decreased synthetic function
  • Itching
    • Due to bile salt accumulation in peripheral nerves
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8
Q

What are signs of chronic liver disease seen on abdominal examination?

A
  • Nails:
    • Leuconychia due to low albumin
    • Clubbing
  • Hands:
    • Palmar erythema
    • Duyputren’s contracture
    • Liver flap
  • Skin
    • Pigmentation
    • Spider naevi
    • Striae
  • Feminization - due to hyperaldosteronism
    • Gynaecomastia
    • Testicular atrophy
    • Loss of body hair
  • Signs of portal hypertension
    • Caput medusae
    • Heprosplenomegaly
    • Ascites
  • Signs of hepatocellular failure
    • Bruising
    • Prolonged clotting
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9
Q

Why to the underlying clinical features of cirrhosis such as hypoproteinanaemia, abnormal clotting, secondary hyperaldosteronism and portal hypertension occur?

A

Hypoproteinanaemia:

  • Damage to hepatocytes results in reduced albumin synthesis (the major protein in blood)

Abnormal clotting:

  • The liver is responsible for production of vitamin K dependent clotting factors (also factor 5)

Secondary hyperaldosteronism

  • The liver is responsible for metabolism (degradation) of steroids, importantly aldosterone and oestrogen, which accumulate in chronic liver disease
  • Also due to activation of the RAAS because hypoalbuminaemia leads to a lower circulating volume

Portal hypertension

  • Damage to liver architecture results in disturbed blood flow through the liver, and portal hypertension
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10
Q

What are the complications of chronic liver disease?

A
  • Hepatocellular failure
  • Portal hypertension
  • Malignant change
  • Renal Failure (hepatorenal syndrome)
  • Respiratory failure (hepatopulmonary syndrome)
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11
Q

What are the complications of cirrhosis and portal hypertension that may occur?

A

Patients with portal hypertension are often asympotmatic, or just show hepatosplenomegaly

Complications that may occur:

  • Ruptured gastro-oesophageal varices
  • Ascites
  • Encephalopathy
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12
Q

Explain what the following complications of cirrhosis and portal hypertension are

  1. Ruptured gastro-oesophageal varices
  2. Ascites
  3. Encephalopathy
A
  1. Ruptured gastro-oesophageal varices
  • Gasto-oesophageal varices are extremely dilated sub-mucosal veins in the lower third of the esophagus or stomach
  • The gastro-oesophageal varies develop due to the cirrhosis (90% of cirrhosis pts get them)
  • 1/3 of patient with gasto-oesophageal varies will suffer a bleed
  1. Ascites
  • Fluid in the peritoneal cavity, which can accumulate slowly or rapidly
  • Mild abdominal pain is common
  1. Encephalopathy
  • Caused by nitrogenous waste building up in the circulation, leading to cerebral oedema when astrocytes attempt to clear it
    • Grade I: Altered mood/behaviour, sleep disturbances
    • Grade II: Increasing drowsiness and confusion
    • Grade III: Stupor (state of near-unconsciousness), incoherence, restlessness
    • Grade IV: Coma
      *
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