Cirrhosis & its Consequences Flashcards Preview

Core Conditions - Abdominal > Cirrhosis & its Consequences > Flashcards

Flashcards in Cirrhosis & its Consequences Deck (76)
Loading flashcards...

What is cirrhosis?


What is the end result of this process?

it is a diffuse process that results from liver cell necrosis followed by fibrosis and nodule formation


the end result is impairment of liver cell function and gross distortion of the liver architecture, leading to portal hypertension


What is the most common cause of cirrhosis?

  • alcohol is the most common cause in the western world


  • viral hepatitis is the most common cause worldwide


What are the 3 most common causes of cirrhosis and what are non-invasive markers of aetiology?


  • history of excess alcohol consumption


Chronic hepatitis B:

  • HBsAg +/- HBeAg/DNA in serum


Chronic hepatitis C:

  • HCV antibodies and HCV RNA in serum


What are 4 other conditions that are commonly seen in clinical practice that can cause cirrhosis?


What are non-invasive markers of aetiology?


  • family history
  • raised serum ferritin + transferrin saturation


Non-alcoholic fatty liver disease:

  • features of the metabolic syndrome
  • hyperechoic liver on ultrasound


Primary biliary cirrhosis:

  • presence of serum antimitochondrial antibodies


Sclerosing cholangitis (primary & secondary):

  • most patients have IBD and serum pANCA
  • multifocal stricturing and dilatation of bile ducts on cholangiography (MRCP or ERCP)


What are non-invasive markers of aetiology for autoimmune hepatitis and cystic fibrosis, which can cause cirrhosis?

Autoimmune hepatitis:

  • circulating autoantibodies 
  • hypergammaglobulinaemia


Cystic fibrosis:

  • presence of extrahepatic manifestations of CF


What non-invasive markers of aetiology are present in Budd-Chiari syndrome, causing cirrhosis?

  • presence of known risk factors 


  • caudate lobe hypertrophy


  • abnormal flow in major hepatic veins on USS


What non-invasive markers of aetiology are present in Wilson's disease, leading to cirrhosis?

  • young age


  • reduced serum caeruloplasmin and total copper


  • increased 24-hour urinary copper excretion


  • Kayser-Fleisher rings 


What are non-invasive markers of aetiology in a1-antitrypsin (AAT) deficiency, leading to cirrhosis?

  • young age


  • associated emphysema


  • reduced serum AAT


What are the 2 different types of cirrhosis histologically?

  • micronodular cirrhosis


  • macronodular cirrhosis


  • there is a mixed picture, with both small and large nodules 


What is micronodular cirrhosis and when is this often seen?

  • characterised by uniform, small nodules up to 3mm in diameter


  • this is often caused by alcohol damage 


What is macronodular cirrhosis and what is this associated with?

  • this involves large nodules that are up to several centimetres in diameter


  • this often occurs following hepatitis B infection


What are the clinical features of cirrhosis a result of?

clinical features are secondary to portal hypertension and liver cell failure


What is the difference between compensated and uncompensated cirrhosis?

Uncompensated cirrhosis:

  • cirrhosis with the complications of encephalopathy, ascites or variceal haemorrhage


Compensated cirrhosis:

  • cirrhosis without any of these complications


Why are investigations carried out in cirrhosis?

  • to assess the severity of the liver disease


  • to identify the aetiology


  • to screen for complications 


What do liver biochemistry and liver function tests usually show in cirrhosis?

Liver biochemistry:

  • may be normal
  • in most people there is at least a slight elevation in serum alkaline phosphatase (ALP) and aminotransferase 


Liver function:

  • serum albumin is reduced
  • prothrombin time is prolonged 
  • these reflect reduced hepatic synthesis


What will serum electrolytes show in cirrhosis?

  • low sodium concentration indicates severe liver disease secondary to either impaired free water clearance or excess diuretic therapy


What is serum a-fetoprotein (AFP) and why is this test performed?

  • usually undetectable after foetal life, but raised levels may occur in chronic liver disease


  • measured to screen for complications of hepatocellular carcinoma (HCC)


  • normal range is 10-20 ng/mL


  • a level > 400 ng/mL is regarded as diagnostic of HCC


How is the aetiology of cirrhosis confirmed?

the cause is determined by the history combined with laboratory investigations


a liver biopsy is performed to confirm the severity and type of liver disease


What further investigations may be carried out in cirrhosis?

  • oesophageal varices are sought with endoscopy


  • USS is useful for detection of hepatocellular carcinoma (HCC)


  • USS is used to assess the patency of the portal and hepatic veins 



What is involved in the management of cirrhosis?


How are the underlying causes commonly corrected?

  • cirrhosis is irreversible, so treatment is aimed at treating the complications seen in decompensated cirrhosis as they arise


  • venesection is used to correct haemochromatosis


  • abstinence from alcohol is used to correct alcoholic hepatitis


  • correcting the underlying cause may halt the progression of liver disease


What 5 variables are used to grade the severity and prognosis of liver disease?


What is 5-year survival like?

  • encephalopathy


  • ascites


  • prothrombin time


  • serum bilirubin


  • serum albumin


  • overall the 5-year survival rate without transplantation is 50%


What are the 7 most common complications of cirrhosis?

  • portal hypertension and variceal haemorrhage


  • ascites
    • this can become infected ascites (spontaneous bacterial peritonitis)


  • portosystemic encephalopathy


  • acute renal failure (hepatorenal syndrome)


  • hepatocellular carcinoma (HCC)


  • malnutrition


  • osteoporosis


What is the role of the portal vein?



  • it carries blood from the gut and the spleen to the liver


  • it accounts for 75% of hepatic vascular inflow
    • the other 25% comes from the hepatic artery


How does blood enter and leave the liver?

  • blood enters the liver via the hepatic artery and the portal vein


  • these blood vessels enter the liver via the hilum (porta hepatis)


  • blood passes into the hepatic sinusoids via the portal tracts 


  • blood leaves the liver via the hepatic veins, which join the inferior vena cava


  • the vena cava returns blood to the right side of the heart


What is normal portal pressure?


What happens in portal hypertension?

  • normal portal pressure is 8 - 10 mmHg


  • portal hypertension occurs when there is an increase in pressure within the portal vein and its branches


  • these are draining blood from the intestines, stomach, pancreas etc. to the liver 


What happens when the inflow of portal blood to the liver is obstructed?


What site is the most significant for collateral formation?

  • the inflow of portal blood to the liver can be partially or completely obstructed at a number of sites


  • this leads to high blood pressure proximal to the obstruction and the diversion of blood into portosystemic collaterals


  • the most important site for collateral formation is at the gastro-oesophageal junction (varices)


  • here the collaterals are superficial and liable to rupture, causing massive gastrointestinal haemorrhage 


What are the 3 main sites of obstruction to the inflow of portal blood to the liver?


  • obstruction of the portal vein before it reaches the liver



  • this results from distortion of the liver architecture



  • this results from obstruction of the hepatic veins


What is the main prehepatic cause of portal hypertension?

portal vein thrombosis


What are the main causes of intrahepatic portal hypertension?

  • cirrhosis


  • alcoholic hepatitis


  • idiopathic non-cirrhotic portal hypertension


  • schistosomiasis