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B - non-alcoholic steatohepatitis


  • she has type II diabetes, is obese and consumes alcohol regularly
    • these are all risk factors


  • simvastatin can be hepatotoxic, but she has only been taking this for 2 years so it is unlikely 


A - full recovery


  • HBsAg shows that they have a current infection 
    • this could be acute or chronic


  • Anti-HBcAg IgM (IgM core antibody) shows that they must currently have an acute infection


  • someone with an acute hep b infection is most likely to make a full recovery


D - IV cefotaxmine and oral lactulose


  • the patient has encephalopathy


  • they also have spontaneous bacterial peritonitis 
    • fever
    • worsening abdominal tenderness / distenstion
    • high neutrophil count


  • IV cefotaxime is an antibiotic that will treat the SBP


  • lactulose reduces ammonia production in the gut to prevent encephalopathy from getting worse 


What is the underlying cause of jaundice?

it is caused by an increased concentration of bilirubin in the blood




What are the steps involved in the bilirubin metabolism pathway?

  • old RBCs are broken down in the spleen 


  • the haemoglobin from RBCs produces iron and unconjugated bilirubin


  • the unconjugated bilirubin travels in the blood, bound to albumin, to the liver


  • in the liver it is conjugated by UDPGT enzyme


  • conjugated bilirubin then enters the biliary system and forms part of the bile


  • conjugated bilirubin enters the duodenum in the bile via the common bile duct


  • here it is converted to urobilinogen and stercobilinogen
    • urobilinogen is excreted in the urine
    • stercobilinogen is excreted in the faeces and gives them a dark colour


What causes pre-hepatic jaundice?


What type of hyperbilirubinaemia is present?

  • caused by excessive RBC breakdown 
    • or impaired uptake of RBCs by the liver 


  • this overwhelms the liver's ability to conjugate bilirubin


  • there is an unconjugated hyperbilirubinaemia


  • any bilirubin that is conjugated will be excreted normally, but the excess unconjugated bilirubin will remain in the bloodstream to cause jaundice 


What are the 2 major causes of pre-hepatic jaundice?


Why do these lead to jaundice?


  • increased RBC breakdown leads to an increase in unconjugated bilirubin concentration


  • the liver cannot conjugate the bilirubin fast enough, leading to an increase in unconjugated bilirubin in the blood
    • there is nothing wrong with the liver, there is just a massive excess of bilirubin


Gilbert's Syndrome:

  • this is a deficiency of the UDPGT enzyme


  • UDPGT enzyme is not working as well as it would in a healthy person, so when this individual becomes stressed / gets an infection they can appear jaundiced


What causes hepatocellular (intrahepatic) jaundice?


What type of hyperbilirubinaemia is produced here?

  • caused by dysfunction of the hepatic cells


  • the liver loses some of its ability to conjugate bilirubin, however this is not the main problem


  • if the liver becomes cirrhotic, it compresses the intra-hepatic portions of the biliary tree to cause a degree of obstruction
    • the conjugated bilirubin cannot get into the biliary system


  • this produces a mixed conjugated and unconjugated hyperbilirubinaemia
    • it is mainly conjugated hyperbilirubinaemia


What are the main causes of hepatocellular jaundice?

Caused by anything that damages the hepatocytes:


  • alcoholic liver disease / cirrhosis 


  • hepatitis
    • viral, autoimmune


  • hepatocellular carcinoma / liver mass


  • haemochromatosis


  • iatrogenic e.g. medication


What causes post-hepatic jaundice?


What type of hyperbilirubinaemia is produced?

  • this is jaundice caused by obstruction of biliary drainage 


  • the liver is still functioning and conjugating bilirubin as normal


  • the conjugated bilirubin cannot get into the duodenum, so it enters the bloodstream instead


  • this produces a conjugated hyperbilirubinaemia 


How can the causes of post-hepatic jaundice be divided into 3 categories? 

Intra-luminal causes:

  • gallstones 


Mural causes:

  • strictures 
  • cholangiocarcinoma
  • drug-induced cholestasis
  • PSC / PBS


Extra-mural causes:

  • pancreatic cancer
  • abdominal masses (e.g. lymphomas)


How can looking at the urine determine what kind of hyperbilirubinaemia might be present?

  • conjugated bilirubin is water soluble and so can be excreted in the urine


  • unconjugated bilirubin cannot be excreted in the urine


  • dark ("coca-cola") urine occurs in conjugated or mixed hyperbilirubinaemia
    • hepatocellular or post-hepatic jaundice


  • normal urine is seen in unconjugated hyperbilirubinaemia
    • pre-hepatic jaundice 


In what type of jaundice do the stools appear different?


Why does this occur?

  • in post-hepatic jaundice the stools will appear paler


  • this occurs when there is an obstructive picture as there are reduced levels of stercobilin entering the GI tract
    • this normally colours the stool


  • there will also be dark urine and pruritis 
    • itching is caused by bile salts, as the blockage affects the drainage of bile salts into the duodenum


What blood tests should anyone presenting with jaundice have?

  • liver function tests


  • coagulation studies
    • prothrombin time can be used as a marker of liver synthetic function


  • FBC
    • anaemia, raised MCV and thrombocytopenia can all be seen in liver disease


  • U&Es


What tests are included in a liver screen?


What does each of these things measure?


  • quantifies the degree of suspected jaundice



  • marker of liver synthetic function


Transaminases - ALT & AST:

  • markers of hepatocellular injury
    • AST : ALT ratio > 2 means likely alcoholic liver disease
    • AST : ALT ratio = 1 means viral hepatitis more likely 


Alkaline phosphatase (ALP):

  • raised in biliary obstruction
    • as well as during pregnancy, bone disease and certain malignancies



  • more specific for biliary obstruction than ALP


What results would you expect to see for each type of jaundice on LFTs?


  • raised bilirubin only 



  • there is damage to hepatocytes so you would expect to see raised AST & ALT



  • there is an obstruction / bile duct damage so you would expect to see raised ALP / GGT


What is meant by hepatitis?


What are the possible causes of this?

  • hepatitis is inflammation of the liver 


  • it presents with raised AST and ALT


  • causes can be acute or chronic and include:
    • alcoholic hepatitis
    • non-alcoholic steatohepatitis (NASH)
    • viruses
    • drugs
    • autoimmune 


How does hepatitis tend to present?

  • all types of hepatitis tend to present with similar symptoms


  • RUQ pain
  • jaundice (hepatocellular)
  • hepatomegaly
  • joint pain
  • nausea
  • fatigue
  • dark urine


How long does hepatitis have to persist for to become chronic?


What are the possible outcomes of acute and chronic hepatitis?

  • acute hepatitis resolves within 6 months
    • it becomes chronic if it lasts for longer than 6 months


  • acute hepatitis can resolve on its own, progress to chronic hepatitis or (rarely) result in acute liver failure


  • chronic hepatitis may progress to cirrhosis, liver failure and hepatocellular carcinoma


What are the 3 conditions that make up the spectrum of alcoholic liver disease?

  • steatosis occurs after a few days of heavy drinking 
    • this is completely reversible


  • alcoholic hepatitis (inflammation) occurs after long term alcohol use (not a binge)
    • this is reversible, especially if mild


  • if alcohol consumption is continued this can cause cirrhosis
    • this is IRREVERSIBLE as it involves scarring of the liver



What are the symptoms of mild and severe alcoholic hepatitis?


  • nausea
  • anorexia
  • weight loss 
  • hepatomegaly



  • fever
  • jaundice
  • tachycardia
  • tender hepatomegaly
  • bruising 
  • encephalopathy
  • ascites


What causes the inflammation associated with alcoholic hepatitis?

  • alcohol metabolism requires NAD+


  • when there is excessive alcohol consumption, there is not enough NAD+ available for glycolysis


  • this promotes fatty infiltration into the liver, leading to inflammation


What would a full blood count show in someone with chronic high alcohol intake?

macrocytic anaemia


  • this presents as low haemoglobin and high mean cell volume (MCV)


What would liver function tests show in someone with chronic high alcohol consumption?

  • AST : ALT ratio > 2
    • remember "alcohol then toAST"


  • increased bilirubin


  • decreased albumin


  • ALP may be normal or raised


  • GGT is raised in someone who drinks a lot of alcohol over long periods of time
    • raised GGT indicates biliary damage, but also chronic alcohol consumption


What would a clotting screen show in someone with chronic alcohol consumption?

  • clotting screen is a functional assessment that tells you how well the liver is working


  • the liver makes clotting factors, so clotting time increases when the liver is damaged


  • increased prothrombin time is a sensitive marker of significant liver damage 


What imaging is performed in alcoholic liver disease?


What would a liver biopsy show?

  • hepatic ultrasound scan is performed


  • liver biopsy is diagnostic, but rarely needed


the presence of Mallory bodies indicates hepatitis 

  • these are damaged intermediate filaments within the hepatocytes


there may also be ballooning degeneration of hepatocytes

  • this is a form of liver parenchymal cell death


What is involved in the management of alcoholic liver disease?

  • alcohol abstinence 


  • diazepam may be given in hospital to manage alcohol withdrawal
    • this prevents withdrawal symptoms and seizures


  • nutrition 
    • enteral preferred - calories and vitamins - alcoholics are often malnourished


  • weight loss / smoking cessation


  • steroids are given in severe alcoholic hepatitis 


What is meant by non-alcoholic fatty liver disease (NAFLD) and how can this progress?

  • the presence of a fatty liver in those who do not consume alcohol in amounts generally considered harmful to the liver 


  • steatosis is completely reversible


  • this progresses to steatohepatitis (NASH), which involves inflammation
    • this is reversible, especially if it is mild


  • this progresses to cirrhosis, which is irreversible


What are the risk factors associated with NAFLD?

  • obesity (truncal)


  • insulin resistance / type II diabetes


  • hyperlipidaemia


  • hypertension


  • metabolic syndrome


  • short bowel syndrome


  • total parenteral nutrition (TPN)


What additional symptoms may someone with NAFLD present with?

  • they may have signs of insulin resistance


  • polyuria


  • polydipsia


  • acanthosis nigricans