Jaundice. Mr Daffodil - 57

Collapsed in the kitchen whilst doing the dishes

HPC

Neurological Causes:

- No headaches

- No Confusion

- No incontinence

- No Loss of Consciousness

- No vision or hearing changes

Chest/heart-No chest

pain- No

breathlessness

Metabolic: -Not a diabetic -Struggling to eat -Very obviously jaundiced

-Further three collapses of similar nature over the last week

-Felt slightly dizzy- legs felt shaky - Felt very tired following the episodes

HPC Contd. Severe loss of appetite

over a 4/5 week period Lost 1-2 stone over a 2

month period Itchy No nausea or vomiting No change in bowel

habits

Jaundice started 2/52 ago Before this – generally fit and well

Similar episode to this happened 7/8 years ago – collapsed several times but without jaundice. No cause found

Chesty cough for 3 weeks and chest infection

DDxJaundice Chronic alcoholic liver disease Gall Stones Pancreatic cancer, pancreatitis Hepatitis Hepatocellular carcinoma Cholangiocarcinoma, cholangitis

Collapse

Alcohol related collapse – alcohol withdrawal

Heart problem

Epilepsy

Management of chronic alcoholic

hepatitis Advise to stop drinking – look at AA forums

etc Provide withdrawal support –antabuse,

acamprosate Manage complications of portal

hypertension High nutrition diet – high fibre, high protein,

low fa Severe alcoholic hepatitis – corticosteroids

- reduce liver inflammation Transplant

Jaundice Derives from french word for yellow – jaune HYPERBILIRUBINAEMIA Total Bilirubin plasma concentrations rise in

all forms of jaundice and can collect in the extracellular fluid, causing skin and sclera to turn yellow

What happens normally?

How is bilirubin made? Bilirubin is a breakdown product of heme. Heme is

broken down into biliverdin by heme oxygenase, which is catalysed to bilirubin by biliverdin reductase. This bilirubin is UNCONJUGATED

Bilirubin is bound to albumin and travels to the liver

Once in the liver, bilirubin is CONJUGATED with gluronic acid by the enzyme glucuronyltransferase. This makes it water soluble

The Entero-hepatic circulation

The conjugated water soluble bilirubin is mainly excreted in bile with the bile salts.

It goes through the small intestine… until it reaches the terminal ileum

Most of the bile is reabsorbed at the terminal ileum (95%) What happens to the bilirubin left in the intestine?

Some conjugated bilirubin in the small intestine is catalysed back to unconjugated bilirubin, which is then further converted to urobilinogen. Any urobilinogen remaining in the small intestine is then converted to stercoblinogen. Stercobilinogen is oxidised to stercobilin.

Some urobilinogen is also reabsorbed. This enters the blood stream and is filtered by the kidneys. It is oxidised to urobilin, giving urine its yellow colour

What happens to the bilirubin that is absorbed? The cycle is repeated and generally it is resecreted in the bile

Pre-hepatic Jaundice

Haemolytic Cause: Genetic Causes

Sickle cell anaemia Spherocytosis Thalassemia Glucose 6-phosphate dehydrogenase

deficiency Kidney

Haemolytic uremic syndrome Defects in bilirubin metabolism

Gilbert’s Syndrome Rotor Syndrome Dubin Johnson Crigler-Najjar Syndrome

Infectious causes: Malaria

Where is the problem?-Spleen/blood/periphery

What is the problem?-Increased production of bilirubin

Is this going to result in increased Conjugated or unconjugated bilirubin or both?-Unconjugated

What symptoms will this produce?-Increased Urobilinogen-Normal Stools -Normal colour urine -Splenomegaly-Normal LFTs

Hepatic Jaundice Hepatocellular Causes:

Acute or Chronic Hepatitis Hepatotoxicity Cirrhosis Drug induced hepatitis Alcohol induced liver disease

Where is the problem?-Hepatocytes

What is the problem?-Swelling, oedema, fibrosis-Leading to a problem in transporting bilirubin from the blood to the biliaryCanaliculi.-Also can lead to problems with bilirubinConjugation

Is this going to result in increased Conjugated or unconjugated bilirubin or both?Both

What symptoms will this produce?-Increased urobilinogen, Increased urobilin (dark urine), Normal/pale stools, splenomegaly, deranged LFTs

Post Hepatic Jaundice

Obstructive Gall stones Pancreatitic cancer Liver flukes Biliary atresia Cholangiocarcinoma Pancreatitis Pancreatitc pseudocysts Mirizzi’s syndrome

Where is the problem?In the biliary tract

What is the problem?Generally obstruction Conjugated bilirubin cannot make it toThe small intestine

Is this going to result in increased Conjugated or unconjugated bilirubin or both?conjugated

What symptoms will this produce?Normal urobilinogen, dark urine (increased urobilin)Pale Stools No splenomegaly Normal LFTs

References Oxford Handbook of Clinical Medicine 2008

edition Kumar and Clark 2005 edition. Vander’s Physiology Marsano et al., 2003; Diagnosis and

Treatment of Alcoholic Chronic Disease and its complications; Alcohol Research and Health; 27; 3

http://www.gpnotebook.co.uk/simplepage.cfm?ID=161087510