1. Collapsed in the kitchen whilst doing the dishes

2. 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

3. 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

4. DDx
Jaundice
 Chronic alcoholic liver disease
 Gall Stones
 Pancreatic cancer, pancreatitis
 Hepatitis
 Hepatocellular carcinoma
 Cholangiocarcinoma, cholangitis
Collapse
Alcohol related
collapse – alcohol
withdrawal
Heart problem
Epilepsy

5. 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

6. 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

7. 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

8. 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

10. 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

11. 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 biliary
Canaliculi.
-Also can lead to problems with bilirubin
Conjugation
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

12. 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 to
The 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

14. 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=1
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