How to Succeed in PBL – GIS

1. Proper history taking is very important

- Relevant questions and detailed
- Assess severity of symptom, for timely intervention: ie diarrhoea, abdominal
pain
- Sort out the systems involved with the symptoms presented
- Identify causes of the problem
2. Skilled clinical examination
3. Formulate management plan according to possible diagnosis

Case 1
45yo Male, chronic smoker, social drinker
No recent drug intake
Black stool (tarry stool, indicates UPPER GI BLEED oesophagus to duodenum part 3), no
abdominal pain, no vomit, no weight loss
Px: hepatomegaly, fatty liver, gastritis, depression, subdural haematoma with burr hole ‘04
Q to ask: are there anymore Important information, how severe is his problem, is it likely to
be malignant?

Need to know enough to ask the right questions. Your own knowledge is the differential
diagnosis
- Family history for upper GI bleed: etiological factor same
- social history (ie Need to document exact drinking habit)
- Are there systemic problems?
- Severity of symptoms: How much blood is loss, is it severe blood loss? Are there
symptoms related? Ie anaemia, dizziness, hypotension with tachycardia (due to
BP drop), shock (severe volume loss)
- Previous drug intake? Chinese medication? Any sort of over the counter?
- Gastritis can be precursor of cancer
- What does black stool mean? Is it clinically significant??
 Benign black stool: iron tablet (acid turns it black), beetroot consumption,
bismuth
 Important to ask the patient to define black stool

GI bleed indications in the population (% of population)

- Coffee ground vomit
- 20% melaena
- 30% haematemesis
- 50% both haematemesis and melaena
- 5% haematochezia
Case 2
M 22yo
Bone marrow transplant in Jan 2009, because of leukaemia (ALL)
 First few months after transplant: bacterial infection prone
 Later months: viral infections or fungal infection common
No GVHD, on prophylactic cyclosporin (immune suppressant)
CMV infection, on antivirals
April 2009 – A&E epigastric pain, watery diarrhoea x10/day undigested food vomit x4
 Can be acute enteritis (can it be weakened immune due to suppressant, from
relatively mild insult? Ie wouldn’t cause problems in normal people? From
food or from infection?)
 Ask patients what they think it is (ICE): any food they ate?
 Usually vom and diarrhoea = food poisoning in normal people
 Likely from infections given his history
AXR (no dilated bowel, +ve dilatation if prominent gastroenteritis, risk of perforation if very
distended), CXR (clear, no fluid)
No fever
Chills
BP is low, pulse is 105 = indicates severity of hypovolaemia
Dehydrated – why? Vomite and diarrhoea – ORAL FLUID AND ELECTROLYTE needed
normal SaO2

immediate: broad spectrum antibiotics to control infection, fluid replacement to restore BP

later: culture

case 3

45male
social drinker
known hep B carrier since childhood
T2DM
Stigmata of chronic liver disease + = spider naevi, white nails (present in cirrhosis)
No hepatic flap (usually caused by hepatic encephalopathy since his hands did not flap when
raised)
Abdomen soft, no ankle odema
Nausea, malaise, jaundice in early September

Questions to ask
- Family history: liver cancer, cirrhosis
- How much is social drinking? Need to clarify
- Other risk factors for viral hepatitis? – tattoo, blood transfusion (Hep C), IV drug
use
- Hep B activation, what caused the reactivation? (is there adequate monitoring in
the years?) + alcoholic use (exacerbate existing weak liver?)  cirrhosis (end
stage liver)  symptoms?
 What triggers flares: drug intake (steroids, can induce flare in hepB), CM
  Are there co-infection of other viral hepatitis (shell fish consumption),
compound the existing HepB
 In this setting: drug and food intake is important (identify Hep ABCD
etiology)
- T2DM – dyslipidaemia, can also contribute to fatty liver  cirrhosis
- What cause the jaundice? Surgical cause (obstruction, accompanied by pale
stool), liver problem?
- I don’t think severity is much: as no hepatic encephalitis, no ascites, no odema
- Also LFT is not indicative of severe disease: normal albumin, normal clotting time

Abdominal distension causes

“屎肥仔氣水”
Odema of other sites also associated with ascites
Painful ascites: indicative of peritonitis
Ascites: indicates poorer prognosis, as indicates very bad liver synthetic function (reflected
by low albumin = low oncotic pressure in blood = fluids leak into interstitial spaces and into
peritoneal cavity leading to ascites, and portal pressure high)
- Low albumin: synthetic function, ascites, immune property = secondary
peritonitis