Upper Gastrointestinal Disease

Question 1

Chronic gastritis

Answer 1

Ongoing inflammation of the stomach mucosa

Compared to acute gastritis, symptoms are less severe but more persistent

Can provide an environment in which dysplasia and carcinoma can arise

Question 2

Chronic gastritis symptoms

Answer 2

upper abdominal pain 
indigestion or bloating 
nausea and vomiting 
belching 
loss of appetite or weight loss 

However, it may be asymptomatic!

Question 3

Chronic gastritis causes

Answer 3

Bacterial- Helicobacter pylori infection
Chemical
Alcohol
Tobacco
Caffeine
A- Autoimmune
		Can lead to pernicious anaemia

Psychological stress

Question 4

Helicobacter pylori

Answer 4

Gram-negative bacterium found in the stomach, particularly antrum
infects over half the world’s population and by age 5.
infection probably acquired via faecal-oral route
untreated, infection persists throughout life

Question 5

H.Pylori - Discovery

Answer 5

It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren
Found that it was present in patients with chronic gastritis and gastric ulcers, conditions not previously believed to have a microbial cause.
It is also linked to the development of duodenal ulcers and stomach cancer.

Question 6

H.Pylori clinical presentation

Answer 6

80% asymptomatic
5-15% peptic ulcer disease
10% non-ulcer dyspepsia
1-3% gastric adenocarcinoma
0.5% gastric MALToma

Question 7

H. Pylori - associations

Answer 7

Strongly associated with Chronic Gastritis
Strongly associated with duodenal ulcer
Fairly strongly associated with gastric ulcer
Associated with gastric carcinoma
Associated with gastric MALT lymphoma

Question 8

Peptic ulcer Disease

Answer 8

Peptic ulcer disease (PUD) usually occurs in D1 or antrum (4:1).
Common causes are H. pylori (80 -100% DU, 65% gastric) and NSAIDs
Most ulcers are solitary
Symptoms include
Pain (gnawing, burning, aching)
Worse at night
Worse after meals

Question 9

Peptic ulcer - complications

Answer 9

Complications include:
Bleeding leading to iron deficiency anaemia
Massive haematemesis
Perforation leading to peritonitis
Long term cancer at edge of ulcer

Question 10

Barrett’s oesophagus

Answer 10

Normal lining of the oesophagus stratified squamous epithelium.
In Barrett’s oesophagus replaced by columnar epithelium with goblet cells (usually found lower in the gastrointestinal tract).
Thought to be an adaptation to chronic acid exposure from reflux oesophagitis
Process of dysplasia: low grade to high grade to invasive carcinoma
Strong association (about 0.5% per patient-year) with oesophageal adenocarcinoma
Need for surveillance

Question 11

Types of Upper GI cancer

Answer 11

Oesophagus	   
Squamous carcinoma
Adenocarcinoma (Barrett’s)
Stomach
Adenocarcinoma
GI Stromal Tumours (GIST)
Small Bowel
Lymphoma
GI Stromal Tumours (GIST)
Neuroendocrine Tumours

Question 12

Oesophageal carcinoma

Answer 12

Squamous cell carcinoma
Adults over 45
M:F 4:1
Risk factors include alcohol, tobacco, caustic injury, achalasia.
Insidious onset with late symptoms
Dysphagia, weight loss, haemorrahge, sepsis, respiratory fistula with aspiration
Overall 5 year survival of 9%

Question 13

Oesophageal Adenocarcinoma

Answer 13

Adenocarcinoma – now more common
Largely from dysplastic change in Barrett’s oesophagus
M:F 7:1
Present with dysphagia, weight loss, haematemesis, chest pain, vomiting.
5 year survival

Question 14

Oesophageal carcinoma spread

Answer 14

DIRECT
into surrounding tissues
LYMPHATIC 
to paraoesophageal, paratracheal and cervical node groups
HAEMATOGENOUS 
to liver or lung

Question 15

Adenocarcinoma stomach

Answer 15

Adenocarcinoma – 90% of gastric malignancies
Precursor lesions
Pernicious anaemia (atrophic gastritis)
Intestinal metaplasia
Neoplastic polyps
Helicobacter associated gastritis

Question 16

Adenocarcinoma stomach symptoms

Answer 16

Early symptoms resemble gastritis
Advanced symptoms
Weight loss, anorexia, anaemia, heamorrhage
Fungating exophytic growth
Prognosis depends on depth of invasion
5 year survival (early) after surgery 90%
Overall 5 year survival 30%

Question 17

Adenocarcinoma stomach spread

Answer 17

Direct infiltration
Duodenum, pancreas, colon, liver, spleen
Lymphatic spread
Local and regional nodes
 Virchow's node
Haematogenous
Liver, lungs
Transcoelomic
 Omentum
 Mesentery
 Ovary (Krukenberg tumour)

Question 18

Small Bowel Neoplasia

Answer 18

Relatively rare compared to other GI malignancy
Different subtypes include:
adenocarcinoma (rare)
gastrointestinal stromal tumor
lymphoma 
carcinoid (neuroendocrine) tumor

Question 19

Risk factors for Small Bowel Neoplasia

Answer 19

Crohn’s disease
Coeliac disease
Radiation exposure
Hereditary gastrointestinal cancer syndromes e.g. familial adenomatous polyposis

Question 20

Coeliac disease

Answer 20

Extensive mucosal disease related to sensitivity to gluten
Prevalence in white Europeans of 0.5 – 1%
Immune mediated villous atrophy and malabsorption
Can be diagnosed via serological blood test (TTG) and biopsy -

Question 21

Coeliac disease symptoms

Answer 21

pain and discomfort in the digestive tract, 
chronic constipation and diarrhoea, 
failure to thrive (in children), 
anaemia 
fatigue 

Intestinal damage begins to heal within weeks of gluten being removed from the diet

Coeliac disease leads to an increased risk of both adenocarcinoma and lymphoma of the small bowel