12. Upper Gastrointestinal Disease Flashcards
Chronic gastritis (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
Chronic gastritis (2)
Symptoms include: upper abdominal pain indigestion or bloating nausea and vomiting belching loss of appetite or weight loss
However, it may be asymptomatic!
Chronic gastritis (3)
Causes include: A, B, C and other Bacterial- Helicobacter pylori infection Chemical Alcohol Tobacco Caffeine A- Autoimmune Can lead to pernicious anaemia
Psychological stress
Helicobacter pylori
H.pylori
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
H.Pylori - Discovery
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.
H. pylori - Clinical presentation
80% asymptomatic 5-15% peptic ulcer disease 10% non-ulcer dyspepsia 1-3% gastric adenocarcinoma 0.5% gastric MALToma
H. Pylori - importance
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
Peptic ulcer
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
Peptic ulcer - complications
Bleeding leading to iron deficiency anaemia
Massive haematemesis
Perforation leading to peritonitis
Long term cancer at edge of ulcer
Barrett’s oesophagus (1)
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
Barrett’s oesophagus (2)
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
Upper GI malignancy
Types of cancer
Oesophagus
Squamous carcinoma
Adenocarcinoma (Barrett’s)
Stomach
Adenocarcinoma
GI Stromal Tumours (GIST)
Small Bowel
Lymphoma
GI Stromal Tumours (GIST)
Neuroendocrine Tumours
Oesophageal carcinoma (1)
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%
Oesophageal carcinoma (2)
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
Oesophageal carcinoma (3)
DIRECT into surrounding tissues LYMPHATIC to paraoesophageal, paratracheal and cervical node groups HAEMATOGENOUS to liver or lung