Upper Gastrointestinal Disease Flashcards
Chronic gastritis
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 symptoms
upper abdominal pain indigestion or bloating nausea and vomiting belching loss of appetite or weight loss
However, it may be asymptomatic!
Chronic gastritis causes
Bacterial- Helicobacter pylori infection Chemical Alcohol Tobacco Caffeine A- Autoimmune Can lead to pernicious anaemia
Psychological stress
Helicobacter 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 - associations
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 Disease
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
Complications include: Bleeding leading to iron deficiency anaemia Massive haematemesis Perforation leading to peritonitis Long term cancer at edge of ulcer
Barrett’s oesophagus
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
Types of Upper GI cancer
Oesophagus Squamous carcinoma Adenocarcinoma (Barrett’s) Stomach Adenocarcinoma GI Stromal Tumours (GIST) Small Bowel Lymphoma GI Stromal Tumours (GIST) Neuroendocrine Tumours
Oesophageal carcinoma
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 Adenocarcinoma
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 spread
DIRECT into surrounding tissues LYMPHATIC to paraoesophageal, paratracheal and cervical node groups HAEMATOGENOUS to liver or lung
Adenocarcinoma stomach
Adenocarcinoma – 90% of gastric malignancies Precursor lesions Pernicious anaemia (atrophic gastritis) Intestinal metaplasia Neoplastic polyps Helicobacter associated gastritis
Adenocarcinoma stomach symptoms
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%
Adenocarcinoma stomach spread
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)
Small Bowel Neoplasia
Relatively rare compared to other GI malignancy Different subtypes include: adenocarcinoma (rare) gastrointestinal stromal tumor lymphoma carcinoid (neuroendocrine) tumor
Risk factors for Small Bowel Neoplasia
Crohn’s disease
Coeliac disease
Radiation exposure
Hereditary gastrointestinal cancer syndromes e.g. familial adenomatous polyposis
Coeliac disease
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 -
Coeliac disease symptoms
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
