Gastro-eosophageal and peptic ulceration Flashcards
Types of acute oesophagitis
- Infection in immunocompromised patients o HSV o Candida o Cytomegalovirus (CMV) - Corrosives
Chronic oesophagitis
- Specific o Tuberculosis o Bullous pemphigoid and epidermolysis bullosa o Crohn’s disease - Non-specific: reflux oesophagitis
Reflux oesophagitis involves
regurgitation of gastric contents and damage to the squamous epithelium
regurgitation of gastric contents due to
- Gastro-oesophageal reflux disease (GORD)
- “incompetente” GO junction
o Alcohol and tobacco
o Obesity
o Durgs (caffeine!)
o Hiatus hernia
o Motility disorders
damage to squamous epithelium due to
- Eosinophils epithelial infiltration
- Basal cell hyperplasia
- Chronic inflammation
Severe reflux leads to
ulceration, may lead to healing by fibrosis: stricture and obstruction.
Barrett’s oesophagus
- Longstanding reflux
- Age 40-60
- Men>women
- Lower oesophagus becomes lined by columnar epithelium
o Intestinal metaplasia
o ? role of gastric/biliary reflux
o ? role of helicobacter pylori - Premalignant: risk of adenocarcinoma of distal oesophagus 100x general population
Inflammatory disorders of the stomach
Acute/chronic gastritic
Acute gastritis causes
Chemical inhjury (NSAIDs, alcohol) H pylori
Chronic
H pyolori
Chemical injury (reflux)
Autoimmune disease
Helicobacter pylori-associated acute gastritis: usually transient phase, often becomes chronic
- Gram -ive spiral shaped or curved bacilli
- Oral-oral, faecal-oral, environmental spread
- Occupied protected niche beneath mucus where pH appox. Neural
- Does not colonise intestinal type epuithelium
- Found in 90 of active chronic gastritis
- Resolves with therapy (double antibiotic and proton pump inhibitors)
H pylori ANTRUM AND BODY
o Atrophy, fibrosis, intestinal metaplasia
o Associated with gastric ulcer and gastric cancer
h pylori ANTRUM ONLY
o Gastric acid secretion increased
o Associated with duodenal ulcer
Detection of H pylori
faecal bacteria, urea breath test, gastric biopsy rapid urease test
Chemical (reflux) gastritis
- Caused by regurgitation of bile and alkaline duodenal secretion
- Loss of epithelial cells with compensatory hyperplasia of gastric foveolae (one of the pits in the embryonic gastric mucosa from which the gastric glands develop)
- Associated with defective pylorus or motility disorders
Autoimmune chronic gastritis
- Autoimmune reaction to gastric parietal cells
o Loss of acid secretion (hypochlorhydia/achlorhydia)
o Loss of intrinsic factor (Vitamin B12 deficiency, macrocytic anaemia – pernicious) - Associated with marked gastric atrophy and intestinal metaplasia
- Increased risk of gastric cancer
- Serum antibodies to gastric parietal cells and intrinsic factor
What is peptic uleration
Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
Major sites for peptic ulceration:
- First part of duodenum
- Junction of antral and body mucosa in stomach
- Distal oesophagus
- Gastro-enterostomy stoma
Aetiological factors for peptic ulceration
- Hyperacidity
- H pylori gastritis
- Duodenal reflux
- NSAIDs
- Smoking
- Genetic factors
- Zollinger-Ellison syndrome
Complications of peptic ulceration
- Haemorrhage
- Penetration of adjacent organs (eg pancreas)
- Perforation
- Anaemia
- Obstruction
- Malignancy
Acute peptic ulcers
- Related to acute gastritis, ful thickness loss of epithelium rather than just erosion
- Related to a stress response (Curling’s ulcer following severe burns)
- A result of extreme hyperacidity (Gastrin-secreting tumours)
Chronic peptic ulcers
- Tend to occur at mucosal junctions (eg antrum-body)
- Pathogenesis: hyperacidity (not whole story) mucosal defence defects
Chronic gastric
- Normal pH of gastric juice 1-2
- Mucosal defences:
o mucus-bicarbonate barrier, dissolved by biliary reflux
o surface epithelium (though less important), damaged by NSAIDs and injured by H Pylori
Chronic duodenal
- increased acid production: more important than for gastric ulcer, can be induced by H pylori
- reduced mucolas resistance: gastric metaplasia occurs in response to hyperacidity, then colonised by H pylori
