3. Gastro-Oesophageal Inflammation and Peptic Ulceration Flashcards
Inflammatory disorders of the oesophagus?
Acute: Infection in immunocompromised patients. E.g. • Herpes simplex viruses • Candida • Cytomegalovirus(CMV) – Corrosives
Chronic: Specific. E.g. • Tuberculosis • Bullous pemphigoid and Epidermolysis bullosa • Crohn’sdisease Non-specific E.g. • Reflux oesophagitis
What is GORD?
Gastro-oesophageal reflux disease
Causes for reflux oesophagitis (6)
Consequence? Leading to 3 pathologies?
• Regurgitation of gastric contents – Gastro-oesophageal reflux disease (GORD) – ‘Incompetent’ GO junction • Alcohol and tobacco • Obesity • Drugs e.g. caffeine! • Hiatus hernia • Motility disorders
Squamous epithelium damaged –>
– Eosinophils epithelial infiltration
– Basal cell hyperplasia
– Chronic inflammation
Consequences of reflux oesophagitis
Severe reflux leads to ulceration. Leading to fibrosis = stricture + obstruction.
Oesophagus narrower and more rigid
What is Barrett’s oesophagus?
Risk?
Diagnosis?
Longstanding reflex
Aged 40-60
Lower oesophagus becomes lined by columnar epithelium due to intestinal metaplasia
Risk? 100 times more likely to get adenocarcinoma of distal oesophagus
Diagnosis: Gastroscopy reveals red appearance of oesophagus
Two classifications of gastric inflammation?
Acute gastritis:
- Usually due to chemical injury (e.g. drugs / alcohol)
- H pylori- associated
Chronic gastritis:
- Active chronic (H pylori associated)
- Auto immume
- Chemical (reflux)
H pylori-associate gastritis:
- Bacteria shape?
- Transmission?
- Occupies?
- Condition associated with?
- Treatment?
- Two distribution patterns?
- Detections?
Bacteria shape?
-Gram negative spiral-shaped or curved bacilli
Transmission;
-Oral-oral, faecal-oral, environmental spread.
Occupies?
- Occupies protected niche beneath mucus where pH approx 7
- Does not colonise intestinal type eptithelium
Condition associated with?
-90% active chronic gastritis
Treatment?
-Resolves with therapy (double antibiotics + proton pump inhibitors)
Two distribution patterns:
1. Diffuse involvement of antrum and body
• Atrophy, fibrosis, intestinal metaplasia
• Associated with gastric ulcer and gastric cancer
2. Antral but not body involvement • Gastric acid secretion increased
• Associated with duodenal ulcer
Detection:
-Faecal bacterial, urea breath test, gastric biopsy rapid urease test
Chemical (reflux) gastritis:
Caused by?
Results in…
Associated with?
Caused by: Regurgitation of bile and alkaline duodenal secretion
Results in loss of epithelial cells with compensatory hyperplasia of gastric foveae
Associated with:
- Defective pylorus
- Motility disorders
Autoimmune chronic gastritis:
What is it? What happens?
Association?
Risk?
What is it? What happens?
Autoimmune reaction to gastric parietal cells. Serum antibodies to gastric patietal cells and intrinsic factor.
Loss of acid secretion (hypochlorhydria/achlorhydria)
Loss of intrinsic factor
–> Vit B12 deficiency
–>Macrocytic anaemia (pernicious anaemia)
Association?
With gastric atrophy and intestinal metaplasia
Risk?
Gastric cancer
What are the 3 causes for chronic gastritis?
- Autoimmune
- Bacterial infection (H pylori)
- Chemical injury
Peptic ulceration:
What is it? Caused by?
Major sites of ulceration?
What is it? Caused by?
Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
Major sites: – First part of duodenum – Junction of antral and body mucosa in stomach – Distal oesophagus – Gastro-enterostomy stoma
Causes for peptic ulcers?
– Hyperacidity – H pylori gastritis – Duodenal reflux – NSAIDs – Smoking – Genetic factors – Zollinger-Ellison syndrome
Complications of peptic ulceration?
– Haemorrhage – Penetration of adjacent organs e.g. pancreas – Perforation – Anaemia – Obstruction – Malignancy
Causes for acute peptic ulcers
Acute gastritis
Stress response
Extremem hyperacidity
Where to chronic peptic ulcers tend to occur?
At mucosal junctions e.g. Antrum- body
