Gastro-Oesophageal Inflammation And Peptic Ulceration Flashcards
Achalasia
Increased tone of the lower oesophagel sphincter due to impaired smooth muscle relaxation. Can cause oesophageal obstruction.
Achalasia triad
- Incomplete lower oesophageal sphincter relaxation.
- Incomplete lower oesophageal sphincter tone
- Aperistalsis of the oesophagus.
Causes of Achalasia: Primary? Secondary?
- Primary - ganglion cell degeneration affecting the vagus nerve.
- Secondary - Chagas disease (Trypanosoma cruzi infection) which destroys myenteric plexus. Diabetic autonomic neuropathy. Amyloidosis. Sarcoidosis. Polio. Down syndrome. Herpes simplex infection.
Treatment of Achalasia
Laparoscopic myotomy, balloon dilatation and botox injection.
Acute Oesophagitis Causes
- Corrosives
- Infection in immunocompromised patients - herpes simplex viruses, candida and cytomegalovirus (CMV).
Chronic Oesophagitis Causes
- Tuberculosis
- Bullous pemphigoid and Epidermolysis bullosa (skin disorders which alos affect the oesophagus).
- Crohn’s disease
- Reflux
Reflux Oesophagitis
- Regurgitation of gastric content. Caused by gastro-oesophageal reflux disease (GORD) or an incompetent gastro-oesophageal junction (due to alcohol, tobacco, drugs e.g. caffeine, hiatus hernia, and motility disorders).
- Squamous epithelium damaged - eosinophils epithelial infiltration, basal cell hyperplasia (increased cell desquamation), chronic inflammation.
- Severe reflux leads to ulceration
- May lead to healing by fibrosis - stricture or obstruction.
Barrett’s Oesophagus
- Longstanding reflux causes metaplasia of the oesophagus epithelium; stratified squamous > columnar epithelium.
- Not sure of exact mechanism - roles of reflux or H.Pylori
- Premalignant - risk of adenocarcinoma of distal oesophagus 100x more likely.
Acute Gastritis Causes
Chemical injury ( alcohol or drugs e.g. NSAIDs) or Helicobacter pylori associated (often becomes chronic, usually transient phase).
Chronic Gastritis Causes
- active chronic (Helicobacter pylori associated)
- autoimmune
- chemical
Helicobacter Pylori-associated Gastritis
- gram negative spiral-shaped or curved bacilli
- oral-oral, faecal-oral, environmental spread
- occupies protected niche beneath mucus where pHapproximately neutral
- does not colonise intestinal type epithelium
- found in 90% of active chronic gastritis
Helicobacter Pylori
- causative factor of gastric and duodenal ulcers
- risk factor for gastric cancer (adenocarcinoma)
- strong link to mucosa-associated lymphoid tissue (MALT) lymphoma.
- associated with dyspepsia, atrophic gastritis, iron deficiency anaemia, and idiopathic thrombocytopenic purpura
Pathogenesis of H.Pylori
- Enters mucosal layer and attaches
- Secretes urease which neutralises gastric acid, allowing it to colonise
- Mucosal damage by bacterial mucinase, creating an unprotected area of gastric epithelium. Which is now inflamed due to contact with gastric acid, proteases snd effector molecules.
- Mucosal cell death by cytotoxins and ammonia
Chemical Gastritis
- Caused by regurgitation of bile and alkaline duodenal secretion.
- Results in loss of wpithelial cells with compensatory hyperplasia of gastric foveolae (cells which produce mucus in stomach).
- Associated with a defective pylorus and motility disorders.
Autoimmune Chronic Gastritis
- Autoimmune reaction to gastric parietal cells which causes loss of acid secretion (hypochlorhydria (decreased HCl production)/ achlorhydria (no HCl production)) and loss of intrinsic factor (causes vitamin B12 deficiency and macrocytic pernicious anaemia).
- Associated with marked gastric atrophy and intestinal metaplasia.
- Increased risk of gastric cancer
- Serum antibodies to gastric parietal cells and intrinsic factor.
Peptic ulceration
Breach in mucosal lining of ailimentary canal as a result of acid and pepsin attack.
Major sites of peptic ulceration
First part of duodenum > junction of antral and body mucosa in stomach > distal oesophagus > gastro-enterostomy stoma
Aetiological factors of peptic ulceration
- Hyperacidity
- H. pylori gastritis
- Duodenal reflux
- NSAIDs
- Smoking
- Genetic factors
- Zollinger-Ellison syndrome(condition where the body produces excess gastrin which means too much acid is produced).
Complications of peptic ulceration
- Haemorrhage - presents as haematoemesis - HCl erodes blood vessels
- Penetration of adjacent organs e.g. pancreas
- Perforation
- Anaemia - loss of blood via ulcer bleed
- Obstruction - especially if close to pyloric sphincter
- Malignancy
Acute Peptic ulcers
-Related to: acute gastritis (full thickness loss of epithelium, rather than just erosion), stress response (e.g. Curling’s ulcer following severe burns), or Extreme Hyperacidity (gastrin-secreting tumours).
Chronic Peptic Ulcers
Tend to occur at mucosal junctions. Hyperacidity + mucosal defence defects (mucus-bicarbonate barrier dissolved by biliary reflux. Surface epithelium damaged by NSAIDs or H.Pylori).
Chronic Duodenal Ulcer
- Caused by increased acid production (could be induced by H.Pylori), and reduced mucosal resistance (gastric metaplasia occurs in response to hyperacidity, which is then colonised by H.Pylori).
- usually small (<20mm), defined structure; defined edges, granulation at base, underlying inflammation and fibrosis, loss of muscularis propria.
- complications - bleed, burst, block, penetrate adjacent organs, malignant (gastric only)
