Gastro-Oesophageal Inflammation and Peptic Ulceration Flashcards
Achalasia
Increased tone of the lower oesophageal sphincter (LES)
• Impaired smooth muscle relaxation
• Can be cause of oesophageal obstruction
Achalasia triad:
- Incomplete LES relaxation
- Increased LES tone and
- Aperistalsis of the oesophagus
Primary achalasia
• Neuronal, ganglion cell degeneration (Vagus N) – rare familiar cases
• Secondary achalasia
- Chagas disease (Trypanosoma cruzi infection) – destruction of myenteric plexuses
- Diabetic autonomic neuropathy, amyloidosis, sarcoidosis, polio, Down syndrome
- Herpes simplex infection
treatment for achalasia
Laparoscopic myotomy, balloon dilatation and Botox injection
Oesophagitis - acute
- Infection in immunocompromised patients
- Herpes simplex viruses
- Candida
- Cytomegalovirus (CMV)
- Corrosives
Oesophagitis - chronic
- Specific
- Tuberculosis
- Bullous pemphigoid and Epidermolysis bullosa
- Crohn’s disease
- Non-specific: reflux oesophagitis
Reflux Oesophagitis
Reflux Oesophagitis
• Regurgitation of gastric contents
• Gastro-oesophageal reflux disease (GORD)
• ‘Incompetent’ GO junction
• Squamous epithelium damaged
causes of reflux oesophagi’s
- Alcohol and tobacco
- Obesity
- Drugs e.g. caffeine!
- Hiatus hernia
- Motility disorders
what kind of squamous epithelium damage
- Eosinophils epithelial infiltration
- Basal cell hyperplasia
- Chronic inflammation
reflux oesophagitis - ulceration
- Severe reflux leads to ulceration
- May lead to healing by fibrosis
- Stricture
- Obstruction
Barrett’s Oesophagus
- Longstanding reflux
- Age 40-60 more men than women
- Lower oesophagus becomes lined by columnar epithelium
Gastric Inflammation - acute gastritis
- Usually due to chemical injury
* H pylori-associated
chronic gastritis
- Active chronic (H pylori-associated)
- Autoimmune
- Chemical (Reflux)
Helicobacter pylori-associated acute gastritis
- Usually transient phase
* Often becomes chronic
H pylori-associated Gastritis
- Gram negative spiral-shaped or curved bacilli
- Oral-oral, faecal-oral, environmental spread
- Occupies protected niche beneath mucus where pH approx. neutral
- Does not colonise intestinal type epithelium
- Found in 90% of active chronic gastritis
Helicobacter pylori
- Causative factor in gastric and duodenal ulcers
- Risk factor for gastric cancer (adenocarcinoma)
- Strong link with MALT (Mucosa Associated Lymphoid Tissue) Lymphoma
H pylori – acute infection
• Can cause acute infection with symptoms that include nausea,
dyspepsia, malaise and halitosis
• Acute infection tends to last about two weeks
• Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration
H pylori –chronic infection
• Local inflammation and gastritis • Outcome depends on: - Pattern of inflammation - Host response - Bacterial virulence - Environmental factors - Patient age
H pylori-associated Gastritis - two distribution patterns
• Diffuse involvement of antrum and body
- Atrophy, fibrosis, intestinal metaplasia
- Associated with gastric ulcer and gastric cancer
• Antral but not body involvement
- Gastric acid secretion increased
- Associated with duodenal ulcer
Chemical (Reflux) Gastritis
• Caused by regurgitation of bile and alkaline duodenal secretion
• Loss of epithelial cells with compensatory hyperplasia of gastric foveolae
• Associated with
- Defective pylorus
- Motility disorders
Autoimmune Chronic Gastritis
• Autoimmune reaction to gastric parietal cells
• Loss of acid secretion (hypochlorhydria / achlorhydria)
• Loss of intrinsic factor
- vit b12 def
- microcytic 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 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
otological 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 e.g. pancreas
- Perforation
- Anaemia
- Obstruction
- Malignancy
Acute Peptic Ulcers
• Related to acute gastritis
- Full thickness loss of epithelium, rather
than just erosion
• Related to a stress response
- e.g. Curling’s ulcer following severe burns
• A result of extreme hyperacidity
- e.g. Gastrin-secreting tumours
Chronic Peptic Ulcers
• Tend to occur at mucosal junctions - e.g. antrum - body • Pathogenesis - Hyperacidity - not whole story - Mucosal defence defects
Chronic Gastric Ulcer
• Normal pH of gastric juice 1-2 • Mucosal defences - Mucus-bicarbonate barrier - Surface epithelium - less important • Mucus-bicarbonate barrier - Dissolved by biliary reflux • Surface epithelium - Damaged by NSAIDs - Injured by H pylori
Chronic Duodenal Ulcer
• Increased acid production - More important than for gastric ulcer - Can be induced by H pylori • Reduced mucosal resistance - Gastric metaplasia occurs in response to hyperacidity - Then colonised by H pylori
pathology of chronic duodenal ulcer
- Usually small (<20 mm)
- Sharply ‘Punched out’ with defined edges
- Defined structure
complications of chronic duodenal ulcer
- ‘Bleed, burst or block’
- Penetration of adjacent organs e.g. pancreas
- Malignant change: rare in gastric ulcer and ‘never’ in duodenal ulcer
