Oesophagus (Robbins pp 776)

Congenital and development disorders

Heterotopias: This is any deviation of any organ from its natural position.

Congenital cysts + duplications: Cysts might develop within wall of the oesophagus. Essentially, they can impinge on the lumen of the oesophagus, causing problems in the passage of food.

Oesophageal atresia: congenital closure of the oesophagus.

Oesophageal fistula: connections between oesaphus ≫ trachea/bronchi. Food enters the lung, and air enters the oesophagus. Major problems.

Oesophageal webs/rings: congenital narrowing ≫ Dysphagia.

Functional disorders

Achalasia: Basically, the lower oesophageal sphincter fails to open during the food passage process. This is because of neurogenic failure (i.e.: defective relaxation, or increased resting tone of sphincter muscle). Therefore you have mega-oesophagus (2^nd year notes).

Mallory Weiss Syndrome: This is a longitudinal tear in the oesophagus at the esophagogastric junction. Associated with: chronic cough, straining at stool, severe hiccups, vomiting and gastric reflux (alcoholism).

Diverticula: Outpouching of the ailementary tract. Can occur in the oesophagus. HIstologically, outpouching contains all visceral layers (mucosa, submucosa, muscularis mucosa, serosa). Three areas: Zenker, Traction, Epiphrenic.

Inflammations – oesophagitis

Reflux oesophagitis:

• Risk factors: smoking, hiatus hernia, obesity, drugs, duodenal ulcer.
  
• Patterns:
  
• 1) Reflux: gastric contents reflux into the lower oesophagus,
• 2) Erosive / ulcerative:erosion of the mucosa due to some other factor other than gastric contents
• 3) Peptic stricture: if there is narrowing of the stomach, then stomach contents will back up and flow into the oesophagus, with help from defective LES.
• 4) Barret’s.
  
• Histopathology: 1) usually basal zone contains squamous epithelial cells that are yet to move into the top zones. In oesophagitis, you see more 20% of the epithelium devoted to this region due to high turnover of cells from destruction. 2) elongation of lamina propria papillae, 3) inflammatory cells present in epithelium: eosinophils, neutrophils, lymphocytes.

Barrett’s oesophagus: This occurs when there is prolonged gastric reflux injury to the oesophagus. The squamous cells are replaced by metaplastic columnar cells (more resistant to acid injury). It resembles gastric mucosa rather than oesophageal mucosa. Histopathology: Three types of mucosa have been described. 1) gastric fundic type mucosa with chief and parietal cells. 2) mucosa resembling the cardia region (more mucous cells), 3) intestinal mucosa with villi and goblet cells. Should search for any dysplasia in the histological section  prevent malignancy. Look for nuclei in the basal aspect of epithelial cell (low grade dysplasia), or apical aspect (high grade dysplasia).

Other causes of oesophagitis: 1) ingestion of mucosal irritants (i.e.: alcohol, corrosive agents, alkaline agents, smoking, excessive hot foods), 2) anticancer therapy that is toxic to tumour cells (i.e.: may also affect normal cells), 3) infection: bacteraemia/viraemia (HSV, CMV), 4) fungal infections: candidiasis, 5) uraemia (setting of renal failure).

Other conditions

Oesophageal varices: This is caused due to increased pressure in the oesophageal veins causing dilated, tortous veins ≫ varices. Associated with alcoholic cirrhosis. The reason for dilated tortous veins is because of portal hypertension. Increase pressure causes the systemic circulation to take up the venous blood (i.e.: oesophageal veins are key area of portal-caval anastomoses).

Hiatus hernia: This is caused by the widening of the space between the muscular crus of the diaphragm and the oesophageal wall. This causes the stomach to herniate through the oesophageal hiatus.

Category: Pathology Notes