T11-L1: Upper GI Pathology Flashcards
Give risk factors of gastro-oesophageal reflux.
- Defective lower oesphageal sphincter
- Hiatus hernia
- Increased intra-abdominal pressure
- Increased gastric fluid volume due to gastric outflow stenosis
Give the aetiology of oesophagitis.
- Infections - Viruses (HSV1, CMV), bacterial occasionally and fungal (particularly in the immunocompromised - usually candida)
What histological appearances do we see in oesophagitis?
Hyperplasia of the basal cell layer, elongation of papillae, elongation of the lamina propria, increased cell desquamation, inflammation and ulceration if severe.
What are complications of oesophagitis?
- Ulceration
- Haemorrhage into the mediastinum
- Perforation particularly into the trachea
- Benign stricture due to repair by fibrosis
- Barret’s oesophagus - dysplasia which predisposes to adenocarcinoma
Give the pathogenesis of Barret’s oesophagus.
Barret’s oesophagus is due to long standing acid reflux. The risk factors therefore are the same as those for reflux (male, Caucasian, overweight). There is extension of the proximal squamoucolumnar junction. squamous mucosa is replaced by columnar mucosa. This is as the columnar epithelium is better adapted to deal with the acidic environment. In complete Barret’s mucosa we see intestinal mucosa - we see goblet cells, mucin etc. It is not gastric lining but intestinal lining. The dysplasia predisposes to adenocarcinoma.
Give risk factors for Oesophageal squamous cell carcinoma.
Risk factors:
• Tobacco and alcohol
• Nutrition (potential sources of nitrosamines)
• Thermal injury (hot beverages)
• Human Papilloma Virus (common cause in the Western World)
• Male
• Ethnicity (black)
Location:
• Middle and lower third (<15% in upper third of oesophagus). It needs to occur in native squamous lining and so you will not see it in Barret’s.
In which part of the stomach is H. pylori most like to infect?
Antrum
Give causes of chronic gastritis.
- H. pylori infection
- Autoimmune such as anti-parietal and anti-IF antibodies
- Chemical injury e.g. NSAIDs, bile reflux, alcohol -direct injury
Compare gastric and duodenal ulcers:
(a) Relative Incidence
(b) Acid levels
(c) H. pylori gastritis
(d) Localisation
(e) Blood group
(a) GU 1 : 3 DU
(b) GU acid levels are normal or low, in DU levels are elevated or normal
(c) GU 70% and DU 95-100%
(d) Gastric ulcer - found in the lesser curve, antrum and prepyloric. In DU they are bulbus
(e) GU in Blood group A and DU in blood group O
Where is peptic ulcer disease localised?
- First part of the duodenum
- The antrum and the body of the stomach
- Distal oesophagus
What are the main aetiology factors of peptic ulcer disease?
- Hyperacidity
- H. pylori (higher incidence in duodenal infection)
- Duodeno-gastric reflux
- Smoking NSAIDs - more common in gastric ulcers
- Smoking
Give complications of peptic ulcers.
- Perforation leading to peritonitis
- Haemorrhage - leading to acute/chronic anaemia
- Penetration into an adjacent organ such as the liver of pancreas
- Sticturing
Give the epidemiological differences between the adenocarcinoma found at the gastro-oesophageal junction and the body/antrum of the stomach.
Adenocarcinoma at the GOJ:
- White males
- An association with gastric reflux
- No association with H. pylori/diet
- Incidence has increased over the years with obesity
Adenocarcinoma of the body/antrum:
- Association with H. pylori
- Association with diet (salt, low fruit &vegetable)
- No association with GI reflux
- Decreased incidence in recent years
What germline mutation can we see in diffuse type gastric adenocarcinoma?
CDH1 mutation - E-Cadherin loss/mutation (loss of cell adhesion protein)
What histopathological features are seen in coeliac disease?
- Villious atrophy
- Crypt elongation
- Increased intraepithelial lymphocytes
