Pathology of the Upper GI Tract

Question 1

Explain the normal structure of the GI tract including the different epithelium’s seen in the mucosa

Answer 1

• Mucosa: mouth and oesophagus have non keratinising stratified squamous epithelium. Stomach SI and colorectum have columnar epithelium. Final anal canal has squamous epithelium.
  -lamina Propria
• Sub-mucosa
• muscularis propria (inner circular layer and outer longitudinal layer)
• Sub-serosa (advantitia in oesophagus)

Question 2

Define dysplasia and explain how squamous dysplasia may present and its risk factors.

Answer 2

Dysplasia is a morphological description where the epithelium shows disordered differentiation.
It presents with red or white patches/plaques or as a non-healing ulcer.
Associated with smoking, alcohol and HPV (mainly affects tonsils and oesophagus)

Question 3

Explain the histological appearence of GORD

Answer 3

This occurs when acid, bile and digestive enzymes injure squamous epithelium. It shows hyperplastic basal layer, elongation of lamina propria papillae and lymphocytes and scanty eosinophils in epithelium.

Question 4

What are some of the pathologies that can occur in the oesophagus

Answer 4

Infections - candidia albicans or herpes simplex virus (mainly in immunocompromised)
Inflammation - peptic oesophagitism, chemicals or pills eg, iron.
- Also get diverticular, achalasia etc

Question 5

Explain the presentation of candida oesophagitis

Answer 5

• White plaques on endoscope.
• Fungal hyphae and spores on histology

Question 6

Explain the presentation of herpes simplex infection of the oesophagus

Answer 6

Presents as oesophageal erosion with atypical squamous cells with nuclear invasion

Question 7

Describe features and presentation of eosinophilic oesophagitis

Answer 7

• Endoscopically appears as ‘feline oesophagus’ with ring like trachealization. Histologically appears with numerous bright red eosinophil infiltrate of epithelium.
• It can cause dysphagia or food bolus obstruction and often have an allergic aetiology

Question 8

What is Barret’s oesophagus?

Answer 8

An intestinal metaplastic response to mucosal injury from long standing GORD. It appears with red and salmon pink tongues endoscopically.
- The normal squamous epithelium becomes glandular usually with intestinal goblet cells.
- Barret’s oesophagus is associated with development of adenocarcinoma.

Question 9

What are the two grades of Barretts oesophagus

Answer 9

Low grade - subtly different in appearence.
High grade - abnormal mitoses, necrosis with rounder nuclei

Question 10

What are the risks of Barrett’s oesophagus and treatment

Answer 10

Over many years can develop into a carcinoma.
Therefore surveillance is required. This can be done via taking four biopsies every 2cm at dysplasia. Or new techniques like cytosponge.
Endoscopic treatment like radiofrequency ablation can reduce need for radical surgery

Question 11

What are the two oesophageal cancers and their associations

Answer 11

• Squamous carcinoma which is associated with smoking and drinking.
• Adenocarcinoma which is associated with GORD and obesity

Question 12

What are the different causes of gastritis?

Answer 12

Acute causes - alcohol, NSAIDs, severe trauma.
Chronic causes - ABC: Autoimmune, bacterial and chemical

Question 13

Explain autoimmune gastritis and what is can lead to

Answer 13

• There is autoimmune destruction of parietal cells due to auto-antibodies targeted to intrinsic factor and parietal cells.
• This can lead to loss of parietal cells with pyloric and intestinal metaplasia. It can cause achlorhydria which causes bacterial overgrowth. It can cause hypergastrinaemia which is due to endocrine cell hyperplasia and it can cause persistent inflammation which can cause epithelial dysplasia

Question 14

What are the two patterns of gastritis caused by H.pylori

Answer 14

• Antral-predominant gastritis which causes hypergastrinaemia and duodenal ulceration. Associated with low IL-8 release from epithelial cells.
• Pangastritis which causes hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia and cancer. Associated with high IL-8 release

Question 15

Explain the role of the host/microbe interface in the development of peptic ulceration

Answer 15

• Microbe factors include variants associated with more severe inflammation eg, CagA.
• Host factors include impaired mucosal defence, often due to NSAIDs or bile reflux.

Question 16

What is the histological appearence of chronic active helicobacter related gastritis

Answer 16

• Lamina propriae is full of plasma cells and lymphocytes.
• Surface erosion and active inflammation.
• Helicobacter organisms on immunohistochemistry

Question 17

What is the histological appearence of chemical gastropathy?

Answer 17

• Fewer inflammatory cells (hense why its not a gastritis)
• Foveolar hyperplasia (corkscrew glands)
• Ectatic mucosal capillaries,
• Muscle spurs in lamina propria,
• More likely to affect the antrum of the stomach than the corpus.
  (caused by chemicals eg, bile reflux, NSAIDs, ethanol or oral iron).

Question 18

Describe features of gastric cancer

Answer 18

• Strongly associated with chronic gastritis (h.pylori or autoimmune causes)
• Histologically has background atrophic mucosa, chronic inflammation, intestinal metaplasia and dysplasia.
• Different classification schemes, eg, Lauren which identifies intestinal or diffuse type (poorly cohesive according to WHO classification).

Question 19

What are the features of diffuse/poorly cohesive gastric cancer

Answer 19

Histologically presents with individual malignant cells with mucin vacuoles (signet ring cells). Diffuse gastric ca may invade extensively without being endoscopically obvious, causing linitis plastica (leather bottle stomach difficult to inflate)
May metastasis to ovaries (Krunkenberg), supraclavicular LNs (Virchow’s node) or sister mary joseph tumour.

Question 20

Describe features of hereditary diffuse gastric cancer

Answer 20

• Caused by germline mutation CDH1.
• Causes small intramucosal foci of diffuse gastric cancer,
• Prophylaxis gastrectomy may be considered.
• Patients at increased risk of lobular carcinoma of the breast