Pathology of the Upper GI Tract Flashcards
Explain the normal structure of the GI tract including the different epithelium’s seen in the mucosa
- 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)
Define dysplasia and explain how squamous dysplasia may present and its risk factors.
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)
Explain the histological appearence of GORD
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.
What are some of the pathologies that can occur in the oesophagus
Infections - candidia albicans or herpes simplex virus (mainly in immunocompromised)
Inflammation - peptic oesophagitism, chemicals or pills eg, iron.
- Also get diverticular, achalasia etc
Explain the presentation of candida oesophagitis
- White plaques on endoscope.
- Fungal hyphae and spores on histology
Explain the presentation of herpes simplex infection of the oesophagus
Presents as oesophageal erosion with atypical squamous cells with nuclear invasion
Describe features and presentation of eosinophilic oesophagitis
- 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
What is Barret’s oesophagus?
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.
What are the two grades of Barretts oesophagus
Low grade - subtly different in appearence.
High grade - abnormal mitoses, necrosis with rounder nuclei
What are the risks of Barrett’s oesophagus and treatment
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
What are the two oesophageal cancers and their associations
- Squamous carcinoma which is associated with smoking and drinking.
- Adenocarcinoma which is associated with GORD and obesity
What are the different causes of gastritis?
Acute causes - alcohol, NSAIDs, severe trauma.
Chronic causes - ABC: Autoimmune, bacterial and chemical
Explain autoimmune gastritis and what is can lead to
- 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
What are the two patterns of gastritis caused by H.pylori
- 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
Explain the role of the host/microbe interface in the development of peptic ulceration
- Microbe factors include variants associated with more severe inflammation eg, CagA.
- Host factors include impaired mucosal defence, often due to NSAIDs or bile reflux.
What is the histological appearence of chronic active helicobacter related gastritis
- Lamina propriae is full of plasma cells and lymphocytes.
- Surface erosion and active inflammation.
- Helicobacter organisms on immunohistochemistry
What is the histological appearence of chemical gastropathy?
- 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).
Describe features of gastric cancer
- 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).
What are the features of diffuse/poorly cohesive gastric cancer
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.
Describe features of hereditary diffuse gastric cancer
- 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
