Pathology of Upper GI Tract

Question 1

What is a classic presentation of mouth cancer?

Answer 1

An ulcer which will not heal and persists without a definite, identifiable cause

Question 2

Name some risk factors for upper GI cancer?

Answer 2

Smoking
Alcohol
HPV

Question 3

What are the components of the GI wall?

Answer 3

Mucosa (non-keratinising stratified squamous epithelium)
Musculatise mucosae
Submucosa 
Muscularis propria 
Advenitia

Question 4

What happens to the histology of the gut wall when it comes into contact with acid?

Answer 4

Injure the squamous epithelium lining of the oesophagus
Increased number of inflammatory cells
Basal, proliferation zone of the epithelium is hyperplasic

Question 5

What infections can you get in the oesophagus?

Answer 5

Candida albicans (fungus)
Herpes simplex virus

Question 6

Name some causes of chemical inflammation of the oesophagus.

Answer 6

Peptic oesophagitis/GORD: relfux of acid or bile
Lye (NaOH, caustic soda)
Iron
Bisposphonates 
Tetracyclines

Question 7

Describe the pathology of a candida oesphagitis infection.

Answer 7

Active chronic inflammation with many neutrophils especially near the luminal surface

Question 8

Describe the pathology of a herpes simplex infection.

Answer 8

Atypical sqaumous cells
- empty looking
Inflammatory exudate and cells (slough)

Question 9

What is eosinophilic oesophagitis?

Answer 9

Overlap with reflex oesphagitits
Causes dysplasis
More common in younger people
May have a dietary sensitiser

Question 10

What is the pathology of an eosinophilic oesophagitis?

Answer 10

Eosinophils infiltrate oesphageal squamous epithelium
Allergic aetiology
- responsive to steriods (Fluticasone)
Trachealisation
- ring-like

Question 11

Which kind of oesophageal cancer is associated with smoking and drinking?

Answer 11

Squamous cell carcinoma

Question 12

Which kind of oesophageal cancer is associated with GORD and obesity?

Answer 12

Oesphageal adenocarcinoma

Question 13

What is Barrett’s oesophagus?

Answer 13

Metaplastic response to mucosal injury

• squamous becomes glandular
• with goblet cells

Question 14

What is Barrett’s oesophagus associated with?

Answer 14

Benign strcitures
Adenocarcinomas
- dysplasia to carcinoma progression over years
- definite low grade and high grade dysplasia increases risk of developing cancer

Question 15

What is the Seattle biopsy protocol?

Answer 15

4 biopsies every 2cm
- effective at finding dysplasia
May be replaced by targeted biopsy as endoscopy improves

Question 16

How is oesophageal cancer treated?

Answer 16

Radiofrequency ablation

Endoscopic treatments

Question 17

Describe the dysplasia spectrum.

Answer 17

Inflammation with reactive changes 
Indefinite for dysplasia
Mild, moderate (low grade) dysplasia
 Severe (high grade) dysplasia
Invasive adenocarcinoma (intramucosal, submucosal)

Question 18

How do you recognise dysplasia?

Answer 18

Architecturally and cytologically abnormal
Low grade
- cells polarised 
- nuclei stratified 
High grade
- polarity lost
- rounder nuclei
- vesicular, prominent nucleoli 
- abnormal mitosis
- necrosis

Question 19

Name some of the acute and chronic causes of gastritis?

Answer 19

Acute
- alcohol, NASIDs, severe trauma (burns and surgery)
Chronic
- Autoimmune
- Bacterial (H.Pylori)
- Chemical

Question 20

Describe the normal absorption of B12.

Answer 20

B12 bound to salivary Haptocorrin is protected from gastric acid
Haptocorrin is digested by the duodenum
B12 binds to intrinsic factor secreted by gastric parietal cells
- absorbed in the terminal ileum via specialised receptors

Question 21

Describe autoimmune gastritis.

Answer 21

Autoimmune destruction of parietal cells
- anti-parietal cell antibodies in the blood
Eventual complete loss of parietal cells with pyloric and intestinal metaplasia
Acholrhydria allows bacterial overgrowth
Persistant inflammation leads to epithelial dysplasia and possibly cancer

Question 22

What is Zollinger-Ellison Syndrome?

Answer 22

Hypersecretion of gastrin by an endocrine tumour (gastrinoma) in the pancreas or duodenum

• increased gastric acid output
• severe peptic ulceration

Question 23

Describe H.Pylori gastritis.

Answer 23

Potentialy lifelone H.Pylori colonises gastric mucosa
- active chronic inflammation
- IL-8 is released from epithelial cells to attract neutrophils
When in the antrum, specifically causes antral-predominant gastritis
- hypergastrinaemia and duodenal ulceration
Pangastritis
- hyperchlorhydria
- multi-focal atrophic gastritis
- intestinal type cancer

Question 24

What is the characteristic morphology of chemical gastritis?

Answer 24

Few inflammatory cells
Surface congestion oedema
Elongation of gastric pits
Tortuosity
Reactive hyperplasia/atypia
Ulceration
Affects the antrum more than the corpus

Question 25

What is the background histology of gastric cancer?

Answer 25

Atrophic mucosa
Chronic inflammation
Intestinal metaplasia
Dysplasia

Question 26

Describe diffuse gastric cancer.

Answer 26

Individual malignant cells with mucin vacuoles
- signet ring cells
May invade extensively without being endoscopically obvious (linitis plastica)
Weak link with gastritis
Commonly metastasises to the ovaries

Question 27

What is familial gastric cancer and how is it managed?

Answer 27

CDH1 (E-Cadherin) mutation
- 70-80% penetrance
Small intramucosal foci of diffuse gastric cancer
Associated risk of lobular carcinoma of the breast
Treated with prophylactic gastrectomy

Question 28

Why are rates of distal gastric cancer decreasing while rates of proximal gastric cancer are increasing?

Answer 28

Distal
- rates of H.Pylori are gradually being reduced
Proximal
- obesity and poor diet is increasing, as are rates of GORD