20 Upper GI pathology

Question 1

What is the structure and history of the normal oesophagus?

Answer 1

Mostly squamous epithelium.
Cricopharyngeal and gastro-oesophageal junctions.
Distal 2cm below diaphragm is glandular mucosa.

Question 2

What is reflux oesophagitis?

Risk factors? (4)

Answer 2

Gastric acid/bile reflux.

Defective LOS, hiatus hernia, increased intra-abdo kPa, gastric outflow stenosis.

Question 3

Differentiate between the two types of hiatus hernia.

Answer 3

Sliding - reflux symptoms.

Paraesophageal - strangulation.

Question 4

What is the histology of reflux oesophagi’s? (4)

Answer 4

Basal cell hyperplasia
Papillae elongation
Increased cell desquamation (shedding).
Inflammatory cell infiltration.

Question 5

What are the complications of reflux oesophagitis? (5)

Answer 5

Ulceration.
Haemorrhage.
Perforation.
Benign stricture.
Barrett's oesophagus.

Question 6

What is Barrett’s oesophagus?

Which types of columnar mucosa do this?

Answer 6

Proximal extension of squamo-columnar junction. Glandular metaplasia.
Gastric cardia/body type, intestinal (‘specialised BM’).

Question 7

What can Barrett’s oesophagus develop into?

Answer 7

Adenocarcinoma.

Question 8

What are the two types of oesophageal carcinoma?

Answer 8

Squamous cell carcinoma.

Adenocarcinoma (most of UK).

Question 9

What is the epidemiology of adenocarcinoma of the oesophagus? (3)

Answer 9

Industrialised countries.
7 M : 1 F.
Caucasians.

Question 10

What are the types of macroscopic appearance of adenocarcinoma of the oesophagus? (6)

Answer 10

Plaque like.
Nodular.
Fungating.
Ulcerated.
Depressed.
Infiltrating.

Question 11

What are the risk factors for squamous carcinoma of the oesophagus? (7)

Answer 11

Tobacco, alcohol.
Nitrosamines.
Thermal injury.
HPV.
Male and black.

Question 12

Differentiate between the position of squamous carcinoma and adenocarcinoma of the oesophagus.

Answer 12

Adenocarcinoma: lower.
Squamous: middle and lower.

Question 13

In the TNM staging for oesophageal carcinoma, what are the T stages?

Answer 13

T1: invades lamina propria/ muscularis mucosa/ submucosa.
T2: invades muscularis propria.
T3: invades adventitia.
T4: invades adjacent structures.

Question 14

What is the pathogenesis of gastritis? (5,5)

Answer 14

Increased aggression: alcohol, smoking, drugs, radiation/chemo, infection
Impaired defences: ischaemia, shock, delayed emptying, duodenal reflux, impaired pepsin secretion.

Question 15

What are the main causes of chronic gastritis? (5)

Answer 15

Autoimmune.
H pylori infection.
Chemical injury.
NSAIDs.
Bile reflux.

Question 16

How des H pylori lead to chronic gastritis?

Answer 16

Damages epithelium -> chronic inflammation.
More common in antrum.
Results in glandular atrophy, fibrosis and intestinal metaplasia.

Question 17

What is peptic ulcer disease?
Sites? (3)
Aetiology? (5)

Answer 17

Local defect at least into submucosa.
Duodenum, antral/body junction, GOJ.
Hyperacidity, H pylori, reflux, NSAIDs, smoking.

Question 18

What is the histology of an acute gastric ulcer? (3)

Answer 18

Full thickness coagulative necrosis.
Covered with ulcer slough - necrotic debris, fibrin, neutrophils.
Granulation tissue on ulcer floor.

Question 19

What is the histology of a chronic gastric ulcer? (4)

Answer 19

Clear cut overhanging edges.
Extensive granulation + scarring.
Scarring breaches muscular propria.
Bleeding.

Question 20

What are the complications of peptic ulcers? (4)

Answer 20

Haemorrhage + anaemia.
Perforation + peritonitis.
Adjacent penetration.
Stricture - hourglass deformity.

Question 21

Differentiate between a gastric and a duodenal ulcer.

Answer 21

1 gastric : 3 duodenal.
Age risk : Only up to 35.
Low acid : Elevated acid.
70%HP : 95% HP caused.
Blood group A : O.

Question 22

Differentiate between adenocarcinoma of the GOJ and the gastric body/antrum.

Answer 22

GOJ: white males, reflux associated, increasing incidence.
Body: H. pylori and diet associated. Decreasing incidence.

Question 23

What are the frequent and non frequent gastric cancers.

Answer 23

Freq: adenocarcinoma.
Non: Endocrine, MALT lymphomas, stromal tumours.

Question 24

What are the two main histological subtypes of adenocarcinoma?

Answer 24

Scattered growth - diffuse type, signet ring cells.

Non-scattered - intestinale type, tubular adenoacarcinoma.

Question 25

Which mutation is involved in hereditary diffuse type gastric cancer?

Answer 25

Germline CDH1/E-cadherin mutations.

Question 26

What is the pathogenesis of coeliac disease?

Answer 26

Gliadin - component of gluten that induces epithelial cells to express IL-15.
Causes CD8+ Intraepithelial lymphocytes (IELs) to activate/proliferate.
IELs kill enterocytes.

Question 27

Why is coeliac disease a difficult diagnosis?

Answer 27

Atypical presentation.
Silent: +ve serology, villous atrophy, no symptoms.
Latent: +ve serology, no atrophy.
Symptomatic: anaemia, diarrhoea, bloating, chronic fatigue.

Question 28

What is coeliac disease associated with? (4)

Answer 28

Dermatitis herpetiformis. Lymphocytic gastritis and colitis.
Enteropathy-associated T-cell lymphoma.
Small intestinal adenocarcinoma.

Question 29

How is coeliac disease diagnosed? (4)

Answer 29

IgA antibodies to transglutaminase.
IgA/IgG to deaminated gliadin.
Anti-endomysial antibodies (specificity>sensitivity).
Tissue biopsy.

Question 30

What are the long term risks of coeliac disease? (4)

Answer 30

Anaemia.
Female infertility.
Osteoporosis.
Cancer.