20 Upper GI pathology Flashcards Preview

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Flashcards in 20 Upper GI pathology Deck (30):
1

What is the structure and history of the normal oesophagus?

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

2

What is reflux oesophagitis?
Risk factors? (4)

Gastric acid/bile reflux.
Defective LOS, hiatus hernia, increased intra-abdo kPa, gastric outflow stenosis.

3

Differentiate between the two types of hiatus hernia.

Sliding - reflux symptoms.
Paraesophageal - strangulation.

4

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

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

5

What are the complications of reflux oesophagitis? (5)

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

6

What is Barrett's oesophagus?
Which types of columnar mucosa do this?

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

7

What can Barrett's oesophagus develop into?

Adenocarcinoma.

8

What are the two types of oesophageal carcinoma?

Squamous cell carcinoma.
Adenocarcinoma (most of UK).

9

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

Industrialised countries.
7 M : 1 F.
Caucasians.

10

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

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

11

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

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

12

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

Adenocarcinoma: lower.
Squamous: middle and lower.

13

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

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

14

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

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

15

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

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

16

How des H pylori lead to chronic gastritis?

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

17

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

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

18

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

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

19

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

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

20

What are the complications of peptic ulcers? (4)

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

21

Differentiate between a gastric and a duodenal ulcer.

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

22

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

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

23

What are the frequent and non frequent gastric cancers.

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

24

What are the two main histological subtypes of adenocarcinoma?

Scattered growth - diffuse type, signet ring cells.
Non-scattered - intestinale type, tubular adenoacarcinoma.

25

Which mutation is involved in hereditary diffuse type gastric cancer?

Germline CDH1/E-cadherin mutations.

26

What is the pathogenesis of coeliac disease?

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

27

Why is coeliac disease a difficult diagnosis?

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

28

What is coeliac disease associated with? (4)

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

29

How is coeliac disease diagnosed? (4)

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

30

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

Anaemia.
Female infertility.
Osteoporosis.
Cancer.

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