20 Upper GI pathology Flashcards

1
Q

What is the structure and history of the normal oesophagus?

A

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

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2
Q

What is reflux oesophagitis?

Risk factors? (4)

A

Gastric acid/bile reflux.

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

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3
Q

Differentiate between the two types of hiatus hernia.

A

Sliding - reflux symptoms.

Paraesophageal - strangulation.

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4
Q

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

A

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

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5
Q

What are the complications of reflux oesophagitis? (5)

A
Ulceration.
Haemorrhage.
Perforation.
Benign stricture.
Barrett's oesophagus.
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6
Q

What is Barrett’s oesophagus?

Which types of columnar mucosa do this?

A

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

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7
Q

What can Barrett’s oesophagus develop into?

A

Adenocarcinoma.

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8
Q

What are the two types of oesophageal carcinoma?

A

Squamous cell carcinoma.

Adenocarcinoma (most of UK).

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9
Q

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

A

Industrialised countries.
7 M : 1 F.
Caucasians.

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10
Q

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

A
Plaque like.
Nodular.
Fungating.
Ulcerated.
Depressed.
Infiltrating.
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11
Q

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

A
Tobacco, alcohol.
Nitrosamines.
Thermal injury.
HPV.
Male and black.
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12
Q

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

A

Adenocarcinoma: lower.
Squamous: middle and lower.

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13
Q

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

A

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

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14
Q

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

A

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

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15
Q

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

A
Autoimmune.
H pylori infection.
Chemical injury.
NSAIDs.
Bile reflux.
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16
Q

How des H pylori lead to chronic gastritis?

A

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

17
Q

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

A

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

18
Q

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

A

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

19
Q

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

A

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

20
Q

What are the complications of peptic ulcers? (4)

A

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

21
Q

Differentiate between a gastric and a duodenal ulcer.

A
1 gastric : 3 duodenal.
Age risk : Only up to 35.
Low acid : Elevated acid.
70%HP : 95% HP caused.
Blood group A : O.
22
Q

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

A

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

23
Q

What are the frequent and non frequent gastric cancers.

A

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

24
Q

What are the two main histological subtypes of adenocarcinoma?

A

Scattered growth - diffuse type, signet ring cells.

Non-scattered - intestinale type, tubular adenoacarcinoma.

25
Q

Which mutation is involved in hereditary diffuse type gastric cancer?

A

Germline CDH1/E-cadherin mutations.

26
Q

What is the pathogenesis of coeliac disease?

A

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

27
Q

Why is coeliac disease a difficult diagnosis?

A

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

28
Q

What is coeliac disease associated with? (4)

A

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

29
Q

How is coeliac disease diagnosed? (4)

A

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

30
Q

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

A

Anaemia.
Female infertility.
Osteoporosis.
Cancer.