Upper GI Pathology Flashcards

1
Q

Describe the oesophageal epithelium

A

Upper 2/3 squamous epithelium, lower 1/3 columnar epithelium, joined by the squamo-columnar junction/ Z-line

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2
Q

What is the most common cause of oesophagitis?

A

Reflux oesophagitis/ gastro-oesophageal reflux disease (GORD)

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3
Q

State some complications of GORD

A

Ulceration, haemorrhage, Barrett’s oesophagus, stricture, perforation

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4
Q

How is GORD managed?

A

Lifestyle changes (weight loss, smoking cessation), proton pump inhibitors (PPIs), H2 receptor antagonists

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5
Q

Name a proton pump inhibitor

A

Omeprazole

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6
Q

Name a H2 receptor antagonist

A

Ranitidine

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7
Q

What is Barrett’s oesophagus?

A

Intestinal metaplasia of squamous epithelium into columnar epithelium following chronic GORD

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8
Q

What % of patients with symptomatic GORD develop Barrett’s oesophagus?

A

10%

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9
Q

What is the main risk of Barrett’s oesophagus?

A

Progression into cancer

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10
Q

State at least 3 risk factors for oesophageal adenocarcinoma

A

Barrett’s oesophagus, smoking, obesity, prior radiotherapy

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11
Q

Which group is oesophageal adenocarcinoma most common in?

A

Caucasian men

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12
Q

State the 2 main and at least 2 other risk factors for oesophageal squamous cell carcinoma

A

Main: Alcohol, smoking
Others: achalasia of cardia, Plummer-Vinson syndrome, nutritional deficiencies, nitrosamines, HPV, Afro-Caribbean ethnicity, male gender

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13
Q

What percentage of squamous cell carcinoma is found in each third of the oesophagus?

A

Proximal: 20%
Middle: 50%
Distal: 30%

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14
Q

Describe the clinical features of oesophageal squamous cell carcinoma

A

Progressive dysphagia (solids then fluids), odynophagia, anorexia, severe weight loss

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15
Q

Where does oesophageal squamous cell carcinoma metastasise to?

A

Lymph nodes, liver, proximal structures

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16
Q

What are oesophageal varices?

A

Engorged dilated veins, usually due to portal hypertension

17
Q

How are bleeding oesophageal varices managed?

A

Emergency endoscopy for sclerotherapy or banding

18
Q

State at least 3 causes of acute gastritis

A

Aspirin and other NSAIDs, bleach, acute H pylori, severe stress

19
Q

Which section of the stomach is chronic H pylori gastritis usually found in?

20
Q

State at least 3 causes of chronic gastritis

A

H pylori, pernicious anaemia, alcohol, smoking, IBD, strongyloides

21
Q

Describe the histology of chemical gastritis

A

Foveolar hyperplasia, chronic inflammation

22
Q

State 2 complications of chronic gastritis

A

Gastric ulcers, cancer

23
Q

What is a gastric ulcer?

A

Breach through the muscularis mucosa into the submucosa

24
Q

Describe the clinical features of gastric ulcers

A

Epigastric pain worse when eating and relieved by antacids, weight loss

25
How are gastric ulcers diagnosed?
Endoscopy showing punched out lesion with rolled margins. Biopsy for H pylori histology status
26
State 3 complications of gastric ulcers
Iron deficiency anaemia, perforation, cancer
27
Which malignancy is associated with H pylori infection?
Gastric lymphoma
28
How is gastric lymphoma managed?
Eradication of H pylori with triple therapy - proton pump inhibitor, clarithromycin, and either amoxicillin or metronidazole
29
State the ratio of gastric to duodenal ulcers
1:4
30
Describe the clinical features of duodenal ulcers
Epigastric pain worse at night and relieved by food and milk
31
Which groups are gastric and duodenal ulcers most common in?
Gastric: elderly Duodenal: young adults
32
Which HLAs are associated with coeliac disease?
HLA-DQ2, HLA-DQ8
33
What is coeliac disease?
T-cell mediated autoimmune disease causing gluten intolerance - gluten intake leads to villous atrophy and malabsorption
34
Which group is mainly affected by coeliac disease?
Females of Irish descent
35
Describe the clinical presentation of coeliac disease
Presents in childhood: Steatorrhoea, failure to thrive, abdominal pain, bloating, nausea, vomiting, fatigue, iron deficiency anaemia, dermatitis herpetiformis
36
State the diagnostic tests for coeliac disease
Anti-endomysial antibodies, anti-tissue transglutaminase IgA antibodies, anti-gliadin antibodies, upper GI endoscopy and duodenal biopsy
37
What % of patients with poorly controlled coeliac disease progress to duodenal T cell lymphoma?
10%