Stomach (GIT) Flashcards

1
Q

What are common causes of gastritis?

A

Drugs (NSAIDs)
Cocaine
Bacterial infection (H. pylori)
Alcohol

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2
Q

Gastritis can be classed as acute, chronic and active chronic.

How can you diffferentiate these microscopically?

A

Acute = neutrophils present
Chronic = plasma cells present
Active chronic = both neutrophils and plasma cells present.

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3
Q

What macroscopic features might you see in gastritis?

A

Eryhtema
Oedema
Intestinal metaplasia
Enlarged folds

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4
Q

What anatomical sites do you find different types of gastritis?

A

H. pylori is often found in the antrum.

Reactive / chemical gastritis involves the greater curvature of the stomach due to gastric contents settling there.

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5
Q

What are the two causes of atrophic gastritis?

What is the effect on acid production in these?

A

H pylori infection - acid production can be increased or decreased

Autoimmune gastritis (AIG) - acid production is decreased.

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6
Q

Why can Vitamin B12 deficiency arise from atrophic gastritis?

A

Chronic inflammation of gastric mucosa causes loss of gastric glands (parietal cells) responsible for creating intrinsic factor.

Without IF we cannot absorb B12.

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7
Q

What is the pathophysiology of H. pylori associated ulcer formation?

What is the relationship between H. pylori infection location and ulcer formation?

A

Antral gastritis from H pylori results in increased gastric acid production, creating environment for ulcer formation.

Antral inflammation causes release of gastrin, causing parietal cells to secrete acid.
H. pylori infection of fundus/body only has modest increase in gastric acid production due to atrophy to gastric glands in this area, and thus are relatively protected from antral/duodenal ulcers.

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8
Q

What are the two anatomical sites that peptic ulcer disease forms ulcers/

A

Stomach (gastric ulcer) or duodenum (duodenal ulcer)>

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9
Q

What are the common presentations of P.U.D and complications?

A

Present with burning after meals and at night.

Complications: Bleeding, perforation, dysplasia –> carcinoma.

Additionally, can casuse lymphoid hyperplasia and MALT lymphoma.

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10
Q

What are the three types of benign gastric tumours, with commonality, dysplastic potential and neoplasm/not neoplasm

A

Hyperplastic polyp - most common, can become dysplastic, not neoplasm

Fundic gland polyp - rarely become dysplastic, not neoplasm

Gastric adenoma - neoplastic polyp with low/high grade dysplasia. Can become gastric carcinoma

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11
Q

What type of carcinoma are most gastric carcinomas?

WHat are some risk factors?

A

Adenocarcinoma.

Risk factors:
Smoked/salted food (dietary carcinogens - Japan = capital of gastric cancer)
H pylori causing intestinal metaplasia

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12
Q

What are the two classifications of gastric carcinoma?

A

Intestinal type adenocarcinoma - forms solitary mass, caused by chronic inflammation that leads to dysplasia/adenoma that develops into adenocarcinoma (e.g. H pylori)

Diffuse adenocarcinoma - infiiltrative, no precursor lesions, due to mutations in genes. Cells have characteristic signet ring shape.

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13
Q

Can gastric carcinoma be ulcerative?

A

Yes

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14
Q

What is the main cause of MALT lymphoma?

A

Chronic inflammation from H pylori infection.

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15
Q

What is the name given to mesenchymal tumours of teh stomach?

From what cells do they arise?

A

Gastrointestinal Stromal Tumours (GISTs)

Cells of Cajal

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