Pathology of the Stomach

Question 1

3 categories of inflammatory stomach disorders?

Answer 1

Acute gastritis - due to irritant chemical injury, e.g: alcohol, NSAIDs

Chronic gastritis (ABC):
Autoimmune
Bacterial
Chemical, e.g: alcohol, NSAIDs and bile reflux

Rare:
Lymphocytic (increase in gastric intra-epithelial lymphocytes)
Eosinophilic (infiltration of eosinophils into the stomach wall; hypersensitivity cause)
Granulomatous (Crohn’s disease, sarcoidosis)

Question 2

Describe autoimmune chronic gastritis

Answer 2

Rarest type; a reaction to intrinsic factor and parietal cells (anti-parietal and anti-intrinsic factor antibodies)

Long-term shows atrophy and intestinal metaplasia in the body of the stomach

Question 3

Consequences of autoimmune chronic gastritis?

Answer 3

Pernicious anaemia, due to B12 deficiency; this can lead to sub-acute combined degeneration of spinal cord and neurological disorders

Increased risk of malignancy

Question 4

Describe bacterial chronic gastritis

Answer 4

Most common type and is due to Helicobacter pylori; it inhabits the niche between the epithelial cell surface and mucous barrier

Lamina propria plasma cells produce anti-H. pylori antibodies, which can cause chronic active gastritis (IL-1, IL-8 and TNFα are critical). This characterised by neutrophil infiltration of the epithelium and lymphocyte/plasma infiltration of the stroma

Epithelium may show metaplasia to a small intestinal type, for a protective effect

Question 5

Consequences of H. pylori gastritis?

Answer 5

Increased risk of:
Duodenal and gastric ulcers
Gastric carcinoma
Gastric lymphoma

Question 6

Describe chemical chronic gastritis

Answer 6

Direct injury to mucous layer by fat-soluble materials

There is marked epithelial hyperplasia in the neck cells of the gastric pits and oedema of the mucosa; there is usually a lack of a inflammatory infiltrate and lack of H. pylori

May produce erosions/ulcers

Question 7

What are peptic ulcers?

Answer 7

Mucosal erosion that penetrates the muscularis mucosae and involves the submucosa, due to acid and pepsin attack

Question 8

Sites of chronic peptic ulcers?

Answer 8

1st part of the duodenum

Stomach (part. at the junction of the body and antrum)

Oesophago-gastric junction

Stromal ulcers

Question 9

Pathogenesis of chronic duodenal ulcers?

Answer 9

Increased acid secretion and sustained secretion of this; there is limited buffering capacity and also a failure of mucosal defence

This produces gastric metaplasia, in the vicinity of the ulcer, and H. pylori infection, inflammation, epithelial damage and ulceration

Question 10

Morphology of peptic ulcers?

Answer 10

2-10 cm across with well-defined edges

Question 11

Microscopic appearance of peptic ulcers?

Answer 11

Layered appearance with a:
Floor of necrotic fibrinopurulent debris and fibrin
Base of granulation tissue
Deepest layer is fibrotic scar tissue

Question 12

Peptic ulcer complications?

Answer 12

Perforation causes peritonitis

Penetration

Haemorrhage due to exposure of major arteries

Stenosis - due to fibrosis

Intractable pain due to nerve stimulation

Question 13

Categories of gastric tumours?

Answer 13

Benign (polyps) - protrusion above the epithelium:
Hyperplastic polyps (occur on a Hx of gastritis)
Cystic fundic gland polyps (due to marked dilatation of the fundic glands and more common in those with FAP)

Malignant (tumours):
(Adeno)carcinoma - malignant epithelial tumours
Lymphomas
Gastrointestinal Stromal Tumours (GISTs) - tumour of connective tissue (mesenchymal origin - sarcoma), the cells of which are similar in appearance to pacemaker cells of Cajal

Question 14

Role of H. pylori in development of gastric adenocarcinoma?

Answer 14

Patients with anti-H. pylori antibodies are at higher risk

Question 15

Pathogenesis of gastric adenocarcinoma?

Answer 15

H. pylori infection leads to chronic gastritis; this causes intestinal metaplasia/atrophy

Dysplasia results and then carcinoma

Question 16

4 pre-malignant conditions assoc. gastric adenocarincoma?

Answer 16

Pernicious anaemia
Partial gastrectomy
HNPCC
Menetrier’s disease

Question 17

Subtypes of adenocarcincoma?

Answer 17

Intestinal type -exophytic/polypoid mass (grows outwards, above the epithelium); these are gland-forming

Diffuse type - ulcerative/infiltrative into the stomach wall; this dis-cohesive cancer cells spreads to all margins of the stomach and so are less resectable (worse prognosis) than intestinal type

Question 18

Appearance of a benign peptic ulcer?

Answer 18

Mimic cancer but are more punched out and lack a raised, rolled edge

Question 19

How do diffuse type adenocarcinomas produce linitis plastica?

Answer 19

Non-cohesive, mucin-containing, signet-ring cells infiltrate widely through the stomach walls, often being assoc. with linitis plastica (macroscopic appearance of thickening/rigidity of the stomach wall)

Question 20

Spread of gastric adenocarcinomas?

Answer 20

Local - into other organs and into peritoneal cavity and ovaries (Kruckenberg spread)

Lymph nodes

Haematogenous - early liver metastases may be seen

Question 21

What are gastric lymphomas?

Answer 21

Maltomas (lymphoma involving MALT and is B-cell derived); assoc. with H. pylori infection

If H. pylori is eradicated, the majority of the time the cancer will regress

Question 22

Pathogenesis of gastric maltoma?

Answer 22

There is continuous inflammation, which induces evolution into a clonal B-cell proliferation (low-grade lymphoma) - lymphocytes will attack the gastric epithelium

If untreated, this evolves into a high-grade B-cell lymphoma