Gastritis and Peptic Ulceration

Question 1

List 6 protective factors of the gastric mucosal barrier

Answer 1

Lipid monolayer
Mucus gel layer
HCO3- secretion from mucous cells
Gastric blood flow carries away H+
Tight junctions of epithelial cells
Rapid cell turnover

Question 2

How do prostaglandins protect the mucosal barrier?

Answer 2

Inhibit HCl secretion
Stimulate HCO3-, phospholipid and mucus secretion
Increase mucosal blood flow
Modify local inflammation

Question 3

What is the acute gastritis?

Answer 3

Acute response to injury which heals in a few days

Question 4

What are the most common causes of gastritis?

Answer 4

Chemical injury, alcohol or drugs
Stress
Shock (decreased mucosal blood flow)
Burns
Head injury
Septicaemia
Staphylococcal food poisoning

Question 5

What histological features are seen in acute gastritis?

Answer 5

Oedema

Erosion with a layer of coagulative necrosis

Question 6

When are PPIs prescribed?

Answer 6

Treatment of gastritis or peptic ulcer

Prophylactically for patients in ICU with head injuries, shock, burns, etc.

Question 7

What is the difference between an erosion and an acute ulcer?

Answer 7

Erosion affects only mucosa

Acute ulcer extends past muscularis mucosae into submucosa

Question 8

What are Curling ulcers?

Answer 8

Ulcers in the duodenum associated with severe burns/trauma

Question 9

What are Cushing ulcers?

Answer 9

Gastric and duodenal ulcers in persons with intracranial injury

Question 10

What are the 3 main types of chronic gastritis?

Answer 10

Autoimmune
Helicobacter-associated
Chemical

Question 11

What is the pathogenesis of autoimmune chronic gastritis?

Answer 11

Immune-mediated destruction of acid-secreting tubules
Atrophy of mucosa, no production of gastric acid
Loss of IF leading to pernicious anaemia
Hypergastrinaemia leads to nodular ECL hyperplasia (can cause malignancy)

Question 12

Describe the regions of the stomach affected by the 3 types of chronic gastritis

Answer 12

AI: corpus only

Question 13

What circulating autoAbs are present in AI gastritis?

Answer 13

To H+/K+ ATPase on parietal cell membrane
To IF
To gastrin receptor

Question 14

What are the histological findings in AI gastritis?

Answer 14

Atrophy of acid secreting tubules
Intestinal and pyloric gland metaplasia
Chronic inflammation
N.B. In corpus only

Question 15

What causes chronic chemical gastritis?

Answer 15

Reflux of bile and alkaline duodenal juice

Longterm aspirin, NSAIDs

Question 16

What are the histological findings in chemical gastritis?

Answer 16

Epithelial desquamation
Hyperplasia of gastric pits
Oedema
Hyperplasia of lamina propria
Mild inflammatory cell infiltrate

Question 17

What occurs in acute H. pylori infection?

Answer 17

Neutrophilic gastritis with acute inflammation

Progresses to chronic infection within 3-4 weeks

Question 18

What are the histological findings in chronic H. pylori infection?

Answer 18

Acute inflammation of gastric pits (foveolitis) with intraepithelial neutrophils and pit abscess
Lymphocytes and plasma cells in lamina propria
Moderate mucosal atrophy
Intestinal metaplasia

Question 19

What are some possible longterm sequelae of chronic H. pylori infection?

Answer 19

PUD
Intestinal metaplasia may predispose to dysplasia and adenocarcinoma
MALToma
IDA
Atrophic gastritis (can cause B12 deficiency)

Question 20

What are the 2 major patterns of H. pylori gastritis and what is the difference between them?

Answer 20

Antrum-predominant: increased acid production with risk of duodenal ulcer and gastric metaplasia
Pan-gastritis: reduced acid production causing atrophy, intestinal metaplasia and gastric ulcer

Question 21

When does intestinal metaplasia occur in the stomach?

Answer 21

With reduced stomach acid (more closely resembles the intestinal environment)