Clinical Case Studies - Gastritis

Question 1

What is Gastritis?

Answer 1

Inflammation of the stomach lining.

Can be acute or chronic.

Question 2

What are the signs and symptoms of gastritis?

Answer 2

• Upper abdominal pain
• Waterbrash
• Reflux
• Belching/vomiting
• Tenderness

Question 3

Names some causes of acute gastritis

Answer 3

• Stress
• Burns - Curling’s ulcer
• NSAIDS
• Alcohol
• Uraemia

Question 4

What types of chronic gastritis are there?

Answer 4

Type A:

• Autoimmune - antibodies are present to parietal cells
• Presents with pernicious anaemia
• Occurs in the fundus or body of the stomach

Type B:

• Most Common
• Associated with Helicobacter pylori infection

Question 5

What type of organism is H Pylori?

Answer 5

• Gram negative spiral bacterium
• Infection begins in childhood
• Increases in prevalence with age
• First discovered in dogs, then humans

Question 6

What diseases are associated with H Pylori?

Answer 6

• Gastritis
• Duodenal ulcer
• Gastric ulcer
• Gastric adenocarcinoma
• Gastric lymphoma
• Potentially Barrett’s Oesophagus

Question 7

What tests are available for diagnosis of H Pylori?

Answer 7

Serum Antibody Test (Blood test)

• Identifies specific IgA or IgG
• Can indicate current or past infection
• Cannot tell if treatment has worked - antibodies can take years to disappear after treatment has worked

Gastric or Duodenal Mucosal Biopsy

• Enzyme test for urease production
• Haematoxylin and Eosin staining/Giemsa staining/Silver Staining

Urease Breath Test

• Radiolabelled Urea (14C or 13C) is broken down by urease
• Labelled CO2 is released and measured
• Unmetabolised is CO2 is excreted in urine

Stool Antigen test

• Can determine if treatment has been successful

Question 8

How Does H Pylori survive in the stomach?

Answer 8

• Bacterial urease hydrolyzes gastric luminal urea to form ammonia
• Helps neutralize gastric acid and enables it to penetrate the gastric mucus layer
• As the pH outside the organism drops, a urea channel permits internal movement of urea to maintain a favorable intracellular pH.
• Spiral shape, flagella, and the mucolytic enzymes facilitate its passage through the mucus layer to the gastric surface epithelium.

Question 9

How does H Pylori cause peptic ulcers?

Answer 9

Increased gastric acid production

• Causes increase of basal and stimulated acid output
• Trophic action on parietal cells and histamine-secreting enterochromaffin-like (ECL) cells
• Stimulates parietal cells largely via the release of histamine

Gastric metaplasia

• Gastric epithelium in the first portion of the duodenum
• May weaken the mucosa, making it more susceptible to acid injury

Immune Response

• Increased production of inflammatory cytokines - interleukin (IL)-1, -6, -8 and tumor necrosis factor alpha.

Mucosal Defense Factors

• Increased epidermal growth factor
• Decreased proximal duodenal mucosal bicarbonate production
• proteases that degrade normally protective mucous glycoproteins