Treatment of peptic ulcers

Question 1

Explain why H Pylori leads to peptic ulcers?

Answer 1

Increased gastric acid formation by increasing gastrin or somatostatin
Gastric metaplasia: cell transformation due to excessive acid exposure- underlying mechanism unknown
Downregulation of defence factors decrease epidermal growth factor (encourage epithelial growth) decrease bicarbonate production

Thus increased acidity and reduced defence cause ulcer

Question 2

Explain 3 aspects of H Pylori virulence?

Answer 2

H Pylori secretes Urease which catalyses urea into ammonium chloride and monochloramine which damage epithelial cells
Urease is also antigenic which evokes immune response and causes local damage
Certain virulent strains produce CagA (antigenic) or VacA (cytotoxic) which leads to more intense tissue inflammation

Question 3

What are two tests that will diagnose a H Pylori infection?

Answer 3

Carbon-urea breath test

Stool antigen test

Question 4

How is a H Pylori infection treated?

Answer 4

Amoxicillin and Clarithromycin/Metronidazole – Antibiotics

Question 5

Explain how the proton pump works?

Answer 5

H+-K+-ATPase (proton pump)
Expressed on secretory vesicles within parietal cells
Increased intracellular Ca causes increase in cAMP which leads to translocation of secretory vesicles to parietal cell apical surface where they can increase H+ secretion

Question 6

Describe another class of drugs used in H Pylori infections?

Answer 6

Proton pump inhibitors e.g. omeprazole

Question 7

Explain how NSAIDs use can cause peptic ulcers?

Answer 7

NSAIDs are
Directly cytotoxic
Reduces mucus production
Increases likelihood of bleeding

Question 8

Explain how you can teat NSAIDs induced ulcers?

Answer 8

Get off NSAIDs

Give H2 receptor antagonists like Ranitidine

Question 9

Describe 4 ways in which gastric acid secretion is regulated?

Answer 9

Acetylcholine (ACh) released from neurones (vagus / enteric) acts on muscarinic (M3) receptors which increase intracellular Ca
Prostaglandins (PGs) released from local cells act on EP3 receptors that increase cAMP
Histamine released from enterochromaffin-like cells (ECL) act on H2 receptors to increase cAMP
Gastrin released from bloodstream acts on cholecystokinin B receptors to increase cAMP

Thus all promote gastric acid secretion.