Treatment of Peptic ulcers

Question 1

What are the 2 types of peptic ulcers and how do they present?

Answer 1

1. Gastric ulcers - epigastric pain worsens upon eating a meal
2. Duodenal ulcers - epigastric pain eases when eating a meal

• Burning pain in both

Question 2

What are 2 tests to test for the presence of H.Pylori?

Answer 2

1. Carbon-urea breath test

• Give the patient lots of urea
• H.Pylori metabolises urea and releases nitrogen in the breath and this can be detected

2. Stool antigen test
   * Test for presence of H.Pylori in the stool

Question 3

Describe the motility and morphology of H.Pylori

Answer 3

• Motile - flagella
• Spirochete

Question 4

Describe the pathophysiology of how H.Pylori causes peptic ulcers

Answer 4

• H.Pylori produces urease - this digests away at the mucous layer lining the stomach cells
• The cells are then exposed to gastric acid
• H.pylori also produces exotoxins that damages cells
• Damage to mucous layer, epithelial layer and interstitial layer
• Formation of peptic ulcers

Question 5

What is the first line treatment for peptic ulcers caused H.Pylori?

Answer 5

• Antibiotics…
• Amoxicillin, Clarithromycin / Metronidazole

Question 6

What other treatments exist for peptic ulcers caused by H.Pylori?

Answer 6

• On top of first line treatment (amoxicillin, clarithromycin / metronidazole)….
• Second line antibiotics - quinolone or tetracycline
• Bismuth
• Proton Pump Inhibitors

Question 7

Which cells in the stomach release histamine?

Answer 7

H-cells

Question 8

Which cells in the stomach produce gastrin?

Answer 8

G-cells

Question 9

What are the various chemical mediators of gastric acid secretion and how do they work?

Answer 9

• Cholinergic system - promotes histamine production from H-cells, which in turn promotes gastric acid secretion from parietal cells
• Histaminergic system - H-cells produce histamine which act on histamine receptors on parietal cells to promote gastric acid secretion
• Somatostatin - reduces parietal cell secretion of gastric acid
• Gastrin - increases parietal cell secretion of gastric acid

Question 10

Which cells in the stomach produce gastric acid?

Answer 10

Parietal cells

Question 11

Describe how the PSNS affects gastric acid secretion

Answer 11

• PSNS via vagus nerve (cholinergic system), stimulates histamine production
• Which in turn acts on histamine receptors on parietal cells to promote gastric acid secretion

Question 12

How does the proton pump inhibitor ‘Omeprazole’ work?

Answer 12

Irreversible inhibition of H+ / K+ ATPase

Question 13

How does the proton pump inhibitor ‘Ranatidine’ work?

Answer 13

• Histamine receptor antagonist
• Therefore, it prevents histamine mediated stimulation of parietal cell gastric acid secretion

Question 14

Describe the pathophysiology of how NSAIDs cause peptic ulcers

Answer 14

• Directly cytotoxic
• Inhibits production of prostaglandins - therefore reduces mucous and bicarbonate production and increases gastric acid production - greater exposure of cells in stomach to acidity
• Increases the likelihood of bleeding

Question 15

Which cells in the stomach produce pepsinogen?

Answer 15

Gastric chief cells

Question 16

What are 3 substances that are protective of the stomach?

Answer 16

1. Mucous - lines the stomach so protective against acidic stomach environment
2. Bicarbonate - at stomach lining - neutralises the stomach acid
3. Prostaglandins - increases blood flow, increases mucous and bicarbonate secretion and reduces gastric acid secretion