Flashcards in Anti-Ulcer Drugs Deck (34)
What are the two types of peptic ulcer?
Describe how gastric ulcers and duodenal ulcers can be distinguished based on their symptoms.
Gastric ulcer – pain at meal times when gastric acid is secreted
Duodenal ulcer – pain relieved by a meal as the pyloric acid closes –pain -3 hours after a meal
What are the protective factors that protect the stomach lining from damage?
Mucous lining the stomach
Bicarbonate produced by cells in the stomach
Prostaglandins facilitate a good blood flow in the stomach, increasemucous and bicarbonate production and inhibit acid secretion
Which cells produce stomach acid?
Explain how the parasympathetic nervous system affects gastric acid production.
The parasympathetic nervous, via the vagus nerve, stimulates histamine production by H cells
Histamine then stimulates an increase in acid production by parietal cells
What are the effects of gastrin?
They trigger the release of histamine from H cells
They also directly trigger acid production by the parietal cells
What do D cells release?
Give an example of a proton pump inhibitor.
What is the mechanism of action of PPIs?
Irreversible inhibitors of H+/K+ ATPase
What are the effects of PPIs?
Inhibits basal and stimulated gastric acid secretion from the parietal cells by >90%
Pathophysiology of peptic ulcers
H pylori dissolves mucus layer causing epithelial cell death from increased exposure to acidic environemnt -> ulcer
Investigations for peptic ulcer
Carbon urea breath test
Stool antigen test
Features of h pylori
How does h pylori increase gastric acid formation
Increase the production of gastrin and reduce that of somatostatin
How does h pylori cause gastric metaplasia
increased exposure to acid causes cell transformation
Defence factors downregulated by h pylori
epidermal growth factors
How is h pylori virulent
Produces urease which catalyses urea into ammonium chloride and monochloramine. These are what can damage the epithelial cells
How can h pylori cause inflammation
Urease is antigenic which evokes an immune response
Exotoxins produced by h pylori
CagA-> is antigenic so increases immune response
VacA-> cytotoxic increasing intensity of tissue inflammation
Treatment for H pylori positive peptic ulcers
Anitbiotics against H pylori
Proton pump inhibitor
Anti-biotics against H pylori
Amoxicillin and clarithomycin
Treatment for chronic peptic ulcer where first line treatment hasnt worked
Quinalone and tetracycline
Chelating agents like bismuth and sucralfate
What else increases number of proton pumps
Increased cytoplasmic Ca2+ which increases cAMP which leads to translocation of secretory vessels which proton pumps inside to apical membrane of parietal cells
What is alternative cause of peptic ulcer to H pylori infection
For example people taking asprin for heart conditions
Pathophysiology of NSAID causing peptic ulcer
Directly cytotoxic as reduces mucus production
Treatment of NSAID causing peptic ulcer
Proton pump inhibitor
Histamine receptor antagonist
Example of histamine receptor antagonist
How do histamine receptor antagonists work
Block H2 receptor
4 things regulating gastric acid regulation