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Flashcards in Anti-Ulcer Drugs Deck (34)
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1

What are the two types of peptic ulcer?

Gastric ulcer
Duodenal ulcer

2

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

3

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

4

Which cells produce stomach acid?

Parietal cells

5

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

6

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

7

What do D cells release?

Somatostatin

8

Give an example of a proton pump inhibitor.

Omeprazole

9

What is the mechanism of action of PPIs?

Irreversible inhibitors of H+/K+ ATPase

10

What are the effects of PPIs?

Inhibits basal and stimulated gastric acid secretion from the parietal cells by >90%

11

Pathophysiology of peptic ulcers

H pylori dissolves mucus layer causing epithelial cell death from increased exposure to acidic environemnt -> ulcer

12

Investigations for peptic ulcer

Carbon urea breath test
Stool antigen test

13

Features of h pylori

Gram negative
Motile
Microaerophilic

14

How does h pylori increase gastric acid formation

Increase the production of gastrin and reduce that of somatostatin

15

How does h pylori cause gastric metaplasia

increased exposure to acid causes cell transformation

16

Defence factors downregulated by h pylori

epidermal growth factors
bicarbonate

17

How is h pylori virulent

Produces urease which catalyses urea into ammonium chloride and monochloramine. These are what can damage the epithelial cells

18

How can h pylori cause inflammation

Urease is antigenic which evokes an immune response

19

Exotoxins produced by h pylori

CagA-> is antigenic so increases immune response
VacA-> cytotoxic increasing intensity of tissue inflammation

20

Treatment for H pylori positive peptic ulcers

Anitbiotics against H pylori
Proton pump inhibitor

21

Anti-biotics against H pylori

Amoxicillin and clarithomycin

22

Treatment for chronic peptic ulcer where first line treatment hasnt worked

Quinalone and tetracycline
Chelating agents like bismuth and sucralfate

23

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

24

What is alternative cause of peptic ulcer to H pylori infection

NSAID use
For example people taking asprin for heart conditions

25

Pathophysiology of NSAID causing peptic ulcer

Directly cytotoxic as reduces mucus production

26

Treatment of NSAID causing peptic ulcer

Remove NSAID
Proton pump inhibitor
Histamine receptor antagonist

27

Example of histamine receptor antagonist

Ranitidine

28

How do histamine receptor antagonists work

Block H2 receptor

29

4 things regulating gastric acid regulation

Ach
Prostaglandins
Histamine
Gastrin

30

How does Ach affect acid secretion

Ach from neurones acts on M3 receptors to increase Ca2+ conc