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Flashcards in Anti-ulcer drugs Deck (20)
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1

Define ulcer

an open sore, break in in/external bodily surface that does not heal

2

Symptoms of a peptic/gastric ucler

epigastric pain, burning, ~30 mins post-prandially

3

Tests used in a suspected peptic ulcer

Carbon-urea breath test
Stool Ag test
H pylori test
Hx of NSAID use

4

2 main causes of peptic ulcers

Helicobacter pylori infection
chronic NSAID use

5

Describe structure of stomach lining

parietal cells
covered by mucous layer (+ HCO3- secretions too)

6

Describe and explain role of parietal cells

secrete H+ into the stomach lumen via apical H+/K+ATPase

7

test results for peptic ulcer caused by H pylori

+ve carbon urea breath test
+ve stool Ag
+ve for H pylori

8

Describe H pylori

gram -ve, spirochaete bacterium
normally inhabits GI tract

9

Describe and explain factors contributing to H pylori's ability to cause peptic ulcers

-Increases H+ secretion by Increasing gastrin secretion and decreasing somatostatin
-Downreg of defences = decreased bicarbonate secretion and protective factors
-gastric metaplasia due to exposure to more acid

10

Enzyme which increases H pylori virulence

urease

11

Actions of urease enzyme

produces toxic products that damage parietal cells
Antigenic and evokes inflammatory response

12

Treatment for H pylori +ve peptic ulcers

Amoxicillin and clarithromycin (quinolone/tetracycline also can beconsidered)
PPIs

13

Give an example of a PPI

Omeprazole

14

MOA of proton pump inhibtors eg omeprazole

Block the H+/K+ ATPase on parietal cell apical membrane, decreases H+ secretion, increases stomach pH and limits damage to ulcer and allows for healing

15

Other hormones/factors controlling gastric acid secretion (origin, ligand, receptor and IC messenger)

neurones -> ACh -> M3AChR -> increased IC[Ca2+]
Enterochromaffin-like cells -> Histamine -> H2R -> increased cAMP
Local cells -> PGE2 -> EP3R -> decreased cAMP
blood stream -> Gastrin -> CCKBR -> increased IC[Ca2+]
All (except PGE2) increase translocation of H+/K+ ATPase to parietal apical surface

16

Pathophysiology of chronic NSAID use in peptic ulcer formation

NSAIDS inhibit PGE2 synthesis which is gastroprotective
Directly cytotoxic
Decrease mucous production
Decreased bicarbonate secretion
Increased gastric acid production
-> increased epithelial damage -> peptic ulcer formation

17

Tests in NSAID

-ve carbon urea breath test
-ve stool Ag
-ve for H pylori
(+ve chronic NSAID use)

18

Treatment for peptic ulcer due to chronic NSAID use (drug type and example)

PPI = omeprazole
H2R antagonist = ranitidine

19

MOA of H2R antagonist

Antagonist for histamine H2R receptor, decreases cAMP, decreases H+/K+ATPase insertion and gastric acid secretion

20

What protein is responsible for the production of gastric acid and where is it found?

H+/K+ ATPase
on apical surface of parietal cells