Anti-ulcer drugs

Question 1

Define ulcer

Answer 1

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

Question 2

Symptoms of a peptic/gastric ucler

Answer 2

epigastric pain, burning, ~30 mins post-prandially

Question 3

Tests used in a suspected peptic ulcer

Answer 3

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

Question 4

2 main causes of peptic ulcers

Answer 4

Helicobacter pylori infection

chronic NSAID use

Question 5

Describe structure of stomach lining

Answer 5

parietal cells

covered by mucous layer (+ HCO3- secretions too)

Question 6

Describe and explain role of parietal cells

Answer 6

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

Question 7

test results for peptic ulcer caused by H pylori

Answer 7

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

Question 8

Describe H pylori

Answer 8

gram -ve, spirochaete bacterium

normally inhabits GI tract

Question 9

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

Answer 9

• 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

Question 10

Enzyme which increases H pylori virulence

Answer 10

urease

Question 11

Actions of urease enzyme

Answer 11

produces toxic products that damage parietal cells

Antigenic and evokes inflammatory response

Question 12

Treatment for H pylori +ve peptic ulcers

Answer 12

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

Question 13

Give an example of a PPI

Answer 13

Omeprazole

Question 14

MOA of proton pump inhibtors eg omeprazole

Answer 14

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

Question 15

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

Answer 15

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

Question 16

Pathophysiology of chronic NSAID use in peptic ulcer formation

Answer 16

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

Question 17

Tests in NSAID

Answer 17

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

Question 18

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

Answer 18

PPI = omeprazole

H2R antagonist = ranitidine

Question 19

MOA of H2R antagonist

Answer 19

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

Question 20

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

Answer 20

H+/K+ ATPase

on apical surface of parietal cells