Anti-ulcer drugs Flashcards
Define ulcer
an open sore, break in in/external bodily surface that does not heal
Symptoms of a peptic/gastric ucler
epigastric pain, burning, ~30 mins post-prandially
Tests used in a suspected peptic ulcer
Carbon-urea breath test
Stool Ag test
H pylori test
Hx of NSAID use
2 main causes of peptic ulcers
Helicobacter pylori infection
chronic NSAID use
Describe structure of stomach lining
parietal cells
covered by mucous layer (+ HCO3- secretions too)
Describe and explain role of parietal cells
secrete H+ into the stomach lumen via apical H+/K+ATPase
test results for peptic ulcer caused by H pylori
+ve carbon urea breath test
+ve stool Ag
+ve for H pylori
Describe H pylori
gram -ve, spirochaete bacterium
normally inhabits GI tract
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
Enzyme which increases H pylori virulence
urease
Actions of urease enzyme
produces toxic products that damage parietal cells
Antigenic and evokes inflammatory response
Treatment for H pylori +ve peptic ulcers
Amoxicillin and clarithromycin (quinolone/tetracycline also can beconsidered)
PPIs
Give an example of a PPI
Omeprazole
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
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
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
Tests in NSAID
-ve carbon urea breath test
-ve stool Ag
-ve for H pylori
(+ve chronic NSAID use)
Treatment for peptic ulcer due to chronic NSAID use (drug type and example)
PPI = omeprazole
H2R antagonist = ranitidine
MOA of H2R antagonist
Antagonist for histamine H2R receptor, decreases cAMP, decreases H+/K+ATPase insertion and gastric acid secretion
What protein is responsible for the production of gastric acid and where is it found?
H+/K+ ATPase
on apical surface of parietal cells
