Treatment of gastric ulcers Flashcards
Are gastric or duodenal ulcers treated differently?
No-different places but pharmacologically the same
What is the most common presentation of peptidic ulcer?
Epigastric pain-burning sensation after meals (or all the time)
NEED TO CHECK if H pylori positive
What are the 2 main tests for ulcers?
Carbon-urea breath test-test if presence in urea in breath-if positive often H pylori
Stool antigen-check for H pylori-check for urease enzyme
check if use NSAIDS-can cause ulcers
How does H pylori cause petidic ulcers?
Normally-mucus over epithelia
H pylori dissolves mucus-increase chance of damage to epithelium by the stomach acid (not all mucus but slowly digs out patches
the damage is what causes the ulcer in the end -> and when cause severe bleeding can be very bad
What is first line treatment can be used to treat stomach ulcers?
first line Usually-pencillin (amoxicilin) and clarythromycin/metrodinazole
usually work with Abx + proton pump inhbitors (second line)
Describe what H.pylori is and how it decreases stomach mucus?
Motile, gram - bacteria-can go to other areas
Normally commensal in GI tract
Increases gastric acid formation-increasing gastrin production or decrease of somatostatin production
also large deregulation of defence factors-like epidermal grwoth factor
=> cause gastric metaplasia
urease-enzyme produced by h pylori-either directly damage cell, or create ammonium chloride (dissolves mucus)
Also cause immune response
Virulence factors-not all strains produce them all. Main one are VacA-cytotoxic, and CagA-antigenic (increase immune response)
What is the main second line treatment for ulcers? if first line didnt work?
Change Abx-quinolone, tetracyclin
if 1st line doesnt work-consider it as chronic disease
also use Bismuth/sucralfate-chelating agents that increase pH of stomach acid-reduce Hpylori love, and damage to cells
proton pumps inhbitors-4-12 weeks
Why are proton pumps inhbitor so good to treat stomach ulcers?
proton pumps inhbitors-H/K/ATPase that send H+ in stomach –and more are expressed in an ulcer
reduce pH-increase acidity
translocation to cell membrane happens after Ca entry to cell
OR ulcer formation-increase activity
What is the most common cause of peptic ulcer if not Hpylori? Why (pathophysiology)
NSAID use-aspirin, ibuprofens ctyotoxic-permanant COX damage Reduce mucus production Increase bleeding chance and increase acidity-ulcer
What is the treatment option for NSAID caused peptic ulcer?
try removal of NSAID (if not used to treat other disease like stroke)
Proton pump inhbitors
Histamine receptor antagonist (ranitadine-over the counter)-4/8 weeks (H2 receptor increase acid secretion)-but pumps are just better
How is gastric acid secretion regulated?
H pumps on lumen/apical side
Other side-many things regulate it
M3R-PSNS-ACh-increase Ca-increase expression
Ep3-Prostaglandins-local cells-reduce cAMP-reduce pump expression
Histamine (ECL)-increase cAMP
Gastrin (G-cell)-increase cellular Ca
Somatostatin-G cells-inhbit cAMP-reduce acidity