123b Peptic Ulcer Flashcards Preview

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Flashcards in 123b Peptic Ulcer Deck (31):

what causes most ulcers?

H Pylori - but a minority of those infected with it get ulcers


Do anti-acid drugs work with h pylori ulcers?

heals, but they come back when drugs stopped


pernicious anmeia

diffuse involvement of entire stomach -- loss of gastric parietal cells --> low IF --> low B12


What increases gastric acid secretion?

Vagal stimulation
Antral distention (most important) (G cells release gastrin)
Increased pH (low pH inhibits gastrin)


what glands are in the body of stomach?

oxyntic/parietal glands
parietal cell - IF and HCl
D cell - somatostatin
Chief Cell - pepsinogen
Enterochromaffin cell - ANP?


Where are g-cells located? what do they secrete?

pyloric gland in antrum of stomach

secrete gastrin --> ECL cells (and parietal cells directly) --> histamine --> parietal cell --> acid secretion


PPI's affect what?

H+/K+ ATPase in parietal cells


D cells - what do they release? in response to what? what does it do?


stops gastrin release from G-cells AND HCl from parietal cells (acts like a break)

low stomach pH


what does stomach acid do?

destroys bacteria


does h pylori cause cancer?

yes, gastric cancer carcinogen and MALT lymphoma (in stomach)


where can H pylori live? is it common in wealthy areas?

stomach and anywhere with gastric metaplasia

no, poor areas


how is hp spread? reservoir? endemic anywhere?

oral-oral; fecal-oral

human reservoir

people in shitty areas get it very early b/c its endemic; wealthy countries have cleaned up water supplies so only old people have it now from when they were kids


duodenal ulcers - what percent from hp? gastric ulcer?

70% - NSAIDs cause gastric ulcers too


pathogenesis of HP infection?

swims thru mucus with flagella
attaches to mucus and multiples
Damages mucosa and internalized in epithelium


what does hp make to protect itself in the acidic stomach?

many things to defeat immune system including:

urease - breaks acid into CO2 and ammonia which protects it as a cloud


how does hp cause duodenal ulcers?

high gastrin postprandial (post meal) release when infected with hp --> D cell (secretes somatostain and prevents secretion) are damaged --> increased acid into duodenal leads to gastric metaplasia which allows hp to live there


what cell type in the stomach does hp preferentially damage? what does this cause?

D cells
less somatostatin (lose break on gastrin release)


what do the majority of duodenal ulcers have for tissue type?

gastric metaplasia

ulcer is a combo of hp and other factors (NSAIDs, smoking, etc)


if you get rid of HP what are the chances of recurrence?

low (~1% per ear)


If someone from a wealthy area presents with dyspepsia should you test for HP?

No, pre test prob low - only test for hp if you think it might be an ulcer (hp can cause dyspepsia but unlikely cause in non-endemic areas)


what are the 2 major patterns of hp induced chronic gastritis? what does theses patterns lead to?

antrum predominant hp; parietal cells still intact so make a lot of acid --> gastric metaplasia/duodenal ulcer

pan-gastritis; hp all over stomach --> decrease parietal cell mass --> low acid production --> gastric ulcer and atrophy


test for HP

urea breath test and stool antigen - active infection

serology - IgG just tells previous exposure not active infection


non-hp ulcers rates are increasing in the us - what else causes ulcers?

NSAIDs and aspirin
zollinger-ellison syndrome
false negative test


What 2 ways can NSAIDs damage the stomach? timeline? pathogenesis?

superficial injury - topical
occurs in minutes, heals rapidly
NSAIDs have low pKa - ionized in stomach and cross into epithelium leading to damage (ion trapping)

chronic (weeks)
lower PGE (lowers blood flow, mucus, bicarb)


Role of COX 1 vs 2?

COX 1 -constitutive; protective in stomach (mucin, HCO3); platelet activity

COX 2 -induced from inflammation; leads to inflammation, pain, fever


what is a risk factor for NSAIDs ucler?

age, coumadin, dose, steroids, other things


gastroprotective strategies for ulcers with NSAID use?

misoprostol - protective against NSAIDs (PGE)


zollinger-ellison syndrome

Pancreatic tumor --> high gastrin secretion

fundus has huge rugaes - parietal cell hyperplasia from high gastrin levels -- make much more acid leading to intractable uclers


z-e syndrome uclers? diarrhea? locations?

intractable, mutiple, diarrhea

present in wierd places like ilieum

acid denatures pancreatic enzymes so malabsorption


gastrin >1000

pernicious anemia or ZES

use secretin stimulation test - normally nothing happens but in ZES there is an increase in gastrin


secretin stimulation test with ZES?

stimulates D cells and G cells - normally balanced out

ZES has few D and a ton of G cells leads to a large rise in gastrin via mass effect