123b Peptic Ulcer Flashcards
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)
Protein
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?
somatostatin
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?
90%
70% - NSAIDs cause gastric ulcers too
pathogenesis of HP infection?
ingestion
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)
Ulcer
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)
PPI
COX-2
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
