123b Peptic Ulcer

Question 1

what causes most ulcers?

Answer 1

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

Question 2

Do anti-acid drugs work with h pylori ulcers?

Answer 2

heals, but they come back when drugs stopped

Question 3

pernicious anmeia

Answer 3

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

Question 4

What increases gastric acid secretion?

Answer 4

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

Question 5

what glands are in the body of stomach?

Answer 5

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

Question 6

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

Answer 6

pyloric gland in antrum of stomach

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

Question 7

PPI’s affect what?

Answer 7

H+/K+ ATPase in parietal cells

Question 8

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

Answer 8

somatostatin

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

low stomach pH

Question 9

what does stomach acid do?

Answer 9

destroys bacteria

Question 10

does h pylori cause cancer?

Answer 10

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

Question 11

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

Answer 11

stomach and anywhere with gastric metaplasia

no, poor areas

Question 12

how is hp spread? reservoir? endemic anywhere?

Answer 12

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

Question 13

duodenal ulcers - what percent from hp? gastric ulcer?

Answer 13

90%

70% - NSAIDs cause gastric ulcers too

Question 14

pathogenesis of HP infection?

Answer 14

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

Question 15

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

Answer 15

many things to defeat immune system including:

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

Question 16

how does hp cause duodenal ulcers?

Answer 16

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

Question 17

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

Answer 17

D cells  
less somatostatin (lose break on gastrin release)

Question 18

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

Answer 18

gastric metaplasia

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

Question 19

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

Answer 19

low (~1% per ear)

Question 20

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

Answer 20

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)

Question 21

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

Answer 21

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

Question 22

test for HP

Answer 22

urea breath test and stool antigen - active infection

serology - IgG just tells previous exposure not active infection

Question 23

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

Answer 23

NSAIDs and aspirin
zollinger-ellison syndrome
false negative test

Question 24

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

Answer 24

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)

Question 25

Role of COX 1 vs 2?

Answer 25

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

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

Question 26

what is a risk factor for NSAIDs ucler?

Answer 26

age, coumadin, dose, steroids, other things

Question 27

gastroprotective strategies for ulcers with NSAID use?

Answer 27

misoprostol - protective against NSAIDs (PGE)
PPI
COX-2

Question 28

zollinger-ellison syndrome

Answer 28

Pancreatic tumor –> high gastrin secretion

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

Question 29

z-e syndrome uclers? diarrhea? locations?

Answer 29

intractable, mutiple, diarrhea

present in wierd places like ilieum

acid denatures pancreatic enzymes so malabsorption

Question 30

gastrin >1000

Answer 30

pernicious anemia or ZES

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

Question 31

secretin stimulation test with ZES?

Answer 31

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