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Clinical Correlation - Peptic Ulcer Disease


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What % of the US population has PUD?
What are the 3 main causes of PUD?
1) H. pylori infection
2) drugs (NSAIDS)
3) chemical (XS Acid)
What is the difference between erosion and an ulcer?
an erosion is more superficial
an ulcer extends into muscularis mucosa
Where do ulcers most likely appear?
at mucosal junctions and near sphincters, especially gastroduodenal junction and oxyntic-antral junction
Is GI ulceration increasing?
primary ulceration down, drug-induced is up
What normally prevents acid from eating up lining of stomach?
mucus-bicarbonate barrier (pH nearly neutral here)
Are acid/gastrin levels the same in most ulcers?
No - the levels vary by ulcer type
Does acid itself normally cause ulcers?
No, but it must be present for an ulcer to exist
What is the main cause of gastric and duodenal ulcers?
Helicobacter pylori
Does everyone with H. pylori develop an ulcer?
No - about 10-15 % do though
Do people with H. pylori often live with others that have it too?
Do normal people have H. pylori and if so, where?
yes, in mucus layer above gastric epithelium
What is the gold standard for diagnosing H. pylori?
gastric biopsy
What does H. pylori do to cause disease?
1) causes inflammation in the mucosa - becomes damages and acid gets from lumen to blood, Na can go into lumen
2) decreases # antral D-cells (decrease amt of SS produced)
3) leads to increase in G-cell activation - more gastrin - more acid released
What is the difference in basal gastric acid secretion?
- high gastric acid secretion in duodenal ulcer patients (2x) (peak acid output on response is higher in DU patients too)
- normal gastric acid levels in gastric ulcer patients
Do most gastric and duodenal ulcer patients have H. pylori present?

95% DU
75% GU
In addition to inflaming the mucosa and making it leaky, what else does H. pylori do?
decreases D cells -> decreases SS --> elevated gastrin --> no negative feedback regulation!
Is Zollinger-Ellison syndrome a common cause of GI ulcers?
no - accounts for 1%
Is H.pylori present in Z-E patients?
What causes ZE?
high gastrin and acid levels -- gastrin is unregulated (it is a chemical pathology)
What % of ZE tumors are associated with multiple endocrine neoplasm syndrom (MEN-1)?
How do you diagnose ZE?
must rule out H.pylori and NSAIDS use to diagnose
What characteristic feature of ZE may be visable by endoscopy or radiographically?
large increase in mucosal growth - may even see obstruction of pylorus
What are the clinical features of GI ulcers?
1) abdominal pain "boring into back" 2-3x day; pain relieved by eating
2) early satiety (due to inflammation of stomach)
3) nausea and vomitting
What are the effects of GI ulcers?
1) bleeding 10-80% patients
2) perforation 10%
3) pyloric outflow obstruction, acute or chronic
How does cigarette smoking change the frequency of PUD in population?
increases incidence and recurrence
What test identifies H. pylori?
Urea breath test
What are the treatments for GI ulcers?
1) antacid
2) H2 receptor blockers
3) Proton pump inhibitor
4) antibiotic treatment
5) surgery
What is the usual chosen treatment for GI ulcers?
antibiotic plus H2 receptor blockers
What is the added benefit of treating PUD with PPIs?
reduce GERD
Is vagotomy or vagotomy plus antrectomy a better treatment?
vagotomy plus antrectomy reduces acid secretion by 85%

(vagotomy only reduces it by 50%)

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