Clinical Correlation - Peptic Ulcer Disease
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- What % of the US population has PUD?
- 5-10%
- What are the 3 main causes of PUD?
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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?
- yes
- 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?
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- 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?
-
yes
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?
- no
- 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)?
- 20%
- 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%)