Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
31 Cards in this Set
- Front
- Back
What % of the US population has PUD?
|
5-10%
|
|
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?
|
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?
|
- 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%) |