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14 Cards in this Set
- Front
- Back
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What is the definition of a peptic ulcer?
What is the most common cause of peptic ulcers? |
Break in the mucosa of stomach >5mm, with depth to the sub-mucosa
Most common cause = H. pylori |
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What are the four major parts of the stomach?
Where are Gastrin and somatostatin primarily made? What about pepsin? |
Fundus > Corpus > Antrum >Pylorus
G&D made in the antrum mainly. Pepsinogen made from chief cells in the corpus. |
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What morphological change occurs in parietal cells when bound by Histamine?
What is the importance of the many mitochondria in parietal cells? |
Cell changes shape (microvili become more prominent and develop microfilaments)
Mitochondria- needed to generate energy (since high amount of H+ needs to be pumped out to generate acid) |
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What three things stimulate the secretion of acid?
Distinguish between direct and indirect stimulation. |
1. vagus nerve --> via Ach (indirect & direct)
2. gastrin --> ECL --> histamine --> parietal cell (indirect) 3. gastrin directly stimulates parietal cells (direct) |
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Name the gastroduodenal defense mechanism found in:
- Pre-Epithelium - Epithelium - Subepithelium |
Pre-epithelium: mucous, HCO3
Eptihelium: tight junctions (apical barrier) Restitution- breaks filled by cell migrating in to gap Replication/ Rapid turnover (replaces lost tissue) Growth factors (EGF, TGFa, etc.) - for repair Subepithelium: Blood flow |
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How do NSAIDS contribute to destruction of the gastric mucosa?
What is the productive role of Prostaglandins? |
NSAIDs directly injure lining of stomach. Indirect (inhibit COX-1), and anti-platelet causing increased bleeding.
Prostaglandins: 1) produce mucous, 2) stimulate bicarb production, 3) decrease acid production, 4) maintain blood flow (needed for repair of GI system) |
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Which of these cell:product pairs is correct?
A. ECL cell: histamine B. Parietal cell: gastrin C: G cell : somatostatin D: Chief cell: H+ E: Chief cell: Intrinsic Factor |
A-
The ECL cells produces histamine which then stimulates parietal cells to secrete HCl and IF |
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T or F
Acid secretion in Gastric ulcer patients is more than that in Duodenal ulcers. |
False
Gastric ulcer pts typically have normal or low acid secretion. The problem is not over production of acid but impaired mucosal defenses. With duodenal ulcers there is inappropriate hypergastrinemia. |
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How does H. Pylori contribute to peptic ulcers?
What type of bacteria is H. Pylori? |
1. Direct cell damage- Secretes exotoxin (VacA) which can kill gastric epithelial cells.
2. Induces immune response- Has Cag pathogenicity island that can be injected into cells causing transcription of inflammatory markers & cytokines 3. Degrades mucus 4. Indirect effects: decreases somatostatin, increases gastrin Gram negative sprial shaped rod. Has multiple flagella. Urease splitting bacteria. |
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What tests can be done to diagnose H-pylori?
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Stool antigen test, Urea-breath test (breathe in radioactive urea and if patient has bacteria they will split urea into ammonia and CO2 which can be detected on breath).
Serology (Ab levels)- have low sensitivity/specificity |
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What percent of people diagnosed with H-pylori actually get gastric pathology? What types of outcomes can one get?
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Very few!
PUD- 10% of people infected Chronic wuperficial gastritis (asymptomatic) 70% lymphoma <1% atrophic gastritis 20% --> carcinoma 1-2% |
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What is the pathogenesis of Zollinge-Ellison syndrome? What are the two types of it?
How would you diagnose it? |
Grastrinoma-- produces gastrin.
Sporadic and MEN I (pit, hyper para, pan). High plasma gastrin, secretin test that has paradoxically ELEVATED gastrin, tumor localization imaging. *remember to have high clinical suspicion (it's a zebra). Think of severe ulcer + diarrhea! |
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What are stress-induced ulcers due to?
What are some sxs? |
Ischemia mainly (decreased blood supply, interferes with repair and restitution). Mainly seen in ICU patients.
Abdominal- epigastric gnawing pain, typically after meal and at night. weight loss, poor appetite, and nausea/vomiting. *note- patients may present with further sxs (bleed or perforation). |
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How do you treat peptic ulcers?
What is the difference between use of PPIs in DU and GU? |
Treat H pylori (with antibiotics- prevpac)
Avoidance of foods, stress, and NSAIDs Surgery for ZE. PPIs- 4 weeks for DU, 8 weeks for GU |
