CM Peptic Ulcer Disease
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| half of people over age 60 have | gastritis
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| Three types of gastritis | Acute and hemorrhagic gastritis, non-erosive (chronic), Distinctive. Endoscopic visualization corresponds poorly. Distinction requires biopsy
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| Petechial hemorrhages and small erosions are seen in which type of gastritis? | Hemorrhagic gastritis
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| Causes of acute hemorrhagic gastritis | stress lesions in seriously ill patients, drugs (NSAIDs, alcohol, corrosive ingestion), Trauma (NG tubes, FB ingestion, radiation), Vascular, Reflux, H. pylori
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| Non-erosive (chronic) gastritis is caused by | H. pylori or NSAIDs and bile reflux(chronic superificial chemical gastritis), autoimmune, environmental
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| H. pylori can cause what kind of gastritis? | acute and chronic
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| Lifetime PUD prevalence | 11-14%
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| 3 most important etiological factors for PUD are | H. pylori, NSAIDs, Acid (excess acid production is a rare cause)
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| Number one cause of PUD | H. pylori. Also a major cause in gastric ulcers
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| H. pylori facts | gram negative rod, spiral, flagellated, stomach is only known reservoir, transmission is suspected fecal-oral
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| Prevalence of H. pylori in developed nations | 80%
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| Populations in which H. pylori is more prevalent | AA and Hispanics
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| Where is H. pylori found? | Resides in the mucosal layer adjacent to the epithelial surface. Usually found in the antrum of the stomach
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| Tests to identify H. pylori | Serology, biopsy with histology, biopsy with urease test, urease breath test, stool antigen
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| Which tests will not be affected by concurrent use of PPI, Abx, or bismuth? | Serology and biopsy with histology. (note: serology can stay positive for years even with treatment)
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| H. pylori Tx | Triple therapy for 2 weeks. PPI, Clarithromycin and amoxicillin. Confirm eradication (urease breath, blood test or stool test)
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| What percentage of people may require retreatment? | 20%
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| H. pylori is associated with | gastric adenoCa and MALT (mucosa associated lymphoid tissue) lymphoma
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| Subepithelial petechiae occur within one hour of ______ ingestion | NSAID. Erosions if repeated doses in 24 hours.
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| Two types of NSAID injury | Topical and Systemic
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| What protects the gastric mucosa? | Prostaglandin (PGE2) by increasing mucin production, increasing mucosal blood flow, increasing bicarb production
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| How do NSAIDs affect PGE2 production | decrease. except Celebrex
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| Syndrome caused by gastrinoma | Zollinger-Ellison syndrome (associated with MEN I syndrome)
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| Where is ZE PUD most common? | majority in duodenal bulb, but also in distal duodenum and jejunum
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| Multiple ulcers in the small bowel and diarrhea (steatorrhea) may suggest: | Zollinger-Ellison syndrome
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| What must you dc before a gastrin test? | your PPI
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| Nl fasting levels of gastrin | <150pg/ml.
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| Fasting level of >1000pg/ml is virtually diagnostic for | gastrinoma
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| What tests can be used for ZE? | fasting gastrin levels, or secretin stim test
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| 90% of gastrinomas in ZE are found in the | gastrinoma triangle
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| Mets are seen in _______ % of patients at diagnosis in ZE | 30-50%
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| Tx of ZE | High dose PPI, Surgical resection if not metastatic, somatostatin, chemo
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| Most discriminating symptom of PUD | presence of pain that awakens the patients from sleep between 2-3 am
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| ____ is worse with meals, while ______is better with meals | GU, DU
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| _________allows characterization of the lesion and biopsy which is important since about 4% of GU are cancerous | EGD (allows you to biopsy, and assess risk of rebleeding if near a vessel)
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| Common site for ulcers | antrum of the stomach. (right near where the stomach leads into the duodenum)
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| Most common complication in PUD | Hemorrhage
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| Complications of PUD | Hemorrhage, Perforation (penetration of ulcer into adjacent viscous or organ), Gastric outlet obstruction
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| Tx for PUD | Antacids, H2 blockers, PPIs
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| Which cell secretes HCL? | Parietal cell.
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| 3 stimuli to the parietal cell to secrete HCL? | histamine, acetylcholine, gastrin. PPIs block out all three mechanisms.
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| Principle inhibitor of HCL production from the parietal cell | Somatostatin
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| How should PPIs be dosed? | 15-30 minutes before meals
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| How do PPIs work? | Block parietal cell H+/K+ ATPase pump
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| Advantage of PPI to H2 | shorter healing period with PPIs. Heals nearly 100% of ulcers refractory to H2 blockers
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| Tx for PUD that is H. pylori negative | 4-6 weeks if asymptomatic
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| tx for PUd that is H. pylori postitive | 2 weeks
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| AE's for PPIs | Diarrhea, Nausea, Abdominal Pain, HA. Increased risk of hip fx with long-term use, Increased risk of C. difficile
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| Surgery procedures for PUD | Gastric patch, Gastrectomy with vagotomy. Surgery is rare now b/c of PPIs
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| Who is at high risk for NSAID complications? | previous GI event, older age, concomitant use of anticoagulants, corticosteroids or other NSAIDs, high-dose NSAID therapy, chronic diseases, if H.pylori positive
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| Who can't use misoprostol? | women of childbearing age
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| In patients with high CV risk and moderate GI risk tx with | PPI/misoprostol and Naproxen
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| _______ is a synthetic prostaglandin E1 analog | Misoprostol
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| Concurrent use of a PPI, abx, or bismuth can cause | false negative results in H. Pylori testing
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| Most common causes of peptic ulcer disease | H. pylori and NSAIDs
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Created by:
ltm12