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