{"type":"rich","version":"1.0","provider_name":"Transistor","provider_url":"https://transistor.fm","author_name":"Board Pearls","title":"Chapter 6, Ep 2 of 2: NSAID Ulcers, Refractory Disease, and Perforation","html":"","width":"100%","height":180,"duration":905,"description":"Episode two of the Peptic Ulcer Disease and H. pylori chapter covers the ulcers that are not driven by H. pylori. It works through NSAID and aspirin injury and its prevention, the sequential exclusion behind refractory and idiopathic ulcers, and the perforation and penetration emergencies that split on whether the leak is free or contained.\n \nTopics covered\n\nNSAID and aspirin ulcer mechanism\nMultiplicative NSAID risk factors and tiers\nAcid-blocker co-prescription and misoprostol\nCelecoxib, the aspirin trap, and dual antiplatelet therapy\nRefractory ulcer sequential exclusion\nGastric cancer and repeat biopsy rule\nZollinger-Ellison and fasting gastrin pitfalls\nFree perforation versus contained penetration\n \n \nKey decisions\n\nNSAID mucosal injury is primarily systemic COX-1 prostaglandin depletion, so suppositories and injections cause ulcers as readily as pills.\nHigh-risk patients (prior complicated ulcer or more than two factors) need a PPI with any non-selective NSAID; standard-dose H2 blockers are inadequate for prevention.\nCelecoxib plus aspirin loses most of the COX-2 GI advantage, so add a PPI when a further risk factor is present; give a PPI alongside dual antiplatelet therapy without fear of clopidogrel interaction.\nA negative H. pylori test on a patient still taking a PPI is a deferred test; retest off acid suppression for one to two weeks and off antibiotics or bismuth for four.\nEvery gastric ulcer gets a follow-up scope at eight to twelve weeks and every non-healing one gets many repeat biopsies from rim and base; duodenal ulcers do not need routine follow-up.\nFasting gastrin is confounded by PPIs (feedback rise) and by atrophic gastritis; gastric pH under two with high gastrin confirms gastrinoma, pH above four points to atrophic gastritis.\nFree perforation goes to a Graham omental patch without added vagotomy; posterior duodenal penetration into the pancreas is managed medically with high-dose acid suppression.\n \n \nThis is an AI-generated podcast, and...","thumbnail_url":"https://img.transistorcdn.com/-FuAdDBcPDLhEoUmroZKtOBRvuBn_FHPpYlh41hOnU4/rs:fill:0:0:1/w:400/h:400/q:60/mb:500000/aHR0cHM6Ly9pbWct/dXBsb2FkLXByb2R1/Y3Rpb24udHJhbnNp/c3Rvci5mbS9iNzlh/ZTU4Y2MzNWExMjQ5/MjA5OWMwMmI3ZTk5/NGFiZS5wbmc.webp","thumbnail_width":300,"thumbnail_height":300}