{"type":"rich","version":"1.0","provider_name":"Transistor","provider_url":"https://transistor.fm","author_name":"Board Pearls","title":"Chapter 26, Ep 2 of 5: Enzyme Replacement, Type 3c Diabetes, Complications","html":"","width":"100%","height":180,"duration":826,"description":"Episode two follows three threads that all trace to the same parenchymal loss the framework episode set up. The acini die and enzyme replacement stands in, but only if dosed with the meal and released at the right duodenal pH, so a proton pump inhibitor enters when the coating fails. The islets die and produce a diabetes defined not by insulin lack but by lost glucagon, which makes hypoglycemia the dominant management feature and steers drug choice away from sulfonylureas. The structural disruption produces complications whose management is read directly off the anatomy, drain the symptomatic pseudocyst, recognize disconnected duct as the exception, and take the spleen out when left-sided portal hypertension bleeds. Mechanism first, management second, throughout.\n \nTopics covered\n\nExocrine reserve and the ten-percent threshold\nEnzyme replacement dosing with meals\nStructured workup for inadequate response\nPancreatogenic diabetes and lost glucagon\nDrug choices: metformin over sulfonylureas\nPseudocyst and disconnected duct syndrome\nDistal bile duct stricture from head fibrosis\nSplenic vein thrombosis and left-sided portal hypertension\nPancreatic ascites and pseudoaneurysm\n \n \nKey decisions\n\nSteatorrhea and fat-soluble vitamin deficiency appear only after exocrine output drops below about ten percent of normal, so clinical insufficiency means roughly ninety percent of acinar capacity is already lost.\nStart enzyme replacement at forty to fifty thousand lipase units with each main meal and half that with snacks, taken with the meal, titrating up to about ninety thousand per meal by clinical response.\nWhen response is inadequate, escalate the dose, then add a proton pump inhibitor because acidic duodenal pH prevents the enteric coating from releasing enzyme, then verify adherence and exclude bacterial overgrowth, bile acid malabsorption, celiac, and mucosal disease.\nPancreatogenic diabetes loses glucagon alongside insulin, making hypoglycemia brittle, so insulin...","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}