{"type":"rich","version":"1.0","provider_name":"Transistor","provider_url":"https://transistor.fm","author_name":"Board Pearls","title":"Chapter 32, Ep 4 of 4: Minerals and Trace Elements","html":"","width":"100%","height":180,"duration":629,"description":"Episode four closes the chapter with the minerals and trace elements, which run on the same logic as the vitamins: each element has a specific biochemical role and a specific exposure or pathology context that produces its phenotype. The boards favor the pairs that turn on a single mechanism, zinc inducing metallothionein to trap copper, cholestasis blocking biliary manganese excretion, and Brazil nuts concentrating selenium. Each element pairs a recognition cue with a population and a replacement strategy, the same teaching unit used for the vitamins.\n \nTopics covered\n\nIron deficiency and malabsorptive anatomy\nPPI-induced hypomagnesemia and TRPM6\nZinc acrodermatitis and dysgeusia\nCopper myeloneuropathy from zinc excess\nCopper deficiency mimicking B12\nManganese toxicity in parenteral nutrition\nSelenium cardiomyopathy and selenosis\nChromium and glucose intolerance\nD-lactic acidosis in short bowel\n \nKey decisions\n\nPPI-induced hypomagnesemia works through impaired TRPM6 channel function, and the testable feature is kinetic asymmetry: magnesium normalizes within about a week of discontinuation but recurs within about two weeks of rechallenge.\nVonoprazan or another potassium-competitive acid blocker is the alternative for the patient with recurrent PPI-induced hypomagnesemia because it does not lower magnesium.\nZinc deficiency is repleted with oral zinc sulfate two hundred twenty milligrams, fifty milligrams elemental, daily, and refractory hepatic encephalopathy in cirrhosis can reflect zinc deficiency through its urea-cycle cofactor role.\nChronic zinc excess from denture cream or supplements induces enterocyte metallothionein that traps copper, producing copper deficiency, so the treatment is copper two milligrams daily plus removing the zinc source.\nCopper deficiency mimics B12 subacute combined degeneration with myeloneuropathy, anemia, and neutropenia, and the discriminators are a normal B12 level and a zinc-excess history.\nManganese is removed from parenteral...","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}