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. Topics covered Iron deficiency and malabsorptive anatomy PPI-induced hypomagnesemia and TRPM6 Zinc acrodermatitis and dysgeusia Copper myeloneuropathy from zinc excess Copper deficiency mimicking B12 Manganese toxicity in parenteral nutrition Selenium cardiomyopathy and selenosis Chromium and glucose intolerance D-lactic acidosis in short bowel Key decisions PPI-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. Vonoprazan or another potassium-competitive acid blocker is the alternative for the patient with recurrent PPI-induced hypomagnesemia because it does not lower magnesium. Zinc 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. Chronic 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. Copper deficiency mimics B12 subacute combined degeneration with myeloneuropathy, anemia, and neutropenia, and the discriminators are a normal B12 level and a zinc-excess history. Manganese is removed from parenteral nutrition once cholestasis develops or globus pallidus T1 hyperintensity appears, because impaired biliary excretion drives basal ganglia accumulation and levodopa-unresponsive parkinsonism. Selenium deficiency on long-term unsupplemented parenteral nutrition produces Keshan cardiomyopathy, while chronic Brazil nut overconsumption, more than three per day, produces selenosis with alopecia, brittle nails, and garlic breath. For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected].

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