Failure to monitor which micronutrient in long-term PN patients is most likely to result in toxicity?

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Multiple Choice

Failure to monitor which micronutrient in long-term PN patients is most likely to result in toxicity?

Explanation:
In long-term parenteral nutrition, the risk of toxicity rises for trace elements that are cleared slowly when liver function is impaired. Manganese stands out because it is excreted primarily through bile. If cholestasis or hepatic dysfunction develops, manganese can accumulate in the brain, especially in the basal ganglia, leading to neurotoxicity such as tremors, gait disturbances, and other movement disorders. MRI may show characteristic basal ganglia T1 hyperintensity due to manganese deposition. Because PN provides a steady, chronic source of manganese, inadequate monitoring can allow toxic levels to build up over time. Other elements like zinc, folate, or molybdenum can cause issues, but their toxicities are less directly tied to liver excretion and long-term PN exposure, making manganese the most concerning in this scenario.

In long-term parenteral nutrition, the risk of toxicity rises for trace elements that are cleared slowly when liver function is impaired. Manganese stands out because it is excreted primarily through bile. If cholestasis or hepatic dysfunction develops, manganese can accumulate in the brain, especially in the basal ganglia, leading to neurotoxicity such as tremors, gait disturbances, and other movement disorders. MRI may show characteristic basal ganglia T1 hyperintensity due to manganese deposition. Because PN provides a steady, chronic source of manganese, inadequate monitoring can allow toxic levels to build up over time. Other elements like zinc, folate, or molybdenum can cause issues, but their toxicities are less directly tied to liver excretion and long-term PN exposure, making manganese the most concerning in this scenario.

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