A nurse manager is discussing social services for older adults during a staff meeting in a long- term acute care (LTAC) facility. Which statement about Medicare made by one of the employees requires correction by the nurse manager?

A. Hypernatremia can indicate dehydration or other electrolyte imbalances. Furosemide can further affect electrolyte balance, especially sodium and potassium. However, this sodium level is only slightly elevated and may not necessarily require immediate action regarding furosemide administration.
B. Furosemide is a diuretic that can further decrease blood pressure due to its effects on fluid volume reduction. Administering it to a patient with already low blood pressure could potentially lead to significant hypotension and compromise perfusion to vital organs.
C. While incontinence itself may not directly contraindicate furosemide administration, it could indicate underlying issues such as bladder dysfunction or fluid overload that need further evaluation. This finding alone would not necessarily require holding the medication, but it warrants further assessment and consideration in the clinical context.
D. Normal serum potassium levels typically range from 3.5-5.0 mEq/L. A level of 5.3 mEq/L indicates hyperkalemia (elevated potassium). While this potassium level is mildly elevated, it would not be a reason on its own to hold furosemide. Monitoring potassium levels closely and potentially adjusting potassium

A. Dopamine is primarily associated with other neurodegenerative disorders such as Parkinson's disease, not Alzheimer's disease. In Alzheimer's disease, the focus is on changes related to beta-amyloid plaques and neurofibrillary tangles rather than alterations in dopamine levels.
B. Glial cells, including astrocytes and microglia, play a role in the brain's immune response and support of neurons. In Alzheimer's disease, there is evidence of increased activation and proliferation of glial cells in response to neuroinflammation and the presence of beta-amyloid plaques and neurofibrillary tangles. This reactive gliosis is a secondary response to the underlying pathology.
C. Glutamate is an excitatory neurotransmitter involved in various brain functions, including memory and learning. In Alzheimer's disease, there is evidence of dysregulation in glutamate metabolism and

signaling pathways. This dysregulation can lead to excitotoxicity, which contributes to neuronal damage and cell death seen in the disease.
D. Neurofibrillary tangles are one of the hallmark pathological features of Alzheimer's disease. These tangles are aggregates of hyperphosphorylated tau protein that accumulate inside neurons, disrupting their normal functioning and eventually leading to cell death. Neurofibrillary tangles, along with beta- amyloid plaques, contribute to the progressive cognitive decline observed in Alzheimer's disease.