Which electrolyte pattern is typical of primary hypoadrenocorticism (Addison's disease)?

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Multiple Choice

Which electrolyte pattern is typical of primary hypoadrenocorticism (Addison's disease)?

Explanation:
The key idea is that primary hypoadrenocorticism disrupts mineralocorticoid and glucocorticoid production, leading to low aldosterone. That causes sodium loss and water loss (hyponatremia and dehydration) and potassium retention (hyperkalemia). The low cortisol also contributes to reduced vascular tone and volume depletion. Hyperkalemia can slow cardiac conduction, producing bradycardia in some cases. Because you’re addressing the underlying electrolyte and volume imbalance, the best approach is to give isotonic IV fluids to correct dehydration and electrolyte disturbances and provide corticosteroids to replace both glucocorticoids and mineralocorticoids (often hydrocortisone). Ongoing monitoring of electrolytes and renal function is essential to guide further treatment. The other patterns don’t fit Addison’s profile: a solitary hyperkalemia finding ignores the concurrent volume depletion and hyponatremia from aldosterone deficiency; hypernatremia with hypokalemia would be opposite to what mineralocorticoid loss causes; hyponatremia with hypokalemia isn’t the typical signature of this disease and wouldn’t reflect the mineralocorticoid deficiency.

The key idea is that primary hypoadrenocorticism disrupts mineralocorticoid and glucocorticoid production, leading to low aldosterone. That causes sodium loss and water loss (hyponatremia and dehydration) and potassium retention (hyperkalemia). The low cortisol also contributes to reduced vascular tone and volume depletion. Hyperkalemia can slow cardiac conduction, producing bradycardia in some cases. Because you’re addressing the underlying electrolyte and volume imbalance, the best approach is to give isotonic IV fluids to correct dehydration and electrolyte disturbances and provide corticosteroids to replace both glucocorticoids and mineralocorticoids (often hydrocortisone). Ongoing monitoring of electrolytes and renal function is essential to guide further treatment.

The other patterns don’t fit Addison’s profile: a solitary hyperkalemia finding ignores the concurrent volume depletion and hyponatremia from aldosterone deficiency; hypernatremia with hypokalemia would be opposite to what mineralocorticoid loss causes; hyponatremia with hypokalemia isn’t the typical signature of this disease and wouldn’t reflect the mineralocorticoid deficiency.

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