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A 4-year-old girl is brought to her pediatrician™s office with lower extremity weakness and inability to walk. She is afebrile, but her blood pressure is 130/80 mm Hg. Routine serum chemistries show profound hypokalemia and metabolic alkalosis. Hypokalemia is the suspected cause of her lower extremity weakness. Further history reveals that the child ate an entire candy dish of authentic black licorice at her grandmother™s house. What hormone caused the syndrome with which this child presents?
Aldosterone
Cortisol
Dihydrotestosterone
Progesterone
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aldosterone?it's excess causes hypokalemia and loss of H + ions so metabollic alkalosis
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answer is B.......cortisol.........
Excessive consumption of licorice causes the syndrome of apparent mineralocorticoid excess. It manifests as hypertension, hypokalemia, and metabolic alkalosis. Licorice contains glycyrrhetinic acid, a substance that inhibits 11ß-hydroxysteroid dehydrogenase. This enzyme normally functions to convert cortisol to cortisone. This is important because cortisol avidly binds the mineralocorticoid receptor in the collecting tubules of the kidney, mimicking aldosterone™s effects (ie, salt retention, potassium excretion). Cortisone is unable to bind the receptor. In patients in whom this enzyme is inhibited, cortisol is not converted to cortisone, inducing a syndrome that presents similarly to mineralocorticoid excess. Aldosterone levels in this situation are suppressed and therefore do not cause hypertension. Dihydrotestosterone and progesterone are not metabolized by 11ß-hydroxysteroid dehydrogenase and have no effect on the mineralocorticoid receptor.
