nida
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Harrison's Q
A 10-year-old girl complaining of profound weakness, occasional difficulty walking, and polyuria is brought to the pediatrician. Her mother is sure the girl has not been vomiting frequently. The girl takes no medicines. She is normotensive, and no focal neurologic abnormalities are found. Serum chemistries include Na+ 142 mmol/L, K+ 2.5 mmol/L, HCO3– 32 mmol/L, and Cl– 100 mmol/L. A 24-h urine collection on a normal diet reveals Na+ 200 mmol/d, K+ 50 mmol/d, and Cl– 30 mmol/d. Renal ultrasound demonstrates symmetrically enlarged kidneys without hydronephrosis. A stool phenolphthalein test and a urine screen for diuretics are negative. Plasma renin levels are found to be elevated. Which of the following conditions is most consistent with these data?
A. Conn's syndrome
B. Chronic ingestion of licorice
C. Bartter's syndrome
D. Wilms' tumor
E. Proximal renal tubular acidosis
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| cyra
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C
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| msyamp
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C
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| som
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| docofthebigapple
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Answer could be B. We know children are fond of licorice. Patient should also have hypertension in that case. I do not know about the enlarged Bilatersl kidneys in licorice consumption.
In barterr's syndrome there is loss of Na K and Cl so all of these should be low instead of only K .
Hco3- is increased showing compensation for consumption of acid from licorice.
I'm not so good in nephro so i will wait for the right answer.
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| msyamp
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you are right its liquorice
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| AAAAA
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Bartter's Syndrome is hypokalemia without hypertension.
The question did not mention hypertension, so I doubt it is Bartter's Sydrome.
(Also Bartter's Syndrome will not even be asked in USMLE Part I, II, III, Internal Medicine !!! Bartter's Syndrome will be asked in the Subspecialtry Examination---Neprology!)
American children (lower-middle class loves to eat licorice !!!!!!!!)
It is a personal story and it is through the life journey that I came across with licorice !
They eat licorice like candy !!!!!!!
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| nida
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The answer is C.
The evaluation of patients with hypokalemia should first include a consideration of redistribution of body potassium into cells such as that which occurs in alkalosis, 2-agonist excess with refeeding syndrome and/or insulin therapy, vitamin B12 therapy, pernicious anemia, and periodic paralysis. In periodic paralysis serum bicarbonate is normal. If the patient is hypertensive and plasma renin is elevated, renovascular hypertension or a renin-secreting tumor (including Wilms) must be considered and appropriate imaging studies must be carried out. If plasma renin levels are low, mineralocorticoid effect may be high as a result of either endogenous hormone (glucocorticoid overproduction or aldosterone overproduction as in Conn's syndrome) or exogenous agents (licorice or steroids). In a normotensive patient a high serum bicarbonate excludes renal tubular acidosis. High urine chloride excretion makes gastrointestinal losses less likely and implies primary renal potassium loss, as may be seen in diuretic abuse (ruled out by the urine screen) or Bartter's syndrome. In Bartter's syndrome, hyperplasia of the granular cells of the juxtaglomerular apparatus leads to high renin levels and secondary aldosterone elevations. Such hyperplasia appears to be secondary to chronic volume depletion caused by a hereditary (autosomal recessive) defect that interferes with salt reabsorption in the thick ascending loop of Henle. Chronic potassium depletion, which frequently presents initially in childhood, leads to polyuria and weakness.
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| AAAAA
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c
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