mahendra
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A 34-year-old female is brought to the emergency room with severe
muscle cramps and carpopedal spasms. The patient was noted to be
extremely irritable and was complaining of tingling around the
mouth and in the hands and feet. A few hours later, laboratory
examination reveals sodium 140 mEq/L, potassium 4.2 mEq/L,
chloride 101 mEq/L, calcium 6.4 mg/dL, phosphate 5.1 mg/dL,
magnesium 2.4 (normal 1.8-3.8 mg/dL) and alkaline phosphatase
67 U/L. A CT scan of the head shows basal ganglia calcifications.
Prolonged QT intervals and T wave abnormalities are noted on
electrocardiogram. The history is pertinent for a thyroidectomy
two months prior to admission. Which of the following conclusions
is most consistent with these data?
A. An increase in dietary vitamin D is warranted
B. Hepatocytes have a low 25-hydroxylase activity
C. Intestinal cells are underexpressing calcium transporter genes
D. Isolated cells from the kidney have high 1-hydroxylase activity
E. The levels of 1,25-dihydroxy vitamin D are normal
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| asmi
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i think its A
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| mahendra
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ITS C
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| asmi
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can you explain it plz
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| mahendra
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Topics: 173
Posts: 419
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The patient presents with the classic symptoms of acute hypocalcemia secondary to hypoparathyroidism, itself the result of overzealous thyroid removal by the surgeon causing damage to the nearby parathyroid glands. Other classic findings would have been Trousseau's sign (carpal spasm after application of a blood pressure cuff) and the Chvostek's sign (facial muscle contraction on tapping in front of the ear). Serum calcium is low and serum phosphate is high, with normal alkaline phosphatase. The magnesium is normal, ruling it out as a cause of the tetany (and also indirectly ruling out chronic alcoholism or renal losses as causes). The calcifications seen on CT scan are a sign of overmineralization due to an unfavorable [calcium] x [phosphate] product. Acute treatment with calcium gluconate and, if possible, 1,25-dihydroxy vitamin D3 (cholecalciferol) is necessary.
Hypocalcemia normally triggers parathyroid hormone (PTH) release from the parathyroid glands. PTH can increase bone resorption by stimulating osteoclastic activity and can promote calcium reabsorption at the level of the kidney distal tubule (to the expense of phosphate), but has no direct effect on intestinal absorption of calcium and phosphate, which are under vitamin D control. However, PTH is required to activate 1-hydroxylase in the kidney, the rate-limiting step in metabolism of Vitamin D3 to its active metabolite, 1,25-dihydroxy-D3. This metabolite helps to raise serum calcium by increasing proximal intestinal absorption of calcium. The lack of 1,25-dihydroxy-D3 would be expected to prevent expression of these calcium transporters. The active metabolite works in concert with PTH to increase osteoclastic activity, promote calcium reabsorption in the kidney, oppose the phosphate losses, and most uniquely, promote calcium and phosphate intestinal absorption.
An increase in dietary vitamin D (choice A) would not be helpful at this time, particularly since the lack of PTH would preclude the activation of the precursor vitamin to the dihydroxylated metabolite. Rather oral calcium would be eventually needed on a chronic basis.
Hepatocytes would not have a low 25-hydroxylase activity (choice B) for two reasons: PTH has no effect on this first hydroxylation step and, more generally, it is not a controlled enzymatic reaction.
Isolated cells from the kidney do not have high 1-hydroxylase activity (choice D) since PTH is no longer present to activate this step.
The levels of 1,25-dihydroxy vitamin D (choice E) would be found to be abnormally low.
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| asmi
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MAHENDER YOU ARE A GENIUS
KEEP IT UP :idea: AND THANKS FOR SUCH A NICE EXPLANATION.
WHEN ARE YOU GIVING STEP 1 ?
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