jean robert
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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 warrante
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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| cirus
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E
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| drgho
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C. low PTH --> Low 1,25DHCC --> Low intestinal calcium absorption.
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| new_n_lost
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A. An increase in dietary vitamin D is warrante
This is hands dowm hypo PTH due to previous thyroid surgery with all the classical symptoms. The parathyroid hormone–dependent renal production of 1,25-dihydroxyvitamin D is deficient in all hypoparathyroid states.
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| drgho
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new_n_lost wrote:
A. An increase in dietary vitamin D is warrante
This is hands dowm hypo PTH due to previous thyroid surgery with all the classical symptoms. The parathyroid hormone–dependent renal production of 1,25-dihydroxyvitamin D is deficient in all hypoparathyroid states.
I don't believe increase in dietary vit D can help this patient. the patient has low level of 1-alpha hydroxylase acitvity and dietary vit D also need to be activated in human's body.
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| silver
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C. Intestinal cells are underexpressing calcium transporter genes
she has acute hypocalcemia sec. to hypoPTH. if she's given oral vit. D it won't get activated because there's no PTH to do that.
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| exambuster
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C
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| doc_clotaire
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C. Intestinal cells are underexpressing calcium transporter genes
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| Misrati
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 C : low vit . D absorption..
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| anzar
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A
Because the vitamin D will increase ca2+ absorption from intestines. the patient probably has hypocalcemia due to permanent destruction of parathyroid due to ischemia.
I deally calcium iv would have been ideal but as per options
A seems to be correct
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| pr20
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I will go with C.
Low Calcium,high Phosphate,prolonged QT interval,basal ganglia calcifications,previous thyroid surgery----all point towards primary hypoparathyroidism.
Low PTH causes---low 1-alpha hydroxylase---leads to low 1-25-diOHD3----which causes decreased intestinal absorption of Ca.
Increase in dietary Vit.D may not help bcas 1-alpha hydroxylase is required to convert dietary form of Vit.D in to active 1-25-diOHD3.
It is important to remember basal ganglia calcifications in primary hypoparathyroidism.
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| jean robert
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The correct answer is C
.
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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