mitty wrote:
For q 22 I think the answer is E.My explanation is since their is mutuation of the PTH hormone receptor on the PTH gland there will not be negative feed back so their will be increase of PTH.And b/c their is no ca receptor in the ascending limb of Henle the effect of the PTH hormone for calicum reabsorption is absent so there will be hypocalcemia and high calcium in urine.
In the question it specified the type of mutation to be "activation of this receptor in the absence of binding of its ligand", in other words, this mutation will give the parathyroid the impression that the serum calcium concentration is too high (persistent presence of calcium) and it will response to decrease PTH secretion.
As far as urine calcium, I believe it has more to do w/ the effect of PTH on the distal tubule to enhance reabsorption. Decreased PTH leads to high calcium level in the urine.
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| webjeee
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g for 22 for sure
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| sjain4
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Answer to 22:
There is a receptor in the thick ascending limb for Ca. When the urine Ca concentration is high, it causes an influx of that Ca into the t.a.l. cells. So in this case, if those receptors are artificially activated due to the mutation in the question, there will be an increased influx of Ca, leading to low Urine concentration of Ca.
The activation of Ca receptors on the parathyroid gland, via the feedback loop would decrease PTH levels. This would cause a state of hypocalcemia.
In my opinion the answer is H.
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| SmokyWaters
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22.G
34.C
4. B
18. E
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