PTH & Calcitonin

[663697]

Current research into the treatment of osteoporosis suggests that high, pulsatile concentrations of PTH could be effective at building bone. It is hypothesized that this may occur by inducing negative feedback of endogenous PTH with a subsequent increase in both calcitonin levels and calcitonin-mediated effects. Which of the following, if true, would disprove this hypothesis?

A. A patient treated with high, pulsatile levels of PTH fails to demonstrate an increase in bone density.
B. A patient treated with high, pulsatile levels of PTH demonstrates an increase in bone density as well as increased renal absorption of calcium.
C. A patient treated with calcitonin fails to demonstrate an increase in bone density.
D. Several patients treated with high, pulsatile levels of PTH demonstrate varying increases in bone density.

Correct answer is B. I can't seem to figure out why A isn't correct. Can somebody explain this?

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[desperadoflakes]

Where's this question from?

 

[663697]

Where's this question from?

TPR ICC book

 

[desperadoflakes]

Very strange if this isn't a mistake. The only thing I'm wondering is that maybe they're defining bone density in some not intuitive way?

 

[desperadoflakes]

Let me give it a shot. I think that A might be incorrect because they're just talking about 1 patient, which wouldn't "disprove" anything. I think this might be important because choice D makes a distinction with multiple patients (with results that would prove the hypothesis).

I think maybe the part about renal absorption is what makes B the correct answer.

They are trying very hard to create a tricky question. Their theory is that HIGH exogenous PTH will inhibit the endogenous PTH, thus AMPLYIFYING calcitonin, which would INCREASE bone density.

So overall we expect to see a decrease in the effects of PTH and an increase in the effects of calcitonin. This is super non intuitive because they're injecting you with PTH, so critically reading and treating a science passage like a CARS passage is more important than your scientific knowledge here.

Inhibiting the effects of PTH and amplifying effects of calcitonin would not induce reabsorption of calcium at the tubules.

That's the only way I can think of explaining this.

I guess also we can rule out A on the basis of n=1 because the result there is the same as regular osteoperosis. But the result here IS an improval, except there's an additional effect we didn't expect which weakens the hypothesis.

Overall a very annoying and weird question though

 

[rabbott1971]

Calcitonin inhibits osteoclasts, which break down bone. So if calcitonin were increased, renal absorption of calcium would decline. That's why B disproves the hypothesis.

 

[eyh]

Calcitonin inhibits osteoclasts, which break down bone. So if calcitonin were increased, renal absorption of calcium would decline. That's why B disproves the hypothesis.

The hormone participates the homeostasis of calcium and phosphorus. You can think of calcitonin as the opposite of PTH.
Calcitonin lowers blood Ca2+ levels in two ways: 1) Major effect: Inhibits osteoclast activity; 2) Minor effect: Inhibits renal tubular reabsorption of Ca2+ and phosphate, allowing them to be excreted. (Remember that calcitonin's role is to regulate blood calcium levels. If blood calcium levels are high, calcitonin wants to decrease it. So it would not promote absorption, but rather excretion).