Chapter 21. Hormonal Control of Calcium & Phosphate Metabolism & the Physiology of Bone
10 days after thyroid surgery, a patient returns to his physician complaining of problems that have gradually developed in the intervening period. It is determined that he has parathyroid deficiency due to inadvertent damage to the parathyroid glands because his signs and symptoms include
A. low plasma phosphate and Ca2+ levels and tetany.
B. low plasma phosphate and Ca2+ levels and tetanus.
C. a low plasma Ca2+ level, increased muscular excitability, and spasm of the muscles of the upper extremity (Trousseau sign).
D. high plasma phosphate and Ca2+ levels and bone demineralization.
E. increased muscular excitability, a high plasma Ca2+ level, and bone demineralization.
The correct answer is C. The lack of PTH results in a steady decline in the levels of circulating Ca2+, in part due to a lack of mobilization of calcium from the bones (rules out options D and E). The reduction in circulating calcium exerts a net excitatory effect on muscle (and nerves), eventually progressing to spasm/tetany. However, phosphate levels increase reciprocally as calcium levels fall (rules out options A and B). One should also distinguish between tetanus (the normal summation of contractile responses, without relaxation, when a muscle receives multiple inputs at high frequency, see Chapter 5) and the pathological condition of tetany, an involuntary contraction of muscle fibers due to their heightened sensitivity.
In an experiment, a rat is infused with a small volume of a calcium chloride solution, or sodium chloride as a control. Compared to the control condition, which of the following would result from the calcium load?
B. Increased formation of 1,25-dihydroxycholecalciferol
C. Decreased secretion of calcitonin
D. Decreased blood coagulability
E. Increased formation of 24,25-dihydroxycholecalciferol
The correct answer is E. Circulating calcium acts directly on the parathyroid glands via binding to CaSR to inhibit secretion of PTH. Thus, the key to understanding this question is to recognize that circulating levels of PTH will be reduced in the experimental animal compared to the control. PTH normally acts on the kidney, via an increase in the expression of 1α-hydroxylase, to trigger the production of 1,25-dihydroxycholecalciferol. When calcium levels are high, therefore, 1,25-dihydroxycholecalciferol synthesis is reduced and the less active metabolite 24,25-dihydroxycholecalciferol is produced instead (rules out option B). PTH also acts on the bone to trigger calcium ...