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Low serum Ca²⁺ triggers PTH release from the parathyroid glands. PTH acts at bone (indirectly via osteoblast signaling) to increase osteoclast activity, mobilizing calcium; at the kidney to increase Ca²⁺ reabsorption (distal nephron) and decrease phosphate reabsorption (to prevent Ca-phosphate precipitation); and in the kidney to stimulate 1α-hydroxylase, converting vitamin D to its active form (calcitriol), which increases intestinal Ca²⁺ absorption. Therefore, B accurately summarizes the integrated response restoring calcium toward normal. Option A reverses calcitonin’s role—calcitonin tends to decrease osteoclast activity, lowering calcium (a minor effect in adult humans). C is the opposite of PTH physiology (it increases, not decreases, vitamin D activation; it decreases, not increases, phosphate reabsorption). D confuses endocrine axes; ADH regulates water balance via aquaporins, not calcium handling. TEAS frequently assesses homeostatic loops: PTH raises Ca²⁺; calcitonin lowers it; vitamin D enhances GI absorption. Recognizing these coordinated adjustments across bone, kidney, and gut helps connect lab patterns (e.g., hypocalcemia with low PTH vs secondary hyperparathyroidism) to underlying physiology and clinical presentation (tetany, paresthesias, or bone changes).