What complication may occur as a result of hyperparathyroidism?

Hyperparathyroidism results from excessive secretion of parathyroid hormone (PTH), which acts on bone, the kidneys, and the intestines to raise serum calcium levels. One of PTH's primary actions on bone is to activate osteoclasts, which break down bone tissue to release calcium into the bloodstream. Prolonged or severe hyperparathyroidism causes significant bone demineralization — a condition called osteitis fibrosa cystica in extreme cases — that weakens bone architecture and dramatically increases the risk of pathological fractures, even with minimal trauma. Options A, B, and D — numbness and tingling, laryngeal spasms, and muscle twitching — are all manifestations of hypocalcemia, not hypercalcemia. Hypoparathyroidism or surgical removal of the parathyroid glands leads to low calcium, causing neuromuscular excitability: paresthesias, tetany, Chvostek's and Trousseau's signs, and laryngospasm. In contrast, hypercalcemia from hyperparathyroidism tends to suppress neuromuscular activity, producing muscle weakness, fatigue, constipation, polyuria, and bone pain — the classic 'bones, stones, groans, and psychic moans' mnemonic. Recognizing that fractures are a consequence of the bone-resorbing action of excess PTH is the key distinction here.