Tertiary hyperparathyroidism is best described as:

• A. Autonomous PTH secretion after prolonged secondary hyperparathyroidism
• B. PTH resistance with elevated PTH
• C. Autonomous PTH secretion after prolonged exposure to secondary hyperparathyroidism
• D. Excess calcitriol production

Answer: (C)

The key idea is that chronic stimulation of the parathyroid glands leads to their growth and becoming self-sufficient in secreting PTH. In long-standing secondary hyperparathyroidism—commonly due to chronic kidney disease—the glands are repeatedly driven to release PTH because low calcium, high phosphate, and other factors persist. Over time, the glands hyperplastically adapt and start producing PTH autonomously, even when the original stimulus (low calcium or CKD-related triggers) is no longer present or is corrected. This autonomous PTH secretion after prolonged exposure shifts the condition into tertiary hyperparathyroidism, which can cause sustained hypercalcemia despite treatment of the initial secondary cause.

Other possibilities describe different scenarios not matching tertiary hyperparathyroidism: PTH resistance with high PTH points to pseudohypoparathyroidism, and excess calcitriol production is seen in conditions with extrarenal vitamin D production or granulomatous diseases.