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Secondary and tertiary hyperparathyroidism are conditions involving overactivity of the parathyroid glands, but they differ in their causes and progression: Secondary Hyperparathyroidism Cause: A compensatory response to low calcium levels, often due to chronic kidney disease (CKD), vitamin D deficiency, or malabsorption syndromes. Mechanism: Low calcium or high phosphate levels stimulate the parathyroid glands to produce more parathyroid hormone (PTH). Symptoms: Bone pain and fractures. Muscle weakness. Calcification in soft tissues. Treatment: Vitamin D Supplements: To correct deficiency and improve calcium absorption. Phosphate Binders: To reduce phosphate levels in CKD patients. Calcimimetics: Medications like cinacalcet to reduce PTH secretion. Surgery: Parathyroidectomy in severe or refractory cases. Tertiary Hyperparathyroidism Cause: Long-standing secondary hyperparathyroidism, where the parathyroid glands become autonomously overactive and continue to produce excessive PTH even after the initial cause is resolved (e.g., after a kidney transplant). Mechanism: Persistent overactivity of the parathyroid glands leads to high calcium and PTH levels. Symptoms: Hypercalcemia-related issues like kidney stones, abdominal pain, and confusion. Bone pain and fractures. Treatment: Medications: Cinacalcet to manage calcium and PTH levels. Surgery: Parathyroidectomy is often required to remove overactive glands #hyperparathyroidism