Hyperparathyroidism for PA

Hyperparathyroidism for the Physician Assistant Licensing Exam

Parathyroid hormone (PTH) regulates calcium and phosphate balance. It increases serum calcium by stimulating osteoclast-mediated bone resorption, increasing renal calcium reabsorption, and enhancing vitamin D-mediated intestinal calcium absorption. PTH also promotes renal phosphate excretion.
Primary Hyperparathyroidism: Results from autonomous overproduction of PTH, leading to hypercalcemia. Most commonly caused by a parathyroid adenoma (85%), with fewer cases caused by parathyroid hyperplasia (10-15%) or parathyroid carcinoma (rare).
Secondary Hyperparathyroidism: Caused by chronic hypocalcemia, most often seen in chronic kidney disease (CKD) or vitamin D deficiency, which leads to increased compensatory PTH secretion.
Tertiary Hyperparathyroidism: Develops after prolonged secondary hyperparathyroidism, typically in CKD patients, resulting in autonomous overproduction of PTH despite normal or elevated calcium levels.

Primary Hyperparathyroidism:
Parathyroid Adenoma: The most common cause.
Parathyroid Hyperplasia: Often associated with familial syndromes like MEN1 or MEN2A.
Parathyroid Carcinoma: Rare but associated with severe hypercalcemia.
Secondary Hyperparathyroidism:
Chronic Kidney Disease (CKD): Reduced renal vitamin D production and phosphate retention lead to hypocalcemia, driving PTH secretion.
Vitamin D Deficiency: Reduces calcium absorption, resulting in increased PTH production.

Primary Hyperparathyroidism:
Many patients are asymptomatic, with hypercalcemia detected incidentally.
Symptomatic Hypercalcemia:
Bone pain: Due to increased bone resorption, leading to osteopenia or osteoporosis.
Nephrolithiasis: Kidney stones from elevated calcium excretion.
Gastrointestinal symptoms: Nausea, constipation, and abdominal pain.
Neuropsychiatric symptoms: Fatigue, depression, and cognitive impairment.
Secondary Hyperparathyroidism:
Symptoms often relate to CKD, including bone pain and muscle weakness, due to chronic hypocalcemia and increased PTH levels.

Serum Calcium: Elevated in primary hyperparathyroidism, low or normal in secondary.
Serum PTH: Elevated in both primary and secondary hyperparathyroidism.
Serum Phosphate: Low in primary hyperparathyroidism due to PTH-induced renal phosphate excretion; elevated in CKD-related secondary hyperparathyroidism.
Vitamin D Levels: Should be measured to rule out vitamin D deficiency.
Imaging:
Sestamibi Scan: Localizes parathyroid adenomas.
Neck Ultrasound: May help identify enlarged parathyroid glands.

Primary Hyperparathyroidism:
Parathyroidectomy: Definitive treatment for symptomatic patients or those with complications such as osteoporosis, nephrolithiasis, or severe hypercalcemia. Also recommended for asymptomatic patients with significantly elevated calcium levels, osteoporosis, or reduced kidney function.
Medical Management:
Hydration: To prevent kidney stones.
Cinacalcet: A calcimimetic that decreases PTH secretion, used in patients who are not surgical candidates.
Bisphosphonates: Used to treat osteoporosis by reducing bone resorption.
Secondary Hyperparathyroidism:
Vitamin D Supplementation: Corrects deficiency.
Phosphate Binders: Used in CKD to reduce serum phosphate levels.
Active Vitamin D Analogues (Calcitriol): Suppress PTH secretion in CKD patients.
Cinacalcet: Lowers PTH in CKD patients who are not candidates for surgery.

Osteoporosis and Fractures: Due to increased bone resorption from elevated PTH.
Nephrolithiasis: Kidney stones due to hypercalciuria.
Hypercalcemic Crisis: Severe hypercalcemia (>14 mg/dL) can lead to dehydration, altered mental status, and cardiac arrhythmias, requiring aggressive treatment with IV fluids, bisphosphonates, and calcitonin.
Renal Impairment: Prolonged hypercalcemia can cause nephrocalcinosis and chronic kidney disease.

Key Points

Primary Hyperparathyroidism is most commonly caused by a parathyroid adenoma, leading to hypercalcemia. Symptoms include bone pain, nephrolithiasis, and neuropsychiatric disturbances. Parathyroidectomy is the definitive treatment for symptomatic or high-risk patients.
Secondary Hyperparathyroidism results from chronic hypocalcemia, commonly seen in CKD or vitamin D deficiency. Treatment involves correcting underlying causes, including vitamin D supplementation and phosphate binders.
Complications of hyperparathyroidism include osteoporosis, nephrolithiasis, and hypercalcemic crisis, which may require aggressive medical intervention.