Parathyroid Hormone PDF

# PARATHYROID GLANDS ## I. BASIC PRINCIPLES - Chief cells regulate serum free (ionized) calcium via parathyroid hormone (PTH) secretion, which - increases bone osteoclast activity, releasing calcium and phosphate - increases small bowel absorption of calcium and phosphate (indirectly by ac...

# PARATHYROID GLANDS ## I. BASIC PRINCIPLES - Chief cells regulate serum free (ionized) calcium via parathyroid hormone (PTH) secretion, which - increases bone osteoclast activity, releasing calcium and phosphate - increases small bowel absorption of calcium and phosphate (indirectly by activating vitamin D) - increases renal calcium reabsorption (distal tubule) and decreases phosphate reabsorption (proximal tubule) - Increased serum ionized calcium levels provide negative feedback to decrease PTH secretion. ## II. PRIMARY HYPERPARATHYROIDISM - Excess PTH due to a disorder of the parathyroid gland itself - Most common cause is parathyroid adenoma (>80% of cases); sporadic parathyroid hyperplasia and parathyroid carcinoma are less common causes. - Parathyroid adenoma is a benign neoplasm, usually involving one gland. - Most often results in asymptomatic hypercalcemia; however, may present with consequences of increased PTH and hypercalcemia such as - Nephrolithiasis (calcium oxalate stones) - Nephrocalcinosis - metastatic calcification of renal tubules, potentially leading to renal insufficiency and polyuria - CNS disturbances (e.g., depression and seizures) - Constipation, peptic ulcer disease, and acute pancreatitis - Osteitis fibrosa cystica - resorption of bone leading to fibrosis and cystic spaces - Laboratory findings include ↑ serum PTH, ↑ serum calcium, ↓ serum phosphate, ↑ urinary cAMP, and ↑ serum alkaline phosphatase. - Treatment involves surgical removal of the affected gland. ## III. SECONDARY HYPERPARATHYROIDISM - Excess production of PTH due to a disease process extrinsic to the parathyroid gland - Most common cause is chronic renal failure. - Renal insufficiency leads to decreased phosphate excretion. - ↑ serum phosphate binds free calcium. - ↓ free calcium stimulates all four parathyroid glands. - ↑ PTH leads to bone resorption (contributing to renal osteodystrophy). - Lab findings include ↑ PTH, ↓serum calcium, ↑ serum phosphate, and ↑ alkaline phosphatase. ## IV. HYPOPARATHYROIDISM - Low PTH - Causes include autoimmune damage to the parathyroids, surgical excision, and DiGeorge syndrome - Presents with symptoms related to low serum calcium - Numbness and tingling (particularly circumoral) - Muscle spasms (tetany) - may be elicited with filling of a blood pressure cuff (Trousseau sign) or tapping on the facial nerve (Chvostek sign) - Labs reveal ↓PTH levels and ↓ serum calcium. - Pseudohypoparathyroidism is due to end-organ resistance to PTH. - Labs reveal hypocalcemia with ↑ PTH levels. - Autosomal dominant form is associated with short stature and short 4th and 5th digits.