Calcium and Parathyroid Flashcards
When Ca receptors on PTgland sense low calcium, what happens
increase in parathyroid hormone release –> will increase renal calcium absorption and increased bone resorption/release of calcium, increase formation of active form of VitD
Vitamin D hydroxylation
2 hydroxylations: 1st in liver, 2nd in kidney (second hydroxylation stimulated by PTH)
Calcitriol/Vitamin D
increases calcium absorption in gut –> increase serum calcium
Hyperparathyroidism
“bones, groans, stones, and psychic moans” –> abnormal PTH hypersecretion –> hypercalcemia
Most primary hyperthyroidism is caused by
solitary (single PT) adenoma (85%), diffuse hyperplasia (15%), parathyroid carcinoma <1%
T/F in pt adenoma, may have hypertrophy of other pt glands
F –> atrophy b/c of negative feedback from high calcium due to hyperactive pt
hypercalcemia can lead to increase/decrease in ECF phosphate
decrease –> increased urinary phosphate is an effect of pth and overrides the phosphate released from bone with calcium
Groans
increased PTH can increase bp, constipation, GI tone
Classical presentation of primary hyperparthyroidism
osteitis fibrosa cystica –> bone demineralization with subperiosteal bone resorption and bone cysts
Realistic presentation of primary hyperparathyroidism
elevated serum calcium, kidney stones, renal dysfunction, reduced bone mineral density (cortical bone)
Tx of hyperparathyroidism
asymptomatic: medical monitoring // surgery for kidney stones, fracture in symptomatic patients or asymptomatic patients<50 years with severe hypercalcemia or reduced creatinine clearance or low bone mass
Secondary hyperparathyroidism
hyperfunctioning Pt glands are compensating for hypocalcemia: renal insufficiency, calcium malabsorption, vitamin D deficiency
Tertiary hyperparathyroidism
gland hyperfunction and hypersecretion due to prolonged secondary hyperparathyroidism –> gland autonomy –> elevated calcium, requires surgery
Familial hypocalciuric hypercalcemia
autosomal dominant –> looks like primary hyperparathyroidism –> abnormal calcium sensor –> increase in calcium setpoint –> increased pth secretion –> elevated calcium –> low urine calcium
Difference between FHH and Primary hyperparathyroidism
low urine calcium in FHH –> calcium sensor in kidney also broken –> cannot flush out calcium
Hypoparathyroidism
following total thyroidectomy or radical neck dissection, infiltrative (hemochromatosis or wilson’s), congenital (digeorge, familial type 1 polyendocrine)
Hypocalcemia effects
cardiac arrhythmia, neuromuscular irritability/tetany
Chvostek sign
irritable facial nerve due to hypocalcemia
Trousessau’s sign
carpal spasm due to hypocalcemia
Trousseau or Chvostek is more specific
Trousseau –> but takes a whole 3 minutes in the clinic
Tx of hypoparathyroidism
oral calcium, vitamin D,monitoring urinary/serum calcium,
Goal is serum calcium level in patient with hypoparahtyroidism
low normal –> will lose a lot of calcium in the urine b/c of absence of pth –> want to avoid kidney stones so go low normal
Vitamin D intoxication
uncommon cause of hypercalcemia –> nausea, vomiting, weakness, AMS
sequelae of Vitamin D intoxication
stored in fat –> cannot chelate it –> prolonged hypercalcemia
Tx of D intoxication
hydration, no dietary calcium
Vitamin D deficiency
lack of sun, decreased intake/absorption of vitamin D, metabolic defects in vitamin D hormone system –> leads to secondary hyperparathyroidism
Sequelae of vitamin d deficiency
rickets in children, osteomalacia in adults –> widened osteoid (demineralized bone) seams and impaired mineralization, risk of osteoporosis
_______ is important in mineralization of devoid bone matrix to lay down calcium.
Vitamin D
Characteristic signs of osteomalaci
diffuse bone pain and tenderness, proximal muscle weakness, Looser-Milkman pseudofractures perpendicular to bone surface
Tx of Vitamin D deficiency
treat underlying disorder, calcium, vitamin D
