Calcium and phosphate are regulated mainly by diet andthree hormones: parathyroid hormone (PTH), vitamin D,and calcitonin. PTH is secreted in response to a decrease inserum ionized calcium level. PTH attaches to its membrane receptor then acts via adenylate cyclase to mobilize calcium from bone into the serum and to enhance fractional reabsorption of calcium by the kidney while inducing phosphateexcretion; all increase the serum calcium concentration and decrease serum phosphate. Lack of PTH effect is heraldedby low serum calcium in the presence of elevated phosphatefor age. PTH stimulates vitamin D secretion by increasing renal 1α-hydroxylase activity and acts indirectly to elevateserum calcium concentration by stimulating the productionof 1,25-dihydroxyvitamin D from 25-hydroxyvitamin D.Calcitonin increases the deposition of calcium into bone; innormal states the effect is subtle, but calcitonin may be usedtemporarily to suppress extremely elevated serum calcium values.
1,25-dihydroxyvitamin D enhances calcium absorption from the gastrointestinal tract, increasing serum calcium levels and bone mineralization. Vitamin D is derived from exposure of the skin to ultraviolet rays (usually via the sun) or from oral ingestion. It is modified first to 25-hydroxyvitamin D in the liver and then 1α-hydroxylated to the metabolically active form (1,25-dihydroxyvitamin D) in the kidney. The serum concentration of 25-hydroxyvitamin D is a better reflection of vitamin D sufficiency than the measurement of 1,25-hydroxyvitamin D (see Chapter 31).
Available @ StudentConsult.com
The clinical manifestations of hypocalcemia result fromincreased neuromuscular irritability and include musclecramps, carpopedal spasm (tetany), weakness, paresthesia, laryngospasm, and seizure-like activity. Tetany can bedetected by the Chvostek sign (facial spasms produced bylightly tapping over the facial nerve just in front of the ear) orby the Trousseau sign (carpal spasms exhibited when arterialblood flow to the hand is occluded for 3 to 5 minutes with a blood pressure cuff inflated to 15 mm Hg above systolic blood pressure). Total serum calcium concentration is usually measured, although a determination of serum ionizedcalcium, the biologically active form, is preferable. Albuminis the major reservoir of protein-bound calcium. Disordersthat alter plasma pH or serum albumin concentration mustbe considered when circulating calcium concentrations arebeing evaluated. The fraction of ionized calcium is inverselyrelated to plasma pH; alkalosis can precipitate hypocalcemiaby lowering ionized calcium without changing total serumcalcium. Alkalosis may result from hyperpnea caused by anxiety or from hyperventilation related to physical exertion.Hypoproteinemia may lead to a false suggestion of hypocalcemia because the serum total calcium level is low even though the ionized Ca2+ remains normal. It is best to measure serum ionized calcium if hypocalcemia or hypercalcemia issuspected.
Primary hypoparathyroidism causes hypocalcemia but does not cause rickets. The etiology of primary hypoparathyroidism includes the following: 1.
Congenital malformation (e.g., DiGeorge syndrome or other complex syndromes) resulting from developmental abnormalities of the third and fourth branchial arches (see Chapters 143 and 144) 2.
Surgical procedures, such as thyroidectomy or parathyroidectomy, in which parathyroid tissue is removed either deliberately or as a complication of surgery for another goal 3.
Autoimmunity, which may destroy the parathyroid gland