Hypercalcemia and Hypocalcemia

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PTH
The dominant hormonal control of serum calcium. A small decrement in serium ionized calcium stimulates PTH release, whereas a small increment in serum ionized calcium suppresses PTH release.
Direct effects of PTH on calcium homeostasis
1) Stimulate osteoclast-mediated release of calcium from bone. 2) Decrease renal calcium clearance (increase tubular reabsorption) 3) Stimulate renal 1-alpha-hydroxylase to convert calcidiol into the far more potent calcitrol, which in turn enhances gut absorption of calcium.
Indirect effects of PTH on calcium
Promotes intestinal absorption of calcium
PTH actions on phosphate
PTH secretion is stimulated by elevated serum phosphate. PTH directly reduces renal tubular reabsorption of phosphate from glomerular filtrate.
Potency of calciferols (Vitamin D group)
Calcitrol >> calcidiol > Vitamin D
Action of calciferols
To promote gut absorption of BOTH calcium and phosphate, thus resulting in INCREASE in the serum levels of both.
Calcitonin
Generally opposes PTH effect on bone, promoting uptake of calcium by bone; to a lesser extent, calcitonin promotes renal calcium excretion.
Thyroxine and triidothyronine
Thyroid hormones that regulate the pace of normal skeletal remodeling; in excess, net osteolysis can produce and increment in serum calcium.
Estrogenic and Androgenic steriods
Generally promote calcium and phosphate deposition in bone, increased bone formation, and reduced osteolysis.
Assessment of protein-bound calcium
For every 1 g/dl decrement below the low-normal serum albumin concentration, serium calcium should be "corrected" by adding 0.8 mg/dl to the raw value. In cases (rare) of very high albumin, you would subtract 0.8 mg/dl from the raw serum calcium value.
PTH in relation to serum calcium
** If serum calcium is HIGH, PTH should be LOW** ** If serum calcium is LOW, PTH should be HIGH**
The "next step" test after confirming hyper- or hypocalcemia
Measure PTH levels and assess its appropriateness or inappropriateness. If its response is inappropriate, a PTH disorder is to blame.
Symptoms of hypercalcemia
Fatigue Depression Mental status changes Coma Anorexia Nausea/vomiting Constipation Short QT interval Nocturia/Polyuria*
Significance of nocturia/polyuria in hypercalcemia
Polyuria is a consequence of hypercalcemia's effect on renal water handling. Hyercalcemia induces a state of nephrogenic diabetes insipidus (the response of the kidney to ADH is impaired). Thus, insensible water loss occurs and can lead to marked volume depletion. The volume depleted states results in a reduced GFR and reduced net calcium excretion, with the net result of hypercalcemia.
Primary Hyperparathyroidism
*the most common form of hypercalcemia, especially in patients who are ambulatory and seem fine* (i.e. the majority of patients with PHP are asymptomatic and only have mild hypercalcemia <12mg/dl)