– medullary thyroid cancer is a calcitonin producing tumour which produces hypocalcemia, not hypercalcemia. Most other malignancies are apt to cause hypercalcemia (esp. Breast), in addition to sarcoidosis and thyrotoxicosis.
– Paget’s disease: can see hypercalcemia and hypercalciuria but this is uncommon.
– dilantin causes osteomalacia in the liver. It induces P-450 mixed function oxidases within hepatic cells that convert vitamin D to inactive polar metabolites, thereby reducing the hydroxylation of cholecalciferol to 25(OH)Vit D
– vitamin D deficient rickets and primary hyperPTH can be distinguished by the urine calcium – in hyperPTH, the urine calcium is increased (hypercalciuria) while in vit D deficient rickets urine calcium is decreased. The calcium levels may not be all that different, but hyperPTH is likely to cause hypercalcemia, while rickets is more likely to have low or normal calcium.
– 99% of calcium in the body is entrapped in bone
– phosphorus is not that tightly controlled, and wide swings are well tolerated
– PTH Action: PTH stimulates kidney to reabsorb calcium (increases serum calcium) while lowering the renal reabsorption threshold for phosphate and thus decreasing the serum phosphate
– Looser’s lines in rickets/osteomalacia are localized collections of OSTEOID that is unmineralized – they appear as ribbonlike linear radiolucent lines that run transversly to the long axis of the bone and are found preferentially on the concave side of long bones including the medial femoral neck, ischium, pubic rami, ribs, and scapula
– fluoride supplementation has been investigated before and found to increase bone mass but make it more brittle – shown to not cause any change in the incidence of vertebral compression fractures, but has been shown to increase the number of nonvertebral fractures (hip, wrist, etc). Fluoride increases cancellous bone, but decreases cortical bone mineral density and therefore increases skeletal fragility.
– hydroxylysine and hydroxyproline: once released from collagen during breakdown of collagen fibers, these are excreted in the urine at a rate that reflects the rate of collagen degradation. The presence of increased urinary excretion of peptides containing hydroxyproline and hydroxylysine in Paget’s disease patients is a useful tool for study of collagen turnover and can be used to assess treatment. The excretion of hydroxyproline is greater than normal in almost all patient’s with Paget’s disease, even with monostotic involvement; in general, the amount excreted is directly correlated with the extent of disease, and treatment of Pagets with agents that effect bone results in decreased hydroxyproline excretion.
– the urinary excretion of calcium, hydroxyproline, and hydroxylysine is, generally speaking, a good marker of bone resorption; in hyperPTH, you would expect all three to be increased.
– Hypophosphatasia is an autosomal recessive disorder caused by low levels of alkaline phosphatase which is important in the formation of inorganic phosphate for bone production. This therefore causes a rickets/osteomalacia syndrome. Serum alk phosphate is low, while serum calcium is high because it is not deposited in bone. Treatment is by phosphate therapy. Increased urinary phosphoethanolamine is diagnostic; they also have hypercalciuria.
– In hypophosphatasia, the low levels of alkaline phosphatase in hypophosphatasia result in high levels of pyrophosphates. Pyrophosphates are naturally occurring inhibitors of bone mineralization; normally, pyrophosphate is cleaved by alkaline phosphatase to form the inorganic phosphate required for hydroxyapatite formation. Pyrophosphate by itself acts as an endogenous inhibitor of crystallization – leads to the rickets/osteomalacia of hypophosphatasia
– Carbonic anydrase facilitates the H20 + CO2 à H+ + HCO3 reaction
– gastrectomy/bowel resection patients can have vitamin D malabsorption and end up with osteomalacia – look for increased unmineralized osteoid,
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