Endocrinology of Calcium, Phosphate and Bone

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Bisphosphonates
Chvosteks Sign
Calcium
Ectopic PTH Production
Parathyroid Adenoma
Phosphate
Trouseaus Sign
Vitamin D

  • Calcium released from sarcoplasmic reticulum in stimulation of skeletal and cardiac muscle
  • calcium released from mitochondria in secretory cells
  • calcium comes in through intestine, some is lost due to enteric secretion
  • excreted in urine
  • resorped and deposited in bone reshaping
  • must be kept constant in blood.
  • in growing period, deposition in bone > resorption of bone therefore gradual loss from blood
  • replaced by decreased excretion in urine and intestine
  • principally controlled by:
  • androgens favour bone formation in childhood and puberty
  • estrogen inhibits PTH-mediated bone resorption in adult female
  • glucocorticoids necessary normally for skeletal growth
    • in excess decrease renal tubular calcium reabsorption
    • interfere with intestinal calcium absorption
    • stimulate PTH secretion
    • inhibit normal osteoblastic bone growth
    • inhibit gonadal androgens
  • thyroid hormones
    • too little causes retarded bone development
    • too much causes excessive bone resorption and hypercalcemia may lead to osteoporosis
  • growth hormone
    • acts through IGF-I (produced in liver and bone)
    • causes mitosis in chondrocytes and osteoblasts
    • also increase intestinal calcium absorption and renal phosphate reabsoption

14.7 HORMONES INFLUENCING CALCIUM, PHOSPHATE, BONE

distribution of calcium: intracellular, plasma, interstitial fluid, bone. phosphate, Mg homeostasis
calcium fluxes via diet, kidney.
systemic effects of lowered and raised plasma calcium
special considerations calcium homeostasis: development, pregnancy, lactation, renal failure

1.1.4 Other hormones that act on bone:

glucocorticoids as cause of osteoporosis bone resorption in malignancy PTH-RP
sex steroids post-menopausal osteoporosis
thyroid hormone, growth hormone & IGFs, local growth factor

 


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