calcium metabolism Flashcards
role of parathryoid hormone (PTH)
provides minute to minute regulation of ECF calcium
- major regulator of PTH hormone (negative feedback loop)
described as the main defender of the serum calcium
components of ECF calcium
50% in ionised calcium form, bioactive
45-50% protein bound, albumin & globulins
5-10% complexed with anions e.g. HCO3
how does PTH restore calcium levels to ‘normal’
- stimulates osteoclastic bone resorption
- stimulates renal tubular reabsorption of calcium
- stimulates renal 1-hydroxylation of 25(OH)D
restores serum calcium by acting on all effector organs
bone and kidney directly; intestine indirectly
PTH release is regulated by
- serum ionized calcium
- serum phosphate
- serum 1,25 dihydroxyvitamin D (-)
what is calcitonin not a regulator of
is NOT a physiological regulator of serum calcium
calcitonin is made in the thyroid
parathyroid hormone-related peptide (PTHrP)
- important paracrine regulator of breast, skin and bone development
- not a physiological regulator of serum calcium
- produced in excess in some cancers, when in the bloodstream it mimics PTH
- acts similarly to PTH signals via PTHR1 = cancer associated hypercalcemia
causes of hypercalcemia
- PTH-dependent
(high Ca2+, normal/high PTH)
- primary hyperparathyroidism
- familial benign hypercalcaemia
- PTH-independent (high Ca2+, suppressed PTH) -cancer -PTHrP -extensive bone reabsorption
- vitamin D-dependent - sarcoidosis = endogenous - vitamin D intoxication = exogenous
causes of hypocalcemia
- hypoparathyroidism
- postsurgical, post neck irradiation, autoimmune - parathyroid hormone resistance
- abnormalities of vitamin D metabolism
- deficiency, renal failure
what plays an important role in phosphate metabolism
- vitamin D (between intestines and ECF)
- PTH (from bone to ECF)
- phosphatonins (regulate in kidneys)
e. g. fibroblast GF 23
important organs involved in phosphate and calcium metabolism
- intestines
- bone
- kidneys
causes of hyperphosphatemia
- increased input - IV phosphate e.g. burn, cell death e.g. tumour
- decreased excretion - *renal failure, PTH deficiency or resistance
causes of hypophosphatemia
- inadequate GI absorption e.g. Vit D deficiency
- intracellular shift
- resp alkalosis - renal loss
- increased PTH, high phosphatonins, alcoholism
vitamin D metabolism
sunlight (UV) exposure causes inactivate precursor = 25 hydroxyvitamin D
the kidneys then hydroxylate this into the active form 1,25 dihydroxyvitmain D
(PTH regulates the enzyme that converts this)
if a patient comes in with hypercalcemia what is the next best step
check PTH levels
blood test results for PTH-dependent hypercalcemia vs PTH-independent hypercalcemia
PTH- dependent
= high sCa++
high/ normal PTH
PTH-independent
=high sCa++
low PTH (appropriate response)