to understand the pathophysiology of diseases , first and foremost , we need to study the normal .
vit d is carried ( by albumin and proteun carriers) to the liver–> inactive form
then to the kidneys where it is transformed into the active form by wn enzyme here.
PTH increase the production of the actve form of vitamin d(calcitriol) by forming the enzyme required for that transformation(25(OH)vitamin D-1α-hydroxylase).
calcitriol will in turn increase absorption of calcium from the small intestine.
other actions of PTH:
increase Ca reabsorption
increase RESORPTION FROM BONES(get out of the bones calcium!!)
increase phosphate excretion
well basically PTH WANTS TO INCREASE THE SERUM CALCIUM.
pssst!!! in renal failure there is lack of prodcution of calcitriol!!! alert: HYPOCALCEMIA, which may be corrected by 2ry hyperparathyroidism
you know whats primary(tumours) and secondary( physiological response to hypocalcemia) .
but what about tertiary??
it is the development of autonomous(doesnt respect the feedback mechanism and keeps secreting PTH) parathyroid hyperplasia AFTER LONG STANDING 2RY HYPERPARWTHYROIDISM( most often in renal failure.
clinical manifestation? —– of hypercalcemia
why is there an increase in urinary cAMP in primary hyperparathyroidism?