ca2+ and phosphate Flashcards
calcium and phosphate levels are regulated by what three main compounds
- parathyroid hormone
- calcitonin
- vitamin D
where is calcitonin created and secreted from
thyroid gland
where is parathyroid hormone created and secreted from
parathyroid
what does humoral secretion of hormones means
- hormone secretion set by concentration of substance in blood and whether it is above or below the setpoint
what triggers parathyroid hormone release
low plasma Ca2+ triggers hormone release from parathyroid gland
PTH is synthesized in what cells
- chief cells
- ca2+ receptors are located on chief cells
PTH is synthesized as
preproPTH
how does increases in extracellular CA2+ inhibit PTH secretion
- ca2+ binds to receptor coupled to G protein -> PLC activated -> IP3 increases Ca2+ which inhibits release of granules containing PTH
- increased Ca2+ also inhibits PTH synthesis
where is parathyroid gland located
four parathyroid glands lie on the posterior side of the thyroid
what is the main effect of PTH
- promote bone resorption releasing both Ca2+ and PO4 into ECF
- also promotes Ca2+ reabsorption at the kidney
PO4 released from bone has what effect on free Ca2+
- PO4 released during bone resorption will bind with Ca2+ in the ECF limiting rise in free Ca2+
- therefore, PTH inhibits PO4 reabsorption at the kidney to limit the rise in ECF PO4
PTH actions on the kidney
- inhibit PO4 reabsorption
- stimulates Ca2+ reabsorption
- net effect: fall in plasma PO4 and rise in plasma free Ca2+
vit D has affects on what organs
- bone
- kidney
- intestine
vit D actions on intestine
- activated vit D stimulatues Calbindin synthesis, which then increases intestinal absorption of Ca2+ and PO4
the small intestine absorbs Ca2+ by two mechanisms. which one is not under control of Vit D
- the passive, paracellular absorption of Ca2+ that occurs throughout the small intestine
the small intestine absorbs Ca2+ by two mechanisms. which one IS under control of Vit D
- active, transcellular absorption of Ca2+ that occurs in the duodenum
- active form of vit D: D-25-dihydroxyvitamin D stimulates all three of the following steps
- ca2+ enters cell across apical membrane through a channel
- inside cell, Ca2+ in buffered by binding proteins and is taken up into intracellular organelles
- Ca2+ exits cell through a Na-Ca exchanger
what enzyme is responsible for making vit D active
1-alpha-hydroxylase
where can vit D come from
- 7-dehydrocholesterol acted on by UV light -> cholecalciferol
- cholecalciferol from diet
actions of vit D on kidney
- promotes Ca2+ reabsorption from distal tubule
- negative feedback: inhibits 1-hydroxylase required for activation of vit D
actions of vit D on bone
- direct effect: mobilize Ca2+ from bone (bone resorption)
- indirect effect: promotes bone mineralization by providing more Ca2+
PTH has what 3 effects on the kidney
- protmoes Ca2+ reabsorption and thus an increase in plasma Ca+
- inhibits Pi reabsorption
- promotes the hydroxylation of 25-hydroxyvitamin D, thereby creating the active metabolite of vit D
PTH effect on bone
promotes net bone resorption and hence increases plasma Ca2+
PTH actions of intestine
- the active form of vit D, produced indurectly as the result of PTH) enhances CA2+ absorption
calcitonin is produced by what cells
parafollicular cells (C cells) of thyroid gland
effects of calcitonin
- ***decrease in plasma Ca2+ levels
- inhibits bone resorption of ca2+ and phosphate
- stimulates excretion of Ca2+ and PO4 in urine
what is rickets
vitamin D deficiency in childhood
- insufficient ca2+ and PO4 to mineralize growing bone
- hypocalcemia from decresed Ca2+ and PO4 absorption from gut
- growth failutre and skeletal anomalies
- elevated PTH
tx of rickets
proper diet and vit D supplements
what is osteomalacia
- deficiency of vit D in adulthood
- causes: dietary deficiency, intestinal sx, lack of sunlight, chronic renal failure
- presentation
- soft, weak bones, frequent fx
tx of osteomalacia
- vit D
- calcium
- phosphate supplements
what is hypocalcemic tetany
- decreased extracellular ca2+ destabilizes neuronal membranes, lowers threshold
- peripheral nerves begin to discharge spontaneously
- skeletal muscles contract tetanically (successive contractions that are fused together)
drinking a lot of colas can have what effect on ca2+ concentration
- excess dietary intake of PO4 can lead to decrease in plasma Ca2+
- PO4 inhibits activation of vit D
- decreased plasma Ca2+ -> increased PTH secretion
- leads to phosphaturia
- ca2+ and PO4 mobilized from bone due to elevated PTH
- leads to phosphaturia
clinical signs of hyperparathyroidism
- “stones, bones, groans”
- hypercalcemia
- hypophosphatemia
- osteoporosis
- kidney stones
- muscle weakness
- decreased muscle excitability
clinical presentation of hypoparathyroidism (usually seen post thyroidectomy)
- hypocalcemia
- hyperphosphatemia
- tetany
- convulsions
- tx: calcium and vit D
what is pseudohypoparathyroidism
- G protein receptors on target tissues not functional
- disturbances
- elevated PTH
- hypocalcemia
- hyperphosphatemia
- growth abnormalities
