Calcium Flashcards
Functions of calcium
Extracellular (maintanence of normal ion product for mineralization, cofactor for prothrombin, maintenance of plasma membrane stability and permeability)
Intracellular (skelatal/cardiac muscle contraction, cell secretion exocrine, endocrine, NT, neural excitation and light transmission, regulation of membrane ion transport, enzyme regulation (gluconeogenosis and glycogenolysis) cell growth and division
calcium mass balance
Calcium intake of 1000 mg/day (intake needs to equal out take so 900 mg in feces and 100 mg in urine)
Absorption: 35% of ingested calcium is absorbed in the small intestine, active vD (1,25 OH 2 D) aka calcitriol stimulates calcium absorption and phosphate absorption
25% of calcium intake is lost as secretions (net calcium absorption)
Deposition/resorption: kg of calcium is stored in bones activity is controlled by resorption (reclaiming calcium and phosphate from bone to extracellular fluid)- stimulated by parathyroid hormone.
Deposition (aka accretion): under normal conditions calcium and phosphorous deposition and resorption rates are equal and there is no net change in the calcium content of the bone. Resorption>deposition=osteoporosis (PTH and estrogens influence bone turnover)
Filtration and reabsorbtion in kidney: 9980 calcium is filtered in kidney, Reabsorption is needed to minimize losses of calcium (PTH is in control of renal in the distal nephron)
Plasma binding of calcium
Calcium is 50% ionized in the free dissolved form and sensed in the parathyroid glands
Calcium also circulates bound to plasma protein (mostly to albumin and a little in anions
Changes in plasma proteins will change calcium more than other hormones
Parathyroid hormone and calcitonin
PTH: secreted from 4 parathyroid glands located behind the thyroid, PTH stimulates bone resorption. (wierd hormone that secretion is inhibited by increases in extracellular Ca) Tight negative feedback loop, so a decrease in Ca triggers PTH release to stimulate calcium resorption from bone
Calcitonin: not really important physiologically (high doses can be used as an antiresorption drug) if plasma Ca is VERY high calcitonin is stimulated and inhibits bone resorption to try to restore ca to normal
Parathyroid glands
Almost all of the PTH is synthesized and secreted by the chief cells
Cheif cells contain a calcium receptor that will inhibit the release of PTH
Calcium receptor
G-protein coupled receptor that when activated by calcium binding inhibits PTH synthesis and secretion from the chief cells
Vitamin D
Activation of Vitamin D to form 1,25 (OH)2 D
D3 (cholecalciferol) animal vitamin D and D2 (ergocalciferol) is plant Vitamin D.
Vitamin D3 is liberated from the skin (stimulated by UV light) Vitamin D intake
Vitamin D is converted to 25 OH D in the liver (25 hydroxylase) unregulated, plasma 25OHD is a reflection of vitamin D intake and stores in the body
Kidney (major regulatory step), PTH stimulates renal 1 hydroxylase to (25 OH D –> 1 25 OH 2 D)
125OH2D stimulates calcium and phosphate absorption in the small intestine
only a very small proportion of 25OH is converted to active form (changes in 1 hydroxylase activity change active D not 25 OH D
Clinical interpretation of Serum Vitamin D metabolite
Serum 25 OHD- index of Vitamin D stores (intake and absorption) not altered by changes in 1 hydroxylase activity
serum 1 255 OH2 D- index of renal 1 hydroxylase activity
Mechanism of Vitamin D
active vitamin D is a steroid hormone, enters receptor in nucleus transcription and translation cause the uptake of calcium and phosphate in small intestine
Phosphate balance
- PTH stimulates (through VD) phosphate absorption in the GI Tract and resorption from the bone
Major effect of PTH is to inhibit phosphate reabsorption in the renal PROXIMAL tubule
hypercalcemia and hypocalcemia
Hyper calcemia:
Primary (increased PTH secretion) via PT adenoma
and results in suppression of PTH VD intoxication
Hypocalcemia:
Primary : not making PTH from PT
Secondary: VERY COMMon renal failure cant make vitamin D or mal absorption (VD deficiency)
