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Calcium Regulation
Physiology
| Question | Answer |
|---|---|
| t/f: calcium is the most abundant positively charged ion | true |
| what are the calcium dietary requirements for pregnant women and why? | 1500 mg/day; increase for development |
| what are the calcium dietary requirements for lactating women and why? | 2000 mg/day; increase to generate milk |
| what are the calcium dietary requirements for postmenopausal women and why? | 1500 mg/day; increase bone loss |
| t/f: bone is the reserve for 99% of the body's calcium | true |
| how much plasma calcium is free vs bound to albumin? | 50% free and 50% bound to albumin |
| why is calcium absorbed in the duodenum by active transport? | keep calcium inside to be rapidly resorbed |
| what is calcium regulated by? | 1,25(OH)2 Vitamin D by passive transport |
| where is calcium resorbed? | proximal tubules of the kidneys |
| t/f: plasma phosphate is bound | false |
| where is phosphate reabsorbed? | proximal tubules of the kidneys |
| t/f: tubular reabsorption of phosphate is decreased by PTH | true |
| What does PTH do to calcium and phosphate? | increase calcium and decrease phosphate absorption |
| what does Calcitonin do to bone resorption and calcium? | inhibits bone resorption (osteoclasts) and decreases calcium |
| what does vitamin D do to calcium and phosphate absorption? | increase calcium and increase phosphate absorption |
| two actions of PTH in the kidneys | return calcium and make vitamin D |
| what happens when vitamin D enters the intestines | calcium is absorbed |
| t/f: low blood calcium indicates an immediate response | true |
| sole function of parathyroid glands | release PTH into systemic circulation in response to variations in serum/blood calcium levels |
| t/f: the effects of PTH on bone and the kidneys occur very slow | false |
| what do osteoblasts and osteoclasts activated by PTH release | RANKL |
| PTH released stimulated by decreased calcium levels acts on what | intestines, kidneys, and bone |
| where is the PTH1 receptor predominantly expressed | bone and kidney |
| two recombinants of PTH | hPTH1-34 (half length) and hPTH1-84 (full length) |
| what are the two recombinants of PTH used to treat? | hypothyroidism |
| t/f: PTH receptor is a g-protein coupled receptor | true |
| why is calcitonin released | increase in calcium serum/blood levels |
| primary function of calcitonin | inhibit bone resorption & decrease serum calcium levels |
| hypocalcemia | PTH released and normalization of calcium |
| hypercalcemia | stimulates thyroid gland to release calcitonin which inhibits bone resorption to suppress hypercalcemia and normalize it |
| what is calcitonin made by | clear parafollicular cells in the thyroid gland |
| what is the calcitonin receptor expressed on | osteoclasts |
| what is calcitonin release stimulated by | increased serum calcium levels |
| t/f: the calcitonin receptor is a g-protein coupled receptor | true |
| what does calcitonin do in the kidneys | inhibit calcium resorption-- calcium excreted in urine |
| what does calcitonin do in the blood | lowers calcium levels |
| what does calcitonin do in the intestines | inhibit calcium absorption |
| what does calcitonin do in the bone | promotes deposition of calcium into bones |
| how does calcitonin act on bone cells | inhibits osteoclasts and stimulates osteoblasts |
| osteoblasts | build bone |
| osteoclasts | break down bone |
| what does decreased plasma calcium levels stimulating parathyroid glands do? | increase PTH and increase plasma calcium |
| what does increased plasma calcium levels stimulating thyroid C cells do? | increase calcitonin and decreased plasma calcium |
| what is the parathyroid gland inhibited by | increased plasma calcium levels |
| what are the thyroid c cells inhibited by | decreased plasma calcium levels |
| what is vitamin D3 hydroxylated into by liver enzymes | 25-(OH)2 vitamin D3 (25-hydroxylase) |
| t/f: decreased hydroxylated vitamin D decreases active vitamin D | true |
| why do we measure hydroxylated vitamin D | it is a stabile metabolite of vitamin D and is considered a nutritional mark |
| two ways the kidney enzymes are stimulated | decrease plasma calcium to stimulate PTH decrease plasma phosphate levels |
| what is the kidney enzyme | 1α-hydroxylase |
| t/f: PTH controls 1α-hydroxylase in the kidneys | true |
| what does active vitamin d promote | intestinal absorption of calcium and phosphate |
| what mediates the release of PTH? | the receptor on the parathyroid gland which senses changes in calcium levels |
| t/f: almost every cell in the body has a calcium receptor | true |
| how do activating mutations lead to hypoparathyroidism | receptor cannot tell if calcium levels are normal so PTH release is prevented and calcium levels fall |
| how do inactivating mutations lead to hyperthyroidism | PTH is continually released because receptors think calcium levels are always low |
| what does decreasing plasma phosphate do to plasma levels and what does this do | increase plasma calcium levels which inhibits the parathyroid glands |
| what does decreasing PTH do to phosphate | increase phosphate reabsorption by the kidneys which decreases urinary excretion of phosphate which increases plasma phosphate levels |
| what does decreasing PTH do to calcium | decrease calcium reabsorption by the kidneys which increases urinary excretion of calcium which works with increased calcium absorption in the intestine (caused by increased active vitamin D) to not change plasma calcium levels |
| what does decreased plasma phosphate do to the kidneys | stimulated the kidneys which increases activated vitamin D |
| what does increased active vitamin D do to phosphate | increase phosphate absorption in the intestine which increased plasma phosphate levels |
| t/f: the skeleton is the store of calcium | true |
| what do osteocytes do? | tell skeleton how to react- signal changes |
| t/f: the central canal is a blood vessel | true |
| where does hematopoiesis occur in the skeleton? | bone marrow |
| how are osteocytes formed? | osteoblasts get trapped in the mineral matrix while repairing the bone |
| t/f: increasing the size of an animal increases the importance of osteonal structures | true |
| t/f: fish and rodents have osteonal structures | false |
| t/f: bone cells require differentiation of molecules like PTH, Interleukin-1, 1,25-dihydroxy-vitamin D | true |
| what do osteoblasts produce | osteoids or bone matrix (mineralizing) |
| what do osteoblasts express | parathyroid hormone receptor |
| t/f: osteoclasts are the only cells that resorb bone | true |
| what are osteoclasts driven by | RANKL |
| how do osteoclasts appear | as a ruffled border formation |
| what do osteoblasts and other precursors secrete | RANKL and Osteoprotegerin (OPG) |
| two functions of RANKL | bind on RANK receptors on macrophages and osteoclasts or bind with OPG |
| what do macrophages and osteoclasts do when bound to RANKL and what does this do | differentiate macrophages into osteoclasts and suppress osteoclast apoptosis which increase osteoclast action |
| what does increasing osteoclast action do? | osteoclast action outpaces osteoblast action which decrease bone mass |
| what happens after RANKL bind to OPG | blocks action of RANK which decreases osteoclast action which causes osteoblasts to outpace osteoclasts to increase bone mass |
| t/f: OPG serves to block RANKL from bind to RANK of macrophages | true |
| t/f: osteocytes are the most abundant cell in bone | true |
| what disease can cause bone resorption to exceed bone formation? | post menopausal osteoporosis |
| what diseases change the balance the balance of bone resorption and bone formation? | metastatic prostate cancer and x-linked hypophosphotemia |
| how does osteoporosis occur? | osteoblasts cannot keep up with the osteoclasts resorbing bone |
Created by:
k.murski
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