P.07 Agents that affect bones

What is the principal role of bones in relation to calcium and phosphate?

What is the main function of osteocalcin in its uncarboxylated form?

Which process contributes to the soluble forms of calcium and phosphate in the body?

Where does most of the absorption of calcium from the diet occur?

What is the fate of a large fraction of filtered calcium and phosphate in the kidneys?

What percentage of calcium and phosphate serve as the principal structural support for the body?

What are potential consequences of disturbances in bone mineral homeostasis?

Which form of calcium is the metabolically active form and tightly regulated?

What are potential cellular dysfunctions associated with abnormalities in bone mineral homeostasis?

Which fraction of total serum calcium primarily binds with albumin?

Which anions can calcium form a complex with in the body?

What is the main role of PTH in the regulation of serum calcium and phosphorus balance?

What is the function of FGF23 in the regulation of serum calcium and phosphorus balance?

Which regulator promotes both increased absorption of calcium and phosphorus in the small intestine?

What is the effect of PTH on phosphorus reabsorption in the kidneys?

What is the net effect of FGF23 on serum phosphorus levels?

What is the serum half-life of intact PTH?

Which enzyme is responsible for producing 1,25 (OH)2D in the parathyroid gland?

What mediates the intracellular accumulation of inositol triphosphate in the parathyroid gland when activated by Ca?

Where is the calcium-sensing receptor (CaR) also expressed?

Which type of protease is capable of cleaving intact PTH into fragments in the parathyroid gland?

What effect does calcium have on PTH production in the parathyroid gland when the calcium-sensing receptor (CaR) is stimulated?

Which hormone makes the parathyroid gland more sensitive to suppression by calcium?

Which receptor is present in the parathyroid gland and promotes increased absorption of calcium and phosphorus in the small intestine?

What effect does PTH have on osteoclasts?

What is the mechanism of action of denosumab in the treatment of osteoporosis?

What is the function of sclerostin in bone physiology?

How does romosozumab work in the treatment of osteoporosis?

What is the specific cellular target of denosumab in bone physiology?

Which cell type does PTH act on to induce the production of RANKL?

What is the role of RANKL in bone physiology?

What is the main source of Vitamin D3 synthesis in humans?

Which organ is responsible for the hydroxylation of 25(OH)D to 1,25(OH)2D?

What is the main form of Vitamin D synthesized in plants?

What is the primary storage site for excess vitamin D in the body?

Which vitamin D metabolite has the longest half-life and is used to measure vitamin D stores in the body?

What condition is associated with increased levels of Vitamin D binding protein (DBP)?

What is the bioactive form of vitamin D that stimulates intestinal calcium and phosphate transport as well as bone resorption?

What is the primary use of calcipotriene (calcipotriol)?

For what condition is doxercalciferol primarily used?

In which country is eldecalcitol approved for the treatment of osteoporosis?

What is the primary function of fibroblast growth factor 23 (FGF23) in the kidney?

What stimulates the production of fibroblast growth factor 23 (FGF23)?

Which cells in bones are the primary site of fibroblast growth factor 23 (FGF23) production?

What is the main effect of calcitonin in the bone?

What is the molecular weight of a human calcitonin monomer?

Which hormone stimulates the secretion of calcitonin?

What role does calcitonin play in the treatment of Paget’s disease, hypercalcemia, and osteoporosis?

What effect does calcitonin have on the reabsorption of calcium and phosphate in the kidneys?

What is the effect of calcitonin on gastrin secretion and gastric acid output?

What is the clearance route for calcitonin in the body?

How do glucocorticoids alter bone mineral homeostasis?

What is the common cause of osteoporosis in adults due to prolonged administration of glucocorticoids?

In what conditions are glucocorticoids useful in reversing hypercalcemia?

What is the mechanism to explain the observation that estrogens prevent accelerated bone loss during the immediate postmenopausal period?

What effect does estrogen administration have on 1,25(OH)2D level in the blood?

Where have estrogen receptors been found, and what is their effect on bone remodeling?

How does denosumab inhibit osteoclast formation and activity?

What is the primary concern associated with the use of denosumab in relation to immune system cells?

In what way is denosumab advantageous over bisphosphonates?

What is the recommended frequency for administering denosumab?

Which condition is denosumab used to limit the development of?

What potential risk is comparable between denosumab and potent bisphosphonates?

What effect can denosumab have on calcium levels in patients with marked bone loss or compromised calcium regulatory mechanisms?

What cell type expresses RANKL and may pose a potential risk when using denosumab?

What is the primary effect of cinacalcet on the parathyroid gland?

For which condition is cinacalcet approved for treatment?

In what conditions may CaSR antagonists be useful?

How do thiazide diuretics reduce the incidence of urinary stone formation in subjects with idiopathic hypercalciuria?

What is the primary mechanism by which thiazide diuretics increase the effectiveness of PTH in stimulating reabsorption of calcium by the renal tubules?

What adverse effects can higher doses of fluoride cause?

What is the role of thiazide diuretics in reducing hypercalciuria and urinary stone formation in subjects with idiopathic hypercalciuria?

How does fluoride affect the resistance of teeth to dental caries?

What do clinical studies suggest about fluoride's effect on fractures?

How can the adverse effects of fluoride be prevented?

How does strontium ranelate affect bone resorption?

What is the primary effect of strontium ranelate on osteoclasts?

Which treatment for hypercalcemia has the potential to cause sudden hypocalcemia, ectopic calcification, acute renal failure, and hypotension if not done properly?

What has been demonstrated in large clinical trials regarding the efficacy of strontium ranelate?

Which medication is used for the management of hypercalcemia of malignancy and proved superior to calcitonin in reducing serum calcium in cancer patients?

Which medication is observed to have an effect on serum calcium within 4-6 hours and lasts for 6-10 hours?

Which medication has no clear role in the immediate treatment of hypercalcemia, but may be effective in chronic hypercalcemia of sarcoidosis, vitamin D intoxication, and certain cancers?

Which medication is used only after other methods of treatment have failed to control symptomatic hypercalcemia and must be given slowly to avoid side effects such as sudden hypocalcemia and acute renal failure?

Which medication is used for the immediate treatment of hypercalcemia and can be administered at high doses without causing toxicity?

Which medication may respond within several days to chronic hypercalcemia of sarcoidosis, vitamin D intoxication, and certain cancers?

Which medication is used for the management of hypercalcemia of malignancy and has potential nephrotoxicity that requires patients to be well hydrated and have good renal output before starting the infusion?

Which medication is the fastest and surest way to reduce serum calcium but is used only after other methods of treatment have failed to control symptomatic hypercalcemia?

Which medication should be switched to oral administration as soon as symptoms of hypercalcemia have cleared to avoid side effects such as sudden hypocalcemia and renal failure?

Which medication is not recommended for the immediate treatment of hypercalcemia but may be used in chronic hypercalcemia of sarcoidosis, vitamin D intoxication, and certain cancers?

What is the first step in reducing serum calcium levels in the treatment of hypercalcemia?

What is the role of furosemide in the treatment of severe hypercalcemia?

What is a potential side effect of repeated doses of pamidronate and zoledronate?

What effects generally persist for weeks after the infusion of pamidronate or zoledronate?

What is the main concern associated with the use of furosemide in severe hypercalcemia?

What is the primary adverse effect associated with repeated doses of pamidronate and zoledronate?

What is the function of saline diuresis in the treatment of hypercalcemia?

What is the main role of pamidronate and zoledronate in treating hypercalcemia of malignancy?

What is a potential side effect following the initial infusion of pamidronate or zoledronate?

What can prevent excretion of more calcium in the urine during severe hypercalcemia due to dehydration?

What enhances urine flow and inhibits calcium reabsorption in the ascending limb of the loop of Henle during treatment for severe hypercalcemia?

What is the preferred intravenous form of calcium for treating hypocalcemia?

What is the recommended oral preparation for treating less severe hypocalcemia?

Which form of vitamin D has rapid action and is capable of raising serum calcium within 24-48 hours?

Which medication is a synthetic PTH used for hypoparathyroidism?

What is the preferred intravenous treatment for severe symptomatic hypocalcemia?

Which oral preparation is often the choice for less severe hypocalcemia due to its high calcium percentage, availability, and low cost?

Which form of vitamin D has rapid action and is capable of raising serum calcium within 24-48 hours?

Which medication is used for hypoparathyroidism?

Which vitamin D form raises serum phosphate levels and requires careful monitoring to prevent ectopic calcification?

Which oral preparation provides approximately 1000–1500 mg of elemental calcium per day for treating less severe hypocalcemia?

What is the primary storage site for excess vitamin D in the body?

What is a potential emergency treatment for hyperphosphatemia?

What is a risk associated with the use of large doses of calcium to control hyperphosphatemia?

What is used in the control of hyperphosphatemia in patients with chronic kidney disease?

Which of the following is a long-term effect of hypophosphatemia?

Which condition is associated with increased bioactive FGF23?

What condition should hypophosphatemia be avoided when using forms of therapy that can lead to it?

What is a consequence of overzealous use of phosphate binders?