50 Calcium and Bone Flashcards
Describe the regulation of plasma calcium and phosphorus including the actions and control of vitamin D, parathyroid hormone and calcitonin.
- Vitamin D: Increases both calcium and phosphorus concentrations in plasma mainly thru affect on GI tract. Causes reabsorption in kidney, bone resorption (osteoclasts) with PTH. Smaller quantities might causes calcification.
- Parathyroid hormone: Made by chief cell. Stimulated by a decreased in ionized calcium. Causes increase in plasma calcium concentration and a decrease in plasma phosphorus. PTH greatly increases phosphate excretion by the kidneys
- Calcitonin: produced by parafollicular cells and stimulated by increase of calcium in plasma or Gastrin. Decreases bone resorption/calcium release. Affects kidney by decreasing reabsorption of Ca and Phosphate.
Describe the effects of parathyroid hormone on the kidney, vitamin D and bone.
- Bone: Stimulates osteoclast activity and bone resorption, stimulates osteoblasts to release OPGL. Inhibits collagen synthesis by osteoblasts. Active Vit. D increases PTH driven bone resorption
- Kidney: controls the amount of calcium reabsorbed in the distal portions of the nephrons and thus the amount of calcium lost in the urine. Inhibits phosphate reabsorption Increased excretion of phosphate. Also, increases activity of enzyme that forms active vitamin D leads to increased uptake of calcium and phosphorus in GI.
List the plasma forms of calcium. Which forms are filtered in the glomerulus? In which form is ~ 50% of the total calcium?
- Free of ionized form (50% and filtered)
- Protein-bound calcium (not filtered in the glomerulus)
- Calcium bound to small diffusible anions (filtered)
Recognize the symptoms of hypocalcemia and hypercalcemia.
- Hypocalcemia = closer to threshold causing hypocalcemic tetany, latent tetany revealed by Trousseu and Chvostek sign , distal extremeity numbness/tingling senstions, laryngospasm, syncope, CHF, angina, epilipsey
- Hypercalcemia = farther away from threshold causing fatigue, muscle weakness, constipation, polyuria, kidney stones, coma, cardiac arrest
Describe bone remodeling. Which cell type is responsible for bone deposition? Bone resorption? What are the roles and alternate names of: OPGL and OPG? Which increases bone resorption? What roles do PTH and vitamin D play in bone resorption?
- Bone deposition: Osteoblasts
- Bone resorption: Osteoclasts
- OPGL (Osteoprotegerin ligand) AKA RANK Ligand: released by osteoblasts with PTH stimulation. It then activates preosteoclasts multinucleated osteoclasts
- OPG (Osteoprotegerin): released by osteoblasts (when stimulated by estrogen) as a decoy receptor for OPGL (preventing it from binding to preosteoclast cells)
Describe where vitamin D precursors are transformed into Vitamin D3 and where vitamin D3 is converted (2 steps, 2 organs) into the most active form of vitamin D. What is the name for this most active form?
Vitamin D3 in liver. Then most active from in kidney. Most active from = 1,25-dihydroxycholecalciferol (calcitol). PTH needed in kidney to make active form of Vit D
Be able to recognize the causes and symptoms of hyperparathyroidism, hypoparathyroidism and pseudohypoparathyroidism.
- Hyperparathyroidism:
- Primary: due to benign adenoma and results in hypercalcemia/hypophosphatemia. Can have calcium-containing kidney stones, weak bones, constipation, constant urination
- Secondary: In patients that have chronically low plasma calcium (renal disease/rickets)
- Hypoparathyroidism: damaged during thyroid surgery results in decline in plasma calcium. Would be fatal if too bad. Low calcium causes hypocalcemic tetany.
- Pseudohypoparathryoidism: Having signs but normal levels of circulating PTH. This is causes by problems with PTH receptor.
Describe how/why renal disease can cause osteomalacia.
Osteomalacia (softening of the bone due to deficient mineralization) can be caused by a type of “renal rickets” due to the failure of the damaged kidney to produce the active form of vitamin D
