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32 Cards in this Set
- Front
- Back
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what are two most impt mineral components of bone?
what is homeostasis of these minerals controlled by? |
Calcium and phorphorus
controlled Parathyroid hormone(PTH) and vit D. also regulated to minor degree by calcitonin, estrogens and glucocoricoids |
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what are exogenous agents clinically used in managing bone mineral disorders such as osteroporosis and pagets dz?
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*bisphosphonates
*SERMS *Estrogens *fluoride |
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what are the physiologic effects of PTH?
intesting? bone? kidney? OVerall effect? |
1. Intestine
-increase ca and po4 absorption 2. Bone -HIGH DOSE=ca and po4 resorption -LOW DOSE=increase bone formation 3. Kidney -decresae ca excretion -INCREASE phosphate excretion what is OVerall effect? *****Increase serum Calcium ****Decrease serum phosphate (this is inverse of kidney) |
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what is a PTH analog used to tx osteoporosis?
how is this drug administered? |
Teriparatide (FORTEO)
(Stimulates new bone formation b/c low dose) sub q |
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what is vit D? how is it produced
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a prohormone produced in skin under control of UV light
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what is mech of action of vit D?
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it activates cytoplasmic and membrane vit D receptors
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what physiologic effects of Vit D on intestine? which form of Vit D is used?
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increase calcium and phosphate absorption w/ 1,25 dihydroxyvitamin D(calcitriol)
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what is physiologic effect of vit D on bone?
what D's are used? |
Net increase in calcium and phosphate resorption with calcitriol
Bone formation enhanced by secalciferol(24,25 dihydroxyvitaminD) |
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what is overall effect in plasma of Vit D?
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Increase both serum calcium and phosphate (PTH decreases phosphate)
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what are the clinical uses of VIt D?
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1. Nutritional rickets(lack of D)
2. Hypocalcemia 3. Hypophosphatemia 4. chronic renal failure 5. Post menopausal osteoporosis |
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what are the physiologic effects of calcitonin?
what is overall effect? |
*decrease bone resorption (help pagets dz)
*increase renal excretion of calcium and phosphate(lower serum Ca) DECREASE SERUM PHOSPHATE AND CALCIUM |
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what are clinical uses of calcitonin?
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*Paget's dz (dz of bone remodeling)
*Hypercalcemia *Postmenopausal osteoporosis when estrogens are C/I |
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what is the #1 clinically used drug to increase duration and potenency of human calcitonin?
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calcitonin-salmon(Miacalcin)
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what is the most efficient tx to inhibit postmenopausal bone loss?
what is Mech of action? |
Estrogen replacement therapy
MOA is that it inhibits PTH stimulated bone resorption |
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what is number 1 estrogen rx'd for inhibiting postmenopausal bone loss?
why? |
Raloxifene(evista)
-a SERM it increases women's bone density w/o increasing risk of endometiral cancer |
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what are glucocoritcoids used to treat regarding calcium levels?
what is problem with extended use of glucocorticoids? |
hypercalcemia (b/c induces pro catabolism)
prolonged use can lead to osteoporosis |
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what are exogenous (non hormonal) agents affecting bone/mineral homeostasis?
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1. Bisphosphonates
2. Fluoride 3. Raloxifene(Evista) 4.Plicamycin(MIthracin) |
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what is physiologic effect of bisphosphonates?
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selectively reduces osteoclastic bone resorption
*induces net bone mass increase in osteoporotic patients |
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what are the three bisphosphonates to know?
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1. Alendronate(Fosamax)#1
2. Risedronate(Actonel)#2 3. Ibandronate(Boniva)#3 is the newest and most popular |
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what is mech of action of bisphosphonates?
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inhibits osteoclastic proton pump requred for dissolution of hydroxyapatite
*hydroxyapatit is what gives bone it's strength |
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what are the clinical uses of bisphosphonates?
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*Tx and prophylaxis of osteoporosis
*Tx Pagets dz *Treat Hypercalcemia of malignancy *tx metastatic bone cancer |
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what is recommendation for administration of this drug and why?
what can happen ifyou dont maintain proper position after taking this drug? |
this drug has low oral bioavailability
take first thing int he morning w/ empty stomach and lots of water. BE UPRIGHT FOR 30 MINUTES if not can have esophageal damage |
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what are adverese effects of bisphosphonates?
what are c/i? |
*esophageal ulcers(reduce by taking and upright for 30 min)
c/is are peptic ulcer or esophageal bnormality |
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what are lcilnical uses of plicamycin(Mithracin)
when is plicamycin used to tx hypercaclemia? |
pagets dz
*hypercalcemia and testicular cancer is used when all other tx's are unsuccessful b/c may lead to serious toxicity |
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what can hypercalcemia cause?
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*CNS depression, coma and possibly death
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what are imp causes of hypercalcemia?
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1. hyperparathyroidism
2. cancer 3. hypervitaminosis D 4. thyrotoxicosis 5. sarcoidosis |
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why would bisphosphonates be a good choice to tx hyper calcemia?
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b/c are efficient in reducing serum calcium levels w/o inducing any observable toxic effects
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why is calcitnon(salmon) not usualy used?
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it rarel is enough to return calcium levels to normal
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what is often ustilized as clinical therapy of hypercalcemia?
what is another condition this med is being studied for use in? |
Gallium nitrate
*it blocks bone resorption clinical studies for pagets dz |
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what are the major sx of hypocalcemia?
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neuromuscular symtpoms(tetany, paresthesias, muscle cramps, convulsions)
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what are major causes leading to hypocalcemia?
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1. hypoparathyroidsm
2. renal failure 3. vit d deficiency(rickets) |
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what is tx of hypocalcemia?
what is preferred metabolite when a rapid increase in serum calcium level is needed? |
calciym gluconate IV
calcium carbonate oral Vit D or metabolites *1,25 dihydroxyvit/calcitriol is preffered for rapid increase |
