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bone disorders-
pharm
| Question | Answer |
|---|---|
| What are some vitamin D metabolites? | cholecalciferol, ergocalciferol, calcitriol, doxercalciferol,paricalcitol, calcipotriene |
| MOA of vitamin D metabolites | Regulate gene transcription via the vitamin D receptor stimulating intestinal calcium absorption, bone resorption, renal calcium and phosphate reaborption-decrease pth-promote innate immunity-inhibit adaptive immunity |
| vitamin d metabolites toxicities | hypercalcemia, hypercalciuria-the vitamin d preparations have much longer half-life than teh metabolites and analogs |
| osteoblasts | cells responsible for anabolic activity of bone |
| osteoclasts | cells responsible for catabolic activity of bone |
| what is the active metabolite of vitamin d | 1,25 dihydroxyvitamin D |
| once released, pth maintains a constant concentration of ionic calcium in the extracellular fluid by several processes: | 1. enhanced intestinal absorption of ca and phos 2. enhanced rate of resorption of ca and phos from the bone 3. increased tubular reabsorption of ca with inhibition of tubular reabsorption of phosphate in the kidney |
| Major androgen by quantity | DHEA |
| FSH in males stimulates -----to produce -----thereby stimulating spermatogenesis | sertoli cells,,,,androgen binding protein |
| FSH also stimulates--- cells to produce ----- which provides neg. feedback to the ant. pituitary to decrease FSH secretion. | Sertoli cells....inhibin |
| LH in men stimulates ---cells to produce---- | leyig cells....testosterone |
| in women what is the major plasma androgen | androstendione--in women androsteindion is teh major plasma androgen and is secreted in teh blood stream or converted into either Testosterone or estradiol by te ovary. |
| because testosterone undergoes extenstive first pass metabolism you should not normally do wat | give terestorone enterally |
| Leuprolide | GnR analog to suppress gonadal function. SC adminitration to treat prostate canncer. |
| Adverse effect of ketoconazole in men | gynecomastia |
| finasteride moa | 5 alpa reductase inhibition/clinical use- benign prostatic hyperplasia /effective in reducing prostate size in men ; treat women with hirstuism |
| cyproterone | antiandrogen that inibit action of androgen at target organ. acetate form has progestational effect that suppresses feedback enhancement of fsh/lh increasing antiandrogen effect-used with estrogen to treat hirstuism, treat excessive sex drive in women |
| flutamide | potent antiandrogen, tx prostate cancer, not a steroid, acts like a competitive antagonist at teh androgen receptor. can cause mild gynecomastia. adv effects; mild reversible hepatic toxicity. |
| Bicalutamid | potent oral antiandrogen adminstered in sinle daily dose. treats prostate caner. |
| spironolactone | competitive inhibitor of aldosterone. competes with dihydroT for androgen receptors in target tissues /lowers plasma levesl of t |
| gossypol | cottonseed derivative MOA: destroys seminiferous epithelium bud does not alter endocrien function of testis. effect-hypokalemia, may lead to transient paralysis. |
| What are some biphosphonates | Ibimdronate, Pamidronate, Alendronate, Risedronate,Zoledronate |
| MOA bisphosphates | Decrease osteoclast mediated Ca resorption |
| what is the most abundant mineral in the body and essential for bone teeth, and muscle, nerve development? | CALCIUM |
| 3 processes that pth maintains a constant ca | 1. enhance intestinal absorption of ca/phos 2. enhanced rate of abosprtion of ca/phos from bone 3.increased tubular reabsopriton of ca with inhibition of tubular reabsoprtion of phosphat in the kidney |
| vitamin d metabolit formed in the liver and major circulating form of the vitamin | calcifidiol |
| the primary active metabolite of vit d3 | calcitriol (1,25 dihydroxyvitamin d) |
| ergocalciferol | plant hormone with similar biologic acitivty |
| which enzyme is responsible for the final conversion of 1,25 ohd | 25 hydroxy chole calciferol 1 hydroxylase |
| remodeling balance | the coupling of bone resorption and formation |
| collagenous substance released by osteoblast | osteoid |
| major causes of hypercalcemia | hyperparathyroidism and cancer |
| goal for hypercalcemia treatment | lowering serum ca concentration and correcting or decreasing the underlying disease |
| 5 approaches for correcting hypercalcemia | 1.increase urinary excretion 2.diminished bone resorption 3. decreased intestinal ca absorption 4. chelation of ionized ca 5. dialysis |
| how do you increase ca excretion | by inhibiting proximal and loop sodium reabsorption thereby reducing the passive reabsorption of ca |
| 3 classes of drugs that lower serum ca concentration | biphosphonates, calcitonin, gallium nitrate and plicamycin or mithramycin but its obsolete |
| calcitonin is secreted by what cells | parafollicular C cells of thyroid gland |
| salmon calcitonin | is used therapeutically in part because it is cleared more slowly from the circulation-high affinity for human calcitonin receptors |
| malignancy related hypercalcemia | zoledronic acid (zometa) iv za is the biphosphonate of choice for malignancy associated hpercalcemia because it is more potent than pamidronate, and can be administered over a shorter period of time |
| treatment for postmenopausal osteoporosis and glucocorticoid induced osteoporosis | alendronate |
| pamidronate | used to treat pagets, mm, hypercalcemia |
| drug of choice for hypoglycemia | iv ca gluconate |
| causes of hyperphosphatemia | massive acute phoshpate load chronic renal failure primary increase in proximal phosphate reabsorption |
Created by:
emorgan03
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