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75 Cards in this Set
- Front
- Back
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What is the extracellular Ca2+ concentration
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9.4 mg/dL only varing by a few percent either way
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what can elevated calcium levels cause
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progressive depression of nervous system
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where is calcium located in the body
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0.1% ECF, 1% in cells, rest stored in bones
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body phosphate stored
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85% bones, 14-15% in cells, less than 1% ECF
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forms of calcium in the plasma
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1) 41% is combines with plasma proteins-not diffusable 2) 9% is with anionic substances, but not ionized-diffusable 3) 50% diffusible and ionized
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total average quantity of inorganic phosphate by both phosphate ions in plasma
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4 mg/dL
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what does chronic hypocalcemia ot hypophosphatemia cause
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greatly decreased bone mineralization
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why does the nervous system become more excitable with low Ca2+
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increased neuronal membrane permeability to sodium ions allowing easy initiation of Aps
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increased Ca2+ effect on heart
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increases QT interval
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what occurs when calcium levels rise above 17 mg/dl
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calcium phosphate crystals are likely to precipitate throughout body
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how much calcium is usually absorbed each day
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35% ingested or 350 mg/day
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how much calcium is lost each day due to GI secretions and sloughed mucosal cells
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250 mg/day
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where is calcium reabsorption selective in the kidney
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late distal tubules and early collecting ducts - depends on concentration in the blood
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most important factor controlling reabsorption of calcium in distal portions of nephron
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PTH (also causes phosphate excretion)
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ground substance of bone
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ECF plus proteoglycans (chondroitin sulfate and hyaluronic acid)
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what additional ions can be conjugated among bone salts
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magnesium, sodium, potassium, and carbonate ions as well as ions normally forgein to bone
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strength of collagen fibers in bones
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great tensile strength
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strength of calcium salts in bones
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great compressional strength
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importance of inhibitors of hydroxyapetite formation
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pyrophosphate - prevent crystal formation in normal tissues despite state of supersaturation of the ions
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What percent of bone is in readily mobilizable salt such as CaHPO4 and other amorphous calcium salts
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0.4-1%
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where are osteoblasts found
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outer surfaces of bone and in bone cavities
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where are osteoprogenitor cells
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in surface tissue lining bone aka "bone membrane"
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what forms after a bone is broken
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callus - large bulge of osteoblastic tissue and new organic bone matrix
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final active product of vitD
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1,25-dihydroxycholecalciferol aka 1,25(OH)2D3
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where is vitD formed (aka cholecalciferol)
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in the skin from 7-dehydrocholesterol via UV rays
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where is cholecalciferol converted to 25-hydroxycholecalciferol
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in the liver
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why is conversion in the liver limited
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feedback inhibition
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why is feedback inhibition in the liver important
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precise regulation of 25-hydroxycholecalciferol in plasma and conserves vitD stored in the lover for future use
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25-hydroxycholecalciferol vs vit D storage
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25-hydroxycholecalciferol persists for a few weeks; vit D can be stored for many months
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what converts 25-hydroxycholecalciferol to 1, 25-dihydroxycholecalciferol
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kidneys in proximal tubules under influence to PTH
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what is 25-hydroxycholecalciferol converted to when there is a high Ca2+ concentration
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24, 25-dihydroxycholecalciferol, which has almost no vitD effect
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3 places where calcium can be absorbed
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intestines, bones, renal tubules
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how does 1, 25-dihydroxycholecalciferol fxn in intestinal calcium absorption
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formation of calcium binding protein over 2 days in intestinal epithelial cells; protein stays in celss for several weeks
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what is the affect on bones with high vitD concentration
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absorption
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PTH action in absence of vitD
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bone absorption greatly reduced or prevented
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vitD action on bone in smaller quantities
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promotes bone calcification
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microscopic appearance of parathyroid glands
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dark brown fat
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cells in parathyroid gland
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chief cells (secrete most/all PTH) and oxyphil cells
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where is PTH synthesized
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on ribosomes, ER modifies, golgi modifies and packages in secretory grnules
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what is a large share of PTH activity caused by
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fragments with PTH activity that aren't removed by the kidney as rapidly as whole 84 aa PTH
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two phases of PTH affect of bone reabsorption
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1) rapid phase of activating already existing cells (mainly osteocytes) to reabsorb calcium phosphate salts 2) days/weeks and causes proliferation of osteoclasts to reabsorb bone
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osteolysis
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absorption of calcium without absorption of fibrous and gel matrix
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PTH ion effects in kidney
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increased absorption of Ca2+, Mg+, H+; decreased reabsorption of phosphate, Na+, K+, and aas
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second messenger commonly used with PTH
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cAMP
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where does synthesis and secretion of calcitonin occur
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parafollicular cells or C cells in the interstitial fluid between follicles of the thyroid gland
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how does calcitonin decrease plasma Ca2+ levels
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1) decrease absorptive activities of osteoclasts 2) decrease formation of new osteoclasts
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why are calcitonin affects transient
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decreased osteoclasts will lead to decreased osteoblast activity
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where are the affects of calcitonin greater
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children due to rapid bone remodeling
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Paget's disease
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osteoclastic activity greatly accelerated
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buffer systems of calcium in the body
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exchangable salt in bones (5-10 g), mitochondria in many tissues of body (10g)
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how many grams of calcium are contained within all the ECF of the body
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~1 g
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osteoteitis fibrosa cystica
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cystic bone disease of hyperparathyroidism
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one of important findings in hyperparathyroidism
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alkaline phosphatase plama levels due to increased osteoblastic activity
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symptoms of extreme elevations in PTH
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CNS and PNS depression, muscle weakness, constipation, abdominal pain, peptic ulcer, lack of appetite, depressed relaxation of heart during diastole
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patients with mild hyperparathyroidism have tendancy to form
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kidney stones - calcium phosphate and calcium oxalate stones; more likely to form in alkaline urine
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secondary hyperparathyroidism
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high PTH due to low plasma calcium levels
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what does vitamin D deficiency lead to
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osteomalacia
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rickets cause
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Vit D or phosphate deficiency in ECF
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phosphate and calcium plasma levels in rickets
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calcium relatively stable due to bone buffer, phosphate low - no adequate system to recover
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when does adult have decreased vit D and calcium level
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steatorrhea - vit D is fat soluble
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congenital hypophosphatemia
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aka vit D resistant rickets; renal tubules have reduced phosphate reabsorption rate
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osteoporosis
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diminished bone matrix (not poor calcification); generally due to decreased osteoblastic activity
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common causes of osteoporosis
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1) lack of physical stress 2) malnutrition 3) lack of vitC 4) postmenopausal lack of estrogen 5)old age 6)Cushing's syndrome (protein deficiency)
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occlusion of teeth
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interdigitation so that upper and lower sets fit together
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what forms the enamel
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ameloblasts
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what makes up the enamel
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very large and dense crystals of hydroxyapatite with absorbed carbonate, magnesium, sodium, potassium, and other ions embedded
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what is the main body of the tooth composed of
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dentin - simliar composition as bone, different histological organization
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what deposits and nourishes the dentin
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odontoblasts along the inner surface of the wall of the pulp cavity
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what does the periodontal membrane secrete
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cementum, lines the tooth socket
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first teeth
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deciduous or milk teeth; 20
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rate of absorption and deposition of minerals in the cementum
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about equal to the surrounding bone
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rate of absorption and deposition of minerals in the dentin
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about 1/3 that of surrounding bone
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enamel mineral exchange
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mostly via exchange with saliva and is extremely slow
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most common bacteria eroding teeth
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streptococcus mutans
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flourine and caries
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fourine replaces hydroxyl ions in the crystals and makes enamel less soluble; makes teeth 3 times more resistant to caries
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