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Bone formation
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cortical bone: dense, compact, hard outer shell, trabecular bone: more metabolically active, higher turnover rate, hips and vertebrae, available for resorption (spongy bone)
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Bone formation
cortical bone: dense, compact, hard outer shell, trabecular bone: more metabolically active, higher turnover rate, hips and vertebrae, available for resorption (spongy bone)
resorption
from the bone to the blood
osteoblasts
bone building, originate in bone marrow, controlled by PTH and calcitriol. Secretes collagen, bone matrix, osteoid. It becomes embedded in the matrix and becomes osteocytes
osteocytes
forms osteocytic membrane system. during mineralization: Ca, phos., Mg enter the bone fluid from the blood and attach to bone proteins and ground substance. Calcium salts make hydroxyapatite (crystal lattice found in bones and teeth made of calcium salts, laid on top of matrix)
calcium
facilitates interactions between proteins or proteins and phospholipids
collagen
proteins in bone
osteonectin
binds to both calcium and collagen
osteopontin
binds hydroxyapatite and bone cells
osteoclasts
resorb bone, large, multinucleated. Contains lysosomes, releases acids, proteases, etc. that break down bone. Responds to PTH, calcitriol, and calcitonin. Helps maintain blood calcium
fibroblasts
form collagen (long rod shaped protein that gives strength), involved in healing
chondrocytes
requires iron, vitamin C and vitamin D. Form ground substances for bone, tendons and ligaments
reticulocytes
bone marrow. Makes red blood cells and leukocytes
bone remodeling
consistently remodeled throughout life; growth and maintenance, fracture repair, maintain serum calcium levels
bone mass
peak = around 27 yrs. Adolescents: greatest activity, best time to add density. Postmenopausal (estrogen): loss of bone mass
DEXA
dual x-ray absorptiometry
factors affecting bone mass
protein intake (increase intake associated with increase calcium excretion), acidosis (increase acidity, increase bone density) caffeine (increased urinary excretion), sodium intake, mechanical loading (more exercise = increased calcium), smoking (decreases absorption), alcohol, calcium intake, vitamin D, phosphorous, weight loss (lose weight = decreased bone density)
calcium DRI's
males 19-30: 1000 mg/d, females 19-30: 1000 mg/d, 9-18 yrs: 1300 mg/d, >50 yrs.: 1200 mg/d
vitamin D DRI's
males 19-30: 5 ug/d, females 19-30: 5 ug/d, 9-18 yrs.: 5 ug/d, >50 yrs.: 10 ug/d
phosphorous DRI's
males 19-30: 700 mg/d, females 19-30: 700 mg/d, 9-18yrs.: 1250 mg/d, >50 yrs.: 700 mg/d
magnesium DRI's
males 19-30: 400 mg/d, females 19-30: 310 mg/d, 9-18 yrs.: 240-410 mg/d, >50 yrs.: 420 mg/d
calcium sources
dairy products (milk, cheese, yogurt), vegetables (turnips or mustard greens, broccoli, cauliflower, legumes, tofu), seafood (salmon, sardines with bones, clams and oysters), fortified foods (orange juice)
calcium supplements
calcium citrate-malate: 35%, calcium monophosphate: 25%, calcium carbonate: 40%
calcium to avoid
calcium carbonate from oyster shell or dolomite, aluminum and lead contamination, bone meal preparation
vitamin D sources
animal sources: beef, eggs, milk and dairy, saltwater fish (salmon, tuna), fortified: breads, cereals, plants, and sunlight
phosphorous and magnesium
readily available and don't usually see a deficiency
phosphorous sources
animal products (organic phosphorous): meat, poultry, fish, milk, eggs, Plant products (inorganic phosphorous): legumes, cereals, whole grains, often in form of phytic acid or phytates
magnesium sources
coffee, tea, cocoa, whole-grains, legumes, nuts, green leafy vegetables, hard water (tap water), supplements
vitamin D
derived from cholesterol
Ergocalciferol
D2, found in plants
Cholecalciferol
D3, found in animal products
vitamin D metabolites
plant sterol --> D2 --> 1,25(OH)2D2 (ercalciol); cholesterol --> D3 --> 25(OH)D3 (calcidiol) --> 1-25(OH)2D3 (calcitriol)
calcidiol
major form found in blood
calcitriol
"active" hormone, found in the kidneys that regulates calcium levels in the blood
calcium and magnesium absorption
enhanced by vitamin D
phosphorous absorption
enhanced by calcitriol
conversion of vitamin D: liver
cholecalciferol --> calcidiol
conversion of vitamin D: kidney
calcidiol --> 1-hydroxylase --> calcitriol
1-hydroxylase
activity is increased by: low plasma calcium, PTH. Activity is decreased by: high calcitriol concentrations and dietary phosphorous
primary functions of vitamin D
regulates calcium an phosphorous (regulators for the enzyme 1-hydroxylase)
nonosseous (non-bone) calcium functions
(1%) Enzyme activation (free calcium induces phospholipase A which liberates fatty acids from glycerol backbone), blood clotting, muscle contraction (requires Mg), nerve impulses, hormones
osseous calcium functions
(99%) bone formation
vitamin D maintains calcium and phosphorous homeostasis
regulation of intestinal absorption of calcium: increased synthesis of CaBP (calbindin) will increase calcium absorption (calcitriol acts as a steroid hormone to stimulate transcription of mRNA's for CaBP), changes to brush border which increases absorption, transcaltachic response (rapid increase in calcium absorption via endocytosis)
vitamin D maintains calcium and phosphorous homeostasis
intestinal absorption of phosphorous: alkaline phosphatase, calcitriol increases enzyme activity and increases absorption
vitamin D maintains calcium and phosphorous homeostasis
bone resorption: calcitriol stimulates resorption of calcium and phosphorous from bone
vitamin D maintains calcium and phosphorous homeostasis
kidney reabsorption: calcitriol stimulates calcium reabsorption in the distal renal tubules of the kidneys
ways blood calcium concentrations are regulated
PTH: secreted in response to low calcium and Mg levels which will increase extra cellular fluid calcium levels, decreases calcitonin secretion, works with bone, kidney and intestine; calcitriol: PTH stimulates conversion of calcidiol to calcitriol, works with bone, kidneys and intestine; calcitonin: secreted from thyroid gland in response to high ECF calcium levels, inhibits kidneys production of calcium from bone
vitamin D deficiency and bone
children: rickets-failure of bone to mineralize, epiphysial cartilage grows but no bone matrix, long bones of legs bow. Spinal, pelvic and thoracic deformities; Adults: osteomalacia- deficiency = decreased calcium absorption, decline in serum calcium = increased PTH, PTH promotes bone resorption, bone matrix is spared but remineralization is impaired, results in bone pain and soft bones, most likely going to have osteoporosis with this
calcium deficiency- osteoporosis
Type I - postmenopausal women (50-65 yrs), vertebrae and distal radius-due to loss of estrogen, affects mostly spongy bone. Type II - men and women over 70, vertebrae, hips, pelvis, long bones
high phosphorous + low calcium
hyperparathyroidism (takes calcium out of bone to put into blood)
other functions of vitamin D
insulin secretion, thyroid hormone synthesis, proliferation and differentiation of immune cells, treatment of psoriasis (inhibits proliferation of keratinocytes, enhances differentiation of epidermis)
those at risk for vitamin D deficiency
elderly: poor dietary intake, more time spent indoors; climate; fat malabsorption; renal disease (decreased renal activity = decrease of renal 1-hydroxylase)
treatment of vitamin D deficiency
vitamin D supplements
vitamin D toxicity
overexposure to sun will not cause toxicity. General symptoms include: weakness, diahhrea, nausea/vomiting, headache. More severe symptoms: hypertension, renal dysfunction, calcification of soft tissues (kidney, heart, lungs, blood vessels)
calcium deficiency
rickets- secondary to vitamin D deficiency; tetany- intermittent muscle contractions that fail to relax (esp. of arms and legs, muscle pain, numbness, and spasms); osteoporosis
calcium toxicity
hypercalcemia- deposition of calcium in soft tissues
large amounts of calcium may result in
constipation, increased risk of kidney stones
magnesium
used in over 300 enzyme reactions. Glycolysis: hexokinase, PFK; krebs: decarboxylation; HMP shunt: tansketolase; beta-oxidation. Provides stability to ATP
magnesium deficiency
hypomagnesemia. Symptoms: anorexia, muscle weakness, spasms, hallucinations and personality changes, changes in cardiovascular and neuromuscular function. Will usually see with: hypokalemia, hypocalcemia, low vit. D levels
those at risk for magnesium deficiency
renal disease, diabetes, excessive alcohol, refeeding syndrome (low phosphorous and magnesium in blood), parathyroid disease
magnesium toxicity
excessive intake will not cause toxicity except in causes of renal failure. High levels of Mg salts can cause: diahhrea and dehydration. Acute toxicity: muscular paralysis, cardiac and/or respiratory failure
phosphorous functions
skeletal: laid down on collagen to form bone; structural: DNA and RNA, cell membranes-phospholipids; energy: creatine phosphate, high-energy phosphate bonds (ATP/GTP); second messengers: cAMP-cyclic andenosine monopohosphate (glycogenolysis and glycogenesis); enzyme regulation: phosphorylase reactions
phosphorous excretion
urine: 67-90%, high intake = increased urinary excretion; feces
phosphorous deficiency
<1.5 mg/dL. General symptoms: anorexia, bone loss, muscle weakness, cardiac dysfunction
those at risk for phosphate deficiency
malnourished. Refeeding syndrome aka hypophosphatemia: follows aggressive refeeding after a period of starvation, abnormal metabolism when body shifts from using fat to CHO for enegy, glucose is taken up rapidly and phosphorous driven into the cells
treatment for refeeding
begin with low calories and CHO, gradually increase kcal and CHO. TPN; add phosphorous and Mg
phosphate toxicity
rare, at risk when on dialysis (kidneys excrete phosphorous, have to be on a low phosphorous diet and/or phosphate binders
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