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DEMS Unit 4 > Dietary Ca and Bone Health > Flashcards

Dietary Ca and Bone Health Flashcards

1
Q

Ca hydroxyapatite

A

what mineralizes bone/teeth

99% of Ca

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2
Q

metabolic functions of extracellular Ca

A
  • 1% of total Ca extracelluarly
  • signal transmitter
  • tertiary structure: activate catalytic and mechanical properties
  • clotting, nerve impulse transmission/relaxation of muscle, mediation of hormones, growth factors

–VERY IMPORTANT!!

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3
Q

low Ca results

A

increases PTH:
- bone resorption, decrease Ca excretion, increased P excretion
activates

itself increases vitamin D hydroxylation in kidney, but increased PTH also does this — increased Ca intestinal absorption and decreased excretion in urine

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4
Q

results of increased serum Ca

A
  • calcitonin increases: deposition of Ca into bone
  • lower PTH
  • lower Ca reabsorption in ascending loop of Henle
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5
Q

2 major ways Ca absorbed

A

1) Active: (3 steps)- vit D dependent
- apical membrane absorption – mostly mediated by TRPV6 (duodenum)
- transport to basal membrane via shuttling – Calbindins mainly
- get into blood: Na/Ca pump and ATP dependent Ca export

2) Passive:

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6
Q

1,25(OH)2 Vit D

A

active form of vitamin D; serves as gene transcription regulator–enters nucleus, and if cell expresses receptor (VDR) will bind and dimerizes with RXR. This complex binds to VDRE (vitamin D response elements) to upregulate genes

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7
Q

where does passive Ca absorption occur

A

duodenum, jejunum, ileum

  • driven by concentration
  • transcellular or paracellular via Ca absorption channels that only work when gradient present
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8
Q

where does active Ca absorption occur

A

duodenum

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9
Q

genes regulating vit D response elements

A

TRPV6, TRPV5, CaBP-9K & 28k, PMCA

increased transcription of all genes involved in getting Ca in

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10
Q

Ca absorption pattern

A
  • generally more Ca intake, more absorbed (passive)
  • lower intake the higher body will regulate active Ca absorption but not perfect, body can only do so much
  • increased Chronic Ca– increased bone accretion
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11
Q

Ca enhanced by

A
  • increased physiologic demand (prego, adolescence)
  • vitamin D status
  • lactose (maintains solubility)
  • gastric acidity–need to release Ca from fod matrix
  • Dietary protein – increase intake assoc with increased absorbed Ca
  • NOT by bone mineral depletion
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12
Q

what drives Ca absorption

A

serum Ca NOT bone mineral depletion

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13
Q

Ca absorption impaired by

A
  • vitamin D deficiency (northern latitudes, limited sun exposure dark pigmentation, elderly)
  • Steatorrhea – unabsorbed fat binds Ca–soaps
  • Gastric alkalinity– esp achlorhydria in elderly
  • Oxalic acid: ex spinach
  • Phytic acid: ex: legumes,
  • Caffeine: increased urine Ca (easy to offset)
  • dietary protein: increased urine Ca (net effect neutral/positive)
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14
Q

dietary protein effects on Ca

A

increases absorption and Ca release in urine; net effect neutral/positive

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15
Q

how does bone form

A

most formed through endochondral bone formation

- cartilage mineralizes and growth plate, which allows for longitudinal bone

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16
Q

types of bone

A
  • trabecular–spongy, much more metabolically active; can absorb impact
  • cortical– much more dense; what gives bone strength due to more hydroxyapatite
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17
Q

Bone turnover

A

happening all over bone; contnual balance between blasts making and clasts breaking down bone
- becomes bad when resorbtion > formation

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18
Q

how often do bones turn over

A

entire skeleton turns over every 10 years

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19
Q

Ca absorption through life cycle

A
  • avg healthy adult about 25%
  • fetus: 80% transfer in 3rd trimester–lots through placenta; doesn’t need much earlier since don’t have cartilage skeleton to mineralize
  • infants: 40-60%
  • early puberty- 34%
  • pregnant women - 50%
  • may decrease in elderly (vit D low, gastric acidity, exercise decreases)
20
Q

Preterm infants and Ca

A

30g crosses placenta

  • 80% transfer in 3rd trimester (endochondral bone formation)
  • risk of osteomalacia of prematurely–bones at high risk of fracture
21
Q

Ca in older children

A

worry about Ca deficiency– Rickets–very severe Ca deficiency, can’t mineralize bones and see bowing of bones supporting weight
- not often in US but more in African diets with less dairy

22
Q

Does Ca intake matter in young children

A

YES

  • probs not big effect with supplementation just acutely
  • Ca intake matters! esp if chronic
23
Q

when do you reach peak bone mass

A

about age 30

- a little you can do to modify

24
Q

Ca absorption in puberty

A

super high early, and slower bone mineralization occurs throughout adolescence

25
Q

Pregnancy and Lactation

A
  • physiologic but not dietary requirements increase due to adaptations
  • Pregnancy: vit D increases – Ca absorption increases (active) to accommodate fetal demand

at birth lose estrogen/progesterone
-Lactation: PTH increases and bone mass loss (for Ca n breastmilke), but recovered with post weaning.

26
Q

are multiple pregnancies putting ppl at risk for bone issues

A

NO; recover after lactation

27
Q

adolescent req for Ca

A

RDA = 1300

1100 = EAR

28
Q

females >51 need how much Ca

A

1200 = RDA

1000-EAR

29
Q

how much Ca do elderly >70 years need

A

1200 = RDA

1000-EAR

30
Q

do pregnant women need to increase Ca intake from RDA

A

no… same
14-18, RDA = 1300
19-50, RDA = 1000

31
Q

where do we get Ca

A
  • dairy
  • Salmon
  • Greens (but have inhibitors–not bioavailable)– spinach, broccoli
  • Salmon
32
Q

Ca supplements

A
  • Ca carbonate: most common (TUMS); 40% elemental Ca in each tablet; best absorbed with meals
  • Ca citrate – more common in multivitamin pills; 21% elemental Ca and best between meals
33
Q

Can Ca supp be harmful

A

YES!

  • increased risk CV events if taken without vitamin D
  • increased MI risk of 30%
  • highest risk if dietary Ca high already
  • no risk associated between dietary Ca
34
Q

High risk populations or Ca needs

A

adolescent females, 71+ males/females not doing great job on population level

35
Q

why worry about adolescent girls

A

want to meet peak bone density

36
Q

are majority of americans getting adequate Ca and vit D

A

yes

37
Q

high risk groups

A

premature infants, adolescents, peri-menopausal women, bariatric surgery (bypass duodenum where active Ca absorption occurs)

38
Q

how does estrogen affect Ca

A

decreased estrogen increases bone resorption

-estrogen stimulates osteoblastic/decreases osteoclastic activity, so low estrogen favors osteoclast

39
Q

osteoporosis

A

reduction in bone mass assd with

40
Q

how common is osteoporosis

A
  • 25% women >50 years

- lots of medical loss

41
Q

Non-nutritional factors assd with bone mineral density

A
  • GENETICS!! (70-80%)
  • hypogonadism–esp low estrogen
  • age: strongest empiric predictor
  • MEDS (corticosteroids)
    glucocorticoids, chronic illness assd with malabsorption, chronic inflammation, steroid use
  • Behaviors (tobacco, EtOH depresses osteoblast activity/impaired nutrition)
  • weight bearing exercise (muscle mass directly related to bone mass; mechanosensors on bone regulate-increase- osteocyte and osteoblast activity)
42
Q

Nutritional factors associated with BMD

A
  • Ca intake
  • Vit D
  • Caffeine
  • Protein
  • Na
  • vegetarian diet (salvage Ca more efficiently)
  • Phosphorous
  • Mg deficiency
  • Vit C/K are cofactors in collagen and osteocalcin, respectively
43
Q

DASH Diet

A

for hypertension but can help decrease turnover of bone and may have benefits to long term bone status

44
Q

Osteoporosis prevention strategies

A
  • achieve peak bone mass when possible (esp adolescence)
  • Dietary focus (Ca, Vit D/K, protein, low Na)
  • maintain ovulation/regular menses
  • weight bearing exercise
  • no smoking, EtOH, steroids
  • supplement judiciously when needed
45
Q

Ca - supplement

A

good when needed

  • especially with low Ca diet, older, institutionalized
  • supplements good when used as recommended

DEMS Unit 4 (16 decks)

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