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VITAMINS & MINERALS > MODULE 1 Week 3: Vitamin D & K > Flashcards

MODULE 1 Week 3: Vitamin D & K Flashcards

1
Q

** Which vitamin also functions as a (steroid) hormone?

A

D

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2
Q

** Main functions of Vitamin D

A
  • Hormone (chemical messenger)
  • CALCIUM homeostasis/bone health
  • Phosphorus homeostasis
  • Cell differentiation, proliferation, growth
  • Muscle tissue/strength/function
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3
Q

** In what populations might vitamin D be considered CONDITIONALLY ESSENTIAL?

A
  • elderly
  • alcoholics
  • People who live in the northeast
  • People with kidney/liver issues
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4
Q

** The DRI of vitamin D between age 9-69 is 600IU, how many cups of milk is that?

A

6

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5
Q

** What 3 vitamins are involved in osteoporosis?

A

A, D, K

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6
Q

** What is osteocalcin? Is is X dependent?

A

BONE gamma-carboxyglutamic acid-containing protein

Vitamin K dependent

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7
Q

** What is gamma carboxylase?

A

Vitamin K dependent enzyme needed to CATALYZE GLA protein

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8
Q

** Bioavailable form of vitamin D

A

1-25 OH (hydroxide)

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9
Q

25(OH) v 1-25(OH) - where are each made?

A

25(OH)= liver

1-25(OH) = kidneys

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10
Q

** Factors required for hydroxylation of vitamin D

A
  • direct sunlight
  • cholesterol
  • good skin
  • FUNCTIONAL LIVER & KIDNEYS
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11
Q

** Are vitamin D receptors located on just the bone or elsewhere?

A

No, on EVERY organ of the body (basically)

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12
Q

** What age group is most susceptible to vitamin D deficiency?

A

Elderly

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13
Q

**Chron’s disease

A

Autoimmune GI disease - part of digestive tract becomes inflamed/ulcerated etc.

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14
Q

** Vitamin D, T cells, autoimmunity

A

Vitamin D regulated hyper active immune response (autoimmune response) by regulating T cell activity in the body

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15
Q

** What part of the intestine is the most vitamin D absorbed ?

A

Distal small intestine

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16
Q

** Vitamin DBP is what?

A

Vitamin D binding protein

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17
Q

What protein is vitamin D transported on ?

A

DBP (vitamin D binding protein)

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18
Q

** Relationship with vitamin D and higher body fat

A

People with higher bod fat store more vitamin D in adipose tissues so requires higher vitamin D intake in order to achieve adequate SERUM vitamin D levels

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19
Q

** Dietary vitamin D is absorbed through passive or active absorption

A

PASSIVE from micelles, incorporated in chylomicrons

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20
Q

** Skin produced vitamin D is absorbed by passive or active?

A

Passive diffusion into blood

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21
Q

** Cholecalciferol (is it active)?

A

D3; not active

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22
Q

** Most abundant vitamin D form in BLOOD

A

25-OH (calcidiol)

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23
Q

*** STEPS IN VITAMIN D METABOLISM/HYDROXYLATION

A
  1. Sunlight hits the skin and converts DEHYDROXYCHOLESTROL to D3(cholecalciferol)
  2. D3 is hydroxylated into 25(OH) in the LIVER
  3. (25(OH) secreted into the blood and transported on DBP)
  4. 25OH travels to KIDNEYS where it is converted to 1,25-OH
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24
Q

** 1-25,OH is regulated by with hormone?

A

PTH (parathyroid)

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25
Q

** Most common test to assess vitamin D status? (What form is measured?)

A

25-OH blood test

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26
Q

** Calcidiol v calcitriol

A

Calcidiol = 25-OH

Calcitriol = 1,25-OH

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27
Q

** Non-genomic interactions of vitamin D involved (hint receptors)

A

Activation of vitamin D receptors in the cell membrane

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28
Q

** Genomic actions of vitamin D (calcitriol)

A

Bind to nuclear receptors and influence DNA sequences/protein transcription

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29
Q

** Vitamin D and serum calcium (eg. what happens with hypocalcemia)

A
  1. Low blood calcium triggers release to PTH from parathyroid gland
  2. ^ PTH causes more calcium to be reabsorbed (from kidneys) AND stimulates conversion to 25-OH to (ACTIVE) 1-25-OH
  3. 1-25-OH travels to intestines to INCREASE Ca from the intestines/gut
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30
Q

** Vitamin D and phosphorus (hint related to calcium regulation)

A
  • PTH released when sense low calcium
  • Kidneys decrease excretion of Ca &(!) increase excretion of phosphorus & increase calcitriol 1-25-OH conversion
  • 1-25-OH travels to INTESTINES where it increased absorption of Ca AND PHOSPHORUS

** PTH travels to bone to release Ca and Phosphorus from bone (to increase serum Ca)

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31
Q

** CELL PROLIFERATION VS. DIFFERENTIATION MEANS

A

P: Increase in the numbers of cells as a result of growth and division

D: process by which a cells changes from one type to another (usually to a more specialized cell)

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32
Q

** Vitamin D deficiency and psoriasis

A

Vitamin D involved in regulating cell differentiation/proliferation; people with psoriasis have an ACCELERATED rate in which new cells rise to the surface of the skin (causing the dry, skin scaling), which may be because they do not have enough vitamin D to regulate the rate of cell growth/rising

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33
Q

** Vitamin D and muscle (development and function)

A

Vit D facilitates normal muscle development and normal contraction/relaxation

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34
Q

** Does vitamin D promote slow and fast twitch muscle fiber development

A

FAST

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35
Q

** vitamin D and myopathy

A

Muscle weakness, increased falls

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36
Q

** Vitamin D and cardiovascular health, immune health, diabetes

A

C: helps regulate blood pressure and lipoprotein metabolism

I: Helps prevent autoimmunity (regulated hyper immune response) and helps mount defense against infection

D: Aids in pancreatic beta cell health and insulin function

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37
Q

** Does dietary or supplementation vitamin K need any digestion?

A

NO

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38
Q

** Symptoms of vitamin D deficiency (as related to muscles, calcium, LOOK UP

A
  • Myopathy
  • ## Calcium deposits
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39
Q

** What might occurs with too much vitamin D in the absence of vitamin K (hint vascular)

A

Calcium deposits - vascular calcification

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40
Q

** Menaquinone v Philoquinone

A

M: BACTERIAL vitamin K (K2)

P: DIETARY vitamin K (K1)

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41
Q

** What causes vitamin K deficiency in infants?

A

Born with STERILE intestines (can’t produce K2) so need bacteria from food/breast feeding etc.

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42
Q

** Can you get toxic amounts of vitamin D from sunlight?

A

No; excess hear on the skin prevents D3 from forming/reaching toxic levels

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43
Q

** SYMPTOMS OF VIT D TOXICITY

A
  • Anorexia
  • Weight loss
  • Renal dysfunction
  • Irregular heart beat
  • VASCULAR CALCIFICATION (happens in absence of vitamin K)
  • Calcification of soft tissues
  • Hypertension
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44
Q

** What is Rickets

A

A condition in infants of soft bones and skeletal deformities caused by failure of bone tissue to harden

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45
Q

**What is osteomalacia

A

A condition in adults of weak and softened bones that can be reversed with supplementation

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46
Q

** SYMPTOMS VIT D DEFICIENCY

A
  • osteomalacia
  • rickets
  • fatigue
  • bone pain
  • myopathy/muscle weakness/cramps
  • depression
  • infertility/reproductive issues
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47
Q

*** D2 v D3; which is more effective at raising blood Vit D levels?

A

D2 = ergocalciferol; made from PLANTS

D3= calciferol; made in human body

  • D3 more effective at raising blood levels
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48
Q

** Non-fortified sources of D3 (calciferol)

A
  • Flesh of fatty fish
  • Fish liver oils
  • eggs, cheese, beef liver (less so)
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49
Q

**Vitamin K absorption is facilitated by bile acid, pancreatic secretions, and X????

A

Presence of dietary fat

50
Q

** Location of absorption of K2 V K3

A

K3 (dietary/supplemental) = Upper intestine (in micelles)

K2 (synthesized by bacteria) = Distal ileum/colon but VARIES by person

51
Q

*** Blood transport of vitamin K occurs on/as part of what?

A
  1. Chylomicrons
  2. When reaches liver (as chylomicron remnant), liver incorporates vit K into VLDL and secrete back into blood (for circulation
52
Q

** Vitamin K primarily stored in which part of cell? Is a large amount stored?

A

Cell membranes; no, only small amounts

53
Q

*** PRIMARY function of vitamin K (hint enzyme activity of GLA)

A

Vitamin K necessary for post-translational carboxylation of GLA (glutamic acid enzyme) to form gamma-carboxylated GLA residue

** Vitamin K is dependent for GLA (enzyme) to add CARBOXYL groups to peptides/proteins after synthesized in cell.

54
Q

** Vitamin K, GLA residues, Ca relationship

A

** Vitamin K needed for GLA enzyme to carboxylate peptides/proteins

** Carboxylated proteins (called residues) are able to bind CALCIUM, which is essential for many mechanisms

55
Q

** While form of vitamin K does majority of vitamin come from in US diet?

A

Phylloquinone/K3 (from dietary sources)

56
Q

** Is vitamin K inhibited by blood thinners?

A

Yes

57
Q

*** 4 Coagulation/clotting factors that vitamin K synthesizes

A

2,7,9,10

58
Q

** Warfarin (Coumadin): how does it interact with vitamin K to prevent clotting?

A

Warfarin inhibits the liver from processing substances into CLOTTING FACTORS (2,7,9,10) that are needed to clot blood

59
Q

** T/F warfarin inhibits the activity of epoxied reductase?

A

T

60
Q

** T/F vitamin D is derived from a steroid?

A

T

61
Q

** Foods often fortified with vitamin D (both 2&3)

A
  • diary products (milk, yogurt, cheese etc.)
  • yogurt
  • breads
  • breakfast cereals
62
Q

** What is 7-dehydrocholesterol?

A

Steroid (derived from cholesterol) that is in SKIN that is involved in absorbing UV rays into the skin (to form vitamin D)

63
Q

** What affects cutaneous production of vitamin D (eg. environmental factors)

A
  • time of day
  • season
  • latitude
  • altitude
  • air pollution etc.
64
Q

*** Melanin and vitamin D

A

Melanin blocks UVB rays so people with dark skin need MORE time in the sun to generate enough vitamin D

65
Q

** What % of dietary vit D is absorbed ?

A

50

66
Q

** Does vitamin D require any digestion?

A

No

67
Q

** What part of intestines is largest amount of vitamin D absorbed?

A

Jejunum

68
Q

** T/F after absorption, DIETARY vitamin D is transported in chylomicrons?

A

T

69
Q

** How is CUTANEOUS vitamin D transported in the blood? (Hint what protein?)

A

DBP (vitamin D binding protein)

70
Q

** Where is calcidiol/25-OH cholecalciferol synthesized?

A

The LIVER

71
Q

** Major “storage site” of vitamin D (as 25-OH) (hint: not an organ)

A

The BLOOD

72
Q

** Where is 1-25-OH synthesized?

A

the KIDNEYS

73
Q

** What 2 hormones regulated the RENAL synthesis of 1,25-OH?

A

PTH (in response to low Ca & Mg) and fibroblast-like growth factors (FGF)

74
Q

** Does DBP bind tighter to 25-OH or 1-25,OH?

A

25-OH

75
Q

** Genomic v Non-genomic (meaning)

A

Genomic = actions mediated through DIRECT DNA BINDING or transcription factor inactivation

Non-Genomic = actions mediated by membrane-receptors/interactions with CELL MEMBRANE

76
Q

** Non-genomic actions of vitamin D (primarily related to what mineral?)

A

Binds to various membrane/intramembrane receptors to causing signals to be transmitted into the cell (signal transduction) that influence various cell functions

**help mediate calcium uptake/calcium concentration etc.

77
Q

** Genomic functions of vitamin D (mechanisms of actions; VDR etc.)

A

Vitamin D can also enter the NUCLEUS and bind to VDR (vitamin D nuclear receptors) which causes changes to the receptor and therefore affecting GENE TRANSCRIPTION (protein making)

78
Q

** Direct genomic action of calcitriol (VDR —> VDRE/transcription etc)

A
  1. Calcitriol enters the nucleus and binds to NUCLEAR VDR,
  2. Binding influences certain DNA sequences called VDRE (vitamin D response elements) which CHANGES GENE TRANSCRIPTION
  3. RESULT = CHANGES IN PROTEIN SYNTHESIS
79
Q

** Calcitriol synthesis stimulated my low X ?

A

CALCIUM

80
Q

** Calcitriol and calcium (does one increase or decrease the other?)

A

Calcitriol INCREASED serum calcium levels

81
Q

** Calcitriol and kidneys (hint calcium)

A

Calcitriol tells kidneys to reabsorb (not excrete) calcium in response to low Ca levels

82
Q

** Calcitriol and intestines (hint calcium)

A

Calcitriol (in response to low calcium) travels to intestines (bound to DBP) and binds to VDRs to upregulate genes involved in calcium uptake

AKA calcitriol tells intestines to absorb MORE calcium

83
Q

** PTH, calcitriol, and bone relationship (hint: RANKL)

A

Hypocalcemia stimulates PTH with stimulates conversion of calcitriol (1,25-OH)

1,25-OH travels to kidneys to and stimulates cytokines RANKL to stimulate osteoCLASTS that break down bone and release Ca from bone in order to raise serum calcium levels

84
Q

** RANK/RANKL/Osteoprogerin system

A

In response to HYPOCALCEMIA

  1. Calcitriol travels to bone
  2. Calcitriol induces production of RANKL (cytokine) within OSTEOBLASTS (bone builder)
  3. RANKL released from osteoblasts and bind to RANK (protein RECEPTOR) located on immature OSTEOCLASTS (bone break downers)
  4. This binding stimulates release of substances that break down bone matrix (HCL) and release CALCIUM into the blood
  5. Osteoprogerin acts to prevent excessive osteoclastogenesis (excessive bone break down/resorption)
85
Q

** When RANKL is upregulated, Osteoprogerin is….?

A

Downregulated

86
Q

** What does Osteoprogerin (OPG) do? How is RANKL involved?

A

Prevents excessive bone breakdown/resorption by BINDING TO RANKL (so RANKL can’t bind to RANK)

87
Q

** Calcitriol and cell differentiation (adequate calcitirol is required for stem cells to differentiate into….?

A

Macrophages, monocytes (that becomes mature osteoclasts)

88
Q

** Calcitriol and muscles (myopathy)

A

Deficiency associated with weak muscles, pain, fails, difficulty walking up stairs

** Involved in fast twitch muscle function and proper contraction and relaxation

89
Q

** Vitamin D and cancer (hint: what does it do to cells? What does it prevent?)

A

Promotes cells differentiation and inhibits proliferation

Promotes apoptosis

90
Q

*** Vitamin D and autoimmunity (hint: what does it do to immune system?)

A

Vitamin D deficiency associated with autoimmune conditions

MECHANISM: Vit D unregulate anti-inflammatory cytokines, immune-modulating (decreased hyper active immune activity) = T-cell differentiation!

91
Q

*Vitamin D excreted through what substance in the feces

A

BILE

92
Q

** Best plant source for vitamin D2

A

Mushrooms

93
Q

** D3 is formed when steroid XXX in skin is broken down by sun

A

7-dehydrocholesterol

94
Q

** Osteocalcin (bone gamma-carboxyglutamic acid-containing protein) & low vitamin K

A

low vitamin D = uncarboxylated osteocalcin

95
Q

** Growth arrest specific gene 6 + vitamin K

A

Gas6 vitamin K dependent; needed for cell regulation/growth

96
Q

** K2 is the traffic cop for ?

A

Calcium ; direct calcium to proper place it needs to be

97
Q

** Vitamin K2 activates proteins that direct XXX to the proper destination

A

CALCIUM

98
Q

** WHAT IS OSTEOCALCIN; is a marker of osteoXXX activity

A

Bone GLA protein

Marker of osteoBLAST activity

99
Q

** Matrix GLA protein is strongest inhibitor of tissue calcification T/F? ** Proteins must be carboxylated by XXX to be physiologically active?

A

T

K2

100
Q

**Why is supplementing with JUST calcium not effective in reversing bone loss (role of osteocalcin/matrix GLA protein)

A

Because without enough K2, calcium will not be directed to the correct location (the bones) which could result in bone loss and tissue calcification

K2 helps drive calcium/vitamin D into the bone by ACTIVATED/CARBOXYLATING osteocalcin (matrix GLA protein) that inhibits calcium into wrong places (soft tissue)

101
Q

** Largest source of K2 in the western diet is?

A

Fatty cuts of ruminant animals/ruminant animals that are GRASS FED

102
Q

** 2 main reasons Americans lack K2 in their diet

A
  • emphasis on LOW FAT DIETS (because is fat-soluble vitamin)
  • Factory feed lot system (not consuming grass which they convert to K2)
103
Q

** Theory about increased heart attacks in winter

A

Because animals are feeding on less grass in winter (than summer) so humans are getting less K2, which contributes to ARTERIAL CALCIFICATION

104
Q

** Dietary sources of vitamin K provided as phylloquinone or menaquinoine?

A

Phylloquinone

105
Q

** Is bacterial synthesis of vitamin K enough to meet body’s needs?

A

No

106
Q

** Is phylloquinone or menaquinone in higher concentrations in the liver?

A

MENAQUINONE (MK-4)

107
Q

** In order for blood to clot, fibrinogen must be converted to X?

A

FIBRIN

108
Q

Intrinsic v extrinsic pathways (collagen v tissue)

A

Intrinsic pathway is activated with collagen damage

Extrinsic pathway activated with tissue damage

109
Q

FIBRINOGEN TO FIBRIN (substances involved in cascade eg. Prothrombin)

A
  1. Prothrombin —> thrombin
  2. Thrombin —> fibrinogen
  3. fibrinogen —> FIBRIN
110
Q

Prothrombin (clotting factor 2) is Vitamin K Xx?

A

DEPENDENT

111
Q

*** All glutamic acid residues must be XXX by vitamin K in order for the protein to function

A

CARBOXYLATED

112
Q

** Is vitamin K in its reduced/oxidized form when it’s involved in the carboxylation process?

A

REDUCED

113
Q

*** Ingestion of diets high in vit K affect the effect of warfarin/Coumadin how??

A

OVERRIDE EFFECTS of warfarin

114
Q

*** Would you need to increase or decrease the amount of warfarin in a client who is taking the medication and eats lots of green leafy vegetables?

A

INCREASE amount if eat a lot of leafy veggies

115
Q

** Severe vitamin K deficiency associated with what disorders?

A
  • Bleeding disorder/ “vitamin K deficiency bleeding/VKDB”
116
Q

** Vitamin D deficiency looks like?

A
  • low BMD
  • increased fracture rates
  • Cardiovascular disease
  • ARTERIAL CALCIFICATION, inflammation
117
Q

** Vitamin K toxicity looks like?

A

No toxicity established (synthetic form causes liver damage)

118
Q

*** Populations where we are likely to see deficiency & why?

A

Infants = sterile intestines (no bacteria), breast milk LOW if vitamin K, low stores

Elderly = Consume small amounts

Chronic antibiotic users = kill bacteria necessary of K2 synthesis

People with fat malabsorption disorders = fat-soluble so needs dietary fat to be absorbed and these people can’t absorb

119
Q

** Which 2 vitamins inhibits vitamin K?

A

A & E

120
Q

**How to test for vitamin K (single test or not)?

A

No single biomarker; need to use:

  • clotting time
  • Prothrombin time
  • measure % of under Carboxylated K-dependent proteins (osteocalcin, prothrombin etc.)

VITAMINS & MINERALS (9 decks)

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