Flash Nutrition Flashcards

Vitamin purpose, deficiency and toxicity

1
Q

Are vitamins organic or inorganic?

A

Minerals INORGANIC vitamins ORGANIC

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2
Q

How many people are effected with v/m deficiencies?

A

1/3 in developing countries

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3
Q

Steroid receptors cytosolic vs nuclear

A

I Cytosolic respond to steoid hormones i.e. estrogen. II nuclear steroid and non-steroid ligands i.e. thyroid hormone

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4
Q

Iodine why an issue? Sources?

A

Foods have low content. NA: iodized salt

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5
Q

Iodine deficiency?

A

TSH signals for T3 and T4. I deficience prolonged elevation of TSH-> hyperplasia of the thyroid (GOITER)

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6
Q

How does iodine make thyroid hormones?

A

Tyrosine in thyroglobulin. Action of iodide peroxidase. Activated to a free radical, chemically attacks thyroglobulinprotein. Spontaneous crosslinking and iodination reactions amongst the side chains. Mess is cut by T3 T4 structures

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7
Q

THS on metabolism and GH’s role?

A

Metabolic effects via mineral ATPases. GH is anabolic, low amount has catabolic effect

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8
Q

Goiter cause, effect, impact?

A

Thyroid enlargement, iodide deficiency 13% of population effected. Cretinism (50 million) mental retardation. Growth and deveopmental abnormalities

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9
Q

Too much iodide?

A

Minamal toxicity effects of iodide at high levels of intake reported although UL established

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10
Q

Vitamin A-> ?

A

Carotenes (plants) and Retinyl Esters (animals)

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11
Q

Carotenes ->?

A

Beta carotene, main. Other carotenes

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12
Q

Retinyl Esters->?

A

Retinol, retinyl palmitate, all-trans retinal, 11-cis Retinal, Retinoic Acid

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13
Q

What cleaves beta-carotene to 2 molecules of retin AL?

A

15, 15’ dioxygenase

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14
Q

What is involved with vit. A and night vision?

A

Retinol-> all-trans retinal-> 11-cis-retinal->rhodopsin (light) ->nerve impulse and all-trans

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15
Q

What can Retinoic acid bind and activate?

A

RAR (retinoic acid receptor) retinoid Xreceptor (RXR) at least 14 members

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16
Q

What causes large variation in RA signaling?

A

homo and heterodimerize

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17
Q

How does vit D increase complexity of gene expression?

A

heterodimerize with vit. D receptors

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18
Q

What is the main effect of vit A deficiency?

A

Imparied epithelial differentation

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19
Q

Where are epithelial cells found?

A

Lungs, trachea, cornea & sclera, GIT, esophagus, skin. Rapidly dividng stem cells are in ALL epithelial tissues

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20
Q

What are the results seen with vit. A deficiency?

A

cornea: Xerophthalmia. Lungs: resp. infections like pneumonia. GI: diarrhea. Skin: folliculosis

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21
Q

What protein accululates with vit. A deficiency?

A

KERATIN

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22
Q

Consequences of Vit. A deficiency?

A

Night blindness, impaired cell differentation (blindness), imparied growth and fertility, fetal developmental defects

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23
Q

Why do fetal development defects differ ?

A

Can occur from too high or too low vit A -> due to loss of control differentation

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24
Q

World effects of vit. A deficiency?

A

100-140 mil childrren deficient. 250 000-500 000 becoming blind, half dying within 12 months of blindness

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25
Q

What is the consequences of vit. A toxicity?

A

liver cell death. Retinyl palmitat stored in stellate cells of liver, cell is full to capacity with excess of vit. A, spills out local hepatocytes damaged and die, fatal liver failure

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26
Q

Excessive intake of beta-carotene?

A

toxic-> cause hypercarotenosis

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27
Q

Acutane -> acne drug causing birth defects?

A

13-cis retinoic acid-> birth defects

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28
Q

Estimated average requirment (EAR)

A

estimated median. Application with planning and assesing intakes for groups of people

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29
Q

Recommended Dietary allowance (RDA)

A

derived from EAR meets or exceeds req. for 97.5 % of pop

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30
Q

Tolerable upper intake level (UL)

A

intake above the UL is potentail risk of adverse effects, highest daily intake that won’t cause harm in general pop

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31
Q

Adequate intake (AI)

A

used when EAR/RDA cannot be developed, average intake level based on observe or exp. Intakes

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32
Q

Vit A DRI

A

RDA 700 W, 900 M ug/day RAE. UL 3000 ug/day retinol

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33
Q

Theraputic Index (TI) Vit. A

A

UL/RDA 3000/900 = 3.3. Small les than 10 TI difficult to maintain

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34
Q

How many vit. D sources are there?

A

5

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35
Q
  1. From plants
A

ergosterol (plant sterol) -UV-> ergocalciferol (D2)

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36
Q
  1. In/from animals
A

7-dehydrocholesterol (made in sebaceous glands of skin)-UV and heat -> cholecalciferol(D3)

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37
Q
  1. SUN
A

7-dehydrocholesterol -> pre vit D3 -> lumisterol, tavhysterol (into skin as D3 in blood DBP- DBP- D3)

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38
Q
  1. Supplementation
A

use D3 form, fat soluble so better absorbed with a lipid

39
Q
  1. Fortification
A

government initiative, relaively low levels, milk and margarine

40
Q

Calcidiol

A

25-OH vit D (circulating is a homeostatic set point)

41
Q

Calcitriol

A

1, 25-diOH vit D

42
Q

Why is calcitriol made?

A

In response to PTH secretion (low blood calcuim)

43
Q

What is the first signaling pathway?

A

enters cell and binds to vit. D receptor (VDR-nuclear) now a transcription facor : VDR can heterodimerize with other receptor families

44
Q

What is the second signaling pathway?

A

binds to a cell surface receptor, causing rapid regulation of existing proteins, inc. calcium transporters

45
Q

Consequences of calcitriol signaling in the bone?

A

acts with PTH to cause osteoblasts, inc. expression of RANK ligand on outer membrane, contace and activates osteoclasts to increase activity (already active in responses to low calcitonin and PTH)

46
Q

Consequences of calcitriol signaling in intestinal mucosal cells or kidney tubules

A

Calcium binding proteins are synthesized and require K dependent gamma-carboxylation. Causes increased absorption and reabsorption of calcuim

47
Q

Where does absorption of D/calcium occur?

A

Small intestine. Minerals need transporters to cross mucosal cell membrane, more transporters to get it ot into the portal blood

48
Q

What does proper absorption of Ca depend on?

A

Expression of a calcium binding protein in epithelial cells

49
Q

Where does reabsorption of D/calcium occur?

A

KIDNEY. Small molecules like CA circulate in blood-> reach kidney -> pass the filter can end up in urine if not reabsorbed. Reabsorption removes molecules from filtrate and puts them back in the blood

50
Q

Where does resorption of D/calcium occur?

A

BONE. Dissolving bone structure to release calcium into the bloodstream. Osteroclasts resorb, ostroblasts build. Balance between synthesis and resorption

51
Q

Parathyroid Hormone and Calcium hormonal control systems.

A

PTH secreted by the parathyroid glands. Serves to INC. blood calcium (1st response)

52
Q

What does PTH stimulate in the Ca hormonal control system?

A

Stimulates production of calcitiol in kidney (activates 1-hydroxylase) Stimulates resorption of bone (activates osteoclasts) Maximized tubular reabsorption of calcium in kidney

53
Q

Vitamin D and calcium hormonal control system.

A

5 sources. INCREASE blood calcium.

54
Q

What does vit. D stimulate in the Ca hormonal control system?

A

stimulates resorption of bone (immediate response) Facilitates absorption of calcium from SI (short term resp.) Maximizes tubular reabsorption of calcium in kidney (short term resp. )

55
Q

Calcitonin and calcium hormonal control systems.

A

Secreted by thyroid parafollicular cells. DECREASE blood calcium (i.e. in response to Ca rebound) Suppreses tubular absorption of Ca in kidney. Inhibs bone resorption and facilitates remineralization

56
Q

Summarize Vit. D deficiency

A

Low vitamin D 1. decreased intestinal Ca absorption. 2. Decreased Tubular Calcium Reabsorption. 3. Decreased Bone Resorption

57
Q

Resoption

A

Bone resorption is the process by which osteoclasts break down bone and release the minerals, resulting in a transfer of calcium from bone fluid to the blood

58
Q

Heatlhy bone contains what % of minerals?

A

60%

59
Q

Vitamin D deficiency?

A

Boneproblems vary depending on life stage. Infants rickets (soft). Teens/adults Osteomalacia (demineralized bone) Adults/elders Osteoporosis

60
Q

RDA of vit D

A

400-800 IU

61
Q

UL of vit D

A

1000-4000 IU

62
Q

Recent changes to RDA of vit D?

A

Recent increases seen, Canadians in general are getting enough. No additional benefits to going above RDA.

63
Q

Why is Vitamin K named?

A

1934 Danish found fat soluble factor involved in coagulation

64
Q

Babies and Vitamin K?

A

little body stoage. Limited amount at birth. Injections given.

65
Q

Why is deficiency rare in adults?

A

Colonic synthesis, fat soluble get passive absorption

66
Q

Plant source

A

Phylloquinone saturated side chains vitamin K1

67
Q

Bacteria source

A

Menaquione unsaturated side chain vitamin k2 N=3-9

68
Q

What is an anti-coagulate drug for humans and Posion in rats?

A

WARAFIN

69
Q

Warafin

A

active K: hydroquinone, inactive: epoxide/ Protein-> gamma-carboxylated protein. Invoved in Ca binding- req. for modification for proper function of at least 4 proteins in cloting cascade

70
Q

vitmain K and Gamma carboxylation

A

protein precursor-> postransationally modified protein -> calcium-binding protein

71
Q

Vitamin K toxicity?

A

virtually no symptoms of toxicity

72
Q

Deficiency of Vitamin K

A

related to role in gamma carboxylation, imparied blood clotting (possible hemorrhagic syndrome-> newborns mostly) Impared activation of Ca binding proteins-> osteoporosis?

73
Q

What are the three types of Ca?

A

Intracellular, blood, bone

74
Q

Intracellular

A

stored in mitochondria and ER, released response to extracellular signal. Transduces signal into an intracellular response i.e. gene expression

75
Q

Blood

A

1/2 bound to protein. Constant level 10 000x conc. Of intracellular. Nearly identical to conc. Of P

76
Q

Bone

A

majority 99% in bone and teeth. In bone 99% mineral phase 1% pool that can exchange with extracellular Ca

77
Q

Mineral Phase in Bone

A

Hydroxyapetite with phosphorus

78
Q

RDA Ca

A

200 (infant) - 1300 (children and lactation)

79
Q

UL Ca

A

1000 (infant)- 3000 (lactation)

80
Q

Ca deficiency

A

Bone: inadequate mineralization, rickets, osteoporosis sometimes osteomalacia, Muscle, hypertension, colon cancer

81
Q

Ca toxicity

A

constipation, hypercalcemia, kidney stones

82
Q

Phosphorus Functions

A

Mostly in bone, metabolism components like ATP, DNA, RNA, Ip3, cAMP, cGMP. Plays role in protein phosphorlation, posttranslational control mechanism for protein f(x)

83
Q

Phosphorus deficiency

A

rare, present in diet

84
Q

Phosphorus Toxicity

A

Very Rare

85
Q

Phosphorus Requirments

A

asumed intake adequate if other nutrients are, RDAs set

86
Q

Florine vs Fluoride

A

fluorine is a gaseous chemical element while fluoride is the anion F-

87
Q

Fluoride Functions

A

Formation of fluoroapatite (in tooth enamel) increased the resistance of the enamel to bacteria-induced damage, if oral health maintained may not be an essential nutrient

88
Q

Fluoride Deficiency

A

causes increased incidence of tooth decay, supplemented in water system, 1ppm in drinking water safe

89
Q

Fluoride Toxicity

A

mainly cosmetic, dusty white patches on teeth, dark mottling. Narrow range between max. protection from cavities to start of fluorosis

90
Q

Flouride Requirments

A

AI increased from 0.01 mg/D in infacnts to 4 mg?d in adults. Almost no range between optimal function and toxicity, neither is life-threatening

91
Q

Micronutrient Basics: Vitamins and Minerals

A

6 characteristive for classification as a Vitamin

92
Q

Vitamin characteristics

A

1) exogenouse supply req. 2) needed in small amounts 3) organic 4) distinct from sugars, fats, and AA in structure and function 5) performs at least one unique essentail biochemical function 6) characteristic deficiency dieased results when compound is lacking or poorly absorbed/utlized

93
Q

Difference between T3 and T4

A

T4 circulatinf form. T3 bioactive form. Free THR (lack T3) depressing effects on gene expression

94
Q

Toxicity of Vitamin D?

A

Sun exposure will not cause risk, limiting factor in skin. Diet excess circulatin 25-OH , absorbed and incorporated into chylomicrons ->liver, hydroxylated at 25. May cause hypercalemia or calcification of soft tissues