Vitamins Flashcards

1
Q

Biotin AI

A

30 mcg

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2
Q

Vitamin K AI

A

120 mcg / 90 mcg

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3
Q

Vitamin B6 RDA

A

1.3-1.7 mg

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4
Q

Folate RDA

A

400 mcg

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5
Q

Vitamin C RDA

A

90 mg / 75 mg

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6
Q

Pantothenic Acid AI

A

5 mg

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7
Q

Riboflavin RDA

A

1.3 mg / 1.1 mg

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8
Q

Vitamin A RDA

A

900 mcg RAE / 700 mcg RAE

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9
Q

Vitamin D RDA

A

15 mcg

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10
Q

Vitamin B12 RDA

A

2.4 mcg

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11
Q

Thiamin RDA

A

1.2 mg / 1.1 mg

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12
Q

Niacin RDA

A

16 mg / 14 mg

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13
Q

Vitamin E RDA

A

15 mg

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14
Q

Differences between macro and micronutrients

A
  1. Energy vs. no energy
  2. Quantity amount (grams vs micro or milligrams)
  3. All vitamins are essential (only essential macronutrients are glucose, linoleic/linolenic acid, and 9 AAs)
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15
Q

Fat-soluble vitamin absorption/transport/storage/excretion

A

Absorbed in the small intestine into the lymphatic system, which requires bile, digestive enzymes and micelles. Transported via chylomicrons to the liver. Excess stored mainly in the liver and fat tissue (except K). Small amounts excreted in bile.

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16
Q

Water-soluble vitamin absorption/transport/storage/excretion

A

Absorbed in the small intestine directly into the blood stream via the portal vein. Transported in the blood, often bound to proteins such as albumin. Very minimal storage. Excreted in the urine (except B12 and B6)

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17
Q

Vitamin A functions

A
  1. Vision: retinal turns visual light into nerve signals, retinoid acid helps maintain normal differentiation of cells in eye (cornea, rod cells)
  2. Growth & development: retinoid acid required for cell formation
  3. Reproduction: requires retinol or retinal
  4. Immunity: retinoids help maintain epithelial layers, differentiation of some cells produced by immune system
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18
Q

Vitamin A deficiency

A
  1. Xerophthalmia (irreversible blindness)
  2. Follicular hyperkeratosis
  3. Impaired immunity
  4. Poor growth
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19
Q

Vitamin A toxicity

A

Hypervitaminosis A (acute, chronic, teratogenic); hypercarotenemia

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20
Q

Rhodopsin

A

A molecule in rod cells: opsin (protein) + cis-retinal

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21
Q

Visual cycle

A

When rhodopsin is exposed to bright light, cis-retinal becomes trans-retinal. Opsin is released from retinal, which sends nerve impulse that carries visual information to the brain. Retinal is reused (some lost), and rhodopsin is reformed.

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22
Q

Xerophthalmia

A

Irreversible blindness caused by vitamin A deficiency. Disease progression:

  1. Night blindness
  2. Decreased mucus production
  3. Development of Bitot’s spots, conjunctival xerosis
  4. Cornea softens
  5. Scarring
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23
Q

Follicular hyperkeratosis

A

Vitamin A deficiency. Normal epithelial cells in the underlying skin layers are replaced with keratinized cells. Hair follicles become plugged with keratin, which causes bumpy, rough, and dry skin.

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24
Q

Acute vitamin A toxicity

A

Caused by ingestion of 100x RDA within a short period. Symptoms include GI upset, headache, blurred vision, muscular uncoordination

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25
Q

Chronic vitamin A toxicity

A

Caused by a large intake of vitamin A over a long time. Symptoms include bone/muscle pain, hip fractures, skin disorders, headache, dry skin, hair loss, increased liver size, double vision

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26
Q

Teratogenic vitamin A toxicity

A

Causes spontaneous abortion or birth defects

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27
Q

Vitamin D nomenclature

A

D3: cholecalciferol, found in animal products
D2: ergocalciferol, found in plants, fortified foods

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28
Q

How active vitamin D is formed in the body

A
  1. Sunlight converts 7-dehydrocholesterol to previtamin D3, and forms D3 with body heat
  2. Liver hydroxylates D3 to 25-OH-D3
  3. Kidney hydroxylates more to 1,25-(OH)2 D3, which is the active form / hormonal form (aka Calcitriol)
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29
Q

Vitamin D functions

A
  1. Regulates blood Ca and P levels. Calcitriol increases intestinal absorption of Ca from foods. With PTH, releases calcium from bone into blood, which increases blood Ca levels. Prevents Ca from being excreted in urine.
  2. Bone growth and development
  3. Cell differentiation
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30
Q

Vitamin D deficiency

A

Rickets (kids), osteomalacia (adults)

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31
Q

Rickets

A

Caused by vitamin D deficiency in kids. Symptoms include bowed legs, outward bowed chest, knobs on ribs, rapid enlargement of head, muscle spasms

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32
Q

Osteomalacia

A

Caused by vitamin D deficiency in adults. Symptoms include loss of Ca, soft, flexible, brittle, deformed bones. Bending of spine, bowed legs.

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33
Q

Vitamin D toxicity

A

Hypercalcemia: over absorption of Ca, which causes irreversible calcification of heart, lungs, and kidneys. Narrows pulmonary arteries, facial changes, mental retardation. Infants most susceptible.

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34
Q

Vitamin K nomenclature

A

K1: phylloquinones (plants)
K2: menaquinones (animal tissue, intestinal bacteria)

35
Q

Vitamin K functions

A

Synthesis of blood clotting factors and bone proteins

36
Q

Vitamin K deficiency

A

Hemorrhage, bone/hip fractures

37
Q

Vitamin K toxicity

A

Not common. High doses can reduce effectiveness of anticoagulant drugs.

38
Q

Vitamin E nomenclature

A

4 tocopherols and 4 tocotrienols. Most active form is alpha-tocopherol

39
Q

Vitamin E functions

A

Antioxidant. Protects PUFAs within cell membrane. Prevents cell lysis/cell death. Prevents the alteration of cell’s DNA and risk for cancer development. Limits LDL oxidation, a contributor to atherosclerosis.

40
Q

Vitamin E deficiency

A

Hemolytic anemia, peripheral neuropathy

41
Q

Hemolytic anemia

A

Hemolysis, ruptured RBCs

42
Q

Vitamin E toxicity

A

Hemorrhagic effect in adults. Inhibits vitamin K metabolism and anticoagulants

43
Q

Antioxidants

A

Compounds that stop the propagation of free radical chain reactions. Free radicals steal electrons from stable compounds, making them unstable. Antioxidants prevent the breakdown of substances in food or the body, particularly lipids, by donating electrons to oxidizing agents. Antioxidants in the body include vitamins C, E, and beta-carotene.

44
Q

Major food sources for fat-soluble vitamins

A
Preformed vitamin A: fish liver oil
Beta-carotene: squash
Vitamin D: salmon (or sunlight)
Vitamin E: almonds
Vitamin K: kale (also intestinal bacteria)
45
Q

Major food sources for water-soluble vitamins

A
Thiamin: pork
Riboflavin: milk
Niacin: poultry
B6: bananas
Folate: orange juice
B12: liver
Pantothenic acid: whole grains
Biotin: egg yolks
Vitamin C: orange
46
Q

Thiamin coenzyme

A

thiamin pyrophosphate (TPP)

47
Q

Riboflavin coenzymes

A
Flavin adrenine dinucleotide (FAD)
Flavin mononucleotidue (FMN)
48
Q

Niacin coenzymes

A

NAD, NADH, NADP, NADPH

49
Q

Vitamin B6 coenzyme

A

Pyridoxal phosphate (PLP)

50
Q

Folate coenzyme

A

tetrahydrofolate (THF)

51
Q

Vitamin B12 coenzymes

A

Methylcobalamin

5-deoxyadenosylcobalamin

52
Q

Pantothenic acid coenzyme

A

part of CoA

53
Q

Thiamin functions

A

Coenzyme in energy metabolism (decarboxylation reaction to convert pyruvate to acetyl-CoA)
Pentose synthesis
Nerve conduction

54
Q

Thiamin deficiency

A

Beriberi, Wernicke-Korsakoff Syndrome

55
Q

Beriberi

A

Caused by deficiency of thiamin. Symptoms include anorexia, weight loss, weakness, peripheral neuropathy, poor memory, confusion.

56
Q

Wernicke-Korsakoff Syndrome

A

Caused by deficiency of thiamin among alcoholics. Alcohol decreases thiamin absorption, alcohol increases thiamin excretion in urine, and alcoholics may consume a poor-quality diet. Symptoms include changes in vision, ataxia (inability to coordinate muscles), and impaired mental functions

57
Q

Thiamin toxicity

A

None

58
Q

Riboflavin functions

A

Coenzyme in numerous oxidation-reduction reactions, including energy metabolism

59
Q

Riboflavin deficiency

A

Ariboflavinosis

  1. Glossitis: inflammation of tongue
  2. Cheilosis: cracks at corner of mouth
60
Q

Riboflavin toxicity

A

None

61
Q

Niacin functions

A

Coenzyme in numerous oxidation-reduction reactions, including energy metabolism. Synthesis and breakdown of fatty acids

62
Q

Niacin deficiency

A

Pellagra (symptoms include diarrhea, dermatitis, dementia, and if untreated, death). Associated with a corn-based diet, used to be a major public health problem in the US.

63
Q

Niacin toxicity

A

No toxicity from food. From nicotinic acid supplementation, can get:

  1. Niacin flush: flushing of the skin
  2. GI upset
  3. Liver damage
64
Q

Vitamin B6 functions

A
Coenzyme in amino acid metabolism
Neurotransmitter synthesis
Heme synthesis
Homocysteine metabolism
Lipid metabolism
65
Q

Vitamin B6 deficiencies

A
Microcytic hypochromic anemia
Confusion
Convulsions
Dermatitis
Depression
66
Q

Microcytic hypochromic anemia

A

Caused by B6 deficiency. Small, pale red blood cells that lack sufficient hemoglobin and thus have reduced oxygen-carrying abilities. Also caused by iron deficiency.

67
Q

Vitamin B6 toxicity

A

None from food. Excess from supplements can cause neuropathy and skin lesions

68
Q

Vitamin B12 functions

A

Coenzyme in DNA synthesis, cell division, folate metabolism, nerve function, homocysteine metabolism

69
Q

Vitamin B12 deficiencies

A
Pernicious anemia (looks like megaloblastic anemia)
Nerve degeneration
Elevated homocysteine (therefore risk of heart disease)
70
Q

Pernicious anemia

A

Caused by B12 deficiency. Associated with nerve degeneration, which can result in eventual paralysis and death

71
Q

Vitamin B12 toxicity

A

None

72
Q

Folate functions

A

Coenzyme in DNA synthesis, amino acid metabolism, homocysteine metabolism

73
Q

Folate deficiencies

A
Megaloblastic anemia
Neural tube defects
Elevated homocysteine (therefore risk of heart disease)
74
Q

Megaloblastic anemia

A

Aka macrocytic anemia. Caused by folate deficiency. Characterized by large, immature RBCs that result from the inability of precursor cells to divide normally.

75
Q

Folate toxicity

A

None

76
Q

Digestion and absorption of vitamin B12

A

In animal-based foods, vitamin B12 is bound to protein. In the stomach, HCl denatures the protein and B12 is released. B12 then binds to R-protein (which is produced in the saliva). In the small intestine, proteases cleave B12 from the R-protein. B12 binds to intrinsic factor (which is produced in the stomach). The B12-IF complex is absorbed by intestinal cells into the bloodstream.

77
Q

Vitamin C functions

A
Antioxidant
Synthesis of collagen, hormones and neurotransmitters
Enhances immune function
Detoxification of drugs/carcinogens
Reactivates vitamin E
78
Q

Vitamin C deficiency

A

Scurvy

79
Q

Scurvy

A

Develops when deficient in vitamin C for 20-40 days. Symptoms include fatigue, pinpoint hemorrhages (aka petichiae), bleeding gums, poor wound healing, joint pain, fractures

80
Q

Vitamin C toxicity

A

GI distress (nausea, abdominal cramps, diarrhea), increased risk of iron overload

81
Q

Vitamins involved in bone health

A

Vitamin A: retinoid acid required for cell formation, thus helps with growth and development
Vitamin D: maintains body’s concentrations of calcium
Vitamin K: synthesizes bone proteins
Vitamin C: synthesizes collagen, which is a fibrous protein found in bone, among other connective tissue

82
Q

Processed grains are enriched with…

A
Thiamin
Riboflavin
Niacin
Folate
Iron
83
Q

Essential nutrient requirements

A
  1. Has a specific biological function
  2. Removing it from the diet leads to a decline in biological function
  3. Adding it back returns function to normal