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Malnourishment and Obesity > Vitamins > Flashcards

Vitamins Flashcards

1
Q

What are vitamins?

A

organic compounds required in small amounts for normal functioning of the body

  • cannot be synthesised in the body
  • must be provided by diet
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2
Q

What are the general outcomes of vitamin toxicity?

A
  • abnormal accumulation in tissues
  • overloading of normal metabolic pathways
  • possibly irreversible lesions
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3
Q

What are some vitamins that are toxic in access?

A
  • vitamin A, D, B6
  • niacin

(possibly Vitamin C, beta-carotene, vitamin E)

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4
Q

What is produced from the reduction of oxygen to water in mitochondria?

A
  • produces ATP

- produces free radicals

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5
Q

What happens to 1-2% of the O2 used by respiratory chain?

A

ends up as superoxide

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6
Q

What are free radicals?

A
  • unstable oxygen species
  • capable of oxidising PUFA/damaging organs/tissues and DNA (@ cell mem = lipid peroxidation)
  • contains one or more unpaired electrons
  • capable of independent existence
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7
Q

What damage do free radicals do?

A
  • nucleic acids
  • nucleotides
  • thiols
  • covalent bonding
  • lipids
  • membrane structure
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8
Q

What diseases can develop from free radicals?

A
  • heart disease
  • cancers
  • parkinsons
  • arthritis
  • cataracts
  • muscular dystrophy
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9
Q

Where can we get some nutrients that act as protective antioxidants in conjunction with body enzymes?

A
  • fruits, nuts
  • leafy greens
  • juices
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10
Q

What are some metal cofactors that contribute to the integrated antioxidant defence system?

A
  • Selenium (GSHPx, X 4)
  • Iron (catalase)
  • Copper (SOD, ceruloplasmin)
  • Zinc (SOD)
  • Manganese (SOD)
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11
Q

What are some antioxidant compounds integrated into antioxidant defence system?

A
  • vitamin E (carotenoids)

- vitamin C (polyphenols)

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12
Q

What are fat soluble vitamins?

A
  • found in fats and oils of food
  • absorbed into lymph and carried in blood with protein transporters (chylomicrons)
  • require bile and fats for absorption
  • stored in liver/body fat
  • can be toxic if large amounts consumed
  • normally not excreted in urine
  • don’t act as coenzymes
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13
Q

What are soluble vitamins?

A
  • found in vegetables, fruits, grains, meat
  • absorbed into bloodstream
  • not stored in body (except B12)
  • toxicity is rare, when large amounts consumed
  • have threshold for urinary excretion
  • act as co-enzymes
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14
Q

Name 4 lipid (fat) soluble vitamins:

A
  • vitamin A
  • vitamin D2
  • vitamin E
  • vitamin K1
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15
Q

What is vitamin A also known as?

A

retinol

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16
Q

What are the requirements, biological activity, and sources of vitamin A?

A
  • 0.8mg
  • eyesight, immune system
  • liver, cheese, eggs and oily fish
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17
Q

What are the requirements, biological activity, and sources of vitamin D?

A
  • 0.01mg
  • bones and teeth
  • oily fish and eggs
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18
Q

What are the requirements, biological activity, and sources of vitamin E?

A
  • 10mg
  • antioxidant activity
  • cereals, vegetable oils, leafy vegetables
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19
Q

What are the requirements, biological activity, and sources of vitamin K?

A
  • (not stated requirement)
  • blood clotting
  • leafy vegetables, dairy products, grains
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20
Q

what is ß-carotene?

A
  • human body converts beta carotene into vitamin A (retinol)

- beta carotene is a precursor of vitamin A.

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21
Q

How much retinol is absorbed by the body (%)?

A

70-90%

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22
Q

How much ß-carotene is absorbed by the body (%)?

A

20-50%

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23
Q

How much ß-carotene is needed for the formation of 1 µg of retinol?

A

6µg

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24
Q

Where is ß-carotene stored?

A

liver

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25
Q

What can retinyl esters form and what is the use of its product?

A
  • 11-cis-retinal

- chromophore for rhodopsin

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26
Q

What can retinoic acid form and what is the use of its product?

A
  • all-trans and 9-cis-retinoic acid

- transcriptionally active vit. A species

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27
Q

How is free retinol esterified to form retinyl esters?

A
  • via ARAT
    or
  • bind to CRBP and esterified by LRAT
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28
Q

Where are retinyl esters stored until needed?

A

in liver stellate cells

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29
Q

Roughly explain the Hepatic vitamin A metabolism:

A
  1. Retinyl esters taken up into liver cells
  2. Free retinol is esterified to retinyl esters
  3. CRBP-retinol has a few pathways
    - converted to retinoic acid
    - released into blood
    - form retinyl ß-glucoronide for excretion in bile
  4. Retinoic acid has few pathways
    - gene expression
    - conjugated to glucaronic acid and excreted in bile
    - 4-oxoretinoic acid
  5. 4-oxoretinoic acid either function like retinoic acid or excretion in bile as glucaronic acid
  6. holo-RBP from retinol, released to blood to form trimolecular complex
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30
Q

Main functions of vitamin A:

A
  1. Vision
    - night vision
    - forms visual molecule rhodopsin
  2. Antioxidant
    - ß-carotene/other carotenoids, reacting with singlet oxygen species
  3. Gene expression (differentiation + growth)
  4. Immune system function
  5. Reproductive process
  6. Bone metabolism
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31
Q

What are two specific vitamin roles in the eye?

A
  1. Process of light perception at retina

2. Maintenance of healthy cornea

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32
Q

What enables the signal that light hits the eyes, to be received by the brain?

A

rhodopsin in rod cells that are transformed and sends signals

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33
Q

How does vitamin A help the immune systems’ function?

A
  • synthesis of glycoproteins

- promotes development of immune cells (NK cells)

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34
Q

How does vitamin A help the reproductive process?

A
  • gene transcription in testis
  • placental development
  • testosterone/oestrogen production
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35
Q

What % of vit. A is egested in faeces?

A

70%

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36
Q

What % of vit. A is excreted in urine?

A

30%

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37
Q

Where else apart from faeces and urine, is vit. A excreted?

A
  • CO2 from lungs and - caretenoid metabolites in bile
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38
Q

What is the require amounts of vitamin A for men and women?

A

men = 1000 µg/day women = 800 µg/day

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39
Q

What is the minimum vitamin A intake per day?

A

600µg

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40
Q

What are the results of high intake/chronic intake of vitamin A?

A
  • in early pregnancy = birth defects
  • anorexia, skin/hair abnormalities, bone/muscle pain
  • ß-carotene cause yellow discolouration of skin (fat pads)
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41
Q

What are the results of vitamin deficiency?

A
  • skin/mucous membrane dryness + infection + keratin deposits
  • anaemia
  • impaired immune response
  • developmental defects (bones, teeth, immune system, vision)
  • eye problems
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42
Q

Name 4 specific ways vitamin A deficiency causes eye problems:

A
  1. Squamous metaplasia + keratinisation of conjunctiva
  2. Dryness wrinkling + thickening of cornea (xerophthalmia)
  3. Ulceration of cornea (blindness)
  4. Impaired colour vision
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43
Q

What are the toxic effects of vit. C?

A
  • fragile RBC, haemmorage
  • bone pain, fractures
  • abdominal pain, diarrhea
  • blurred vision
  • dry skin, hair loss
  • liver englargement
  • death
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44
Q

What are the (animal) sources of retinol?

A
  • egg yolk
  • butter
  • whole milk
  • liver/fish liver oils
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45
Q

What are the (plant) sources of ß-carotene?

A
  • dark green leafy vegetables

- yellow/orange vegetables = carrots

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46
Q

What is vitamin D?

A
  • steroid pro hormone

- made under the skin in UV light presence

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47
Q

What is the mean vitamin D intake required?

A

serum 25(OH)D concentration ≥ 25 nmol/L

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48
Q

General outcome of vit. D deficiency?

A
  • rickets (children)

- osteomalacia (adults)

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49
Q

Which vitamin is the most potentially toxic?

A

vitamin D

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50
Q

Explain how we synthesise vitamin D:

A
  1. UV light shines on cholesterol compound in human skin
  2. Transformed into vit. D precursor + absorbed to blood
  3. Next day, liver and kidneys finish converting precursor to vit. D
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51
Q

25(OH)D (vitamin D) compound is needed in 4 areas, what are they?

A
  1. Intestine - increase absorption of Ca2+ and P
  2. Bone - increase boe mineralisation
  3. Immune cells - induces differentiation
  4. Tumour microenvironment
    - inhibits proliferation
    - induces differentiation
    - inhibits angiogenesis
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52
Q

What is the final form of vitamin D when synthesised?

A

calcitroic acid

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53
Q

Which form of vit. D doesn’t require digestion?

A

D2 and D3

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54
Q

Vit. D is absorbed via a _____ with the aid of ____ by _____ into the intestinal cell.

A
  • micelle
  • bile salts
  • passive diffusion
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55
Q

What is vit. D incorporated into for transport into lymphatic system and blood?

A

chylomicrons

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56
Q

What is the % of dietary vit. D absorbed?

A

50%

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57
Q

How is excessive production of vit. D in skin prevented?

A

through inactive metabolite generation (lumisterol)

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58
Q

In liver, what hydroxylates vitamin D to active form?

A

cytochrome p450 hydroxylases

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59
Q

What is the half life of active vitamin D?

A

15 days to 3 weeks

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60
Q

What are the genomic and non-genomic functions of vitamin D?

A
  1. Serum calcium homeostasis (kidney, bone)
  2. Phosphorus homeostasis
  3. Cell differentiation, proliferation, growth
  4. Calcitriol and muscle
  5. Blood pressure regulation
  6. Immune function
  7. Pancreatic beta-cell production, insulin secretion
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61
Q

What does vitamin E refer to?

A

group of 8 tocopherols

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62
Q

Which tocopherol is the biologically active form?

A

A-tocopherol

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63
Q

What are the functions of Vit. E?

A
  1. Antioxidant
  2. Prevent damage to lungs, RBCs, WBCs (immunity), heart
  3. Necessary for normal nerve development
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64
Q

What is the result of vitamin E deficiency?

A
  • Decreased absorption of fats
  • liver disease
  • low fat diets
  • premature babies - fragile RBCs (haemolysis)
  • Loss muscle coordination, vision, immune function
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65
Q

What is the exceeding upper intake of vit. E?

A

1000 mg/day

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66
Q

Which vitamin is the least toxic from the fat-soluble vitamin list?

A

Vitamin E

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67
Q

What might extreme doses of vitamin E cause?

A
  • affect blood clotting effects of vit K
  • increased haemmorage
  • increase effects of anticoagulants (coumadin, warfarin)
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68
Q

What can destroy vit. E?

A

high temperatures

69
Q

What is the daily recommended intake for Vit. E?

A

15mg

70
Q

What are some sources of vit. E?

A
  • safflower oil
  • mayonnaise
  • canola oil
  • wheat germ
  • sunflower seeds
71
Q

What and which part produces vitamin K?

A

produced by bacteria, in the large intestines

72
Q

What are the functions of vitamin K?

A
  1. Coagulation
  2. Promotes synthesis of blood clotting proteins (interfere with anti-coagulants
  3. Bone formation
73
Q

What was vitamin K named after?

A

Danish word, “koagulation”

74
Q

What are the recommended daily intakes of vit. K for men and women?

A 
men = 120µg
women = 90µg
75
Q

What are good sources of vit. K?

A
  • cauliflower
  • cabbage
  • canola oil
  • spinach (steamed)
  • salad greens
  • soybeans (dry roasted)
76
Q

Are there any vitamin K deficiencies?

A

rare, unlikely in healthy adult

77
Q

Which populations are at risk of vitamin K deficiency?

A
  • infants (after prolonged antibiotic therapy)
  • patients with decreased bile production
  • patients with chronic malabsorptive disorders
78
Q

Why are infants given vit. K injection?

A
  • milk is low in vit K
  • low vit K stores at blood
  • GI not populated with vit K producing bacteria
79
Q

What is the result of vit. K toxicity?

A
  • ingestion of large amounts doesn’t cause toxicity but maybe above >1000mg/d
  • haemolytic anaemia (rupture of RBCs)
  • liver damage (jaundice)
80
Q

What are the water-soluble vitamins?

A

non-B complex (vit. C) and B-complex

81
Q

Who cannot synthesise vit. C?

A
  • humans

- guinea pigs, primates, birds

82
Q

Why can’t humans synthesise vit. C?

A

have congenital absense of gulonolactone oxidase

83
Q

What was used in the experiment to cure scurvy, 250 years ago?

A

lemons

84
Q

Vitamin C is also known as?

A

ascorbic acid

85
Q

What are the main food sources of vitamin C?

A

fruits and vegetables

86
Q

What are the main deficiency symptoms of vit. C?

A
  • scurvy

- capillary fragility

87
Q

Does vitamin require digestion prior to absorption?

A

No

88
Q

What assists absorption of ascorbic acid?

A
  • sodium dependent vit. C transporters (SVCT 1 and 2)
89
Q

What is SVCT1?

A
  • main carrier responsible for vit C absorption
  • enables intestinal absorption of vitamin in excess of cell needs
  • downregulated by ascorbic acid
90
Q

What is SVCT2?

A

present in most metabolically active tissues except muscle/lungs

91
Q

What is involved in transport of dehydroascorbic uptake into cells?

A

GLUT transporters

92
Q

What generally happens in interconversion of ascorbic acid and dehydroascorbic acid?

A
  1. Ascorbyl radical formed but has short half-life - doesn’t form ROS
  2. Oxidation of this radical forms vit. C
  3. Dehydroascorbic acid reduced to ascorbin acid with H provided from reduced glutathione (GSH)
93
Q

What is the range of recommended vit. C intake per day?

A

30-180mg

94
Q

What is the % of absorption?

A

70-90%

95
Q

What is the relationship of absorption and intake?

A

Absorption decreases with increased intake

96
Q

At what levels of vit. C is is there 98% absorption?

A

> 20mg

97
Q

What is the normal plasma ascorbic acid concentration range?

A

0.4-1.7mg/dL

98
Q

Where in the body are is the highest level of vit C plasma concentration and how much?

A

adrenal and pituitary glands

30-50mg/100g

99
Q

But where in the body contains the most vitamin C?

A

liver

100
Q

What is the maximum vitamin C pool taken per day?

A

2g

101
Q

What can result from taking more than 2g vit. C a day?

A
  • alteration of insulin response to carbohydrate
  • interference with blood clotting medications
  • kidney stones
  • gout
  • digestive upsets
102
Q

How is vit C excreted?

A

in urine after chemical reactions as various metabolites, 25% in form of oxalic acid

103
Q

What can high doses of vit. C result in?

A
  • formation of kidney stones, from overproduction of oxalate

- DNA damage (500mg/d)

104
Q

In terms of its function as antioxidant, what roles do vit. C play?

A
  1. React with many reactive free radicals
  2. Powerful, non-specific reducing agent, H donator
  3. Protects water soluble compartments
  4. Neutralises free radicals
  5. Regenerates Vit. E (H donor)
105
Q

How can the vit E radical be converted back to vit E?

A

reaction with vit C

106
Q

Explain the amidation of peptides with c-terminal glycine (involves vit. C):

A
  1. Vit. C = reducing agent, converts copper to reduced form
  2. enzyme cleaves carboxyl-terminal residue, residue released as glyoxylate
  3. Amidated peptides are active hormones/hormone-releasing factors/neurotransmitters
107
Q

What are other functions of vit. C?

A
  1. Collagen/carnitine synthesis
  2. Facilitates Fe (non haem) absorption
  3. Co-factor in mono-oxidase reactions - neurotransmitter synthesis
  4. Activation of peptide hormones
  5. Tyrosine synthesis (liver and kidney - from phenylalanine)
  6. Cholesterol catabolism
  7. Bile acid formation
108
Q

What is the function of ascorbate?

A

hydroxylation of peptide-bound proline and lysine in the synthesis of collagen

109
Q

What are the 3 interwoven chains of collagen?

A

glycine, proline and hydroxyproline

110
Q

What is the use of carnitine?

A

transfer long chain FAs to inner mitochondria mem. for energy production

111
Q

Tyrosine is synthesised from?

A

amino acid phenylalanine

112
Q

What are the symptoms of vit. C deficiency?

A
  • bleeding gums
  • small skin discolouration (ruptured blood vessels)
  • sub-lingual haemmorages
  • easy bruising
  • impaired wound and fracture healing
  • joint pain
  • loose/decaying teeth
113
Q

How many b-complex vitamins do we know of?

A

8

114
Q

What are the b-complex vitamins?

A

water-soluble, chemically distinct vitamins that coexist in same foods

115
Q

What is the function of the b-vitamins?

A
  • coenzymes

- important for cells to generate energy, make protein/new cells, metabolise carbs/fats/proteins

116
Q

What is a coenzyme?

A

molecule that combines with enzyme to make it active

117
Q

What is vitamin B1 known as?

A

Thiamine

118
Q

What does the deficiency of thiamine cause?

A
  • beri-beri
  • possible edema
  • muscle wasting, weakness
  • pain, apathy
    etc (so much)
119
Q

What is beri-beri?

A

disease that was widespread in Asia, leg paralysis (polyneuritis)

  • primary symptom = anorexia
  • progresses to cardiovascular/neurological problems
120
Q

What is the recommended intake for vit. B1 (thiamine)?

A

0.5mg/1000kcal

121
Q

What is the dose at which vit. B1 is toxic?

A

300mg

122
Q

What are the sources of vit. B1?

A
  • meats (pork, beef)
  • salmon
  • legumes, grain products
  • cereals, breads
  • yeast, wheat germ, soy milk
123
Q

What are the 3 functions of thiamine (vit. B1)?

A
  1. Energy transformation
  2. Synthesis of pentoses and NADPH
  3. Membrane/nerve conduction
124
Q

How many metabolites does degradation break thiamine to?

A

20 or more

125
Q

What does wet beri-beri cause (reversible)?

A
  • cardiomegaly
  • edema
  • waxy skin
126
Q

What does dry beri-beri cause (reversible)?

A
  • peripheral neuropathy

- weakness

127
Q

What is the results of irreversible beri-beri?

A
  • cerebral beri-beri like:
  • Wernicke-Kosakoff syndrome
  • brain tissue damage
128
Q

How does alcoholism affect thiamine?

A
  • thiamine deficiency related to alcohol consumption
  • alcohol inhibits absorption of thiamine in mucosal cells + conversion to TPP
  • symptoms: mental confusion, loss recent memory, ataxia
129
Q

What is vitamin B2 known as?

A

Riboflavin

130
Q

Explain vit. B2 absorption:

A
  • digested from protein prior to absorp.
  • via saturable, energy-dependent Na+-independent carrier (9RTF2)
  • in large amounts, absorbed via diffusion
  • bile facilitates absorp.
  • alcohol impairs digestion + absorp.
  • 95% absorp.
131
Q

What is the maximum in g of vit. B2 absorbed per day?

A

25g

132
Q

What are the functions of vit. B2?

A
  • energy metabolism

- flavoproteins (fatty acid beta-oxidation)

133
Q

Is B2 affected by B1?

A

Yes, it is low when B1 is low.

134
Q

What are the daily recommendations of vit. B2 for men and women?

A 
men = 1.2mg/d
women = 1.1mg.d
135
Q

What are the results of vit. B2 deficiency?

A
  • cracks/redness at mouth corners
  • sore throat
  • inflamed eyes/eyelids
  • sensitivity to light/skin rashes
136
Q

What is Vitamin B3 known as?

A

Niacin

137
Q

How was niacin discovered?

A

through its deficiency - pellagra

138
Q

Niacin is a generic term for?

A

nicotinin acid and nicotinamide

139
Q

Niacin absorption is dependent on…?

A

Na+-dependent, carrier mediated diffusion

140
Q

At what g is there complete absorption of B3 (niacin)?

A

3-4g

141
Q

What are the functions of niacin?

A
  1. Coenzyme
    - b-oxidation of fatty acids
    - fatty acid/cholesterol/hormone synthesis
  2. Non-redox roles (donor of ADP)
  3. Energy metabolism
  4. Cell respiration
  5. DNA repair/synthesis
  6. Act as secondary messenger
  7. Stimulate increased Ca2+
142
Q

What are the symptoms of pellagra (hint: 4Ds)?

A
  • Dermatitis (sunburn-like skin)
  • Dementia (neurological, headache, memory loss)
  • Diarrhoea (+ vomiting)
  • Death
143
Q

What re the recommended daily intakes of vit. B3 (niacin) for men and women?

A 
men = 16mg
women = 14mg
144
Q

What is the tolerable upper intake level of B3?

A

35mg/day

145
Q

What is pantothenic acid bound as?

A

coenzyme A (CoA)

146
Q

What reactions do CoA participate in?

A
  • nutrient metabolism
  • energy production (TCA cycle)
  • Acyl-carrier protein (ACP)
147
Q

What results from pantothenic acid deficiency?

A

Burning feet syndrome

148
Q

What was biotin usually called?

A

Vitamin H or B7

149
Q

Although rare, when the biotin deficiency occur?

A

in patients treated with anticonvulsnts/antibiotics

150
Q

What synthesises significant quantities of biotin?

A
  • intestinal flora
151
Q

What does avidin do?

A
  • irreversibly binds to biotin

- prevents biotin absorption (not heat resistant)

152
Q

What is the tightest non-covalent bond found in nature?

A

avidin binding with biotin

153
Q

What are the coenzyme forms of folate?

A

DHF and THF

154
Q

What is folate known as?

A

Vitamin B9

155
Q

What are the functions of folate?

A
  1. Amino acid metabolism

2. Purine and pyrimidine synthesis/nucleotide metabolism

156
Q

What is the recommended daily intake of folate (vit. B9) for adults?

A

400μg/d

157
Q

When would there be requirement of additional dietary intakes of folate?

A

during pregnancy and lactation

158
Q

What are the sources of folate?

A
  • leafy green vegetables
  • liver, kidney beans, lima beans
  • leaf beef, potatoes, whole grain bread
  • excludes oranges and root vegetables
159
Q

What destroys half of folate in foods?

A

heat and oxidation during cooking/storage

160
Q

What is the % of dietary folate that is nutritionally available?

A

25-50%

161
Q

What are the results of folate (B9) deficiency?

A
  • anaemia, mental confusion
  • increase of neural tube defects, anencephaly, absence of cerebral hemisphere
  • alterations in DNA metabolism
  • changes in cellular nuclear morphology
  • poor growth, GI tract disturbances
162
Q

How does a women achieve maximum benefit from folate supplementation?

A

enhance her folic acid intake before she becomes pregnant

163
Q

Why is vitamin B12 unique?

A

contains metal ion, cobalt

164
Q

What is required for B12 absorption?

A

intrinsic factor

165
Q

What are the functions of B12?

A
  1. Methyl transfer reactions (with folate)
  2. Homocysteine to methionine
  3. DNA/RNA
  4. L-methylmalonyl-coA to succinyl-coA
  5. Fat and protein metabolism
  6. Haemoglobin metabolism
166
Q

What are sources of B12?

A
  • food from animals
  • liver and kidney
  • milk, egg, fish, cheese, meat
167
Q

When how much B12 is lost % when milk is pasteurised or evaporated?

A

40-90%

168
Q

What is the recommended intake of B12 in adults?

A

2.4μg/d

169
Q

What are the results of vitamin B12 deficiency?

A
  • reflects inadequate absorption and not poor intake
  • lack of HCL (development of atrophic gastritis esp. in elderly)
  • Lack intrinsic factor (defective gene of IF)
  • impaired DNA synthesis
  • defective proliferation of rapidly dividing cells (megalobasltic anaemia, glossitis, hypospermia.. etc)

Malnourishment and Obesity (21 decks)

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