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Nutrition and Metabolism > Vitamins > Flashcards

Vitamins Flashcards

1
Q

What are Vitamins?

A

A complex organic substance required in the diet in small amounts , compared to other dietary components such as protein carbohydrate and fat, and whose absence leads to a deficiency disease.

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2
Q

How are vitamins divided?

A
  1. Water soluble: B group, C
  2. Fat soluble: A D E K
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3
Q

What are the diffrences between water soluble and fat soluble?

A
  1. Water soluble: B group, C
    * not stored extensively - needed regularly in diet
    * needed regularly
    * generally not toxic in excess (within reason)
  2. Fat soluble: A D E K
    stored
    * not absorbed easily
    * not excreted easily
    * may be toxic in excess (A, D)
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4
Q

Sources of Vitamin C?

A

Citrus fruits, tomatoes, berries

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5
Q

function of vitamin c?

A
  1. An anti-oxidant nutrient
  2. Hydroxylation of proline and lysine in collagen formation.
    needed to maintain the Fe(II) necessary for proline and lysine
    hydroxylase activity in the reduced, active state.
  3. Reduction of dietary Fe in the stomach for absorption
  4. Possibly, in vivo, as an anti-oxidant protecting vitamins A, E, K from oxidation
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6
Q

What is the vitamin C defieciency?
When does this present?

A

Scurvy
* The well fed human body has a 6 month store of vitamin C
* Signs of scurvy after three months on vitamin C free diet.
* impaired wound healing, haemorrhages and anaemia (also
from decreased Fe and folate absorption).

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7
Q

Presentation of scurvy?

A
  • impaired wound healing, haemorrhages and anaemia (also
    from decreased Fe and folate absorption).
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8
Q

Vitamin C status in the uk?

A
  • Low status in the elderly, in alcoholics and in adolescents
    especially on ‘junk’ food.
  • Smokers need twice the normal intakes (80 mg/day) as the
    turnover of ascorbic acid is greatly increased by smoking.
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9
Q

Viatmin A Consequences of megadoses?

A

Benefits uncertain and under review
* cholesterol turnover, immune function, male fertility, cancer prevention, Se and Fe utilisation, physical working capacity

  • Supplements may ease symptoms
  • Commen cold: No evidence that megadoses have an effect
  • Heart disease, cancer, eye diseases - no clear pattern
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10
Q

Risks of megadoses of vitamin C?

A
  • Oxalate (major metabolite)) kidney stones in susceptible individuals
  • diarrhoea
  • systemic conditioning- Pregnant women on high doses may have infants with unusually high requirements and individuals on high intakes are at risk of deficiency if the intake is lowered to levels which are adequate for most people.​
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11
Q

Causes of fat soluble vitamin deficiency?

A

Causes of deficiency​

Primary:​

  • dietary deficiency​
  • low fat diet​
  • (usually by choice in developed societies)​
  • fat malabsobtion absorption
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12
Q

Sources of Vitamin A?

A

Sources

  • as retinol
  • Animal liver and fish liver oils, whole milk and egg yolk
  • plant carotenoids (mainly b- carotene)
  • Green/yellow/ orange vegetables and fruit.
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13
Q

Absorption of Vitamin A sources?

A

Absorption
diffrerents between plant and aminal sources

  • Carotenoids (plant sources) are cleaved to 2 retinol molecules
  • conversion is inefficient,
  • ratio carotene : retinol not 1:2 but 6:1
  • Potency is expressed as retinol equivalents

1 RE = 1 ug retinol

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14
Q

Active forms of Vitamin A

A

Active forms
* retinoic acid - acts as a hormone
* retinal - in vision
* (b - carotene - antioxidant)

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15
Q

What are two main functions of vitamin A?

A
  1. control of protein synthesis
  2. in vision
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16
Q

How does Vitamin A control protein synthesis?

A
  • retinoic acid binds specific receptor protein in cytosol, then
  • binds chromatin and affects synthesis of proteins involved in cell growth and differentiation.
  • acts in a similar way to steroid hormones
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17
Q

How is Vitamin A used in vision?

A
  • best understood function
  • at low light intensity (scotopic vision) 11-cis retinal participates in conversion of light energy to impulses in the optic nerve in the rod cells of the retina
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18
Q

Transport and Storage of Vitamin A?

A
  • From the gut to the liver in chylomicrons
  • From the liver to the tissues bound to a specific retinol binding protein, and pre-albumin.
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19
Q

Where is Vitamin A presented?

A
  • rarely seen in developed countries, but common in developing
    countries e.g. India & SE Asia
  • Usually associated with inadequate protein diets.
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20
Q

What does Vitamin A deficiency affect?

A
  • Affects synthesis of retinol binding protein and therefore transport to the tissues.
    Administration of vitamin A alone often does not help.
  • Night blindness(role in vision), followed by: progressive keratinisation of the cornea (xerophthalmia), and finally keratomalacia and irreversible blindness. - progresses without treatment
    The development of xerophthalmia and keratomalacia
    relates to its role in the function of epithelial cells and
    mucopolysaccharide synthesis.
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21
Q

Vitamin A requirements

A
  • In pregnancy no more than 3.3mg/day are recommended
  • RNI is 0.7 mg/day for men and 0.6mg/day for women

UK animal livers: 13 - 40 mg/100g​

  • Pregnant women should not take supplements or eat liver regularly - can lead to birth defects
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22
Q

If too much Vitamin A is taken? What happens?

A

Toxicity
*Dermatitis, hair loss, mucous membrane defects, hepatic dysfunction, thinning and fracture of long bones.
Unlikely with normal sources but possible with supplements e.g. for acne or colds.​

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23
Q

Sources of vitamin E?

A

Source
* Associated with beauty and fertility
* Vegetable oils especially wheat germ oil, nuts, green
vegetables.

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24
Q

Bad sources of Vitamin E

A
  • Canned and frozen foods severely depleted
  • includes family of tocopherols
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25
Q

What is Vitamin E?
What is a safe level for Vitamin E?

A

includes family of tocopherols
most potent: a-tocopherol –
naturally occurring ANTIOXIDANT
Safe level - up to 1 g/day

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26
Q

Function of vitamin E?

A
  1. Prevents oxidation of unsaturated/poly-unsaturated fatty acids (PUFA) in cell membranes and circulating lipoproteins
    * PUFA are particularly susceptible to attack by free radicals (generated in body)
  2. Destruction disrupts membrane structure and cell integrity.
  3. Some polyunsaturated fatty acids are precursors of prostaglandins and so prostaglandins metabolism is also disturbed.
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27
Q

How does Free radical scavenging occur with vitamin E?

A
  • Polyunsaturated fatty acids are susceptible to attack by free
    radicals
    other radicals are generated in this process.
  • Reaction of a fatty acid radical with oxygen gives a peroxyl radical.
  • This continues chain reaction by attacking other PUFAs
  • it can react with an anti-oxidant – e.g vitamin E - thus
    terminating the chain reaction
    itamin E can be regenrated
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28
Q

Why is Vitamin E a radical?

A

vitamin E becomes a radical itself,
* stable
* can be reduced to original form by other antioxidant nutrients,
possibly ascorbic acid.

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29
Q

What does Vitamin E deficiency cause?

A

Deficiency
* Known in animals as a cause of sterility and muscular dystrophy.

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30
Q

Who does Vitamin E deficincey occur in and why?

A
  • Virtually unknown except in premature, low birth
    weight infants. vitamin E does not cross the placenta
    easily;
  • human milk is not a good source of vitamin E.
  • Haemolytic anaemia due to fragility of red cell
    membranes is characteristic.
  • Vitamin E is now included in infant formulae
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31
Q

Proposed benefits in vitamin E?

A
  • Requirements difficult to establish, likely to be higher with high PUFA intake.
  • A protective effect against cardiovascular disease and cancer?
  • Vitamin E is thought to protect fatty acids and apoprotein B in LDL from oxidative damage.
  • evidence that damaged LDL in arterial wall is part of mechanism that leads to atherosclerotic damage.
  • Studies inconclusive
  • Cancer? May reduce risk in men but not in women.
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32
Q

What is Vitamin D?

A
  • a group of similar compounds.
    *Cholecalciferol (vitamin D3)
  • occurs naturally in animals.
    *functions by binding to intra-cellular receptors that eventually interact with DNA –
    *i.e. acts like most steroid hormones.
    Vitamin as it needed in diet but can still be synthesised
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33
Q

What is Vitamin D2?

A

Vitamin D2 (ergocalciferol)
* derived from ergosterol widely found in plants, fungi and moulds.
* important pharmaceutically and commercially as a food additive because of ready availability of ergosterol.

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34
Q

Sources of D2?

A

Sources:
* Milk and dairy products, fortified margarine, eggs.
* Cholecalciferol formed in skin by UV light on 7- dehydrocholesterol,
* ergocalciferol is formed from ergosterol by the action
of UV light, prepared commercially

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35
Q

Function of vitamin D?

A
  • Acts to maintain correct levels of calcium and phosphate in the blood so that proper mineralisation of bone is achieved.
  • Biggest influence on calcuim and phosphate absoption
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36
Q

Vitamin D Deficiency?

A
  • Rickets in children and osteomalacia in adults
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37
Q

What is Rickets?

A

Rickets
* mineral : matrix ratio decreases in bone
* bending of long bones and kyphosis.
* Tooth eruption delayed

38
Q

What is Osteomalacia? Symptoms? Where is found?

A
  • muscle weakness
  • bone pain
  • decalcification of long bones
  • ** mineral : matrix ratio decreases in bone **- but doesnt show as bones are fully formed
  • nearly always due to Vit D deficiency and rarely a calcium deficiency
  • Borderline cases of deficiency common in the UK especially in the elderly and
    also in Asian children and women especially in the north of England and Scotland
39
Q

Reccomedation and toxitiy level of vitamin D?
What happens if too much vitamin D taken?

A

Consider taking 10 microg between October and March for adults and
children over 4 years

Toxicity
* Excessive consumption of vitamin D is toxic.
* Hypercalcaemia, GI tract disturbances and calcification of soft tissues
(heart, lungs, kidney).
* fatal when severe
* Intakes of 10 x RNI produce toxicity (100 g).

40
Q

Good sources of Vitamin K

A

Sources
* Green leafy vegetables best, small amounts in milk,
meat, eggs and cereals
* A considerable amount from the bacterial flora of the
jejunum and ileum.

41
Q

Why may newbons have a vitamin k deficiency?

A
  • Human milk has a low vitamin-K content
  • infants may have marginal insufficiency
  • it does not cross the placenta efficiently
  • the neonatal gut is sterile
42
Q

How is blood clotting come about?

A

Blood clotting is defective. This process depends on a cascade system of interacting proteins.
* Deficiency resulting in increased blood clotting time is rare except:
* In long term antibiotic therapy

43
Q

Vitamin K disease?

A

haemorrhagic disease of the new-born
* poor placental transfer and no gut flora.
* Some affected babies develop intracranial haemorrhages.
* Of these, 50% die and the other 50% tend to have neurological malfunction.
In the UK babies have been given vitamin K at birth since the 1950s.

44
Q

What are the B group of vitamins?
What is the deficiency?

A

ALL B VITAMINS ACT AS CO-ENZYMES IN METABOLIC PATHWAYS

  • THIAMIN (B1)
  • thiamin deficiency is the 5th commonest cause of dementia
45
Q

Good sources of vitamin B?

A

Good sources: whole grain, pork, poultry, fish, vegetables, dairy produce.

46
Q

Bad sources of vitamin B

A

Food stuffs deficient in the vitamin: polished rice, sugar, fat, refined and processed foods.

47
Q

Requirements of Vitamin B?

A

DRV 1.4 mg / day ( male) 1.0 mg / day (female)
0.5 mg / day / 1000 kcal

Requirement high if carbohydrate intake is high
Note thiaminases (raw fish) and anti-thiamin factors (coffee, tea).

48
Q

Main manifistation of thiamin deficiency?

A

B1 Deficiency
In the West main manifestation of thiamin deficiency
‘Wernicke - Korsakoff syndrome’
mainly associated with alcoholism.

49
Q

Biochemical role of thiamine?

A

Biochemical role:
* Needed as as thiamin pyrophosphate (TPP) ‘coenzyme’
* e.g. pyruvate → acetyl CoA
* pyruvate dehydrogenase complex
* deficiency results in accumulation of lactate in muscles

50
Q

Presentation of thiamin deficiency?

A

Beri-beri - diffrent varities
1. Infantile beri-beri
* Sudden onset, cardiovascular symptoms
2. Acute cardiac beri-beri
* congestive heart failure, enlarged heart, liver,engorged neck veins,sudden heart failure
3. chronic dry beri-beri
* symmetrical ascending peripheral neuropathy weakness, numbness, ataxic gait, painful extremities

51
Q

What is Wernicke/Korsakoff syndrome?
Symptoms?

A

Wernicke’s encephalopathy
* 1930’s recognised as cerebral beri-beri
* confusion , ataxia, polyneuropathy ,disorientation in space and time.
* If untreated, progresses into:
* Korsakoff’s psychosis
* principal feature: loss of memory of recent events.

52
Q

Where is W/K syndrome seen mainly?
Why?

A

W/K syndrome is seen mainly in alcoholics
* Alcohol leads to anorexia,
* inhibition of active transport (absorption) of thiamin from the
intestine,
* inhibition of the enzyme which converts thiamin into TPP

53
Q

Why do Alcoholics suffer many B vitamin
deficiencies?

A
  • may have adequate energy intake but as ‘empty
    calories’ from alcohol
  • inadequate levels of vitamins and other nutrients.
    *** GI tract **malfunctions are common.
    * Cirrhotic liver affects storage, transport and metabolism
    of many vitamins.
  • storage and transport of fat soluble vitamins ,e.g. vitamin A, may be impaired
54
Q

What is B2?
Main source?

A

RIBOFLAVIN (B2)
* UV sensitive, mainly in milk, usually associated with
protein.

55
Q

Vitamin B2 function?

A

Function
* As FAD and FMN in redox reactions.

56
Q

Who is vitamin B2 deficiency found in?
Symptoms?

A
  • Rare (due to asocaition with proteins), except in alcoholics.
  • Symptoms mild : cheilosis, angular stomatitis and cataracts.
  • It is protein bound. diets adequate in protein will be
    adequate in riboflavin.
  • In UK, low status in alcoholics, the elderly and some adolescents ( British schoolchildren diet survey).
  • It is not toxic in excess.
57
Q

What are NIACIN?

A

genetic term for Nicotinic acid /nicotinamide : vitamers (different structural forms of a vitamin).

58
Q

Function of niacin?

A

As NAD and NADP in redox reactions

59
Q

Sources of niacin?

A
  • in cereals in small amounts, its bioavailability is low.
  • high protein diets have no requirement for niacin can be formed from tryptophan
  • Not vitamin as that is always neccessary
60
Q

What a Deficiency in niacin could lead to?

A
  1. Pellagra
    * maize eating people in Europe and USA.
    * fatal if severe
    * maize contains niacin but its not available (low bioavailability)
  2. Dermatitis photosensitive
    (Casal’s necklace) - appears where skin is exposed to sun
  3. Diarrhoea
  4. Dementia
61
Q

What is B6?

A

PYRIDOXINE (B6)
* Pyridoxine, pyridoxamine, pyridoxal

62
Q

Function of B6?

A

Function
* Active form: pyridoxal phosphate
* essential for amino acid metabolism (transaminations,
deaminations etc.). and haem synthesis

63
Q

Vitamin B6 deficiency?
Cause?
Treatment

A

Deficiency
* commonest is secondary, caused by the** presence of
antagonistics**
* Isoniazid, in treatment of TB combines with PP and
renders it unavailable. Patients given** B6 supplements.**
* no evidence that oral contraceptives increase
requirement

64
Q

Therapeutic uses of B6?

A
  • treatment of seizures
  • Down’s syndrome
  • autism,
  • pre-menstrual tension syndrome (PMS)
  • (with variable success)
65
Q

Toxicity of B6?

A

Women, self-medicating for PMS, taking 500-5000 mg
/day have shown peripheral neuropathy within one to
three years.

66
Q

What is B12?

A

Vitamin B12 (cobalamin) a carrier of methyl groups in mammalian
metabolism

67
Q

B12 Function?

A

r treatment of pernicious anaemia with
raw liver (oral liver therapy).

68
Q

Folate structure and function?

A

Folate structure and function:
* carrier of 1C units
* Active form : tetrahydrofolate,
* dihydrofolate reductase important in maintenance of this form.

69
Q

Examples of Folate?

A
    • CHO N5 formyl THFA
    • CHO N10 formyl THFA
    • CH= NH N5 formimino
  • = CH - N5,10 methenyl
    • CH2 - N5,10 methylene
    • CH3 N5 methyl
70
Q

Where is B12?

A
  • B12 only in animal tissues.
  • Vegan diets, no B12. DRV: 1 g /day
71
Q

How does absorption of B12 occur?

A
  • binds to glycoprotein secreted from gastric cells, the intrinsic factor
  • needed for absorption and transport of B12.
  • Pharmacological doses absorbed by diffusion along the entire length of the small intestine, only 1% is absorbed in this way, but it enables oral therapy
72
Q

What is B12 deficiency named? What is the cause?

A
  • commonest cause of pernicious anaemia is lack of intrinsic factor.
73
Q

Where is folate? Requirements?

A
  • mainly in green vegetables, liver and whole grains.
  • DRV 50 g / day
  • normal serum levels are 5 - 15 ng/ml
74
Q

Metabolic function of B12?

A

1-C transfer reactions in:
* purine and pyrimidine synthesis
* amino acid metabolism
* e.g. homocysteine to methionine

75
Q

Metabolic function of folate?

A
  • conversion of homocysteine to methionine
  • in branched chain amino acid metabolism
76
Q

METHOTREXATE

A

Chemotherapy
* As immunosuppressant in autoimmune
diseases
* Ectopic pregnancies

77
Q

Megaloblastosis:
Explanation of symptoms

A

B12 and folate needed for thymidylate synthesis and therefore DNA
* B12 dependent methionine synthetase only means of Me THF
return to the folate pool.
* B12 deficiency ‘traps’ THF in the Me THF form producing functional THF deficiency
* explains why haematological picture of B12 deficiency identical to
folate deficiency
* In both cases, lack of 5,10 methylene THF and hence lack of
adequate DNA synthesis:
* haemopoietic cells die in bone marrow without completing cell cycle.
* Megaloblastosis: giant germ cells.

78
Q

What are the symptoms of Inadequate myelin synthesis?

A

Symptoms:
* numbness fingers hands and forearms
* tingling hands and feet
* loss of position sense
* unsteadiness, ataxia, confusion, moodiness, depression.
* spinal cord, brain and peripheral nerve lesions

79
Q

How does a deficiency come about?

A

Inadequate intake, inadequate absorption

80
Q

Deficiencies of B12?

A

B12
* absent IF,
* defective IF,
* gastric atrophy,
* gastrectomy,
* coeliac disease (ileum)
* Crohn’s disease (terminal ileum most commonly
affected)

81
Q

Deficiencies of folate?

A

folate
* malabsorption,
* tropical sprue,
* drugs e.g. barbiturates and anti-convulsants,
* ethanol,
* ?oral contraceptives

82
Q

Folate and Neural tube defects link?

A

UK : one of the world’s highest rates of neural tube defects.
* 1991 blind trial
* folate supplementation or mixture of other vitamins around conception time
* ?could prevent neural tube defects (anencephaly, spina bifida, encephalocele) in women who already had one
affected pregnancy
* 72 % reduction in the incidence of neural tube defects in the groups supplemented with folic acid.
* In the UK all pregnant women attending ante-natal
clinics are routinely prescribed folate supplements.

83
Q

Folate, B6 and B12 and
cardiovascular mortality

A

Hyperhomocysteinaemia and CVD*
Some studies show link between high
homocysteine conc and some not
* Is it a link or a cause?
* Some studies show lower risk of CVD with high
dose supplements of the B’s and some do not.

84
Q

link of Folate, B6 and B12 and Alzheimer’s?

A
  • certain B vitamins can** halve the rate of brain shrinkage** in elderly
    people who suffer from** mild memory problems**, an Oxford University
    study has shown. Sep 2010.
  • 168 volunteers aged 70 or over with mild memory problems, half of
    whom took high dose B vitamin tablets for two years and the other
    half a placebo tablet. The researchers assessed disease progression in this group by using MRI scans to measure the brain atrophy rate over a two-year period.
85
Q

Source of PANTOTHENIC ACID?

A

Ubiquitous - present, appearing, or found everywhere.
Deficiency is Rare

86
Q

Functions of PANTOTHENIC ACID?

A
  • Component of the coenzyme-A (CoASH) in the metabolism and transfer of carbon chains
  • e.g. fatty acid oxidation
87
Q

Source of biotin?

A

Widely distributed; peanuts, chocolate and egg yolk
* normally sufficient quantities provided by intestinal
bacterial synthesis.

88
Q

Function of biotin?

A
  • Prosthetic group for carboxylations
  • pyruvate → oxaloacetate
  • acetyl CoA → malonyl CoA
89
Q

Cause of Deficiency of biotin?

A

Deficiency
* Rare on a normal diet unless eating raw egg whites.
* Long term antibiotic therapy resulting in sterilisation of the abdominal tract is the commonest cause of deficiency.

90
Q

SLIDE 35 OF VITAMIN A

A

Nutrition and Metabolism (14 decks)

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