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biochem term 2 quiz 4 > vitamins > Flashcards

vitamins Flashcards

1. learn the biochemical function of each vitamin 2. learn the clinical significance of each vitamin

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1
Q

what does recommended daily allowance (RDA) reflect?

A

they do not reflect the nutritional needs of individuals but rather provide a tool to compare the contribution of specific food items to the overall diet - what each person needs is an individual things - can actually convert to mg - so really just a unit of measure - approximation of what the average person may need

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2
Q

in what kinds of patients do vitamin deficiencies normally occur?

A

alcohol abusers, elderly patients, patients with small bowel resections, food faddists, and malnourished people in the developing world

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3
Q

where can we get water-soluble vitamins in our diets?

A

all water soluble vitamins except for B12 are in vegetables

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4
Q

water-soluble vitamins (summary)

A

1: most are precursors of coenzymes involved in intermediary metabolism
2: all water soluble vitamins except for vitamin B12 are present in vegetables
3: deficiency of all water soluble vitamins except for vitamin b12 produces clinical symptoms within weeks due to low body stores

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5
Q

what are most water-soluble vitamins precursors to?

A

most are precursors of coenzymes involved in intermediary metabolism

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6
Q

how long does it take for symptoms of vitamin deficiency to occur?

A

deficiency of all water-soluble vitamins except for B12 produces clinical symptoms within weeks due to low body stores

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7
Q

vitamin B1 (summary)

A

thiamine pyrophosphate is a coenzyme for enzymes involved in carbohydrate metabolism, specifically pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase
deficienys causes korsakoff’s in alcohol abusers

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8
Q

what enzymes is thiamine pyrophosphate (vitamin B1) a coenzyme for?

A

enzymes involve in carbohydrate metabolism

  • pyruvate dehydrogenase
  • alpha-ketoglutarate dehydrogenase
  • transketolase
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9
Q

what is the result of vitamin B1 deficiency?

A

beriberi-peripheral neuropathy and dilated cardiomyopathy
deficiency results in korsakoff’s syndrome in alcohol abusers
administer thiamine with glucose to alcohol abusers
would see impaired eye movements (mystagmus) and ataxia

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10
Q

what patient population would you expect to see korsakoff’s syndrome in?
what should be administered with thiamine to these patients?

A

alcohol abusers

administer thiamine with glucose to alcohol abusers

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11
Q

what is vitamin B2 (riboflavin) a precursor for?

A

flavin mononucleotide (FMN) and flavin dinucleotide (FAD) coenzymes

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12
Q

what is the result of riboflavin/vitamin B2 deficiency?

A

fissuring at the angles of the mouth
dermatitis
purple tounge

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13
Q

what two compounds can vitamin B3/niacin be found as?

A

nicotinamide or nicotinic acid

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14
Q

what enzymes is vitamin B3/niacin a precursor for?

A

nicotinaminde adenine dinucleotide (NAD)

nicotinamide adenine dinucleotide phosphate (NADP)

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15
Q

why isn’t vitamin B3/niacin technically a vitamin?

A

because humans can synthesize niacin from tryptophan

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16
Q

what does vitamin B3/niacin deficiency cause?

A

pellagra (italian for sour skin)

dermatitis, diarrhea, dementia and death

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17
Q

in what types of patients would you expect to see vitamin B3/niacin deficiency?

A

patients with Hartnup disease (diminshed tryptophan uptake)

patients with carcinoid syndrome (altered tryptophan metabolism)

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18
Q

what can vitamin B3/niacin be used for theraputically? in what disorder is this treatment used?

A

used to lower LDL and VLDL cholesterol in type IIb hyperlipoproteinemia

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19
Q

what coenzyme is vitamin B5/pantothenic acid a component of?

A

coenzyme A

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20
Q

what is the result of vitamin B5/pantothenic acid deficiency?

A

none yet discovered - it’s widely available in food and so deficiency syndrome has not been characterized

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21
Q

what three molecules does vitamin B6 collectively describe?

A

pyridoxine, pyridoxal and pyridoxamine

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22
Q

what coenzyme is vitamin B6 a precursor for and what does it do?

A

precursors of pyridoxal phosphate, which catalyzes reactions involving amino acids

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23
Q

what drug does vitamin B6 bind to and what is done about this?

A

it binds to the antituberculosis drug isoniazid

as a result, B6 is routinely perscribed with anti-TB drugs to prevent a deficiency in B6

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24
Q

what does a deficiency in vitamin B6 cause?

A

seizures

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25
Q

what is vitamin B7/biotin a coenzyme for?

A

in carboxylation reactions

in these, it’s covalently bound to specific lysine residues of biotin-containing enzymes

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26
Q

what is the result of a vitamin B7/biotin deficiency?

A

dermatitis
glossitis
nausea

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27
Q

how would someone acquire a biotin/vitamin B7 deficiency?

A

by eating greater than 20 raw eggs per day
raw eggs contain a biotin-binding protein called avidin - in the egg whites
apparently people use egg whites as supplements, so could see this in body builders, etc.

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28
Q

what molecules is vitamin B9/folate necessary for?

A

for one-carbon metabolism, including the synthesis of purine and thymidine (and therefore DNA)

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29
Q

what does vitamin B9/folate deficiency cause? how would these deficiencies be acquired?

A

in adults: megaloblastic anemia,
patients taking chemo drugs (methotrexate) - causes shortness of breath due to anemia
pregnant women because fetus is using so much folate
alcohol abusers
in fetuses: neural tube defects -mother didn’t get enough folate during first trimester - part of brain or spinal cord can become externalized (spina bifida, anencephaly)

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30
Q

how is folate deficiency prevented in our diets?

A

it has been supplemented in “enriched” foods since 1998 - for people who are alcohol abusers

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31
Q

what is vitamin B12/cobalamin a precursor for?

what products is that used to synthesize?

A

precursor for methylcoalamin
needed to synthesize methionine from homocysteine in blood cells
also precursor for deoxyadenosylcobalamin, which is needed for fA metabolism in brain cells

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32
Q

what is required for intestinal absorption of vitamin B12/cobalamin?

A 
intrinsic factor
(as a result, deficiency is seen in patients with pernicious anemia, meaning they lack intrinsic factor)
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33
Q

in what organism is vitamin B12/cobalamin not produced?

A

plants

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34
Q

in what patients would you expect to see a deficiency in vitamin B12/cobalamin?

A

in vegans

in patients with pernicious anemia (lacking intrinsic factor)

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35
Q

what is the result of deficiency in vitamin B12/cobalamin?

A

megaloblastic anemia by functionally trapping folate
subacute combined degeneration of the spinal cord
dementia

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36
Q

why does vitamin B12/cobalamin deficiency cause megaloblastic anemia?

A

this is the folate trap hypothesis:
during methionine synthesis, N5-methyl-THF transfers a methyl group to vitamin B12 = methylcobalamin
reaction also required to metabolize N5-methyl-THF
lack of B12 blocks metabolism of N5-methyl THF so it can’t be used to make DNA

37
Q

how long does it take for the clinical symptoms of vitamin B12/cobalamin deficiency to manifest?

A

years because there are large body stores of the vitamin

38
Q

how is pernicious anemia treated?

A

with intramuscular B12 injections - circumvents the need for intrinsic factor (couldn’t give B12 orally because the problem is that it’s not being absorbed by parietal cells properly, so that wouldn’t help)

39
Q

which clinical manifestations of folate/vitamin B12 deficiency can be treated with folate supplementation and which cannot?

A

pernicious anemia with intermuscular B12 injections
megaloblastic anemia due to deficiencies of vitamin B12 or folate can be ameliorated by supplementation
the subacute combined degeneration of the spinal cord can’t be treated by supplementation

40
Q

what is vitamin C/ascorbic acid necessary for?

A

post-translational hydroxylation of proline, especially in collagen
required for hydroxylation of lysine and proline residues in collagen, promoting cross-links
note: only required in primates and guinea pigs

41
Q

what does vitamin C/ascorbic acid deficiency result in?

A

scurvy: bleeding gums, hemorrhages around corkscrew hair follicles, bone pain caused by bleeding underneath periosteum, poor wound healing - connective tissue breakdown

42
Q

what can overdose of vitamin C/ascorbic acid cause?

A

oxalic acid kidney stones

43
Q

which vitamins are water soluble?

A 
the B vitamins
- 1: thiamine
- 2: riboflavin
- 3: niacin
- 5: pantothenic acid
- 6: (just itself)
- 7: biotin
- 9: folate
- 12: cobalamin
Vitamin C: ascorbic acid
44
Q

which vitamins are fat soluble?

A

vitamins A, D, E, and K

45
Q

fat soluble vitamins (summary)

A

in the US, deficiencies of fat-soluble vitamins are often present in patients with fat malabsorption syndromes
fat-soluble vitamins are stored in the body and metabolized slowly - therefore deficiency usually develops only after months of inadequate intake
excess consumption of either vitamin A or D leads to toxicity

46
Q

in what type of patients would you expect to see deficiencies in fat-soluble vitamins in the US?

A

in patients with fat malabsorption syndromes

47
Q

how long does it take for symptoms of a deficiency of a fat-soluble vitamin to appear?

A

months, since fat-soluble vitamins are stored in the body and metabolized slowly

48
Q

which fat-soluble vitamins can cause toxicity if consumed in excess?

A

vitamins A or D

49
Q

what three molecules are categorized as vitamin A?

A

retinol, retinal, and retinoic acid

50
Q

what is retinal essential for?

A

vision - it’s the pigment in rods and cones that senses light

51
Q

what is retinoic acid essential for?

A

to maintain differentiation of epithelial cells

52
Q

how is vitamin A obtained?

A

from animal sources or derived from beta-carotene in plants

53
Q

what is the result of vitamin A deficiency?

what is the first symptom and how can it be improved?

A

deficiency causes 1.2 million cases of permanent blindness each year in the developing world
the first symptom is night blindness - this can be rapidly improved with emergency vitamin A therapy

54
Q

what are the physical signs of vitamin A deficiency?

what causes these?

A

xeropthalmia and Bitot’s spots

caused by corneal epithelial cells dedifferentiation/keratinization

55
Q

what is vitamin A used to treat?

A

acne

psoriasis

56
Q

what occurs when too much vitamin A is consumed?

A

called hypervitaminosis A

results in skin rash, liver damage, raised intracranial pressure

57
Q

what patients should you avoid giving vitamin A to and why?

A

vitamin A is teratogenic and so should not be given to pregnant patients

58
Q

how is vitamin D produced?

A

endogenously in the skin by uv irradiation

obtained from animal (D3) or plant (D2) tissues

59
Q

how is vitamin D converted to its active form?

where does this conversion occur?

A

it’s active form is calcitriol
requires two successive hydroxylation reactions
the first is in the liver
the second is in the kidney, bone or placenta

60
Q

what does calcitriol do in the body?

A

it’s a steroid hormone that increases calcium absorption by the intestine epithelium

61
Q

how is vitamin D deficiency prevented in our diets?

A

in the US, milk is fortified with it

62
Q

what does vitamin D deficiency result in?

A

in adults: demineralization of formed bone, leading to osteomalacia (bone pain, microfractures, compression fractures)
in children: failure to mineralize developing bones, leading to rickets (bowed legs)

63
Q

what are the risk factors for vitamin D deficiency?

A

lack of milk consumption (often due to lactose intolerance)
dark skin color
low sun exposure

64
Q

what can theraputic calcitriol treatment cause?

A

hypercalcaemia: causes “bones, stones, and abdominal moans”

65
Q

what is vitamin E/tocopherol important for?

A

it’s an antioxidant that protects lipid membranes

66
Q

what can vitamin E/tocopherol deficiency cause?

A

red blood cell fragility in infants

67
Q

what biochemical reaction is vitamin K needed for?

what is this reaction needed for?

A

post translational carboxylation of glutamate
this is required for calcium binding by several blood clotting factors, including prothrombin
adds carboxyl group to several clotting factors - gives them a second negative charge - allows it to bind to Ca2+ which brings the clotting factor to the center of the cell

68
Q

where does vitamin K come from?

A

it’s produced by intestinal bacteria

69
Q

what is the result of a vitamin K deficiency?

A

hemorrhage with a long prothromin time (PT)

70
Q

to what patients is vitamin K clinically adminstered and why?

A

to premature infants who lack the intestinal bacteria to provide vitamin K
to adults on long-term antibiotic therapy

71
Q

how is vitamin K blocked and why?

A

it can be blocked by the drug coumadin, which is a vitamin K antagonist
it prevents clotting, for example in patients with prosthetic heart valves

72
Q

vitamin classifications (list)

A 
water soluble
      - non-b-complex
                     ascorbic acid
      - b-complex
             - energy-releasing
                     thiamine (B1)
                     riboflavin (B2)
                     niacin (B3)
                     biotin
                     pantothenic acid
             - hematopoietic
                     folic acid
                     vitamin B12
              - other
                     pyridoxine (B6)
                     pyridoxal
                     pyridoxamine
fat-soluble
                     vitamin A (retinol; beta-carotenes)
                     vitamin D (cholecalciferol)
                     vitamin K (phylioquinonoes, menaquinones)
                     vitamin E (tocopherols)
73
Q

what would happen if you give a patient with vitamin B1 deficiency glucose?

A

if you gave it without thiamine, would get degeneration of mammillary bodies in brain which would result in korsakoff’s disease

74
Q

what would be the symptoms of beriberi? what causes it? in what patient population would you see it?

A

seen in malnourished patients from the developing world
will be short of breath, look warm and flushed
weakness and loss of touch sensation in both feet
due to thiamin deficiency that causes dilated cardiomyopathy

75
Q

what are the symptoms of riboflavin deficiency?

A

cheliosis (fissuring at angle of mouth)
dry skin, rash
smooth, purple tongue
not that important clinically because not deadly

76
Q

why can we get niacin deficiency even if we can make it?

A

synthesis from tryptophan is very slow

can also have disorders where you don’t make enough tryptophan

77
Q

what are the symptoms of niacin deficiency?

A

pellagra: confusion, diarrhea, hyperpigmented skin rash that’s photosensitive, death
four Ds

78
Q

what can vitamin B6 be used to treat?

A

TB - isoniazid

79
Q

what would be the symptoms of pernicious anemia? what causes it?

A

caused by B12 deficiency
would likely have autoimmune disease - destruction of parietal cells so can’t absorb B12
fatigue
anemic - smear shows megaloblasts - smear looks like someone with folate deficiency
decreased sense of vibration in both feet

80
Q

what are the symptoms of subacute combined degeneration?

A 
increase in clumsiness
decreased sense of vibration in both feet on physical examination
history of autoimmune disease
not anemic
normal peripheral blood smear
B12 deficiency
81
Q

what is the cause of subacute combined degeneration?

A

get folate supplemenation but have megaloblastic anemia - the supplementation masks the effects of the anemia
but the folate supplementation doesn’t prevent spinal cord damage
this damage is irreversable
destroys areas of spinal cord that are responsible for vibration sense in lower extremities
so still need B12 even though getting folate

82
Q

why do people die of scurvy?

A

can’t heal their wounds

lack of immune function

83
Q

what is retinol necessary for?

A

reproduction

deficiency results in sterility

84
Q

what are the symptoms/clinical presentation of vitamin A deficiency?

A

starts with night blindness

dry eyes - wrinkles and loss of shine

85
Q

what can hypervitaminosis cause?

A

dry skin
liver damage
raised intracranial pressure

86
Q

what would be the clinical presentation of vitamin D deficiency?

A 
osteomalacia in adults = 
fractures in bone
bone pain
microfractures 
compression fractures
rickets in children
87
Q

what would be the clinical presentation of vitamin K deficiency?

A

premature infant in nicu begins bleeding spontaneously at venous puncture sites
prothrombin time is prolonged
could be internal bleeding

88
Q

why do patients in the NICU have vitamin K deficiency?

A

born with sterile guts so can’t get vitamin K

biochem term 2 quiz 4 (7 decks)

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