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Molecular and Cellular Princples of Medicine > Unit 6 - Vitamins and Minerals > Flashcards

Unit 6 - Vitamins and Minerals Flashcards

1
Q

what are the optimal amounts of vitamins?

A

occur in a range, from toxicity symptoms&raquo_space; nutrient-nutrient or nutrient-drug interactions > average dietary intake > biochemical parameters of deficiency (detectable, but mild)&raquo_space; deficiency symptoms

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2
Q

how is the RDA fixed?

A

RDA is set 2 standard deviations above normal, to meet the needs of 97-98% of the population

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3
Q

how do deficiencies arise?

A
  1. poor nutrition
  2. increased demand
  3. problem with absorption of 1+ vitamins
  4. interactions with medications
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4
Q

how do the fat and water soluble vitamins differ in terms of deficiency VS toxicity?

A

fat: stored more efficiently (resemble lipids), so deficiencies «< toxicities
water: not stored (hydrophilic), so deficiencies&raquo_space;> toxicities

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5
Q

functions of vit A

A
  • visual cycle (carotenoids are precursors for rhodopsin and cone opsins)
  • synthesis of certain glycoPRO and mucopolysaccharides
  • retinoic acid acts as a hormone
  • antioxidant
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6
Q

vit A deficiency VS toxicity

A

deficiency: night blindness (early), xeropthalemia (advanced); follicular hyperkeratosis; anemia (although normal Fe); poor child growth; increased infection/cancer
toxicity: accumulates in liver for nausea, diarrhea, bone pain, scaly/orange skin

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7
Q

what are susceptible groups for vit A deficiency?

A

poor, malnourished, or premature babies

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8
Q

what form of vit A do plants have?

A

carotenoids (pro-vitamin A); require further processing for biological activity in humans

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9
Q

progression of vit A deficiency

A

extreme dryness and thickening of conjunctiva mucus membrane lining inner surface of eyelid and exposed eyeball (xerophthalmia), that progresses to corneal ulceration, perforation, and destruction of eye (keratomalacia)

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10
Q

functions of vit D

A
  • maintains bone
  • Ca++ homeostasis
  • acts as hormone; receptors in many tissues, but full range of activity unknown
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11
Q

vit D deficiency VS toxicity

A

deficiency: rickets (children), osteomalacia (adults), increased susceptibility to breast and other cancers, metabolic syndrome/diabetes, infection
toxicity: rare, but causes hypercalcemia and bone loss

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12
Q

what are susceptible groups to vit D deficiency?

A

poor, elderly, alcoholics

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13
Q

relationship of vit D and cancer

A

low serum vit D in post-menopausal women are correlated with increased risk of breast cancer
-some correlation between polymorphisms in vit D receptor and certain cancers

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14
Q

function of vit K

A
  • localization of enzymes for blood clotting

- helps catalyze addition of gamma-carboxyglutamate to clotting enzymes (GLA modification)

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15
Q

vit K deficiency and susceptible gruops

A

easy bruising, bleeding, hemorrhage

  • newborns: lack intestinal bacteria that makes vit K, so need supplementation
  • adults: long-term antibiotics kill intestinal bacteria that make vit K
  • patients with poor fat absorption are also insufficient
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16
Q

structure of vit K and its forms (K1/2)

A

quinone ring
K1 = phylloquinone in plants (esp. green vegetables)
K2 = menaquinone from intestinal bacteria

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17
Q

vit E functions

A

antioxidants (scavenge free radicals)

  • protect membranes from damage
  • prevent LDL oxidation
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18
Q

deficiency of vit E

A

cardiovascular disease and neurological symptoms

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19
Q

what are susceptible groups to vit E deficiency?

A

patients with severe, prolonged defects in absorption (celical) or genetic defects

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20
Q

what are the overall vit E structures and what is the major form in plasma?

A

called tocopherols and tocotrienols

-major forms are alpha and gamma

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21
Q

how does vit E exert its protective effect?

A

vit E is located in all cell and organelle membranes
-alpha-tocopherol in membrane will intercept ROS and other FR to prevent chain reaction of lipid destruction of especially unsaturated lipids

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22
Q

functions of vit C

A
  • cofactor for oxidases in collagen formation
  • -hydroxylation of pro, lys, and epinephrine
  • required for synthesis of steroids in stress response (trauma will decrease vit C)
  • aids Fe absorption
  • antioxidant activity
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23
Q

mild VS severe cit C deficiency

A

mild: bruising, immunocompromised
severe: scurvy (decreased wound healing, osteoporosis, pinpoint hemorrhage, anemia, fatigue, corkscrew hairs, severe peridontal disease)

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24
Q

who are susceptible groups for vit C deficiency?

A

people with poor diet (Widower’s scurvy); smokers; long-term treatment of aspirin, oral contraceptives, and corticosteroids (esp. Devlin); severe stress/trauma

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25
Q

how much vit C is absorbed from food?

A

almost all of it (readibly absorbed)

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26
Q

what are common deficiencies for energy-releasing B vitamins?

A

symptoms show up in rapidly growing tissues (dermatitis, glossitis, diarrhea), then affect nervous system (peripheral neuropathy, depression, confusion, lack of coordination, malaise)

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27
Q

what are B1 functions?

A

required cofactor for enzymes in cellular energy metabolism as TPP)
-particularly critical in nervous system

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28
Q

what are 3 enzymes that involve thiamine pyrophosphate (TPP)?

A
  1. transketolase/transaldolase (pentose phosphate shunt)
  2. pyruvate dehydrogenase (TCA)
  3. a-KG dehydrogenase (TCA)
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29
Q

what are mild, moderate, and severe B1 deficiency symptoms, and their susceptible groups?

A

mild: GI symptoms, depression, fatigue (poor, elderly)
moderate: Wernicke-Korsakoff syndrome (alcoholics; may get CHF)
severe: beriberi (sometimes alcoholics, mostly if only polished rice)

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30
Q

dry VS wet beriberi

A

both have extreme muscle weakness, poly neuropathy, and CHF, but only wet has pitting edema

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31
Q

functions of riboflavin

A

precursor of FAD and FMN for REDOX energy reactions

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32
Q

what does deficiency of B2 cause? susceptible group?

A

ariboflavinosis - rash around nose, inflammation of mouth and tongue, burning/itchy eyes, and light sensitivity
-in alcoholics, but deficiency is usually uncommon

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33
Q

functions of niacin

A

precursor of NAD and NADP for REDOX energy reactions

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34
Q

what kinds of patients are given niacin for treatment?

A

patients with hypercholesterolemia or hypertriglyceridemia

-also given if have deficiency (along with tryptophan)

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35
Q

what groups are susceptible to niacin deficiency?

A

people with corn or millet based diets (deficient in tryptophan)

36
Q

function of biotin

A

coenzyme for several carboxylases

37
Q

biotin deficiency

A

rare, but caused by eating raw eggs with avidin (binds biotin tightly)
-biotin in many food sources, and made by intestinal bacteria, so deficiencies are rare

38
Q

function of pantothenic acid (B5)

A

required for synthesis of CoA, and TCA cycle, metabolism of all fats and PRO

39
Q

deficiency of B5 (pantothenic acid) and susceptible groups

A

very rare, but if present, have typical symptoms of B vit deficiency
-usually in patients taking isoniazid

40
Q

pyridoxine (B6) function?

A

precursor of pyridoxal phosphate (PLP) cofactor required for glycogen breakdown and GABA/heme synthesis

41
Q

mild and severe B6 (pyridoxine) deficiency?

A

mild: irritability, nervousness, depression
severe: peripheral neuropathy, convulsions, decreased glucose tol`erance, hyper-homocysteinemia (CVD risk), anemia

42
Q

E-releasing VS hematopoietic B vitamins

A

E-releasing: B1-6 + biotin

hematopoietic: folate + cobalamin

43
Q

folate function

A

precursor of THF coenzyme in making precursors for DNA and PRO synthesis

44
Q

folate deficiency

A
  • NTDs if deficient mothers,
  • macrocytic anemia
  • hyperhomocysteinemia (CVD risk)
45
Q

susceptible groups to folate deficiency

A

pregnant women, elderly, alcoholics, pts with long-term drug treatments, or people with genetic polymorphisms in folate metabolism

46
Q

why does folate deficiency inhibit DNA synthesis?

A

decreases availability of purines and dTMP

47
Q

what makes cobalamin unique as a water-soluble vitamin?

A

it can be stored in the liver (up to 6-year supply)

48
Q

cobalamin function

A
  1. methionine synthesis
  2. mmCoA –> SCoA conversion
  3. needed in folate metabolism
49
Q

what does B12 deficiency cause?

A

pernicious (megaloblastic) anemia with demyelination

-usually due to lack of IF

50
Q

susceptible groups to cobalamin deficiency

A

elderly, malabsorptive diseases, and long-term vegetarians (although debate b/c have stores)

51
Q

how is B12 released and absorbed?

A

released from PRO by acid hydrolysis in stomach, then bound to IF to be absorbed in ileum

52
Q

what element does cobalamin contain?

A

cobalt

53
Q

what makes it macrocytic VS microcytic anemia?

A

macro (megaloblastic): from folate or B12 (specifically pernicious) deficiency

  • large RBC due to deficiency in nucleotides, so decreased DNA and RNA synthesis
  • cells increase in size w/o division, and large immature RBCs can’t carry enough O2

micro: from Fe deficiency (as well as vit C and Cu)
- small, pale RBC b/c less hemoglobin made, so RBC undergo more cell divisions in bone marrow while waiting for hemoglobin
- fatigue, pallor, weakness, and dizziness

54
Q

what is the general role of minerals?

A

enzyme cofactors, but also can play structural roles in PRO or on their own

55
Q

functions of calcium

A
  • major component of bone
  • signaling
  • coagulation
  • muscle contraction
  • neurotransmission
56
Q

mild VS severe calcium deficiency and susceptible groups

A

mild: muscle cramps, osteoporisis
severe: rickets

in children, adult women, and elderly

57
Q

what sources does calcium come from?

A

solely from diet, and distribution highly regulated

58
Q

when is calcium intake important to prevent osteoporosis?

A

when bone is reaching max density (10-35 in women); even higher amounts needed to maintain bone mass in postmenopausal women (exercise can also maintain bone density)

59
Q

functions of magnesium

A

essential chelator for many enzymes (F1Fo synthase, Na/K-ATPase, SERCA Ca++ pumps) that use MgATP or MgADP as substrate
-if Mg not complexed, many transporters fail to recognize ATP or ADP

60
Q

what does deficiency of Mg cause? susceptible groups?

A

weakness, tremors, cardiac arrythmias

in alcoholics and patients taking diuretics, or severe vomit and diarrhea

61
Q

phosphorus functions

A

mostly in phosphates, and major part of hydroxyapatite

  • constituent of nucleic acids, membrane lipids
  • required in all E-producing reactions
62
Q

phosphorus deficiency

A

rare (since abundant in food supply), but causes rickets, muscle weakness/breakdown, and seizure

63
Q

what is the most common nutrient deficiency worldwide? what is the most common mineral in humans?

A

deficiency: Fe

present in humans: Ca

64
Q

Fe functions

A
  1. O2/CO2 transport in hemoglobin
  2. oxidative phosphorylation
  3. cofactor in several nonheme Fe proteins and cytochromes (REDOX properties important)
65
Q

what does Fe deficiency cause? susceptible groups?

A

microcytic hypochromic anemia, decreased immunity

common in children, menstruating women, pregnant women (almost impossible to get from diet alone, so need supplements), elderly

66
Q

how is Fe absorption and distribution tightly regulated?

A
  • reduction from 3+ to 2+ promoted by vit C
  • low pH in stomach releases 3+ from ligands to make bioavailable
  • uptake via mucosal cells is regulated in response to Fe-deficient or overload states
  • Fe is carefully “escorted” in circulation and cells b/c of potential REDOX damage
67
Q

what are the 2 major barriers to Fe absorption?

A
  1. release of 3+ from food (usually tightly chelated, so need acidic stomach to release)
  2. need reducing agent (like vit C) to convert 3+ to 2+
68
Q

what is hepcidin?

A

signals Fe sufficiency and prevents export of Fe++ from duodenal mucosal cell by downregulating exporter

69
Q

what is MCV and what is it used for?

A

mean corpuscular volume

  • provides measure of average RBC size
  • what is reported in lab
70
Q

long term VS chronic Fe toxicity

A

long term: hemochromatosis; Fe deposits in multiple tissues

  • compromised liver, pancreas, and heart function
  • ultimately compromises mitochondrial function causing lactic acidosis (due to oxidative damage)

acute: Fe overdose in kids
- most common cause of death due to toxicity in kids under 6 yo (b/c eat adult Fe supplements)

71
Q

copper functions

A
  • assists Fe absorption via ceruloplasmin
  • cofactor for enzymes in collagen synthesis (lysyl oxidase needs Cu and vit C), FA metabolism, and elimination of reactive O2 species
72
Q

copper deficiency? susceptible patients?

A

rare, but includes microcytic anemia, hypercholesterolemia, fragile large arteries, demineralization, demyelination

those with Menkes syndrome, or consuming excessive zinc

73
Q

why does excess zinc cause copper deficiency?

A

they compete for the same transporter in initial uptake

74
Q

Menkes disease VS Wilson’s disease

A

Menkes: mutations in Cu transporter ATP7A causes deficiency
-needed to transport Cu to Golgi for enzymes; if not attached to Cu, enzymes are secreted

Wilson: mutations in Cu transporter ATP7B causes overload

  • Cu not sequestered properly, and accumulates in liver with severe liver and nervous system symptoms
  • -causes liver failure/cancer due to REDOX damage
  • -forms brown ring around iris if accumulated in brain
75
Q

function of zinc

A
  • cofactor for over 300 metalloenzymes

- plays structural role in many PRO as Zn finger domains

76
Q

deficiency in zinc? susceptible groups?

A

poor wound healing, dermatitis, reduced taste acuity, poor growth, impaired sexual development in kids

in alcoholics, elderly, or people with malabsorptive or kidney disease

77
Q

what is the earliest symptom of Zn deficiency?

A

scaly dermatitis

  • early and easily detectable
  • can be reversed before more severe
78
Q

chromium functions? deficiency? susceptible groups?

A
  • component of chromodulin that facilitates insulin binding to its receptor
  • impaired glucose tolerance (from reduced insulin effectiveness)
  • those with impaired glucose tolerance, but Cr+++ hasn’t been proven helpful in DM2
79
Q

iodine function and deficiency

A
  • incorporated into T3/4 to regulate BMR

- goiter enlarges thyroid gland (b/c low I- causes increased TSH), and either hyperthyroidism or hypothyroidism

80
Q

selenium function and deficiency

A
  • component of antioxidant enzymes (glutathione peroxidase) and deiodinase enzymes (T3/4 metabolism)
  • Keshan disease (in areas with little Se in soil); cardiomyopathy and cretinism
81
Q

manganese functions

A

in arginase, pyruvate carboxylase, superoxide dismutase

82
Q

molybdenum functions

A

in xanthene oxidase

83
Q

fuoride functions

A

incorporated into bones and teeth to strengthen

84
Q

boron functions

A

involved in bone formation

85
Q

sulfer functions

A

component of AA, used in post-translational modifications

86
Q

what are the most common deficiencies in:

  • children
  • teens
  • women
  • elderly
  • alcoholics
A
  1. Fe, Ca
  2. Ca, Mg, vit A/C/B6
  3. Fe, Ca, Mg, B6, B9
  4. B6, B12, D, Zn, Cr
  5. susceptible to many, but especially B1, B6, B9
87
Q

most common reasons for vit/min deficiencies?

A
  • drug-nutrient interactions
  • compromised liver function
  • poor absorption

Molecular and Cellular Princples of Medicine (42 decks)

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