Micronutrients (Fe, Zn, I) Flashcards

1
Q

describe the body’s abosorption rate when deficient

A

absorbs nutrients that are deficient faster

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2
Q

excess of vit can lead to…

A

potential toxicity ie. gummy bears

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3
Q

metabolic interactions:

A

vitamins can compete w/ binding sites

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4
Q

what are metalloenzymes?

A

Enzymes that contain one or more minerals as part of their structures.

common in redox rxns because metal ions can exist in multiple states

ie. catalase has Fe in it. Can’t function without Fe

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5
Q

what are approx amounts of major minerals in a 60kg person?

A
  1. Ca 1150g
  2. Phosphorus 600g
  3. Potassium 210g
  4. Sulphur 150g
  5. Sodium 90g
  6. Chloride 90g
  7. Magnesium 30g
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6
Q

what are the fat soluble or water soluble vits?

A

fat soluble: DEAK

water soluble: Bs and C

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7
Q

define a vitamin

A

essential organic nutrients required in small amounts (mg or ug) for specific functions that promote growth, reproduction ,maintenance of health/life.

generally function as coenzymes

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8
Q

what is a vitamer

A

different forms of a vitamin can have diff functions.

conversion between forms, and from precursors

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9
Q

factors that affect bioavailability of vitamins

A
  • efficiency of digestion
  • other foods consumed at the same time
  • method of food prep
  • source of nutrient
  • previous nutrient intake and nutrition status
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10
Q

what are the 9 B vitamins?

A
thiamin
riboflavin
niacin
biotin
pantothenic acid
vit B6
folate
vit B12
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11
Q

how does the solubility of fat or water soluble vitamins affect metabolism?

A

water soluble vit:

  • found in watery compartments of food
  • moves directly into blood when absorbed
  • travels freely in blood
  • excess is removed in urine
  • possible to reach toxic levels if consumed from supplements
  • needed in more frequent doses (every 1-3 days)

fat soluble vits:

  • must first enter the lymph and then the blood
  • need protein carriers for transport in the blood
  • less readily excreted (tends to remain in fat storage sites)
  • likely to reach toxic levels from supplements
  • needed in less frequent doses: (weeks of months)
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12
Q

are vitamins easily degraded?

A

yes. ie by light or o2

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13
Q

describe process of co enzyme use with enzymes

A

enzyme is inactive without enzyme because substrate can’t bind

enzyme is activated by adding coenzyme

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14
Q

example of hormonal function of vitamins?

A

vit A as retinoic acid in cell differentiation

vit D as calcitriol in calcium availability

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15
Q

What type of anemia does a Fe deficiency lead to?

A

hypochromic microcytic anemia

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16
Q

what type of anemia does folate or vit B12 deficiency lead to?

A

megaloblasitic or pernicious anemia

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17
Q

functions of Fe

A

To transfer oxygen

part of a heme group in 2 types of protein

  1. hemoglobin (in RBC) for transport of o2 to tissues. hemoglobin accounts for 80% of body’s iron
  2. myoglobin: oxygen holding protein in muscle cells
    - transport of electrons through resp chain (cytochromes)
    - enzymes such as peroxidase, catalase, etc
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18
Q

what are the two ionic states of iron?

A

ferrous iron: Fe2+ (reduced)
ferric iron: Fe3+ (oxidized)

can easily be reduced or oxidized between the forms. Thus Fe is a good cofactor to REDOX enzymes

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19
Q

what is ferritin

A

the iron storage protein

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20
Q

what is transferrin

A

iron transport protein

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21
Q

what is heme

A

iron holding part of the hemoglobin and myglobin proteins. Found only in animal protein products (40%). Nonheme Fe (60%) is found in plant and animal sources

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22
Q

What are vulnerable stages of life that are high risk for FE deficiency?

A

women in reproductive years (repeated blood loss from menstruation)

pregnant women (needs extra Fe to support added blood volume for growth of fetus and blood loss during childbirth)

infants and young children( need extra Fe to support fast growth)

teens

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23
Q

What is an iron deficiency anemia

A

microcytic hypochromic anemia

severe depletion of iron stores that results in less hemoglobin and small and pale RBC

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24
Q

signs and symptoms of Fe deficiency anemia?

A

tiredness
low work performance
low childhood development (psychomotor and intellectual)
high lead poisoning susceptibility

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25
Q

stages of iron deficiency

A
  1. Fe stores diminish: serium ferritin (in the blood) reflect iron stores
  2. decrease in transport iron: serium iron falls and transferrin (iron-carrying protein) increases. as the severity of the deficiency increases: more transferring and less iron
  3. hemoglobin production declines: lack of iron limits hemoglobin production. Hemoglobin precursor (erythrocyte protoporphyrin) accumulates
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26
Q

describe RBC without anemia (healthy)

A

normochromic and normocytic cells (dark and bigger compared to anemic cells)

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27
Q

hemoglobin count of iron deficiency anemia for men and women?

A

HGB < 140g/L

Hgb < 120 g/L

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28
Q

what is usually tested for when evaluating iron status? How is this limiting?

A

hemoglobin level.

lower hemoglobin levels = lower ability to carry o2

limiting because it only tests for 3rd step of deficiency (shows only advance Fe deficiency, not earlier stages where problems begin)

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29
Q

what is hematocrit?

A

measurement of the volume of RBC in a specific volume of blood

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30
Q

difference between iron deficieny and anemia?

A

people can be deficient wihtout being anemic

iron def: depleted body iron stores without presence of anemia

iron def anemia:

  • hemoglobin synthesis decreases. Results in low hemoglobin and small, pale RBC (hyprochronic and microcytic cells).
  • These cells can’t carry enough O2 from lungs to the tissues (results in lower energy metabolism. Ie. fatigue, weakness, headache)
  • impared neurotransmitter synthesis results in slower work performance and productivity. Can begin in the 1st stage of iron deficiency, even when no outward symptoms are showing. Can be easily mistaken for behaviour problems
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31
Q

why are women more at risk of IDA?

A

women have higher EAR because of menstruation

high percent of women are under EAR

32
Q

describe iron metabolism

A
  1. Fe2+ binds to Fe3+ (ferritin) and crosses membrane to transferring (needs to be bound in ferric state)
  2. transferrin brings iron to bone marrow where stem cells become RBC. Involves Fe2+ and protoporphyrin (precursor)
  3. Heme is made. Becomes hemoglobin in RBC. Circulates for approx 120 days in the blood
  4. RBC is taken up by the liver where it is broken down
  5. Heme is converted to billirubin (toxic compound) and goes out into bile and excreted in feces (billirubin makes it brown). Some is excreted in urine (makes it yellow. higher billirubin = higher dehydration)
  6. Fe is recycled back into transferrin
33
Q

sources of heme and nonheme iron in foods?

absorption of these sources?

A

animal sources: contain heme and nonheme iron. (heme iron)

plant sources: only nonheme iron (elemental iron)

heme iron is 25% absorbed
Nonheme iron is 17% absorbed

heme iron is 10% of average daily iron intake.
non heme is 90%.

34
Q

how is iron recycled in the body?

A
  • RBC lives approx 4 months before the spleen and liver removes it from the blood
  • RBC are taken apart and parts are prepared for excretion/recycling
  • iron is salvaged and attached to transferrin (protein that carries iron in blood) which transports it back to bone marrow to be reused for making new RBC

only small amounts of iron are lost in urin, sweat and shed skin

35
Q

why do vegetarians/vegans need more Fe in diet?

A

lower absorption in nonheme iron sources (approx 10% absorption)

don’t have MFP peptide to enhance absorption (only found in animal products)

36
Q

what are factors that inhibit or enhance nonheme iron absorption?

A

enhance: MFP factor ( a peptide in Meat, Fish, Poultry). Vit C
inhibits: phytates (legumes and grains), veg proteins, calcium, phosphate, tannic acid and polyphenols (in tea and coffee)

37
Q

where does RBC synthesis occur?

A

in bone marrow (stem cells become RBC)

38
Q

difference between EAR and how much iron you absorb?

A

EAR is the amount that you need. How much iron you actually absorb is less.

Must take into account the bioavailability of the iron source to see if there is adequate iron in the diet

ie. spinach is very high high in iron, but also high in oxalates. The oxalates bind to Fe and lowers bioavilability of the Fe source. Thus spinach is not a good source of Fe

39
Q

primary vs secondary deficiency?

A

primary: caused by inadequate intake of that nutrient
secondary: caused by other problems inside the body that affect absorption/metabolism of that nutrient

both results in declining nutrient stores which results in symptoms of deficiency

40
Q

What changes in Fe transport occurs when deficient in Fe?

A
  1. iron is drawn from ferritin stores
  2. plasma ferritin decreases
  3. efficiency of transporting Fe increases
  4. transferrin production increases
  5. absorption efficiency increases (transferrin binding capacity and # of receptors increases)
  6. intestinal epithelial cells absorb Fe better when Fe is present
  7. defective erythropoiesis (no production of RBC). Not enough iron for protoporphyrin (precursor). Results in hemoglobin being made without Fe.
  8. RBC doesn’t function properly without hemoglobin. Results in hypochromic and microcytic cells (IDA)

ie. when someone is deficient or requires more Fe, they absorb more and faster (higher efficiency)

41
Q

Describe causes of iron deficiency

A
  1. Decreased dietary iron (less iron absorbed or from vegetarian diet which lacks heme)
  2. inhibition of absorption. From mineral interactions where Ca and zinc supplements decrease absorption or other absorption inhibitors (ie. phytates and oxalates)
  3. increased red cell mass (pregnancy and growth)
  4. increased losses (hemolysis, GI bleeding, heavy menstrual losses)
42
Q

Name of iron overload disorder (toxicity)

A

hemochromatosis: caused by a genetic failure to prevent unneeded iron in diet from being absorbed

characterized by:

  • tissue and liver damage
  • infections are likely because bacteria thrive on iron-rich blood

too much vit C can reduce transferrin to free ferrous iron. results in potential toxicity

43
Q

calculate EAR for iron for healthy individuals

how much is the assumed percent of ingested iron that is absorbed?

A

1.5mg (iron needed) / 0.18 (% iron absorbed) = 8mg of iron (EAR)

assumed that 18% of ingested iron is absorbed

44
Q

RDA for healthy women in reproductive years?

RDA for healthy men?

A

18mg/day (loses iron through menstruation)

men: 8mg/d

45
Q

RDA for vegetarian men and women?

A

to calculate RDA for vegetarians: multiply by 1.8

veg men: 8mg x 1.8 = 14mg/d

veg women: 18mg x 1.8 = 32mg/day

46
Q

supplements for IDA treatment?

A

ferrous sulphate (Fe2+) because higher solubility and absorption than dietary ferric (Fe3+)

47
Q

why do vegetarians need more iron?

A

to make up for low bioavailability of their diets

only nonheme sources are found in plants, which have a lower absorption rate

48
Q

how to treat a widespread deficiency across a population?

A

fortify food supply

ie. Fe sulphate in wheat flour

but need to be careful of toxicity for some population groups (because men have much lower EAR and UL)

49
Q

where is iron stored?

A

mostly in the liver. Also in bone marrow and spleen

Most is circulating RBC

50
Q

UL of iron for adults?

A

45mg/d

51
Q

how does a deficiency of copper affect iron absorption?

A

copper is needed for iron to be absorbed.

deficiency of copper results in secondary Fe deficiency

Not very common to occur because we receive copper from water pipes

52
Q

functions of zinc?

A
  • required as a cofactor for many enzyme metabolic reactions to occur (ie. gene regulation)
  • important for immune system, growth and development, synthesis and storage of hormones, activation of vit A, taste perception

zinc deficiency impairs many normal body functions. but zinc deficiency is hard to diagnose and easily seen as a general protein deficiency

53
Q

what does saturation of transferring indicate about iron levels?

A

low saturation of transferrin indicates deficiency of iron

high saturation indicates over-supply of iron

the number of transferrin receptors is highly regulated (there is more transferrin when there is more Fe)

54
Q

basal daily iron losses?

A

men: 1.0mg
premenopausal women: 1.4mg

loss from:
-GI blood, GI mucose, bile, skin cells and sweat, unire, menstrual losses

55
Q

total Iron DRIs of all categories?

A

men: 8mg/d (14mg if vegan)

women: 18mg/d
27mg if pregnant
33mg if vegan

56
Q

RDA of women and men?

UL?

A

men: 11mg/d
women: 8mg/d

UL: 40mg/d

57
Q

good sources of zinc

A

beef: 5mg
eggs: 1mg
seafood: more than 5mg
legumes/nuts: 1.5mg
whole grains and foritifed cereals

58
Q

describe zinc absorption

A
  • if more zinc is needed, more is absorbed (higher absorption if deficient)
  • approx 33% absorption efficiency
  • primarily absorbed in small intestine (carrier mediated process)
  • bioavailability is affected by consuming with other foods (ie. phytates bind with zinc and decrease bioavailability)
  • 2 options of absorption:
    1. involves itself in the metabolic functions of the cell
    2. retained in the cell by metallothionein (binds and transports metals. Regulates zinc absorption by storing the zinc until the body needs it. Zinc is released into the blood stream where it is transported around the body)
59
Q

what are factors that enhance/inhibits zinc absorption?

A

enhance: acids, AA
inhibits: phytate, oxalate, polyphenols, fibre, folate

60
Q

describe zinc deficiency and the results of it

A
  • difficult to diagnose. Usually misdiagnosed as general protein deficiency deficieincy
  • no specific test because zinc has so many roles
  • children are most vulnerable (immune system dysfunction compromised growth, poor appetite)
  • also vulnerable to pregnant women, elderly and the poor

results of chronic zinc deficiency:

  • growth retardation and slow sexual development
  • slow digestion and absorption
  • worsens malnutrition
  • impairs immune response (infections are likely)
  • damages central nervous system and brain
  • impairs vit A metabolism
61
Q

what is parakeratosis?

A

skin rash resulting from zinc deficiency

62
Q

describe enteropancreatic circulation of zinc

A

refer to diagram

63
Q

why do children have high zinc needs

A

growing rapidly and synthesizing many zinc containing proteins

64
Q

what factors control homeostatic regulation of zinc?

A

zinc content is controlled between:

  1. absorption efficiency of dietary zinc
  2. endogenous secretions in pancreatic fluid (ie. fecal losses)
65
Q

describe steps in dietary zinc deficiency

A
  1. increased absorption and decreased losses
  2. tissue zinc conservation
  3. mobilization of zinc from exchangeable pool
  4. general tissue dysfunction
66
Q

describe zinc recycling in enteropancreatic circulation

A

intestine receives two doses of zinc with each meal:

  1. one from dietary zinc from food
  2. from zinc-rich pancreatic secretions

zinc can be excreted in shed intestinal cells or absorbed into the body when circulating in the blood

67
Q

describe symptoms of acute zinc toxicity?

chronic toxicity?

A

acute: nausea, vomiting, diarrhea

chronic toxicity:

  1. increase of metallothionein in intestine
  2. induces absorption
  3. copper is not released in blood
  4. copper is lost in shed mucosal cells

copper deficiency has similar symptoms to iron deficiency

68
Q

why is it hard to diagnose copper deficiency?

A

it has similar symptoms to an iron deficiency

69
Q

What are the roles of iodide in the body?

A

-thyroid hormones (T3 and T4) that regulate body temp, metabolism, reproduction, growth, RBC production, brain development, nerve and muscle function

70
Q

describe iodine deficiency

A

without dietary iodine:

  1. thyroid hormone (T3 and T4) production declines
  2. body responds by secreting more TSH to accelerate iodide uptake by the thyroid gland
  3. if deficiency persists, thyroid gland cells enlarge to trap as much iodide as possible (one of the causes of goiter)

Refer to diagram fo full

71
Q

What is the average intake of iodide?

sources of iodine?

A

9g/d

sources: iodized salt

72
Q

what is cretinism

A

mental and physical retardation caused by maternal iodine deficiency during pregnancy

affects approx 6 million people worldwide

73
Q

describe how increase of iron affects zinc (mineral interactions)

A

increase Fe = Fe occupies all transferrin binding sites = lower Zn absorption and transport

74
Q

how does increasing zinc affect copper (mineral interactions_

A

increase zinc = high metallothionein = Cu binds more strongly = Cu not released from mucosal cell

75
Q

how does decreasing protein affect zinc

A

decrease protein = decrease albumin = decrease Zn release from mucosal cell = more growth failure = immune dysfunction