Iron deficiency and Folate/Vitamin b12 deficiency Flashcards

1
Q

Define hypochromic.

A

Low in colour red cells

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2
Q

Define microcystic.

A

Small, low hemoglobin

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3
Q

How are the red blood cells in iron deficiency?

A

Hypochromic and microcystic

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4
Q

How are the red blood cells in folate or vitamin B12 deficiency?

A

Megaloblastic or pernicious anemia

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5
Q

Name examples of structures made from amino acids but are NOT a protein.*

A

Heme

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6
Q

Iron functions

A
  • Transfer oxygen
  • As part of a Heme group in the protein to transfer oxygen around the body
  • Myoglobin in muscles for oxygen storage
  • Transport of electrons in the electric transport chain( cytochromes)
  • Many enzymes like peroxidase,myeloperoxidase,catalse
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7
Q

Where is hemoglobin is made?

A

In the bone narrow

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8
Q

Why too much iron is not a good thing?

A

Because it can increase lipid peroxidation and other reactions that can cause damage to our body

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9
Q

How many oxygens on hemoglobin and myoglobin

A

Hemoglobin-4

Myoglobin-1

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10
Q

What is interesting about the structure of the hemoglobin molecule?

A

It does not have nucleus and other organelles to maximize the space for oxygen

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11
Q

What happens to the cells with iron deficiency?

A

Alteration of DNA sythesize->hypochromic microcytic anemia

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12
Q

What is pika?

A

A term to describe a craving to chew substances that have no nutritional value(ice,clay,soil,paper). A sigh of severe iron deficiency

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13
Q

Signs and symptoms of iron deficiency

A
  • Tiredness
  • Lower work performance
  • Problems with memory, mental capacity and decline in intellect in children
  • Higher lead poising susceptibility( as there will be no competition for absorption)
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14
Q

What level of hemoglobin in blood should be to diagnose as anemic?

A

Men -<140g/L

Women -<120 g/L

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15
Q

Compare the prevalence of iron deficiency in developed vs. developing countries.

A

Developing: 50% women + children, 25% men Developed: 7-12% women + children

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16
Q

What percentage of low income infants in Montreal have iron deficiency?

A

25%

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17
Q

How many people worldwide have iron deficiency anemia?

A

4-5 billion people

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18
Q

What should iron metabolism be if an individual is healthy?

A

Iron intake = Iron losses

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19
Q

Describe free iron.

A

Toxic (oxidative stress)

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20
Q

What happens to the iron when it gets into our body?

A
  • Mucosal cells in the intestine store excess iron in mucosal ferritin
  • Of the body does not need it, it will be excreted with mucosal cells in 3-5 days
  • If needed , will be given to transferrin that travels around the body
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21
Q

Where are the primer storage for iron?

A

Liver,bone marrow,spleen

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22
Q

What will be done in the body, if there is not enough Fe?

A

Increased in transferrin sythesize+ transferrin will have more binding sites->maximize the space available for iron binding and transport

  • Less ferritin sythesize
  • Increase efficiency of absorption and release from IEC (intestinal epithelial cells)
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23
Q

Transferrin delivers iron to

A

Bone marrow and other tissues

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24
Q

Iron stored in the form of

A

Ferritin -plasma,IEC and hemosiderin-liver

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25
Q

What is hepcidin?

A

Regulating hormone,that keeps in balance between ferritin and transferrin

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26
Q

Describe the recycle circuit of iron in the body

A

Liver and spleen dismantles RBC, packages iron into transferrin and stores excess iron in ferritin and hemosiderin

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27
Q

How much transferrin is occupied by iron usually?

A

1/3

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28
Q

What does different saturation of transeferrin mean?

A

-Low saturation indicates deficiency of iron

High saturation indicates over-supply of iron

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29
Q

What happens to trasnferrin receptors in iron rich environment

A

Decrease

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30
Q

How much is the number of the total body iron?

A

2.5 to 3.8 grams

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31
Q

1 micrograma ferrtin/L is equal to how much storage of iron

A

10 mg

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32
Q

What are the total iron loses for men and women?

A

Men -1 mg

Women -1.4 mg

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33
Q

How iron can be lost?

A
  • Gi losses( Gi blood, Gi mucosal,bile)
  • Desquamented skin cells and sweat
  • Urinary losses
  • Menstrual losses
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34
Q

Where iron is incorporated into hemoglobin?

A

Bone marrow

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35
Q

How long do circulating RBCs live?

A

120 days

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36
Q

In what state does iron function in?

A

2+ state

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37
Q

Why does vitamin C help iron absorption?

A

It is a reducing agent: Fe3+ to Fe2+ = more absorbed

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38
Q

Describe the pathway of iron in the body

A

Ferritin->transferrin->Bone marrow+protoporphyrn(a precursor for hemoglobin)->heme->hemoglobin->RBCs->Liver->Bilirubin or Iron back to transferrin

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39
Q

At what stages iron can be measured?

A

Transferrin level+how iron binds to it

  • Hemoglobin levels
  • RBCs and their size
  • Bilirubin in the urea or in the blood
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40
Q

What is bilirubin?

A

A yellow compound that occurs in the normal catabolic pathway that breaks down heme . Used in bile synthesize and also excreted in urine

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41
Q

Deficiency or excess of iron over time leads to

A

Malnutrition

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42
Q

Symptoms of malnutrition with iron

A

-Diarrhea
Skin rashes
Fatigue
Others

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43
Q

Define the 4 components of iron balance.

A

1) Iron intake (dietary iron + bioavailability) 2) Amount of iron in storage 3) Rate of erythrocyte production 4) Iron losses

44
Q

What should we know for a total picture of the individual for iron deficiency?

A
  • Historical information ( like health status, social economic status,drug use, diet history)
  • Anthropometric measurements
  • Physical examination (hair,skin,eyes,tongue,finger nails)
  • Laboratory tests
45
Q

What happens to the tongue and to the nails during iron deficiency?

A

Tongue-change of color
Pale skin
Spoon finger nails

46
Q

How can you assess primary deficiency

A

Diet history

47
Q

How can you assess secondary deficiency

A

Health history

48
Q

How can you assess declining nutrient stores

A

Laboratory tests

49
Q

How do you measure abnormal functions inside the body

A

Laboratory tests

50
Q

Physical signs and symptoms

A

Physical examination and anthropometric measure

51
Q

What is the first step in developing iron deficiency ?

A

Depletion of iron stores->decline in serum ferritin in the IEC, liver and spleen

52
Q

What is the second step in developing iron deficiency?

A
  • Increased absorption deficiency
  • Increased transferrin iron binding capacity
  • Decreased transferrin saturation %( more receptors, but less binding )
  • Increased transferrin receptors
53
Q

What happens at the third stage of developing iron deficiency ?

A

Defective erythropoiesis(red cell production)
Decreased plasma iron
Decreased Erythrocyte protoporphyrin

54
Q

When iron deficiency is considered as anemia?

A

At the last 4th stage , when there is microcytic hypochromic erythrocytes and associated behavioral signs (fatigue,etc.)

55
Q

Causes of iron deficiency

A
Decreased dietary iron
Less iron absorbed( Ca, fibre)
Vegetarian diets lack heme
2.Inhibition of absorption
Mineral Interactions: Calcium, zinc supplements can iron absorption
Absorption inhibitors
3.Increased red cell mass
Pregnancy, growth
4.Increased losses
Hemolysis (rupturing of RBC)
GI bleeding (occult)
Heavy menstrual losses
56
Q

What are the most iron rich foods

A

Broccoli,Tomato juice,Clams,beef liver,parsley

57
Q

Two types of iron of food, where it can be found and bio-availability

A

Heme( meat sources) and non-heme( vegetables)
In meat 40% is heme iron, 60% is non-heme
Vegetables have only non-heme iron
Heme is 25% absorbed
Non-heme is 17% absorbed

58
Q

Non-heme iron is increased by

A

Vitamin C,sugars,acids including AA

59
Q

Non-heme iron is decreased by

A

Ca, P, phytates(grains, legumes, nuts),oxalates(spinach),polyphenols ( beans, nuts), tannins( tea),EDTA(preservative)

60
Q

Why chilli with beans is better than just beans for iron

A

Because heme iron helps the absorption of non-heme iron

61
Q

What is the iron situation in Canada

A

Men are fine

Women are struggling to get the iron( only 25 % are meeting the requirement)

62
Q

RDA for normal men and premenopausal women

A

Men-8 mg/d

Women -18 mg/day

63
Q

RDA for men and women who are vegan

A

M-14 mg

Women -33 mg

64
Q

RDA for women woth oral contraceptives and pregnancy

A

OCs- 11 mg

Pregnancy -27 mg

65
Q

UL for iron

A

45 mg/day

66
Q

Treatment for iron deficiency

A

-Diet
supplement
•ferrous sulphate or gluconate
retest

67
Q

Iron deficiency prevention

A

Fortify food supply

68
Q

Iron overload and toxicity

A

Acute iron toxicity or poisoning, especially kids
Iron overload from repeated transfusions: Hemosideros->cirrhosis
Megadoses of Vitamin C –Pro-oxidant
can reduce ferric iron bound to transferrin to free ferrous iron
free iron is a powerful oxidant: Fenton reaction

69
Q

What is Hemochromatosis

A

Autosomal recessive, most common geneticdisorder in US (1.5 million people)
More common in men than iron deficiency
Very efficient iron absorption due to defective hepcidin production (hormone that inhibits iron release from IECs)
TX: phlebotomy, desferroxamine, low iron diet, low vitamin C

70
Q

What is the name of vitamin B12 and its structure

A

Cobalamin-B-12

Large molecule with cobalt in the middle

71
Q

B 12 absorption

A

Released from proteins by HCl+pepsin, absorbed in the small intestine with the help of intrinsic factor

72
Q

Name 2 functions of folate and vitamin B 12

A
  • DNA synthesis and repair - Plays important role in cell division and growth
73
Q

What is the correlation between folate and vitamin B12

A

They need each other for activation

74
Q

What is one individual role for vitamin B12?

A

Protect nerve fibers and bone cell activity

75
Q

Why vitamin B12 is needed in small amounts and the danger connected with it

A

It can reabsorbed and it takes 3 years to develop the deficiency, but it is very crucial for pregnant women and her baby

76
Q

Food sources of vitamin B12

A

Animal sources. Best availability in fish and milk

77
Q

How should vegan get vitamin B 12

A

Fortified plant beverages and cereals , B 12 fortified nutritional yeast( only a specific species grown in vitamin B 12 rich environment)

78
Q

Symptoms of vitamin B 12 and folate deficiency

A

Fatigue, dementia,peripheral nerve degeneration

79
Q

What is folate?

A

Vitamin B9

80
Q

Name some sources of folate.

A

• Leafy green vegetables • Fresh, uncooked vegetables & fruits • Eggs • Orange juice & legumes

81
Q

In foods, how does folate naturally occur?

A

Polyglutamate (multiple glutamates)

82
Q

What is the chemical structure of folate?

A

3 rings and a glutamate

83
Q

In enriched foods and supplements, how does folate naturally occur?

A

Monoglutamate Absorbed 2x as efficienctly

84
Q

Explain B 12 and folate metabolism

A

Folate with multiple glutamates-> in the intestine folate monoglutamate+methyl group( inactive form)-> to be activated, B 12 takes methyl to itsself. Now both folic acid and B 12 are activated

85
Q

What happens with B 12 and homocysteine?

A

B12 converts homocysteine in methionine. Low folate and B 12 -> high homocesteine-> high oxidative stress

86
Q

What can stop folate from being recycled?

A

Folate cannot be recycled unless b12 takes it out of its trapped inactive form

87
Q

How do red blood cells during folate OR vitamin B12 deficiency?

A
  • DNA strands break and cell division diminishes - RNA synthesis continues, resulting in a large cell and large nucleus - Megaloblastic anemia: large, immature, nucleated cells
88
Q

Why does megaloblastic B12 and folate anemia look the same?

A

Since the methyl group transfer is the issue

89
Q

What is the difference between megaloblastic anemia and pernicious anemia

A

Megaloblastic anemia-> primary deficiency (lack of dietary folate and B12)
Pernicious Anemia->secondary deficiency ( intrinsic factor deficiency, low acidity in the stomach)

90
Q

How megaloblastic and pernicious anemias are cured?

A

Megaloblastic anemia - quiet rare, slow to develop, only if inadequate intake

Pernicious Anemia-given injections or nasal spray of vitamin B 12

91
Q

How can folate affect birth defects? What is the neural tube?

A

Neural tube will not develop properly with low folate The neural tube is the embryonic tissue that forms the brain and the spinal cord

92
Q

Three neural tube defects diseases

A

Spina bifida( gap or split int he spinal cord)
Anecephaly( partial or complete absence of brain)
Encephalocoele (brain and skull are malformed)

93
Q

Why are all pregnancies at risk for neural tube defects?

A

95% of pregnancies with it have no previous histories

94
Q

Name 3 risk factors for folate deficiency during pregnancy.

A

1) Diet-Preconceptional Folate status 2) Genetic Link (family history with NTD on either side) 3) Ethnic Background (northern European and Hungarian ancestry)

95
Q

What did Health Canada suggest pregnant women do to avoid NTD? What did they opt for instead?

A

Multivitamin contain 0.4 mg of folate to take starting BEFORE pregnant = unrealistic - Fortify food supply instead

96
Q

Name 3 reasons why you would fortify the food supply.

A

1) To correct or prevent widespread nutrient deficiency 2) To restore nutrients lost in processing 3) To add nutrients normally supplied in the food the product replaces (soy beverage)

97
Q

Name 2 fortification controversies.

A

• Targeting the at-risk population • Optimal intake (fix problem without endangering others)

98
Q

How can folate supplements mask B12 deficiency?

A
  • Additional folate will erase megaloblastic anemia - Does not fix neurological problem of B12 deficiency - High intake of folate, don’t need to bother recycling folate WE JUST USE NEW FOLATE, then we have healthy looking RBCs, we don’t know whether it is fresh folate all the time or if it is because we recycled it
99
Q

What is the link between Alzheimer’s and folate intake?

A

Characterized by brain atrophy associated with low plasma folate - Highest levels of folate show lowest cognitive decline

100
Q

High levels of folate decreases the risk of what?

A

Stroke and depression

101
Q

What is associated to lower levels of vitamins B6, B12 and folate?

A

High homocysteine

102
Q

What are high levels of homocysteine a risk factor for?

A

Independent risk factor for heart diseases (atherosclerosis, formation of blood clots)

103
Q

How does vitamin deficiency cause high levels of homocysteine?

A

Causes a bottleneck of homocysteine removal, build up and the homocysteine damages arteries Vitamin B12 and folate are implicated in the synthesis of methionine from homocysteine, if there is less of these nutrients, there will be more homocysteine and less methionine

104
Q

Folate in food

A

Lentils, Asparagus,brocolli, tomato juice

105
Q

Fortification with iron pros and cons

A

-prevent anemia( if the grains are fortified with iron , need to take vitamin C to maximize the effect
-But the toxicity for men with hemochromatosis( need to choose not fortified food without vitamin C)
-