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iron Flashcards

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1
Q

where is iron found

A

center of hemoglobin in ferrous 2+ state

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2
Q

iron can REVERSIBLY bind with

A

oxygen

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3
Q

heme binds with _________ in lungs and carries to tissues

A

oxygen

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4
Q

oxidized iron in ferric state

A

methemoglobin (doesn’t carry oxygen)

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5
Q

how much do humans have of iron (all forms)

A

3-5 grams

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6
Q

how much iron is transported to bone marrow for heme molecules

A

80%

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7
Q

if you can’t get iron

A

iron deficiency anemia (IDA)

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8
Q

what is the center of myoglobin (muscles)

A

iron

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9
Q

massive breakdown of muscle=

A

lots of free iron released (toxic to the body)

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10
Q

iron storage places

A

bone marrow, liver, and spleen

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11
Q

2 forms of iron storage

A

ferritin and hemosiderin

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12
Q

how does iron get into RBC?

A

via transferrin receptors

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13
Q

where does iron go

A

depending on the needs of the cell
-shuttle for storage
-mitochondria for hemoglobin

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14
Q

how is iron regulated

A

absorption in intestine

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15
Q

how can absorption be disrupted

A

gasteric bypass surgery
chrone’s disease

if lining of intestine disrupted- absorption disrupted

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16
Q

what state of iron does absorption occur in

A

ferrous 2+

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17
Q

what state is iron after absorption

A

ferric 3+ bu gut mucosa

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18
Q

normal serum iron levels

A

60-170 mg/dL

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19
Q

body iron distribution

A

1) functional iron– needed for metabolic processes
2) Transport iron finish

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20
Q

body iron distribution

A

1) functional iron
2) transport iron
3) storage iron

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21
Q

functional iron

A

needed for metabolic processes (ex. Hgb)

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22
Q

transport iron

A

transferrin helps iron
-serves as way to get iron where needed
-prevents toxicity
-keeps iron soluble

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23
Q

storage iron

A

ferritan– 800 mg in the body

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24
Q

where is ferritin found

A

liver
spleen
bone marrow
macrophages

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25
Q

what moves to beta region on electrophoresis

A

transferrin

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26
Q

where is transferrin secreted?

A

apoferritin molecule (shell helps transport ferritan)

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27
Q

how many molecules of ferric iron does transferrin bind

A

2

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28
Q

what is the saturation rate of transferrin with iron

A

30%

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29
Q

in IDA saturation rate ____ because no iron to bind to

A

decreases

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30
Q

in IDA serum levels _______ because un bound transferrin

A

increased

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31
Q

what is saturation in iron overload

A

increased

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32
Q

in iron overload serum transferrin _______ because bound

A

decreased

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33
Q

main iron storage form

A

ferritan

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34
Q

most diagnostic indicator of IDA

A

ferritan

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35
Q

DO NOT look at serum iron as indicator of IDA because

A

serum levels remain normal because pulling from storage so look at ferritan

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36
Q

main iron storage site

A

liver

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37
Q

if there is liver damage

A

can’t hang onto iron

-release ferritin
-increase in serum iron

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38
Q

end stage hepatitis = iron toxicity

A

liver lets go of iron and dumped everywhere

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39
Q

APR acute phase reactant

A

ferritin

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40
Q

how is ferritin an acute phase reactant

A

increased in inflammation, malignancy, infection

COVID people have increased ferritin levels

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41
Q

ferritin woman levels

A

10-120

42
Q

men ferritin levels

A

20-250

43
Q

2nd form of storage iron

A

hemosideran

44
Q

how is hemosiderin released from the body

A

slowly

45
Q

granules in liver and macrophage help diagnose with prussian blue stain

A

hemosiderin granules

46
Q

anemia has decreased

A

iron granules

47
Q

protein made only in liver

A

hepcidin

48
Q

what is main iron regulatory hormone

A

hepcidin (nothing to do with iron)

changes of mutations lead to IDA or iron overload

49
Q

where is hepcidin found

A

serum or urine

50
Q

function of hepcidin

A

control amount of extracellular iron that gets into body

51
Q

how does hepcidin regulate

A

1) decrease or increase dietary iron absorption
2) control amount of iron released, enterocytes, gut cells, and macrophages
3) either destroying or not destroying ferroportin

52
Q

ferroportin channels

A

in order iron inside cells to outside goes through ferroportin tube to extracellular

53
Q

hepcidin can break down ferro protein to

A

decrease release

54
Q

iron deficient in serum:

A

hepcidin levels decrease because need fetoprotein tubes are needed

55
Q

iron overload in serum:

A

hepcidin increases because break down ferroportin so iron can’t exit

56
Q

_______ follows iron levels

A

hepcidin

57
Q

another APR

A

hepcidin

58
Q

when hepcidin increased due to inflammation

A

will decrease serum iron levels

59
Q

appear iron anemic but not

A

anemia of chronic inflammation

don’t give more iron! need to decrease inflammation

60
Q

all cells have _______ receptors on them

A

transferrin

(bind transferrin and iron complex)– receptors turn inward release and turn back outward

61
Q

once iron released

A

cleaved by enzymes and become soluble in serum

62
Q

increase receptor

A

go along with decrease in available iron (wants every molecule it can find to attach to transferrin)

63
Q

increase in iron= decrease in receptors

A

don’t need to go out and looks for them, it comes to them

64
Q

NOT APR

A

soluble transferrin receptors

advantage because won’t increase in inflammation only in relation to iron status

65
Q

look at chart in book

A
66
Q

average iron balance in male

A

4 grams of body iron

67
Q

average iron body woman

A

2.5 grams – lower RBC count

68
Q

daily requirement of iron depends on

A

age, infant, toddlers, puberty, gender

69
Q

lose 2 mg of iron everyday through

A

stool
urine
cells - dying

70
Q

where does iron regulation – absorption occur

A

intestine

body uses what it needs and get rids of rest

71
Q

major factors of iron abs

A

rate of RBC production
rate of myoglobin production
iron stored

72
Q

what vitamin stored in combo with iron

A

vitamin C– helps with absorption

alcohol also increases absorption

73
Q

interfering sources of absorption

A

dairy foods
tea
iron and calcium taken at same time
certain antibiotics

74
Q

leading cause of anemia

A

iron deficiency

75
Q

1 reason for IDA

A

nutrition

76
Q

other reasons for IDA

A

-lead poisoning
-gastric bypass
-crohn’s disease
-celiac disease
-parasitic infection

77
Q

how does IDA develop

A

serum iron first lowered

don’t see because call on ferritin to pull out reserve
-no symptoms until serum iron levels are low upon testing (ferritin also low)

78
Q

test levels full blown IDA

A

decreased MCV, MCH, MCHC

increased transferrin, total binding iron capacity

decreased percent saturation

increased soluble transferrin receptors

decrease hepcidin– no inflam.

79
Q

what happens in body during IDA

A

-lack of energy(oxygen not getting around)
-decrease mental capacity in child
-decrease growth
-large tongues
-sores in mouth
impairment of GI tract

80
Q

main reason for iron overload

A

MAIN: hereditary hemochromatosis

81
Q

hereditary hemochromatosis

A

not everyone homozygous- show expression later in life

men 5x to display symptoms because aren’t getting rid of iron like women

can absorb more iron than body needs

82
Q

hereditary hemochromatosis symptoms

A

tan
liver problems
diabetes

83
Q

if not dealt with how much iron can be in body

A

20 g

84
Q

look at lab test for hereditary hemochromatosis

A
85
Q

lots of patients get liver biopsy

A

prussian blue stain for hemosiderin

86
Q

treatment for hereditary hemochromatosis

A

therapeutic phlebotomies
-chelation therapy

87
Q

what occurs in celation therapy

A

deferoxamine

88
Q

other reason for Iron overload

A

hemosiderosis

89
Q

hemosiderosis

A

iron over load due to repeated blood transfusions

ex. sickle cell

have to monitor for diabetes, liver disease (pancreas destroyed bc iron overload)

use celation?

90
Q

specimen for iron testing

A

serum tube and heparin

no oxalate, citrate, or EDTA : binds iron

91
Q

combine detection … color metric

A

dissociation ferric iron from transferrin through addition of acid

ferric– ferrous= chromagin + ferrus = color proportional to amount of serum iron

92
Q

serum iron levels

A

60-170

93
Q

amount of iron that transferrin can bind if all binding sites saturated

A

TIBC

94
Q

TIBC reflects

A

unsaturated transferrin (UIBC)

95
Q

total iron binding capcity=

A

unsaturated iron binding capacity + serum iron

96
Q

TIBC procedure?

A

1) saturate serum with per determined amount of iron that will saturate all transferrin sites

2) add agent that complex will all unbound iron

97
Q

normal TIBC

A

250-425

98
Q

amount of transferrin saturated with iron at any given moment

A

% saturation

99
Q

% saturation equation

A

serum iron/ TIBC. x 100

100
Q

normal % sat

A

20-50 %

below 20= IDA
above 50 = iron overload

101
Q
A

chem (5 decks)

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