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Hematology Exam 2 > Diseases of Iron Metabolism > Flashcards

Diseases of Iron Metabolism Flashcards

1
Q

iron metabolism disorders

A

defect in hemoglobin synthesis due to a deficiency of iron or abnormal utilization of iron

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2
Q

microcytic hypochromic anemia

A

red cell disorders

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3
Q

types of iron metabolism disorders

A

microcytic hypochromic anemias

iron overload

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4
Q

types of microcytic hypochromic anemias

A

iron deficiency anemia
anemia of chronic disease
sideroblastic anemia

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5
Q

type of iron overload

A

hemochromatosis

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6
Q

causes of iron deficiency

A

insufficient dietary intake of iron
absorption is impaired
increased loss of iron through bleeding

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7
Q

causes of iron overload

A

absorption abnormally increases
individual receives multiple transfusions
individual receives iron injections

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8
Q

disturbances in heme & globin synthesis can cause

A

defective hb production

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9
Q

types of disturbances in heme synthesis

A

deficient iron
defective iron metabolism
defect in porphyrin synthesis

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10
Q

iron is found associated with or as

A

functional iron
transport
storage

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11
Q

types of functional iron

A

hemoglobin

myoglobin

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12
Q

type of transport iron

A

transferrin

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13
Q

types of storage iron

A

hemosiderin

ferritin

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14
Q

total iron concentration in the body

A

40-50 mg of iron/kg of body weight

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15
Q

iron homeostasis depends on balance of

A

absorption of iron

total body requirements

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16
Q

two forms of dietary iron

A 
nonheme iron (ferric, fe3+)
heme iron (ferrous, fe2+)
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17
Q

where is nonheme iron found

A

vegetables, whole grains

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18
Q

where is heme iron found

A

red meats

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19
Q

nonheme iron

A

ferric, fe3+

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20
Q

heme iron

A

ferrous, fe2+

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21
Q

how is nonheme iron different from heme iron

A

nonheme is not easily absorbed
gastric acid solubilizes the iron complex
reduces ferric iron to ferrous form
low pH allows transport of iron across the enterocyte membrane

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22
Q

where is ferrous iron form absorbed

A

through the mucosal cells (enterocytes) of the intestine

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23
Q

how is ferrous iron absorbed

A

fe2+ is oxidized to fe3+ for binding to transferrin
transferrin distributes to body tissues or for storage
absorption increased when erythropoiesis increased & iron stores depeleted

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24
Q

where is ferric iron form absorbed

A

enters through the blood stream

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25
Q

transferrin

A

plasma iron transport protein mediates iron exchange between tissues

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26
Q

what is transferrin made of

A

a single polypeptide
two homologous lobes
two atoms of ferric iron can bind to one transferrin molecule

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27
Q

what do the two atoms of ferric iron bound to one transferrin molecule do

A

maintains iron in soluble form

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28
Q

what does transferrin do

A

assists iron delivery to erythroblasts in bone marrow by plasma circulation

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29
Q

transferrin receptor 1 (TfR1)

A

expressed on virtually all cells

one molecule of transferrin binds to TfR1

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30
Q

transferrin/TfR1 complex

A

enters cell
iron is released
TfR1 available for recycling

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31
Q

iron not used for erythropoiesis

A

stored in the reticuloendothelial cells of BM, liver, spleen, as ferritin or hemosiderin

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32
Q

ferritin

A

major form of iron storage
stores up to 4500 molecules of Fe3+
primary storage compound for iron
readily available for erythropoiesis

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33
Q

ferritin stores what type of iron

A

nonheme - ferric, fe3+

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34
Q

hemosiderin

A

found in macrophages
aggregate of iron, carbohydrate, lipid, protein
iron from hemosiderin is released slowly - not readily available for cellular metabolism

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35
Q

BM macrophages contain hemosiderin if

A

iron stores are normal or high

stains with prussian blue

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36
Q

percent saturation in males & females in transferrin

A

20-50% males

15-50% females

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37
Q

total serum iron test

A

forces transferrin to let go of the iron

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38
Q

how many ferric irons can transferrin hold

A

2

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39
Q

total binding capacity

A

indirecty measures how much transferrin you have

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40
Q

transferrin is measured functionally as

A

TIBC - maximum amount of Fe able to be bound in serum

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41
Q

what is transferrin percent saturation

A

amount of transferrin complexed with iron - usually about 30%

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42
Q

the quality of storage iron accompanied by changes in serum iron & TIBC

A

when storage iron increases, serum iron increases, & TIBC decreases
when storage iron decreases or is absent, serum iron decreases, TIBC increases

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43
Q

transferrin saturation in IDA

A

<16%

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44
Q

transferrin saturation in iron overload or hemochromatosis

A

> 55%

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45
Q

unsaturated binding capacity test

A

approximates how many transferrin molecules are present by finding out how much iron can be bound

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46
Q

when leftover iron reacts with reagent to make a color, what is the relationship

A

darker the color, more was available

the less empty the slots were

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47
Q

total iron capacity

A

sum of the:
total serum + unsaturated iron binding capacity
approximates the amount of transferrin

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48
Q

transferrin saturation

A

~1/3 (33%) of transferrin is saturated with iron

indicator of amount of iron available for erythropoiesis

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49
Q

% transferrin saturation

A

serum iron / TIBC x 100

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50
Q

serum iron normal range

A

50 - 160 ug/dL

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51
Q

TIBC normal range

A

250 - 400 ug/dL

52
Q

% saturation of transferrin

A

20 - 55%

53
Q

in an iron deficient patient is there more or less transferrrin

A

more

54
Q

total iron binding capacity increases in what type of patient

A

iron deficient patient

55
Q

ferritin

A

much better measurement than serum iron & TIBC for assessment of iron stores
directly proportional to the amount of storage iron
acute phase reactant

56
Q

what is the amount of serum ferritin in depletion of iron stores

A

<12 mcg/L

57
Q

what is the amount of serum ferritin in iron overload

A

> 1000 mcg/L

58
Q

low ferritin can be the first indicator of what

A

iron deficiency anemia

59
Q

transferrin receptor - sTfR

A

inversely proportional to the amount of body iron
TfR synthesis increases in iron deficiency - only after iron stores are depleted
not affected by inflammation/infection

60
Q

zinc protoporphyrin - ZPP

A

when iron not available for incorporation into the protoporphyrin ring to form Fe, zinc is incorporated forming ZPP
reflects iron supply over preceding weeks

61
Q

CBC in IDA

A

normocytic-normochromic cells are replaced by microcytic-hypochromic cells
RDW increased

62
Q

what biochemical transports ferric in the blood stream

A

transferrin

63
Q

what biochemical has ferrous iron and binds oxygen & CO2

A

hemoglobin

64
Q

what biochemical is the best indicator of iron stores

A

ferritin

65
Q

what biochemical is used for deposits of iron in tissues & cells

A

hemosiderin

66
Q

prussian blue stains

A

iron

67
Q

erythroblastic island

A

erythroid progenitors clustering around a central macrophage

68
Q

iron can only enter cells that have a

A

transferrin receptor

69
Q

free erythricyte protoporphyrin

A

a heme precursor

70
Q

without iron, porphyrins will

A

build up “FEP” & complex with zinc to make ZPP

71
Q

serum iron/TIBC x 100% =

A

transferrin saturation

72
Q

the amount of transferrin can be estimated by the

A

total iron binding capacity

73
Q

increased ZPP indicates that

A

the patient is deficient in iron, so zinc takes its place

74
Q

most common anemia

A

iron deficiency aneia

75
Q

etiology of IDA

A

diet & increased need
blood loss - GI bleeds & menstruation
malabsorption - celiac disease, gastric bypass, etc

76
Q

stage 1 iron depletion

A

ferritin decreased
transferrin increased
total iron binding capacity increased

77
Q

stage 2 iron deficient erythropoiesis

A

FEP & ZPP increased
H&H decreased with microcytes
TfRs increased

78
Q

stage 3 iron deficient anemia

A

H&H mycrocytic hypochromic very low

79
Q

clinical features of IDA

A

glossitis
koilonychias
chellitis
blue sclera

80
Q

treatment for IDA

A

correction of primary disease
oral supplements
transfusion

81
Q

the most common cause of hypochromic anemia is

A

iron deficiency anemia

82
Q

anemia of chronic disease

A

common complication in inflammation/infection

principal pathogenesis is related to hepcidin

83
Q

hepicidin

A

peptide hormone that is involved in iron absorption & recycling
block release of iron from cells

84
Q

hepicidin’s expression is dependent upon

A

iron availability

IL-6 mediated inflammatory signaling

85
Q

hepicidin is released by

A

the liver

86
Q

hepicidin induces

A

iron sequestration & hypoferremia

87
Q

hepicidin prevents

A

iron availability for RBC production

88
Q

1-3 months after anemia of chronic disease hypothesis

A

activated immune system produces cytokines that reduce iron in the circulation

89
Q

1-3 months after anemia of chronic disease characteristics

A

low serum iron, TIBC decreased, transferrin saturation decreased, ferritin is normal or increased (it’s an acute phase protein)
lower EPO; response to EPO is blunted

90
Q

ACD blood smear characteristics

A

60-70% are normocytic, normochromic & rest are microcytic
retic count not appropriate for degree of anemia
bone marrow has increased stainable iron
FEW & ZPPincrease

91
Q

differential diagnosis of IDA vs ACD is

A

measurement of plasma transferrin receptors

92
Q

tratement of ACD

A

treat the disease

transfuse if needed

93
Q 
IDA characteristics
hgb
mcv
iron
TIBC
ferrin
rbc
rdw
sTfR
A 
hgb - low
mcv - low, <80
iron - low
TIBC - high
ferrin - low
rbc - low
rdw - high
sTfR - high
94
Q 
ACD characteristics
hgb
mcv
iron
TIBC
ferrin
rbc
rdw
sTfR
A 
hgb - low
mcv - normal or <80
iron - low
TIBC - low
ferrin - normal or increased
rbc - low
rdw - normal to slight increase
sTfR - normal
95
Q

TfR is elevated in ___ but not in ___

A

IDA not in ACD

96
Q

types of sideroblastic anemia

A

inherited

acquired

97
Q

sideroblastic anemia

A

iron is incorporated into heme through a series of enzymatic steps
iron is abundant, but heme synthesis is poor

98
Q

inherited sideroblastic anemia

A

iron incorporated into heme has a defect in one or more of the enzymes

99
Q

inherited sideroblastic anemia is caused by

A

sex linked form

autosomal recessive form

100
Q

acquired sideroblastic anemia

A

iron incorporated into heme blocks one or more of the steps

101
Q

acquired sideroblastic anemia is caused by

A

drugs, chloraphenicol

lead poisoning

102
Q

in sideroblastic anemia, prussian blue stain of marrow shows

A

ringed sideroblasts

103
Q

ringed sideroblasts

A

normoblasts with iron deposits surrounding the nucleus, awaiting incorporation into heme

104
Q

siderobastic anemia may be improved with

A

pyridoxing to stimulate heme synthesis

105
Q 
sideroblastic anemia characteristics
hgb
mcv
iron
TIBC
ferrin
rbc
rdw
sTfR
A 
hgb - low
mcv - normal
iron - increased
TIBC - decreased
ferrin - increased
rbc - decreased
rdw - increased
sTfR - normal or low
106
Q

lead poisoning is what type of anemia

A

acquired sideroblastic anemia

107
Q

lead poisoning

A

lead interferes with conversion of ALA to porphobilinogen & incorporation of iron into protoporphyrin IX

108
Q

lead poisoning anemia may be

A

normochromic/normocytic or microcytic hypochromic

109
Q

lead poisoning characteristics

A

retic count is high

basophilic stippling

110
Q

ringed sideroblasts have iron deposits in the

A

mitochondria

111
Q

defect in the conversion of d-ALA to porphobilinogen can lead to

A

sideroblastic anemia

112
Q

basophilic stippling

A

representation of precipitation of rRNA

113
Q

porphyria

A

enzyme block in porphyrin production
porphyrin precursors build up in tissue
excreted in urine & feces

114
Q

porphyria causes

A

photosensitivity, motor dysfunction, mental disturbances

115
Q

hemochromatosis

A

excess iron builds up in tissues

116
Q

types of hemochromatosis

A

primary

secondary

117
Q

primary hemochromatosis

A

hereditary hemochromatosis HFE mutation

118
Q

secondary hemochromatosis

A

to RBC destruction & transfusion

119
Q

hereditary hemochromatosis

A

caucasian genetics

HFE glycoprotein binds transferrin receptors to regulate their affinity for transferrin

120
Q

common mutations in hereditary hemochromatosis

A

C282Y & H63D

121
Q

hemochromatosis symptoms

A

joint pain
fatigue
iron ferritin, & transferrin are increased

122
Q

hallmark of hemochromatosis

A

transferrin saturation
>50% = females
>60% = males
then HFE analysis

123
Q

what is the most common mutation causing hereditary hemochromatosis

A

C282Y HFE

124
Q

therapy for primary iron overload

A

therapeutic phlebotomy

125
Q

therapy for secondary overload

A

therapeutic phlebotomy

desferrioxamine iron chelation therapy

Hematology Exam 2 (2 decks)

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