Iron Deficieny Anemia in Pregnancy

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    IRON DEFICIENCY ANEMIA in PREGNANCY

    Nyoman Arya Adi Wangsa

    030.09.171

    FAC!"Y OF MEDICINE "RI#A$"I NI%ER#I"Y

    &A$AR"A

    D'('m)'r *+ ,01,

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    Pr'-a('

    Firstly I would say thanks to Ida Sang Hyang Widhi Wasa, finally my paper has been completed

    to fulfill the english assignment.

    I would also say thanks to Prof. Muzief (????) as my supervisor. With his guidance, this paper

    has been done.

    In this paper, I would present a discussion about Iron Deficiency nemia in !regnancy. I hope

    that this paper can provide ade"uate information for the readers.

    Finally, I apologi#e if there are some mistakes in this paper, and I am looking forward any

    suggestions and criticisms to improve in the future.

    &aar/a+ D'('m)'r *+ ,01,

    Nyoman Arya Adi Wangsa

    2

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    CON"EN"#

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    3

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    CAP"ER I

    In/rod(/ion

    Iron deficiency anemia @IDA is a type of anemia that affects most people in developing

    countries, including in Indonesia. s many as '>

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    CAP"ER II

    IRON ME"A2O!I#M

    0ost of the iron within the body is found in hemoglobin within erythrocytes @about '577 mg of

    ironA. Iron is stored in macrophages @and to a lesser e9tent in hepatocytesA, which represents the

    storage pool of iron @about '>77 mg of ironA. Small amounts of iron are found in myoglobin and

    in plasma @bound to transferrin. Iron is conserved within the body. *he typical adult human body

    contains about -777

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    diet cannot be transferred to plasmaA. Hepcidin, a main iron regulating protein, decreases

    ferroportin and thus decreases iron absorption.

    Iron "rans-'r5r'(y(4ing

    Iron is not free in the circulation but

    e9ists as transferrin @bound to

    apotransferrinA. 0ost of the iron

    used for red blood cell hemoglobin

    production is obtained from

    hemoglobin breakdown of senescent

    $&s @called recyclingA. When red

    blood cells reach the end of their lifespan @senescentA, they are phagocyti#ed by macrophages @in

    the spleen, liver, bone marrowA. Hydrolytic en#ymes in macrophages degrade the ingested $&s

    and release hemoglobin. !roteolytic digestion of hemoglobin liberates heme and globins. 6lobins

    are broken down to amino acids which can be used for protein production. *he iron is released

    from heme, leaving a porphyrin ring which is converted to bilirubin. (nce iron is released from

    the heme, it is utili#ed by the cell @iron is an essential component of many en#ymesA, e9ported

    @via ferroportinA, or stored as ferritin @like enterocytes < see above figureA. In macrophages,

    ceruloplasmin @which like hephaestin in intestinal cells also re"uires copperA is a ferro9idase and

    facilitates the transfer of macrophage iron to transferrin. So copper deficiency decreases iron

    release from macrophages and affects iron absorption. 1ike enterocytes, hepcidin downregulates

    ferroportin causing iron se"uestration in macrophages.

    7

    Pic 2. Iron Transfer

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    Iron /a' )y Ey/6roid Prog'ni/ors

    *ransferrin

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    IRON DEFICIENCY ANEMIA

    Iron deficiency is defined as a decreased total iron body content. Iron deficiency anemia occurs

    when iron deficiency is severe enough to diminish erythropoiesis and cause the development of

    anemia. Iron deficiency is the most prevalent single deficiency state on a worldwide basis. It is

    9

    *able '. )ormal Distribution of Iron &omponent in 0en and Women@mg=kgA

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    important economically because it diminishes the capability of individuals who are affected to

    perform physical labor, and it diminishes both growth and learning in children.@+A

    Cas's

    Iron deficiency anemia occurs when your body doesnEt have enough iron to produce hemoglobin.

    Hemoglobin is the part of red blood cells that gives blood its red color and enables the red blood

    cells to carry o9ygenated blood throughout your body. If you arenEt consuming enough iron, or if

    youEre losing too much iron, your body canEt produce enough hemoglobin, and iron deficiency

    anemia will eventually develop. &auses of iron deficiency anemia include? lood loss, a lack of

    iron in diet, an inability to absorb iron, pregnancy.

    #ym/oms

    Initially, iron deficiency anemia can be so mild that it goes unnoticed. ut as the body becomes

    more deficient in iron and anemia worsens, the signs and symptoms intensify. Iron deficiency

    anemia symptoms may include?

    %9treme fatigue Irritability

    !ale skin Inflammation or soreness of your tongue

    Weakness rittle nails

    Shortness of breath Fast heartbeat

    Headache nusual cravings for non

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    en#ymes, also known as cytochromes. dults lose appro9imately ' mg @menA to '.3 mg

    @premenopausal womenA a day in faeces and des"uamated mucosal and skin cells. *he haem from

    destroyed or senescent red blood cells is recycled back into new $&s. Iron, which is absorbed

    mostly in the 8e8unum, is transported by transferrin and stored in either ferritin or haemosiderin

    forms. If more iron is lost or needed than can be absorbed, iron stores are used up, and the patient

    becomes iron deficient. !oor iron stores result in impaired haemoglobin synthesis and a

    hypochromic, microcytic anaemia. naemia then results in decreased o9ygen

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    carry o9ygen throughout your body. reticulocyte count shows whether your bone marrow is

    making red blood cells at the correct rate.

    P'ri6'ra4 sm'ar.For this test, a sample of your blood is e9amined under a microscope. *he

    characteri#e of Iron Deficiency nemia is microcytic hypochrom.

    "'s/s /o m'asr' iron 4'8'4s.*hese tests can show how much iron has been used from your

    bodyGs stored iron. *ests to measure iron levels include?

    Serum iron. *his test measures the amount of iron in your blood. *he level of iron in your

    blood may be normal even if the total amount of iron in your body is low. For this reason,

    other iron tests also are done.

    Serum ferritin. Ferritin is a protein that helps store iron in your body. measure of this

    protein helps your doctor find out how much of your bodyGs stored iron has been used.

    *ransferrin level, or total iron

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    CAP"ER III

    IRON DEFICIENCY ANEMIA in PREGNANCY

    P6ysio4ogy o- Pr'gnan(y

    !regnancy causes physiologic changes in all maternal organ systems such as cardiovascular,

    13

    Table 4. Normal Hemo lobin Consentration WHO

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    hematologic, respiratory, endocrine, urinary, dermatology, and othersC most return to normal after

    delivery. In general, the changes are more dramatic in multifetal than in single pregnancies.

    'ma/o4ogi(*otal blood volume increases proportionally with &(, but the increase in plasma

    volume is greater @close to 37:, usually by about '>77 m1 for a total of 3+77 m1A than that in

    $& mass @about +3:AC thus, Hb is lowered by dilution, from about '-.- to '+.' g=d1. *his

    dilutional anemia decreases blood viscosity. With twins, total maternal blood volume increases

    more @closer to >7:A. W& count increases slightly to B,777 to '+,777=1. 0arked leukocytosis

    @ +7,777=1A occurs during labor and the first few days postpartum.

    Iron re"uirements increase by a total of about ' g during the entire pregnancy and are higher

    during the +nd half of pregnancyJ> to ; mg=day. *he fetus and placenta use about -77 mg of

    iron, and the increased maternal $& mass re"uires an additional 377 mg. %9cretion accounts for

    +77 mg. Iron supplements are needed to prevent a further decrease in Hb levels because the

    amount absorbed from the diet and recruited from iron stores @average total of -77 to 377 mgA is

    usually insufficient to meet the demands of pregnancy. @/,'7A

    R'g4a/ion o- Iron "rans-'r /o "6' F'/s

    *ransfer of iron from the mother to the fetus is supported by a substantial increase in maternal

    iron absorption during pregnancy and is regulated by the placenta. Serum ferritin usually falls

    markedly between '+ and +3 week of gestation, probably as a result of iron utili#ation for

    e9pansion of the maternal red blood cell mass. 0ost iron transfer to the fetus occurs after week

    -7 of gestation, which corresponds to the time of peak efficiency of maternal iron absorption.

    Serum transferrin carries iron from the maternal circulation to transferrin receptors located on the

    apical surface of the placental syncytiotrophoblast, holotransferrin is endocytosed, iron is

    14

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    released, and apotransferrin is returned to the maternal circulation. *he free iron then binds to

    ferritin in placental cells where it is transferred to apotransferrin, which enters from the fetal side

    of the placenta and e9its as holotransferrin into the fetal circulation. *his placental iron transfer

    system regulates iron transport to the fetus. When maternal iron status is poor, the number of

    placental transferrin receptors increases so that more iron is taken up by the placenta. %9cessive

    iron transport to the fetus may be prevented by the placental synthesis of ferritin. s discussed

    later in this review, evidence is accumulating that the capacity of this system may be inade"uate

    to maintain iron transfer to the fetus when the mother is iron deficient. @3A

    Pa/6og'n'sis 'mog4o)in Con('n/ra/ion C6ang's in Pr'gnan(y

    nemia in pregnancy is a condition with elevated maternal hemoglobin values below '' g in

    first trimester and third trimester, or levels of hemoglobin values of less than '7.3 g: in trimester

    two @&enters for Disease &ontrol, 'BB5A. Difference above the limit value associated with the

    incidence of hemodilution

    During pregnancy, blood volume increases dramatically in order to nourish and grow of the baby.

    !lasma volume rises 37:, but red blood cells increase only about -7:, resulting in a physiologic

    dilution of red blood cells called Khemodilution of pregnancyL that can look a lot like anemia.

    *his is a normal process that occurs throughout the first +5

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    n e9panded plasma volume

    decrease hematocrit, blood

    hemoglobin concentration and

    erythrocyte count, but did not

    reduce the absolute amount of

    hemoglobin or red blood cells in

    circulation. Decrease in hematocrit, hemoglobin concentration, erythrocyte count and can usually

    be seen at week

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    E--'(/s o- Iron D'-i(i'n(y An'mia in Pr'gnan(y

    '. )egative %ffects on the 0other During !regnancy and the !erinatal !eriod.

    a) epro!"ction#relate! mortalit$.

    It has been clearly demonstrated that the anemic pregnant woman is at greater risk of death

    during the perinatal period. &lose to 377,777 maternal deaths ascribed to childbirth or early post;5B=+'3;B. ccessed on 0ay '5, +7'+.

    / 6//55>>>./rans-siongid'4in's.org.5do(s5d-s5r/(?>mids@'d@r's@'44io//.d-

    http://www.blackwellpublishing.com/content/BPL_Images/Content_store/Sample_chapter/9781405134880/9781405134880.pdfhttp://www.blackwellpublishing.com/content/BPL_Images/Content_store/Sample_chapter/9781405134880/9781405134880.pdfhttp://vivantemidwifery.com/sitebuildercontent/sitebuilderfiles/IncreasingIronDuringPregnancy.pdfhttp://vivantemidwifery.com/sitebuildercontent/sitebuilderfiles/IncreasingIronDuringPregnancy.pdfhttp://vivantemidwifery.com/sitebuildercontent/sitebuilderfiles/IncreasingIronDuringPregnancy.pdfhttp://repository.usu.ac.id/handle/123456789/21579http://www.transfusionguidelines.org.uk/docs/pdfs/rtc-wmids_edu_pres_elliott.pdfhttp://www.blackwellpublishing.com/content/BPL_Images/Content_store/Sample_chapter/9781405134880/9781405134880.pdfhttp://vivantemidwifery.com/sitebuildercontent/sitebuilderfiles/IncreasingIronDuringPregnancy.pdfhttp://vivantemidwifery.com/sitebuildercontent/sitebuilderfiles/IncreasingIronDuringPregnancy.pdfhttp://repository.usu.ac.id/handle/123456789/21579http://www.transfusionguidelines.org.uk/docs/pdfs/rtc-wmids_edu_pres_elliott.pdf