Paper Inggris Nyoman

8/12/2019 Paper Inggris Nyoman

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IRON DEFICIENCY ANEMIA IN PREGNANCY

Nyoman Arya Adi Wangsa

030.09.177

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

&A$AR"A

DECEM'ER 7( )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?? , MS as my supervisor. With his guidance, this paper

has been done.

In this paper, I would present a discussion about he !elationship "etween Iron #eficiency

$nemia and %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.

&a-ara( D*s,*m/*r 7( )01)

Niyoman Arya Adi Wangsa

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CON"EN"#

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CAP"ER I

I.I I!+#/)I+ ..................................................................................... 0

CAP"ER II

II.I I!+ M($"+1ISM 22222222222222222222..3

II.II I!+ #(FI)I()4 $(MI$ 22222222222222222..5

CAP"ER III

III.I I!+ #(FI)I()4 $(MI$ I %!(6$)4

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)+)1/SI+ 222.................................................................................-7

!(F(!()(S .................................................................................................-*

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A'#"RAC"

$nemia is one of the four ma8or problem in Indonesia that e9perienced by appro9imately 3*: of

pregnant women. $ccording to WH+, anemia in pregnancy is the cause of 07: of deaths of

mothers in developing countries such as Indonesia. In addition to the mother, anemia in

pregnancy also adversely affects to the fetus. #eficiency of nutrients have been suggested as the

most common cause of anemia. $bout ;3: of anemia in pregnancy caused by iron deficiency.

WH+ reported the prevalence of pregnant mothers who e9perience iron deficiency appro9imately

3 people who had anemia with distribution according to gestational age, * person in the first

trimester, 0 people in the second trimester and -* people in the third trimester. Iron deficiency

anemia in pregnancy is a risk factor for preterm delivery and subse&uent low birth weight, and

possibly for inferior neonatal health. For women with reasonable iron stores, iron supplements

improve iron status during pregnancy and for a considerable length of time postpartum, thus

providing some protection against iron deficiency in the subse&uent pregnancy.

$*y Words ? $nemia, iron deficiency anemia, pregnancy, trimester, preterm delivery, birth

weight

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CAP"ER I

Inrod,ion

Iron deficiency anemia @I#$A 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"A'O!I#M

Most 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+*r4r*,y,ing

Iron is not free in the circulation but

e9ists as transferrin @bound to

apotransferrinA. Most 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 2a-* /y Ey5roid Prog*niors

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

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.

#ym2oms

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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such as ice, dirt or starch

#i''iness or lightheadedness %oor appetite, especially in infants and children

with iron deficiency anemia

)old hands and feet $n uncomfortable tingling or crawling feeling in

your legs @restless legs syndromeA

Pa5o25ysioogy

Iron is re&uired for the formation of the haem moiety in haemoglobin, myoglobin, and haem

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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another condition. Finally, the )") looks at mean corpuscular volume @M)A and the

mean corpuscular hemoglobin concentration @M)H)A have values below the normal

range for the laboratory performing the test. !eference range values for M) and M)H)

are 5


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your blood. otal iron


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CAP"ER III

IRON DEFICIENCY ANEMIA IN PREGNANCY

P5ysioogy o+ Pr*gnan,y

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

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.

*maoogi,6otal 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. Marked 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. @0,*7A

R*gaion o+ Iron "rans+*r o "5* 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

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

e9pansion of the maternal red blood cell mass. Most 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

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

Pa5og*n*sis *mogo/in Con,*nraion C5ang*s in Pr*gnan,y

$nemia in pregnancy is a condition with elevated maternal hemoglobin values below ** gr : in

first trisemester and third trimester, or levels of hemobglobin values of less than *7,3 : in two

trisemester @)enters for #isease )ontrol, *BB5A. #ifference above the limit value associated with

the incidence of hemodilution

#uring 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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e9panding. $ falling hemoglobin

and a healthy well


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mother and the fetus increases during pregnancy. his increased demand cannot be met without

iron supplementation. #uring pregnancy the total maternal need for e9tra iron averages close to

577 < *777 mg @elemental ironA, of which about 77 mg is for the fetus and the placenta, 77A

E++*,s o+ Iron D*+i,i*n,y An*mia in Pr*gnan,y

*. egative (ffects on the Mother #uring %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

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