paper inggris nyoman
TRANSCRIPT
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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
$nemia and %regnancy. I hope that this paper can provide ade&uate information for the readers.
Finally, I apologi'e if there are some mistakes in this paper, and I am looking forward any
suggestions and criticisms to improve in the future.
&a-ara( D*s,*m/*r 7( )01)
Niyoman Arya Adi Wangsa
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CON"EN"#
%!(F$)( ................................................................................................. *
)+(S ................................................................................................. -
$"S!$) .................................................................................................
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
22222222222222222222222*-
)+)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.
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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