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Apa etiologi dan mekanisme dari hematoschezia ?

Interpretasi dan mekanisme abnormal Hb dan Ht ?

Indikasi permeriksaan feses

Adanya diare dan konstipasi

Adanya ikterus

Adanya gangguan pencernaan

Adanya lendir dalam tinja

Kecurigaan penyakit gastrointestinal

Adanya darah dalam tinja

manisfestasi klinis

hematopoesis

Patients with iron deficiency anemia may report the following:

atigue and diminished capability to perform hard labor

!eg cramps on climbing stairs

"ra#ing ice $in some cases% cold celery or other cold #egetables& to suck or chew

Poor scholastic performance

"old intolerance

'educed resistance to infection

Altered beha#ior $eg% attention deficit disorder&

(ysphagia with solid foods $from esophageal webbing&


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)orsened symptoms of comorbid cardiac or pulmonary disease

indings on physical e*amination may include the following:

Impaired growth in infants

Pallor of the mucous membranes $a nonspecific finding&

+poon,shaped nails $koilonychia&

A glossy tongue% with atrophy of the lingual papillae

issures at the corners of the mouth $angular stomatitis&

+plenomegaly $in se#ere% persistent% untreated cases&

Pseudotumor cerebri $a rare finding in se#ere cases&

Iron is #ital for all li#ing organisms because it is essential for multiple metabolic

processes% including o*ygen transport% (-A synthesis% and electron transport. Iron

e/uilibrium in the body is regulated carefully to ensure that sufficient iron is absorbed in

order to compensate for body losses of iron $see the image below&. )hereas body loss

of iron /uantitati#ely is as important as absorption in terms of maintaining iron

e/uilibrium% it is a more passi#e process than absorption.

0he total body iron in a 12,kg man is about 3 g. 00he total body iron in a 12,kg man is

about 3 g. 0his is maintained by a balance between absorption and body losses.

Although the body only absorbs 4 mg daily to maintain e/uilibrium% the internal

re/uirement for iron is greater $52,56 mg&. An erythrocyte has a lifespan of 452 days so

that 2.78 of red blood cells are destroyed and replaced each day. A man with 6 ! of

blood #olume has 5.6 g of iron incorporated into the hemoglobin% with a daily turno#er of

52 mg for hemoglobin synthesis and degradation and another 6 mg for other

re/uirements. 9ost of this iron passes through the plasma for reutilization. Iron in e*cess

of these re/uirements is deposited in body stores as ferritin or hemosiderin.

In healthy people% the body concentration of iron $appro*imately 2 parts per million

;ppm


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9ucosal cells in the pro*imal small intestine medi9ucosal cells in the pro*imal small

intestine mediate iron absorption. Intestinal cells are born in the crypts of !ieberkuhn and

migrate to the tips of the #illi. 0he cells are sloughed into the intestinal lumen at the end

of their 5, to >,day lifespan. Absorpti#e cells remain attuned to the body re/uirement for

iron by incorporating proportionate /uantities of body iron into the absorpti#e cells. 0his

iron and recently absorbed iron decrease uptake of iron from the gut lumen by satiationof iron,binding proteins with iron% by stimulating an iron regulatory element% or both. 0he

incorporation of iron into these cells in /uantities proportional to body stores of iron also

pro#ides a limited method of increasing iron e*cretion in indi#iduals replete in iron.

ither diminished absorbable dietary iron or e*cessi#e loss of body iron can cause iron

deficiency. (iminished absorption usually is due to an insufficient intake of dietary iron in

an absorbable form. Hemorrhage is the most common cause of e*cessi#e loss of body

iron% but it can occur with hemoglobinuria from intra#ascular hemolysis. 9alabsorption of

iron is relati#ely uncommon in the absence of small bowel disease $sprue% celiacdisease% regional enteritis& or pre#ious @I surgery.

Iron uptake in the pro*imal small bowel occurs by > separate pathways $see the image

below&. 0hese are the heme pathway and 5 distinct pathways for ferric and ferrous iron.

0hree pathways e*ist in enterocytes for uptake of 0hree pathways e*ist in enterocytes

for uptake of food iron. In the nited +tates and urope% most absorbed iron is deri#ed

from heme. Heme is digested enzymatically free of globin and enters the enterocyte as a

metalloporphyrin. )ithin the cell iron is released from heme by heme o*ygenase to pass

into the body as inorganic iron. 9ost dietary inorganic iron is ferric iron. 0his can enter

the absorpti#e cell #ia the integrin,mobilferrin pathway $I9P&.+ome dietary iron is

reduced in the gut lumen and enters the absorpti#e cell #ia the di#alent metal

transporter,4 $(90,4B("0,4B-ramp,5&. 0he proteins of both pathways interact within the

enterocyte with paraferritin% a large protein comple* capable of ferrireduction. *cess

iron is stored as ferritin to protect the cell from o*idati#e damage. Iron lea#es the cell to

enter plasma facilitated by ferroportin and hephaestin% which associate with an

apotransferrin receptor. 0he enterocyte is informed of body re/uirements for iron by

transporting iron from plasma into the cell using a holotransferrin receptor.

In -orth America and urope% one third of dietary iron is heme iron% but two thirds of

body iron is deri#ed from dietary myoglobin and hemoglobin. Heme iron is not chelated

and precipitated by numerous dietary constituent that render nonheme iron

nonabsorbable $see the image below&% such as phytates% phosphates% tannates%

o*alates% and carbonates. Heme is maintained soluble and a#ailable for absorption by

globin degradation products produced by pancreatic enzymes. Heme iron and nonheme


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iron are absorbed into the enterocyte noncompetiti#ely.

(ietary iron contains both heme and nonheme iron. (ietary iron contains both heme and

nonheme iron. =oth chemical forms are absorbed noncompetiti#ely into duodenal and

jejunal mucosal cells. 9any of the factors that alter the absorption of nonheme iron ha#e

little effect upon the absorption of heme iron because of the differences in their chemical

structures. Iron is released from heme within the intestinal absorpti#e cell by heme

o*ygenase and then transferred into the body as nonheme iron. actors affecting

#arious stages of iron absorption are shown in this diagram. 0he simplest model of iron

absorption must consider intraluminal% mucosal% and corporeal factors.

Heme enters the cell as an intact metalloporphyrin% presumably by a #esicular

mechanism. It is degraded within the enterocyte by heme o*ygenase with release of iron

so that it tra#erses the basolateral cell membrane in competition with nonheme iron to

bind transferrin in the plasma.

erric iron utilizes a different pathway to enter cells than ferrous iron. 0his was shown by

competiti#e inhibition studies% the use of blocking antibodies against di#alent metal

transporter,4 $(90,4& and beta>,integrin% and transfection e*periments using (90,4

(-A. 0his research indicated that ferric iron utilizes beta>,integrin and mobilferrin% while

ferrous iron uses (90,4 to enter cells.

)hich pathway transports most nonheme iron in humans is not known. 9ost nonhemedietary iron is ferric iron. Iron absorption in mice and rats may in#ol#e more ferrous iron

because they e*crete moderate /uantities of ascorbate in intestinal secretions. Humans%

howe#er% are a scorbutic species and are unable to synthesize ascorbate to reduce ferric

iron.

Cther proteins appear to be related to iron absorption. 0hese are stimulators of iron

transport $+0&% which are reported to increase the absorption of both ferric and ferrous

iron% and hephaestin% which is postulated to be important in the transfer of iron from

enterocytes into the plasma. 0he relationships and interactions among the newlydescribed proteins are not known at this time and are being e*plored in a number of

laboratories.

0he iron concentration within enterocytes #aries directly with the bodyDs re/uirement for

iron. Absorpti#e cells of iron,deficient humans and animals contain little stainable iron%


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whereas those of subjects who are replete in iron contain significantly higher amounts.

ntreated phenotypic hemochromatosis creates little stainable iron in the enterocyte%

similar to iron deficiency. Iron within the enterocyte may operate by up,regulation of a

receptor% saturation of an iron,binding protein% or both.

In contrast to findings in iron deficiency% enhanced erythropoiesis% or hypo*ia% endoto*in

rapidly diminishes iron absorption without altering enterocyte iron concentration. 0his

suggests that endoto*in and% perhaps% cytokines alter iron absorption by a different

mechanism. 0his is the effect of hepcidin and the balance of hepcidin #ersus

erythropoietin.

9ost iron deli#ered to nonintestinal cells is bound to transferrin. 0ransferrin iron is

deli#ered into nonintestinal cells #ia 5 pathways: the classical transferrin receptor

pathway $high affinity% low capacity& and the pathway independent of the transferrin

receptor $low affinity% high capacity&. Ctherwise% the nonsaturability of transferrin binding

to cells cannot be e*plained.

In the classical transferrin pathway% the transferrin iron comple* enters the cell within an

endosome. Acidification of the endosome releases the iron from transferrin so that it can

enter the cell. 0he apotransferrin is deli#ered by the endosome to the plasma for

reutilization. 0he method by which the transferrin receptorEindependent pathway

deli#ers iron to the cell is not known.

-onintestinal cells also possess the mobilferrin integrin and (90,4 pathways. 0heir

function in the absence of an iron,saturated transferrin is uncertainF howe#er% their

presence in nonintestinal cells suggests that they may participate in intracellular

functions in addition to their capability to facilitate cellular uptake of iron.

Pre#ious

-e*t +ection: tiology

'ead more about Iron (eficiency Anemia on 9edscape

'elated 'eference 0opics


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