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    BLOOD GROUPS ANDTRANSFUSION

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    The A and B Antigens:

    The membranes of human red cells contain avariety of antigens called agglu t inogens. The

    most important and best known of these are A

    and B agglu t inogens, and individuals are

    divided into 4 major blood types

    O 47 %

    A 41 %

    B 9 %

    AB 3 %

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    The ABO blood groups are genetically determined.The type O gene is apparently functionless in

    production of a red cell antigen.

    Each of the other antigens is expressed by thepresence of a strong antigen on the surface of the

    red blood cell.

    Six genoty pes, or gene combinations result in fourphenotypes,or blood type expressions.

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    Two genes, one on each of two paired chromosomes,determine the A-B-O blood groups.

    These two genes are allelomorphic genes that can be anyone of three different types, but only one type on each

    chromosome.

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    Six possible combinations of genes (genotypes) are:

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    Inheritance of ABO blood typeAO AO

    A O A O

    AA AO AO OO

    AA AO

    A A O

    AA AO

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    Group A

    There are about 20 different known subgroups. A1

    and A2 individuals make up the vast majority of

    people with A blood type, all other subgroups equal

    less than 1% of A's.

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    A1 and A2 Subgroups

    These are the most important subgroups in the system.

    A1 equals approximately 80% of the entire A blood type

    population, and A2 makes up the remaining 20%, under

    current data. This means that all other subgroups must be

    rare.

    Differences between A1 and A2

    A1 red blood cells have about one million A antigens percell.

    A2 red cells have only 250,000 A antigens per cell, or one-fourth the amount that A1 cells have.

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    A1 and A2 Blood Cell and Antigens

    A1 Red Cell A2 Red Cell

    Red blood Cell Ceramide Glucose Galactose N-Acetyl Glucosamine Fucose N-Acetyl Galactosamine

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    Agglutinins

    Antibodies against agglutinogens are calledagglu t in ins (most of them are IgM and IgG molecules).

    Immediately after birth the quantity of agglutinins inthe plasma is almost zero. Two to 8 months after birth,

    the infant begins to produce agglutinins. The

    maximum titer is usually reached at 8 to 10 years of

    age.

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    Why are these agglu t in ins pro du ced in the indiv id uals

    who do n ot have the ant igenic subs trates in thei r

    RBCs?

    Probably small amounts of group A and B antigens

    enter the body in the food, in bacteria and in other

    waysand initiate the development of the anti-A or

    anti-B agglutinins.

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    The Agglutination Process in Transfusion Reactions:

    Dangerous hemolytic transfusion reactions occur whenblood is transfused into an individual with an

    incompatible blood type, ie. an individual who has

    agglutinins against the red cells in the transfusion.

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    The plasma in the transfusion is usually so diluted in the

    recipient that it rarely causes agglutination even when

    the titer of agglutinins against the recipients cells is

    high.

    However, when the recipient's plasma has agglutinins

    against the donor's red cells, the cells agglutinate and

    hemolyze

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    Hemolysis occur as ear ly hemolysis (activation ofcomplement system) or as a result of phagocytosis of

    agglutinated cells(la te hemo lysis).

    Free hemoglobin is liberated into the plasma. Theseverity of resulting transfusion reaction may vary from

    an asymptomaticminor rise in the plasma bilirubin level

    tosevere jaundiceandrenal tubular damage(caused in

    some way by the products liberated from hemolyzedcells), with anur ia and d eath.

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    Blood Typing:

    Blood typing is performed by mixing an individual's

    red cells with appropriate antisera on a slide and

    seeing if agglutination occurs.

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    Persons with type AB blood areun iversal recipients

    Type O individuals areuniversal donors

    This does not mean, however, that blood should ever be transfusedwithout being cross matched except in the most extreme

    emergencies, since the possibility of reactions or sensitization due

    to incompatibilities other than ABO incompatibilities always exist.

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    In cros s-matchin g,donor red cells are mixed withrecipient plasma on a slide and checked for

    agglutination.It is advisable to check the action of the donor's

    plasma on the recipient cells even though this is

    rarely a source of trouble.

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    The Rh Blood Types:

    Along with the A-B-O system the most important othersystem in the transfusion of bloods is the Rh system.

    The Rh blood group system consists of 50 definedblood-group antigens

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    There are six common types of Rh antigens each ofwhich is called an Rh factor. These types are

    designatedC, D, E, c, d, and e. A person who has a C

    antigen will not have the c antigen, but the person

    missing the C antigen will always have the c antigen.

    The type D antigen is widely prevalent in thepopulation and it is also considerably more antigenic

    than other Rh antigens.

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    Therefore anyone who has this type of antigen is

    said to beRh posi t ive,whereas those persons who

    do not have the type D antigen are said to be Rh

    negative

    Approximately 85 % of all whites are Rh positive,

    and 15 percen t, Rh negative.

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    The one major difference between the A-B-O system and

    the Rh system:

    - In the A-B-O system , the agglutinin s respons ible

    for causing transfus ion reactions develop s pontaneously,

    whereas in the Rh system spon taneous agglutinins almos t

    never occur. Instead th e person must first be massively

    exposed to an Rh antigen.

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    D-negative individuals (Rh-) who have received atransfusion of D-positive blood (even years previously)

    can have appreciable anti-D titers and thus may

    develop transfusion react ions wh en transfu sed again

    wi th D-posi t ive b lood.

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    Hemolytic Disease of Newborn:

    Another complication due to Rh incompatibility arises when anRh-

    negative mothercarries an Rh-posit ive fetus. Small amounts of fetal

    blood leak into the maternal circulation at the time of delivery, and

    some mothers develop significant titers of anti-Rh agglutininsduring the postpartum period.

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    During the next pregnancy, the mother's agglutinins cross theplacenta to the fetus. In addition, there are some cases of

    fetal maternal hemorrhage during pregnancy and

    sensitization can occur during pregnancy.

    In any case, when anti-Rh agglutinins cross the placenta toan Rh positive fetus, they can cause hemolysis and various

    forms of hemolyt ic disease of newborn (erythroblastosis

    fetalis).

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    +

    +

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    About 50% of Rh-negative individuals are sensitized

    (developed an anti-Rh titer) by transfusion of Rh-positive

    blood.

    Since sensitization of Rh-negative mothers by carrying an

    Rh-positive fetus generally occurs at birth, the first child is

    usually normal.

    However, hemolytic disease occurs in about 17% of the Rh-

    positive fetuses born to Rh-negative mothers who have

    previouslypregnant to Rh-positive fetuses.

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    It is possible to prevent sensitization from occurring the firsttime by administering a single dose ofant i -Rh ant ibo diesin the

    form of Rh immune globul in (gamma-globul in-contain ing Rh

    ant ibody), Rh D-immune globulin during the post partum period.

    Such passive immunization does not harm the mother and has

    been demonstrated to prevent active antibody formation by the

    mother.

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    After sensitization has developed, the immune globulinis of no value.

    Treatment with a small dose during pregnancy will alsoprevent sensitization due to fetal maternal hemorrhage

    before delivery.

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    The Physiologic Jaundice:

    In the first week of life, about 60% of term and 80% of pretermneonates are jaundiced. This physio log ic jaundice appears in

    term infants on the second o r th i rd days of l i fe, and bilirubin

    levels peak at less than 12 mg/dl.

    This complication probably is

    related to the increased fetal

    red cell breakdown and inability

    of the immature liver to conjugate

    bilirubin.

    Exposure of the skin to white l ight

    converts bi l i rubin to lumirubin, which

    has a shorter half l i fe than bi l i rubin

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    When jaundice appears at atypical t imes (i .e., at bi r th oafter 1 week) the cause is sought to prevent exaggerated

    hyperbilirubinemia and its toxic consequences. Many

    factors cause elevated bilirubin levels in the neonate:

    Breast feeding (4-7 days after birth, fatty acids in milkinhibit bilirubin conjugation and there is an increased

    absorption of bilirubin in the duodenum).

    Hemo lyt ic disease of n ewbornHypoxiaInfect ionsAcidos isAlbumin bind ing drugsLiver dis easeBi l iary obstruct ion

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    Apheresis (ay-fur-ee-sis) is a special kind of blood donation that allows

    a donor to give specific blood components, such as platelets

    After donating blood, you replace these red blood cells within four

    weeks. It takes eight weeks to restore the iron lost after donating.

    Cancer, transplant and trauma patients, and patients undergoing open-

    heart surgery require platelet transfusions to survive.

    There is no substitute for human blood.

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