Blood Typing Lab Test Simulation

Both A and B surface antigens are oligosaccharides (short sugar chains), differing in structure only at their terminal (last) sugars. They are also categorized as glycoproteins or glycolipids because they link to proteins or lipids in the RBC plasma membrane. A third ABO oligosaccharide, designated as H, appears on all RBCs but does not have a terminal sugar, nor is it antigenic.

A single gene (the ABO gene) controls an individual’s ABO blood type, and there are three alleles (or versions) of the gene: A, B, and O. An individual inherits an ABO allele from each parent, and the pair of alleles determines the individual’s blood type.

The A and B alleles are codominant. Thus, if both alleles are present, the RBCs express both antigens. The O allele is recessive, and either the A or the B allele will dominate.

The body makes antibodies to RBC surface antigens that it considers foreign. Usually, the body must first be exposed to a foreign antigen before antibody production begins. However, for ABO blood group antigens, prior exposure to incompatible blood is not required.

Instead, the generation of antibodies occurs naturally. Blood type A individuals make anti-B antibodies, and blood type B individuals make anti-A antibodies. Blood type AB individuals do not make anti-A or anti-B antibodies. Individuals with type O blood, who lack A and B antigens, make anti-A and anti-B antibodies.

The natural production of anti-A and anti-B antibodies begins a few months after birth, peaking around 5 to 10 years of age.

Anti-A and anti-B antibodies are of the IgM class in structure, each with ten binding sites. When encountering the opposing RBC surface antigens, these relatively large antibodies cause rapid agglutination (or clumping).

Unlike the ABO antigen, Rh antigens are transmembrane proteins that coil and loop along the RBC plasma membrane. The arrangement of amino acids on the extracellular loops determines the Rh type. Fifty Rh antigens are now recognized, but the D antigen is the most clinically significant.

The Rh+ allele is dominant over the Rh- allele, and about 85 percent of Americans are Rh-positive (Rh+). The rest of the American population is Rh-negative (Rh−)

Note that the Rh group is distinct from the ABO group, so that any individual may have or lack this Rh antigen, no matter their ABO blood type. When identifying a person’s blood type, a positive or negative is added to the ABO type to designate the Rh group. For example, A positive (A+) means ABO group A blood with the Rh antigen present, and AB negative (AB−) means ABO group AB blood without the Rh antigen.

Antibodies to the Rh antigen are produced only in Rh-negative individuals after exposure to incompatible Rh+ blood. The antibodies produced are mostly of the IgG class, each having only two antigen-binding sites.

Sensitization is the term given to exposure-activated antibody production. Rh sensitization most frequently happens with the birth of an Rh+ baby to an Rh− mother. Problems are rare in a first pregnancy because the baby’s Rh+ cells rarely cross the placenta (the organ of gas and nutrient exchange between the baby and the mother). However, the mother may become exposed to the baby’s Rh+ cells during or immediately after birth. Research has shown this occurs in 13−14 percent of such pregnancies.

After exposure, the mother’s immune system begins to generate anti-Rh antibodies. If the mother should conceive another Rh+ baby, the small IgG Rh antibodies can cross the placenta and enter the fetal bloodstream, destroying the fetal RBCs. This condition is known as hemolytic disease of the newborn (HDN) or erythroblastosis fetalis.  The result may be mild anemia. However, agglutination and hemolysis can be so severe that the fetus may die without treatment in the womb or shortly after birth.

A drug containing anti-Rh antibodies, called RhoGAM (Rh immune globulin), can temporarily prevent the development of Rh antibodies in the Rh-negative mother, thereby averting this potentially severe disease for the fetus. RhoGAM antibodies destroy any fetal Rh+ erythrocytes that may cross the placental barrier. The administration of RhoGAM typically occurs during weeks 26−28 of pregnancy and within 72 hours following birth. It has proven remarkably effective in decreasing the incidence of HDN. Earlier, we noted that the incidence of HDN in an Rh+ subsequent pregnancy to an Rh− mother is about 13–14 percent without preventive treatment. Since the introduction of RhoGAM in 1968, the incidence has dropped to about 0.1 percent in the United States.