Blood Typing

Procedure
1. Materials were prepared. Glass slide was wiped with clean tissue paper.
2. After washing hands with soap and water, fingertip was sterilized with alcohol and was
pricked with a sterile lancet.
3. 3 drops of blood was placed separately on a glass slide. Punctured area was then pressed with
cotton ball soaked in alcohol.
3. One drop of anti-A serum, anti-B serum and anti-D serum was added to each blood drop
respectively.
4. Serum and cells were mixed with an applicator stick. Agglutination was noted.
Genotype
OO
AA, AO
BB, BO
AB

Phenotype
O
A
B
AB

1. The ABO blood group Antigens are encoded by one genetic locus, the ABO locus. The ABO
Locus has three alternative (allelic) formsA, B, and O. A child receives one of the three
alleles from each parent, giving rise to six possible genotypes and four possible blood types
(phenotypes).
Erythrocytes have surface projecting H antigens that Are subject to
modification by an enzyme. The ABO locus, which is located on chromosome 9, contains
seven exons that span more than 18 kb of genomic DNA. Exon 7 is the largest and contains
most of the coding sequence. The ABO locus (chromosome 9), encodes a glycosyltransferase.
The ABO locus has three main alleleic forms: A, B, and O. The A allele encodes
a glycosyltransferase that bonds -N-acetylgalactosamine to the D-galactose end of the H
antigen, producing the A antigen. The B allele encodes a glycosyltransferase that bonds -Dgalactose to the D-galactose end of the H antigen, creating the B antigen. In the case of the O
allele, when compared to the A allele, exon 6 lacks one nucleotide (guanine), which results in
a loss of enzymatic activity. This difference, which occurs at position 261, causes
a frameshift that results in the premature termination of the translation and, thus,
degradation of the mRNA. This results in the H antigen remaining unchanged in the case of O
groups. (Note: nice to know nalang yung mga exon chuva diyan)
2. An antigen/agglutinogen is a substance, usually a membrane (ie surface) protein that
has the ability to provoke an immune response and the ability to react with the ANTIBODIES
(or cells) that result from the immune response.
3.

ANTIBODIES/immunoglobulins/agglutinin are protein molecules produced by certain

cells, as part of the immune response, against a
specific antigen. The ANTIBODIES
combine with (they latch onto) that specific antigen to neutralize, inhibit, or otherwise

destroy it. The combination of an ANTIBODY with the antigen for which it is specific is
called an antigen/ANTIBODY complex and the process of antigen/ANTIBODY-complexformation is called agglutination. Each IgG molecule consists of two heavy chains and two
light chains. The two heavy chains are linked to each other by disulfide bonds and each heavy
chain is linked to a light chain by a disulfide bond. In any given immunoglobulin molecule, the
two heavy chains and the two light chains are identical, giving an antibody molecule two
identical antigen-binding sites and thus the ability to bind simultaneously to two identical
structures.
Anti-A & Anti-B are not naturally occurring antibodies. They are not present at
birth and only appear 2-8/12 months. These antigens are Triggered by A & B antigens
in food and bacteria
4. Once antigen/ANTIBODY complexes form, they now stick out quite a long ways from the
cells surface and make the cells hang-up on each other as they pass by. This causes bunches
of these similar cells to clump-up, or agglutinate. Agglutination renders cells useless and
easier for macrophages to come along, engulf large quantities of them, and destroy/digest
them.
5. Organisms possess antibodies to antigens they DO NOT possess. Example: If you have
antigens A, C and E but NOT antigens B, D or F.then you would have Anti- bodies b, d, and
f. You would NOT, of course, have antibodies a, c nor e.because you would NOT want to
agglutinate your own cells!! Organisms may be born with many of these antibodies; they may
acquire some from nursing, or they may manufacture many more upon exposure to various
antigenic agents. (It is the activated B-lymphocytes,
maturing into plasma cells, that
manufacture these antibodies or Igs).
6. Landsteiners Law
Only applicable to the ABO system
2 laws :
(I)
1st Law: When an Agglutinogen is present on the membrane of RBC, the corresponding
agglutinin must be absent in the plasma of the person.
Eg: RBC contains A Ag; plasma must not contain agglutinin; otherwise there will be
death!
(i)
2nd Law: When the RBCs in an individual is devoid of agglutinogen, plasma shall
contain the corresponding agglutinin.
Eg: RBCs contain no B or A antigen. In the plasma of this individual; there must be antiA and anti-B agglutinins.
Therefore: A group blood must contain -agglutinin in the plasma and Group O blood must
contain both and agglutinins in the plasma.
7. Before blood cells can be transfused, they must be typed and cross-matched so that
transfusion reactions are avoided. People have different blood types and transfusion of
incompatible blood can be fatal. RBC cell membranes, just as do ALL body cells, bear highly
specific glycoproteins (antigens) on their external surfaces, which identify each of us as
unique from all others. One persons RBC proteins may be recognized as foreign if transfused
into someone with a different RBC type, and the transfused cells may be agglutinated and
destroyed. At least 30 varieties of naturally occurring RBC antigens are common in humans.
Besides these, perhaps 100 others occur in individual families (private antigens) rather
than in the general population. The presence or absence of each antigen allows each
persons blood cells to be classified into several different blood groups.
Antigens
determining the ABO and Rh blood groups cause vigorous transfusion reactions (destroying
foreign erythrocytes) when they are improperly transfused. Thus, blood typing for these
antigens is always done before blood is transfused. Additional antigens (such as the M, N,
Duffy, Kell, and Lewis factors) are mainly of legal or academic importance. Because these
factors cause weak or no transfusion reactions, blood is not specifically typed for them unless
the person is expected to need several transfusions, in which case the many weak transfusion
reactions could have cumulative effects. The most important blood groups for RBCs must be
typed are the ABO and Rh groups which will be described now.
8. the ABO blood groups are named based on the presence or absence of two antigens: type A
and type B. A person has blood type A if there are A antigens present on the RBCs
membranes; blood type B if there are B antigens present on the RBCs membranes, blood

type AB if there are BOTH A antigens and B antigens on the RBCs membrane, and type O if
there are NEITHER A antigens nor B antigens on the RBCs membranes. (Note: this is read
O, as in the letter O; but there is NO SUCH THING AS O antigens. Hence, this really
stands for zero, zilch, nada, none NO ANTIGENS!!)
9. The other half of the blood typing story involves the ANTIBODIES present in the plasma.
Again, as shown in a person has the ANTIBODIES opposite of the antigens he/she possesses.
That is, someone with type A blood has anti-B antibodies; while someone with type B blood
has anti-A antibodies; persons with type AB would have neither antibody, those with type O
blood would have BOTH anti-A and anti-B antibodies.
10. When mismatched blood is infused, a transfusion reaction occurs in which the donors
RBCs are attacked bythe recipients plasma antibodies. (Note: the donors plasma antibodies
may also be agglutinating the hosts RBCs, but they are so diluted in the recipients circulation
that this does not usually present a serious problem.) The initial event, agglutination of the
foreign RBCs, clogs small blood vessels throughout the body. During the next few hours, the
clumped RBCs begin to rupture or are destroyed by phagocytes, and their hemoglobin is
released into the bloodstreamwhen the rxn is exceptionally severe, the RBCs are lysed
almost immediately. These events lead to two easily recognized problems: (1) the O 2 carrying
capability of the transfused blood cells is disrupted, and (2) the clumping of RBCs in small
vessels hinders blood flow to tissues beyond those points. Less apparent, but more
devastating, is the consequence of hemoglobin escaping into the bloodstream. Circulating
hemoglobin passes freely into the kidney tubules where it may precipitate, blocking the
kidney tubules and causing renal shutdown. If shutdown is complete (aka acute renal failure),
the person may die! (Transfusion rxns can also cause fever, chills, low blood pressure, rapid
heartbeat, nausea, vomiting, and general toxicity; but in the absence of renal shutdown,
these rxns are rarely lethal. Tx of transfusion rxns is directed toward preventing kidney
damage by infusing alkaline fluids to dilute and dissolve the hgb and flush it out of the body.
Diruretics, which urine output, are also given.)