0% found this document useful (0 votes)
15 views28 pages

Blood Groups

Uploaded by

Paul King
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
15 views28 pages

Blood Groups

Uploaded by

Paul King
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 28

BLOOD GROUPS

PIO 201
MONDAY 2-4 PM
OUTLINE
❑ ABO and Rh blood group systems

❑ Hazards and complications of blood


transfusions
OBJECTIVES
At the end of this class, you should be able
to:
❑List and differentiate the blood groups
❑Explain the importance of cross matching
and blood transfusion
Antigens and Antibodies
❑ Antigens are substances that the body does not recognize
as belonging to the “self” which trigger a defensive
response from the leukocytes of the immune system.
▪ Generally large proteins, but may include carbohydrates, lipids, and
nucleic acids.
❑ Antibodies (immunoglobulins) are proteins produced by
certain B lymphocytes (plasma cells).
▪ Attach to the antigens on the plasma membranes of the transfused
erythrocytes and cause them to adhere to one another.
Antigens and Antibodies
❑ Antigens: isoantigens or agglutinogens
❑ Antibodies: isoantibodies or agglutinins
❑ Following a transfusion of incompatible blood, erythrocytes
with foreign antigens appear in the bloodstream and trigger
an immune response.
❑ More than 50 antigens have been identified on erythrocyte
membranes, but the most significant are classified in two
groups:
▪ the ABO blood group
▪ Rh blood group.
Transfusion Reactions
• Antibodies attach to the antigens on the plasma membranes
of the transfused erythrocytes and cause them to adhere to
one another.
• Because the arms of the Y-shaped antibodies attach randomly
to more than one nonself erythrocyte surface, they form
clumps of erythrocytes - Agglutination.
• These clumps block small blood vessels throughout the body,
depriving tissues of oxygen and nutrients.
• As the clumps are degraded (hemolysis) their hemoglobin is
released into the bloodstream.
• This hemoglobin travels to the kidneys but excess hemoglobin
released can easily overwhelm the kidney’s capacity to clear
it, and the patient can quickly develop kidney failure.
Definition of Terms
❑ Agglutination: collection of separate RBCs into clumps or
masses

❑ Agglutinogen: antigen, on the surface of the erythrocyte

❑ Agglutinin: antibody, found in the plasma

❑ Hemolysis: is the degradation of the erythrocyte clumps


ABO Blood Group
❑ Discovery: Karl Landsteiner, an Austrian scientist, in 1901.
❑ Determined by the presence or absence of specific marker
molecules on the plasma membranes of erythrocytes
❑ ABO blood typing designates the presence or absence of
just two antigens, A and B.
❑ Both are glycoproteins.
▪ People whose erythrocytes membrane surface have A antigens are
blood type A,
▪ Those whose erythrocytes have B antigens are blood type B.
▪ People with both A and B antigens are blood type AB.
▪ People with neither A nor B antigens are designated blood type O.
❑ ABO blood types are genetically determined.
ABO Blood Group
• Normally the body must be exposed to a foreign antigen
before an antibody can be produced.
• This is not the case for the ABO blood group. Individuals
with:
– Type A have preformed antibodies to the B antigen
circulating in their plasma. Anti-B (β-antibody) antibodies, will
cause agglutination and hemolysis if they ever encounter
erythrocytes with B antigens.
– Type B blood have pre-formed anti-A (α-antibody) antibodies.
– Type AB blood having both antigens do not have preformed
antibodies to either of these.
– Type O blood lack antigens A and B on their erythrocytes, but
both anti-A and anti-B antibodies circulate in their plasma.
LANDSTEINER LAW
❑ The law states that if a particular
agglutinogen (antigen) is present in the
RBCs, corresponding agglutinin (antibody)
must be absent in the serum.
❑ If a particular agglutinogen is absent in
the RBCs, the corresponding agglutinin
must be present in the serum.
Antigen and Antibody present in ABO blood groups
Rh Blood group
❑ Rh factor is an antigen present in RBC.
❑ Discovered by Landsteiner and Wiener in Rhesus monkey
and hence the name ‘Rh factor’.
❑ The Rh blood group is classified according to the
presence or absence of a second erythrocyte antigen
identified as Rh. Known is designated D.
❑ Those who have the Rh D antigen present on their
erythrocytes are described as Rh positive (Rh+) and
those who lack it are Rh negative (Rh−).
Rh Blood group
❑ When identifying a patient’s blood type, the Rh group is
designated by adding the word positive or negative to the
ABO type.
▪ A positive (A+) means ABO group A blood with the Rh
antigen present
▪ AB negative (AB−) means ABO group AB blood without
the Rh antigen.
❑ In contrast to the ABO group antibodies, which are
preformed, antibodies to the Rh antigen are produced only
in Rh− individuals after exposure to the antigen -
Sensitization.
Rh Blood group
• This occurs following a transfusion with Rh-incompatible
blood or with the birth of an Rh+ baby to an Rh− mother
• The Rh group is distinct from the ABOs, in spite of their
ABO blood type, there is a presence or absence of this Rh
antigen.
• Rh group system is also different from ABO group system
because, the antigen D does not have corresponding
natural antibody (anti-D).
• If Rh+ blood is transfused to a Rh− person, anti-D is
developed in that person.
• However, there is no risk of complications if the Rh +
person receives Rh− blood.
DETERMINATION OF ABO GROUP
• A.k.a blood grouping, blood typing or blood matching.
• Agglutination occurs if an antigen is mixed with its
corresponding antibody.
– A antigen is mixed with anti-A or when B antigen is mixed with
anti-B.
• To determine the blood group of a person, a suspension of
one’s RBC and testing antisera are required.
• Suspension of RBC is prepared by mixing blood drops with
isotonic saline (0.9%)
• Test sera are: Antiserum A (anti-A or α-antibody),
Antiserum B, (anti-B or β-antibody)
DETERMINATION OF ABO GROUP
• Method:
– One drop of antiserum A is placed on one end of a glass
slide (or a tile) and one drop of antiserum B on the
other end.
– One drop of RBC suspension is mixed with each
antiserum. The slide is slightly rocked for 2 minutes.
– The presence or absence of agglutination is observed by
naked eyes.
– Presence of agglutination is confirmed by the presence
of thick masses (clumping) of RBCs.
– Absence of agglutination is confirmed by clear mixture
with dispersed RBCs.
MATCHING AND CROSS-MATCHING

❑ Blood typing is a laboratory test done to determine the blood


group of a person.
❑ When the person needs blood transfusion, another test called
cross-matching is done after the blood is typed.
❑ Cross-matching is done by mixing the serum of the recipient
and the RBCs of donor.
❑ Cross-matching is always done before blood transfusion.
❑ Matching = Recipient’s RBC + Test sera.
Cross-matching = Recipient’s serum + Donor’s RBC.
TRANSFUSION REACTIONS DUE TO ABO
INCOMPATIBILITY
❑ In mismatched transfusion, the transfusion reactions occur
between donor’s RBC and recipient’s plasma.
❑ If the donor’s plasma contains agglutinins against
recipient’s RBC, agglutination does not occur because these
antibodies are diluted in the recipient’s blood.
❑ But, if recipient’s plasma contains agglutinins against
donor’s RBCs, the immune system launches a response
against the new blood cells.
❑ Donor RBCs are agglutinated resulting in transfusion
reactions.
❑ The reactions may be mild causing only fever and or may
be severe leading to jaundice, renal failure, cardiac shock
and death.
TRANSFUSION REACTIONS DUE TO Rh
INCOMPATIBILITY
❑ A Rh- person receives Rh+ for the first time, and isn’t
affected much as the reactions don’t occur immediately.
❑ But the Rh antibodies develop within one month.
❑ The transfused RBCs, which are still present in the recipient’s
blood, are agglutinated but lysed by macrophage.
❑ So, a delayed transfusion reaction occurs but usually mild and
does not affect the recipient. However, antibodies developed
in the recipient remain in the body forever.
❑ So, when this person receives Rh+ blood for the 2nd time, the
donor RBCs are agglutinated and severe transfusion reactions
occur immediately.
❑ These reactions are similar to the reactions of ABO
incompatibility
ERYTHROBLASTOSIS FETALIS
❑ Hemolytic disease of the newborn.
❑ Hemolytic disease is the disease in fetus and newborn,
characterized by abnormal hemolysis of RBCs.
❑ It is due to Rh incompatibility
❑ Hemolytic disease leads to erythroblastosis fetalis.
❑ Erythroblastosis fetalis is a disorder in fetus, characterized
by the presence of erythroblasts in blood.
❑ When a mother is Rh negative and fetus is Rh positive,
usually the first child escapes the complications of Rh
incompatibility.
ERYTHROBLASTOSIS FETALIS
❑ Problems are rare in a first pregnancy, since the baby’s Rh+
cells rarely cross the placenta
❑ At the time of parturition, the Rh antigen from fetal blood
may leak into mother’s blood because of placental
detachment.
❑ During postpartum period, the mother develops Rh
antibody in her blood.
❑ With the 2nd Rh+ fetus, the Rh antibody from mother’s
blood crosses placental barrier and enters the fetal blood.
❑ This causes agglutination of fetal RBCs resulting in
hemolysis.
ERYTHROBLASTOSIS FETALIS
❑ To compensate for this hemolysis, there is rapid production
of RBCs, not only from bone marrow, but also from spleen
and liver.
❑ Many large and immature cells in proerythroblastic stage
are
released into circulation.
❑ The agglutination and hemolysis can be so severe that
without treatment the fetus may die in the womb or shortly
after birth.
❑ Ultimately due to excessive hemolysis severe complications
develop: Severe anemia, Hydrops fetalis, Kernicterus
ERYTHROBLASTOSIS FETALIS

❑ A drug known as (RhoGAM) Rh immune globulin, can


temporarily prevent the development of Rh antibodies in the
Rh− mother averting this fetal disease.
❑ RhoGAM antibodies destroy any fetal Rh+ erythrocytes that
may cross the placental barrier.
❑ RhoGAM is normally administered to Rh− mothers during
weeks 26−28 of pregnancy and within 72 hours following
birth.
❑ The introduction of RhoGAM was in 1968.
References

❑ https://open.oregonstate.education/aandp/chapter/18-6-blo
od-typing/

❑ K Sembulingam. Essentials of Medical Physiology. Blood


Clotting Chapter 20

You might also like