BLOOD TYPES; TRANSFUSION;

TISSUE AND ORGAN TRANSPLANTATION

BY DR. MUHAMMAD UMAIR

BLOOD TYPES Multiplicity of Antigens in the Blood Cells.

At least 30 commonly occurring antigens O-A-B system and the Rh system.

Antigenicity & Immune Reactions of Blood The bloods of different people have different antigenic and immune properties, so that antibodies in the plasma of one blood will react with antigens on the surfaces of the red cells of another blood type causing a transfusion reaction.

O-A-B BLOOD TYPESA and B Antigens—AgglutinogensMajor O-A-B Blood Types. depend on the

presence or absence of A and B agglutinogens.

Genetic Determination of the Agglutinogens. Two genes, one at a time on each of two

paired chromosomes Any one of three types

Type O (functionless)Type A or Type B

Relative Frequencies of the Different Blood Types.

AGGLUTININS (ANTIBODIES)

Anti-A agglutininsAnti-B agglutinins

Type O blood, containing no agglutinogens,does contain both anti-A and anti-B agglutinins

Type A blood contains type A agglutinogens and anti-B agglutinins

Type B blood contains type B agglutinogens and anti-A agglutinins.

Type AB blood contains both A and B agglutinogens but no agglutinins.

Origingamma globulins produced in bone marrow and

lymph gland cells Mostly IgM and IgG

QUESTION: Why are these agglutinins produced in people who do not have the respective agglutinogens in their red blood cells ?

The answer to this is that small amounts of type A and B antigens enter the body in food, in bacteria, and in other ways, and these substances initiate the development of the anti-A and anti-B agglutinins.

AGGLUTININS TITER AT DIFFERENT AGES.

Immediately after Birth its almost zero.

Two to 8 months — begins to produce agglutinins.

8 to 10 years — maximum titer.

gradually declines with aging.

AGGLUTINATION PROCESS IN TRANSFUSION REACTIONS

In mismatched blood transfusion, the agglutinins of recipient’s blood are mixed with the agglutinogens of the donar RBCs.

Agglutinis having binding sites attach to RBCs

This binding causes the RBCs to clump.these clumps plug small blood vessels

throughout the circulatory system

“Delayed Hemolysis” ( during hours to days)physical distortion of the cells or Destruction of the agglutinated cells

membranes, releasing hemoglobin into the plasma

‘‘Acute Hemolysis’’activation the complement system, which

releases proteolytic enzymes (the lytic complex)

Far less common because it requires high titer of antibodies for lysisHemolysins. (IgM antibodies)

BLOOD TYPING

PROCEDUREThe red blood cells are first separated from the

plasma and diluted with saline.One portion is then mixed with anti-A agglutinin

and another portion with anti-B agglutinin. After several minutes, the mixtures are observed

under a microscope.An antibody antigen reaction: If the red blood

cells have become clumped—“agglutinated”

RH BLOOD TYPES

O-A-B system VS the Rh system massive exposure to an Rh antigen(blood transfusion)

before enough agglutinins production to cause a significant transfusion reaction.

Rh Antigens Rh factor (six common types of Rh antigens) C,D, E, c, d, and e A person who has a C antigen does not have the c antigen

and vice versa each person has one of each of the three pairs of antigens. Type D antigen— widely prevalent and more antigenic

“Rh-Positive” and “Rh-Negative” People. +ve = having D antigen -ve = no D anitgen

RH IMMUNE RESPONSE Formation of Anti-Rh Agglutinins.

When RBCs containing Rh factor are injected into Rh-negative person—(with no Rh factor)

Develop slowly.Reach maximum conc. In about 2 to 4 months.With multiple exposures to the Rh factor, an Rh-

negative person eventually becomes strongly “sensitized” to Rh factor.

Characteristics of Rh Transfusion Reactions.Rh +ve blood transfusion

in previously unexposed Rh –ve person = no immediate but delayed reaction ( after 2-4 weeks ) due to anti Rh antibodies development

In previously exposed Rh –ve person = immediate and severe

ERYTHROBLASTOSIS FETALIS (“HEMOLYTIC DISEASEOF THE NEWBORN”)

disease of the fetus and newborn child characterized by agglutination and phagocytosis of the fetus’s red blood cells.Mother = Rh -ve Father = Rh +veBaby = Rh +ve

mother develops anti-Rh agglutinins from exposure to the fetus’s Rh antigen.

Which then diffuse through the placenta into the fetus and cause red blood cell agglutination.

Incidence of the Disease rises progressively with subsequent pregnancies

Clinical Picture of Erythroblastosis.Anemic , jaundice, kernicterus.Hepatomegally and spleenomegallynucleated blastic red blood cells in blood pictureMental retardationDeath

Treatment of the Erythroblastotic Neonate.Exchange Transfusion

Prevention of Erythroblastosis Fetalis.Rh immunoglobulinglobin, an anti-D antibody at 28 to 30 weeks of gestation and after delivery inhibit antigen-induced B lymphocyte antibody

production in the expectant mother.anti-D antibody also attaches to D antigen sites on

Rh-positive fetal RBCs hence interfere with immune response to D antigen.