This document discusses blood types and transfusions. It explains that there are multiple blood group antigens, including the A, B, and Rh antigens. A person's blood type depends on which antigens are present on their red blood cells. Improper blood transfusions can cause agglutination and hemolysis reactions as antibodies attack mismatched antigens. The Rh system is also described, including how Rh-negative mothers can produce antibodies against a Rh-positive baby in later pregnancies, potentially causing hemolytic disease of the newborn. Prevention and treatment methods are mentioned.

1. BLOOD TYPES; TRANSFUSION;
TISSUE AND ORGAN TRANSPLANTATION
BY DR. MUHAMMAD UMAIR

2. 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.

3. O-A-B BLOOD TYPES
A and B Antigens—Agglutinogens
 Major 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

4. Relative Frequencies of the Different Blood Types.

5. AGGLUTININS (ANTIBODIES)
Anti-A agglutinins
 Anti-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.

6.  Origin
 gamma 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.

7. 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.

8. 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

9.  “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 lysis
Hemolysins. (IgM antibodies)

10. BLOOD TYPING
 PROCEDURE
 The 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”

11. 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

12. 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

13. ERYTHROBLASTOSIS FETALIS (“HEMOLYTIC DISEASE
OF 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 +ve
 Baby = 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

14.  Clinical Picture of Erythroblastosis.
 Anemic , jaundice, kernicterus.
 Hepatomegally and spleenomegally
 nucleated blastic red blood cells in blood picture
 Mental retardation
 Death
 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.