1. Karl Landsteiner discovered the main blood group systems (ABO and Rh) in 1900 and 1940 respectively. The ABO system categorizes blood into A, B, AB and O groups based on antigens on red blood cells. 2. Blood typing and cross-matching are important to ensure safe and compatible blood transfusions. Transfusing incompatible blood can cause hemolytic or allergic reactions in the recipient. 3. Other minor blood group systems have been discovered including MNS, Duffy, Kell and Lewis systems which are important for transfusion medicine and anthropological research. Understanding blood groups is crucial for blood banking and preventing diseases like hemolytic disease of the newborn.

1. Blood Groups

2. I. INTRODUCTION
II. BLOOD GROUP SYSTEMS
III. LANDSTEINER’S LAW
IV. CLASSICAL ABO BLOOD GROUPING SYSTEM
V. RHESUS BLOOD GROUPING SYSTEM
VI. CLINICAL IMPLICATION OF BLOOD GROUPING
VII. BLOOD TRANSFUSION
INDEX

3. Austrian Karl Landsteiner(1900) discovered -
•Human blood possess different antigenic and immune properties
•Blood clumping was an immunological reaction.
Nobel Prize in Physiology and Medicine in 1930.
Introduction

4. CLASSIFICATION-
Major blood group system
Minor blood group system
Familial blood group system-
Kell, Duffy, Lutheran, Lewis, Deigo, kidd Etc.
Blood Group System

5. LANDSTEINER’s LAW-
1.If an agglutinogen is present on red blood cell membrane ,the corresponding agglutinin
must be absent in the plasma.
2.If an agglutinogen is absent on red blood cell membrane, then corresponding agglutinin
must be present in the plasma.

6. I. Discovery
II. Antigen and Antibodies
III. Inheritance
ABO Blood Group System

7. • Karl Landsteiner(1900) classified human blood into A,B,O groups.
• Von Decastello and Sturli (1902) discovered AB blood group.
• Von Dungern and Hirszfeld(1911) divided group A into 2 subgroups A1 and A2.
Discovery

8. Appear in the sixth week of fetal life.
Present on red cell membrane and in other tissues like salivary glands, pancreas, kidney
EXCEPT CNS also in body fluids.
H antigen is also present usually in all individuals.
Antigens

9. • Basic precursors for ABH antigens.
• Type-1 chain beta (1-3) linkage
• Type-2 chain beta (1-4) linkage
Biochemistry
Glucose
Galactose
Nacetylglucosamine
Galactose
Precursor
Substance
(stays the
same)

10. Formation of H Antigen
Glucose
Galactose
N-
acetylglucosamine
Galactose
H antigen
RBC
Fucose
L Fucosyl Transferase Enzyme (product of H gene)

11. Glucose
Galactose
N-
acetylglucosamine
Galactose
RBC
Fucose N-
acetylgalactosamine
N-acetylgalactosaminyl Transferase (product of A gene)
Formation of the A antigen

12. Formation of the B antigen
Glucose
Galactose
N-
acetylglucosamine
Galactose
RBC
Fucose Galactose
D-galactosyl Transferase(product of B gene)

13. O GENE
Group O Group A
Fewer
H
antigen
sites
A
A A
AA
Many H antigen sites
Why do Group O individuals have more
H antigen than the other groups?
The O gene is a silent allele. It does not alter the
structure of the H substance….that means more
H antigen sites.

14. • Mostly IgM type.
• Produced by bone marrow and lymph gland cells .
• Known as cold antibodies.
Anti-A and Anti-B agglutinins
Titre of antibodies

15. Why antibodies produced in people who do not have the
respective antigens in their red blood cells?
Immune system form antibodies against the antigens recognised as non-self(i.e. not
present in the own body).

16. Alpha -agglutinins- alpha-1 and alpha -proper.
20% 40% 8% 32%
Group A has 2 subgroups -A1 and A2.
Group AB -A1B and A2B.
Types of ABO Blood Group

17. Inheritance of ABO blood group
Follows Mendelian Law.
In 1924, Felix Bernstein proposed presently accepted theory.
Heterozygous: AO or BO
Homozygous: AA or BB

18. Mom Dad Offsprin
g Blood
Group
AA BB 100%
AB
BO OO 50%
each of
B or O
OO OO 100% O
OO AO 50%
each of
A or O
Examples-

19. Genotype And Phenotype
BLOOD
GROUP
ANTIGEN ANTIBODY GENES at
9q34.1
GENES at 19
q13.2
A A Anti-B AA,AO HH
B B Anti-A BB,BO HH
AB AB None AB HH
O Neither(H) Anti-A and
anti-B
OO HH
Bombay
phenotype
No ABH
Antigen
Anti-A
,Anti-B,
Anti -H
any hh

20. The Rhesus Blood Group System
I. Discovery of Rh system
II. Antigen and antibodies
III. Inheritance
IV. Haemolytic disease of newborn

21. History of the Rh System
Levine and Stetson(1939) described a hemolytic transfusion reaction in an obstetric
patient following delivery of stillborn infant.
An antibody was isolated from the mother’s serum. It was postulated that the fetus and the
father possessed a common factor that the mother lacked.

22. While the mother carry the fetus, the mother was exposed to this factor and developed
antibody against the transfused red cells from the father and resulted in transfusion
reaction.
At that time ,the responsible antibody was not named.
Landsteiner and Wiener(1940) injected RBC’s of rhesus monkeys in rabbits- developed
antibodies.
The antibody was named as anti-Rh.

23. When resulting antiserum was mixed with human RBC’s, then agglutination occurred.
The RBC antigen responsible for this reaction was called as Rh factor.
The antibody discovered by Levin and Stetson in the mother was subsequently re-
examined and found identical in activity as the anti-Rh antibody found by Landsteiner and
Weiner.
So this work led to discovery of Rh system.

24. Anti-rhesus formed by the animals was renamed anti-LW (Landsteiner and Wiener).
Fisher and Race(1943 and 1944) discovered C, E, c, e Ag and their corresponding antibodies
anti-C , anti -E ,anti- c ,anti -e.

25. Rh Antigens
• Rh system involves 6 Rh
antigens D,d,C,c,E,e
Rh positive
Presence of rh D
85% occurrence
Rh negative
Absence of rhD
15% Occurrence
Integral membrane proteins with an active phoshpholipid component.
Present on red blood cells.
D antigen is commonest and most immunogenic.

26. • IgG type.
• Known as warm antibodies.
• Produced by exposure to foreign Rh antigen .
Rh Antibodies

27. • D Ag is inherited as a dominant gene D.
• Genotype of individual may be:
DD
Dd
dd
Inheritance

28. Examples-
Heterozygous Rh +
Homozygous Rh-
50% hetrozygous rh+
50% homozygous rh-

29. • ABO Incompatibility- immediate reaction as antibodies are naturally present.
• Rh Incompatibility-
First exposure-
Primary response
Immunological memory
Second exposure-
Immediate and severe response.
Incompatibility

30. Agglutination
No complications
But Rh antibody is produced
To Rh negative personFrom Rh positive person
Rh antigen reacts with Rh antibody
First transfusion
Second transfusion

31. Haemolytic Disease Of Newborn

32. I.Erythroblastosis fetalis-
• Erythroblastosis
Mechanism- Rapid production of red blood cells by haematopoeitic tissues of baby in order
to replace haemolysed RBC’s.
• Anaemia
II.Icterus gravis neonatorum
III.Kernicterus
IV.Hydrops fetalis
Manifestations

33. HYDROPS FETALIS
ERYTHROBLASTOSIS
FETALIS
ICTERUS GRAVIS
NEONATORUM
KERNICTERUS

34. I. Anti-D Prophylaxis –
• Based on principle antibody mediated immunosuppression.
• Inject anti-D antibody in mother soon after child birth.
• Fetal Rh typing, then give anti- D antibody to expectant mother between 28 to 30 weeks.
II. Exchange transfusion
Prevention And Treatment

35. • THE Ii SYSTEM-
Weiner et al (1956)
2 antigens –I and i
Difference-
• At birth , RBC’s are rich in i Ag ,not I Ag.
• In first second years of life, gradual changeover from i to I.
Other Blood Group Systems

36. • THE DUFFY SYSTEM
Cutbush , Mollison and Parkin(1950).
System has 3 blood groups-Fya ,Fyb and Fyab.
Fyab blood groups are resistant to plasmodium vivax whereas Fya and Fyb are susceptible
to vivax malaria.
Cont…

37. • KELL SYSTEM-
Coombs ,Mourant , Race(1946).
Antigen - K
Rare In India(.3 To .7%)
• P BLOOD GROUP SYSTEM-
Landsteiner and Levine in(1927).
2 blood groups- P positive
P negative
Cont…

38. • MN SYSTEM-
Landsteiner and Levine(1927).
Required for-
• Paternity tests
• Anthropological and genetic studies.
Cont…

39. • LEWIS SYSTEM-
Mourant and Andresen(1946,1948)
2 antigens- Lea and Leb.
Ceppelline(1955) showed, Lea substance in saliva was controlled by dominant gene Le
and its allele le.
Not real antigens because they are present in plasma and saliva, RBCs acquire by
adsorption from plasma.
Cont…

40. I. In blood transfusion.
II. In preventing HDN due to Rh Incompatibility.
III. In paternity disputes.
IV. In medicolegal cases.
V. In knowing susceptibility to diseases.
Clinical Implications

41. I. Indications
II. Donor and Recepeints
III. Precautions
IV. Hazards
Blood Transfusion

42. I. Blood loss.
II. For quick restoration of Hb.
III. Exchange transfusion.
IV. Blood diseases like- aplastic anaemia, leukaemia,hemophilia,purpurae,clotting defects.
V. Acute poisoning.
VI. Acute infections or fever when gamma globulin is needed.
VII. Shock
Indications

43. • Donor selection-
I. Healthy and age between 18 to 60 years.
II. Haemoglobin > 12 gm%
III. Weight more than 45 kg.
IV. Females should not be Pregnant, lactating and menstruating.
V. No diseases like AIDS, Viral Hepatitis ,Malaria, Syphilis.
VI. No past H/O jaundice , HTN,TB, and cardiac diseases.
Donor And Recepient

44. Blood transfusion-who can receive
blood from whom?
Blood
Group
Antigens Antibodies Can give
blood to
Can
receive
blood from
AB A and B None AB AB, A, B, O
A A B A and AB A and O
B B A B and AB B and O
O None A and B AB, A, B, O O

45. • For safe and compatible blood transfusion-
• ABO and Rh typing
• Cross matching
• Antibody screening
Investigations

46. Determination Of Blood Group
Blood Typing

47. Under Microscope
Human RBC before (left) and after (right) adding serum containing antibodies.

48. II. Cross Matching-
Major cross matching -Donor’s RBCs are mixed with recepient’s plasma.
Minor cross matching- Recepients RBC’s are mixed with donor’s plasma.
When no agglutination then only donors blood can be transfused.
Cross Matching

49. III. Antibody Screening –
Antibody Screening

50. IV. Rh positive blood should never be transfused to Rh negative blood.

51. V. Check blood bag for correct label.
VI. Transfuse blood at slow rate(not >20 drops/min) under proper aseptic measures.
VII. Careful watch on recepient’s condition.
VIII. Stop transfusion if reaction occurs.

52. • Hemoglobinemia
• Haemoglobinuria
• Chestpain and chills
• Fever
• Shock
• Renal failure
• Death
Haemolytic
• Cardiorespiratory symptoms
• Acute left ventricular failure
• Immunological reaction
• Pulmonary edema
• Allergic reactions.
• Transmission of diseases.
• Thrombophlebitis,air embolism.
Non- Haemolytic
Transfusion reactions