Blood group and typing Dr Shamshad Loni

1. Lecture 35:Blood Groups
Dr Shamshad

2. 1. Classify and describe different types of blood groups.
2. Restate the Landsteiner’s law.
3. Enumerate the uses of blood grouping .
4. Explain the importance of blood grouping in blood transfusion.
5. Relate the uses of blood grouping in hemolytic diseases of
newborn.
Objectives

3. Blood Groups Classification
Based on:-
The presence or absence of Antigens on the surface of RBCs
The antigens are :-
Integral proteins :- e.g., rhesus [Rh], Kell..,
Glycoproteins or glycolipids:- e.g., ABO.
About 33 blood gp systems representing over 300 antigens listed
by the International Society of Blood Transfusion(ISBT).

4. Blood group systems
Major system Minor system
P system
MN type
Rhesus system
ABO system
Familial blood groups:
Lewis,Duffy,Kell,
Bombay blood group
Based on presence of agglutinogens
Widely prevelant among population

5. Most commonly used

6. ABO Agglutinogens (Antigens)
 Present on surface of RBCs: A & B
 Genetic Determination of the Agglutinogens.
• Genetic locus has three alleles,
• Three different forms of the same gene.
• These alleles “A,” “B,” and “O,”
• Inherited two surface chromosomes
OO,OA,AA,BB, or AB.

7. Gene expression is not restricted to RBC they code for the
particular enzymes that catalyze formation of the carbohydrates.
But occurs universally in most:-
 Epithelial and endothelial cells,
 WBC ,platelets,
 Body tissue: lungs,pancreas,salivary glands,
Body fluids (Depending of presence or absence of Ags)
Secretors 80% Ags:Saliva,Sweat,Tears,
Semen,& Serum
Se genes:
(SeSe or Sese)
Nonsecretors 20% Ags:Absent Absent

8. Agglutinins (Antibodies)
Naturally occuring : anti-A, anti-B : Origin:IgM,IgG
• Cannot cross the placenta
• Cold antibodies : Act best at 5oC to 20oC
• Absent at birth:Appear within 2 mths after birth
• Reach peak b/w 5-10 years of age
• Triggered by A & B antigens
• Present in food and bacteria

9. If A agglutinogen absent in person’s RBCs,
antibodies, anti-A agglutinins develop in the plasma.
Also, If B agglutinogen is absent in the RBCs,
antibodies, anti-B agglutinins develop in the plasma.

11. Landsteiner’s law
1:If an agglutinogen (antigen) is present on the RBCs the
corresponding agglutinin (antibody) must be absent in the plasma
2:If an agglutinogen (antigen) is absent on the RBCs the
corresponding agglutinin (antibody) must be present in the plasma.
Note: The First part is applicable to all blood groups but the second
part is not necessary always , its true for ABO blood groups.

12. Rh System:
 Depends on presence/absence of Rhesus antigen D on surface of
RBCs
 Rh antigens: Dd,Cc,Ee
 D play important role.
Rh system D antigen on
surface of RBCs
% of population
Rh+ve Present 85% [American blacks 95%,African blacks 100%]
Rh-ve Absent 15%

13. Anti-D (Antibodies)
➢ Acquired type antibodies
➢ Belongs to IgG class
➢ Can cross the placenta
➢ Can be acquired by
• Transfusion of Rh -ve individual with Rh+ve blood
• Rh-ve pregnancy with Rh +ve fetus

14. Significance of blood grouping
➢ In blood transfusion
➢ In preventing hemolytic diseases
➢ Prevent incompatibility
➢ In medicolegal cases : paternal disputes
➢ Research: anthropological & racial studies
➢ Statistically divide the population
➢ Knowing susceptibility to diseases
➢ Case of infertility and rejection of organ transplant

15. O blood gp A blood gp B blood gp AB blood gp
47% 41% 9% 3%

16. Transfusion reaction
 Due to agglutination reaction of donar and recepient blood
 Agglutination of RBCs leads to activation of complement
stystem
 Agglutinated RBCs hemolysed and destroyed by WBCs
 Thus release of Hb, bilurubin and Iron pigments into circulatioin

17. Transfusion Reactions
 Acute hemolytic transfusion reaction
 Allergic reactions Immediate intravascular hemolysis
 Febrile, chills,
 Nonhemolytic transfusion reaction
 Transfusion-related acute lung injury
 Shock,
 Renal failure, Hepatic failure
 Jaundice
Acute Immunological Reaction

18. Transfusion Reactions
 Delayed hemolytic transfusion reaction
 Post transfusion purpura
Delayed immunologic reaction

19. Transfusion Reactions
 Volume overload
 Citrate toxicity
 Hypothermia
 Bacterial contamination
Acute Non immunological reaction

20. Transfusion Reactions
 Infectious disease transfusion
 Ex: Malaria, AIDS, Hepatitis B…
Delayed nonimmunologic reaction

21. Diference b/w transfusion reactions of ABO & Rh system
➢ In the ABO system, the plasma agglutinins responsible for causing
transfusion reactions develop spontaneously.
➢ In the Rh system, spontaneous agglutinins almost never occur.
● The person must first be massively exposed to an Rh antigen, such as by transfusion
of blood containing the Rh antigen, before enough agglutinins to cause a significant
transfusion reaction will develop.
● Anti-Rh antibodies can develop in sufficient quantities during the next 2 to 4 weeks to
cause agglutination of the transfused cells that are still circulating in the blood.
● Cells are then hemolyzed by the tissue macrophage system.

22. Hemolytic Disease of the Newborn/Erythroblastosis Fetalis
 Disease of the fetus and newborn child
 Characterized by agglutination and phagocytosis of the fetus’s
RBCs.
 The mother is Rh -ve and the father is Rh +ve
 The baby has inherited the Rh+ve antigen from the father, and
the mother develops anti-Rh agglutinins from exposure to the
fetus’s Rh antigen.

26. Effect of the Mother’s Antibodies on the Fetus.
➢ After anti-Rh antibodies (IgG) have formed in the mother, they
diffuse slowly through the placental membrane into the fetus’s
blood.
➢ There they cause agglutination of the fetus’s blood.
➢ Agglutinated RBCs then hemolyze, releasing Hb into blood.

27. ➢ The fetus’s macrophages then convert Hb into bilirubin, which
causes the baby’s skin to become yellow (jaundiced) and
anemia.
➢ The antibodies can also attack and damage other cells of the
body.

28. ➢ The hematopoietic tissues of the infant attempt to replace the
hemolyzed RBCs.
➢ The liver & spleen become greatly enlarged & produce RBCs .
➢ Due to rapid production of RBCs, nucleated blastic forms, are
passed from the baby’s bone marrow into the circulatory
system.

29. ➢ Hence due to the presence of these nucleated blastic RBCs the
disease is called erythroblastosis fetalis.
➢ Severe cases precipetation of bilirubin in the neuronal cells
[basal ganglia and motor areas of brain] causes permanent
mental impairment leading to kernicterus.

30. Fetus at risk
➢ About 3 % of second Rh-positive babies exhibit some signs of
erythroblastosis fetalis.
➢ About 10 % of third babies exhibit the disease.
➢ The incidence rises progressively with subsequent pregnancies.

31. Treatment of Neonates with Erythroblastosis Fetalis.
1: To replace the neonate’s blood with Rh-negative blood.
About 400 ml of Rh-ve blood infused over a period of 1.5 or more
hours while the neonate’s own Rh+ve blood is being removed.
This procedure may be repeated several times during the first few
weeks (about 6wks)of life, mainly to keep the bilirubin level low
and thereby prevent kernicterus.

32. Treatment of Neonates with Erythroblastosis Fetalis.
Thus anti-Rh agglutinins that had come from the mother will have
been destroyed

33. Treatment of mother with Erythroblastosis Fetalis.
2: Rh -ve mother is treated with Anti-D vaccination within
24 to 48 hours of parturation or abortion.
This prevents the formation of antibodies in the mother’s blood
Thus protecting the future pregnany and fetus from agglutination
reation.

34. Bombay blood group
1.Rare ABO group name "Bombay" first discovered to exist in
Bombay, India.
2. H gene is very rare, in which parents are blood relatives
3.RBC lacks ABH antigens and their sera contain anti-A and anti-
B and anti-H.
4.The anti-H would not be detected in the ABO group.