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Lecture 35:Blood Groups
Dr Shamshad
Objectives
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.
Classification of the blood groups is based on
The presence or absence of Antigen on the surface of RBCs
The antigens can be integral proteins where polymorphisms lie in
the variation of amino acid sequence (e.g., rhesus [Rh], Kell),
glycoproteins or glycolipids (e.g., ABO).
About 33 blood gp systems representing over 300 antigens are
listed by the International Society of Blood Transfusion(ISBT).
Blood group systems
Major system
Minor system
P systemMN typeRhesus systemABO system
Familial blood groups:
Lewis,Duffy,Kell,
Bombay blood group
Based on presence of
agglutinogens widely
prevelant in population
Most commonly used
ABO Agglutinogens(Antigens):
-Present on surface of RBCs:A, B
Genetic Determination of the Agglutinogens.
-Genetic locus has three alleles,
-which means three different forms
of the same gene.
-These alleles “A,” “B,” and “O,”
-Inherited two surface chromosomes
OO,OA,AA,BB, or AB
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 (weakened form),
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:NON nS
Agglutinins (Antibodies): Naturally occuring :anti-A, anti-B
● Origin:Gamma globulins:IgM,IgG.
● Cannot cross the placenta
● Cold antibodies 5 to 20 0C
● Not present at birth
● Appear within 2 months,
● Reach peak b/w 5-10 years of age
● Triggered by A and B antigens
present in food and bacteria
● When type A agglutinogen is not present in a person’s RBCs, antibodies known as anti-A agglutinins
develop in the plasma. Also, when type B agglutinogen is not present in the RBCs, antibodies
known as anti-B agglutinins develop in the plasma.
Blood group and typing
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.
The First part is applicable to all blood groups but the second part is not necessary always ,its true for ABO
blood groups
Rh system:
Depends on presence or absence of Rhesus antigen (D) on the
surface of RBCs
Rh antigens: Dd,Cc,Ee:(D play important role)
Rh system D antigen on
surface of RBCs
% of population
Rh+ve type Present 85%[American blacks,95%,African blacks 100%]
Rh-ve type Absent 15%
Anti-D (Antibodies)
➢ Acquired type antibodies
➢ Are considered as IgG class
➢ Can cross the placenta.
➢ Aquired by transfusion of Rh -ve individual with Rh+ve blood
➢ Rh-ve pregnancy with Rh +ve fetus
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
O blood gp A blood gp B blood gp AB blood gp
47% 41% 9% 3%
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
Transfusion reactions
Acute
immunological
reaction
● Acute hemolytic
transfusion reaction
● Allergic reactions
● Febrile, chills,
● Nonhemolytic
trasnfusion reaction
● Transfusion-related
acute lung injury
● Shock,
● Renal failure
● Heptic failure
● Jaundice
Delayed
immunologic
reaction
● Delayed
hemolytic
transfusion
reaction
● Posttransfusion
purpura
Delayed
nonimmunologic
reaction
● Infectious
disease
transfusion
● Such as
malaria
● AIDS
● Heptitis B
Acute nonimmunologic
reaction.
● Volume overload
● Citrate toxicity
● Hypothermia
● Bacterial
contamination
Acute
Non immunological
reaction
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.
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.
Blood group and typing
Blood group and typing
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.
➢ 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.
➢ 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.
➢ 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.
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.
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.
Thus anti-Rh agglutinins that had come from the mother will have
been destroyed
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.
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.

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Blood group and typing

  • 2. Objectives 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.
  • 3. Classification of the blood groups is based on The presence or absence of Antigen on the surface of RBCs The antigens can be integral proteins where polymorphisms lie in the variation of amino acid sequence (e.g., rhesus [Rh], Kell), glycoproteins or glycolipids (e.g., ABO). About 33 blood gp systems representing over 300 antigens are listed by the International Society of Blood Transfusion(ISBT).
  • 4. Blood group systems Major system Minor system P systemMN typeRhesus systemABO system Familial blood groups: Lewis,Duffy,Kell, Bombay blood group Based on presence of agglutinogens widely prevelant in population
  • 6. ABO Agglutinogens(Antigens): -Present on surface of RBCs:A, B Genetic Determination of the Agglutinogens. -Genetic locus has three alleles, -which means 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 (weakened form), 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:NON nS
  • 8. Agglutinins (Antibodies): Naturally occuring :anti-A, anti-B ● Origin:Gamma globulins:IgM,IgG. ● Cannot cross the placenta ● Cold antibodies 5 to 20 0C ● Not present at birth ● Appear within 2 months, ● Reach peak b/w 5-10 years of age ● Triggered by A and B antigens present in food and bacteria ● When type A agglutinogen is not present in a person’s RBCs, antibodies known as anti-A agglutinins develop in the plasma. Also, when type B agglutinogen is not present in the RBCs, antibodies known as anti-B agglutinins develop in the plasma.
  • 10. 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. The First part is applicable to all blood groups but the second part is not necessary always ,its true for ABO blood groups
  • 11. Rh system: Depends on presence or absence of Rhesus antigen (D) on the surface of RBCs Rh antigens: Dd,Cc,Ee:(D play important role) Rh system D antigen on surface of RBCs % of population Rh+ve type Present 85%[American blacks,95%,African blacks 100%] Rh-ve type Absent 15%
  • 12. Anti-D (Antibodies) ➢ Acquired type antibodies ➢ Are considered as IgG class ➢ Can cross the placenta. ➢ Aquired by transfusion of Rh -ve individual with Rh+ve blood ➢ Rh-ve pregnancy with Rh +ve fetus
  • 13. 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 O blood gp A blood gp B blood gp AB blood gp 47% 41% 9% 3%
  • 14. 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
  • 15. Transfusion reactions Acute immunological reaction ● Acute hemolytic transfusion reaction ● Allergic reactions ● Febrile, chills, ● Nonhemolytic trasnfusion reaction ● Transfusion-related acute lung injury ● Shock, ● Renal failure ● Heptic failure ● Jaundice Delayed immunologic reaction ● Delayed hemolytic transfusion reaction ● Posttransfusion purpura Delayed nonimmunologic reaction ● Infectious disease transfusion ● Such as malaria ● AIDS ● Heptitis B Acute nonimmunologic reaction. ● Volume overload ● Citrate toxicity ● Hypothermia ● Bacterial contamination Acute Non immunological reaction
  • 16. 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.
  • 17. 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.
  • 20. 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. ➢ 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.
  • 21. ➢ 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. ➢ 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.
  • 22. 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.
  • 23. 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. Thus anti-Rh agglutinins that had come from the mother will have been destroyed
  • 24. 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.
  • 25. 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.