Blood group and typing

lecture on blood groups and its significance

1. Lecture 35:Blood Groups Dr Shamshad

2. Objectives Classify and describe different types of blood groups. Restate the Landsteiner’s law. Enumerate the uses of blood grouping . Explain the importance of blood grouping in blood transfusion. 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 RBC s 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 system MN type Rhesus system ABO system Familial blood groups: Lewis,Duffy,Kell, Bombay blood group Based on presence of agglutinogens widely prevelant in 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, -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. A gglutinins (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 .

9. 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

10. 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%

11. 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

12. Significance o f 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%

13. 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

14. 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

15. 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.

16. Hemolytic Disease of the Newborn/Erythroblastosis Fetalis D isease 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.

17. 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.

18. 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.

19. Fetus at risk A bout 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.

20. 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

21. 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.

22. 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.

23. Individuals belonging to Bombay blood group (oh) are homozygous for the absence of H gene i.e., they are of the genotype 'hh', so that they are unable to bring about the initial part of conversion of the precursor blood group substance Even if 'A' and 'B' genes are present they have no substrate for their normal function of producing 'A' and 'B' blood group substances The ABO genes cannot therefore be expressed and such individuals appear to belong to 'O' but their true state can be detected because of the presence in their serum of anti-H . Thus the 'Bombay phenotype' , lack 'A', 'B' and 'H' antigens on their erythrocytes and in secretions. Nevertheless they appear to have normal 'A' and 'B' genes that can be expressed in the next generation if their children acquire an 'H' gene from the other parent . It follows that there is no 'O' antigen; group 'O' erythrocytes and the saliva of group 'O' secretors contain 'H' antigen, but the designation group 'O' erythrocytes has been retained for historical reasons