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Blood group
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- 2. I. INTRODUCTION II. BLOODGROUP 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 groupsystem Minor blood group system Familial blood group system- Kell, Duffy, Lutheran, Lewis, Deigo, kidd Etc. Blood Group System
- 5. LANDSTEINER’s LAW- 1.If anagglutinogen 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. Antigenand 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 thesixth 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 precursorsfor 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 HAntigen 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 theB antigen Glucose Galactose N- acetylglucosamine Galactose RBC Fucose Galactose D-galactosyl Transferase(product of B gene)
- 13. O GENE Group OGroup 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 IgMtype. • Produced by bone marrow and lymph gland cells . • Known as cold antibodies. Anti-A and Anti-B agglutinins Titre of antibodies
- 15. Why antibodies producedin 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-1and 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 ABOblood group Follows Mendelian Law. In 1924, Felix Bernstein proposed presently accepted theory. Heterozygous: AO or BO Homozygous: AA or BB
- 18. Mom Dad Offsprin gBlood 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 ANTIGENANTIBODY 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 BloodGroup System I. Discovery of Rh system II. Antigen and antibodies III. Inheritance IV. Haemolytic disease of newborn
- 21. History of theRh 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 mothercarry 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 antiserumwas 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 bythe 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 • Rhsystem 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 Agis inherited as a dominant gene D. • Genotype of individual may be: DD Dd dd Inheritance
- 28. Examples- Heterozygous Rh + HomozygousRh- 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 Rhantibody is produced To Rh negative personFrom Rh positive person Rh antigen reacts with Rh antibody First transfusion Second transfusion
- 31. Haemolytic Disease OfNewborn
- 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.
- 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 IiSYSTEM- 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 DUFFYSYSTEM 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- Landsteinerand Levine(1927). Required for- • Paternity tests • Anthropological and genetic studies. Cont…
- 39. • LEWIS SYSTEM- Mourantand 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 bloodtransfusion. 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. Donorand 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 canreceive 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 safeand compatible blood transfusion- • ABO and Rh typing • Cross matching • Antibody screening Investigations
- 46. Determination Of BloodGroup Blood Typing
- 47. Under Microscope Human RBCbefore (left) and after (right) adding serum containing antibodies.
- 48. II. Cross Matching- Majorcross 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 positiveblood should never be transfused to Rh negative blood.
- 51. V. Check bloodbag 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