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Blood presentation1

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MUHAMMAD UMAIR KHAN
MUHAMMAD UMAIR KHAN

This document discusses blood types and transfusions. It explains that there are multiple blood group antigens, including the A, B, and Rh antigens. A person's blood type depends on which antigens are present on their red blood cells. Improper blood transfusions can cause agglutination and hemolysis reactions as antibodies attack mismatched antigens. The Rh system is also described, including how Rh-negative mothers can produce antibodies against a Rh-positive baby in later pregnancies, potentially causing hemolytic disease of the newborn. Prevention and treatment methods are mentioned.

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BLOOD TYPES; TRANSFUSION; TISSUE AND ORGAN TRANSPLANTATION BY DR. MUHAMMAD UMAIR
BLOOD TYPES Multiplicity of Antigens in the Blood Cells. At least 30 commonly occurring antigens O-A-B system and the Rh system. Antigenicity & Immune Reactions of Blood The bloods of different people have different antigenic and immune properties, so that antibodies in the plasma of one blood will react with antigens on the surfaces of the red cells of another blood type causing a transfusion reaction.
O-A-B BLOOD TYPES A and B AntigensAgglutinogens Major O-A-B Blood Types. depend on the presence or absence of A and B agglutinogens. Genetic Determination of the Agglutinogens. Two genes, one at a time on each of two paired chromosomes Any one of three types Type O (functionless) Type A or Type B
Relative Frequencies of the Different Blood Types.
AGGLUTININS (ANTIBODIES) Anti-A agglutinins Anti-B agglutinins Type O blood, containing no agglutinogens, does contain both anti-A and anti-B agglutinins Type A blood contains type A agglutinogens and anti-B agglutinins Type B blood contains type B agglutinogens and anti-A agglutinins. Type AB blood contains both A and B agglutinogens but no agglutinins.
Origin gamma globulins produced in bone marrow and lymph gland cells Mostly IgM and IgG QUESTION: Why are these agglutinins produced in people who do not have the respective agglutinogens in their red blood cells ? The answer to this is that small amounts of type A and B antigens enter the body in food, in bacteria, and in other ways, and these substances initiate the development of the anti-A and anti-B agglutinins.
AGGLUTININS TITER AT DIFFERENT AGES. Immediately after Birth its almost zero. Two to 8 months begins to produce agglutinins. 8 to 10 years maximum titer. gradually declines with aging.
AGGLUTINATION PROCESS IN TRANSFUSION REACTIONS In mismatched blood transfusion, the agglutinins of recipients blood are mixed with the agglutinogens of the donar RBCs. Agglutinis having binding sites attach to RBCs This binding causes the RBCs to clump. these clumps plug small blood vessels throughout the circulatory system
Delayed Hemolysis ( during hours to days) physical distortion of the cells or Destruction of the agglutinated cells membranes, releasing hemoglobin into the plasma Acute Hemolysis activation the complement system, which releases proteolytic enzymes (the lytic complex) Far less common because it requires high titer of antibodies for lysis Hemolysins. (IgM antibodies)
BLOOD TYPING PROCEDURE The red blood cells are first separated from the plasma and diluted with saline. One portion is then mixed with anti-A agglutinin and another portion with anti-B agglutinin. After several minutes, the mixtures are observed under a microscope. An antibody antigen reaction: If the red blood cells have become clumpedagglutinated
RH BLOOD TYPES O-A-B system VS the Rh system massive exposure to an Rh antigen(blood transfusion) before enough agglutinins production to cause a significant transfusion reaction. Rh Antigens Rh factor (six common types of Rh antigens) C,D, E, c, d, and e A person who has a C antigen does not have the c antigen and vice versa each person has one of each of the three pairs of antigens. Type D antigen widely prevalent and more antigenic Rh-Positive and Rh-Negative People. +ve = having D antigen -ve = no D anitgen
RH IMMUNE RESPONSE Formation of Anti-Rh Agglutinins. When RBCs containing Rh factor are injected into Rh-negative person(with no Rh factor) Develop slowly. Reach maximum conc. In about 2 to 4 months. With multiple exposures to the Rh factor, an Rh-negative person eventually becomes strongly sensitized to Rh factor. Characteristics of Rh Transfusion Reactions. Rh +ve blood transfusion in previously unexposed Rh ve person = no immediate but delayed reaction ( after 2-4 weeks ) due to anti Rh antibodies development In previously exposed Rh ve person = immediate and severe
ERYTHROBLASTOSIS FETALIS (HEMOLYTIC DISEASE OF THE NEWBORN) disease of the fetus and newborn child characterized by agglutination and phagocytosis of the fetuss red blood cells. Mother = Rh -ve Father = Rh +ve Baby = Rh +ve mother develops anti-Rh agglutinins from exposure to the fetuss Rh antigen. Which then diffuse through the placenta into the fetus and cause red blood cell agglutination. Incidence of the Disease rises progressively with subsequent pregnancies
Clinical Picture of Erythroblastosis. Anemic , jaundice, kernicterus. Hepatomegally and spleenomegally nucleated blastic red blood cells in blood picture Mental retardation Death Treatment of the Erythroblastotic Neonate. Exchange Transfusion Prevention of Erythroblastosis Fetalis. Rh immunoglobulinglobin, an anti-D antibody at 28 to 30 weeks of gestation and after delivery inhibit antigen-induced B lymphocyte antibody production in the expectant mother. anti-D antibody also attaches to D antigen sites on Rh-positive fetal RBCs hence interfere with immune response to D antigen.

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Blood presentation1

  • 1. BLOOD TYPES; TRANSFUSION; TISSUE AND ORGAN TRANSPLANTATION BY DR. MUHAMMAD UMAIR
  • 2. BLOOD TYPES Multiplicity of Antigens in the Blood Cells. At least 30 commonly occurring antigens O-A-B system and the Rh system. Antigenicity & Immune Reactions of Blood The bloods of different people have different antigenic and immune properties, so that antibodies in the plasma of one blood will react with antigens on the surfaces of the red cells of another blood type causing a transfusion reaction.
  • 3. O-A-B BLOOD TYPES A and B AntigensAgglutinogens Major O-A-B Blood Types. depend on the presence or absence of A and B agglutinogens. Genetic Determination of the Agglutinogens. Two genes, one at a time on each of two paired chromosomes Any one of three types Type O (functionless) Type A or Type B
  • 4. Relative Frequencies of the Different Blood Types.
  • 5. AGGLUTININS (ANTIBODIES) Anti-A agglutinins Anti-B agglutinins Type O blood, containing no agglutinogens, does contain both anti-A and anti-B agglutinins Type A blood contains type A agglutinogens and anti-B agglutinins Type B blood contains type B agglutinogens and anti-A agglutinins. Type AB blood contains both A and B agglutinogens but no agglutinins.
  • 6. Origin gamma globulins produced in bone marrow and lymph gland cells Mostly IgM and IgG QUESTION: Why are these agglutinins produced in people who do not have the respective agglutinogens in their red blood cells ? The answer to this is that small amounts of type A and B antigens enter the body in food, in bacteria, and in other ways, and these substances initiate the development of the anti-A and anti-B agglutinins.
  • 7. AGGLUTININS TITER AT DIFFERENT AGES. Immediately after Birth its almost zero. Two to 8 months begins to produce agglutinins. 8 to 10 years maximum titer. gradually declines with aging.
  • 8. AGGLUTINATION PROCESS IN TRANSFUSION REACTIONS In mismatched blood transfusion, the agglutinins of recipients blood are mixed with the agglutinogens of the donar RBCs. Agglutinis having binding sites attach to RBCs This binding causes the RBCs to clump. these clumps plug small blood vessels throughout the circulatory system
  • 9. Delayed Hemolysis ( during hours to days) physical distortion of the cells or Destruction of the agglutinated cells membranes, releasing hemoglobin into the plasma Acute Hemolysis activation the complement system, which releases proteolytic enzymes (the lytic complex) Far less common because it requires high titer of antibodies for lysis Hemolysins. (IgM antibodies)
  • 10. BLOOD TYPING PROCEDURE The red blood cells are first separated from the plasma and diluted with saline. One portion is then mixed with anti-A agglutinin and another portion with anti-B agglutinin. After several minutes, the mixtures are observed under a microscope. An antibody antigen reaction: If the red blood cells have become clumpedagglutinated
  • 11. RH BLOOD TYPES O-A-B system VS the Rh system massive exposure to an Rh antigen(blood transfusion) before enough agglutinins production to cause a significant transfusion reaction. Rh Antigens Rh factor (six common types of Rh antigens) C,D, E, c, d, and e A person who has a C antigen does not have the c antigen and vice versa each person has one of each of the three pairs of antigens. Type D antigen widely prevalent and more antigenic Rh-Positive and Rh-Negative People. +ve = having D antigen -ve = no D anitgen
  • 12. RH IMMUNE RESPONSE Formation of Anti-Rh Agglutinins. When RBCs containing Rh factor are injected into Rh-negative person(with no Rh factor) Develop slowly. Reach maximum conc. In about 2 to 4 months. With multiple exposures to the Rh factor, an Rh-negative person eventually becomes strongly sensitized to Rh factor. Characteristics of Rh Transfusion Reactions. Rh +ve blood transfusion in previously unexposed Rh ve person = no immediate but delayed reaction ( after 2-4 weeks ) due to anti Rh antibodies development In previously exposed Rh ve person = immediate and severe
  • 13. ERYTHROBLASTOSIS FETALIS (HEMOLYTIC DISEASE OF THE NEWBORN) disease of the fetus and newborn child characterized by agglutination and phagocytosis of the fetuss red blood cells. Mother = Rh -ve Father = Rh +ve Baby = Rh +ve mother develops anti-Rh agglutinins from exposure to the fetuss Rh antigen. Which then diffuse through the placenta into the fetus and cause red blood cell agglutination. Incidence of the Disease rises progressively with subsequent pregnancies
  • 14. Clinical Picture of Erythroblastosis. Anemic , jaundice, kernicterus. Hepatomegally and spleenomegally nucleated blastic red blood cells in blood picture Mental retardation Death Treatment of the Erythroblastotic Neonate. Exchange Transfusion Prevention of Erythroblastosis Fetalis. Rh immunoglobulinglobin, an anti-D antibody at 28 to 30 weeks of gestation and after delivery inhibit antigen-induced B lymphocyte antibody production in the expectant mother. anti-D antibody also attaches to D antigen sites on Rh-positive fetal RBCs hence interfere with immune response to D antigen.