Blood Types and Transfusions PDF

 UNIT VI Chapter 36: Blood Types; Transfusion Ebaa M Alzayadneh, PhD Associate Professor of Physiology  Early transfusions Red cell agglutination and lysis Severe transfusion reactions, often fatal In other cases, wel...

 UNIT VI Chapter 36: Blood Types; Transfusion Ebaa M Alzayadneh, PhD Associate Professor of Physiology  Early transfusions Red cell agglutination and lysis Severe transfusion reactions, often fatal In other cases, well-tolerated and beneficial Led to the discovery of red blood cell antigens and the practice of cross-matching >30 common antigens, many rare ones  Early transfusions Red cell agglutination and lysis Severe transfusion reactions, often fatal In other cases, well-tolerated and beneficial Led to the discovery of red blood cell antigens and the practice of cross-matching >30 common antigens, many rare ones  The ABO System Red blood cell surface antigens: glycolipids or glycoproteins Present on all cells in the body, not just blood cells Agglutinogens: surface antigens (A,B) - Genes: A, B, O (maternal, paternal alleles) - Genotypes: OO, OA, OB, AA, BB, AB Agglutinins (immunoglobulins): anti-A, anti-B Occurance: O: 47% A: 41% B: 9% AB: 3%  Agglutinins Antibodies, mostly IgM and IgG Begin developing age 2-8 months, peak ~age 10 years Response to A and B antigens in foods, bacteria; initial exposures are environmental  Blood Groups Genotype Blood Type Agglutinogens Agglutinins OO O ------ ANTI-A and ANTI-B OA or AA A A ANTI-B OB or BB B B ANTI-A AB AB ------ AB  Blood Typing Blood Type Anti-A Anti-B O A B AB  The Rh (rhesus) antigens Requires prior exposure to incompatible blood Six common antigens (“Rh factors”) C, D, E, c, d, e - Each person is CDE, CDe, Cde, CdE, cDE, cDe, or cde D (“Rh positive”) is prevalent (85% EA, 100% Africans) and particularly antigenic C and E can also cause transfusion reactions, generally milder Activation of complement ABO activation is immediate Delayed due to Rh  Anti-Rh Transfusion Reactions Rh+ blood into Rh- recipient: -delayed mild transfusion reaction -sensitization to further Rh+ transfusion - agglutinins peak after 2- 4 months 50% of Rh- are sensitized by 1st exposure - 20% after a second exposure - 30% are non-responders Rh matching to prevent immunization  Anti-Rh Transfusion Reactions Naïve Rh- recipient → usually no reaction initially Within 2-4 weeks sufficient Ig for agglutination → delayed reaction, usually mild hemolysis within tissue macrophages Any subsequent transfusion with Rh+ blood → potentially severe transfusion reaction  Hemolytic Disease of the Newborn Clinical Perspective (Erythroblastosis fetalis) ABO incompatibility (O mother and A or B fetus) - Unusual: - Most anti-A is IgM, does not cross placenta - ABO antigens not well developed in fetus Rh incompatibility (RhD+ fetus and Rh- mother) - Immunization due to fetal-maternal bleeding during delivery - Mother develops Anti-D agglutinins - Usually not a problem with first pregnancy - Worse with subsequent pregnancies (3% EF second pregnancy, 10% with third) Hemolytic Disease of the Newborn (Erythroblastosis fetalis)  Hemolytic Disease of the Newborn Clinical Perspective (Erythroblastosis fetalis) Maternal antibodies cross the placenta and cause agglutination and lysis of fetal erythrocytes Fetal macrophages convert hemoglobin to bilirubin → jaundice Anemic at birth; continued hemolysis 1-2 months Hepato- splenomegaly from extramedullary erythropoiesis May have permanent neurologic damage from deposition of bilirubin in neural tissues (“kernicterus”)  Hemolytic Disease of the Newborn: Clinical Perspective Treatment Repetitive removal of Rh-positive blood, replacement with Rh negative (400 ml exchange over 90 minutes) May be done several times over a few weeks Maternal antibodies disappear over 1-2 months so newborn’s Rh-positive cells cease to be a target  Hemolytic Disease of the Newborn: Clinical Perspective Prevention Provide exogenous anti-D antibodies to the mother in late pregnancy and just after birth These bind to D antigenic sites on fetal erythrocytes that enter the mother’s circulation, preventing an immune response  Blood Component Transfusion Clinical Perspective Single donation is 450 ml Processed into components - Packed Red Cells; Stored ~ 30- 40 days - Plasma (clotting factors); Frozen - Platelets; Stored for 8-10 days - White blood cells; Rarely used  Transfusion reactions Red cells agglutinate Plug small vessels Physical distortion, phagocytic attack → hemolysis In some cases, immediate, complement- dependent hemolysis (depends on Ig type …IgM “hemolysins”)  Clinical Perspective Transfusion Reactions Occur because of mismatched blood Recipient antibodies react against donor antigens Either immediate or delayed agglutination and hemolysis Fever, chills, shortness of breath; potentially shock, renal shutdown Macrophages produce bilirubin With normal liver function, no jaundice unless ≥ 400 ml blood hemolyzed in < 1 day  Clinical Acute Renal Failure After Perspective Transfusion Reaction Products of hemolysis cause powerful renal vasoconstriction Immune-mediated circulatory shock Free hemoglobin can leak through glomerular membranes into tubules → high quantities may block tubules May require acute or even chronic hemodialysis