Immunohematology and Blood Banking PDF

Summary

This document provides an overview of immunohematology and blood banking. It covers various blood group systems, common tests, antibodies, transfusion reactions, and autoimmune hemolytic anemia. This document is suitable for healthcare professionals or students studying this subject.

Full Transcript

Common tests for immunohematology 1. Coomb’s test (Antiglobulin Test or called Anti-Human Globulin Test “AHG”) 2. RBC typing (O= 45%; A= 40%; B= 11%; AB= 4%... Rh + = 85%; USA) 3. Cross-matching 4. Antibody screening 5. Compatibility testing Antibodies attached to RBC a...

Common tests for immunohematology 1. Coomb’s test (Antiglobulin Test or called Anti-Human Globulin Test “AHG”) 2. RBC typing (O= 45%; A= 40%; B= 11%; AB= 4%... Rh + = 85%; USA) 3. Cross-matching 4. Antibody screening 5. Compatibility testing Antibodies attached to RBC as in erythroblastosis fetalis or hemolytic anemia Anti-Rh antibodies # Anti- C, anti-c # Anti-E, Anti-e # Anti-D (only) Potency (From strongest to weakest) # Anti-D, anti-c, anti-E, anti-C, and anti-e Do not bind complement (incomplete hemolysin or antibodies) IgG, active at 37 Degree Celsius. # Rh is a protein antigen Tested by indirect Coomb’s test (anti-globulin test) Lewis Blood Group (Antigen) Le gene: Codes L-fucosyltransferase, to attach fucose to subterminal unit (N-acetylglucosamine) of ABH precursor : (Lea ) Se gene: Codes a-2-L-fucosyltransferase to attach a second fucose to terminal unit (galactose) of ABH Precursor: (Leb) Lele: Co-dominant Soluble antigens, produced by tissues and found in body fluids (plasma) cont./… Lewis Antibodies IgM Can activate complement (C) leading to hemolysis at room temperature (RT). Lewis antibodies are almost always clinically insignificant because: 1. Transfused RBC shed their Lewis antigens & acquire Lewis phenotype of the recipient 2. Lewis antibodies are quickly adsorbed by free serum Lewis antigens Very rarely cause Hemolytic Transfusion Reaction (HTR) P Antigen Three types of antigens: P, P1, and Pk P antigen is a binding site for Parvovirus B19 Found in secretions as plasma & hydatid fluid cont./… P Blood Group Autoanti-P Antibodies - IgG - Can cause Paroxysmal Cold Hemoglobinuria (PCH) - Produced after some viral infections M and N Blood Group (Antigen) Rich in sialic acid TWO coding genes: Glycophorin A and B on chromosome 4 coding FIVE antigens: - M, N, S, s, and U MN system Antibodies: - IgM or IgG - Do not bind C, and active at RT Kell Blood Group (Antigen) K antigen: - Second in immunogenicity after D antigen Kell antibodies: - Anti-Kell is common - IgG (AHG test) - 20% bind complement - Can cause HDN &HTR; Linked to AID Duffy Blood Group (Antigen) Three alleles: Fya, Fyb, and Fy (silent) Four antigens: Fy3, Fy4, Fy5, and Fy6 (all normal RBC are positive for them) Duffy Antibodies: - IgG; reacts best via AHG - Do not bind complement - Cause acute and delayed HTR; & HDN Kidd Blood Group (Antigen) Three alleles: Jka (JK1), JKb (JK2), & JK3 Kidd antigens transport urea in RBC Kidd antibodies: - IgG - Can cause HDN, and delayed HTD - Anti-JK3: Jka- JKb- (rarest type) Autoimmune Hemolytic Anemia (AIHA) RBC destruction by autoantibodies (Aab): # IgG or IgM, or more rarely IgE or IgA If fix C, it causes intravascular hemolysis, but if not, it causes extravascular hemolysis Ab coated RBC: Lose membrane by Mc in the spleen, then forming spherocytosis. AIHA, according to thermal specificity of Aab: 1. Warm Ab: Bind at 37o C, 80% of cases, and majority are IgG against Rh antigens 2. Cold Ab: Bind at 4o C, 20% of cases and are IgM and fix complement (see next slide). Warm autoimmune hemolysis Common in middle age and females 50% no underlying cause, but others are due to lymphoid neoplasms, solid tumors, C.T. disease as SLE, drugs as penicillin & others. Cold autoimmune hemolysis 1. Chronic : Affects elderly; with B cell lymphoma; antibody is monoclonal against Ii antigens 2. Acute: With Mycoplasma pneumoniae, IMN, & PCH*; Ab is polyclonal against P antigen * In children with congenital syphilis

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