RED BLOOD CELL AND PLATELET PRODUCTION Whole Blood 450mL blood + 63ml blood AC - 500 mL blood + 70ml

l blood AC DONOR gives blood every 8 weeks - blood tested for 9 screening tests for infectiioys markers RBC 90% ATP (glycolysis) 10% (pentose phosphate pathway) - 92-95% HbA, 2-3% HbA, 1-2% HbF - 75% postrtransfusion survival of RBC successful transfusion (SUCCESSFUL TRANSFUSION) Collection of Donor Blood - >16yrs old - Temp: <37.5 or <99.5 - BP: 180/100 - Hgb/Hct: >12.5/>38 - Pulse: 100 beats per minute - Weight: min 110 lb/50 kg Common Anticoagulants, Additives and Rejuvenating Soln Anticoagulants: ACD, CPD, C2PD 21 days expiration CPDA-1 35 days expiration Additives: Rejuvenating: Adsol, Nutricel, Optisol 42 days expiration Rejuvesol only FDA-approved

Immunodominant sugars L-fucose - for H specificity N-acetylgalactosamine for A specificity D-galactose - for B specificity hh genotype Bombay phenotype/ Oh - lacks normal expression of ABH antigens - Patients serum + Ulex europaeus = agglutination Group O persons contains the greatest amount of H substance Group A1B persons contains the least amount of H substance Type 1 precursors glycoproteins in secretions are formed Type 2 precursors ABH Ag on RBCs are formed (4+) yielded by FORWARD and REVERSE Grouping Group A contain anti-B in their serum Group B contain anti-A in their serum Group AB-contain neither anti-A or anti-B in their serum Group O contain both anti-A and anti-B in their serum Secretors inherit the Se gene (78% of population) Nonsecretors inherit the se gene (22% of population) Se gene codes for the production of L-fucosyltransferase RH BLOOD GROUP SYSTEM Rh antigens characterized as nonglycosylated proteins in the RBC membrane - inherited as codominant alleles Rh antibody named on the basis of Ab production by guinea pigs and rabbits when transfused with rhesus monkey RBCs - most are IgG immunoglobulins and react with 37OC - Exposure to <0.1 mL of Rh(+) RBCs can stimulate Ab production in an Rh (-) person. Rh antibodies are IgG and can cross placenta to coat fetal (Rhpositive) RBCs

Antiglobulin Test -detect RBC sensitized by IgG alloantibodies, autoantibodies and complement components -AHG reacts with human globulin molecules bound to RBCs or free in serum Polyspecific AHG sera Ab + C3d component of complement Monospecific AHG sera 1 Ab specificity (anti-IgG/ Ab to anti-C3b-C3d) Anti-Jka clinically significant antibody whose detection may be dependent on anticomplement activity in polyspecific AHG

Hybridoma technology produce monoclonal antiglobulin serum Rh primary cause of HDN, Erythroblastosis fetalis and hemolytic transfusions reactions DAT in-vivo sensitization of RBCs w/ IgG and/or complement Rhnull person who expresses no Rh antigens on RBC components (+) DAT = HDN, HTR, AIHA Controls the expression of Rh --> followed by DAT panel (monospecific anti-IgG and anti-C3d to (1) RHD codes for the presence/absence of D determine the specific type of protein sensitizing the RBC (2) RHCE codes for the expression of CcEe antigens FALSE POSITIVE: Use of refrigerated, clotted blood sample in which complements coat RBCs in vitro Fisher-Race DCE terminology - based on the theory that Ag of the system are produced by three EDTA used to collect to avoid in-vitro complement attachment closely linked sets of alleles and that each gene is responsible for associated with refrigerated clotted specimens producing a product or antigen on the RBC surface. IAT in-vitro sensitization of RBCs and can be applied to compatibility testing, antibody screen, antibody identification, RBC phenotyping, and titration studies (+)IAT Identification of alloantibody specificity using panel of reagent RBCs *RBCs must be washed in SALINE at least 3 times to remove traces of free serum globulins Coombs control cells = Type O(+) coated with anti-D ABO BLOOD GROUP SYSTEM ABO frequencies: Group O 45%, Group A 40%, Group B 11%, Group AB 4% IgM naturally occurring antibodies ABO genes inherited in a codominant manner ABH soluble Ag secreted by tissue cells and found in all body secretions. These secretions depend on the persons ABO group. ABO reverse grouping omitted from cord blood testing on newborns because their AB titer levels are generally too low for detection ABO RBC antigens glycolipids, glycoproteins or glycosphingolipids ABO-secreted substances glycoproteins Wiener Rh-Hr nomenclature - gene responsible for defining Rh actually produces an agglutinogen that contains a series of blood factors, in which each factor is an Ag recognized by an Ab. Rosenfield alpha/numeric terminology - a number is assigned to each antigen of the Rh system in order of its discovery Rh 1 = D Rh 4 = c Rh 2 = C Rh 5 = e Rh 3 = E Genotypes: R1r 31% (whites) R0r 23% (blacks) R0R0 19% Partial D individual characterized as lacking one or more pieces or epitopes of the total D antigen and may produce alloantibody to the missing fraction if exposed to RBCs with the complete D antigen Blood transfusion: Rh (+) D or weak D test is positive Rh (-) Both the D and weak D tests are negative. Rh mediated hemolytic transfusion reactions can result in extravascular hemolysis

Lewis System Lewis blood group Ag not synthesized by the RBCs - made by tissue cells, secreted into body fluids and plasma and adsorbed onto the RBC membrane Glycoproteins Lewis antigens present in secretions Glycolipids Lewis cell-bound antigens absorbed from plasma onto RBC membrane Le gene code for L-fucosyltransferase (adds L-fucose to type 1 chain) Lea needs the Le gene formed by the addition of Lfucose to the number 4 carbon of N-acetyl-D-glucosamine for type 1 H Leb needs the Le and Se gene Formed when a second L-fucose is added to the number 4 carbon of the subterminal N-acetyl-Dglucosamine of type 1 H

(3) THE I AND i ANTIGENS I and i antigens not antithetical, but reciprocal relationship Adult I antigen Infant i antigen (after 18 months) develops I antigen Anti I benign, weak, naturally occurring, saline-reactive IgM autoagglutinin, usually detectable at 4OC Pathogenic anti-I strong cold autoagglutunin - demonstrates high titer at 4OC - Reacts over a wide thermal range (up tp 30-32OC) Potent cold autoantibodies - can mask clinically significant underlying alloantibodies and complicate pre-transfusion testing - Patients with M.pneumoniae Anti-I is a rare IgM agglutinin that reacts optimally at 4OC - potent examples may be associated with infectious mononucleosis (4) THE KELL BLOOD GROUP SYSTEM - well developed at birth and are not destroyed by enzymes - destroyed by DTT, ZZAP, and glycine-acid-EDTA K-antigen - rated 2nd only to D antigen in immunogenicity - high-incidence antigen Anti-K -IgG Ab reactive in the AHGA phase - made in response to pregnancy or transfusion of RBCs - implicated in severe hemolytic transfusion reactions and HDN McLeod phenotype - affecting only males - rare phenotype with DECREASED Kell system antigen expression McLeod Syndrome Abnormal RBC morphology and compensated hemolytic anemia and neurologic and muscular abnormalities. Associated with X-linked chronic granulomatous disease. (5) THE DUFFY BLOOD GROUP SYSTEM Fya and Fyb antigens - destroyed by enzymes and ZZAP Fy(a-b-) - prevalent in blacks, nonexistent in whites - RBCs were shown to resist infection by the malaria organisms P.knowlesi and P.vivax

Le (a+b-) ABH nonsecretors; only Lea substance in secretions Le (a-b+) ABH secretors; have both Lea and Leb in secretions - common in whites and blacks - commonly associated with H.pylori infection lele genotype Le (a-b-) common among blacks than whites Lewis antigens - poorly expressed at birth - do not demonstrate dosage in serologic reactions Lewis antibodies - generally IgM - capable of binding complement and enhanced by enzymes - frequently encountered in pregnant women - not considered significant in transfusion medicine OTHER MAJOR BLOOD GROUP SYSTEMS (1)THE MNS BLOOD GROUP SYSTEM Anti-M and Anti-N - cold reactive saline agglutinins that do not bind complement or react with enzyme-treated cells Anti-N found in renal patients undergoing dialysis treatment Anti-S and Anti-s - IgG antibodies reactive at 370C and the antiglobulin phase - may bind complement - associated with HDN and hemolytic transfusion reactions S-s-U- phenotype found in blacks Anti-U IgG Ab associated with hemolytic transfusion and HDN (2) THE P BLOOD GROUP - consist of biochemically related antigens, P, P1, Pk and LKE - biochemical relationship with ABH and I antigens

Anti-Fya and Anti Fyb - IgG antibodies - React optimally at the antiglobulin phase of testing - Implicated in Delayed hemolytic transfusion P1 Ag expression is variable; poorly developed at birth reactions and HDN Anti P1 common naturally occurring IgM Ab in the sera of P1 (6) THE KIDD BLOOD GROUP SYSTEM Individuals Anti Jka and Anti-Jkb weak and found in combination with other - weak, cold reactive saline agglutinin seldom detected in routine antibodies - can be neutralized with soluble P1 found in hydatid cyst fluid Anti-PP1Pk produced by all p individuals early in life without RBC sensitization and reacts with all RBCs except those of other p individuals Antibodies may be a mixture of IgM and IgG, efficiently bind complement and may demonstrate in-vitro hemolysis Anti-P naturally occurring alloantibody in the sera of all Pk indv Paroxysmal cold hemoglobinuria (PCH) - caused by autoantibodies that demonstrate anti-P specificity PCH autoantibodies - IgG biphasic hemolysins - demonstrable only by Donath-Landsteiner test