MUST TO KNOW. IMMUNOHEMATOLOGY (BLOOD BANKING) ISBT 001 ‘ABO. ISBT 002 MNS ISBT 003 P ISBT 004 Rh. ISBT 005 Lutheran ISBT 006 Kell ISBT 007 Lewis ISBT 008 Duty ISBT 009 Kidd ISBT 010 Diego ISBT O11 Cartwright ISBT 012 Xg ISBT 013 Scianna ISBT 014 Dombrock ISBT 015 Colton ISBT 016 Landsteiner-Weiner ISBT 017 Chido/Rodgers ISBT 018 H ISBT-019 Kx, ISBT 020 Gerbich ISBT 021 (Cromer, ISBT 022 Knops ISBT 023 Indian Chromosome 1 Rh Duffy Scianna Cromer Knops Chromosome2 Gerbich Chromosome 4 MNS Chromosome 6 Chido/Rodgers ‘Chromosome 7 Cartwright Colton Kell Chromosome 9 ‘ABO Chromosome 11 Indian Chromosome 17 Diego Chromosome 18 Kidd Chromosome 19 H Lewis Landsteiner-Weiner Lutheran Chromosome 22 P Chromosome X Xg Kx. Chromosome: Not known | Dombrock Von Descatello (Decastello) | AB ‘Sturle (Sturli) Blood groups (Most common) 0 > A> B > AB (Least common) Page | 237Cell typing Forward/direct typi Specimen: RBCs (Ag) Reagents: nti-A (blue: trypan blue) nti-B (yellow: acroflavin dye) nti-AB (colorless) Uses of anti-AB Checks for the reaction of anti-A and anti-B Detects weak subgroup of A and B because it has higher titer of anti-A & anti-B ‘Serum typing Reverse/indirect typing Specimen: Serum (Ab) = 3-6 months (development) Reagents: Gel typing Major Advantage: Standardization Medium: Dextran-acrylamide gel 0 = Unagglutinated Cells --- (media)---> Battam of the jttube (microtube) > May concentrate at the bottom of ptube Throughout the length of the tube Concentrate near the tap of the jitube ‘Top of the media Mixed-field: gglutinated cells --(media)—-> Top inagglutinated cells --(media)---> Bottom Red cell Ag-Ab reactions jo agglutination/hemolysis ‘ny agglutinates, turbid BG 1+= Small agglutinates, turbid BG (25% agglutination) 2+ = Medium agglutinates, clear BG (50% agglutination) 3+=Large agglutinate, clear BG (75% agglutination) 4+ = One solid agglutinate (100% agglutination) Universal donor Group 0. Universal recipient Group AB Universal donor for RBCs Group 0 (No Ag) Universal recipient for RBCs Group AB (No Ab) Universal donor for plasma Group AB (No Ab) Universal recipient for plasma Group AB (No Ag) RCS: Red cell suspension BB =2-5% RCS Approximate = Tomato red Exact % RCS = [Vol. RBCs (mL) + TV (mL)] x 100 Genotype One's genetic makeup Phenotype Expression of one’s genes Homozygous. In double dose Heterozygous In single dose Dominant. Always expressed even in the heterozygous state Recessive Not expressed when (+) dominant gene To be expressed, it should be in the homozygous state Allele One of two or more different genes that may occupy a specificlocus on a chromosome Silent/amorph Only indicates the absence of the Ag Von Dungern Hirafeld ‘Subgroups of A = A; (80%) and Az (20%) Page | 238Dolichos biflorus Lectin source of anti-A Phenotype Possible Genotypes AL AA Aida. AO Ao AcAz A,0 AB AB ADB ABB. B oO Gene Glycosyltransferase ‘Ag | Acceptor molecule H L-fucosyltransferase H_|_ Precursor subs. A N-acetylgalactosaminyltransferase N-acetyl-D-galactosamine | A H B D-galactosyltransferase D-galactose B H ‘AB | _ N-acetylgalactosaminyltransferase N-acetyl-D-galactosamine | A H D-galactosyltransferase D-galactose B oO 7 7 ~ Unchanged H Amount of H Ag (Greatest) 0 > Az > B > AoB > A > A:B (Least) Bombay individual Bhende (-) Hgene hh or Hout Lack H, A and B Ag’s Designated as On w/ anti-H, anti-A and anti-B Ab's Mistyped as group 0 Parabombay Inherit weak H gene w/ detectable A and B Ag's but no detectable H Ag ‘Ay, By, AB) Anti-H Differentiates Group 0 from Oy individuals Ulex europaeus Lectin source of anti-H ‘ABO Histoblood group = present on all tissues and organs of the body May be expressed in secretions depending on the secretor status (SeSe or Sese) Determination of Secretor Status ‘Specimen: Saliva Principle: Hemagglutination-inhibition ‘ABO antibodies Mixture of lgM. 1gG and IgA (Henry) Anti-A Anti-B Predominantly IgM React at room temp Naturally occurring ‘Anti-A.B (Group 0) Predominantly IgG React at 37°C Immune Ab Immune Ab’s, Production is stimulated by: 1. Pregnancy 2. Incompatible transfusion and transplant ‘ABO HDN Mother: Group 0 Child: Group A or B Group | discrepancies ‘Weak reacting/missing Ab’s Newborns Elderly patients Hypogammaglobulinemia/agammaglobulinemia Page | 239Group discrepancies ‘Weak reacting/missing Ag's (Less frequent) Leukemia Acquired B phenomenon Subgroups of A Hodgkin's disease BGSS (Remedy: Wash RBCs) Group III discrepancies Plasma abnormalities resulting to Rouleaux formation (Plasma factor) % globulins: MM, WM, HL, ‘fibrinogen Dextran and PVP Wharton's jelly (Remedy: Wash cord cells 6-8x (7x) Group IV Miscellaneous: Polyagglutination Anti-I (cold agglutinin) Cis “AB phenotype” Unexpected ABO isoagglutinins: inti-H: produced by Ai and AB (YH Ag) inti-A,: produced by Az and AcB (No Ai Ag) A Subgroups Ay MF agglutination w/ anti-A & anti-A.B Ac Weak MF agglutination w/ anti-A& anti-A,B ‘Acnd MF agglutination w/anti-A,B ‘An (- Agglutination, (+) AH substance in secretions A, (-) Agglutination, / AH substance in secretions, ‘Aci (-) Agglutination, [+] H substance in secretions B Subgroups Ba MF agglutination w/ anti-B & anti-A.B B, MF agglutination w/anti-A,B Bm (-)Agglutination, (+) BH substance in secretions Bu, (-) Agglutination, (+) H substance in secretions Rh Nomenclatures 1 Rosenfield = no genetic basis, indicates the presence or absence of Rh Ag’s 2. Fisher-Race (DCE) = inheritance of 3 genes (d= amorph/silent) 3. Wiener (Rh-hr) = inheritance of 1 gene (Ex. R®), w/c codes for an agglutinogen (Ex. Rha), w/c contains 3 blood factors (Ex. Rhohr’hr”) Immunogenicity of Rh Ag’s (Most immunogenic) D > c>E > C> e (Least immunogenic) Rorr Dord tor’ Ce 2or” cE Zory CE G D+C+ red cell Rh: 13,14, 15, 16 4 different parts of the D mosaic Genetic weak D D Ag's expressed appear to be complete, but few in number D Mosaic (Partial D) Ifone or more parts of D Ag is missing > weakened expression of D Ag May produce anti-D (Ab against missing fragment) 4 fragments Trans D-(trans)—> C (Ex. Dee/dCe) f (ce) c ---(cis)---> e [Ex. Dce/DCE] rh (Ce) ‘C—(cis)---> e [Ex. DCe/DcE] Hro “Common” Rh phenotypes (RiRi, RoRo, rr) Rh Ab’s IgG: and IgGs React at 37°C Immune Ab’ Page| 240()C binding = extravascular hemolysis (delayed HTR) RhADN Mother: Rh (-) Child: Rh (+), 24 pregnancy RhoGam or Rhig Purified anti-D Administer w/in 72 hrs after 1% delivery Full dose RhoGam 300 jig anti-D (212 weeks gestation) Protect up to 30mL D+ WB or 15mL D+ RBCs Minidose/Microdose 50 wg anti-D RhoGam Protect up to Sml. of D+ WE or 2.5ml. D+ RBCs (<12 weeks gestation) Ex. Abortion # Rhig vials Volume of EMH (mL) = 30 Vol. FMH = % fetal cells x 50 x= (% Fetal cells x 50) + 30 x=_+1=#Rhigvials As little as Iml Rh(+) RBC Rh+ Produces anti-D RBCs + anti-D = (+) agglutination Perform test for D® (IAT) IE RBCs + anti-D = (-) agglutination = IAT is (+) agglutination = +D" (weak D) Rh- RECs + anti-D + AHG reagent = (-) agglutination 2 conditions wherein an Rh- pt. can be transfused w/ Rh+ blood 1.No prior exposure to D Ag (males) or past childbearing age (females) 2. Administer RhoGam “Anti-LW (Landsteiner-Weiner) Originally identified as anti-Rh in early experiments involving rabbits, immunized w/ Rhesus monkey blood Anti-LW agglutinates Rh+ and Rh- cells except Rhyui cells Rlina No Rh Ag Designated as -~ Stomatocytes Rhdeleted No C/cand E/e Ag Designated as D--/D-~ Lewis system Le gene codes for the production of fucosyltransferase enzyme that catalyzes addition of fucose to the 4° C of N-acetylglucosamine of type 1 precursor Lewis Ag’s Le®---(Se)—-> Le? Produced by tissue cells, Not well developed at birth = NB/cord cells = Le(a-b-) Decreased expression during pregnancy Genotype ‘Substances (Secretion) Phenotype Le Ab's ABH, lele, sese None. ABH, Le(a-b-) Anti-Le® & Anti-Le® ABH, lele, SeSe/Sese ‘ABH ‘ABH, Le(a-b-) Anti-Le® & Anti-Le? ABH, LeLe/Lele, sese Let ABH, Le(a+b-) ‘ABH, LeLe/Lele, SeSe/Sese ABH, Le®, Le? ABH, Le(a-b+) Lewis Ab's ‘Anti-Le* & Anti-Le® Naturally occurring IgM Activates the C’ MNAg’s Glycophorin A (MN-SGP) M= Ser-Ser-Threo-Threo-Gly N= Leu-Ser-Threo-Threo-Glu Well developed at birth Important in paternity testing ‘Anti-M IgM, pH-dependent (6.5), glucose-dependent Page | 241“Anti-N-like Ab IgM Found in renal patients dialyzed w/ formaldehyde sterilized equipment SSAg’s Glycophorin B (Ss-SGP) = Methionine (29) = Threonine (29) SS AD'S IgG React at 37°C and AHG Severe HTR w/ hemoglobinuria and HD. Phenotype Detectable Ag’s, Possible Ab’s Pi Pyand P ‘None Pe P Anti-P) p(pnull) ‘None ‘Anti-P, Py, PF (anti-T}>) Pik Ps and P: ‘Anti-P Poi Pk Anti-P, anti-Py Pylike Plasma, pigeon and turtledove droppings, turtledove egawhit P, substance Hydatid cyst fluid, Lumbricoides terrestris, Ascaris suum Anti-P; IgM Naturally occurring Strong anti-P; = Hydatid disease (E. granulosus) Associated w/ fascioliasis, C. sinensis and O. viverrini infections. Anti-T? Anti-P, Pi, PF Spontaneous abortions in early pregnancy Anti-P, IgG Naturally occurring Biphasic hemolysin (PCH) ‘Test: Donath-Landsteiner TiBlood Group I: Individuality Neonates = VII (Ag) Adults (18 mos.-adult} THEMPAS 4 Agin adults Anti-l Interfere w/ reverse typing (Group IV) Benign anti-I = normal, IgM, naturally occurring, react at 4’C Pathologic anti-I = IgM, react at 30/32'C (CAS = PAP) Autoanti-1= M. pneumoniae, L. monocytogenes Anti IgM Reactat 4'C EBV caused Diseases of RES: - Alcoholic cirrhosis - Myeloid leukemia - Reticuloses Anti-T? Transition: from i> 1 Yanomama Indians Hodgkin’slymphoma K Kell k Kp* Cellano Penney Kp Rautenberg, Js* Sutter Is Matthews Kell Ags Immunogenicity: 2% to D (D>K>c>E>C>e) Synthesized on precursor Kx Page | 242in WBCs: remain unconverted. If (-) > CGD \n RBCs: converted to Kell Ag’s. If (-) -> MacLeod phenotype Macleod phenotype ‘Acanthocytosis Muscular dystrophy ‘Anti-K IgG React at 37'Cand ANG Fy(atb-) Chinese (90.8%) Fy(a-b-) ‘American blacks Resistant to P. vivax/P. knowlesi (malaria) Fy and Fy Receptors for malaria Duffy gene 1 human gene to be assigned to specific chromosome (1) Anti-Fy= IgG Anti-Fy? React at AHG Jk and Jk Enhanced by enzymes Anti-jke Notorious antibody = not easily detected Antik? Immune Ab's (IgG) Common cause of delayed HTR Autoanti-Jk= Methyldopa (Aldomet) Lu®and Lu Development at age of 15 Anti-Lu? IgG, IgM, IgA Naturally occurring React at room temp ‘Anti-Lub IgGs, IgM, IgA Immune Ab React at 37°C Diego (Di) Mongolian ancestry AE=-1 = HCOs <--> Ch Defect in AE molecule “ASO” Acanthocytosis Hereditary Spherocytosis SEA Ovalocytosis Cartwright (Yt) Erythrocyte acetylcholinesterase = neurotransmission Xe Sex-linked 4% Females Short arm of X chromosome Scianna Sel, Sc2, Se3. Dombrock Colton (Co) Gregory (Gy*) Holley (Hy) Joseph (Jo*) CHIP, Aquaporin = water permeability Chido/Rodgers (Ch/Re) HLA system (Bg) C4A (Rg) and C4B (Ch) = C’ component HTLA = exhibit reaction only at high dilution DAF (Cr) Gerbich (Ge) GPC and GPD Leach phenotype (GE: -2, -3, -4) = Elliptocytosis Cromer (Cr) DAF CROM Ab's = black individuals | Knops (Kn) Indian (In) CRI (C' receptor 1) CD44 (immune adhesion) Benneth-Goodspeed (Bg) HLA g's on RBCs (Class I MHC) Bge = HLA-A7 Page | 243LA-B28 Public Ag idence Ag’s En: (99.9%) Private Ag. Low-incidence Ag's (<1%) HTLA Ab's ‘Anti-Ch Anti-Rg Anti-Kn Anti-Yke Anti-Cs* Anti-McC Anti-JMH. Soures of Substances for Neutralization for Certain Antibodies Hydatid cyst fluid, pigeon droppings, turtledoves’ egg whites Plasma/serum, secretor saliva ‘Anti-Ch, Anti-Rg, Plasma/serum Urine, guinea pig urine Anti-l Mother's milk ‘Anti-H Saliva Effect of Proteolytic Enzymes on Select Antigen-Antibody Reactions Enhanced Ph Rh I Kidd Lewis Destroyed MNS Duffy Chido Rodgers Cartwright Xg Donation Process ‘At least 2 persons Bleeder Head (BB) Donor registration 1 stop Interview & physical exam 2n4 step ‘Actual donor selection and blood collection 3% step Collection <15 mins (7-10mins) >15 mins = (-) cryoprecipitate Donor bleeding 45° angle > 10-20° angle (Venipuncture: 15" angle) Basic Qualifications of the Potential Blood Donor. Good health Purplish blue lesions > Kaposi's sarcoma (HIV, HHV-8) ‘Age 118-65 yrs old <18 yrs old = w/ parent's consent >65 yrs old = w/ physician's consent Body weight Max: 10.5mL./kg Ideal: 110 Ibs (SOkg) 450mL blood + 30mL blood (serologic tests) 63mL anticoagulant Page | 244Donor “<110 Ibs ( sink w/in 15 secs (Hgb: 212.5 g/dL) Donor Deferral Permanent Chagas’ disease Babesiosis Tegison (Tx: Psoriasis) = teratogenic Recipient of human (pituitary)-derived Gi [Recombinant GH = no deferral] Recipient of cornea/dura mater = risk of transmitting CJD isk of transmitting CD 3 years Malaria refugee/immigrant ‘year (12 months) Recipients of blood known to be possible sources of hepatitis, ‘Tattoo Rape Incarceration in jail (3 days/72 hrs) Blood transfusion Major operation including dental surgery Syphilis Gonorrhea Traveler > malaria-endemic places Rabies vaccine ‘9 months (DOH) Childbirth (AABB: 6 weeks) 3 months (12 weeks) [DoH] Recent blood donation (AABB: 8 weeks) = 450ml blood: 12 weeks .00mL blood: 6-8 weeks ‘Tmonth (4 weeks) Rubella vaccine Isotretinoin Accutane (Tx: Acne) = teratogenic Proscar (Tx: Benign prostatic hyperplasia 2-3 weeks After febrile episodes Page | 2452 weeks Rubeola vaccine Polio vaccine Mumps vaccine 2 days (48 hrs) ter hemapheresi: 12hrs ‘After alcohol intake Cause: Arterial puncture | Jet-like pulsating bleeding w/ bright red blood Citrate Binds Ca2* Massive transfusion (8-10 units) ~ Citrate toxicity > Hypocalcemia Milk= Ca? Dextrose/Glucose Provides energy for red cells Citric acid Prevents caramelization (WpH) Adenine For improved survival of red cells Phosphate buffer 4 ATP ShelF-life: 21 days ACD (Apheresis) CPD CP2D Shelf-life: 35 days CPDA-1 Shelf 42 days CPDA-2 (DOH) Additive solutions: -Adsol (AS-1) -Nutricel (AS-3) -Optisol (AS-5) ‘Additive solutions SAGM: Saline -Adenine -Glucose -Mannitol = RBC membrane stabilizing agent Rejuvenation solutions ‘ATP & 2,3-DPG (Rejuvesol) PIGPA = Phosphate, Inosine, Glucose, Pyruvate, Ade PIPA = Phosphate, Inosine, Pyruvate, Adenine Heavy spin 5000g for Smins = pRBC, platelet concentrate 5000g for 7mins = cryo, cell-free plasma Light spin 2000g for 3mins = platelet-rich plasma 6-8 hours processing ‘To maximize the number of components derived from 1 unit of blood Platelet concentrate Light spin > Heavy spin Centrifuge at 20-24°C [Other blood components: Ref. centrifuge (1-6'C)] ‘Bacterial contamination Separate from WB w/in 6-8 hrs Blood Indication Storage | Transport Shelf-life Other Info ‘Component Whole blood T.Blood vol. expansion& ® | 1-6'C Tie | 21d (ACD,CPD) | Tunit: RBC mass 35d (CPDA-1) ‘High by 1 to 2. Massive transfusion & 424 (CPDA-2) 15g/dl. acute blood loss 2d (Heparin AHict by 3-5% Packed RBCS | 1.4 RBC mass 16C T10C | Opensystem: 24h | *80% plasma (Normovolemicpatients) Closed syster removed 21d(ACD,CPD) —_| (Het: 65-80% but 354 (CPDA-1) not >80%) Luni ‘High by 1 to 1Sg/dl. AHiet by 3-5% Page| 246Blood Indication ‘Storage | Transport Shelf-life Other Info ‘Component Leukoreduced | 1. FNHTR (Leuko. Ab’s) = 16C rive | Sameas WB Preparation: RBCs ‘NVC in temp. 1. Centrifugation 2. Prevent CMV 2, Filtration 3.Saline washing Washed RBCs | 1. Allergic (plasma w/ 16C 24h Also for foreign protein) ‘polyagglutination 2, FNHTR (Leuko, Ab's) Anaphylactic: VigA w/ anti ga Frozen RBCS 1.Prolongstorage ofrare | -65'Cor 10 years units “125°C 2. Prolong storage of autologous units Deglycerolized 24h RBCS Fresh frozen 1. Multiple coag. factor def, | -18C Tyear (18°C) Contains plasma, plasma (liver disease) -65'C 7 years (-65'°C) | all coag. factors and 2, Replace isolated factor ‘complement def. when specific PRP: Thaw at 37°C components not available Thawed plasma: 3. Reverse effects of store at 1-6°C coumarin/warfarin Administer w/in 24hrs once thawed Cryoprecipitate | 1. Fibrinogen det. =18'C or Tyear ‘Contains: 2.Memophilia A colder -150mg fibrinogen 3.vWD -80 U AHF 4. Factor XIll det. “vWF -Factor XII 4Cryoppt: Thaw at 37C “Thawed cryoppt (<15mt; notgroup- spec): store at RT Administer w/in 6 hrs Granulocyte T. Granulocyte dysfunction | 20-24 24h Contains 1x 10 ‘concentrate (cab) w/o granulocytes, 2. Myeloid hypoplasia agitation Platelet 1. Thrombocytopenia 20-24 5d(20-2#Cw/ | Tunitwill ® concentrate w/ agitation) platelet count by agitation 2d (1-6'C) 5,000- 10,000/ul 16°C Irradiated blood | 1. Prevent GVHD 28 days from Usually RBCS and ‘component irradiation or orig. | plateletsare exp. date irradiated whichever comes first Factor Vil 1. ForhemophiliaA T6C Varies Stored in ‘concentrate lyophilized form Factor IX T. For hemophilia B T6C Varies “Aka. prothrombin concentrate complex Contains factors Il, Vil, and X NSA T. Hypovolemieshock 2A0C S years 96% Albumin 4% Globulin Page | 247Blood Indication ‘Storage | Transport Shelf-life Other Info Component PPF T. Hypovolemieshock ZAC Syears 80-85% Albumin 10-15% Globulin ‘SDP 5 years SDP: Single donor plasma Methods of Freezing RBCs Concentration Frozen at Stored at Equipment High glycerol 40% w/v glycerol | -80'C “65°C Mechanical (Slow freezing) freezer Low glycerol 20% w/v glycerol | -196'C =120°C Liquid nitrogen (Fast freezing) ‘Agglomeration Glycerol “80°C ~65C Mechanical Glucose freezer Fructose EDTA Cryoprotective agent Prevents rupture of RBCs during freezing Ex. Glycerol Deglycerolization Removal of glycerol Hypertonic solution followed by an isotonic solution High glycerol (DG) 1.6% NaCl -----> 0.9% NaCl Low glycerol (DG) 45% NaCl in 15% mannitol ‘Agglomeration (DG) 50% Glucose + 5% Fructose -----> 0.9% NaCl Cryoprecipitate After thawing = administer w/in 6 hours After pooling = administer w/in 4 hours Leukapheresis HES (Hydroxyethylstarch) = Separation bet. WBCs and RBCS Donor: administered w/ corticosteroids 12-24 hrs before donation = ¥ of circulating granulocytes Plateletpheresis Usually takes 1-2 hours Donor: = Platelet count: 2150 x 10°/L spirin-free: 3 days Single donor platelets (SDP) ‘Aka. super packed platelets From plateletpheresis For patients who are refractory or unresponsive to RDP Limit patient exposure to multiple donors RDP: Random Donor Platelets ‘SDP: Single Donor Platelets Preparation From WB: Light spin > Heavy spin Plateletpheresis Amount 5.5 x 10! platelets 3.0.x 10" platelets Vol. of plasma 50-75mL 300ml. pH 2 6.0 (New: 6.2) 26.0 (New: 6.2) Storage 20-24'C w/ agitation 20-24'C w/ agitation ‘Shelf-life 5 days 5 days ‘Atrisk of TA-GVHD Recipient of BM transplant Patients w/ hematologic or oncologic disease Patients w/ congenital immunodeficiency Recipient of blood from 1: degree relative (direct) Irradiation Radiation source: 25-35 Gy (Gy: Gray | 1Gy = 100 rads) a, Cesium (Ce) b. Cobalt (Co) Infusion IV fluids: a. NSS = the only fluid allowed to start an IV line prior to transfusion Page | 248’b. DSW (5% dextrose in 1120) = Not allowed to start (hypotonic > hemolysis) Ringer's lactate =not allowed to start (contains Ca?* > promote coagulation) Blood warmers 37°C Temp. >42'C = hemolyzed Filters 1. Clot screen filter (170m) = to remove gross clots 2. Leukocyte depletion filter ‘Speed of infusion 1Sgtts = ImL 1 unit must be completed w/in 4hrs of blood transfusion Polyagglutination (Hubener-Thomsen-Fridenrich Phenomenon) Cryptantigens Hidden Ag's Covered w/ NANA (N-acetylneuraminic acid) or sialicacid When NANA is destroyed (by neuraminidase) > Ag's are exposed Exposed Ag's > Agglutination = React w/ tetrasaccharide of Thomas & Winzler (Treceptor) Acquired Microbially-Associated Polyagglutination C.perfringens V. cholerae S. pneumoniae All produce neuraminidase Th E.coli Proteus sp. Produce weaker neuraminidase Tx Bacterial and viral Unknown mechanism. Te “CABS” C.albicans A niger B. fragilis S.marcescens All produce enda/exogalactosidase Altered precursor substances (Altered: ABH, Le, |, P) ‘Acquired B phenomenon Bacteria: Deacetylase enzyme N-acetylgalactasamine--(Deacetylase)--> N-acetyl + galactosamine Galactosamine = Group B Remedy: Add acetic anhydride VA Vienna, Virginia Microbial fucosidase = Wfucose = WH ‘Acquired Non-Microbially Associated Polyagglutination Th (-) B-3-D-galactosyltransferase enzyme needed for the normal structure of T receptor (Tetrasaccharide of Thomas and Winzler) Inherited Polyagglutination Cad sae HEMPAS/CDAI Adult iAg= VH Ag VSialicacid Others HbM - Hyde Park NOR = Norfolk, Virginia Page| 249Tm Cad T Tk Arachis hypogaea - = + + Salvia sclarea + : - : Salvia horminum + + : : Glycine soja + + + = Predeposit AD Autologous Donation icipated transfusion “No age limit *No strict we “Hgb= 11g/dL *Het 2 33% *Frequency: every > 3days ht requirement (Wvol. by 4mL/1 pound below 110) Intraoperative AD_ Collect blood during surgical procedure > reinfused immediately Immediate preoperative hemodilution. Collect blood > replace patient volume w/ colloid crystalloid > reinfuse during surgical procedure Postoperative salvage Drainage tube Postoperative bleeding > salvaged (saved) > clean and reinfused Immediate Immune Transfusion Reactions FNHTR A 1Cin temperature Cause: anti-leukocyte Ab's (leukoagglutinins) Prevention: Leukopoor RBCs Allergic Cause: Donor plasma w/ foreign proteins Prevention: Washed RBCs ‘Anaphylactic ‘Afebrile (no fever) Signs and symptoms occur only after the infusion of only few mL of blood IgA deficiency w/ anti-Iga antibody Prevention: Washed RBCs | IgA-deficient donor (rare) ‘Anaphylactoid Afebrile Normal IgA w/ anti-IgA to donor IgA Prevention: Washed RBCs | IgA-deficient donor (rare) ‘TRALI (NCPE) Cause: Anti-leukocyte Ab's (leukoagglutinins) Signs and symptoms resemble respiratory distress Prevention: Leukopoor RBCs Hemolytic Bleeding, hypotension, hemoglobinuria, anuria Delayed Immune Transfusion Reactions TA-GVHD Cause: T lymphocyte proliferation Prevention: Irradiated RBCs PTP DHTR Onset of thrombocytopenia Cause: anti-platelet Ab’s (HPA-1a negative platelets) Prevention: Therapy a. Administration of corticosteroid , Exchange transfusion c.1V immunoglobulins Tdays Immediate Nonimmune Transfusion Reactions TACO ‘Administration of blood w/o equivalent blood loss Iatrogenic: physician-caused Atrisk: a. Young children b Elderly patients Page | 250Patients w/ cardiac disease Prevention: Therapy a. Therapeutic phlebotomy b.IV diuretics 0; therapy Bacterial contamination Cause: Endotoxin production by psychrophilic/cryophilic bacteria ¥. enterocolitica (most common) E.coli P. aeruginosa Factors: a. During phlebotomy b, During preparation /processing . During thawing Prevention: a. Sterile technique b. Visual inspection of unit — Blood unit = Brown, purple, hemolysis, clot — Plasma = Murky (dark brown) purple, red. PCITR Causes: - Small bore needle - Warming blood above 50°C - Freezing blood w/o cryoprotective agent - Citrate toxicity Delayed Nonimmune Transfusion Reactions Iron Overload (Hemosiderosis) Patients w/ normovolemic anemia ‘Transfusion-dependend patients: - Aplastic anemia = Congenital hemolytic anemia Prevention a. Iron-chelating agent = Deferroxamine b, Neocytes = young RBCs, has longer lifespan Disease transmi HBV, HCV, HDV, CMY, EBV, HTLV-1 and Il, HIV, T. pallidum, Plasmodium spp., B. microti, T. cruzi, T. gondii Hemolytic Disease of the Newborn Inutero ‘Anemia ( immature RBCs, enlarged spleen & liver = extramedullary hematopoiesis) Hydrops fetalis = cardiac insufficiency, edema Neonatal period. 4 Unconjugated bilirubin > Brain > Kernicterus ‘Treatment 1. Intrauterine transfusion -Inutero - Corrects anemia - X-match: Mother's serum 2. Exchange transfusion - Neonatal period - Removes bilirubin & Ab-coated RBCs - X-match: Mother's serum (preferred) or infant's serum Cross-Matching Full X-mateh. Zhours Can be shortened to 30 mins ‘Abbreviated X-match Electronic X-match Type/screen + immediate spin DC/PS = no agglutination/hemolysis Patient blood type is determined on 2 occasions Page | 251Emergency situation Patient blood type is unknown Group 0 (Rh-) pRBCs (#4) Major X-match ( Alloantibody control (+) Autoantibody, autocontrol Ratio of serum to cells Routine = 40:1 Det. weak Ab’s = 133:1 Saline for washing pH 7.2-7.4 Incubation period 30-120 mins (majority: 30 mins) Enhancement media 1. Albumin 2. PEG 3. LISS (Incubation pd: 5-15 mins) Lectin Sources ‘Anti-Ay Dolichosbiflorus ‘Anti-H Ulex europaeus ‘Anti-M Iberisamara Iberis umbellate Iberis semperivens Macluraaurantiaca ‘Ant-N Bauhinia variegate Bauhinia purpura Bauhinia bonatiana Bauhinia candicans Vicia graminea Anti-B Bandeiraesimplicifolia Quality Control Annually Mercury thermometers Quarterly (Every 3 months) ell washers (speed, timer) Blood warmers Monthly ‘Alarm Activation (refrigeration and freezers) Temperature (refrigerated centrifuge) Daily Refrigerators and freezers (continuous monitors) Platelet incubators (enclosed, monitored chambers) Daily when in use Transfusion service: - Heating blocks = Water baths Donor facility: - Donor unit agitators Scales - Balances = Hemoglobinometer - Microhematocrit centrifuges Every 4 hours Platelet incubators (ambient temperature storage) Other Topi “Apheresis/Hemapheresis Whole blood is withdrawn, a desired component separated, and the remainder of the tube returned to the donor Intermittent-flow centrifugation (IFC) ‘venipuncture Blood is withdrawn and reinfused through the same needle Once the desired component is separated, the remaining components are reinfused to the donor Continuous-flow centrifugation (CFC) 2 venipunctures Withdraw, process and return the blood to the individual simultaneoush Page | 252Antibody screen Collect new specimen every 3 days in a series of transfusion Donor & recipient samples Keep for 7 days after transfusion (at1-6'¢) Compatibility testing Series of tests that ensure safety of transfusion to recipient and donor 1. Review of BB records 2. ABO and Rh 3. Ab screen 4, Cross matching DHTRs. Occur 3 to 7 days after transfusion Virus inactivation in plasma products Heating in a liquid state w/ LMW stabilizers Heating in lyophilized state UVirradiation ¥. enterocolitica 44 Bacterial contamination of blood. Dei Separates neocytes from mature RBCs Requirementsforblood | 1.(-) HbS products to be transfused | 2. <7 days to infants 3.y-irradiated 4.) CMV, ‘Allogeneic donor blood from outside sources Repeat ABO and Rh typing ‘w/in 30 mins Time limit when a unit of blood is removed from 2-8'Cand returned back to the refrigerator Procedure when HTR| occurs 1. Stop transfusion 2. Keep IV line open 3. Notify the physician and BB ‘Specimens for investigation of HTR 1. Patient pre-transfusion blood sample 2. Patient post-transfusion blood sample PT/PTT/DAT = Pink: Hgb 0.2 g/L or 20 mg/dL. ed: Hgb >1 g/L. or 100 me/dL. 3. Patient post-transfusion urine = Bilirubin/Urobilinogen 4.Blood bag = GS/CS LISS Glycine/glucose+ saline 5=15 mins incubation ‘ZZAP Cysteine-activated papait Mixture of DTT and papain True chimerism Presence of 2 cell population Ex. Twins Mixed-field agglutination ‘Artificial chimerism ‘After: -BM transplantation -Blood transfusion -Exchange transfusion -Fetomaternal hemorrhage ‘AB cis genotype Group IV discrepancy Inheritance of 3 ABO genes (AB/O) ‘Acquired A antigen 1. Tn activation 2. P. mirabilis Pace 126%‘Acquired B antigen “EPIC” 1. E.coli Oss 2. P. vulgaris 3. Intestinal obstruction 4. Carcinoma of the colon and rectum HAT medium Hypoxanthine, Aminopterin, Thymidine medium, Culture for hybridoma cells Hybridoma cells, Plasma cells (mouse + myeloma cells + PEG Polyspecific AHG reagent | Anti-IgG and anti-C3d_ Prepared by conventional technique (rabbits) Monospecific ANG reagent | Anti-IgG or anti-C3d Prepared by monoclonal Ab production (mice) ‘Type 1 precursor substance | B 1> 3 ABH substance in secretions (glycoproteins) HAB, Se, Le genes Type 2 precursor substance | B 1>4 ‘ABH on RBC (glycoproteins) HAB genes Agglutination in Gel Incompatible technology ‘Affinity column technology | Affinity adherence of IgG-sensitized RBCs to immunologically active matrix (Gamma ReACT) ‘Wash RBCs 2-3x to remove unbound globulins # cryobags [Desired level of Factor VIII x volume of plasma (ml)] + 80 # units to test # units required + frequency of donors (-) for relevant Ag Enzyme technique 1 Papain = papaya 2. Bromelin = pineapple 3.Ficin = figs 4. Trypsin = pig's stomach Elution Breaking of bonds between Ag and Ab by: a, Physical: heating, shaking b. Chemical: ether, acid ‘Adsorption. Removal of Ab in serum using appropriate RBC Biphasic hemolysin Cold = attaches to RBCs Warm = RBC lysis, Perfluorocarbons Oz carrying capacity RBC substitute Page | 254