MUST TO KNOW BLOOD BANKING PDF

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MUST TO KNOW IN IMMUNOHEMATOLOGY (BLOOD BANKING)ISBT 001 ABOISBT 002 MNSISBT 003 PISBT 004 RhISBT 005 LutheranISBT 006 KellISBT 007 LewisISBT 008 DuffyISBT 009 KiddISBT 010 DiegoISBT 011 CartwrightISBT 012 XgISBT 013 SciannaISBT 014 DombrockISBT 015 ColtonISBT 016 Landsteiner-WeinerISBT 017 Chido/Ro...

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MUST TO KNOW IN IMMUNOHEMATOLOGY (BLOOD BANKING) ABO MNS P Rh Lutheran Kell Lewis Duffy Kidd Diego Cartwright Xg Scianna Dombrock Colton Landsteiner-Weiner Chido/Rodgers H Kx Gerbich Cromer Knops Indian Rh Duffy Scianna Cromer Knops Chromosome 2 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 Xg Chromosome X Kx Chromosome: Not known Dombrock Von Descatello (Decastello) AB Sturle (Sturli) ISBT 001 ISBT 002 ISBT 003 ISBT 004 ISBT 005 ISBT 006 ISBT 007 ISBT 008 ISBT 009 ISBT 010 ISBT 011 ISBT 012 ISBT 013 ISBT 014 ISBT 015 ISBT 016 ISBT 017 ISBT 018 ISBT 019 ISBT 020 ISBT 021 ISBT 022 ISBT 023 Chromosome 1

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Blood groups

(Most common) O > A > B > AB (Least common)

Cell typing

Forward/direct typing Specimen: RBCs (Ag) Reagents: = Anti-A (blue: trypan blue) = Anti-B (yellow: acroflavin dye) = Anti-AB (colorless) 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 Reverse/indirect typing Specimen: Serum (Ab) = 3-6 months (development) Reagents: = A1 cells = B cells Major Advantage: Standardization Medium: Dextran-acrylamide gel 0 = Unagglutinated Cells ---(media)---> Bottom of the μtube (microtube) 1+ = Agglutinated cells ---(media)---> May concentrate at the bottom of μtube 2+ = Agglutinated cells ---(media)---> Throughout the length of the μtube 3+ = Agglutinated cells ---(media)---> Concentrate near the top of the μtube 4+ = Agglutinated cells ---(media)---> Top of the media Mixed-field: = Agglutinated cells ---(media)---> Top = Unagglutinated cells ---(media)---> Bottom 0 = No agglutination/hemolysis W+ = Tiny 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) Group O Group AB Group O (No Ag) Group AB (No Ab) Group AB (No Ab) Group AB (No Ag)

Uses of anti-AB Serum typing

Gel typing

Red cell Ag-Ab reactions

Universal donor Universal recipient Universal donor for RBCs Universal recipient for RBCs Universal donor for plasma Universal recipient for plasma RCS: Red cell suspension

Genotype Phenotype Homozygous Heterozygous Dominant Recessive Allele

BB = 2-5% RCS Approximate = Tomato red Exact % RCS = [Vol. RBCs (mL) ÷ TV (mL)] x 100 One’s genetic makeup Expression of one’s genes In double dose In single dose Always expressed even in the heterozygous state Not expressed when (+) dominant gene To be expressed, it should be in the homozygous state One of two or more different genes that may occupy a specific locus on a chromosome Page | 2

Silent/amorph Von Dungern Hirzfeld Dolichos biflorus Phenotype A1

Only indicates the absence of the Ag Subgroups of A = A1 (80%) and A2 (20%) Lectin source of anti-A1

Possible Genotypes A1A1 A1A2 A1O A2 A2A2 A2O A1B A1B A2B A2B B BB BO O OO Gene Glycosyltransferase Immunodominant Sugar Ag Acceptor molecule H L-fucosyltransferase L-fucose 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 O ---Unchanged H Amount of H Ag (Greatest) O > A2 > B > A2B > A1 > A1B (Least) Bombay individual Bhende (-) H gene hh or Hnull Lack H, A and B Ag’s Designated as Oh w/ anti-H, anti-A and anti-B Ab’s Mistyped as group O Parabombay Inherit weak H gene w/ detectable A and B Ag’s but no detectable H Ag Ah, Bh, ABh Anti-H Differentiates Group O from Oh 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 Specimen: Saliva Status Principle: Hemagglutination-inhibition ABO antibodies Mixture of IgM, IgG and IgA (Henry) Anti-A Predominantly IgM Anti-B React at room temp Naturally occurring Anti-A,B (Group O) 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 O Page | 3

Group I discrepancies

Group II discrepancies

Group III discrepancies

Group IV

A3 Ax Aend Am Ay Ael B3 Bx Bm Bel Rh Nomenclatures

Immunogenicity of Rh Ag’s R or r 1 or ‘ 2 or ‘’ Z or y G Rh: 13, 14, 15, 16 Genetic weak D D Mosaic (Partial D)

Child: Group A or B Weak reacting/missing Ab’s Newborns Elderly patients Hypogammaglobulinemia/agammaglobulinemia Weak reacting/missing Ag’s (Less frequent) Leukemia Acquired B phenomenon Subgroups of A Hodgkin’s disease BGSS (Remedy: Wash RBCs) 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) Miscellaneous: Polyagglutination Anti-I (cold agglutinin) Cis “AB phenotype” Unexpected ABO isoagglutinins: = Anti-H: produced by A1 and A1B (H Ag) = Anti-A1: produced by A2 and A2B (No A1 Ag) A Subgroups MF agglutination w/ anti-A & anti-A,B Weak MF agglutination w/ anti-A& anti-A,B MF agglutination w/ anti-A,B (-) Agglutination, (+) AH substance in secretions (-) Agglutination, AH substance in secretions (-) Agglutination, (+) H substance in secretions B Subgroups MF agglutination w/ anti-B & anti-A,B MF agglutination w/ anti-A,B (-) Agglutination, (+) BH substance in secretions (-) Agglutination, (+) H substance in secretions 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. R0), w/c codes for an agglutinogen (Ex. Rh0), w/c contains 3 blood factors (Ex. Rh0hr’hr’’) (Most immunogenic) D > c > E > C > e (Least immunogenic) D or d Ce cE CE D+C+ red cell 4 different parts of the D mosaic D Ag’s expressed appear to be complete, but few in number If one or more parts of D Ag is missing weakened expression of D Ag May produce anti-D (Ab against missing fragment) 4 fragments Page | 4

C Trans f (ce) rhi (Ce) Hr0 Rh Ab’s

Rh HDN RhoGam or RhIg Full dose RhoGam (>12 weeks gestation) Minidose/Microdose RhoGam ( C (Ex. Dce/dCe) c ---(cis)---> e [Ex. Dce/DCE] C ---(cis)---> e [Ex. DCe/DcE] “Common” Rh phenotypes (R1R1, R2R2, rr) IgG1 and IgG3 React at 37’C Immune Ab’s (-) C’ binding = extravascular hemolysis (delayed HTR) Mother: Rh (-) Child: Rh (+), 2nd pregnancy Purified anti-D Administer w/in 72 hrs after 1st delivery 300 μg anti-D Protect up to 30mL D+ WB or 15mL D+ RBCs 50 μg anti-D Protect up to 5mL of D+ WB or 2.5mL D+ RBCs Ex. Abortion Volume of FMH (mL) ÷ 30 Vol. FMH = % fetal cells x 50 --------------------------------------------x = (% Fetal cells x 50) ÷ 30 x ≈ __ + 1 = # RhIg vials Produces anti-D RBCs + anti-D = (+) agglutination If RBCs + anti-D = (-) agglutination = IAT is (+) agglutination = +Du (weak D) RBCs + anti-D + AHG reagent = (-) agglutination 1. No prior exposure to D Ag (males) or past childbearing age (females) 2. Administer RhoGam Originally identified as anti-Rh in early experiments involving rabbits immunized w/ Rhesus monkey blood Anti-LW agglutinates Rh+ and Rh- cells except Rhnull cells No Rh Ag Designated as ---/--Stomatocytes No C/c and E/e Ag Designated as D--/D-Le gene codes for the production of fucosyltransferase enzyme that catalyzes addition of fucose to the 4th C of N-acetylglucosamine of type 1 precursor Lea ---(Se)---> Leb Produced by tissue cells Not well developed at birth = NB/cord cells = Le(a-b-) Decreased expression during pregnancy Le Ab’s Substances (Secretion) Phenotype Anti-Lea & Anti-Leb None ABH, Le(a-b-) ABH ABH, Le(a-b-) Anti-Lea & Anti-Leb a Le Anti-Leb ABH, Le(a+b-) ABH, Le(a-b+) none ABH, Lea, Leb a b Anti-Le & Anti-Le Page | 5

MN Ag’s

Anti-M Anti-N-like Ab SS Ag’s

Ss Ab’s

Phenotype P1 P2 p (p null) P1k P2k P1-like P1 substance Anti-P1

Anti-Tja Anti-P

Ii Blood Group

HEMPAS Anti-I

Anti-i

Naturally occurring IgM Activates the C’ Glycophorin A (MN-SGP) M = Ser-Ser-Threo-Threo-Gly N = Leu-Ser-Threo-Threo-Glu Well developed at birth Important in paternity testing IgM, pH-dependent (6.5), glucose-dependent IgM Found in renal patients dialyzed w/ formaldehyde sterilized equipment Glycophorin B (Ss-SGP) S = Methionine (29th) s = Threonine (29th) IgG React at 37’C and AHG Severe HTR w/ hemoglobinuria and HDN Detectable Ag’s Possible Ab’s P1 and P None P Anti-P1 Anti-P, P1, Pk (anti-Tja) None k Anti-P P and P1 Pk Anti-P, anti-P1 Plasma, pigeon and turtledove droppings, turtledove eggwhite Hydatid cyst fluid, Lumbricoides terrestris, Ascaris suum IgM Naturally occurring Strong anti-P1 = Hydatid disease (E. granulosus) Associated w/ fascioliasis, C. sinensis and O. viverrini infections Anti-P, P1, Pk Spontaneous abortions in early pregnancy IgG Naturally occurring Biphasic hemolysin (PCH) Test: Donath-Landsteiner I: Individuality Neonates = I I (Ag) = I-i+ Adults (18 mos.-adult) = I I = I+ii Ag in adults 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-I = M. pneumoniae, L. monocytogenes IgM React at 4’C EBV caused Diseases of RES: - Alcoholic cirrhosis - Myeloid leukemia - Reticuloses Page | 6

Anti-IT

K k Kpa Kpb Jsa Jsb Kell Ag’s

MacLeod phenotype Anti-K Fy(a+b-) Fy(a-b-) Fya and Fyb Duffy gene Anti-Fya Anti-Fyb Jka and Jkb Anti-Jka Anti-Jkb

Lua and Lub Anti-Lua

Anti-Lub

Diego (Di) Defect in AE molecule

Cartwright (Yt) Xg

Scianna Dombrock

Transition: from i I Yanomama Indians Hodgkin’s lymphoma Kell Cellano Penney Rautenberg Sutter Matthews Immunogenicity: 2nd to D (D>K>c>E>C>e) Synthesized on precursor Kx = On WBCs: remain unconverted. If (-) CGD = On RBCs: converted to Kell Ag’s. If (-) MacLeod phenotype Acanthocytosis Muscular dystrophy IgG React at 37’C and AHG Chinese (90.8%) American blacks Resistant to P. vivax/P. knowlesi (malaria) Receptors for malaria 1st human gene to be assigned to specific chromosome (1) IgG React at AHG Enhanced by enzymes Notorious antibody = not easily detected Immune Ab’s (IgG) Common cause of delayed HTR Autoanti-Jk = Methyldopa (Aldomet) Development at age of 15 IgG, IgM, IgA Naturally occurring React at room temp IgG4, IgM, IgA Immune Ab React at 37’C Mongolian ancestry AE-1 = HCO3- Cl“ASO” Acanthocytosis Hereditary Spherocytosis SEA Ovalocytosis Erythrocyte acetylcholinesterase = neurotransmission Sex-linked Females Short arm of X chromosome Sc1, Sc2, Sc3 Gregory (Gya) Holley (Hy) Joseph (Joa) Page | 7

Colton (Co) Chido/Rodgers (Ch/Rg)

CHIP, Aquaporin = water permeability 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) CR1 (C’ receptor 1) Indian (In) CD44 (immune adhesion) Benneth-Goodspeed (Bg) HLA Ag’s on RBCs (Class I MHC) Bga = HLA-A7 Bgb = HLA-A17 Bgc = HLA-B28 Public Ag High-incidence Ag’s Ena (99.9%) Private Ag Low-incidence Ag’s ( 0.9% NaCl After thawing = administer w/in 6 hours After pooling = administer w/in 4 hours HES (Hydroxyethylstarch) = Separation bet. WBCs and RBCs Donor: administered w/ corticosteroids 12-24 hrs before donation = # of circulating granulocytes Usually takes 1-2 hours Donor: = Platelet count: ≥150 x 109/L = Aspirin-free: 3 days A.k.a. super packed platelets From plateletpheresis For patients who are refractory or unresponsive to RDP Limit patient exposure to multiple donors Page | 12

Preparation Amount Vol. of plasma pH Storage Shelf-life At risk of TA-GVHD

Irradiation

Infusion

Blood warmers Filters Speed of infusion

Cryptantigens

T

Th

Tx Tk

RDP: Random Donor Platelets SDP: Single Donor Platelets From WB: Light spin Heavy spin Plateletpheresis 5.5 x 1010 platelets 3.0 x 1011 platelets 50-75mL 300mL ≥ 6.0 (New: 6.2) ≥6.0 (New: 6.2) 20-24’C w/ agitation 20-24’C w/ agitation 5 days 5 days Recipient of BM transplant Patients w/ hematologic or oncologic disease Patients w/ congenital immunodeficiency Recipient of blood from 1st degree relative (direct) Radiation source: 25-35 Gy (Gy: Gray | 1Gy = 100 rads) a. Cesium (Ce) b. Cobalt (Co) IV fluids: a. NSS = the only fluid allowed to start an IV line prior to transfusion b. D5W (5% dextrose in H2O) = Not allowed to start (hypotonic hemolysis) c. Ringer’s lactate =not allowed to start (contains Ca2+ promote coagulation) 37’C Temp. >42’C = hemolyzed 1. Clot screen filter (170μm) = to remove gross clots 2. Leukocyte depletion filter 15gtts = 1mL 60gtts = 1min 1min = 4mL 1hr = 240mL Rate = 240mL/hr 1 unit must be completed w/in 4hrs of blood transfusion Polyagglutination (Hubener-Thomsen-Fridenrich Phenomenon) Hidden Ag’s Covered w/ NANA (N-acetylneuraminic acid) or sialic acid When NANA is destroyed (by neuraminidase) Ag’s are exposed Exposed Ag’s Agglutination = React w/ tetrasaccharide of Thomas & Winzler (T receptor) Acquired Microbially-Associated Polyagglutination C. perfringens V. cholerae S. pneumoniae All produce neuraminidase E. coli Proteus sp. Produce weaker neuraminidase Bacterial and viral Unknown mechanism “CABS” C. albicans A. niger B. fragilis S. marcescens All produce endo/exogalactosidase Page | 13

Acquired B phenomenon

VA

Tn

Cad HEMPAS/CDA II Others

Altered precursor substances (Altered: ABH, Le, I, P) Bacteria: Deacetylase enzyme N-acetylgalactosamine --(Deacetylase)--> N-acetyl + galactosamine Galactosamine = Group B Remedy: Add acetic anhydride Vienna, Virginia Microbial fucosidase = fucose = H Acquired Non-Microbially Associated Polyagglutination (-) β-3-D-galactosyltransferase enzyme needed for the normal structure of T receptor (Tetrasaccharide of Thomas and Winzler) Inherited Polyagglutination Sda Adult i Ag = H Ag, Sialic acid HbM – Hyde Park NOR = Norfolk, Virginia

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Arachis hypogaea Salvia sclarea Salvia horminum Glycine soja

Predeposit AD

Intraoperative AD Immediate preoperative hemodilution Postoperative salvage

FNHTR

Allergic Anaphylactic

Anaphylactoid

TRALI (NCPE)

Hemolytic TA-GVHD PTP

DHTR TACO

Tn + + +

Cad + +

T + +

Tk + -

Autologous Donation Before anticipated transfusion Requirements: *No age limit *No strict weight requirement (vol. by 4mL/1 pound below 110) *Hgb ≥ 11g/dL *Hct ≥ 33% *Frequency: every ≥ 3days Collect blood during surgical procedure reinfused immediately Collect blood replace patient volume w/ colloid/crystalloid reinfuse during surgical procedure Drainage tube Postoperative bleeding salvaged (saved) clean and reinfused Immediate Immune Transfusion Reactions 1’C in temperature Cause: anti-leukocyte Ab’s (leukoagglutinins) Prevention: Leukopoor RBCs Cause: Donor plasma w/ foreign proteins Prevention: Washed RBCs 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) Afebrile Normal IgA w/ anti-IgA to donor IgA Prevention: Washed RBCs | IgA-deficient donor (rare) Cause: Anti-leukocyte Ab’s (leukoagglutinins) Signs and symptoms resemble respiratory distress Prevention: Leukopoor RBCs Bleeding, hypotension, hemoglobinuria, anuria Delayed Immune Transfusion Reactions Cause: T lymphocyte proliferation Prevention: Irradiated RBCs Onset of thrombocytopenia Cause: anti-platelet Ab’s (HPA-1a negative platelets) Prevention: Therapy a. Administration of corticosteroid b. Exchange transfusion c. IV immunoglobulins 7 days Immediate Nonimmune Transfusion Reactions Administration of blood w/o equivalent blood loss Iatrogenic: physician-caused At risk: Page | 15

Bacterial contamination

PCITR

Iron Overload (Hemosiderosis)

Disease transmission

In utero Neonatal period Treatment

Full X-match

a. Young children b. Elderly patients c. Patients w/ cardiac disease Prevention: Therapy a. Therapeutic phlebotomy b. IV diuretics c. O2 therapy Cause: Endotoxin production by psychrophilic/cryophilic bacteria Y. enterocolitica (most common) E. coli P. aeruginosa Factors: a. During phlebotomy b. During preparation/processing c. During thawing Prevention: a. Sterile technique b. Visual inspection of unit → Blood unit = Brown, purple, hemolysis, clot → Plasma = Murky (dark brown) purple, red Causes: - Small bore needle - Warming blood above 50’C - Freezing blood w/o cryoprotective agent - Citrate toxicity Delayed Nonimmune Transfusion Reactions 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 HBV, HCV, HDV, CMV, EBV, HTLV-I and II, HIV, T. pallidum, Plasmodium spp., B. microti, T. cruzi, T. gondii Hemolytic Disease of the Newborn Anemia ( immature RBCs, enlarged spleen & liver = extramedullary hematopoiesis) Hydrops fetalis = cardiac insufficiency, edema Unconjugated bilirubin Brain Kernicterus 1. Intrauterine transfusion - In utero - 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 2 hours Can be shortened to 30 mins Page | 16

Abbreviated X-match Electronic X-match Emergency situation (+) Major X-match Ratio of serum to cells Saline for washing Incubation period Enhancement media

Anti-A1 Anti-H Anti-M

Anti-N

Anti-B Annually Quarterly (Every 3 months)

Monthly Daily Daily when in use

Every 4 hours Apheresis/Hemapheresis Intermittent-flow

Type/screen + immediate spin DC/PS = no agglutination/hemolysis Patient blood type is determined on 2 occasions Patient blood type is unknown Group O (Rh-) pRBCs (-) Alloantibody control (+) Autoantibody, autocontrol Routine = 40:1 Det. weak Ab’s = 133:1 pH 7.2-7.4 30-120 mins (majority: 30 mins) 1. Albumin 2. PEG 3. LISS (Incubation pd: 5-15 mins) Lectin Sources Dolichos biflorus Ulex europaeus Iberis amara Iberis umbellate Iberis semperivens Maclura aurantiaca Bauhinia variegate Bauhinia purpura Bauhinia bonatiana Bauhinia candicans Vicia graminea Bandeirae simplicifolia Quality Control Mercury thermometers Speed timer (centrifuge) Cell washers (speed, timer) Blood warmers Alarm Activation (refrigeration and freezers) Temperature (refrigerated centrifuge) Refrigerators and freezers (continuous monitors) Platelet incubators (enclosed, monitored chambers) Transfusion service: - Heating blocks - Water baths Donor facility: - Donor unit agitators - Scales - Balances - Hemoglobinometer - Microhematocrit centrifuges Platelet incubators (ambient temperature storage) Other Topics Whole blood is withdrawn, a desired component separated, and the remainder of the tube returned to the donor 1 venipuncture Page | 17

centrifugation (IFC)

Continuous-flow centrifugation (CFC) Antibody screen Donor & recipient samples Compatibility testing

DHTRs Virus inactivation in plasma products Y. enterocolitica Density Requirements for blood products to be transfused to infants Allogeneic donor blood from outside sources w/in 30 mins Procedure when HTR occurs

Specimens for investiga...