Must to Know in Immunohematology (Blood Bank) PDF

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MUST TO KNOW IN IMMUNOHEMATOLOGYISBT 001 ABOISBT 002 MNSISBT 003 PISBT 004 Rh ISBT 005 Lutheran ISBT 006 Kell ISBT 007 Lewis ISBT 008 Duffy ISBT 009 Kidd ISBT 010 Diego ISBT 011 Cartwright ISBT 012 Xg ISBT 013 Scianna ISBT 014 Dombrock ISBT 015 Colton ISBT 016 Landsteiner-Weiner ISBT 017 Chido/Rodge...

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MUST TO KNOW IN IMMUN OHEMATOLOGY

ISBT 001

ABO

ISBT 002

MNS

ISBT 003

P

ISBT 004

Rh

ISBT 005

Lutheran

ISBT 006

Kell

ISBT 007

Lewis

ISBT 008

Duffy

ISBT 009

Kidd

ISBT 010

Diego

ISBT 011

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

Chromosome 2

Gerbich

Chromosome 4

MNS

Chromosome 6

Chido/Rodgers

Chromosome 7

Cartwright Colton Kell

Chromosome 9

ABO

Chromosome 11

Indian pg. 1

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) 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)

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

pg. 2

Specimen: Serum (Ab) = 3-6 months (development) Reagents: = A 1 cells = B cells Gel typing

Major Advantage: Standardization Medium: Dextranacrylamide 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 Red cell Ag-Ab reactions

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)

Universal donor

Group O

Universal recipient

Group AB

Universal donor for RBCs

Group O (No Ag)

Universal recipient for Group AB (No Ab) RBCs Universal donor for plasma

Group AB (No Ab)

Universal recipient for Group AB (No Ag) plasma 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

pg. 3

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 specific locus on a chromosome

Silent/amorph

Only indicates the absence of the Ag

Von Dungern

Subgroups of A = A 1 (80%) and A 2 (20%)

Hirzfeld Dolichos biflorus

Lectin source of anti-A 1

Phenotype

Possible Genotypes

A1

A 1A 1 A1 A2 A1O

A2

A 2A 2 A2 O

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

NN-acetyl-Dacetylgalactosaminyltransferase galactosamine

A

H

B

D-galactosyltransferase

B

H

AB

NN-acetyl-Dacetylgalactosaminyltransferase galactosamine

A

H

D-galactosyltransferase

D-galactose

D-galactose

B

pg. 4

O

--

--

--

Amount of H Ag

(Greatest) O > A 2 > B > A 2 B > A 1 > A 1 B (Least)

Bombay individual

Bhende

Unchanged H

(-) H gene hh or H null

Lack H, A and B Ag’s Designated as O h 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 A h , B h , ABh

Anti-H

Differentiates Group O from O h 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 Principle: Hemagglutination-inhibition

Status ABO antibodies

Mixture of IgM, IgG and IgA (Henry)

Anti-A Anti-B

Predominantly IgM 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: Pregnancy Incompatible transfusion and transplant

ABO HDN

Mother: Group O Child: Group A or B

Group I discrepancies Weak reacting/missing Ab’s Newborns Elderly patients Hypogammaglobulinemia/agammaglobulinemia

pg. 5

Group II 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: = Anti-H: produced by A 1 and A 1 B (H Ag) = Anti-A 1 : produced by A 2 and A 2 B (No A 1 Ag)

A Subgroups A3

MF agglutination w/ anti-A & anti-A,B

Ax

Weak MF agglutination w/ anti-A& anti-A,B

A end

MF agglutination w/ anti-A,B

Am

(-) Agglutination, (+) AH substance in secretions

Ay

(-) Agglutination, AH substance in secretions

A el

(-) Agglutination, (+) H substance in secretions

B Subgroups

pg. 6

B3

MF agglutination w/ anti-B & anti-A,B

Bx

MF agglutination w/ anti-A,B

Bm

(-) Agglutination, (+) BH substance in secretions

B el

(-) Agglutination, (+) H substance in secretions

Rh Nomenclatures

Rosenfield = no genetic basis, indicates the presence or absence of Rh Ag’s Fisher-Race (DCE) = inheritance of 3 genes (d= amorph/silent) Wiener (Rh-hr) = inheritance of 1 gene (Ex. R 0 ), w/c codes for an agglutinogen (Ex. Rh 0 ), w/c contains 3 blood factors (Ex. Rh 0 hr’hr’’)

Immunogenicity of (Most immunogenic) D > c > E > C > e (Least immunogenic) Rh Ag’s R or r

D or d

1 or ‘

Ce

2 or ‘’

cE

Z or y

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)

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

C Trans

D --- (trans) --- > C (Ex. Dce/dCe)

f (ce)

c --- (cis) --- > e [Ex. Dce/DCE]

rh i (Ce)

C --- (cis) --- > e [Ex. DCe/DcE]

Hr 0

“Common” Rh phenotypes (R 1 R 1 , R2 R 2 , rr)

Rh Ab’s

IgG1 and IgG3 React at 37’C I mmune Ab’s (- ) C’ binding = extravascular hemolysis (delayed HTR)

Rh HDN

Mother: Rh (-) Child: Rh (+), 2 nd pregnancy

RhoGam or RhIg

Purified anti-D Administer w/in 72 hrs after 1 st delivery

Full dose RhoGam

300 μg anti -D

pg. 7

(>12 weeks gestation) Protect up to 30mL D+ WB or 15mL D+ RBCs Minidose/Microdose RhoGam

50 μg anti -D Protect up to 5mL of D+ WB or 2.5mL D+ RBCs Ex. Abortion

( Le b

pg. 8

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 a & Anti- Le b

ABH, lele, SeSe/Sese

ABH

ABH, Le(a-b-)

Anti-Le a & Anti- Le b

ABH, LeLe/Lele, sese

Le a

ABH, Le(a+b-)

Anti-Le b

ABH, LeLe/Lele, SeSe/Sese

ABH, Le a , Le b

ABH, Le(a-b+)

none

Lewis Ab’s

Anti-Le a & Anti- Le b Naturally occurring IgM

Activates the C’ MN Ag’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

Anti-N-like Ab

IgM Found in renal patients dialyzed w/ formaldehyde sterilized equipment

SS Ag’s

Glycophorin B (Ss-SGP) S = Methionine (29 th ) s = Threonine (29 th )

Ss Ab’s

IgG

React at 37’C and AHG Severe HTR w/ hemoglobinuria and HDN Phenotype

Detectable Ag’s

Possible Ab’s

P1

P 1 and P

None

P2

P

Anti-P 1

p (p null)

None

Anti-P, P 1 , P k (anti- Tj a )

P1k

P k and P 1

Anti-P

P2k

Pk

Anti-P, anti-P 1

P 1 -like

Plasma, pigeon and turtledove droppings, turtledove eggwhite

P 1 substance

Hydatid cyst fluid, Lumbricoides terrestris, Ascaris suum

Anti-P 1

IgM Naturally occurring

Strong anti P 1 = Hydatid disease ( E. granulosus) pg. 9

Associated w/ fascioliasis, C. sinensis and O. viverrini infections Anti-Tj a

Anti-P, P 1 , P k Spontaneous abortions in early pregnancy

Anti-P

IgG Naturally occurring Biphasic hemolysin (PCH) Test: Donath Landsteiner

Ii Blood Group

I: Individuality Neonates = I I (Ag) = I- i+ Adults (18 mos.-adult) = I I = I+i-

HEMPAS

i Ag in adults

Anti-I

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

Anti-i

IgM

React at 4’C EBV caused Diseases of RES: Alcoholic cirrhosis Myeloid leukemia Reticuloses Anti-I T

Transition: from i I

pg. 10

Yanomama Indians

Hodgkin’s lymphoma K

Kell

k

Cellano

Kp a

Penney

Kp b

Rautenberg

Js a

Sutter

Js b

Matthews

Kell Ag’s

Immunogenicity: 2 nd 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 MacLeod phenotype

Acanthocytosis Muscular dystrophy

Anti-K

IgG

React at 37’C and AHG Fy(a+b-)

Chinese (90.8%)

Fy(a-b-)

American blacks Resistant to P. vivax/P. knowlesi (malaria)

Fy a and Fy b

Receptors for malaria

Duffy gene

1 st human gene to be assigned to specific chromosome (1)

Anti-Fy a

IgG

Anti-Fy b

React at AHG

Jk a and Jkb

Enhanced by enzymes

Anti-Jk a Anti- Jk b

Notorious antibody = not easily detected Immune Ab’s (IgG) Common cause of delayed HTR Autoanti-Jk = Methyldopa (Aldomet)

Lu a and Lu b

Development at age of 15

Anti-Lu a

IgG, IgM, IgA Naturally occurring React at room temp

Anti-Lu b

IgG4 , IgM, IgA Immune Ab React at 37’C

Diego (Di)

Mongolian ancestry

pg. 11

AE-1 = HCO 3 - Cl Defect in AE molecule “ASO” Acanthocytosis Hereditary Spherocytosis SEA Ovalocytosis Cartwright (Yt)

Erythrocyte acetylcholinesterase = neurotransmission

Xg

Sex-linked Females Short arm of X chromosome

Scianna

Sc1, Sc2, Sc3

Dombrock

Gregory (Gy a ) Holley (Hy) Joseph (Jo a )

Colton (Co)

CHIP, Aquaporin = water permeability

Chido/Rodgers (Ch/Rg) 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)

pg. 12

Benneth-Goodspeed (Bg)

HLA Ag’s on RBCs (Class I MHC) Bg a = HLA-A7 Bg b = HLA- A17 Bg c = HLA-B28

Public Ag

High- incidence Ag’s En a (99.9%)

Private Ag

Low- incidence Ag’s (...