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Kell major antigens
K, k, Kp a/b, Js a/b
Kidd major antigens
Jk a/b
Duffy major antigens
Fy a/b
Kell high frequency antigens
k, Kpb, Jsb
Kidd high frequency antigens
Jka in black people
Frequency of K in caucasian/african american populations
9% vs 2%
Kidd/Kell/Duffy mode of stimulation
transfusion and pregnancy
Kidd/Kell/Duffy optimal phase of reactivity
AHG
Kell effect of enzymes
none
Kidd effect of enzymes
enhanced
Duffy effect of enzymes
destroyed
Kell implication in HDN/HTR
yes
Kidd implication in HDN/HTR
delayed HTR
Duffy implication in HDN/HTR
HTR, uncommon in HDN
Dosage in Kell
no
Dosage in Kidd
yes
Dosage in Duffy
yes
How is the Mcleod phenotype related to the kell system
red cells lack Kx (precursor), no kell ags are expressed, acanthocytes
Duffy genotype that confers resistance to malaria
fy(a-b-), lack glycoprotein receptor needed for malaria to enter RBC, protect against p. vivax
Frequency of the 4 lutheran phenotypes
Lub, Luab, Lua, Lu(a-b-)
Antigen characteristics of Lua/Lub
poorly developed at birth, show dosage, destroyed by enzymes
Characteristics of anti-Lua
mostly IgM, mixed field agglutination, clinically insignificant
Characteristics of anti-Lub
rare, mostly IgG, weak mixed field, causes HTR/HDN
Relationship of Lewis antigens w/ secretors
se status affects type of lewis
Lewis phenotype of nonsecretor
Lea, LeLe, no ABO in saliva
Lewis phenotype of secretor
Leb, Lele, ABO in saliva
Only Lewis phenotype to build antibodies
lele, still a secretor
Major antigens of I system
I, i, Oi
I/i specificity of adult/newborn cells
adult: I, newborn: i
Sources of I and i antigens used in serologic testing
plasma, serum, saliva, milk
Antibodies associated w/ I system
Auto anti-I, Allo anti-I, anti-i
Auto anti-I characteristics
weak IgM, strong RT or AHG, warm supplies before testing
Allo Anti-I characteristics
in adult i individuals
Anti-i characteristics
IgM, associated w/ mono, myeloid leukemia, anemia, cirrhosis
Disease states associated w/ Auto anti-I
cold agglutination syndrome, mycoplasma pneumoniae
5 possible phenotypes in P1 blood group system
P1, P2, p, P1K, P2K
Recount 3 attributes of the P1 antigen
not fully developed at birth, strength varies, neutralized by pigeon eggs
General characteristics of Anti-P1
IgM, seen in P2, neutralized by P1 substance, enhanced by cold/enzymes
General characteristics anti-PP
produced by Pnull/p individuals, reacts w/ all other RBCs, wide temp range
General characteristics of anti-P
found in Pk individuals, potent IgM hemolysin
Clinical significance of Anti-P1
ahg reactive may cause in vivo rbc destruction
Clinical significance of Anti-PP
spontaneous abortion
Clinical significance of Anti-P
paroxysmal cold hemoglobinuria (binds in the cold)
How to detect anti-P
donath-lansteiner test, spectrophotometer
MN antigen glycoprotein
glycophorin A
Ss antigen glycoprotein
glycophorin B
Order of frequency of MNSs gene complexes
Ns, Ms, MS, NS
Frequency of U antigen
high
Associate antigen phenotype S-s-U- w/ black population
1%
Anti-M lectin
iberis amara
Anti-N lectin
vicia graminea
General characteristics of Anti-M
mostly IgM, no complement, destroyed by enzymes, dosage, pH dependent
Which antibody likes acidity
anti-M
General characteristics of Anti-N
cold reactive, no complement, insignificant, dosage
Where is anti-Nf seen
dialysis patients
General characteristics of Anti-S/s
IgG, cause HDN/HTR, maybe enzymes/dosage
Xga characteristics
sex-linked, X
Dia characteristics
south american indians
Vel characteristics
rare HTR (IgM)
Sda charateristics
mixed field, shiny refractile agglutination, neutralized w/ pos urine
Principle of antiglobulin reaction
based on a reagent prepared by injecting rabbits w/ human ab and complement proteins, animal produces abs which are manufactured and agglutinate w/ IgG-coated red cells
Source of AHG
rabbits
Types of AHG
poly and monospecific
Polyspecific AHG
screening for anti-IgG and Anti-C3d
Applications of Poly AHG
complete crossmatching, alloantibody screening/ID, DAT
Monospecific AHG
specify anti-IgG or anti-C3d
Anti-IgG AHG
reacts w/ heavy chain (Fc) of IgG
Anti-C3d AHG
component of complement associated w/ immune hemolysis
Applications of anti-IgG AHG
detects almost all clinically significant coating antibodies
Applications of anti-C3d AHG
AIHA, DAT fractionation
Importance of Coombs control
ensure testing was completed/valid
What is in coomb’s check cells
Group O pos RBC’s coated w/ IgG anti-D
Causes of false pos in AHG testing
bacterial contamination, overcentrifugation, dirty glassware
Causes of false neg in AHG testing
inadequate washing, AHG reagent not added, expired AHG, undercentrifugation
Purpose of DAT
detects in vivo IgG or complement sensitized red cells
Procedure for DAT
cell suspension, wash, AHG, SRR, microscope if neg
Applications for DAT
HDN, HTR, AIHA, Drug-induced abs
Purpose of IAT
detects in vitro Ag/Ab reactions
Procedure for IAT
incubate, wash, AHG, SRR, microscope neg except for weak D
Applications of IAT
ab screening/ID, crossmatching, phenotyping, weak D
Why is an EDTA tube required for DAT
anticoagulant removes Ca needed for agglutination to occur
False positive DAT cause
specimen taken from IV line, pt w/ septicemia
Characteristics of clinically significant alloantibody
decrease survival of RBCs, HTR/HDN
Always clinically significant antibodies
ABO, Rh, Kell, Kidd, Duffy, S/s, U
Occasionally clinically significant antibodies
Leb, MN, P1, L
Rarely clinically significant antibody
Lea
High frequency antigens
k, Jsb, Kpb, U, e
Low frequency antigens
Jsa, Kpa, K, Lua
IgG blood groups
Rh, S, Kell, Kidd, Duffy, LuB, sometimes Lewis
IgM blood groups
MN, Lewis, Lua, P1, I
Antigens exhibiting dosage
MNSs, Duffy, Kidd, Rh
Antigens developed at birth
ABO, MN, Lutheran, P, Lewis
Complement binding blood groups
ABO, duffy?, kidd, lewis
Warm blood groups
Rh, Kell, Duffy, Kidd
Cold blood groups
MN, P1
Cells destroyed by enzymes
MN, Duffy
Cells enhanced by enzymes
Rh, Kidd
Clinical Significance of Rh System
D antigen is second in immunogenicity, Abs are immune stimulated
How are Rh genes inherited
codominantly
Phenotype of Rh
D pos or neg