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86 Cards in this Set
- Front
- Back
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non rbc immune
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H I M N Lea Leb
IgM rxn at IS |
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IgM
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IS, decr at 37
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IgG
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rbc immune
at 37 and incr at AHG Rh Duffy Xga Kale Kidd Lub Ss |
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Dosage
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Mn
Ss Duffy Kidd |
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Destroyed by enzymes
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MN
Duffy Xga |
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Incr with enzymes
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Rh
P Lewis Kidd |
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Fy(null)
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Fy/Fy
incr in black popl resistant to Malaria |
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Fyx
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weak Fyb
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Fy3, 4, 5, 6
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closer to RBC memb
rare not destroyed by enzymes decr (13000) Ag sites on RBC = difficult to ID |
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Fy Ags
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well developed at birth
50% White Fya and b pos 68% blacks Fy a and b neg |
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ag weaken over time, dont store well in saline > flase neg
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Fy
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Fy a and b destroyed by
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proteolytic enzyme ZZAP
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reduced expr of Fyb Fy 3 and 5
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Fyx
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produces basic precursor to Fya and b
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Fy3
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is single ab and weaker in mix with others
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Anti Fya
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less common and occurs in mix of abs
have to have had incr exposure (transf) |
Anti Fyb
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IgG
reacts at AHG binds compl enhanced with LISS dosage acute and delayed HTR and HDN |
Fy
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24 ags
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Kell
Kell and cellano (hi) |
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Kell
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Kk
Jsa and b Kpa and b |
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Ko
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null
rare prod anti Ka |
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Kmod
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weak expr of Kell ags
rare |
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Kx
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separate blood group
inhert by Kx gene on X chrom weak expr nerve, muslce, and heart probls CGD |
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Mcleod synd
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absence of K on X
compensated HA and incr Ck neuro males can be x link |
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Ko or Kmod have
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stronger rxn than Kx
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ag destroyed by AET and ZZAP
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Kell
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IgG
at AHG doesnt bind compl mild-mod HTR and HDN can be poor with LISS |
Kell
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57% blacks
28% whites |
Jkb neg
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null is very rare
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Jk
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develop at birth = HDFN
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Jk
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Papain and Ficin enhance
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Jk
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looks like deletion, behaves like anti- Jka and b, types as Jka and b neg
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Jk3
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dosage
weak ab, incr with exposure delayed HTR IgG possible part IgM enhance with LISS in vitro heme bind compl detect by Anti C' |
Jk
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Jka=b=
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null
in orientals, Polynesians inhibs prod of inherited Jk genes |
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severe immediate and delayed HTR, mild HDN
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anti Jk3
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alleles and prod structures near end of glycophorin A chain
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MN
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easily destroyed bu enzymes
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MN
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alleles and prod is closer to the RBC on the chain
on short glycophorin B resistant to enzymes, unless excessive |
Ss
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high inc
most neg for it > Anti |
Ena
of MNSs |
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null for MNSs
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Mk
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non rbc immune
can be IgG ir rxn at 37= clin sig dont bind compl dont react with enzyme dosage some at 6.5 pH rare HTR and HDN |
anti M and N
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igg at 37 and AHG
dosage may bind compl HTR, hgburia HDN |
anti Ss
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IgG
no compl mild-severe HDFN and HTR Ag not destr by enzymes |
anti U
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U neg RBC are
in Blacks |
S=s=
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P, P1, Pk
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P and Globside
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p is
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null for P
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is expr on all cells except p/p
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Pk
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not expr on newborn cell until 7
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P1
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vary in strength
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P ag
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more P1
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blacks
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suppresses P ag expr
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In(Lu)
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deteriorates rapidly in storage
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P1
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Ag- P1,P,Pk
no ab |
P1
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ag- P,pk,
ab- anti P1 |
P2
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ag- none
ab- Anti P, P1, Pk |
p
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ag- P1, Pk
Ab- anti P |
P1k
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ag- Pk
ab- Anti P,P1 |
P2k
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non rbc immune
weak rare at 37 rare bind compl immediate and delayed HTR no HDN enhanced with enzyme |
anti P
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prod by p/p
non immune IgM,G wide thermal range binds compl extreme heme incr rate of spontaneous abortion |
Anti P,P1,Pk
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non immune
in sera of Pk rare wide thermal range strong heme clin sig |
Allo anti P
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cold reactive IgG
viral infs Donath Landstiner test |
Auto Anti- P
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biphasic
binds RBC in cold, activates compl at 37 |
Auto anti-P
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arent antithetical ag
both high enhance with enzyme |
I and i
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at birth, ___ incr on RBC for 18 months, replace by ___
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i, I
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auto, in all people
test at 4C or wiht enzymes usually benign |
Anti I
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doesnt react with cord cells
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i+
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assoc with cold agglu synd
broad thermal range IgM HA or heme in room temp parts of body M pnemoniae |
Pathological Auto Anti I
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masks clin sig Ab
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Patho Auto Anti I
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IgM or G with i/i
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Allo Anti I
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IgM
wide thermal range can heme bad |
Anti i
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not expr at birth
absorbed on to surface of RBC, not ag |
Le
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22% blacks
pregnant females freq and prod Ab suring pregnancy |
Le a=b=
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non immune
IgG,M activate compl in vivo and vitro heme incr with enzymes |
anti Le
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high or low incidence
Abs rare b more common poorly dev at birth |
Lu
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IgM
non immune some bind compl IgA,G,M shows mf with SCI or II clin insig rare HDN |
Anti Lua
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IgG, can be A or M
RBC shorter survival HTR, mild HDN |
Anti Lub
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Dominant ln(Lu), Rec. LuLu, Rec xlink inhib
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Lu a=b=
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small amount of Lu ag
inherited at diff site interfers with expr of P1,i abn RBC shape |
Dom ln(Lu)
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rare lack all Lu ag
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Rec LuLu
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Mongolians
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Dia
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Diego
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Di a/b
Wr a/b |
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anti a more freq
IgM or G IgG> HTR and HDN |
Wr a/b
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strond as, hign incidence
ab freq seen IgG |
Yta
cartwright |
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hemizygous, males
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Xga+
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on short arm of X chrom
IgG doesnt react with enzyme binds compl |
Xg
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behaves as high titer low avidity ab, detected at AHG and react vary
in multi transf and preg ab cab be abs out using plasma Ag inherited via genes closely linked to HLA sys absorbed on RBC |
Chido/ Rodgers
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Bg a/b/c
ab reacts with the ag are directed against HLA ags weak and obscure rxns weak and vari at IAT with only 1-2 cells |
WBC Ag, Bg
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