chapter 6 Flashcards
(32 cards)
antigens enhanced by enzymes
ABO/H
lewis
I
P
RH
Kidd
antigens destroyed by enzymes
duffy
MNSs
Xga
unaffected by enzymes
Kell
IgM antibodies
ABO, Lewis, I, P1, M,N
IgG antibodies
Rh, K, k, Kidd,Duffy, S,s,
Lutheran ( not clinically significant )
which antibodies are high incidence and not shown on antigrams
H & I
anti-H,anti- I and anti-IH are autoantibodies that can interfere with alloantibody ID ( esspecially with enzyme treated cells)
which antigens arent on fetal cells
Lewis, I
weakly P1& lutheran
K and k clinical significance
HTR & HDFN
percentage of people with K and k
K ~9%
k >99%
when may anti K be an IgM antibody
rare but may occur and associated with bacterial infections
what other antithetical pairs are associated with Kell system
penny ( Kpa & Kpb)
sutter ( Jsa & Jsb)
both b’s are high incidence
a’s are low incidence
what destroys Kell
the disulfide bonds may be broken by DTT or 2ME
( not affected by enzymes )
which antigens are associated with KIdd system
Jka, Jkb
& Jk3 ( high incidence bc present as long as either JKa or Jkb is there )
which group binds complement as an IgG class that is almost as good as an IgM
Kidd
clinical significance of kidd
HTR & HDFN
why does the kidd system often cause severe delayed HTR
it drops below serologically detetctable levels within months of production
which antigen should you never transfuse to a women within child bearing years
Rh pos if they are Rh neg
Kell pos if they are Kell neg or if theyre unknown
Fy a clinical significance
HTR & HDFN
Fy b clinical significance
HTR
which blood group can cause resistance to malaria P.vivax
Fya- Fyb-
will have a cell membrane change
commonin african ethnicity
MNS system clinical significance
M- none unless IgG ( rare)
N- none
S- HTR & HDFN
s- HDNF
GYPA gene controls which antigens
M & N
GYPB gene controls which antigens
S & s
when is P1 fully expressed
age 7
