Blood Groups (After exam 1) Flashcards
Describe reaction grades
0
W+ (weak)
H (hemolysis)
1+
RBC ags Attributes
how many groups recognized by ISBT
unique?
common features?
36 groups recognized by blood bank society
>250 unique rbc ags
Ab/Ag in the blood group share common features
RBC Ags chemically
trasnferases attach….
sequence
intrinsic or extrinsic
transferases attaches oligosaccharide to glycoproteins (ABO, Lewis, P)
amino acid sequence of glycoproteins
What chromosome are Rh genes on?
Chromosome 1
Intrinsic
passes through cellular membrane (ex Rhag/Rh)
Extrinsic example
ABO outside of cell
Blood group
ag is expression is controlled by….
Ag expression is controlled by single locus gene or closely linked homologous genes w/ little to no recombination
Alleles
snp
SNPs single nucleotide polymorph altern form of gene
Ag
requirements
phenotypes expression of allels that are significantly different
1.) must be inheritable/sequenced
antithetical
co-dominent
2.) must be expressed on cell surface
Systems
same…
same genetic locus and related glycoprotein placement
Collections
sero/bio/chemically related Ag that do not fit the definition of system
700 series
low incidence Ag w/an incidence less than 1% and cannot be included in system
rare in population
901 series
high incidence ag w incidence greater than 90% cannot be included in system
Null
absence of Ag expression
due to silencer or amorph
Usual suspects
have variable frequency, can cause severe problems
Naming Ags
Genes
Ag
Alleles
Genes - italics or underlined
Ag - numbers or letters superscript
Alleles-ISBT terminology gene included with * and ISBT #
Phenotype
how a person serologically presents ag (not collections) regardless of genetics
Kell Sytem
antetheicals
single mutation….
only?
second most immunogenic
K and k antethetical
Jsa -Jsb
kpa -kpb
single mutation of KEL (big K) on chrom 7 separate anthethetical ag inherited as glycoprotein
only high/low incidence
What is big K called in Kell and Little k called?
K = Kell
little k = cellano
mother group of Kell system
little k/Kpb/Jsb
K ag
2nd most immunogenic next to D ag
Kpa ag
supresses other Ag in expression in haplotype
Jsa Ag
prevelance is unique to african population
XK
like rhag, holds onto KEL,
x linked
What does DTT chemical disrupt?
disrupts cystine bonds that hold the ag
What does Kell cause
disease
what kind of glycoprotein?what does it do?
null ?
What syndrome?
enhanced with?
severe hemolytic disease
kell glycoprotein is a single pass transmembrane protein in rbc
Null for kell is acanthocytes
MCLEOD SYNDROME - CGD
enhanced with ficin and papain
Kell Ab
immunoglobulin
compliment relationship
AHG phase?
Rxns?
IgG
no compliment doesnt cause hemolysis
AHG no detection
severe hemolytic rxns
Anti- K
Anti-Ku
Anti-Kx+ km
an- K: most common Ab seen in Blood bank
An-Ku: detects all ag in Kell system
An-Kx+: Km rxn stronger w Ko weaker w normal kell
Kidd system
notorious for….
rxns?
ag?
Ab are notorious for extreme dosage and quick titer in vivo
delayed hemolytic transfusion rxns
Jka Jkb
Kidd system compliment and immunoglobulin
ag developed as early as?
binds to compliment - extravascular hemolyiss
IgG immune stimulated
Ag developed as early as 7 (jkb) - 11 (jka) weak gestation/ not destroyed by most treatments
Where is Kidd expressed
expressed on rbc, endothelial surface of kidney, NOT on other blood cells
Kidd ag frequencies and chromosomes
Jk3 high frequency with jka/jkb
jk null silent alleles
Chrom 18 multipass - HUT11
Special feature of Jk null (kidd system)
resistent rbc to 2m urea lysis
Duffy system
protection from?
glycoprotein? location? acronym?
begins to form around?
what organs affected?
protection from malaria vivax
intrinsic membrane glyco - ACKRI
begins to form at 6wk
on organs like brain,colon,spleen
Fya Fyb
Duffy system special feature
destroyed by common enzymes
Duffy chromosome
1
Duffy null
common in what population
independently….”
point maturation on?
no?
common in west africans inherited independently “syntenic”
point maturation GATA-1 on rbc ONLY
no anti-fyb made
Duffy Ab
immunoglobulin?
compliment?
complications?
rxns?
IgG
rare compliment binding
dosage complicated due to unknown serology of black donors
transfusion rxn/HDN
T/F P. falciparum can infect duffy people
true, it can make it through the cell
Lutheran group
two proteins
immuno?
chromosome?
Lu gene linked with?
development w birth?
High incidence ag?
two proteins one gene
lua lub
not immunogenic
Chrom 19
Lu gene linked to H and Lewis
poor develop at birth
Lub high incidence
Lutheran special features
resistant to enzyme treatment but NOT DTT
BCAM basal adhesion molecule
Lutheran null phenotype
dominannt inherited suppresor LU3-
Lutheran Ab
common?
Lua - ig
characteristics?
Lub - ig
characteristics?
rare
anti-lua characterisic mixed field
IgM not great at compliment
anti-lub
IgG post transfusion jaundice
variable rxn
