COMMON Flashcards
(165 cards)
1
Q
● The 2nd blood group system identified after ABO.
A
MNS BLOOD GROUP SYSTEM (ISBT NO. 002)
2
Q
● MNS blood group antigens are expressed only on
A
.r
3
Q
M, N, S, s, U Antigens
prevalence
well developed or not?
A
● Usually Low prevalence Antigens
● Well developed at birth
4
Q
Usually detected as Room temperature saline agglutinins
Naturally occurring antibodies of IgM isotype
A
Anti-M and Anti-N
5
Q
can be used in paternity testing, reactive to Vicea
graminea.
A
Anti-N
6
Q
○ Commonly encountered in Blood Bank
A
● Anti-M
7
Q
Observed in GYPB deficient patients
phenotype and antibody
A
Alloanti-N
in GYPB deficient patients
(M+N-S-s-phenotype)
8
Q
In these patients, Severe Hemolytic Transfusion
Reaction and HDFN can occur after transfusion of N+
RBC.
A
Alloanti-N
9
Q
● Reported in hemodialysis patient in the past.
A
Autoanti-N
10
Q
● Caused by the use of formaldehyde to sterilize membranes.
A
Autoanti-N (Anti-Nƒ)
Formaldehyde reacted with the terminal leucine on N
and ‘N’ antigens, creating a neoantigen
11
Q
Enzymatic modification of RBC with proteases but not
neuraminidase can decrease the reactivity of some
A
Anti-S
and Anti-s.
12
Q
● s unaffected by proteolytic enzymes.
A
Anti-U i
13
Q
○ Is the most common, observed exclusively in blacks.
A
U
14
Q
○ complete loss of glycophorin B
A
S-s-U-
15
Q
recombinant (modified)
glycophorin B.
A
Henshaw phenotype -
16
Q
Can react weakly with some examples of human
anti-U and are known as
A
U variants (S-s-Uvar)
17
Q
○ Results from recombination of glycophorin A and B
genes
A
En(a-)
18
Q
○ Shows resistance to P. falciparum.
A
● En(a-)
19
Q
Lacks all MNSs Antigens, result of recombination and
deletion of GPYA and GPYB.
A
Mᵏ
20
Q
Contribute significantly to the zeta potential of red cells,
decreasing homotypic and heterotypic red cell
adhesion.
A
● Glycophorin A and Glycophorin B
21
Q
Glycophorin A
○ Also known as
A
Membrane Inhibitor of Reactive Lysis
(MIRL): CD59
22
Q
■ Prevents C9 polymerization.
A
MIRL
23
Q
ncreased Band 3 expression and osmotic resistance
can be observed with Miltenberger type Ill red cells, a
GYP B-A-B hybrid.
A
● Glycophorin A
24
Q
○ Receptor for pyelonephritogenic E. coli (UPEC).
A
● Glycophorin A
25
● GPA and GPB are receptors for
PLASMODIUM FALCIPARUM
26
P BLOOD GROUP SYSTEM ISBT NO.
○ 1 antigen: P1(ISBT 003)
○ 2 antigens of the GLOB: Pk and P (ISBT 028)
27
Antigens are glycosphingolipids, consisting of an
antigenically active carbohydrate moiety covalently linked to a
ceramide lipid tail
P BLOOD GROUP SYSTEM (ISBT NO. 003 AND 028)
28
○ P:
○ Pk and P1:
○ Pk and P1: galactose
○ P: N-acetylgalactosamine
29
poorly expressed at birth (up to 7 years). However,
expression is high in fetus.
P1
30
Approximately 79% of Caucasian and 94% of black
donors express this.
P1
31
expression is variable between individuals and can
be lost with in vitro storage.
P1
32
○ High-frequency antigen on most donor RBC (>99.9%)
○ RBC are particularly rich in P antigen, which makes up
nearly 6% of the total RBC lipid.
● Pᵏ and P
33
P and Pk also found in:
■ Plasma as glycosphingolipids
■ Glycoproteins in hydatid cyst fluid
34
○ Resistant to treatment with ficin and papain
P AND PK
35
● Naturally occurring antibody of lgM isotype.
● May cause immediate and delayed HTRs.
Anti-P1
36
Often detected as a weak, cold-reactive saline agglutinin
(reacts optimally at 4°C)
Anti-P1
37
● May be detected in the IAT if AHG is used.
Anti-P1
38
ANTI P1 IS ELEVATED WHENN
Titers are often elevated in patients with.
○ Parasitic infections (e.g. Hydatid disease, and
fascioliasis, C. sinensis, O. viverrini infections)
○ Bird Fancier's Lung
39
● Sources of Substances for NEUTRALIZATION
Hydatid Cyst fluids, Pigeon Droppings. Turtledoves' egg
whites, Lumbricoides terrestris, Ascaris suum
40
● Separable mixture of anti P, Anti P1 and Anti Pk
● Historically known as anti Tja
41
● Naturally occurring in "p" (P Null) phenotypes
Anti-P, P1, Pᵏ
42
Naturally occurring IgM alloantibody in the serum of Pk
(and p) individuals
Alloanti-P
43
○ Can cause in vivo hemolysis following transfusion of P
positive (P1 and P2) RBCs
Alloanti-P
44
○ Associated with spontaneous abortions.
Alloanti-P
45
● Donath Landsteiner antibody
Autoanti-P
46
● Seen in patients with Paroxysmal Cold Hemoglobinuria (PCH)
Autoanti-P
47
● IgG, biphasic hemolysin.
Autoanti-P
48
Capable of binding RBCs at colder temperatures,
followed by intravascular hemolysis at body
temperature
Autoanti-P
49
characteristic can be demonstrated in vitro in the Donath
Landsteiner test.
Autoanti-P
50
may be associated with
the c-interferon and major histocompatibility class l receptors
and may modulate cell signaling via lipid rafts
Pk antigen
51
may also play a role in cellular
differentiation and neoplasia
P blood group antigens
52
● Pk and P antigens are differentially expressed during.
○ Embryogenesis
○ Hematopoiesis
○ Intestinal mucosal differentiation
53
○ A marker of apoptosis in germinal center B cells, Burkitt
lymphoma, and lymphoblastic leukemia.
Pk antigen
54
LKE (Luke Antigen)
○ Formed with the addition two additional sugars:
???
LKE (Luke Antigen)
○ Formed with the addition two additional sugars:
■ Galactose and sialic acid
55
■ Galactose and sialic acid
○ A marker of embryonic and mesenchymal stem cells implicated in adhesion, cell signaling, and metastasis in
renal cell and breast carcinoma
LKE (Luke Antigen)
56
is the receptor for
Parvovirus B19, a single stranded DNA virus
associated with multiple clinical sequelae, including
aplastic crises.
P blood group antigen
57
can bind human immunodeficiency virus (HIV) and
may confer resistance to HIV infection.
Pk
58
are receptors for Shiga toxins,
produced by Shigella dysenteriae and Enterohemorrhagic Escherichia coli (EHEC /
O157:H7) strains
P1 and Pk antigens
59
on uroepithelium
are cell receptors for P-fimbriae, a bacterial adhesin
and colonization factor expressed on Uropathogenic E.
coli strains
P, Pk,and LKE blood group antigens
60
serves as a receptor for Streptococcus
suis and Pseudomonas aeruginosa
Pk antigen
61
LUTHERAN BLOOD GROUP SYSTEM (ISBT NO. )
005
62
Poorly developed at birth and don't reach adult levels until the
age of 15.
LUTHERAN
63
Lutheran appears on red cells at the ??? concurrent with binding of red cells to
laminin.
Lutheran appears on red cells at the orthochromatic
erythroblast stage, concurrent with binding of red cells to
laminin.
64
A minor constituent of RBC membranes –
lutheran
65
Lu(a-b-) phenotype can occur in 3 settings with distinct
patterns of inheritance:
○ Autosomal recessive
○ Autosomal dominant (In [Lu])
○ X-linked Recessive
66
Characterized by complete absence of all
Lutheran
○ Autosomal recessive
67
These individuals can make an alloantibody to
Lutheran glycoprotein (anti Lu3) which reacts
with all Lu positive RBCs.
○ Autosomal recessive
68
■ You will inherit the inhibitor.
○ Autosomal dominant (In [Lu])
69
Can show weakened expression of P1, i,
Indian/CD44, and Knops/CD35 antigens and
enhanced expression of CDw75
○ Autosomal dominant (In [Lu])
70
Can display subtle abnormalities, including
increased poikilocytosis and increased
hemolysis, during in vitro storage
○ Autosomal dominant (In [Lu])
71
Has weakened Lutheran, enhanced i and
CDw75, and normal P1, i, and CD44
expressioN
○ X-linked Recessive
72
● Not clinically significant
● Rarely associated with HDFN and hemolytic transfusion
reactions
● Activity can be inhibited by enzyme pretreatment of RBCs
○ Chymotrypsin, trypsin, 2 aminoethyl isothiouronium
bromide (AET), dithiothreitol (DTT)
LUTHERAN ANTIBODIES
73
Most common Lutheran alloantibody encountered in the
blood bank
Anti-Lua
74
● Often an IgM, room temperature agglutinin
that can display mixed field agglutination because not all RBCs express detectable Lu antigens
Anti-Lu a
75
● Discovered in patient with systemic lupus diffuses.
Anti-Lu ^a
76
● Reacting best in the IAT
Anti Luᵇ and other Lutheran antibodies
77
77
KELL AND KX BLOOD GROUP SYSTEM (ISBT NO. ??
KELL AND KX BLOOD GROUP SYSTEM (ISBT NO. 006 AND 019)
78
● First BGS discovered through AHG testing.
KELL AND KX BLOOD GROUP SYSTEM
79
Immunogenicity
(D>K>c>E>C>e)
80
● Acquired ?? like Ag in Streptococcus faecium infection.
KELL AND KX BLOOD GROUP SYSTEM (ISBT NO. 006 AND 019)
81
is found on erythroid & megakaryocyte
progenitors, skeletal muscle, lymphoid organs and testis.
XK (gene) protein
82
K, k,
kel antigen tas cellano antigen
83
○ Completely lacks all Kell antigens.
K0K0
84
As a consequence, these individuals can make an
alloantibody to the Kell glycoprotein (anti Ku)
K0K0
85
Have enhanced expression of Kx antigen, present on the XK protein and have no decrease in CO2 permeability.
K0K0
86
Can be produced in the laboratory by treating Kell
positive RBCs with sulfhydryl reducing agents.
koko
87
○ Have significantly depressed/absent Kell antigens
● McLeod RBCs
88
An X linked recessive phenotype characterized by the
absence of XK protein on RBCs, acanthocytes, and neuromuscular disorders.
● McLeod RBCs
89
are incompatible with both Kell
positive and KoKo RBCs
McLeod individuals
90
○ Depressed Kell expression
● Kmod and Gerbich-negative RBC
91
Transient depression and masking of Kell antigens have
been reported due to
anti Kell autoantibodies.
92
Often characterized by reticulocytopenia, with little or
no bilirubinemia
anti-k1
93
Reports have also described neonatal thrombocytopenia due
to suppression of marrow megakaryocytes
anti-k1
94
● Antibody against K.
Anti-K1
95
Most commonly encountered antibody against the Kell blood
group system.
Anti-K1
96
Present in approximately 1% of pregnancies, with HDFN
affecting 40% of positive infants.
Anti-K1
97
A vasoactive peptide that functions in endothelial cell
migration, neovascularization, axonal growth, and
neural crest development
endothelin-3
98
to suppress fetal erythropoiesis also
suggests a possible role for Kell during erythroid
differentiation and maturation
anti-Kell
99
○ Decreased permeability to water.
○ Abnormal morphology (acanthocytes)
● McLeod RBCs
100
○ Hematologic neuromuscular abnormalities
Late onset muscular dystrophy and cardiomyopathy
can also be seen.
● McLeod Syndrome
101
Can also be associated with Chronic Granulomatous
Disease
● McLeod Phenotype
102
in 2/3 of patients, it results from a deletion or
mutation of the cytochrome b gene (CYBB) on the X
chromosome.
cgd
103
It is speculated that they could play a role in renal graft
rejection
Anti-Lea and Anti-Leb
in black, Le(a-b-) individual only
104
104
Sources of Substances for NEUTRALIZATION
lewis
○ Plasma or Serum, Saliva (px should be a secretor)
105
● Naturally occurring IgM, Room temp
O
● Seldom Clinically significant (HTR rare, does not cause
HDFN)
● Although uncommon, some examples demonstrate in vitro
hemolysis.
Anti-Lea and Anti-Leb
106
Binds H, Leb, and Ley antigens via BabA recognition of a
terminal Fuca1-2 Gal. epitope
● Helicobacter pylori
107
Has been linked with a higher incidence of recurrent
Candida vaginitis and urinary tract infection
● Lewis null and/or non-secretor phenotype
108
○ Protects against Norovirus infection.
● Lewis null and/or non-secretor phenotype
109
phenotype associated with an increased
incidence of heart disease
Le (a-b-)
110
○ A ligand for the endothelial adhesion molecule E
selectin and may mediate tumor cell endothelium
interactions
Sialyl-Lea
111
serologic marker for monitoring patients with
gastrointestinal and other malignancies
CA 19 9,
112
DUFFY BLOOD GROUP SYSTEM (ISBT NO. ??)
DUFFY BLOOD GROUP SYSTEM (ISBT NO. 008)
113
Inheritance is autosomal codominant with 3 predominant
phenotypes.
KIDD BLOOD GROUP SYSTEM (ISBT NO. 009)
114
Fya and Fyb - ______ antigens.
○ Differs in location ?//
○ Fya: ____
○ Fyb: ____
Fya and Fyb - autosomal codominant antigens.
○ Differs in location 42
○ Fya: glycine
○ Fyb: aspartate
115
high incidence antigens (so not clinically
significant) present on all RBCs except the Duffy null
phenotype.
Fy3, Fy5, and Fy6
116
○ originally described on Fy (a-b-) RBCs
● Fy4 antigen
117
marker for African black race.
Fy (a-b-)
duffy
118
● 90.8% frequency among Chinese
Fy (a+b+)
119
○ Characterized by extremely weak Fyb expression
somewhat rare.
● Fyx
120
○ Can cause or produce autoantibodies.
Fyx
121
are relatively resistant to protease
digestion.
Fy5 and Fy3 antigens
122
Most common alloantibody encountered clinically can
be observed in Fy (a-) individuals of all races.
● Anti-Fya
123
○ Relatively uncommon and is observed primarily in
nonblacks.
● Anti-Fyb
124
○ occasionally produced by sickle cell, Fy (a-b-) patients
despite the expression of Fyb on nonerythroid tissues
anti-fy3
125
○ behaves like an anti-Fya+b, reacting with all Duffy positive RBCs.
anti-fy3
126
○ Also reacts like an anti Fy a+b
○ Requires the presence of Rh antigens for reactivity.
Anti-Fy5
127
The epitope for an anti-Duffy monoclonal antibody that
blocks Plasmodium vivax binding
● Anti-Fy6
128
may facilitate leukocyte recruitment to the sites of
inflammation by establishing a chemokine across activated
endothelium
DARC
129
The role of DARC and Fy phenotype in renal transplantation is
mixed,with some studies showing an
increase in rejection and
chronic lesion
130
In humans, no distinct clinical syndrome is associated with a
Fy null phenotype, however, the Fy nu phenotype has been
linked to:
○ Lower neutrophil counts
○ Susceptibility to infection
○ Renal disease
○ Reduced graft survival following renal transplantation.
131
In patients with sickle cell disease, is associated with
increased chronic organ damage and proteinuria.
● Fy null phenotype
132
Resistant to most Plasmodium vivax strains and
Plasmodium knowlesi
● Fynu individuals
133
○ is the receptor for Plasmodium vivax
DARC
134
○ binds DARC at the Fy6 epitope
Plasmodium vivax
135
● 3 antigensof kidd
● 3 antigens Jka, Jkb, Jk3
136
A 4th phenotype of kidd blood group , J___________, is very rare, except among
Polynesians (<1%) and Finns.
A 4th phenotype, Jk null or Jk (a-b-), is very rare, except among
Polynesians (<1%) and Finns.
137
Resistant to lysis by 2M urea, a lytic agent used by some
automated hematology analyzers
JK NULL
138
○ Second Jk (a-b-) phenotype
● In (Jk)
139
Autosomal dominant owing to a suppressor gene at a
distant, unrelated locus, similar to In (Lu)
● In (Jk)
140
○ Characterized by very weak Kidd expresion
○ Have intermediate resistance to urea.
● In (Jk)
141
● Common cause of hemolytic transfusion reactions,
○ Accounting for nearly one quarter of all delayed
hemolytic transfusion reactions and 75% of those with
true hemolytic sequelae
ANTI-Jk
142
ANTI-Jk
ISOTYPE
● Usually of lgGl or lgG3 isotype
143
● causes formation of autoanti-Jk
Methyldopa
144
● Reacts with all RBCs except Jk,ul.,
ANTI-Jk3
145
● Observed in JKu individuals.
ANTI-Jk3
146
● functions in the facilitated transport of urea
JK/UT-B
147
may help preserve the osmotic
stability of RBCs as they pass through the kidney.
JK/UT B
148
Exhibit a slightly decreased capacity to concentrate
urine.
● Jk null individuals
149
I BLOOD GROUP SYSTEM (ISBT NO. ??)
I BLOOD GROUP SYSTEM (ISBT NO. 027)
150
● Resistant to treatment with DTT and glycine acid EDTA.
I BLOOD GROUP SYSTEM (ISBT NO. 027)
151
strongly expressed on cord cells because of developmental
delays in the enzyme responsible for l antigen synthesis
I BLOOD GROUP SYSTEM (ISBT NO. 027)
152
Increases in I antigen are accompanied by
parallel increases
in A and B antigens.
153
A rare, autosomal recessive phenotype found in <1/10,000
donors in Asia, can be associated with congenital cataracts.
i adult (Null) phenotype
154
HEMPAS
(hereditary
erythroblastic multinuclearity with positive acidified serum
test)
155
A congenital dyserythropoietic anemia associated with
chronic hemolysis, binucleated erythroblasts, and
altered red cell glycosylation.
HEMPAS
156
The molecular basis of HEMPAS was recently identified
as
altered Golgi trafficking due to mutation in SEC23B, a
COPll protein.
157
○ Usually low titered cold agglutinins
● Autoantibodies to I
158
observed in cold autoimmune hemolytic
anemia (CAIHA)
● Autoantibodies to I
159
Found as a naturally occurring antibody in i adult
individuals.
● Alloanti-I
160
○ Also uncommon
○ Has been reported in CAIHA, infectious mononucleosis,
choriocarcinomatosis, and alcoholic cirrhosis.
Anti-i
161
164
165
