OTHER MAJOR BLOOD GROUP SYSTEM Flashcards
(130 cards)
1
Q
Lewis antigens are not intrinsic to RBCs but are produced by ____ and coded by the production of ____ enzyme.
A
tissues, fucosyltransferase
2
Q
The genes coding for fucosyltransferase enzymes in the Lewis system.
A
FUT1 (H gene), FUT2 (Se gene), FUT3 (Le gene)
3
Q
The glycosphingolipid type associated with Lewis antigens, adsorbed onto the RBC membrane.
A
Type 1 glycosphingolipids
4
Q
The two antigens of the Lewis system.
A
Le^a and Le^b
5
Q
The chromosome where the Lewis gene (Le) is located.
A
Chromosome 19
6
Q
Le(a-b-) is commonly found in these conditions.
A
Cord blood, cancer, pregnant women
7
Q
Phenotype of non-secretors with Lewis gene present.
A
Le(a+b-)
8
Q
Phenotype of secretors with Lewis gene present.
A
Le(a-b+)
9
Q
The function of the Lewis positive gene (Le).
A
Converts precursor material to Le^a substance
10
Q
The result of inheriting Lewis negative genes (lele).
A
Le(a-b-) phenotype
11
Q
The phenotype of a person with at least one Le gene and one Se gene.
A
Le^b positive
12
Q
The phenotype of a person with at least one Le gene and sese genes.
A
Le(a+b-)
13
Q
The gene controlling ABH secretion but not Lewis secretion.
A
Se gene
14
Q
Reaction characteristics of anti-Le^bH.
A
Reacts best when both Le^b and H antigens are present
15
Q
Reaction characteristics of anti-Le^6L.
A
Recognizes any Le^b antigen regardless of ABO type
16
Q
Characteristics of Lewis antibodies.
A
Naturally occurring, generally IgM, neutralizable by plasma
17
Q
Role of Le^a^b in pathogen interactions.
A
Associated with H. pylori and Norwalk virus receptor
18
Q
Marker associated with Reed-Sternberg cells in Hodgkin’s lymphoma.
A
Le^x
19
Q
Clinical implications of Le(a-b-) phenotype.
A
Increased renal graft survival, heart disease risk, susceptibility to Candida and uropathogenic E. coli
20
Q
The most common Lewis antibody.
A
“Anti-Le^a” - seen in nonsecretors
21
Q
Le^a+b+ phenotype is rare in which population?
A
East Asian descent
22
Q
Genes involved in Le^a+b+ phenotype
A
Lewis (FUT3) and weak secretor (FUT2)
23
Q
Characteristic of Le^a+b+ phenotype
A
Both Le^a and Le^b antigens on RBCs
24
Q
Effect of weak secretor status on Le^a+b+ phenotype
A
Reduced conversion of Le^a to Le^b
25
Antigens in the P blood group system
P, P1, Px, LKE
26
Biochemical relation of P1PK (003), Globoside (028), and Related Antigens
P1PK - P1,PK, Globoside - P, Px, LKE
27
Antigens formed in the P blood group system
P1, Px, P
28
Receptor for Parvovirus B19
P antigen
29
Prevalence of P1 antigen on red cells
Present in 79% of the population
30
Individuals lacking P1 antigen are called
P2
31
Phenotype of individuals lacking P1, PK, and P antigens
P null or p
32
Time of P1 antigen presence on fetal red cells
Present as early as 12 weeks, weakens with gestational age
33
Storage effect on P1 antigen
Deteriorates rapidly
34
Substances containing Pl antigen
Hydatid cyst fluid, earthworm (Lumbricoides terestris), Ascaris suum
35
Anti-P1 antibodies are found in which sources
Liver flukes, tapeworms, earthworms, pigeons, turtledoves
36
Anti-P1 antibody type
Naturally occurring IgM
37
Anti-P, P1Pk antibody is associated with which condition
Spontaneous abortions
38
Original name of Anti-P, P1Pk antibody
Anti-Tja
39
Alloanti-P antibody characteristics
Rare, hemolytic, reacts over a wide thermal range
40
Autoanti-P is found in which disease
Paroxysmal Cold Hemoglobinuria (PCH)
41
Test for Autoanti-P
Donath-Landsteiner Test(expose blood at 4°C, then 37°C, check for hemolysis)
42
Anti-Pk antibody is isolated from which cells
P1 cells
43
Anti-Pk antibody is reported in which conditions
Biliary cirrhosis, autoimmune hemolytic anemia
44
Luke (LKE) antigen is a marker for which cells
Embryonic and mesenchymal stem cells
45
Luke (LKE) antigen disease associations
Hemolytic uremic syndrome (HUS), HIV protection, apoptosis in B cells, Burkitt lymphoma, lymphoblastic leukemia
46
I antigen can also be found on which cells
WBC, platelets, cord blood cells
47
Prevalence of I antigen
High in adults (trace i antigen in adults)
48
Transition of i to I antigen
i decreases, I increases by 1.5 to 2 years
49
Rare phenotype of I antigen
i adult or I negative
50
Anti-I association
Cold hemagglutinin disease, M. pneumoniae
51
Anti-i association
Infectious mononucleosis
52
I and i antigens sources
Plasma, serum, saliva, human milk, amniotic fluid, urine, ovarian cyst fluid
53
Conditions with increased I antigen
Acute leukemia, (hypoplastic anemia i antigen), megaloblastic anemia, sideroblastic anemia, thalassemia, sickle cell disease, PNH, chronic hemolytic anemia, HEMPAS
54
MNSs system location
Chromosome 4
55
Effect of enzymes on MNSs antigens
Destroyed by enzymes
56
Antigen type of MNSs system
Red cell antigens, not in secretions
57
Anti-M antibody type
Naturally occurring IgM
58
Optimal pH for Anti-M reaction
pH 6.5
59
Anti-Nf antibody associated condition
Renal patients, IgM
60
Anti-S/Anti-s antibody reaction temperature
37°C, antiglobulin test phase
61
MN antigens location
Glycoprotein A
62
M and N antigen amino acid differences
M: Serine at 1, Glycine at 5; N: Leucine at 1, Glutamate at 5
63
Development of MN antigens
Well developed at birth, enzyme-sensitive
64
Ss antigens location
Glycophorin B
65
Critical amino acid for Ss antigen expression
Methionine at position 29 for S, Threonine for s
66
Resistance of Ss antigens to enzymes
Less easily degraded by enzymes
67
U antigen presence
Always present with S or s inheritance, resistant to ficin
68
SsU phenotype genetic basis
GYPB deletion
69
En(a) phenotype genetic basis
GYPA deletion
70
MNSs null phenotype
GYPA + GYPB - MkMk
71
Parasite receptor function of M and N
Receptor for Plasmodium falciparum
72
Resistance to malaria in M-N- phenotype
Resistant to P. falciparum
73
Order of immunogenicity among ABO, D, and Kell
ABO > D > Kell
74
Kell system chromosome location
Chromosome 7
75
First blood group system discovered after antiglobulin testing
Kell
76
Antithetical antigens in Kell system
K-Kell, k-Cellano; Kpa-Penney, Kpb-Routenberg; Jsa-Sutter, Jsb-Matthews
77
Kell antigen dependency
Dependent on the presence of Kx protein
78
Kx antigen system characteristic
Kx is the only antigen in the Kx system
79
K0 phenotype characteristic
Null phenotype in the Kell system
80
Most common antibody in Kell system (excluding ABO and Rh)
Anti-K
81
Bacteria associated with anti-K production
E. coli O125:B15
82
McLeod phenotype characteristic
Absence of Kx, Km; depression of all Kell antigens, associated with GD defect
83
Blood abnormalities in McLeod phenotype
Presence of acanthocytes
84
Gender most affected by McLeod phenotype
Male
85
Source of Kell antigen identification
Serum of Mrs. Keller
86
Duffy system similarity to other blood groups
Similar to MNS, Sirbon, Mulligans, and P. knowlesi systems
87
Duffy antigens
Fya and Fyb
88
Effect of enzymes on Duffy antigens
Destroyed by common proteolytic enzymes (ficin and papain)
89
Duffy antigen expression during development
Identified on fetal red cells as early as 6 weeks gestation and expressed at birth
90
Receptor role of Duffy antigens
Receptors for Plasmodium vivax and Plasmodium knowlesi
91
Malaria resistance associated with Duffy phenotype
Fya-b- is resistant to Plasmodium vivax and P. knowlesi
92
Null phenotype in Duffy system
Fy null (Fya-b-) confers resistance to Plasmodium vivax and P. knowlesi
93
Function of Fya-b-
Acts as a chemokine receptor
94
Duffy antigen polymorphism amino acid positions
Fya has glycine, Fyb has aspartic acid at position 42
95
Duffy system characteristic regarding dosage
Demonstrates dosage effect
96
Type of antibodies for Anti-Fya and Anti-Fyb
Usually IgG
97
Reaction phase of Anti-Fya and Anti-Fyb
Best at antiglobulin phase
98
Effect of low ionic strength medium on Anti-Fya and Anti-Fyb
Activity is enhanced
99
Reaction of Anti-Fya and Anti-Fyb with enzyme-treated red cells
No reaction
100
Clinical significance of Anti-Fya and Anti-Fyb
Associated with hemolytic transfusion reactions; hemolysis is usually mild
101
Anti-Fya and HDFN severity
Often mild, occasionally severe
102
Prevalence of Anti-Fya vs Anti-Fyb
Anti-Fya is more commonly observed
103
Function of Kidd antigens
RBC urea transporter
104
Kidd antigens
Jka, Jkb, Jk3
105
Development of Kidd antigens
Well-developed at birth; Jka detected at 11 weeks, Jkb at 7 weeks
106
Effect of enzymes on Kidd antigens
Enhanced by enzymes
107
Silent allele in Kidd system
Jk allele; common in Polynesians, Filipinos, and Chinese
108
Phenotype resulting from JkJk genotype
Jk(a-b-)
109
Practical test for Jk(a-b-) phenotype
Resistance to 2M urea
110
Clinical significance of anti-Jka and anti-Jkb
Common cause of delayed hemolytic transfusion reactions (HTR)
111
Characteristic of anti-Jka and anti-Jkb in vitro
Titer quickly declines
112
Notorious reputation of anti-Jka and anti-Jkb
Difficult to detect in the blood bank
113
Clinical significance of anti-Jk3
Associated with severe immediate and delayed HTR and mild HDFN
114
Lutheran antigens
Lua, Lub
115
Development of Lutheran antigens
Poorly developed at birth; reach adult levels by age 15
116
Incidence of most Lutheran antigens
High incidence
117
Discovery of Lutheran blood group
Named due to a labeling error of donor 'Lutteran'
118
Antibody classes in anti-Lua
IgG, IgM, IgA
119
Antibody class in anti-Lub
IgG (immune antibody)
120
Effect of enzymes on Lutheran antigens
Affected by enzymes
121
ISBT number for Lutheran system
ISBT 005
122
Immunoglobulin classes of Anti-Lua
IgM and IgG
123
Optimal temperature for Anti-Lua agglutination
Room temperature
124
Clinical significance of Anti-Lua
No clinical significance in transfusion; mild HDFN reported
125
Characteristic pattern of Anti-Lua agglutination
Mixed-field pattern
126
Immunoglobulin class of Anti-Lub
IgG
127
Phase of agglutination for most Anti-Lub reactions
Antiglobulin phase
128
Clinical significance of Anti-Lub
Associated with transfusion reactions and mild HDFN
129
Why is Anti-Lub rare?
Due to the high incidence of Lub antigen
130
Mixed-field agglutination in Anti-Lub
Some examples show mixed-field agglutination
