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BLOODBANK/IMMUNOHEMATOLOGY > OTHER MAJOR BLOOD GROUP SYSTEM > Flashcards

OTHER MAJOR BLOOD GROUP SYSTEM Flashcards

1
Q

Lewis antigens are not intrinsic to RBCs but are produced by ____ and coded by the production of ____ enzyme.

A

tissues, fucosyltransferase

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2
Q

The genes coding for fucosyltransferase enzymes in the Lewis system.

A

FUT1 (H gene), FUT2 (Se gene), FUT3 (Le gene)

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3
Q

The glycosphingolipid type associated with Lewis antigens, adsorbed onto the RBC membrane.

A

Type 1 glycosphingolipids

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4
Q

The two antigens of the Lewis system.

A

Le^a and Le^b

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5
Q

The chromosome where the Lewis gene (Le) is located.

A

Chromosome 19

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6
Q

Le(a-b-) is commonly found in these conditions.

A

Cord blood, cancer, pregnant women

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7
Q

Phenotype of non-secretors with Lewis gene present.

A

Le(a+b-)

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8
Q

Phenotype of secretors with Lewis gene present.

A

Le(a-b+)

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9
Q

The function of the Lewis positive gene (Le).

A

Converts precursor material to Le^a substance

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10
Q

The result of inheriting Lewis negative genes (lele).

A

Le(a-b-) phenotype

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11
Q

The phenotype of a person with at least one Le gene and one Se gene.

A

Le^b positive

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12
Q

The phenotype of a person with at least one Le gene and sese genes.

A

Le(a+b-)

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13
Q

The gene controlling ABH secretion but not Lewis secretion.

A

Se gene

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14
Q

Reaction characteristics of anti-Le^6H.

A

Reacts best when both Le^b and H antigens are present

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15
Q

Reaction characteristics of anti-Le^6L.

A

Recognizes any Le^b antigen regardless of ABO type

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16
Q

Characteristics of Lewis antibodies.

A

Naturally occurring, generally IgM, neutralizable by plasma

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17
Q

Role of Le^a^b in pathogen interactions.

A

Associated with H. pylori and Norwalk virus receptor

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18
Q

Marker associated with Reed-Sternberg cells in Hodgkin’s lymphoma.

A

Le^x

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19
Q

Clinical implications of Le(a-b-) phenotype.

A

Increased renal graft survival, heart disease risk, susceptibility to Candida and uropathogenic E. coli

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20
Q

The most common Lewis antibody.

A

“Anti-Le^a” - seen in nonsecretors

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21
Q

Le^a+b+ phenotype is rare in which population?

A

East Asian descent

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22
Q

Genes involved in Le^a+b+ phenotype

A

Lewis (FUT3) and weak secretor (FUT2)

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23
Q

Characteristic of Le^a+b+ phenotype

A

Both Le^a and Le^b antigens on RBCs

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24
Q

Effect of weak secretor status on Le^a+b+ phenotype

A

Reduced conversion of Le^a to Le^b

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25
Q

Antigens in the P blood group system

A

P, P1, Px, LKE

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26
Q

Biochemical relation of P1PK (003), Globoside (028), and Related Antigens

A

P1PK - P1,PK, Globoside - P, Px, LKE

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27
Q

Antigens formed in the P blood group system

A

P1, Px, P

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28
Q

Receptor for Parvovirus B19

A

P antigen

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29
Q

Prevalence of P1 antigen on red cells

A

Present in 79% of the population

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30
Q

Individuals lacking P1 antigen are called

A

P2

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31
Q

Phenotype of individuals lacking P1, PK, and P antigens

A

P null or p

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32
Q

Time of P1 antigen presence on fetal red cells

A

Present as early as 12 weeks, weakens with gestational age

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33
Q

Storage effect on P1 antigen

A

Deteriorates rapidly

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34
Q

Substances containing Pl antigen

A

Hydatid cyst fluid, earthworm (Lumbricoides terestris), Ascaris suum

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35
Q

Anti-P1 antibodies are found in which sources

A

Liver flukes, tapeworms, earthworms, pigeons, turtledoves

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36
Q

Anti-P1 antibody type

A

Naturally occurring IgM

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37
Q

Anti-P, P1Pk antibody is associated with which condition

A

Spontaneous abortions

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38
Q

Original name of Anti-P, P1Pk antibody

A

Anti-Tja

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39
Q

Alloanti-P antibody characteristics

A

Rare, hemolytic, reacts over a wide thermal range

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40
Q

Autoanti-P is found in which disease

A

Paroxysmal Cold Hemoglobinuria (PCH)

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41
Q

Test for Autoanti-P

A

Donath-Landsteiner Test(expose blood at 4°C, then 37°C, check for hemolysis)

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42
Q

Anti-Pk antibody is isolated from which cells

A

P1 cells

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43
Q

Anti-Pk antibody is reported in which conditions

A

Biliary cirrhosis, autoimmune hemolytic anemia

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44
Q

Luke (LKE) antigen is a marker for which cells

A

Embryonic and mesenchymal stem cells

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45
Q

Luke (LKE) antigen disease associations

A

Hemolytic uremic syndrome (HUS), HIV protection, apoptosis in B cells, Burkitt lymphoma, lymphoblastic leukemia

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46
Q

I antigen can also be found on which cells

A

WBC, platelets, cord blood cells

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47
Q

Prevalence of I antigen

A

High in adults (trace i antigen in adults)

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48
Q

Transition of i to I antigen

A

i decreases, I increases by 1.5 to 2 years

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49
Q

Rare phenotype of I antigen

A

i adult or I negative

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50
Q

Anti-I association

A

Cold hemagglutinin disease, M. pneumoniae

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51
Q

Anti-i association

A

Infectious mononucleosis

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52
Q

I and i antigens sources

A

Plasma, serum, saliva, human milk, amniotic fluid, urine, ovarian cyst fluid

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53
Q

Conditions with increased I antigen

A

Acute leukemia, (hypoplastic anemia i antigen), megaloblastic anemia, sideroblastic anemia, thalassemia, sickle cell disease, PNH, chronic hemolytic anemia, HEMPAS

54
Q

MNSs system location

A

Chromosome 4

55
Q

Effect of enzymes on MNSs antigens

A

Destroyed by enzymes

56
Q

Antigen type of MNSs system

A

Red cell antigens, not in secretions

57
Q

Anti-M antibody type

A

Naturally occurring IgM

58
Q

Optimal pH for Anti-M reaction

A

pH 6.5

59
Q

Anti-Nf antibody associated condition

A

Renal patients, IgM

60
Q

Anti-S/Anti-s antibody reaction temperature

A

37°C, antiglobulin test phase

61
Q

MN antigens location

A

Glycoprotein A

62
Q

M and N antigen amino acid differences

A

M: Serine at 1, Glycine at 5; N: Leucine at 1, Glutamate at 5

63
Q

Development of MN antigens

A

Well developed at birth, enzyme-sensitive

64
Q

Ss antigens location

A

Glycophorin B

65
Q

Critical amino acid for Ss antigen expression

A

Methionine at position 29 for S, Threonine for s

66
Q

Resistance of Ss antigens to enzymes

A

Less easily degraded by enzymes

67
Q

U antigen presence

A

Always present with S or s inheritance, resistant to ficin

68
Q

SsU phenotype genetic basis

A

GYPB deletion

69
Q

En(a) phenotype genetic basis

A

GYPA deletion

70
Q

MNSs null phenotype

A

GYPA + GYPB - MkMk

71
Q

Parasite receptor function of M and N

A

Receptor for Plasmodium falciparum

72
Q

Resistance to malaria in M-N- phenotype

A

Resistant to P. falciparum

73
Q

Order of immunogenicity among ABO, D, and Kell

A

ABO > D > Kell

74
Q

Kell system chromosome location

A

Chromosome 7

75
Q

First blood group system discovered after antiglobulin testing

A

Kell

76
Q

Antithetical antigens in Kell system

A

K-Kell, k-Cellano; Kpa-Penney, Kpb-Routenberg; Jsa-Sutter, Jsb-Matthews

77
Q

Kell antigen dependency

A

Dependent on the presence of Kx protein

78
Q

Kx antigen system characteristic

A

Kx is the only antigen in the Kx system

79
Q

K0 phenotype characteristic

A

Null phenotype in the Kell system

80
Q

Most common antibody in Kell system (excluding ABO and Rh)

A

Anti-K

81
Q

Bacteria associated with anti-K production

A

E. coli O125:B15

82
Q

McLeod phenotype characteristic

A

Absence of Kx, Km; depression of all Kell antigens, associated with GD defect

83
Q

Blood abnormalities in McLeod phenotype

A

Presence of acanthocytes

84
Q

Gender most affected by McLeod phenotype

A

Male

85
Q

Source of Kell antigen identification

A

Serum of Mrs. Keller

86
Q

Duffy system similarity to other blood groups

A

Similar to MNS, Sirbon, Mulligans, and P. knowlesi systems

87
Q

Duffy antigens

A

Fya and Fyb

88
Q

Effect of enzymes on Duffy antigens

A

Destroyed by common proteolytic enzymes (ficin and papain)

89
Q

Duffy antigen expression during development

A

Identified on fetal red cells as early as 6 weeks gestation and expressed at birth

90
Q

Receptor role of Duffy antigens

A

Receptors for Plasmodium vivax and Plasmodium knowlesi

91
Q

Malaria resistance associated with Duffy phenotype

A

Fya-b- is resistant to Plasmodium vivax and P. knowlesi

92
Q

Null phenotype in Duffy system

A

Fy null (Fya-b-) confers resistance to Plasmodium vivax and P. knowlesi

93
Q

Function of Fya-b-

A

Acts as a chemokine receptor

94
Q

Duffy antigen polymorphism amino acid positions

A

Fya has glycine, Fyb has aspartic acid at position 42

95
Q

Duffy system characteristic regarding dosage

A

Demonstrates dosage effect

96
Q

Type of antibodies for Anti-Fya and Anti-Fyb

A

Usually IgG

97
Q

Reaction phase of Anti-Fya and Anti-Fyb

A

Best at antiglobulin phase

98
Q

Effect of low ionic strength medium on Anti-Fya and Anti-Fyb

A

Activity is enhanced

99
Q

Reaction of Anti-Fya and Anti-Fyb with enzyme-treated red cells

A

No reaction

100
Q

Clinical significance of Anti-Fya and Anti-Fyb

A

Associated with hemolytic transfusion reactions; hemolysis is usually mild

101
Q

Anti-Fya and HDFN severity

A

Often mild, occasionally severe

102
Q

Prevalence of Anti-Fya vs Anti-Fyb

A

Anti-Fya is more commonly observed

103
Q

Function of Kidd antigens

A

RBC urea transporter

104
Q

Kidd antigens

A

Jka, Jkb, Jk3

105
Q

Development of Kidd antigens

A

Well-developed at birth; Jka detected at 11 weeks, Jkb at 7 weeks

106
Q

Effect of enzymes on Kidd antigens

A

Enhanced by enzymes

107
Q

Silent allele in Kidd system

A

Jk allele; common in Polynesians, Filipinos, and Chinese

108
Q

Phenotype resulting from JkJk genotype

A

Jk(a-b-)

109
Q

Practical test for Jk(a-b-) phenotype

A

Resistance to 2M urea

110
Q

Clinical significance of anti-Jka and anti-Jkb

A

Common cause of delayed hemolytic transfusion reactions (HTR)

111
Q

Characteristic of anti-Jka and anti-Jkb in vitro

A

Titer quickly declines

112
Q

Notorious reputation of anti-Jka and anti-Jkb

A

Difficult to detect in the blood bank

113
Q

Clinical significance of anti-Jk3

A

Associated with severe immediate and delayed HTR and mild HDFN

114
Q

Lutheran antigens

A

Lua, Lub

115
Q

Development of Lutheran antigens

A

Poorly developed at birth; reach adult levels by age 15

116
Q

Incidence of most Lutheran antigens

A

High incidence

117
Q

Discovery of Lutheran blood group

A

Named due to a labeling error of donor ‘Lutteran’

118
Q

Antibody classes in anti-Lua

A

IgG, IgM, IgA

119
Q

Antibody class in anti-Lub

A

IgG (immune antibody)

120
Q

Effect of enzymes on Lutheran antigens

A

Affected by enzymes

121
Q

ISBT number for Lutheran system

A

ISBT 005

122
Q

Immunoglobulin classes of Anti-Lua

A

IgM and IgG

123
Q

Optimal temperature for Anti-Lua agglutination

A

Room temperature

124
Q

Clinical significance of Anti-Lua

A

No clinical significance in transfusion; mild HDFN reported

125
Q

Characteristic pattern of Anti-Lua agglutination

A

Mixed-field pattern

126
Q

Immunoglobulin class of Anti-Lub

A

IgG

127
Q

Phase of agglutination for most Anti-Lub reactions

A

Antiglobulin phase

128
Q

Clinical significance of Anti-Lub

A

Associated with transfusion reactions and mild HDFN

129
Q

Why is Anti-Lub rare?

A

Due to the high incidence of Lub antigen

130
Q

Mixed-field agglutination in Anti-Lub

A

Some examples show mixed-field agglutination

BLOODBANK/IMMUNOHEMATOLOGY (22 decks)

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