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Immunohematology Lec > [14] CHAPTER VI LESSON 2 > Flashcards

[14] CHAPTER VI LESSON 2 Flashcards

1
Q

*Named after the first antibody maker in a Venezuelan family.

A

Diego (010)

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2
Q
  • Expressed on RBCs of newborns.
A

Diego (010)

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3
Q

*Named in 1956 for the first antibody maker and used the last letter “t” in the patient’s last name, which was Catwright.

A

Cartwright (011)

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4
Q

*Named after the first antibody maker

A

Scianna (013)

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5
Q

*The antigens are expressed on cord RBCs.

A

Scianna (013)

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6
Q

*Named for the first antibody maker, Mrs. Dombrock.

A

Dombrock (014)

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7
Q

22 antigens: Dia , Dib, Wra, Wrb and Wu/DISK and 17 low-prevalence antigens.

A

Diego (010)

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8
Q

Yta – high prevalence

A

Cartwright (011)

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9
Q

Ytb – low prevalence

A

Cartwright (011)

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10
Q

Xga and CD99

A

Xg (012)

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11
Q

7 antigens: SC:1, SC:2, SC:3, Sc4, Sc5 (STAR), Sc6 (SCER), Sc7 (SCAN)

A

Scianna (013)

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12
Q

Doa, Dob, Gya, Hy, Joa

A

Dombrock (014)

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13
Q

*Carried on Band 3 or also known as Red Cell anion exchanger (AE1) or solute carrier family-4.

A

Diego (010)

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14
Q

*Dia is rare in most populations but is polymorphic in people of Mongolian Ancestry.

A

Diego (010)

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15
Q

In South American Indians, the prevalence can be as high as 54%.

A

Diego (010)

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16
Q

*Anti-Wra is commonly found with other antibodies.

A

Diego (010)

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17
Q

*Resistant to enzyme treatment.

A

Diego (010)

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18
Q

Anion exchanger, member 1 (SLC4A1)

A

Diego (010)

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19
Q

*The Yt antigens are antithetical and represent an amino acid substitution on the glycosylphosphatidylinositol (GPI)-linked RBC glycoprotein acetylcholinesterase (AChE).

A

Cartwright (011)

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20
Q

*Variably sensitive to enzymes (Ficin and Papain)

A

Cartwright (011)

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21
Q

Sensitive to DTT

A

Cartwright (011)

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22
Q

*The antigens are developed at birth but are expressed more weakly on cord RBCs than on adult RBCs, and are absent from RBCs of people with PNH III.

A

Cartwright (011)

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23
Q

*Inherited on X chromosome; frequency varies with sex.

A

Xg (012)

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24
Q

*Sensitive to Ficin and Papain; Resistant to DTT treatment.

A

Xg (012)

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25
Q

*The SC gene is located on chromosome 1 at 1p34.

A

Scianna (013)

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26
Q

The product of the gene is a protein called erythroid membrane- associated protein.

A

Scianna (013)

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27
Q

*Resistant to Ficin and Papain; slightly weakened by DTT.

A

Scianna (013)

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28
Q

*The antigens are carried on a mono-ADP-ribosyltransferase 4 (ART4) attached to the RBC membrane by the GPI anchor.

A

Dombrock (014)

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29
Q

*Hy phenotype is found only in blacks

A

Dombrock (014)

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30
Q

anti-Doa and anti-Dob antibodies are rarely found as a single specificity.

A

Dombrock (014)

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31
Q
  • Antigens are present on cord RBCs, but are absent from PNH III RBCs.
A

Dombrock (014)

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32
Q

Resistant to Ficin, Papain and Glycine Acid EDTA

A

Dombrock (014)

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33
Q

Sensitive to 0.2 M DTT treatment.

A

Dombrock (014)

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34
Q

Named after the first antibody maker Calton, but the tube was misread.

A

Colton (015)

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35
Q

Expressed on RBCs of newborns

A

Colton (015)

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36
Q

4 antigens: Coa, Cob, Co3, Co4

A

Colton (015)

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37
Q

The antigens are carried on an integral membrane protein aquaporin 1 (AQP1).

A

Colton (015)

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38
Q

Anti-Cob is rarely found as a single specificity

A

Colton (015)

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39
Q

Resistant to enzyme treatment.

A

Colton (015)

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40
Q

3 LW Antigens: LWa, LWab – highprevalence LWb- lowprevalence

A

Landsteiner-Wiener (016)

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41
Q

The structure that carries the LW antigens is a glycoprotein known as intracellular adhesion molecule 4 (ICAM-4), a membrane of the immunoglobulin superfamily.

A

Landsteiner-Wiener (016)

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42
Q

The LW antigens may be depressed during pregnancy and in some diseases, such as lymphoma and leukemia.

A

Landsteiner-Wiener (016)

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43
Q

Resistant to treatment with enzymes and Glycine Acid EDTA.

A

Landsteiner-Wiener (016)

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44
Q

*Named after the 2 antibody producers, Ch for Chido and Rg for Rodgers.

A

Chido/Rodgers (017)

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45
Q

are clinically insignificant for transfusion.

A

Anti-Ch and Anti-Rg

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46
Q

Ch, Rg

A

Chido/Rodgers (017)

Anti-Ch and Anti-Rg

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47
Q

Ch and Rg antigens are not intrinsic to the RBC membrane, they are on the fourth component of complement C4, and are adsorbed onto RBCs from plasma.

A

Chido/Rodgers (017)

Anti-Ch and Anti-Rg

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48
Q

Antigens are sensitive to enzymes and found in plasma; antibodies have HTLA characteristics.

A

Chido/Rodgers (017)

Anti-Ch and Anti-Rg

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49
Q

Destroyed by Ficin and Papain

A

Chido/Rodgers (017)

Anti-Ch and Anti-Rg

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50
Q

Resistant to treatment with DTT and Glycine Acid EDTA.

A

Chido/Rodgers (017)

Anti-Ch and Anti-Rg

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51
Q

The antigens are carried on sialoglycoprotein structures GPC and GPD.

A

Gerbich (020)

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52
Q

The Leach type is the Gerbich null phenotype (Ge: -2,-3,-4)

A

Gerbich (020)

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53
Q

All antigens except for Ge4 are sensitive to enzymes.

A

Gerbich (020)

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54
Q

Resistant to treatment with DTT and Glycine Acid EDTA.

A

Gerbich (020)

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55
Q

Ge2 and Ge4: Ficin and Papain Sensitive

A

Gerbich (020)

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56
Q

Ge3: Ficin Resistant

A

Gerbich (020)

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57
Q

Named after Mrs. Gerbich, the first antibody producer.

A

Gerbich (020)

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58
Q

Expressed at birth

A

Gerbich (020)

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59
Q

6 high prevalence antigen (Ge2, Ge3, Ge4, GEPL, GEAT and GETI)

A

Gerbich (020)

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60
Q

5 low prevalence antigen (Wb, Lsa, Ana, Dha, and GEIS)

A

Gerbich (020)

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61
Q

An antibody was found in a black prenatal patient, Mrs. Cromer, that reacted with all RBCs except her own and 2 siblings.

A

Cromer (021)

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62
Q

DAF is strongly expressed on placental tissue and will adsorb Cromer antibodies.

A

Cromer (021)

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63
Q

Cra, Tca, Tcb, Tcc, Dra, Esa, IFC, WESa, WESb, UMC

A

Cromer (021)

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64
Q

Antigen is also found in plasma

A

Cromer (021)

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65
Q

located on Decay Accelerating Factor (CD55).

A

Cromer (021)

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66
Q

Distributed in body fluids and on RBCs, WBCs, platelets and placental tissue.

A

Cromer (021)

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67
Q

PNH III RBC’s are deficient in DAF so they lack Cromer antigens.

A

Cromer (021)

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68
Q

The Cr(a-) phenotype is typically found in blacks and is not found in whites.

A

Cromer (021)

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69
Q

Resistant to treatment with Ficin and Papain and Glycine Acid EDTA

A

Cromer (021)

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70
Q

Destroyed by achymotrypsin

A

Cromer (021)

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71
Q

Weakened with DTT.

A

Cromer (021)

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72
Q

Named after the first antibody maker, Mrs. Knops.

A

Knops (022)

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73
Q

Antigens are weakly expressed on cord RBCs and weaken upon storage of adult RBCs.

A

Knops (022)

74
Q

Kna, Knb, McCa, Sla, Yka

A

Knops (022)

75
Q

Located on Complement Receptor 1

A

Knops (022)

76
Q

are clinically insignificant and have weak & “nebulous” reactivity at the antiglobulin phase

A

Knops antibodies

77
Q

they are not inhibited by plasma.

A

Knops antibodies

78
Q

Antibody reactivity is enhanced with longer incubation (e.g., 1 hour at 37oC)

A

Knops (022)

79
Q

The “Helgeson phenotype”- null

A

Knops (022)

80
Q

Antigen depression in SLE, PNH, and AIDS

A

Knops (022)

81
Q

antigens are weakened by ficin treatment

A

Knops (022)

82
Q

antibodies have HTLA characteristics

A

Knops (022)

83
Q

Weakened by treatment with Ficin and Papain

A

Knops (022)

84
Q

Destroyed by DTT.

A

Knops (022)

85
Q

Antigen: Resistant to Glycine Acid EDTA

A

Knops (022)

86
Q

The Indian blood group system was named because the first In(a+) individuals were from India.

A

Indian (023)

87
Q

Ina, Inb are weakly expressed on cord RBCs

A

Indian (023)

88
Q

4 antigens: Ina, Inb and the other 2 high prevalence antigens

A

Indian (023)

89
Q

Antibodies are usually IgG and reactive in the antiglobulin test.

A

Indian (023)

90
Q

Do not bind the complement.

A

Indian (023)

91
Q

The Ina antigen is more prevalent in Arab and Iranian populations with Ina and Inb antigen expression being depressed on the dominant type Lu(a-b-).

A

Indian (023)

92
Q

Sensitive to treatment with Ficin and Papain, DTT

A

Indian (023)

93
Q

Resistant to Glycine Acid EDTA.

A

Indian (023)

94
Q

Named after the antibody maker, Mrs. Kobutso

A

Ok (024)

95
Q

Oka is well developed on RBCs from newborns Oka, OKGV, OKVM

A

Ok (024)

96
Q

The OK antigens are carried on CD147, a member of the immunoglobulin superfamily that mainly functions as receptors and adhesion molecules.

A

Ok (024)

97
Q

Anti-Oka has not been reported to cause HDFN. *Resistant to enzyme treatment.

A

Ok (024)

98
Q

Raph for the first patient to make the alloanti-MER2.

A

Raph (025)

99
Q

The antigen name (MER2) is derived from monoclonal and Eleanor Roosevelt, the laboratory where the antibody was produced.

A

Raph (025)

100
Q

It was shown that MER2 is located in CD151, a tetraspanin.

A

Raph (025)

101
Q

MER2 is abundant in on platelets and is expressed on erythroid precursors of individuals with either MER2+ and MER2-RBCs.

A

Raph (025)

102
Q

Resistant to treatment with ficin and Papain

A

Raph (025)

103
Q

Sensitive to treatment with Trypsin, achymotrypsin, pronase, and AET.

A

Raph (025)

104
Q

MER2

A

Raph (025)

105
Q

Named after the first antibody maker John Milton Hagen

A

JMH (026)

106
Q

Weakly expressed on cord RBCs

A

JMH (026)

107
Q

JMH; JMH2-JMH6

A

JMH (026)

108
Q

Autoanti-JMH is often found in elderly patients with absent or weak antigen expression

A

JMH (026)

109
Q

antibodies have HTLA characteristics

A

JMH (026)

110
Q

antigens are sensitive to enzymes and DTT

A

JMH (026)

111
Q

JMH antibodies are generally considered clinically insignificant.

A

JMH (026)

112
Q

Destroyed by treatment with Ficin, Papain and DTT

A

JMH (026)

113
Q

Antigens: Resistant to treatment with Glycine Acid EDTA.

A

JMH (026)

114
Q

is genetically discrete from all other blood group systems

A

Gill (029)

115
Q

GIL

A

Gill (029)

116
Q

The antigen is found on the glycerol transporter aquaporin 3 (AQP3).

A

Gill (029)

117
Q

The GILnull phenotype results from a frameshift and a premature stop codon.

A

Gill (029)

118
Q

Enhanced with Ficin, Papin treatment of RBCs.

A

Gill (029)

119
Q

Antigens: Resistant to DTT and Glycine Acid EDTA

A

Gill (029)

120
Q

Newest blood group system

A

RH-Associated glycoprotein (030)

121
Q

The Rh associated glycoprotein (RhAg) does not have Rh blood group antigens.

A

RH-Associated glycoprotein (030)

122
Q

Two antigens assigned to the RHAG system:
1. Duclos (RHAG1)
2. Ola (RHAG2) *DSLK (Duclos type)

A

RH-Associated glycoprotein (030)

123
Q

RHAG4

A

RH-Associated glycoprotein (030)

124
Q

Part of a blood group collection rather than a system.

A

Cost (Csa and Csb)

125
Q

Named after the first antibody maker

A

Vel

126
Q

Variable antigen expression on red cells

A

Vel

127
Q

both IgG and IgM antibodies are associated with hemolytic reactions (in vitro hemolysis)

A

Vel

128
Q

antibodies react best with enzyme treated red cells.

A

Vel

129
Q

High prevalence antigen named for Sid, who was the head of maintenance department at the Lister Institute in London.

A

Sda

130
Q

Not expressed on RBCs of newborns but is in their saliva, urine and meconium

A

Sda

131
Q

Antigen found in guinea pig and human urine

A

Sda

132
Q

antibodies are typically weak and agglutination is mixed field

A

Sda

133
Q

reduction of Sda expression during pregnancy

A

Sda

134
Q

The soluble form of Sda is Tamm Horsfall glycoprotein found in urine.

A

Sda

135
Q

Reactivity is described as small, refractile (shiny) agglutinates in a sea of free RBCs.

A

Sda

136
Q

Resistant to treatment with enzymes.

A

Sda

137
Q

First described in the serum of a black woman named Mrs. Augustine.

A

Ata

138
Q

The antigen is fully developed at birth.

A

Ata

139
Q

The antibody is usually IgG, reactive in the antiglobulin test and has caused severe HTRs.

A

Ata

140
Q

has caused severe severe HTRs and one reported cause of HDFN.

A

Anti- Ata

141
Q

Resistant to treatment with enzymes.

A

Ata

142
Q

High prevalence antigen

A

Jra

143
Q

The antigen is fully developed at birth.

A

Jra

144
Q

Resistant to treatment with enzymes.

A

Jra

145
Q

is usually IgG.

A

Anti-Jra

146
Q

Appreciating the unique characteristics of each blood group system is helpful in understanding the serologic and clinical features of the associated [?].

A

antibodies

147
Q

With the exception of the ABO system, antibodies that are [?] are usually not clinically significant and react at room temperature, whereas antibodies that are [?] require the antiglobulin test and are clinically significant.

A

IgM

IgG

148
Q

Clinically significant

A

ABO, Rh, Kell, Kidd; Duffy; S, s, and U, Lutheran (Lub)

149
Q

Usually clinically insignificant

A

I, Lewis, M, N, P1, Lutheran (Lua)

150
Q

IgM

Antigens
White
Black
Phase
Enzyme
Class
Comments
Kell

9
2
AHG
→
IgG
IgG
IgG
IgG
lgG
IgG
Antigens in the Kell system
k
99.9
99.8
AHG
→
are destroyed by DTT
Кр°
2
<1
AHG
→

Kph
99.9
>99.9
AHG
→

Js*

20
AHG

Jsb
>99.9
99
AHG

Duffy
Fy*
66
10
AHG

IgG
Fy（a-b-） is protective
against malaria
Fyb
83
23
AHG

IgG
Kidd
Jk°
77
91
AHG

IgG
Associated with delayed transfusion reactions
Jk’
73
49
AHG

IgG
Lutheran
Lu*
7.6
5.3
RT
→
IgM
May exhibit mixed-field reactions
Lu’
99.8
99.9
AHG
→
IgG
Lewis

22
23
RT

IgM
Lewis antigens are found in plasma and red cells

72
55
RT
↑
IgM
Le” arises from H, Le, and Se genes

> 99.9
99.9
RT

IgM
Frequently found as a cold autoantibody
P1PK

<1
RT

IgM
I is negative on cord cells
P1
79
94
RT

IgM

MNS

78
74
RT

IgM
Antigens M and N show dosage

N
72
75
RT

S-s- are also U-negativ-

55
31
AHG
var
IgG

89
93
AHG
var
IgG

A
151
Q

9
2
AHG
IgG

A

K

152
Q

99.9
99.8
AHG
IgG

A

k

153
Q

2
<1
AHG
IgG

A

Кpa

154
Q

99.9
>99.9
AHG
IgG

A

Kpb

155
Q

<1
20
AHG
IgG

A

Jsa

156
Q

> 99.9
99
AHG
IgG

A

Jsb

157
Q

66
10
AHG
IgG

A

Fya

158
Q

83
23
AHG
IgG

A

Fyb

159
Q

77
91
AHG
IgG

A

Jka

160
Q

73
49
AHG
IgG

A

Jkb

161
Q

7.6
5.3
RT
→
IgM

A

Lua

162
Q

99.8
99.9
AHG

IgG

A

Lub

163
Q

22
23
RT
IgM

A

Lea

164
Q

72
55
RT
个
IgM

A

Leb

165
Q

> 99.9
99.9
RT
IgM

A

I

166
Q

<1
<1
RT
IgM

A

i

167
Q

79
94
RT
IgM

A

P1

168
Q

78
74
RT
IgM

A

M

169
Q

72
75
RT
IgM

A

N

170
Q

55
31
AHG
var
IgG

A

S

171
Q

89
93
AHG
var
IgG

A

s

172
Q

Antigens in the Kell system are destroyed by DTT

A

Kell

173
Q

Fy(a-b-) is protective against malaria

A

Duffy

174
Q

Associated with delayed transfusion reactions

A

Kidd

175
Q

May exhibit mixed-field reactions

A

Lutheran

176
Q

are found in plasma and red cells

A

Lewis antigens

177
Q

arises from H, Le, and Se genes

A

Leb

178
Q

Frequently found as a cold autoantibody

A

I

179
Q

is negative on cord cells

A

I

180
Q

show dosage

A

Antigens M and N

181
Q

are also U-negative

A

S-s-

Immunohematology Lec (35 decks)

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