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Transfusion Medicine 2 > Module # 1 - Other Blood Group Systems > Flashcards

Module # 1 - Other Blood Group Systems Flashcards

1
Q

K frequency

A

9%

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2
Q

k frequency

A

99.8%

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3
Q

Kpa frequency

A

2%

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4
Q

Kpb frequency

A

100%

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5
Q

Jsa frequency

A

Rare

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6
Q

Jya frequency

A

100%

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7
Q

Fya frequency

A

66%

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8
Q

Fyb frequency

A

83%

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9
Q

Jka frequency

A

77%

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10
Q

Jkb frequency

A

72%

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11
Q

M frequency

A

78%

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12
Q

N frequency

A

72%

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13
Q

S frequency

A

55%

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14
Q

s frequency

A

89%

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15
Q

P frequency

A

100%

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16
Q

P1 frequency

A

79%

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17
Q

Pk frequency

A

Rare

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18
Q

Lua frequency

A

8%

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19
Q

Lub frequency

A

100%

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20
Q

I frequency

A

Adults

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21
Q

i frequency

A

Babies

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22
Q

Are Kell antigens expressed at birth?

A

Yes

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23
Q

Are Duffy (Fya and Fyb) antigens expressed at birth?

A

Yes

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24
Q

Are Kidd (Jka and Jkb) antigens expressed at birth?

A

Yes

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25
Q

Are MNSs antigens expressed at birth?

A

Yes

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26
Q

Are the P antigens expressed at birth?

A

Poor expression

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27
Q

Are the Lu antigens expressed at birth?

A

Yes, but poorly.

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28
Q

Are the I and i antigens expressed at birth?

A

i yes, I no.

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29
Q

Where are Kell antigens found?

A

Red blood cells

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30
Q

Where are Duffy antigens found?

A

Red blood cells and tissues.

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31
Q

Where are Kidd antigens found?

A

Only red blood cells.

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32
Q

Where are the MNSs antigens found?

A

Only red blood cells.

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33
Q

Where are the P antigens found?

A

RBC, platelets, WBC, epithelial cells, fibroblasts.

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34
Q

Where are Lu antigens found?

A

Red blood cells.

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35
Q

Where are I and i antigens found?

A

Red blood cells, White blood cells and platelets.

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36
Q

Do Kell antigens exhibit dosage?

A

No

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37
Q

Do Duffy antigens exhibit dosage?

A

No

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38
Q

Do Kidd antigens exhibit dosage?

A

Yes

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39
Q

Do MNSs antigens exhibit dosage?

A

Yes

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40
Q

Do P antigens exhibit dosage?

A

No - although the strength of the antigen varies between individuals.

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41
Q

Do Lu antigens exhibit dosage?

A

No

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42
Q

Do I antigens exhibit dosage?

A

No

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43
Q

In what ways are Kell antigens modified?

A

Kell antigens are the most antigenic antigens compared to A, B and D. They are destroyed by trypsin and chymotrypsin. Thiol reducing agents (DDT, 2-ME, AET and ZZAP) destroy Kell antigens.

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44
Q

In what ways are Duffy antigens modified?

A

Duffy antigens are destroyed by proteolytic enzymes and by ZZAP. Duffy antigens are not destroyed by thiol reagents.

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45
Q

In what ways are Kidd antigens modified?

A

Kidd antigens are enhanced by enzymes, unaffected by others.

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46
Q

In what way are MNSs antigens modified?

A

MNSs antigens are destroyed by ZZAP (S and s less sensitive to enzyme destruction.

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47
Q

In what ways are the P antigens modified?

A

P antigens resist enzymes, DDT, chloroquine and glycine acid-EDTA.

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48
Q

In what way are Lu antigens modified?

A

There are no noted ways that Lu antigens are modified. They are low density on the RBCs.

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49
Q

In what way are I and i antigens modified?

A

I and i antigens are enhanced by enzymes.

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50
Q

Are Kell antibodies natural or immune?

A

Immune

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51
Q

Are Duffy antibodies natural or immune?

A

Immune

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52
Q

Are Kidd antibodies natural or immune?

A

Immune

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53
Q

Are MNSs antibodies natural or immune?

A

Both

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54
Q

Are P antibodies natural or immune?

A

Natural

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55
Q

Are Lu antibodies natural or immune

A

Lua - Both, Lub - immune

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56
Q

Are I and i antibodies natural or immune?

A

Anti-I - Alloantibody, IgG/IgM

Anti-i - Autoantibody, IgG

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57
Q

Antibody class of Kell antibodies?

A

IgG

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58
Q

Antibody class of Duffy antibodies?

A

IgG

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59
Q

Antibody class of Kidd antibodies?

A

IgG

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60
Q

Antibody class of MNSs antibodies?

A

IgG and IgM

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61
Q

Antibody class of Anti-P?

A

IgM

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62
Q

Antibody class of PP1/PK?

A

IgG and IgM

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63
Q

Antibody class of P?

A

IgG and IgM

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64
Q

Antibody class of Auto-P?

A

IgG

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65
Q

Antibody class of Anti-Lua?

A

IgG

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66
Q

Antibody class of Anti-Lub?

A

IgM

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67
Q

Antibody class of Anti-I?

A

IgG or IgM

68
Q

Antibody class of Anti-i?

A

IgM

69
Q

Temp range of sensitivity for Anti-Kell?

A

37

70
Q

Temp range of sensitivity for Anti-Duffy?

A

37

71
Q

Temp range of sensitivity for Anti-Kidd?

A

37

72
Q

Temp range of sensitivity for Anti-MNSs?

A

Anti-M/N are cold (4)

Anti-S (37)

73
Q

Temp range of sensitivity for Anti-P?

A

4

74
Q

Temp range of sensitivity for Anti-PP1/PK?

A

37

75
Q

Temp range of sensitivity for Auto-P?

A

4

76
Q

Temp range of sensitivity for Anti-Lua?

A

Cold (4)

77
Q

Temp range of sensitivity for Anti-Lub?

A

37

78
Q

Temp range of sensitivity for Anti-i?

A

4 to 37

79
Q

Favoured reaction conditions for Anti-Kell?

A

PEG/IAT

80
Q

Favoured reaction conditions for Anti-Duffy?

A

IAT/LISS

81
Q

Favoured reaction conditions for Anti-Kidd?

A

IAT/LISS/PEG

82
Q

Favoured reaction conditions for Anti-MNSs?

A

Increase or decrease incubation time, pH of 6.5, 4 drops of plasma, albumin/LISS/PEG

83
Q

Favoured reaction conditions for Anti-P?

A

Cold, saline reactive.

84
Q

Favoured reaction conditions for Anti-PP1/PK?

A

IAT

85
Q

Favoured reaction conditions for Anti-P?

A

IAT

86
Q

Favoured reaction conditions for Auto-P?

A

Siphasic

87
Q

Favoured reaction conditions for Anti-Lua/b?

A

N/A

88
Q

Favoured reaction conditions for Anti-I/i?

A

Avoid using room temperature resting and Anti-IgG (AHG).

89
Q

Does Anti-Kell bind complement?

A

Yes, but no lysis.

90
Q

Does Anti-Duffy bind complement?

A

Some do.

91
Q

Does Anti-Kidd bind complement?

A

Many bind complement.

92
Q

Does Anti-M/N bind complement?

A

Rarely.

93
Q

Does Anti-S bind complement?

A

Yes

94
Q

Does Anti-P bind complement?

A

No

95
Q

Does Anti-PP1/PK or Auto-P bind complement?

A

Yes

96
Q

Does Anti-Lua bind complement?

A

Yes

97
Q

Does Anti-Lub bind complement?

A

No

98
Q

Does Anti-I bind complement?

A

No

99
Q

Does Anti-i bind complement?

A

Yes

100
Q

Other characteristics of Anti-Kell are…

A

Can cause HDN and transfusion reactions.

101
Q

Other characteristics of Anti-Duffy are…

A

Are destroyed by treatment of reagent red blood cells. Are associated with mild to severe HDN and hemolytic transfusion reactions.

102
Q

Other characteristics of Anti-Kidd are…

A

Not commonly enhanced by enzymes. Associated with HDN and transfusion reactions.

103
Q

Other characteristics of Anti-MNSs are…

A

Exhibit dosage. Anti-S causes hemolytic transfusion reactions and HDN.

104
Q

Other characteristics of Anti-P and associated antibodies are…

A

Cause severe hemolytic transfusion reactions and HDN. Women who have Anti-P or Anti-PP1PK and have suffered multiple abortions may be plasmaphersed to reduced the level of antibody in their plasma during pregnancy.

105
Q

Other characteristics of Anti-Lua/Lub are…

A

Has a characteristic loose field appearance.

106
Q

Other characteristics of Anti-i are…

A

Can cause agglutinin syndrome and hemolytic anemia. Anti-i is very uncommon. Is associated with the Epstein Barr Virus, myeloid leukemias and alcoholic cirrhosis. The antibodies are IgM and react best at 4 degrees celsius, so they seldom cause significant hemolysis. IgG forms of Anti-i will cause HDN.

107
Q

H Antigen Frequency

A

99.99%

108
Q

A Antigen Frequency

A

40%

109
Q

B Antigen Frequency

A

11%

110
Q

AB Antigen Frequency

A

4%

111
Q

O Antigen Frequency

A

45%

112
Q

Are ABO antigens expressed at birth?

A

Yes

113
Q

Where are ABO antigens found?

A

RBCs

114
Q

Do ABO antigens exhibit dosage?

A

No

115
Q

Are ABO antigens modified by enzymes?

A

No

116
Q

Rh D antigen frequency

A

85%

117
Q

Rh C antigen frequency

A

70%

118
Q

Rh E antigen frequency

A

30%

119
Q

Rh c antigen frequency

A

80%

120
Q

Rh e antigen frequency

A

98%

121
Q

Are Rh antigens expressed at birth?

A

Yes

122
Q

Where are Rh antigens found?

A

Chromosome 1, RBC membrane

123
Q

Do Rh antigens exhibit dosage?

A

Yes

124
Q

Are Rh antigens modified by enzymes?

A

Enzymes allow Rh antigens to migrate within membrane to form clusters. Enzymes enhance the activity of Rh antigens.

125
Q

What is the frequency of lewis Le(a-b+)?

A

72%

126
Q

What is the frequency of lewis Le(a+b-)?

A

22%

127
Q

What is the frequency of lewis Le(a-b-)?

A

6%

128
Q

What is the frequency of lewis Le(a+b+)?

A

Rare

129
Q

Are Lewis antigens expressed at birth?

A

No, infants are Le(a-b-) until around 2 years old. If they have either antigen; adult concentrations will be not be attained until at least 6 years old.

130
Q

Where are Lewis antigens found?

A

Secretions (e.g. saliva or plasma) Not an integral part of the RBC. They elute off the surface and are not involved in transfusion reactions.

131
Q

Do Lewis antigens exhibit dosage?

A

No

132
Q

Are Lewis antigens modified by enzymes?

A

Enzymes enhance the activity of Lewis antigens. Le gene produces Le glycosyltransferase: Type 1 precursor –> Lea. Need both H and Se gene to convert Lea –> Leb.
Decreased expression of Lewis antigens during pregnancy.

133
Q

Anti-A (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgM, regular, naturally occurring, binds complement, saline, room temp or cold, intravascular hemolysis.

134
Q

Anti-B (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgM, regular, naturally occurring, binds complement, saline, room temp or cold, intravascular hemolysis.

135
Q

Anti-AB (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgM, regular, naturally occurring, binds complement, saline, room temp or cold, intravascular hemolysis.

136
Q

Anti-H (Bombay) (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgM, regular, naturally occurring (very rare), binds complement, 4 degrees celsius, usually harmless may be found in A1/A1B individuals.

137
Q

Anti-A1 (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgM, regular, naturally occurring (very rare), binds complement, react below 37 degrees celsius, not clinically significant.

138
Q

Anti-D (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in HDN and transfusion reactions (is the most antigenic.)

139
Q

Anti-C (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.

140
Q

Anti-c (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.

141
Q

Anti-E (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.

142
Q

Anti-e (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)

A

IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.

143
Q

Explain why the frequency and prevalence of blood group antigens is important.

A

The percent occurrence of the antigen allows the technologist to better determine how difficult it will be to find antigen negative donor blood for a patient with a blood group antibody.

144
Q

Explain why it is important to know if an antigen is expressed at birth.

A

If an antigen is expressed at birth, or earlier it is possible for the antigen to stimulate antibody production in the mother. If IgG the antibody will be able to cross the placenta and can bind to the antigen on the fetus causing destruction of fetal cells. Some antigens are expressed at birth, others are not.

145
Q

Explain why it is important to know where an antigen can be found in the body.

A

Blood group antigens (ABO) are found in the RBCs. Some are also present in the plasma, platelets, white cells or on various tissues (HLA antigens)

146
Q

Why would it be important to know if an antigens demonstrates dosage?

A

If a blood group gene is inherited in a homozygous fashion, the red cell may demonstrate that antigen more strongly that if the blood group gene is inherited in a heterozygous fashion. Not all blood group antigens demonstrate dosage.

147
Q

Why would a technologist want to modify an antigen in the lab? AKA Destroy the antigen?

A

Modification of an antigen is accomplished through the use of various chemicals in vitro (in the lab). Enzymes are the most common example. They destroy M, N, S and S and Duffy (Fya and Fyb). DDT, AET and 2ME destroy the disulphide bonds. Some antigens are destroyed, while some are enhanced by chemical treatments. It is useful in destroying a clinically insignificant antibody to determine if a clinically significant antibody is present in the patient’s plasma.

148
Q

What is the equation to determine the number of donor units that would have to be screened in order to find the required number of antigen negative units?

A

Number of units to screen = number of units required/ Probability (%) of finding that antigen negative unit.

E.g. Patient with an Anti-C requires 2 units of blood
# of units = 2/0.30 = 7 units or 7 units.  The C antigen has a prevalence of 70% which means that 30% of donors would be C antigen negative.)
149
Q

The following are High Prevalence antigens carried on the RBCs of most individuals

A

Lan, Ata, Jra, Emm, AnWj, Sda (91%), PEL and MAM.

150
Q

The following are low prevalence antigens (less than 1% of the population)

A

By, Chra, Bi, Bxa, Toa, Pta, Rea, Jet, Lia, Milne, RASM, JFV, Kg, Jones, HJK, HOFM, SARA, REIT

151
Q

Temperature Range of Reactivity

A

IgG antibodies tend to require warm (37 degrees celsius) conditions, IgM are cold reactive (at room temp or lower), Clinically significant antibodies are always IgG and react at 37 degrees celsius and require the use if Anti-IgG to detect that they have bound to red cells.

152
Q

Complement Binding

A

IgM antibodies bind complement and so do IgG antibodies. Two antibodies in close proximity are required to bind complement and the adjacent CH2 regions of the IgG’s. The outcome of complement binding includes opsonization, inflammation and lyses.

153
Q

Complement Binding

A

IgM antibodies bind complement and so do IgG antibodies. Two antibodies in close proximity are required to bind complement and the adjacent CH2 regions of the IgG’s. The outcome of complement binding includes opsonization, inflammation and lyses.

154
Q

What is the frequency of the K antigen?

A

9%

155
Q

What are HLA antibodies?

A

Are antibodies directed against human leukocyte antigens. They are distributed on all nucleated cells as well as some non-nucleated cells. Red blood cells and platelets carry residual HLA antigen on their cells because they contained nuclei during development.
HLA antibodies do not cause HDN and very rarely a hemolytic transfusion reaction. They are clinically insignificant.

156
Q

What is human platelet concentration?

A

It is used to absorb unwanted anti-Bg antibodies and other HLA antibodies from a patient’s plasma. Human platelets contain variable amounts of HLA-A, HLA-B and HLA-C antigens.

157
Q

What is AET (2-aminoethylisothiuronium bromide)?

A

A sulfhydryl reagent used to weaken class 1 antigens on reagent red cells.

158
Q

Classifying Reagent Antisera

A

Saline media incubated at 20 degrees or 4 degrees - Anti-M, N, Lea, Leb.
Saline media incubated at 37 degrees - Rh antisera.
High protein media incubated at 37 degrees - modified and rapid tube reagents.
IAT (incubated at 37 degrees celsius) - Anti-K, k, Fya, Jka and Jkb.

159
Q

Classifying Reagent Antisera

A

Saline media incubated at 20 degrees or 4 degrees - Anti-M, N, Lea, Leb.
Saline media incubated at 37 degrees - Rh antisera.
High protein media incubated at 37 degrees - modified and rapid tube reagents.
IAT (incubated at 37 degrees celsius) - Anti-K, k, Fya, Jka and Jkb.

160
Q

Why must we ensure cells are not DAT positive before performing the IAT procedure.

A

If the patient cells are DAT positive this means their red blood cells are already coated with complement or antibody in vivo. They will react with the AHG used in the IAT phenotyping procedure.

161
Q

Negative control (antigen)

A

Must lack the corresponding antigen for the antisera you are using, and preferably demonstrate the antithetical antigen.

162
Q

Negative control (antigen)

A

Must lack the corresponding antigen for the antisera you are using, and preferably demonstrate the antithetical antigen.

163
Q

What is the protocol if a patient has an antibody that is no longer detectable?

A

The red blood cells of all subsequent transfusions to that patient should still lack the antigen to prevent a secondary immune response.

164
Q

Why is an anti globulin crossmatch required on donor units to a patient who has or previously had a clinically signifiant antibody?

A

To help ensure the safety of the transfusion.

165
Q

How can the IAT crossmatch can be performed on donor units right away?

A

It save expensive reagents when using a panel to identify the antibody again. If the units are not compatible and another antibody is suspected, a panel will have to be set up.

166
Q

If a unit comes from CBS with antigen typing already performed on it, what must be done in the lab prior to receiving the donation into inventory?

A

The lab will have to confirm the antigen typing, except for ABO and D typing results. The antigen typing may or may not be on the donor label, although it must be found on a paper copy or in the computer.

167
Q

What is present on donor units that have been antigen typed?

A

Antigen typed and result. Initials of the person who did the typing and the institute in which the typing was performed.

Transfusion Medicine 2 (1 decks)

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