1
Q
K frequency
A
9%
2
Q
k frequency
A
99.8%
3
Q
Kpa frequency
A
2%
4
Q
Kpb frequency
A
100%
5
Q
Jsa frequency
A
Rare
6
Q
Jya frequency
A
100%
7
Q
Fya frequency
A
66%
8
Q
Fyb frequency
A
83%
9
Q
Jka frequency
A
77%
10
Q
Jkb frequency
A
72%
11
Q
M frequency
A
78%
12
Q
N frequency
A
72%
13
Q
S frequency
A
55%
14
Q
s frequency
A
89%
15
Q
P frequency
A
100%
16
Q
P1 frequency
A
79%
17
Q
Pk frequency
A
Rare
18
Q
Lua frequency
A
8%
19
Q
Lub frequency
A
100%
20
Q
I frequency
A
Adults
21
Q
i frequency
A
Babies
22
Q
Are Kell antigens expressed at birth?
A
Yes
23
Q
Are Duffy (Fya and Fyb) antigens expressed at birth?
A
Yes
24
Q
Are Kidd (Jka and Jkb) antigens expressed at birth?
A
Yes
25
Are MNSs antigens expressed at birth?
Yes
26
Are the P antigens expressed at birth?
Poor expression
27
Are the Lu antigens expressed at birth?
Yes, but poorly.
28
Are the I and i antigens expressed at birth?
i yes, I no.
29
Where are Kell antigens found?
Red blood cells
30
Where are Duffy antigens found?
Red blood cells and tissues.
31
Where are Kidd antigens found?
Only red blood cells.
32
Where are the MNSs antigens found?
Only red blood cells.
33
Where are the P antigens found?
RBC, platelets, WBC, epithelial cells, fibroblasts.
34
Where are Lu antigens found?
Red blood cells.
35
Where are I and i antigens found?
Red blood cells, White blood cells and platelets.
36
Do Kell antigens exhibit dosage?
No
37
Do Duffy antigens exhibit dosage?
No
38
Do Kidd antigens exhibit dosage?
Yes
39
Do MNSs antigens exhibit dosage?
Yes
40
Do P antigens exhibit dosage?
No - although the strength of the antigen varies between individuals.
41
Do Lu antigens exhibit dosage?
No
42
Do I antigens exhibit dosage?
No
43
In what ways are Kell antigens modified?
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.
44
In what ways are Duffy antigens modified?
Duffy antigens are destroyed by proteolytic enzymes and by ZZAP. Duffy antigens are not destroyed by thiol reagents.
45
In what ways are Kidd antigens modified?
Kidd antigens are enhanced by enzymes, unaffected by others.
46
In what way are MNSs antigens modified?
MNSs antigens are destroyed by ZZAP (S and s less sensitive to enzyme destruction.
47
In what ways are the P antigens modified?
P antigens resist enzymes, DDT, chloroquine and glycine acid-EDTA.
48
In what way are Lu antigens modified?
There are no noted ways that Lu antigens are modified. They are low density on the RBCs.
49
In what way are I and i antigens modified?
I and i antigens are enhanced by enzymes.
50
Are Kell antibodies natural or immune?
Immune
51
Are Duffy antibodies natural or immune?
Immune
52
Are Kidd antibodies natural or immune?
Immune
53
Are MNSs antibodies natural or immune?
Both
54
Are P antibodies natural or immune?
Natural
55
Are Lu antibodies natural or immune
Lua - Both, Lub - immune
56
Are I and i antibodies natural or immune?
Anti-I - Alloantibody, IgG/IgM
| Anti-i - Autoantibody, IgG
57
Antibody class of Kell antibodies?
IgG
58
Antibody class of Duffy antibodies?
IgG
59
Antibody class of Kidd antibodies?
IgG
60
Antibody class of MNSs antibodies?
IgG and IgM
61
Antibody class of Anti-P?
IgM
62
Antibody class of PP1/PK?
IgG and IgM
63
Antibody class of P?
IgG and IgM
64
Antibody class of Auto-P?
IgG
65
Antibody class of Anti-Lua?
IgG
66
Antibody class of Anti-Lub?
IgM
67
Antibody class of Anti-I?
IgG or IgM
68
Antibody class of Anti-i?
IgM
69
Temp range of sensitivity for Anti-Kell?
37
70
Temp range of sensitivity for Anti-Duffy?
37
71
Temp range of sensitivity for Anti-Kidd?
37
72
Temp range of sensitivity for Anti-MNSs?
Anti-M/N are cold (4)
| Anti-S (37)
73
Temp range of sensitivity for Anti-P?
4
74
Temp range of sensitivity for Anti-PP1/PK?
37
75
Temp range of sensitivity for Auto-P?
4
76
Temp range of sensitivity for Anti-Lua?
Cold (4)
77
Temp range of sensitivity for Anti-Lub?
37
78
Temp range of sensitivity for Anti-i?
4 to 37
79
Favoured reaction conditions for Anti-Kell?
PEG/IAT
80
Favoured reaction conditions for Anti-Duffy?
IAT/LISS
81
Favoured reaction conditions for Anti-Kidd?
IAT/LISS/PEG
82
Favoured reaction conditions for Anti-MNSs?
Increase or decrease incubation time, pH of 6.5, 4 drops of plasma, albumin/LISS/PEG
83
Favoured reaction conditions for Anti-P?
Cold, saline reactive.
84
Favoured reaction conditions for Anti-PP1/PK?
IAT
85
Favoured reaction conditions for Anti-P?
IAT
86
Favoured reaction conditions for Auto-P?
Siphasic
87
Favoured reaction conditions for Anti-Lua/b?
N/A
88
Favoured reaction conditions for Anti-I/i?
Avoid using room temperature resting and Anti-IgG (AHG).
89
Does Anti-Kell bind complement?
Yes, but no lysis.
90
Does Anti-Duffy bind complement?
Some do.
91
Does Anti-Kidd bind complement?
Many bind complement.
92
Does Anti-M/N bind complement?
Rarely.
93
Does Anti-S bind complement?
Yes
94
Does Anti-P bind complement?
No
95
Does Anti-PP1/PK or Auto-P bind complement?
Yes
96
Does Anti-Lua bind complement?
Yes
97
Does Anti-Lub bind complement?
No
98
Does Anti-I bind complement?
No
99
Does Anti-i bind complement?
Yes
100
Other characteristics of Anti-Kell are...
Can cause HDN and transfusion reactions.
101
Other characteristics of Anti-Duffy are...
Are destroyed by treatment of reagent red blood cells. Are associated with mild to severe HDN and hemolytic transfusion reactions.
102
Other characteristics of Anti-Kidd are...
Not commonly enhanced by enzymes. Associated with HDN and transfusion reactions.
103
Other characteristics of Anti-MNSs are...
Exhibit dosage. Anti-S causes hemolytic transfusion reactions and HDN.
104
Other characteristics of Anti-P and associated antibodies are...
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
Other characteristics of Anti-Lua/Lub are...
Has a characteristic loose field appearance.
106
Other characteristics of Anti-i are...
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
H Antigen Frequency
99.99%
108
A Antigen Frequency
40%
109
B Antigen Frequency
11%
110
AB Antigen Frequency
4%
111
O Antigen Frequency
45%
112
Are ABO antigens expressed at birth?
Yes
113
Where are ABO antigens found?
RBCs
114
Do ABO antigens exhibit dosage?
No
115
Are ABO antigens modified by enzymes?
No
116
Rh D antigen frequency
85%
117
Rh C antigen frequency
70%
118
Rh E antigen frequency
30%
119
Rh c antigen frequency
80%
120
Rh e antigen frequency
98%
121
Are Rh antigens expressed at birth?
Yes
122
Where are Rh antigens found?
Chromosome 1, RBC membrane
123
Do Rh antigens exhibit dosage?
Yes
124
Are Rh antigens modified by enzymes?
Enzymes allow Rh antigens to migrate within membrane to form clusters. Enzymes enhance the activity of Rh antigens.
125
What is the frequency of lewis Le(a-b+)?
72%
126
What is the frequency of lewis Le(a+b-)?
22%
127
What is the frequency of lewis Le(a-b-)?
6%
128
What is the frequency of lewis Le(a+b+)?
Rare
129
Are Lewis antigens expressed at birth?
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
Where are Lewis antigens found?
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
Do Lewis antigens exhibit dosage?
No
132
Are Lewis antigens modified by enzymes?
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
Anti-A (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgM, regular, naturally occurring, binds complement, saline, room temp or cold, intravascular hemolysis.
134
Anti-B (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgM, regular, naturally occurring, binds complement, saline, room temp or cold, intravascular hemolysis.
135
Anti-AB (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgM, regular, naturally occurring, binds complement, saline, room temp or cold, intravascular hemolysis.
136
Anti-H (Bombay) (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgM, regular, naturally occurring (very rare), binds complement, 4 degrees celsius, usually harmless may be found in A1/A1B individuals.
137
Anti-A1 (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgM, regular, naturally occurring (very rare), binds complement, react below 37 degrees celsius, not clinically significant.
138
Anti-D (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
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
Anti-C (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.
140
Anti-c (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.
141
Anti-E (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.
142
Anti-e (Class, regular/irregular, natural or immune, bind complement?, reaction conditions, clinical significance.)
IgG, Immune, does not bind complement, enhanced with enzymes and enhancement medium. Reacts well with AHG, implicated in transfusion reactions.
143
Explain why the frequency and prevalence of blood group antigens is important.
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
Explain why it is important to know if an antigen is expressed at birth.
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
Explain why it is important to know where an antigen can be found in the body.
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
Why would it be important to know if an antigens demonstrates dosage?
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
Why would a technologist want to modify an antigen in the lab? AKA Destroy the antigen?
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
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?
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
The following are High Prevalence antigens carried on the RBCs of most individuals
Lan, Ata, Jra, Emm, AnWj, Sda (91%), PEL and MAM.
150
The following are low prevalence antigens (less than 1% of the population)
By, Chra, Bi, Bxa, Toa, Pta, Rea, Jet, Lia, Milne, RASM, JFV, Kg, Jones, HJK, HOFM, SARA, REIT
151
Temperature Range of Reactivity
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
Complement Binding
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
Complement Binding
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
What is the frequency of the K antigen?
9%
155
What are HLA antibodies?
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
What is human platelet concentration?
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
What is AET (2-aminoethylisothiuronium bromide)?
A sulfhydryl reagent used to weaken class 1 antigens on reagent red cells.
158
Classifying Reagent Antisera
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
Classifying Reagent Antisera
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
Why must we ensure cells are not DAT positive before performing the IAT procedure.
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
Negative control (antigen)
Must lack the corresponding antigen for the antisera you are using, and preferably demonstrate the antithetical antigen.
162
Negative control (antigen)
Must lack the corresponding antigen for the antisera you are using, and preferably demonstrate the antithetical antigen.
163
What is the protocol if a patient has an antibody that is no longer detectable?
The red blood cells of all subsequent transfusions to that patient should still lack the antigen to prevent a secondary immune response.
164
Why is an anti globulin crossmatch required on donor units to a patient who has or previously had a clinically signifiant antibody?
To help ensure the safety of the transfusion.
165
How can the IAT crossmatch can be performed on donor units right away?
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
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?
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
What is present on donor units that have been antigen typed?
Antigen typed and result. Initials of the person who did the typing and the institute in which the typing was performed.
Transfusion Medicine 2
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