[12] CHAPTER V LESSON 2 Flashcards
(306 cards)
1
Q
The number of IgG molecules that sensitize an RBC and the rate at which sensitization occurs can be influenced by several factors, including:
A
- Ratio of serum to cells
- Reaction Medium: Albumin, LISS, PEG
- Temperature
- Incubation Time
- Washing of RBCs
- Saline for washing
- Addition of AHG
- Centrifugation for Reading
2
Q
- Reaction Medium
A
a. Albumin
b. Low Ionic Strength Solution
c. PEG
3
Q
- can detect a level of 100 to 500 IgG molecules per RBC and 400 to 1,100 molecules of C3d per RBC
A
DAT
4
Q
- 100 to 200 IgG or C3 molecules on the cell to obtain a positive reaction
A
IAT
5
Q
Ratio of serum to cells Minimum ratio of
A
40:1
6
Q
achieved by using [?] of serum and [?] of a 5% volume of solute per volume of solution (v/v) suspension of cells.
A
2 drops
1 drop
7
Q
When using cells suspended in saline- it is often advantageous to increase the ratio of serum to cells- to [?]
A
detect weak antibodies
8
Q
Macromolecules of [?] allow antibody-coated cells to come into closer contact with each other so that aggregation occurs.
A
albumin
9
Q
In 1965, Stroup and MacIlroy reported on the increased sensitivity of the IAT if [?] was incorporated into the reaction medium.
A
albumin
10
Q
Stroup and MacIlroy’s reaction mixture, consisting of [?] of serum, [?] of 22% (w/v) bovine albumin, and [?] of 3% to 5% (v/v) cells, was shown to provide the same sensitivity at [?] of incubation as a [?] salineonly test
A
2 drops
2 drops
1 drop
30 minutes
60-minute
11
Q
Introduced by Low and Messeter
A
Low Ionic Strength Solution
12
Q
Enhance antibody uptake and allow incubation times to be decreased- from 30 to 60 minutes incubation to 10-15 minutes- by reducing the zeta potential surrounding the RBC.
A
Low Ionic Strength Solution
13
Q
- showed that optimum reaction were obtained using 2 drops of serum and 2 drops of a 3% (v/v) suspension of cells in LISS.
A
Moore and Mollison
14
Q
Increasing the serum-to-cell ratio increased the [?] of the reaction mixture, leading to a decrease in sensitivity and counteracting the shortened incubation time of the test.
A
ionic strength
15
Q
A LISS medium may be achieved by either [?] or using a [?], with the latter being the more common practice.
A
suspending RBCs in LISS
LISS additive reagent
16
Q
Water soluble linear polymer
A
Polyethylene Glycol (PEG)
17
Q
Used as an additive to increase antibody uptake.
A
Polyethylene Glycol (PEG)
18
Q
Its action is to remove water molecules surrounding the RBC, thereby effectively concentrating antibody.
A
Polyethylene Glycol (PEG)
19
Q
is the AHG reagent of choice with PEG testing to avoid false-positive reactions
A
Anti-IgG
20
Q
may cause aggregation of RBCs reading for agglutination following 37°C incubation in the IAT is omitted.
A
PEG
21
Q
The rate of reaction for the majority of IgG antibodies is optimal at [?]
A
37 degrees Celsius
22
Q
usual incubation temperature for the IAT
A
37 degrees Celsius
23
Q
optimum temperature for complement activation
A
37 degrees Celsius
24
Q
Cells suspended in saline: incubation times vary between
A
30-120 minutes
25
Majority of clinically significant antibodies- detected after [?] of incubation and extended incubation times are usually not necessary.
30 minutes
26
If LISS or PEG technique is being used- incubation times may be shortened to
10 to 15 minutes
27
With these shortened times, it is essential that tubes be incubated at a temperature of
37°C
28
When both the DAT and IAT are performed, RBCs must be saline-washed a minimum of [?] before adding the AHG reagent.
3 times
29
remove free unbound serum globulins
Washing RBCs
30
One of the most important steps in testing
Washing of RBCs
31
The wash phase can be controlled using
check cells, or group O cells sensitized with IgG.
32
The saline used for washing should be fresh and buffered to a pH of
7.2 to 7.4.
33
Saline stored for long periods in plastic containers has been shown to [?] in pH, which may [?] the rate of antibody elution during the washing process, yielding a [?] result.
decrease
increase
falsenegative
34
should be added immediately after washing to minimize the chance of antibody eluting from the cell and subsequently neutralizing the AHG reagent.
AHG
35
The [?] added should be as indicated by the manufacturers.
volume of AHG
36
However, Voak and associates have shown that adding [?] of AHG may overcome washing problems when low levels of serum contamination remain.
two volumes
37
[?] of the cell button for reading of hemagglutination along with the method used for [?] is a crucial step in the technique.
Centrifugation
resuspending the cells
38
The CBER recommended method for the evaluation of AHG uses
1000 RCF for 20 seconds
500 RCF for 15 to 20 seconds- HARMENING
39
The use of [?] more sensitive results; however, depending on how the button is resuspended, it may give weak false-positive results because of [?], or may give a negative result if [?]
higher RCFs yields
inadequate resuspension
resuspension is too vigorous
40
a. Improper specimen (refrigerated, clotted) may cause in vitro
False-positive Results
41
b. complement attachment
False-positive Results
42
c. Overcentrifugation and overreading
False-positive Results
43
d. Centrifugation after the incubation phase when PEG or other
False-positive Results
44
e. positively charged polymers are used as an enhancement medium
False-positive Results
45
f. Bacterial contamination of cells or saline used in washing
False-positive Results
46
g. Dirty glassware
False-positive Results
47
h. Presence of fibrin in the test tube may mimic agglutination.
False-positive Results
48
a. Inadequate or improper washing of cells
False negative Results
49
b. Failure to wash additional times when increased serum volumes are used
False negative Results
50
c. Contamination of AHG by extraneous protein (i.e., glove, wrong dropper)
False negative Results
51
d. High concentration of IgG paraproteins in test serum
False negative Results
52
e. Early dissociation of bound IgG from RBCs due to interruption in testing
False negative Results
53
f. Early dissociation of bound IgG from RBCs due to improper testing g. temperature (i.e., saline or AHG too cold or hot)
False negative Results
54
i. Cells with a positive DAT will yield a positive IAT.
False-positive Results
55
j. Polyagglutinable cells
False-positive Results
56
k. Saline contaminated by heavy metals or colloidal silica
False-positive Results
57
l. Using a serum sample for a DAT (use EDTA, ACD, or CPD anticoagulated blood)
False-positive Results
58
m. Samples collected in gel separator tubes may have unauthentic complement attachment.
False-positive Results
59
n. Complement attachment when specimens are collected from infusion
False-positive Results
60
o. lines infusing dextrose solutions
False-positive Results
61
p. Preservative-dependent antibody directed against reagents
False-positive Results
62
h. AHG reagent nonreactive because of deterioration or neutralization (improper reagent storage)
False negative Results
63
i. Excessive heat or repeated freezing and thawing of test serum
False negative Results
64
j. Serum nonreactive because of deterioration of complement
False negative Results
65
k. AHG reagent, test serum, or enhancement medium not added
False negative Results
66
l. Undercentrifuged or overcentrifuged
False negative Results
67
m. Cell suspension either too weak or too heavy
False negative Results
68
n. Serum-to-cell ratios are not ideal.
False negative Results
69
o. Rare antibodies are present that are only detectable with polyspecific AHG and when active complement is present.
False negative Results
70
p. Low pH of saline
False negative Results
71
q. Inadequate incubation conditions in the IAT
False negative Results
72
r. Poor reading technique
False negative Results
73
may be used for performing antiglobulin tests.
Solid-phase technology
74
Solid-phase technology
75
Antibody is attached to a microplate well, and RBCs are added.
Direct Test
76
Known RBCs are bound to a well that has been treated with glutaraldehyde or poly Llysine.
Indirect Test
77
If antibody is specific for antigen on RBCs, the bottom of the well will be covered with suspension; if no such specificity occurs, RBCs will settle to the bottom of the well.
Direct Test
78
Test serum is added to RBC-coated wells, and if antibody in serum is specific for antigen on fixed RBCs, a positive reaction occurs as previously described.
Indirect Test
79
is a process that detects RBC antigen-antibody reactions by means of a chamber filled with polyacrylamide gel
Gel Test
80
The [?] acts as a trap; [?] form buttons in the bottom of the tube, whereas [?] are trapped in the tube for hours.
gel
free unagglutinated RBCs
agglutinated RBCs
81
Therefore, negative reactions appear as [?] in the bottom of the microtube, and positive reactions are fixed in the [?].
buttons
gel
82
• No additives
Saline-tube testing
83
• Reduced cost
Saline-tube testing
84
• Avoids reactivity with auto Abs
Saline-tube testing
85
• Ability to assess multiple phases of reactivity
Saline-tube testing
86
• Long incubation
Saline-tube testing
87
• Least sensitive
Saline-tube testing
88
• Requires highly trained staff
Saline-tube testing
89
• Most procedural steps
Saline-tube testing
90
• Fewer methoddependent Abs detected
Saline-tube testing
91
• Reduced cost
LISS-tube testing
92
• Avoids reactivity with auto Abs
LISS-tube testing
93
• Shortest incubation time
LISS-tube testing
94
• Increased Ab uptake
LISS-tube testing
95
• Most common tube method
LISS-tube testing
96
• Ability to assess multiple phases of reactivity
LISS-tube testing
97
• Inability to be automated
LISS-tube testing
98
• Requires highly trained staff
LISS-tube testing
99
• Many procedural steps
LISS-tube testing
100
• Fewer methoddependent Abs detected
LISS-tube testing
101
• Reduced cost
PEG- tube testing
102
• Decreased incubation time
PEG- tube testing
103
• Increased Ab uptake
PEG- tube testing
104
• Enhances most Abs
PEG- tube testing
105
• Ability to assess multiple phases of reactivity (not 37° C)
PEG- tube testing
106
• Requires highly trained staff
PEG- tube testing
107
• Many procedural steps
PEG- tube testing
108
• Detects more unwanted Abs
PEG- tube testing
109
• Inability to be automated
PEG- tube testing
110
• Fewer methoddependent Abs detected
PEG- tube testing
111
• More sensitive DAT method
Gel
112
• No washing steps
Gel
113
• No need for check cells
Gel
114
• Stable endpoints
Gel
115
• Small test volume
Gel
116
• Enhanced anti-D detection
Gel
117
• Ability to be automated
Gel
118
• Warm auto Abs enhanced
Gel
119
• Mixed-cell agglutination with cold Abs
Gel
120
• Increased costs
Gel
121
• Increased need for additional instrumentation
Gel
122
• Increased chances of detected unwanted Abs
Gel
123
• No need for check cells
Solid phase
124
• Stable endpoints
Solid phase
125
• Small test volume
Solid phase
126
• Enhanced anti-D
Solid phase
127
• Increased sensitivity for all Abs
Solid phase
128
• Ability to be automated
Solid phase
129
• Increased sensitivity for all Abs
Solid phase
130
• Detects unwanted Abs
Solid phase
131
• Warm auto Abs enhanced
Solid phase
132
• Increased costs
Solid phase
133
• Increased need for additional instrumentation
Solid phase
134
• The [?] used in the immunohematology laboratory provide the tools to detect
reagents
135
• Principles of routine testing are based on the combination of a [?] in a test environment.
source of antigen and a source of antibody
136
• Sources of antigen and antibody are derived from [?].
commercially available reagents and patient or donor samples
137
is indicative of Ag-Ab recognition.
• Agglutination or hemolysis
138
• The purposes of reagents used in the immunohematology laboratory are to:
a. Determine the [?] of donors and patients
b. Detect antibodies produced by patients or donors who have been exposed to red cells through [?]
c. Identify the [?] detected in the antibody screen procedure
d. Determine the presence or absence of additional antigens on the red cells in addition to the [?]
e. Perform [?] to evaluate serologic compatibility of donor and patient before transfusion
ABO/Rh-type
transfusion or pregnancy
specificity of antibodies
A, B, and D antigens
crossmatches
139
• [?] in blood banking reagents refers to the strength of an AgAb reaction.
Potency
140
[?] in blood banking reagents refers to recognition of antigen and antibody to make the Ag-Ab reaction.
Specificity
141
are made from several different clones of B cells that secrete antibodies of different specificities.
Polyclonal antibodies
142
are made from a single clone of B cells that secrete antibodies of the same specificity
Monoclonal antibodies
143
Reagents for ABO typing are derived from [?] and may be blended to create reagents that recognize the corresponding A or B antigen. These reagents contain [?] in a low-protein environment.
monoclonal antibody sources
IgM antibodies
144
• Reagents for D typing are derived from [?] and may be [?]. The reagents can contain either [?] in a low-protein environment.
monoclonal antibody sources
monoclonal antibody blends or monoclonalpolyclonal antibody blends
IgM or IgG antibodies
145
• The [?] checks for the presence of spontaneous agglutination of patient or donor red cells in testing.
low-protein control reagent
146
The [?] should always show no agglutination.
control
147
are used as sources of antigen in antibody screens, ABO reverse grouping, and antibody identification tests.
• Reagent red cells
148
• The antiglobulin test detects [?] that have attached (sensitized) to red cells but have not resulted in a visible agglutination reaction.
IgG molecules and complement protein molecules
149
• The [?] detects antibody or complement molecules that have sensitized red cells as a result of a clinical event within the body.
DAT
150
• The [?] requires an incubation step for sensitization and is an invitro test.
IAT
151
The [?] is commonly used in antibody screens, antibody identification, and testing of donor and recipient compatibility.
IAT
152
The AHG test can possess sources of error that cause [?]. Recognition and prevention of these sources of error aid the correct interpretation of the AHG test result.
false-positive or false-negative AHG test results
153
are used primarily in direct antiglobulin testing to determine whether IgG or complement molecules have attached to the red cells in vivo
Polyspecific AHG reagents
154
This reagent contains both anti-IgG and antiC3d antibodies and detects both IgG and C3d molecules on red cells.
Polyspecific AHG reagents
155
are used in the investigation of a positive DAT to determine the nature of the molecules attached to the red cells
Monospecific AHG reagents
156
are prepared by separating the specificities of the polyspecific AHG reagents into individual sources of anti-IgG and anti-C3d/anti-C3b.
Monospecific AHG reagents
157
are commercially available reagents that enhance the detection of IgG antibodies by increasing their reactivity
Antibody potentiators, or enhancement medi
158
Examples of enhancement media include
AHG reagents, LISS, PEG, and enzymes
159
can reduce the zeta potential of the red cell membrane by adjusting the in-vitro test environment to promote agglutination.
• Enhancement media
160
are added to improve the detection of Ag-Ab complex formation. In this role, potentiators may enhance antibody uptake (first stage of agglutination), promote direct agglutination (second stage of agglutination), or serve both functions.
Enhancement media
161
are plant extracts that bind to carbohydrate portions of certain red cell antigens and agglutinate the red cells.
Lectins
162
Although no antibodies exist in these reagents, [?] can be useful in identifying antigens present on patient or donor red cells.
lectins
163
uses gel particles combined with diluent or reagents to trap agglutination reactions within the gel matrix.
Gel technology
164
use a microtiter plate with 96 wells to serve as the substituted test tubes. The microplate technique can be adapted to red cell antigen testing or serum testing for antibody detection
Microplate techniques
165
The principles that apply to agglutination in test tubes also apply to testing in
microplate methods
166
In [?], the antigen or antibody is immobilized to the bottom and sides of the microplate wells.
solid-phase red cell adherence testing
167
adhere to the microplate wells if an Ag-Ab reaction is observed.
IgG antibodies or red cell antigens
168
An awareness of the [?] enhances the ability of laboratory personnel to provide accurate interpretations of results generated in testing and ultimately affects overall transfusion safety.
proper use and limitations of reagents
169
46 antigens have been included in the
MNS system
170
: anti-M and anti-N
Landsteiner and Levine
171
: discovered S (its antithetical partner “s” was discovered in 1951)
Walsh and Montgomery
172
an antibody to a high-prevalence antigen, was named by Wiener.
U (for “Universal” distribution)
173
Demonstrates “Dosage Effect”
MNS
174
may serve as the receptor by which certain pyelonephrogenic strains of E.coli gain entry to the urinary tract
GPAM
175
The malaria parasite Plasmodium falciparum appears to use alternative receptors, including [?] for cell invasion.
GPA and GPB
176
The major RBC sialic-rich glycoprotein (sialoglycoprotein, SGP)
Glycophorin A (GPA): M and N Antigens
177
GPA consists of [?] amino acids, with [?] outside the cell membrane.
131
72
178
are antithetical and differ in their amino acids at positions 1 and 5
M and N antigens
179
M:
Serine, Serine, Threonine, Threonine, Glycine
180
The antigens are well developed at birth.
Glycophorin A (GPA): M and N Antigens
181
N:
Leucine, Serine, Threonine, Threonine, Glutamic acid
182
They do not bind complement regardless of their immunoglobulin class, and they do not react with enzyme treated RBCs.
Anti-M
183
It rarely causes HTRs, decreased red cell survival, or HDFN.
Anti-M
184
Examples of N-like antibody have been found more frequently in dialysis patients exposed to formaldehyde-sterilized dialyzer membranes.
Anti-N
185
Clinically significant IgG antibodies that can cause decreased red cell survival and HDFN.
Anti-S, Anti-s, and Anti-U
186
They may bind complement, and they have been implicated in severe HTRs with hemoglobinuria.
Anti-S, Anti-s, and Anti-U
187
Typically IgG
U phenotype
188
Has been reported to cause severe and fatal HTRs and HDFN.
U phenotype
189
RBCs usually type S-s-U-
U phenotype
190
these individuals can make anti-U in response to transfusion or pregnancy.
S-s-U-
191
is resistant to enzyme treatment.
U antigen
192
consists of 32 high-prevalence and low-prevalence antigens.
The Kell blood group system
193
was identified in 1964 in the serum of Mrs. Kelleher.
Anti-K
194
The associated antigen Kx is the only antigen in the Kx system, ISBT number[?] and symbol [?].
019
XK
195
are found ONLY on RBCs.
Kell blood group antigens
196
is found in erythroid tissues and in other tissues, such as brain, lymphoid organs, heart, and skeletal muscle.
Xk protein
197
The K antigen can be detected on fetal RBCs as early as [?] and is well developed at birth.
10 weeks
198
The k antigen has been detected at [?].
7 weeks
199
Other antigens:
Kpa, Kpb, and Kpc, Jsa and Jsb Antigens
200
The antigens are not denatured by enzymes [?] but are destroyed by [?] when combined.
ficin and papain
trypsin and chymotrypsin
201
Thiol- reducing agents such as [?] destroy Kell antigens but not Kx.
100 to 200 mM DTT, 2mercaptoethanol (2-ME), AET, and ZZAP
202
also destroys Kell antigens.
Glycine-acid EDTA
203
Excluding ABO, K is rated second only to D in immunogenicity.
K and k Antigens
204
Most [?] appears to be induced by pregnancy and transfusion.
anti-K
205
Outside the ABO and Rh antibodies, anti-K is the most common antibody seen in the blood bank.
Anti-K
206
The antibody is usually made in response to antigen exposure through pregnancy and transfusion and can persist for many years.
Anti-K
207
It has been associated with HTRs and HDFN.
Anti-K
208
The most reliable method of detection is the IAT
Anti-K
209
Antibodies usually do not bind the complement.
Anti-K
210
Depressed reactivity of anti-K is observed in some LISS reagents.
Anti-K
211
Antibodies to the low-prevalence Kell antigens are rare because so few people are exposed to these antigens.
Antibodies to Kpa, Jsa, and Other Low-Prevalence Kell Antigens
212
The serologic characteristics and clinical significance of these antibodies parallel anti-K.
Antibodies to Kpa, Jsa, and Other Low-Prevalence Kell Antigens
213
Antibodies to high-prevalence Kell system antigens are rare because so few people lack these antigens.
Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens
214
They also parallel anti-K in serologic characteristics and clinical significance.
Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens
215
is present on all RBCs except those of the rare McLeod phenotype.
Kx
216
have increased Kx antigen.
Ko and Kmod phenotype RBCs
217
Red cells with normal Kell phenotypes carry trace amounts of
Kx antigen.
218
lack expression of all Kell antigens.
Ko RBCs
219
Immunized individuals with the Ko phenotype typically make an antibody called [?] that recognizes the “Universal” Kell antigen (Ku) present on all RBCs except Ko.
anti-Ku (K5)
220
has caused both HDFN and HTRs.
Anti-Ku
221
It is very rare and is seen almost exclusively in males as a result of the X chromosome-borne gene
McLeod phenotype
222
lack Kx and another high-prevalence antigen, Km, and have marked depression of all Kell antigens.
McLeod phenotype RBCs
223
Significant proportions of the RBC in individuals with the [?] are acanthocytic with decreased deformability and reduced in vivo survival.
McLeod phenotype
224
Individuals with the said phenotype have a chronic but well compensated hemolytic anemia characterized by reticulocytosis, bilirubinemia, splenomegaly, and reduced serum haptoglobin test
McLeod phenotype
225
It is associated with Chronic Granulomatous Disease (CGD).
McLeod phenotype
226
is characterized by the inability of phagocytes to make NADH oxidase, an enzyme important in generating H2O2, which is used to kill ingested bacteria.
CGD
227
Not all males with the [?] have CGD, nor do all patients with CGD have the [?].
McLeod phenotype
McLeod phenotype
228
McLeod individuals develop a slow, progressive form of [?] between ages 40 to 50 years and [?] (leading to cardiomyopathy) as well as elevated [?] of the MM type (cardiac/skeletal muscle) and serum creatinine phosphokinase levels [?]
muscular dystrophy
cardiomegaly
serum creatinine phosphokinase levels; carbonic anhydrase III levels
229
It was first discovered in the serum of a hemophiliac who received multiple transfusions, Mr. Duffy.
Duffy Blood Group System
230
is the first human gene to be assigned to a specific chromosome.
The Duffy gene
231
can be identified on fetal RBCs as early as 6 weeks gestational age and are well developed at birth.
Duffy antigens
232
The antibodies possess clinical significance in transfusion and are an uncommon cause of HDFN.
Duffy Blood Group System
233
antigens are considered of greatest importance in transfusion purposes.
Fya and Fyb
234
Some examples of [?] show dosage, reacting more strongly with RBCs that have a double dose than RBCs from heterozygotes.
anti-Fya and anti-Fyb
235
It was discovered that [?] resist infection by Plasmodium knowlesi and also Plasmodium vivax.
Fy (a-b-) RBCs
236
Antithetical antigens
Fya and Fyb
237
Sensitive to ficin or papain treatment
Fya and Fyb
238
Receptors for Plasmodium vivax and Plasmodium knowlesi
Fya and Fyb
239
Resistant to ficin or papain treatment
Fy3
240
Red cells that are Fy(a-b-) are also Fy:-3
Fy3
241
Anti-Fy3- rare antibody made by Fy(a-b-)
Fy3
242
Resistant to ficin and papain treatment
Fy5
243
Common in Whites
Fy5
244
Altered expression in Rhnull phenotype
Fy5
245
Possible antigen interaction between Duffy and Rh proteins
Fy5
246
Red cells that are Fy(a-b-) are also Fy:-6
Fy6
247
Sensitive to ficin or papain treatment
Fy6
248
Antigen has been defined by murine monoclonal antibodies
Fy6
249
no human anti-[?] has been described
Fy6
250
Reactions with Anti-Fya: +
Reactions with Anti-Fyb: 0
251
Reactions with Anti-Fya: 0
Reactions with Anti-Fyb: +
Fy (a-b+)
252
Reactions with Anti-Fya: +
Reactions with Anti-Fyb: +
Fy (a+b+)
253
Reactions with Anti-Fya: 0
Reactions with Anti-Fyb: 0
Fy (a-b-)
254
White: 17
Black: 9
Chinese: *90.8
Fy (a+b-)
255
White: 34
Black: 22
Chinese: 0.3
Fy (a-b+)
256
White: *49
Black: 1
Chinese: 8.9
Fy (a+b+)
257
White: Rare
Black: *68
Chinese: 0
Fy (a-b-)
258
In 1951, [?] reported finding an antibody in the serum of Mrs. Kidd, whose infant had HDFN.
Allen and colleagues
259
-commonly found on RBCs of most individuals
Jka and Jkb
260
are well developed on the RBCs of neonates
Jka and Jkb antigens
261
has been detected on fetal RBCs as early as 11 weeks
Jka
262
has been detected at 7 weeks
Jkb
263
is a silent allele that produces neither Jka nor Jkb antigens
Jk allele
264
it is a common allele in Polynesians, Filipinos, and Chinese
Jk allele
265
the JkJk genotype results in a
Jk (a-b-) phenotype
266
Jk (a-b-) phenotype can also be derived by the action of a dominant suppressor gene, [?].
In (Jk) – for “Inhibitor”
267
has been associated with severe immediate and delayed HTRs and with mild HDFN
Anti-Jk3
268
Kidd antibodies have a notorious reputation in the blood bank.
Anti-Jka and Anti-Jkb
269
They demonstrate dosage are often weak, and are found in combination with other antibodies, all of which make them difficult to detect.
Anti-Jka and Anti-Jkb
270
Agglutination reactions are best observed by the IAT
Anti-Jka and Anti-Jkb
271
Antibody reactivity can also be enhanced by using, by using 4 drops of serum instead of 2 (to increase antibody-to-antigen ratio) or by using enzymes such as ficin or papain.
Anti-Jka and Anti-Jkb
272
The antibodies are produced in response to antigen exposure through transfusion or pregnancy.
Anti-Jka and Anti-Jkb
273
The antibodies do not store well; antibody reactivity quickly declines in vitro and the difficulty in detecting Kidd antibodies are reasons why they are common cause of HTRs, especially of the delayed type.
Anti-Jka and Anti-Jkb
274
Red cell stimulated
KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM (weak antibody)
275
IgG
KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM
276
Reactive with AHG
KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM
277
Clinical Significance YES
KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM
278
Effect of Enzymes NO EFFECT
KELL SYSTEM
279
Effect of Enzymes NO REACTIVITY
DUFFY SYSTEM
280
Effect of Enzymes ENHANCED
KIDD SYSTEM
281
Anti-K most common
KELL SYSTEM
282
Anti-Jsb more common in blacks
KELL SYSTEM
283
Anti- Kpb more common in whites
KELL SYSTEM
284
Fy(a-b-) resist infection by P. knowlesi and P. vivax
DUFFY SYSTEM
285
Bind complement
KIDD SYSTEM
286
Common cause of Delayed HTRs
KIDD SYSTEM
287
was found in the serum of a patient with lupus erythematosus, following the transfusion of a unit of blood carrying the corresponding low-prevalence antigen.
Anti-Lua
288
The donor’s last name was
Lutteran
289
20 antigens are part of the
Lutheran system
290
Although the antigens have been detected on fetal RBCs as early as 10 to 12 weeks of gestation, they are poorly developed at birth.
Lutheran Blood Group System
291
Presence of [?] on placental tissue may result in adsorption of maternal antibodies to Lutheran antigens decreasing the likelihood of HDFN.
Lutheran glycoprotein
292
: Produced by allelic codominant genes.
Lua and Lub Antigens
293
Are IgM naturally occurring saline agglutinins that react better at room temperature than at 37oC.
Anti-Lua
294
has a characteristic mixed field pattern of agglutination; small agglutinates are surrounded by unagglutinated free red cells.
Anti-Lua
295
It has no clinical significance in transfusion; mild cases of HDFN have been reported.
Anti-Lua
296
Immunoglobin class is mostly IgG, but IgM and IgA antibodies have also been noted.
Anti-Lub
297
Most examples of anti-Lub are IgG and reactive at 37oC at antiglobulin phase.
Anti-Lub
298
Made in response to pregnancy or transfusion.
Anti-Lub
299
has been implicated with shortened survival of transfused cells and post transfusion jaundice, but severe or acute hemolysis has not been reported.
Anti-Lub
300
Rarely occurs and may manifest itself in any of the following three unique genetic mechanisms
Lunull phenotype or Lu(a-b-)
301
: only true Lunull phenotype; homozygosity for a rare recessive amorph, Lu, at the LU locus.
a. Recessive
302
: heterozygosity for a rare dominant inhibitor gene, In(Lu), that is not located at the LU locus.
b. Dominant inhibitor or In(Lu) phenotype
303
: inherited in a recessive manner.
c. X-linked suppressor gene
304
Rare antibody that reacts with all RBCs except Lu(a-b-) RBCs.
Anti-Lu3
305
Usually antiglobulin reactive.
Anti-Lu3
306
Made only by individuals with the recessive type of Lu(a-b-).
Anti-Lu3
