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[Immunohematology] Lec > [12] CHAPTER V LESSON 2 > Flashcards

[12] CHAPTER V LESSON 2 Flashcards

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
  1. Ratio of serum to cells
  2. Reaction Medium: Albumin, LISS, PEG
  3. Temperature
  4. Incubation Time
  5. Washing of RBCs
  6. Saline for washing
  7. Addition of AHG
  8. Centrifugation for Reading
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2
Q
  1. Reaction Medium
A

a. Albumin

b. Low Ionic Strength Solution

c. PEG

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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

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4
Q
  • 100 to 200 IgG or C3 molecules on the cell to obtain a positive reaction
A

IAT

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5
Q

Ratio of serum to cells Minimum ratio of

A

40:1

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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

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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

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8
Q

Macromolecules of [?] allow antibody-coated cells to come into closer contact with each other so that aggregation occurs.

A

albumin

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9
Q

In 1965, Stroup and MacIlroy reported on the increased sensitivity of the IAT if [?] was incorporated into the reaction medium.

A

albumin

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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

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11
Q

Introduced by Low and Messeter

A

Low Ionic Strength Solution

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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

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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

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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

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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

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16
Q

Water soluble linear polymer

A

Polyethylene Glycol (PEG)

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17
Q

Used as an additive to increase antibody uptake.

A

Polyethylene Glycol (PEG)

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18
Q

Its action is to remove water molecules surrounding the RBC, thereby effectively concentrating antibody.

A

Polyethylene Glycol (PEG)

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19
Q

is the AHG reagent of choice with PEG testing to avoid false-positive reactions

A

Anti-IgG

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20
Q

may cause aggregation of RBCs reading for agglutination following 37°C incubation in the IAT is omitted.

A

PEG

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21
Q

The rate of reaction for the majority of IgG antibodies is optimal at [?]

A

37 degrees Celsius

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22
Q

usual incubation temperature for the IAT

A

37 degrees Celsius

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23
Q

optimum temperature for complement activation

A

37 degrees Celsius

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24
Q

Cells suspended in saline: incubation times vary between

A

30-120 minutes

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25
Q

Majority of clinically significant antibodies- detected after [?] of incubation and extended incubation times are usually not necessary.

A

30 minutes

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26
Q

If LISS or PEG technique is being used- incubation times may be shortened to

A

10 to 15 minutes

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27
Q

With these shortened times, it is essential that tubes be incubated at a temperature of

A

37°C

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28
Q

When both the DAT and IAT are performed, RBCs must be saline-washed a minimum of [?] before adding the AHG reagent.

A

3 times

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29
Q

remove free unbound serum globulins

A

Washing RBCs

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30
Q

One of the most important steps in testing

A

Washing of RBCs

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31
Q

The wash phase can be controlled using

A

check cells, or group O cells sensitized with IgG.

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32
Q

The saline used for washing should be fresh and buffered to a pH of

A

7.2 to 7.4.

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33
Q

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.

A

decrease

increase

falsenegative

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34
Q

should be added immediately after washing to minimize the chance of antibody eluting from the cell and subsequently neutralizing the AHG reagent.

A

AHG

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35
Q

The [?] added should be as indicated by the manufacturers.

A

volume of AHG

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36
Q

However, Voak and associates have shown that adding [?] of AHG may overcome washing problems when low levels of serum contamination remain.

A

two volumes

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37
Q

[?] of the cell button for reading of hemagglutination along with the method used for [?] is a crucial step in the technique.

A

Centrifugation

resuspending the cells

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38
Q

The CBER recommended method for the evaluation of AHG uses

A

1000 RCF for 20 seconds

500 RCF for 15 to 20 seconds- HARMENING

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39
Q

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 [?]

A

higher RCFs yields
inadequate resuspension
resuspension is too vigorous

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40
Q

a. Improper specimen (refrigerated, clotted) may cause in vitro

A

False-positive Results

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41
Q

b. complement attachment

A

False-positive Results

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42
Q

c. Overcentrifugation and overreading

A

False-positive Results

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43
Q

d. Centrifugation after the incubation phase when PEG or other

A

False-positive Results

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44
Q

e. positively charged polymers are used as an enhancement medium

A

False-positive Results

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45
Q

f. Bacterial contamination of cells or saline used in washing

A

False-positive Results

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46
Q

g. Dirty glassware

A

False-positive Results

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47
Q

h. Presence of fibrin in the test tube may mimic agglutination.

A

False-positive Results

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48
Q

a. Inadequate or improper washing of cells

A

False negative Results

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49
Q

b. Failure to wash additional times when increased serum volumes are used

A

False negative Results

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50
Q

c. Contamination of AHG by extraneous protein (i.e., glove, wrong dropper)

A

False negative Results

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51
Q

d. High concentration of IgG paraproteins in test serum

A

False negative Results

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52
Q

e. Early dissociation of bound IgG from RBCs due to interruption in testing

A

False negative Results

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53
Q

f. Early dissociation of bound IgG from RBCs due to improper testing g. temperature (i.e., saline or AHG too cold or hot)

A

False negative Results

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54
Q

i. Cells with a positive DAT will yield a positive IAT.

A

False-positive Results

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55
Q

j. Polyagglutinable cells

A

False-positive Results

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56
Q

k. Saline contaminated by heavy metals or colloidal silica

A

False-positive Results

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57
Q

l. Using a serum sample for a DAT (use EDTA, ACD, or CPD anticoagulated blood)

A

False-positive Results

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58
Q

m. Samples collected in gel separator tubes may have unauthentic complement attachment.

A

False-positive Results

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59
Q

n. Complement attachment when specimens are collected from infusion

A

False-positive Results

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60
Q

o. lines infusing dextrose solutions

A

False-positive Results

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61
Q

p. Preservative-dependent antibody directed against reagents

A

False-positive Results

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62
Q

h. AHG reagent nonreactive because of deterioration or neutralization (improper reagent storage)

A

False negative Results

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63
Q

i. Excessive heat or repeated freezing and thawing of test serum

A

False negative Results

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64
Q

j. Serum nonreactive because of deterioration of complement

A

False negative Results

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65
Q

k. AHG reagent, test serum, or enhancement medium not added

A

False negative Results

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66
Q

l. Undercentrifuged or overcentrifuged

A

False negative Results

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67
Q

m. Cell suspension either too weak or too heavy

A

False negative Results

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68
Q

n. Serum-to-cell ratios are not ideal.

A

False negative Results

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69
Q

o. Rare antibodies are present that are only detectable with polyspecific AHG and when active complement is present.

A

False negative Results

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70
Q

p. Low pH of saline

A

False negative Results

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71
Q

q. Inadequate incubation conditions in the IAT

A

False negative Results

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72
Q

r. Poor reading technique

A

False negative Results

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73
Q

may be used for performing antiglobulin tests.

A

Solid-phase technology

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74
Q

Solid-phase technology

A
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75
Q

Antibody is attached to a microplate well, and RBCs are added.

A

Direct Test

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76
Q

Known RBCs are bound to a well that has been treated with glutaraldehyde or poly Llysine.

A

Indirect Test

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77
Q

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.

A

Direct Test

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78
Q

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.

A

Indirect Test

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79
Q

is a process that detects RBC antigen-antibody reactions by means of a chamber filled with polyacrylamide gel

A

Gel Test

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80
Q

The [?] acts as a trap; [?] form buttons in the bottom of the tube, whereas [?] are trapped in the tube for hours.

A

gel

free unagglutinated RBCs

agglutinated RBCs

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81
Q

Therefore, negative reactions appear as [?] in the bottom of the microtube, and positive reactions are fixed in the [?].

A

buttons

gel

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82
Q

• No additives

A

Saline-tube testing

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83
Q

• Reduced cost

A

Saline-tube testing

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84
Q

• Avoids reactivity with auto Abs

A

Saline-tube testing

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85
Q

• Ability to assess multiple phases of reactivity

A

Saline-tube testing

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86
Q

• Long incubation

A

Saline-tube testing

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87
Q

• Least sensitive

A

Saline-tube testing

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88
Q

• Requires highly trained staff

A

Saline-tube testing

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89
Q

• Most procedural steps

A

Saline-tube testing

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90
Q

• Fewer methoddependent Abs detected

A

Saline-tube testing

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91
Q

• Reduced cost

A

LISS-tube testing

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92
Q

• Avoids reactivity with auto Abs

A

LISS-tube testing

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93
Q

• Shortest incubation time

A

LISS-tube testing

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94
Q

• Increased Ab uptake

A

LISS-tube testing

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95
Q

• Most common tube method

A

LISS-tube testing

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96
Q

• Ability to assess multiple phases of reactivity

A

LISS-tube testing

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97
Q

• Inability to be automated

A

LISS-tube testing

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98
Q

• Requires highly trained staff

A

LISS-tube testing

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99
Q

• Many procedural steps

A

LISS-tube testing

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100
Q

• Fewer methoddependent Abs detected

A

LISS-tube testing

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101
Q

• Reduced cost

A

PEG- tube testing

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102
Q

• Decreased incubation time

A

PEG- tube testing

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103
Q

• Increased Ab uptake

A

PEG- tube testing

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104
Q

• Enhances most Abs

A

PEG- tube testing

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105
Q

• Ability to assess multiple phases of reactivity (not 37° C)

A

PEG- tube testing

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106
Q

• Requires highly trained staff

A

PEG- tube testing

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107
Q

• Many procedural steps

A

PEG- tube testing

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108
Q

• Detects more unwanted Abs

A

PEG- tube testing

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109
Q

• Inability to be automated

A

PEG- tube testing

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110
Q

• Fewer methoddependent Abs detected

A

PEG- tube testing

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111
Q

• More sensitive DAT method

A

Gel

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112
Q

• No washing steps

A

Gel

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113
Q

• No need for check cells

A

Gel

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114
Q

• Stable endpoints

A

Gel

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115
Q

• Small test volume

A

Gel

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116
Q

• Enhanced anti-D detection

A

Gel

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117
Q

• Ability to be automated

A

Gel

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118
Q

• Warm auto Abs enhanced

A

Gel

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119
Q

• Mixed-cell agglutination with cold Abs

A

Gel

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120
Q

• Increased costs

A

Gel

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121
Q

• Increased need for additional instrumentation

A

Gel

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122
Q

• Increased chances of detected unwanted Abs

A

Gel

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123
Q

• No need for check cells

A

Solid phase

124
Q

• Stable endpoints

A

Solid phase

125
Q

• Small test volume

A

Solid phase

126
Q

• Enhanced anti-D

A

Solid phase

127
Q

• Increased sensitivity for all Abs

A

Solid phase

128
Q

• Ability to be automated

A

Solid phase

129
Q

• Increased sensitivity for all Abs

A

Solid phase

130
Q

• Detects unwanted Abs

A

Solid phase

131
Q

• Warm auto Abs enhanced

A

Solid phase

132
Q

• Increased costs

A

Solid phase

133
Q

• Increased need for additional instrumentation

A

Solid phase

134
Q

• The [?] used in the immunohematology laboratory provide the tools to detect

A

reagents

135
Q

• Principles of routine testing are based on the combination of a [?] in a test environment.

A

source of antigen and a source of antibody

136
Q

• Sources of antigen and antibody are derived from [?].

A

commercially available reagents and patient or donor samples

137
Q

is indicative of Ag-Ab recognition.

A

• Agglutination or hemolysis

138
Q

• 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

A

ABO/Rh-type

transfusion or pregnancy

specificity of antibodies

A, B, and D antigens

crossmatches

139
Q

• [?] in blood banking reagents refers to the strength of an AgAb reaction.

A

Potency

140
Q

[?] in blood banking reagents refers to recognition of antigen and antibody to make the Ag-Ab reaction.

A

Specificity

141
Q

are made from several different clones of B cells that secrete antibodies of different specificities.

A

Polyclonal antibodies

142
Q

are made from a single clone of B cells that secrete antibodies of the same specificity

A

Monoclonal antibodies

143
Q

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.

A

monoclonal antibody sources

IgM antibodies

144
Q

• Reagents for D typing are derived from [?] and may be [?]. The reagents can contain either [?] in a low-protein environment.

A

monoclonal antibody sources

monoclonal antibody blends or monoclonalpolyclonal antibody blends

IgM or IgG antibodies

145
Q

• The [?] checks for the presence of spontaneous agglutination of patient or donor red cells in testing.

A

low-protein control reagent

146
Q

The [?] should always show no agglutination.

A

control

147
Q

are used as sources of antigen in antibody screens, ABO reverse grouping, and antibody identification tests.

A

• Reagent red cells

148
Q

• The antiglobulin test detects [?] that have attached (sensitized) to red cells but have not resulted in a visible agglutination reaction.

A

IgG molecules and complement protein molecules

149
Q

• The [?] detects antibody or complement molecules that have sensitized red cells as a result of a clinical event within the body.

A

DAT

150
Q

• The [?] requires an incubation step for sensitization and is an invitro test.

A

IAT

151
Q

The [?] is commonly used in antibody screens, antibody identification, and testing of donor and recipient compatibility.

A

IAT

152
Q

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.

A

false-positive or false-negative AHG test results

153
Q

are used primarily in direct antiglobulin testing to determine whether IgG or complement molecules have attached to the red cells in vivo

A

Polyspecific AHG reagents

154
Q

This reagent contains both anti-IgG and antiC3d antibodies and detects both IgG and C3d molecules on red cells.

A

Polyspecific AHG reagents

155
Q

are used in the investigation of a positive DAT to determine the nature of the molecules attached to the red cells

A

Monospecific AHG reagents

156
Q

are prepared by separating the specificities of the polyspecific AHG reagents into individual sources of anti-IgG and anti-C3d/anti-C3b.

A

Monospecific AHG reagents

157
Q

are commercially available reagents that enhance the detection of IgG antibodies by increasing their reactivity

A

Antibody potentiators, or enhancement medi

158
Q

Examples of enhancement media include

A

AHG reagents, LISS, PEG, and enzymes

159
Q

can reduce the zeta potential of the red cell membrane by adjusting the in-vitro test environment to promote agglutination.

A

• Enhancement media

160
Q

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.

A

Enhancement media

161
Q

are plant extracts that bind to carbohydrate portions of certain red cell antigens and agglutinate the red cells.

A

Lectins

162
Q

Although no antibodies exist in these reagents, [?] can be useful in identifying antigens present on patient or donor red cells.

A

lectins

163
Q

uses gel particles combined with diluent or reagents to trap agglutination reactions within the gel matrix.

A

Gel technology

164
Q

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

A

Microplate techniques

165
Q

The principles that apply to agglutination in test tubes also apply to testing in

A

microplate methods

166
Q

In [?], the antigen or antibody is immobilized to the bottom and sides of the microplate wells.

A

solid-phase red cell adherence testing

167
Q

adhere to the microplate wells if an Ag-Ab reaction is observed.

A

IgG antibodies or red cell antigens

168
Q

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.

A

proper use and limitations of reagents

169
Q

46 antigens have been included in the

A

MNS system

170
Q

: anti-M and anti-N

A

Landsteiner and Levine

171
Q

: discovered S (its antithetical partner “s” was discovered in 1951)

A

Walsh and Montgomery

172
Q

an antibody to a high-prevalence antigen, was named by Wiener.

A

U (for “Universal” distribution)

173
Q

Demonstrates “Dosage Effect”

A

MNS

174
Q

may serve as the receptor by which certain pyelonephrogenic strains of E.coli gain entry to the urinary tract

A

GPAM

175
Q

The malaria parasite Plasmodium falciparum appears to use alternative receptors, including [?] for cell invasion.

A

GPA and GPB

176
Q

The major RBC sialic-rich glycoprotein (sialoglycoprotein, SGP)

A

Glycophorin A (GPA): M and N Antigens

177
Q

GPA consists of [?] amino acids, with [?] outside the cell membrane.

A

131

72

178
Q

are antithetical and differ in their amino acids at positions 1 and 5

A

M and N antigens

179
Q

M:

A

Serine, Serine, Threonine, Threonine, Glycine

180
Q

The antigens are well developed at birth.

A

Glycophorin A (GPA): M and N Antigens

181
Q

N:

A

Leucine, Serine, Threonine, Threonine, Glutamic acid

182
Q

They do not bind complement regardless of their immunoglobulin class, and they do not react with enzyme treated RBCs.

A

Anti-M

183
Q

It rarely causes HTRs, decreased red cell survival, or HDFN.

A

Anti-M

184
Q

Examples of N-like antibody have been found more frequently in dialysis patients exposed to formaldehyde-sterilized dialyzer membranes.

A

Anti-N

185
Q

Clinically significant IgG antibodies that can cause decreased red cell survival and HDFN.

A

Anti-S, Anti-s, and Anti-U

186
Q

They may bind complement, and they have been implicated in severe HTRs with hemoglobinuria.

A

Anti-S, Anti-s, and Anti-U

187
Q

Typically IgG

A

U phenotype

188
Q

Has been reported to cause severe and fatal HTRs and HDFN.

A

U phenotype

189
Q

RBCs usually type S-s-U-

A

U phenotype

190
Q

these individuals can make anti-U in response to transfusion or pregnancy.

A

S-s-U-

191
Q

is resistant to enzyme treatment.

A

U antigen

192
Q

consists of 32 high-prevalence and low-prevalence antigens.

A

The Kell blood group system

193
Q

was identified in 1964 in the serum of Mrs. Kelleher.

A

Anti-K

194
Q

The associated antigen Kx is the only antigen in the Kx system, ISBT number[?] and symbol [?].

A

019

XK

195
Q

are found ONLY on RBCs.

A

Kell blood group antigens

196
Q

is found in erythroid tissues and in other tissues, such as brain, lymphoid organs, heart, and skeletal muscle.

A

Xk protein

197
Q

The K antigen can be detected on fetal RBCs as early as [?] and is well developed at birth.

A

10 weeks

198
Q

The k antigen has been detected at [?].

A

7 weeks

199
Q

Other antigens:

A

Kpa, Kpb, and Kpc, Jsa and Jsb Antigens

200
Q

The antigens are not denatured by enzymes [?] but are destroyed by [?] when combined.

A

ficin and papain

trypsin and chymotrypsin

201
Q

Thiol- reducing agents such as [?] destroy Kell antigens but not Kx.

A

100 to 200 mM DTT, 2mercaptoethanol (2-ME), AET, and ZZAP

202
Q

also destroys Kell antigens.

A

Glycine-acid EDTA

203
Q

Excluding ABO, K is rated second only to D in immunogenicity.

A

K and k Antigens

204
Q

Most [?] appears to be induced by pregnancy and transfusion.

A

anti-K

205
Q

Outside the ABO and Rh antibodies, anti-K is the most common antibody seen in the blood bank.

A

Anti-K

206
Q

The antibody is usually made in response to antigen exposure through pregnancy and transfusion and can persist for many years.

A

Anti-K

207
Q

It has been associated with HTRs and HDFN.

A

Anti-K

208
Q

The most reliable method of detection is the IAT

A

Anti-K

209
Q

Antibodies usually do not bind the complement.

A

Anti-K

210
Q

Depressed reactivity of anti-K is observed in some LISS reagents.

A

Anti-K

211
Q

Antibodies to the low-prevalence Kell antigens are rare because so few people are exposed to these antigens.

A

Antibodies to Kpa, Jsa, and Other Low-Prevalence Kell Antigens

212
Q

The serologic characteristics and clinical significance of these antibodies parallel anti-K.

A

Antibodies to Kpa, Jsa, and Other Low-Prevalence Kell Antigens

213
Q

Antibodies to high-prevalence Kell system antigens are rare because so few people lack these antigens.

A

Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens

214
Q

They also parallel anti-K in serologic characteristics and clinical significance.

A

Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens

215
Q

is present on all RBCs except those of the rare McLeod phenotype.

A

Kx

216
Q

have increased Kx antigen.

A

Ko and Kmod phenotype RBCs

217
Q

Red cells with normal Kell phenotypes carry trace amounts of

A

Kx antigen.

218
Q

lack expression of all Kell antigens.

A

Ko RBCs

219
Q

Immunized individuals with the Ko phenotype typically make an antibody called [?] that recognizes the “Universal” Kell antigen (Ku) present on all RBCs except Ko.

A

anti-Ku (K5)

220
Q

has caused both HDFN and HTRs.

A

Anti-Ku

221
Q

It is very rare and is seen almost exclusively in males as a result of the X chromosome-borne gene

A

McLeod phenotype

222
Q

lack Kx and another high-prevalence antigen, Km, and have marked depression of all Kell antigens.

A

McLeod phenotype RBCs

223
Q

Significant proportions of the RBC in individuals with the [?] are acanthocytic with decreased deformability and reduced in vivo survival.

A

McLeod phenotype

224
Q

Individuals with the said phenotype have a chronic but well compensated hemolytic anemia characterized by reticulocytosis, bilirubinemia, splenomegaly, and reduced serum haptoglobin test

A

McLeod phenotype

225
Q

It is associated with Chronic Granulomatous Disease (CGD).

A

McLeod phenotype

226
Q

is characterized by the inability of phagocytes to make NADH oxidase, an enzyme important in generating H2O2, which is used to kill ingested bacteria.

A

CGD

227
Q

Not all males with the [?] have CGD, nor do all patients with CGD have the [?].

A

McLeod phenotype

McLeod phenotype

228
Q

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 [?]

A

muscular dystrophy

cardiomegaly

serum creatinine phosphokinase levels; carbonic anhydrase III levels

229
Q

It was first discovered in the serum of a hemophiliac who received multiple transfusions, Mr. Duffy.

A

Duffy Blood Group System

230
Q

is the first human gene to be assigned to a specific chromosome.

A

The Duffy gene

231
Q

can be identified on fetal RBCs as early as 6 weeks gestational age and are well developed at birth.

A

Duffy antigens

232
Q

The antibodies possess clinical significance in transfusion and are an uncommon cause of HDFN.

A

Duffy Blood Group System

233
Q

antigens are considered of greatest importance in transfusion purposes.

A

Fya and Fyb

234
Q

Some examples of [?] show dosage, reacting more strongly with RBCs that have a double dose than RBCs from heterozygotes.

A

anti-Fya and anti-Fyb

235
Q

It was discovered that [?] resist infection by Plasmodium knowlesi and also Plasmodium vivax.

A

Fy (a-b-) RBCs

236
Q

Antithetical antigens

A

Fya and Fyb

237
Q

Sensitive to ficin or papain treatment

A

Fya and Fyb

238
Q

Receptors for Plasmodium vivax and Plasmodium knowlesi

A

Fya and Fyb

239
Q

Resistant to ficin or papain treatment

A

Fy3

240
Q

Red cells that are Fy(a-b-) are also Fy:-3

A

Fy3

241
Q

Anti-Fy3- rare antibody made by Fy(a-b-)

A

Fy3

242
Q

Resistant to ficin and papain treatment

A

Fy5

243
Q

Common in Whites

A

Fy5

244
Q

Altered expression in Rhnull phenotype

A

Fy5

245
Q

Possible antigen interaction between Duffy and Rh proteins

A

Fy5

246
Q

Red cells that are Fy(a-b-) are also Fy:-6

A

Fy6

247
Q

Sensitive to ficin or papain treatment

A

Fy6

248
Q

Antigen has been defined by murine monoclonal antibodies

A

Fy6

249
Q

no human anti-[?] has been described

A

Fy6

250
Q

Reactions with Anti-Fya: +
Reactions with Anti-Fyb: 0

A
251
Q

Reactions with Anti-Fya: 0
Reactions with Anti-Fyb: +

A

Fy (a-b+)

252
Q

Reactions with Anti-Fya: +
Reactions with Anti-Fyb: +

A

Fy (a+b+)

253
Q

Reactions with Anti-Fya: 0
Reactions with Anti-Fyb: 0

A

Fy (a-b-)

254
Q

White: 17
Black: 9
Chinese: *90.8

A

Fy (a+b-)

255
Q

White: 34
Black: 22
Chinese: 0.3

A

Fy (a-b+)

256
Q

White: *49
Black: 1
Chinese: 8.9

A

Fy (a+b+)

257
Q

White: Rare
Black: *68
Chinese: 0

A

Fy (a-b-)

258
Q

In 1951, [?] reported finding an antibody in the serum of Mrs. Kidd, whose infant had HDFN.

A

Allen and colleagues

259
Q

-commonly found on RBCs of most individuals

A

Jka and Jkb

260
Q

are well developed on the RBCs of neonates

A

Jka and Jkb antigens

261
Q

has been detected on fetal RBCs as early as 11 weeks

A

Jka

262
Q

has been detected at 7 weeks

A

Jkb

263
Q

is a silent allele that produces neither Jka nor Jkb antigens

A

Jk allele

264
Q

it is a common allele in Polynesians, Filipinos, and Chinese

A

Jk allele

265
Q

the JkJk genotype results in a

A

Jk (a-b-) phenotype

266
Q

Jk (a-b-) phenotype can also be derived by the action of a dominant suppressor gene, [?].

A

In (Jk) – for “Inhibitor”

267
Q

has been associated with severe immediate and delayed HTRs and with mild HDFN

A

Anti-Jk3

268
Q

Kidd antibodies have a notorious reputation in the blood bank.

A

Anti-Jka and Anti-Jkb

269
Q

They demonstrate dosage are often weak, and are found in combination with other antibodies, all of which make them difficult to detect.

A

Anti-Jka and Anti-Jkb

270
Q

Agglutination reactions are best observed by the IAT

A

Anti-Jka and Anti-Jkb

271
Q

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.

A

Anti-Jka and Anti-Jkb

272
Q

The antibodies are produced in response to antigen exposure through transfusion or pregnancy.

A

Anti-Jka and Anti-Jkb

273
Q

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.

A

Anti-Jka and Anti-Jkb

274
Q

Red cell stimulated

A

KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM (weak antibody)

275
Q

IgG

A

KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM

276
Q

Reactive with AHG

A

KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM

277
Q

Clinical Significance YES

A

KELL SYSTEM
DUFFY SYSTEM
KIDD SYSTEM

278
Q

Effect of Enzymes NO EFFECT

A

KELL SYSTEM

279
Q

Effect of Enzymes NO REACTIVITY

A

DUFFY SYSTEM

280
Q

Effect of Enzymes ENHANCED

A

KIDD SYSTEM

281
Q

Anti-K most common

A

KELL SYSTEM

282
Q

Anti-Jsb more common in blacks

A

KELL SYSTEM

283
Q

Anti- Kpb more common in whites

A

KELL SYSTEM

284
Q

Fy(a-b-) resist infection by P. knowlesi and P. vivax

A

DUFFY SYSTEM

285
Q

Bind complement

A

KIDD SYSTEM

286
Q

Common cause of Delayed HTRs

A

KIDD SYSTEM

287
Q

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.

A

Anti-Lua

288
Q

The donor’s last name was

A

Lutteran

289
Q

20 antigens are part of the

A

Lutheran system

290
Q

Although the antigens have been detected on fetal RBCs as early as 10 to 12 weeks of gestation, they are poorly developed at birth.

A

Lutheran Blood Group System

291
Q

Presence of [?] on placental tissue may result in adsorption of maternal antibodies to Lutheran antigens decreasing the likelihood of HDFN.

A

Lutheran glycoprotein

292
Q

: Produced by allelic codominant genes.

A

Lua and Lub Antigens

293
Q

Are IgM naturally occurring saline agglutinins that react better at room temperature than at 37oC.

A

Anti-Lua

294
Q

has a characteristic mixed field pattern of agglutination; small agglutinates are surrounded by unagglutinated free red cells.

A

Anti-Lua

295
Q

It has no clinical significance in transfusion; mild cases of HDFN have been reported.

A

Anti-Lua

296
Q

Immunoglobin class is mostly IgG, but IgM and IgA antibodies have also been noted.

A

Anti-Lub

297
Q

Most examples of anti-Lub are IgG and reactive at 37oC at antiglobulin phase.

A

Anti-Lub

298
Q

Made in response to pregnancy or transfusion.

A

Anti-Lub

299
Q

has been implicated with shortened survival of transfused cells and post transfusion jaundice, but severe or acute hemolysis has not been reported.

A

Anti-Lub

300
Q

Rarely occurs and may manifest itself in any of the following three unique genetic mechanisms

A

Lunull phenotype or Lu(a-b-)

301
Q

: only true Lunull phenotype; homozygosity for a rare recessive amorph, Lu, at the LU locus.

A

a. Recessive

302
Q

: heterozygosity for a rare dominant inhibitor gene, In(Lu), that is not located at the LU locus.

A

b. Dominant inhibitor or In(Lu) phenotype

303
Q

: inherited in a recessive manner.

A

c. X-linked suppressor gene

304
Q

Rare antibody that reacts with all RBCs except Lu(a-b-) RBCs.

A

Anti-Lu3

305
Q

Usually antiglobulin reactive.

A

Anti-Lu3

306
Q

Made only by individuals with the recessive type of Lu(a-b-).

A

Anti-Lu3

[Immunohematology] Lec (35 decks)

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