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Transfusion > Trans lecture 1 > Flashcards

Trans lecture 1 Flashcards

1
Q

How can the genotype be determined from the phenotype?

A

The genotype can only be inferred or derived by deduction from the phenotype.

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2
Q

What techniques can be used to determine the genotype?

A

The genotype can be determined by molecular techniques or family studies.

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3
Q

What is specificity in immunology?

A

Specificity refers to the recognition of the antigen and its corresponding antibody molecule.

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4
Q

Give an example of specificity in immunology.

A

A commercial anti-sera anti-B will react with red cells that possess the B antigen and will not react with cells that lack the B antigen.

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5
Q

What does potency describe in immunology?

A

Potency describes the strength of the agglutination reaction.

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6
Q

Which blood group system is the most important?

A

The ABO system is the most important of all blood groups.

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7
Q

Why is ABO typing important for blood donors and patients who may require transfusion?

A

ABO typing is important to determine compatibility and prevent red cell lysis or death from incompatible transfusions.

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8
Q

What is the ABO reciprocal relationship?

A

The forward + reverse must be opposite for it to be valid.

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9
Q

Why is the ABO reciprocal relationship important?

A

The inverse reciprocal relationship between forward and reverse testing is a ‘check’ or ‘validation’ of the patient’s blood type.

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10
Q

What should be done if a discrepancy exists in ABO typing?

A

A discrepancy in ABO typing must be resolved before any transfusion can occur.

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11
Q

What populations may have variation in ABO group frequencies?

A

Selected populations and different ethnic populations may have variation in ABO group frequencies.

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12
Q

Which population is Group B blood type seen more frequently in?

A

Group B blood type is seen more frequently in the Black and Asian populations than in Caucasian populations.

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13
Q

What are some examples of red cell antigen differences seen by ethnicity?

A

Examples include U and Duffy antigens, which are more common in African Americans and protect from malaria.

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14
Q

What are the immunoglobulins of the ABO system and how do they develop?

A

The immunoglobulins of the ABO system are IgM and ‘naturally’ occurring. They develop due to exposure to bacteria or substances with a similar chemical make-up as the A and B antigens.

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15
Q

What can ABO antibodies activate and when do they react strongly?

A

ABO antibodies can activate complement and they react strongly at room temperature or even colder.

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16
Q

What are isoagglutinins and when are they detected in newborns?

A

Isoagglutinins are antibodies anti-A, anti-B, and anti-AB. They start to develop in newborns at birth but are not detected until 3 to 6 months of age.

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17
Q

Why are reverse testing not done on newborns?

A

Reverse testing is not done on newborns as maternal antibodies will be detected on cord cells, making the results invalid.

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18
Q

How is ABO typing determined in newborns?

A

ABO typing in newborns is determined solely on the forward reactions, as reverse testing is not performed.

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19
Q

What happens to ABO antibody production as we age?

A

ABO antibody production declines as we age, sometimes to the point where it is too low to detect, resulting in a discrepancy in ABO typing.

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20
Q

When does ABO antibody production typically peak?

A

ABO antibody production typically peaks around the age of 5 to 10.

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21
Q

How are most blood group antigens inherited?

A

Most blood group antigens are inherited co-dominantly.

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22
Q

What are some examples of blood group inheritance patterns?

A

Most blood group antigens are inherited co-dominantly.

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23
Q

What is the reaction pattern observed when red cells are transfused to a Bombay patient?

A

Immediate red cell lysis

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24
Q

What antigens do Bombay individuals lack on their red cells?

A

A, B, and H antigens

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25
Q

What antibodies do Bombay individuals possess in their sera?

A

Anti-A, anti-B, and anti-H

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26
Q

When is anti-H detected in routine ABO grouping?

A

It is detected in pre-transfusion testing

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27
Q

Which red cells would agglutinate when Bombay sera is tested with group O screening cells and group O donor cells?

A

Group O screening cells and group O donor cells

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28
Q

What is the significance of the Bombay phenotype in blood transfusion?

A

All normal ABO groups are incompatible when cross-matched for Bombay individuals

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29
Q

What is the recommended source of blood for transfusion to a Bombay patient?

A

Blood from another Bombay individual

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30
Q

Where can donors for Bombay individuals be sought?

A

Among blood relatives (especially siblings) or from the CBS rare donor file

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31
Q

What confirmatory testing can be done to identify Bombay phenotype?

A

Agglutination of A, B, AB, and O cells and negative anti-H lectin

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32
Q

Which lectin is most important for determining A1 antigen specificity?

A

Dolichos biflorus

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33
Q

What does the agglutination of Dolichos biflorus lectin indicate?

A

A1 antigen (if no agglutination, indicates A2 antigen)

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34
Q

What is the H antigen specificity of Ulex europaeus lectin?

A

Secretor or Bombay phenotype

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35
Q

What is the N antigen specificity of Vicia graminea lectin?

A

Renal dialysis patients have N- and will have to transfuse N-

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36
Q

Which lectin belongs to MNS-sU-u and has M antigen specificity?

A

Iberis amara

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37
Q

What type of activation does Arachis hypognea lectin cause in polyagglutination syndromes?

A

T activation

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38
Q

Which lectin agglutinates B cells?

A

Bandeiraea simplicifolia

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39
Q

What are ABO subgroups and how do they differ from other ABO blood types?

A

Subgroups are phenotypes that differ in the amount of antigen on red cells and the secretions present in body fluids

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40
Q

How are ABO subgroups classified?

A

Based on different levels of expression of A or B antigens on red blood cells

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41
Q

What are the major subgroups of group A individuals?

A

A1 and A2

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42
Q

What is the approximate percentage of group A individuals who are A1?

A

Approximately 80%

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43
Q

What is the approximate percentage of group A individuals who are A2?

A

Approximately 20%

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44
Q

How does the amount of antigen expressed on red cell membrane differ between group A1 and A2 subgroups?

A

Group A1 individuals have approximately 2 million antigen sites per red cell, while group A2 individuals have approximately 500,000 sites

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45
Q

Which subgroup of group A individuals has more H antigen on their red cells?

A

Group A2 individuals

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46
Q

Can group A2 subgroup be determined serologically?

A

No, it can only be determined based on genetic testing

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47
Q

What is the qualitative difference between A1 and A2 subgroups?

A

A2 subgroup has more H antigen on their red cells than A1 subgroup

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48
Q

What percentage of individuals belong to ABO subgroups?

A

1% to 8%

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49
Q

What group does acquired B phenomenon fall into?

A

Group II discrepancies

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50
Q

What diseases is acquired B phenomenon commonly seen in?

A

Digestive tract diseases like cancer of the colon

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51
Q

Which patients with a lower GI tract disease state are commonly associated with acquired B phenomenon?

A

Group A patients

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52
Q

What are some examples of lower GI tract diseases associated with acquired B phenomenon?

A

Colon or rectal cancers, bowel obstruction, gram negative septicemia

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53
Q

What is the cause of acquired B phenomenon?

A

Removal (deacetylation) of the acetyl group of the group A immunodominant sugar into D-galactosamine

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54
Q

What sugar does the modified immunodominant sugar in acquired B phenomenon resemble?

A

D-galactose (group B immunodominant sugar)

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55
Q

What is the term for weak agglutination caused by the cross-reaction of D-galactosamine with anti-B antisera?

A

Pseudo-B

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56
Q

What happens to the A1 antigen in acquired B phenomenon?

A

It is produced at the expense of the pseudo B antigen

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57
Q

What happens to the ABO type once the patient has recovered from acquired B phenomenon?

A

It returns to normal

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58
Q

What type of reactions are observed in acquired B? (AUTO test)

A

Negative reactions - anti-B in serum does not agglutinate autologous RBC’s with the acquired B antigen

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59
Q

Under what pH conditions will acquired anti-B not agglutinate?

A

pH > 8.5 or < pH 6.0

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60
Q

What reduces the reactivity of cells tested against anti-B in acquired B phenomenon?

A

Treating RBC’s with acetic anhydride

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61
Q

How are normal B cells affected by acetic anhydride treatment?

A

They are not affected

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62
Q

What can occur with some anti-B antisera in acquired B phenomenon?

A

Cross-reaction

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63
Q

What should be transfused if transfusion is required in acquired B phenomenon?

A

Group A blood

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64
Q

What causes Category III discrepancies?

A

Protein or plasma abnormalities

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65
Q

What does the presence of abnormal protein in plasma result in category III discrepancies?

A

Rouleaux formation or pseudoagglutination

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66
Q

What may increased levels of globulin indicate in Category III discrepancies?

A

Patients with Multiple Myeloma, Waldenström’s macroglobulinemia, other plasma cell dyscrasias, and possibly advanced cases of Hodgkin’s lymphoma

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67
Q

What can cause category III discrepancies in individuals?

A

High levels of fibrinogen, treatment with plasma expanders like dextran, and presence of Wharton’s jelly - cord cells

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68
Q

What is the resolution for category III discrepancies due to rouleaux formation?

A

Washing the patient cells several times with 0.9% saline and retest

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69
Q

What is the method of resolving category III discrepancies caused by excess Wharton’s jelly in cord cells?

A

Wash cells 6-8 times with 0.9% saline

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70
Q

What causes category IV discrepancies?

A

Discrepancy between forward and reverse typing

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71
Q

What are some possible causes of category IV discrepancies?

A

Cold reacting autoantibodies, unexpected ABO isoagglutinins, unexpected non-ABO alloantibodies, and more than one ABO type circulating due to transfusion or BM/stem cell transplant

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72
Q

How can forward typing discrepancies in category IV be resolved?

A

By incubating cells at 37°C, washing at least 3 times with saline, and then repeat testing

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73
Q

What can disperse IgM agglutination in category IV discrepancies?

A

Treat cells with dithiothreitol (DTT)

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74
Q

What is the method of resolving forward typing discrepancies in serum/plasma testing?

A

Perform strict pre-warmed technique and then perform testing, potentially converting to the AHG phase of testing

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75
Q

Which ABO phenotype possesses the most H antigens?

A

Group O RBC’s

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76
Q

Which ABO phenotype possesses the fewest H antigens?

A

Group A1B RBC’s

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77
Q

In which ABO phenotype are H antibodies almost never detected?

A

Group B individuals

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78
Q

What are the characteristics of anti-H antibodies?

A

Relatively weak reacting, primarily react at room temperature, considered clinically insignificant

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79
Q

What can cause discrepant results in reverse testing?

A

H antibodies

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80
Q

What is the term used to refer to the secretion of blood type antigens A, B, and H soluble antigens into body fluids?

A

Secretor

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81
Q

Which fluids can be used to detect A, B, and H soluble antigens in secretors?

A

Saliva, sweat, tears, semen, breast milk, amniotic fluid, urine, bile

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82
Q

What are the two alleles that control ABH secretion?

A

Se (dominant) and se (recessive)

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83
Q

What percentage of the population are secretors?

A

Approximately 80%

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84
Q

What is the inheritance pattern of secretor genes relative to ABO and H genes?

A

Inherited independently

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85
Q

What soluble antigens are secreted by group O individuals?

A

H soluble antigen

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86
Q

What soluble antigens are secreted by group A individuals?

A

A and H soluble antigens

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87
Q

What soluble antigens are secreted by group B individuals?

A

B and H soluble antigens

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88
Q

What soluble antigens are secreted by group AB individuals?

A

A, B, and H soluble antigens

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89
Q

What is the practical application of the interaction between ABO, H, and secretor genes?

A

Expression of soluble antigens in body fluids

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90
Q

What is the purpose of the inhibition neutralization test for the detection of ABH substances in saliva?

A

To determine secretor status

91
Q

What happens during antibody neutralization in the inhibition neutralization test?

A

Soluble antigens in saliva neutralize the antibodies

92
Q

What happens during agglutination inhibition in the inhibition neutralization test?

A

Soluble antigens prevent agglutination with known antigens

93
Q

In the inhibition neutralization test, how is the reaction interpreted for secretors?

A

Negative for agglutination but positive for secretor status

94
Q

In the inhibition neutralization test, how is the reaction interpreted for non-secretors?

A

Positive for agglutination but negative for secretor status

95
Q

What is the first part of the inhibition/neutralization test procedure?

A

Mixing saliva with diluted commercial antisera

96
Q

What is the second part of the inhibition/neutralization test procedure?

A

Testing for agglutination inhibition using commercial red cells

97
Q

What fluids can be used to collect samples for the inhibition-neutralization test?

A

Saliva

98
Q

What are the possible indications of a positive antibody screen?

A

Possible indications of a positive antibody screen include spontaneous agglutination, significant hemolysis, and a decrease in agglutination strength over time.

99
Q

How many screening cells are typically used in an antibody screen?

A

Depending on the hospital, you might only have 2 screening cells.

100
Q

What is the significance of a positive antibody screen?

A

A positive antibody screen indicates the presence of antibodies in the patient’s plasma/serum due to exposure to red cell antigens through pregnancy or transfusion.

101
Q

What is the purpose of performing an antibody identification?

A

Antibody identification is performed to determine the specific antibodies present in the patient’s plasma/serum, which helps in selecting compatible blood for transfusion.

102
Q

What is the difference between warm and cold antibodies?

A

Warm antibodies are IgG antibodies, while cold antibodies are IgM antibodies.

103
Q

What is the purpose of testing patient red cells?

A

Patient red cells are used to identify patient red cell antigens, such as ABO and Rh typing, and phenotype testing.

104
Q

How are patient red cells prepared for testing?

A

Patient red cells are prepared into a 3-5% cell suspension for tube testing or 0.8% for GEL methodology, and the suspension must be in an EDTA tube.

105
Q

What is the purpose of testing blood donor cells?

A

Blood donor cells are used to identify blood donor red cell antigens, such as ABO and Rh typing, and phenotype testing.

106
Q

What are the sources of antibodies used in routine testing?

A

Sources of antibodies include patient plasma/serum, commercial anti-sera, and commercially known antibodies.

107
Q

How is ABO/Rh typing performed?

A

ABO/Rh typing is performed by combining commercial antisera (known antibodies) with patient red cells (unknown antigens).

108
Q

What is the purpose of ABO serum typing?

A

ABO serum typing detects the presence or absence of ABO antibodies (anti-A, anti-B) in a patient’s plasma using commercial red cells with known antigens.

109
Q

What does an antibody screen test for?

A

An antibody screen test detects the presence of pre-formed antibodies in a patient’s plasma/serum due to exposure to red cell antigens through pregnancy or transfusion.

110
Q

How are immune red cell antibodies developed?

A

Immune red cell antibodies develop in individuals who lack a specific red cell antigen and are exposed to the foreign antigen through pregnancy or transfusion.

111
Q

What is the purpose of using Rogan for O- moms during pregnancy?

A

Rogan is given to O- moms to prevent the development of antibodies against the baby’s red cells, which can lead to hemolytic disease of the newborn.

112
Q

What are the two antigens responsible for ABO types?

A

A and B

113
Q

What are the two antibodies responsible for ABO types?

A

Anti-A and Anti-B

114
Q

How many genes are associated with the ABO system?

A

Three

115
Q

What type of inheritance is associated with gene A in the ABO system?

A

Co-dominant

116
Q

What type of inheritance is associated with gene B in the ABO system?

A

Co-dominant

117
Q

What type of inheritance is associated with gene O in the ABO system?

A

Silent gene or amorph – NO detectable antigens

118
Q

When both A and B genes are inherited, how are the antigens expressed on red blood cells?

A

Equally

119
Q

Are recessive or dominant inheritance patterns common in blood group system genetics?

A

No

120
Q

On which chromosome are the A and B genes found?

A

Chromosome 9

121
Q

How many alleles are co-dominant in the ABO system?

A

Two

122
Q

Will an A or B gene always be expressed when inherited?

A

Yes

123
Q

What will be expressed if an individual inherits the O gene?

A

No A or B antigens

124
Q

What type of gene is the O gene?

A

Amorph (silent gene)

125
Q

When does the O gene get expressed?

A

When inherited from both parents (OO)

126
Q

What gene can an A/A parent pass along?

A

An A gene

127
Q

What genes can an A/O parent pass along?

A

An A or O gene

128
Q

What gene can a B/B parent pass along?

A

A B gene

129
Q

What genes can a B/O parent pass along?

A

A B or O gene

130
Q

What gene can an O/O parent pass along?

A

An O gene

131
Q

What genes can an AB parent pass along?

A

An A or B gene

132
Q

What is the H antigen controlled by?

A

The H gene

133
Q

Is the H gene dominant or recessive?

A

Dominant

134
Q

What is critical for the ability to express A and B antigens?

A

Formation of H antigen

135
Q

Which antigens are found on a common carbohydrate structure?

A

ABO antigens

136
Q

What do the gene products of ABO alleles need as the acceptor molecule?

A

H antigen

137
Q

What is the common structure for the A, B, and H antigens?

A

Oligosaccharide chain

138
Q

What do the A and B genes code for?

A

Enzymes that add sugars to the H antigen

139
Q

What is the immunodominant sugar for group A specificity?

A

N-acetylgalactosamine

140
Q

What is the immunodominant sugar for group B specificity?

A

D-galactose

141
Q

What is the type O rich in?

A

Unconverted H antigen

142
Q

Why are Group O individuals rich in H antigens?

A

Because they have no A or B genes to convert the H antigen to A or B antigens

143
Q

What is the result of autoantibodies in patient cells?

A

Spontaneous agglutination resulting in a positive DAT.

144
Q

If a cold autoantibody reacts with all adult cells, what will the reverse cells show?

A

Agglutination.

145
Q

What can you do if you are expecting agglutination in reverse but it is still negative?

A

Perform autoabsorption - patient serum + patient cells.

146
Q

What are unexpected isoagglutinins?

A

Naturally occurring anti-A1 or A1 and A1B in individuals who are A2 or A2B.

147
Q

How can you determine the specificity of an antibody?

A

Test at least 3 samples of A1, A2, B, O cells and auto control, and look at the reaction pattern.

148
Q

What may the presence of anti-A1 antibody indicate?

A

If antibody agglutinates only A1 cells, it can be identified as anti-A1 present.

149
Q

If anti-A1 is detected, what additional test should be performed?

A

The patient must be tested with Dolichos biflorus.

150
Q

What cold-reacting antibodies may be detected in reverse testing?

A

Anti-M, anti-N, anti-Lea, and anti-Leb.

151
Q

Why might reverse cells possess certain antigens?

A

Reverse cells are pooled, so they may possess antigens if the patient has a specific antibody.

152
Q

If a patient has a specific antibody, how can you test for it?

A

Perform a panel ID on the patient serum and test A1 and/or B cells negative for the specific antibody.

153
Q

What can cause agglutination in forward typing?

A

Ag/AB complexes (acriflavine/anti-acriflavine) adsorbing onto patient RBC’s.

154
Q

How can you resolve agglutination in forward typing caused by ag/AB complexes?

A

Wash in saline several times and repeat testing.

155
Q

What is the cis-AB phenotype?

A

Inheriting both A and B genes from one parent on the same chromosome, while the other parent is group O.

156
Q

What is the discrepancy in serum of most cis-AB people?

A

Weak anti-B.

157
Q

Where can you find a chart for discrepancies between forward and reverse grouping?

A

Page 143 -144 of ‘Modern Blood Banking and Transfusion Practices, 7th Edition’.

158
Q

What should you look for in the chart for discrepancies between forward and reverse grouping?

A

Reaction pattern, cause, and resolution.

159
Q

What is Landsteiner’s Rule or Law based on?

A

Mendel’s theories/laws.

160
Q

According to Landsteiner’s Rule, what happens if you possess a red cell antigen?

A

You will not have the corresponding antibody, except for alloantibodies.

161
Q

What does Landsteiner’s Rule state about the coexistence of antigens and antibodies?

A

Corresponding antigens and antibodies will not coexist in individuals.

162
Q

In the ABO system, what antibodies are found in the plasma if the A antigen is absent on the patient’s red cells?

A

Anti-A antibodies.

163
Q

What antibodies are found in the plasma if the B antigen is absent on the patient’s red cells?

A

Anti-B antibodies.

164
Q

If both A and B antigens are absent from red cells, what antibodies will be found in the plasma?

A

Both anti-A and anti-B antibodies.

165
Q

Which blood group is considered the Universal Donor for red cells?

A

Group O.

166
Q

Which blood group can receive all blood types, A, B, AB, and O?

A

Group AB.

167
Q

What are lipids and proteins that cause lysis of red blood cells?

A

Potent hemolysins.

168
Q

Why must the ABO of a patient and blood donor be compatible during transfusion?

A

Mismatch can lead to death - 10 cc of ABO mismatched blood can kill.

169
Q

Which blood group is considered the Universal Donor for plasma?

A

Group AB.

170
Q

Where are antigens found and where are antibodies found?

A

Antigens are found on red cells, and antibodies are found in plasma or serum.

171
Q

What must be known if the unknown variable is the antibody?

A

The known variable must be the antigen.

172
Q

What are the sources of antigens in routine testing?

A

Red cells, reagent red cells, patient, blood donor.

173
Q

What are reverse cells used for?

A

Reverse typing to determine the presence/absence of corresponding antibodies.

174
Q

What are screening cells used for?

A

AB Screen, to test for the presence of A or B antigen or antibodies.

175
Q

What are panel cells used for?

A

Antibody identification to determine the specificity of antibodies.

176
Q

What are Coombs Control cells used for?

A

To verify if it is a true negative result in antigen testing.

177
Q

What is the evidence of reagent red cell deterioration?

A

Not mentioned in the course notes.

178
Q

What is the best resolution for Category I discrepancies in ABO blood typing?

A

Enhancing weak or missing reaction by incubating reverse tubes with A1 and B cells.

179
Q

What is chimerism in the context of ABO blood typing discrepancies?

A

It refers to individuals with two distinct cell populations existing in one person.

180
Q

What is the difference between true and artificial chimerism?

A

True chimerism occurs only in twins and is lifelong, while artificial chimerism is common but not lifelong.

181
Q

What can cause artificial chimerism?

A

Artificial chimerism can occur due to transfusion, BM transplant, exchange transfusion, or fetal-maternal bleed.

182
Q

What are the possible causes for weak or missing red cell antigens in Category II discrepancies?

A

Possible causes include subgroups of A or B, weakened antigens in leukemias, Hodgkin’s disease, acquired ‘B’ phenomenon.

183
Q

What are blood group-specific soluble substances (BGSS) and their effect on blood typing?

A

BGSS substances neutralize anti-A/anti-B antisera, resulting in a negative reaction in forward grouping.

184
Q

How can discrepancies due to BGSS be resolved?

A

Patient RBC’s can be washed with saline to remove the substance, correcting the forward and reverse discrepancy.

185
Q

What can cause weak or missing reactions in RBC grouping besides BGSS?

A

Antibodies to low-incidence antigens or low incidence antibody in antisera can cause such discrepancies.

186
Q

How can discrepancies due to weak or missing reactions be resolved?

A

Repeat testing using reagents from different lots or different manufacturers can help identify low-incidence antibodies.

187
Q

How can weak reacting antigens in Category II discrepancies be enhanced?

A

Extending the incubation at room temperature to 30 minutes can enhance antigen/antibody association.

188
Q

What is the Acquired B Phenomenon?

A

It refers to weakened expression of the B antigen in the forward typing, often caused by disease states like leukemia.

189
Q

What percentage of A2B individuals produce anti-A1?

A

22% to 35%

190
Q

What is the main feature of the A3 subgroup?

A

Mixed field reaction with anti-A and anti-A,B antisera

191
Q

Which gene is dominant over the A2 gene?

A

A1 gene

192
Q

What is the purpose of A1 lectin?

A

To differentiate between A1 and A2 subgroups

193
Q

What percentage of A2 people naturally have A1 antibody?

A

Approximately 8%

194
Q

Is it necessary to distinguish between A1 and A2 phenotypes for transfusion purposes?

A

No, unless the patient has a reacting A1 antibody

195
Q

What is the main characteristic of the A3 subgroup?

A

Mixed field (MF) reaction with anti-A and anti-A,B antisera

196
Q

Which subgroup is very rare, approximately 1/40,000?

A

Ax

197
Q

How can weak A subgroups be differentiated serologically?

A

Perform forward typing for presence of A and H antigens, perform reverse typing of ABO isoagglutinins, perform adsorption and elution testing with anti-A, perform saliva testing (neutralization/inhibition) to detect A and H substances

198
Q

What does a weak A phenotype indicate?

A

Several ways to differentiate weak A subgroups serologically

199
Q

What is the significance of a 2+ reaction in weak A subgroups?

A

It is a significant but weak reaction

200
Q

What type of reaction does anti-A1 antibody cause?

A

IgM, agglutinates at RT (room temperature) and binds complement well

201
Q

What can clinically significant anti-A1 cause?

A

Red cell destruction of transfused cells or HDFN (hemolytic disease of the fetus and newborn)

202
Q

What is the cause of ABO discrepancies?

A

Most discrepancies are caused by technical/clerical errors

203
Q

Do transfusions with ABO discrepancies need to be resolved?

A

Yes, ABO discrepancies must be resolved

204
Q

What is the purpose of adsorption-elution methods in ABO discrepancies?

A

To determine the presence of B substance in saliva

205
Q

What should you give in emergency situations if there is no time to rematch?

A

O- unmatched blood

206
Q

When may a discrepancy be seen in both the forward and reverse typing?

A

When there is a discrepancy in both the serum and cells

207
Q

What is the first step in identifying the source of an ABO discrepancy?

A

Identifying the source of the problem

208
Q

What should you always suspect with an ABO discrepancy?

A

The weakest reaction

209
Q

What may indicate an ABO discrepancy?

A

Agglutination strength of typing anti-sera is weaker than expected

210
Q

What technical errors can result in ABO discrepancies?

A

Blood sampling errors, tube labelling errors, failure to add sample, reagents not added or incorrect reagent added, contaminated reagents, presence of hemolysis, incorrect sample tested/sample mix-up, not following manufacturer’s instructions, using uncalibrated centrifuge, over or under centrifugation

211
Q

What should be added to tubes first, before adding reagent or patient cells?

A

Anti-sera/plasma

212
Q

What is the general rule to resolve ABO discrepancies?

A

Check for technical/clerical errors, check patient transfusion history, repeat testing using a fresh cell suspension

213
Q

What is the most common category of ABO discrepancy?

A

Unexpected Reverse Reactions

214
Q

What is associated with category I ABO discrepancies?

A

Unexpected weakly reacting or missing reverse reactions

215
Q

What can cause category I ABO discrepancies?

A

Patients with depressed ABO antibody production, certain disease states, immunosuppressive medication, BM or hematopoietic progenitor stem cell transplants

216
Q

What is the significance of the K antigen?

A

The presence of the K antigen indicates that the person will not possess anti-K antibodies.

217
Q

How are screening cells used to detect unexpected antibodies?

A

Patient plasma is mixed with commercial screening cells to identify the presence of unexpected antibodies.

218
Q

What antigens should be included on screening cells for antibody detection?

A

The antigens expressed on screening cells should include: D, C, E, c, e, M, N, S, s, P1, Lea, Leb, K, k, Fya, Fyb, Jka, and Jkb.

219
Q

What is the purpose of using group O cells in testing?

A

Group O cells are used because they do not react with ABO antibodies present in patient or donor plasma.

220
Q

When should an antibody panel be performed?

A

An antibody panel should be performed when a new unexpected antibody is detected or when testing suggests a new antibody.

221
Q

What is the purpose of crossmatch or compatibility testing?

A

Crossmatch or compatibility testing is used to determine compatibility between the patient and donor before transfusion.

222
Q

When should phenotype testing be performed?

A

Phenotype testing should be performed when a patient has a previously identified antibody or when confirming a newly identified antibody.

223
Q

What is the difference between phenotype and genotype testing?

A

Phenotype testing detects the physical expression of inherited traits, while genotype testing determines the genetic makeup.

Transfusion (7 decks)

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