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Blood Bank > Blood Bank Exam 3 > Flashcards

Blood Bank Exam 3 Flashcards

1
Q

List the cold antibodies. Are these clinically significant?

A

Lewis (anti-Le)
anti-I
anti-P1
anti-M
anti-A, anti-B, anti-H
anti-N
Not clinically significant

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2
Q

Are anti-M and anti-N cold or warm antibodies? Are they IgG or IgM?

A

Cold antibodies. IgM.

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3
Q

T/F: IgG/warm antibodies are naturally occurring.

A

False. IgM are naturally occurring

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4
Q

List the warm antibodies. Are they clinically significant?

A

Rh antibodies (Anti-D,C,E)
Duffy (Anti-Fya, Fyb)
Kidd (Anti-Jk)
Kell (Anti-Kp, Anti-Js)
Anti-S, Anti-s
They are clinically significant

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5
Q

What are clinically significant antibodies associated with?

A

Decreased RBC survival, causing HDFN and transfusion reactions

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6
Q

Which antibodies are enhanced by enzymes?

A

Kidd
Rh
Lewis
I
P

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7
Q

Which antibodies are destroyed by enzymes?

A

Duffy
M
N
S,s

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8
Q

Is Kell destroyed or enhanced by enzymes?

A

Neither!

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9
Q

Which antibodies exhibit dosage?

A

Kidds, Duffy, Rh, M, N, S
(Kidds and Duffy the Monkey (Rh) eat a lot of M & N’S)

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10
Q

What antibody is warm IgG, associated with Glycophorin B, destroyed by enzymes, exhibits dosage, and causes HDFN/HTRXN?

A

Anti-S and Anti-s

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11
Q

What antibody is warm IgG, enhanced by enzymes, exhibits dosage, causes DELAYED HDFN/HTRXN, and is associated with complement fixation/activation?

A

Kidd antibodies

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12
Q

What antibody is a cold IgM, associated with Glycophorin A, exhibits dosage, and is destroyed by enzymes?

A

Anti-M and anti-N

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13
Q

What antibodies are capable of crossing placenta, warm IgG, exhibits dosage, enhanced by enzyme, and do not bind complement?

A

Rh antibodies

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14
Q

Which blood group antigens are present at birth, capable of HDFN/HTRXNs, associated with resistance to malarial infections?

A

Duffy antigens

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15
Q

Which antigen group is poorly present at birth, weakly immunogeneic, capable of delayed HDFN/HTRXNs, and is associated with resistance to ZM urea testing?

A

Kidd antigens

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16
Q

O blood group - antibodies it has and antigens it has.

A

O has no antigens on its surface
O has anti-A and anti-B and anti-A,B

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17
Q

AB blood group - antigens and antibodies that it has

A

AB has A and B antigens on its surface
AB has no antibodies

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18
Q

What is the universal donor for pRBC?
What is the universal recipient for pRBC?

A

Type O - universal donor
Type AB - universal recipient

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19
Q

What is the universal donor for FFP?
What is the universal recipient for FFP?

A

Universal donor - AB
Universal recipient - O

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20
Q

What enzyme does the A gene encode for?

A

N-acetyl-galactosamine enzymes

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21
Q

What enzyme does the B gene encode for?

A

D-galactose enzymes

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22
Q

What enzyme does the O gene encode for?

A

L-fucose enzymes

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23
Q

What do ABO genes code for? What do they do?

A

Glycosyltransferases that add sugars to a precursor substance (H antigen)

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24
Q

what is hh phenotype called? what will they type as? what does this mean?

A

Bombay phenotype - they will type as O but they cannot receive regular O blood because of the lack of H antigen

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25
Q

T/F: ABO antigens are fully developed at birth.

A

False

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26
Q

At birth, neonates will have ____% the number of adult ABO antigens on the RBC surface. When are they fully developed?

A

50%; at 2-4 years they are fully developed

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27
Q

When do ABO antibodies develop? Are ABO antibodies naturally occurring? Does this make them IgG or IgM (cold or warm)

A

ABO antibodies develop around 6 months after birth. They are naturally occurring, cold IgM antibodies.

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28
Q

Are ABO antigens produced by the baby?

A

No, all antibodies in baby’s plasma are maternal in origin.

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29
Q

Can you do a reverse type on cord blood specimens? (neonates)

A

No because there are no antibodies yet.

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30
Q

When will you have the highest ABO antibody titers?

A

5-10 years old; they will decline with age

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31
Q

What are the most common blood types in order?

A

O is most common, A, B, AB

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32
Q

ABO antibodies: IgG or IgM? Naturally occurring? Complement binding? Placenta crossing? Developed at birth? Does it exhibit dosage?

A

ABO can be IgG or IgM. They are both naturally occurring. IgM can bind complement. IgG can cross placenta. ABO antibodies are not developed at birth and they do not exhibit dosage.

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33
Q

ABO - forward typing

A

“what you are” - antigens on RBC surfaces
Anti-A = positive with type A
Anti-B = positive with type B
Anti-A,B = positive with type AB
O will not react with any anti-sera because it has no antigens.

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34
Q

% of the population with type O blood

A

44%

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35
Q

% of the population with type AB blood

A

4%

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36
Q

% of the population with type A blood

A

37%

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37
Q

% of the population with type B blood

A

15%

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38
Q

ABO reverse typing

A

“what you are not” - tests antibodies in plasma
Reaction with A1 cells = type B
Reaction with B cells = type A
Reaction with both A1 and B cells = type O
Reaction with neither = AB

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39
Q

SeSe or Sese gene

A

Secretor gene - secrete ABO/H in saliva and body fluids

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40
Q

Rank H antigen concentration depending on ABO blood group.

A

O > A2 > B > A2B > A1 > A1B > Oh

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41
Q

What is used in blood banks to confirm suspected cases of Bombay phenotype (Oh)? What plant is it made from?

A

Anti-H lectin made from Ulex europaeus

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42
Q

What does a Bombay serum contain?

A

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

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43
Q

What happens if we add Anti-H lectin to someone that is bombay phenotype?

A

No agglutionation - negative reaction (positive for bombay)

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44
Q

What happens if we add anti-H lectin to someone that is not bombay phenotype?

A

Agglutination - postive reaction (no bombay)

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45
Q

What percent of people have the A1 allele? A2?

A

80% have A1
18% have A2

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46
Q

What is used to determine A1 subgroups? What plant is it from?

A

Anti-A1 lectin from plant Dolichos biflorus

47
Q

What is an ABO discrepancy?

A

When forward and reverse typing do not match

48
Q

What pRBC blood type would you give for an emergency where the patient is an unresponsive female patient that is approximately 24 years old? 70 years old?

A

O negative for women in child-bearing ages to prevent HDFN
O positive for women past child-bearing ages

49
Q

If an ABO discrepancy is due to RBC properties, is this reverse or forward?

A

Forward - antigens are on RBC

50
Q

IF an ABO discrepancy is from plasma/serum properties, is this a forward or reverse type issue?

A

Reverse type - antibodies found in plasma/serum

51
Q

If the forward type is 4+ with anti-A and 4+ with anti-B (strong AB)
And the reverse type is 4+ with B cells (strong A)
What discrepancy could this be?
How could you resolve it?

A
  1. Forward Type discrepancy: Cord blood - excessive serum proteins/Wharton’s Jelly
    Wash cord blood with saline before testing the forward type
  2. Poly-agglutination of RBCs
    Perform DAT and if + can confirm polyagglutination
52
Q

If the forward type is O (no reaction with anti-A or anti-B)
And the reverse type is A (4+ reaction with B cells)
What ABO discrepancy could this be?
How would you resolve it?

A

Forward Type discrepancy: Weak or missing antigens - A subgroups, Diseases, BMTs, Leukemias
Check patient medical history and transfusion history, test for secretor status

53
Q

If the forward type is AB (4+ anti-A, 1+ Anti-B) so weak B
And the reverse type is A (4+ B cells)
What ABO discrepancy could this be?
How to resolve this?

A

Forward Typing: Acquired B antigen –> extra specificity that was not real
Perform an auto-crossmatch, if there is no reaction in the crossmatch, then B was not actually there.

54
Q

Reverse type discrepancies are most commonly caused by:

A

Rouleaux, unexpected antibodies other than ABO, and weak/missing isoagglutinin

55
Q

If the forward type is 4+ for Anti-A (A)
And the reverse type is 4+ for Anti-A and Anti-B (O)
What ABO discrepancy will this be?
How do you resolve it?

A

Reverse Type: Rouleaux - resolve through Saline replacement technique

56
Q

If the forward type is 4+ Anti-A (Type A)
And the reverse type is 2+ A1 and 4+ B cells (Type O)
What ABO discrepancy may this be?
How do you resolve this?

A

Reverse Type: unexpected antibodies other than ABO - could be a cold autoantibody that reacts at room temp
Incubate at room temp

57
Q

If the forward type is Anti-A: 4+ (Type A)
And the reverse type is no reaction (Type AB)
What ABO discrepancy may this be?
How to resolve this?

A

Reverse Type: Weak or missing immunoglobulins due to age/immunocompromised patient
Incubate at room temp or cold temp

58
Q

% of people that are D

A

85%

59
Q

% of people that are d

A

15%

60
Q

Immunogenicity of Rh antigens from high to low

A

D > c > E > C > e

61
Q

Rosenfield Numericals

A

1 = D is present
2 = C is present
3 = E is present
4 = c is present
5 = e is present

62
Q

Wiener genes - ‘ or 1

A

represents C present
use ‘ with d
use 1 with D

63
Q

Wiener genes ‘’ or 2

A

represents E is present
use ‘’ with d
use 2 with D

64
Q

Wiener genes: r vs R

A

R = D present
r = d present

65
Q

Wiener genes: y and z

A

means that both C and E are present
use z with D
use y with d

66
Q

What antibodies could an R1R1 person make if they are given R2r blood?

A

R1R1 = DCe/DCe
R2r = DcE/dce

R1R1 person could make anti-E antibodies and anti-c antibodies (are lacking E and c antigens)

67
Q

Why might someone have a weak D antigen?

A

Hereditary weakened expression of the D antigen (positional effect - D allele is in trans to the C allele
Classic D mosaic or partial D - Genetic loss of D nucleotide may result in a D antigen that is missing subunits

68
Q

If Rh control is positive, results are _____.

A

invalid

69
Q

When is someone tested for weak D?

A

If Anti-D is negative

70
Q

Compound antigens: what is the f antigen of the Rh system?

A

when c and e are in cis
(Dce and dce)

71
Q

Dce/dce
DCe/DcE
Which is f positive and which is f negative? why?

A

Dce/dce is f positive because c and e are in cis
DCe/DcE is f negative because c and e are in trans

72
Q

Compound antigens: what is the g antigen in the Rh system?

A

when D and C are in cis (Dce and DCE)

73
Q

Dce/DCE
DcE/dCe
Which is g positive? g negative? Why?

A

Dce/DCE are g positive because D and C are in cis
DcE/dCe are g negative because D and C are in trans

74
Q

What is the Rh null phenotype?

A

Lacking all Rh phenotypes

75
Q

What antigens are destroyed by DTT and ZZAP?

A

Kell antigens

76
Q

Kell Antigens: are they well developed at birth? are they destroyed by enzymes? Does it cause HTRXNs and HDFN?

A

They are well developed at birth
NOT destroyed by enzymes, but destroyed by DTT and ZZAP
It can cause HDFN and HTRXNs

77
Q

Kell:
k antigen prevalence
K antigen prevalence

A

k prevalence = 91%
K prevalence = 10%

78
Q

What is McLeod phenotype?

A

Individuals who lack Kx and Km antigen (precursor for Kell antigens) and causes RBC abnormalities.

79
Q

What is McLeod phenotype?

A
80
Q

What other rare x-linked disorder is linked to McLeod phenotypes?

A

Chronic granulomatous disease

81
Q

What is the difference between McLeod phenotype and McLeod syndrome?

A

McLeod phenotype’s show acanthocytes and decreased RBC survival, but when it is accompanied by muscle and nerve disorders it is known as McLeod syndrome.

82
Q

Kell Antibodies:
IgG or IgM?
Binds complement?
HDFN/HTRXs?
Enzyme affect?
Most common antibody?

A

IgG
No complement binding
Yes causes HDFN/HTRXs
No effect from enzymes
Anti-K is the most common

83
Q

Duffy Blood group antigens:
Well developed at birth?
Enzyme affect?
IgG or IgM?
Dosage?
Complement binding?
HDFN?
Fun fact?

A

Yes, well developed at birth.
Destroyed by enzymes.
IgG.
Demonstrates dosage
Does not bind complement.
HDFN may occur.
Fy(a-b-) phenotype is prevalent in black populations to have resistance to malaria.

84
Q

What antigen gives increased survival odds for malaria? Which antigen group is it under?

A

FyFy (Fya-b-) Duffy Antigen Group 68% prevalence in black community

85
Q

Kidd antigens: which is more common, Jka or Jkb?

A

Jka

86
Q

Which blood group antigens is associated with 2M urea lysis?

A

Kidd

87
Q

Kidd antigens:
Immunogenicity?
Well developed at birth?
Enzyme affect?
HDFN?
IgG or IgM?
Complement binding?

A

Not very immunogeneic
Not well developed at birth
Enhanced by enzymes
Causes HDFN
IgG
Can bind complement

88
Q

MNS antigens:
Well developed at birth?
Enzyme affect?

A

Well developed at birth
Destroyed by enzymes

89
Q

Anti-M and Anti-N: IgG or IgM?

A

IgM

90
Q

Anti-S and Anti-s:
IgG or IgM?
Bind complement?
HDFN/HTRXNs?

A

IgG
Yes
Yes

91
Q

When does someone have anti-U?

A

When they are lacking S and s antigen.

92
Q

What antigens are found on Glycophorin A?

A

M and N antigens

93
Q

What antigens are located on glycophorin B?

A

S and s antigens 1

94
Q

What does the Le gene code for?

A

L-fucosyltransferase

95
Q

If someone has Le Se hh, what antigens will be in their secretions and why?

A

Only Le-a because even though they have the secretor genes, since H is not present, they cannot make Le-b.

96
Q

If someone has Le Se H genes, what antigens will be in their secretions? What will their red cell phenotype be?

A

Le-a, Le-b, and H antigens in secretions.
Red cell phenotype is Le(a-b+)

97
Q

If someone has Le sese H, what antigens will be in their secretions, what is their red cell phenotype?

A

Antigens in secretions: Le-a
Phenotype: Le(a+b-)

98
Q

If someone has the genes lele Se H, what antigens will be present? What is the red cell phenotype?

A

H
Le(a-b-)

99
Q

If someone has the genes lele sese hh, what antigens in secretions? red cell phenotype?

A

No antigens in secretions.
Le(a-b-)

100
Q

lele Se H red cell phenotype and antigens in secretions

A

phenotype: Le(a-b-)
antigens: H

101
Q

What is a common cause of initial spin XM incompatibilities?

A

Lewis antibodies

102
Q

Cord cells are abundant in _____ I, but poorly developed in _____ I.

A

little, big

103
Q

Adult cells are abundant in ____ I, but have very little ______ I.

A

big, little

104
Q

What can anti-little I be associated with?

A

Epstein Barr Virus

105
Q

What can autoanti-I specificity be associated with?

A

Mycoplasma pneumoniae infections and cold agglutinin disease

106
Q

T/F: I and little I antigens are antithetical; they have a direct relationship.

A

False; they are not antithetical. they have an indirect realtionship

107
Q

Pathological conditions associated with increased little I antigen on adult RBCs

A

cancers/anemias

108
Q

What is associated with Paroxysmal Cold Hemoglobinuria (PCH)?

A

Auto anti-P

109
Q

What is also called the Donath-Landsteiner antibody?

A

Autoanti-P

110
Q

What is also known as Anti-Tja and is found in null P antigen patients?

A

Anti-PP1Pk

111
Q

What is the most common P antibody?

A

Anti-P1

112
Q

The most common platelet antibody is directed against _____.

A

HPA-1a

113
Q

A biphasic antibody:

A

activates complement at cold temps and lyses cells at warm temps

Blood Bank (7 decks)

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