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Immunohematology - 4444 > Test 3: Other Blood Group Systems > Flashcards

Test 3: Other Blood Group Systems Flashcards

1
Q

What are the naturally occurring carbohydrate blood group systems?

A

-ABO
-Lewis
-P
-I

(IgM)

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2
Q

What are the immune stimulated protein blood group systems?

A

-RH
-MNSs (IgM)
-Kell
-Duffy
-Kidd
-Lutheran

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3
Q

What causes unexpected antibodies in a patient?

A

the patient being “challenged” (exposure to antigens)

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4
Q

What is the most common Lewis phenotype?

A

Le (a-b+)

72% whites
55% blacks

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5
Q

What is the least common Lewis phenotype?

A

Le(a+b+)

rare for all populations

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6
Q

How do Lewis antigens get on RBCs?

A

they are passively absorbed

they are not of erythroid origin

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7
Q

Why do newborns type as Le(a-b-)?

A

not expressed on cord RBCs

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8
Q

What is diminished on maternal RBCs that will seroconvert after the birth of the baby? ***

A

Lewis antigens

-mothers will type as Le(a-b-) while pregnant

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9
Q

Where are Lewis antigens found?

A

all throughout the body: lymphocytes, platelets, tissues (organs),
saliva

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10
Q

Are Lewis antigens affected by enzymes?

A

no, resist enzymes

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11
Q

Lewis antigen _______ cause HRTs, _______ HDFN.

A

rarely, never

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12
Q

What are two reasons Lewis antigens never cause HDFN?

A

-IgM, cannot cross the placenta
-baby will not have antigens

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13
Q

Are Le(a) and Le(b) alleles?

A

No. (gene says yes or no)

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14
Q

What genes does the Lewis system depend on?

A

Hh, Se, and Le genes

-le, h, and se do not produce
products

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15
Q

If the Le gene is inherited, ____ substance is produced

A

Le(a)

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16
Q

What must all be inherited to convert Le(a) to Le(b)?

A

Le, H, and Se

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17
Q

Le(a+b+) RBCs are rare, except in what population?

A

Asian populations (10-40%)

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18
Q

Phenotype if Inherit only FUT3 (Lewis gene)?

A

Le(a+b-)

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19
Q

FUT 1 is ______ gene
FUT 2 is ______ gene
FUT 3 is ______ gene

A

H
secreter
Lewis

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20
Q

Phenotype if Inherit both FUT3 and FUT2
(Secretor gene)?

A

Le(a-b+)

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21
Q

True or False?

Lea does not turn into Leb

A

True

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22
Q

Why is anti-Le(a) not made with Le(a-b+)?

A

still produces small
amounts of Le(a)

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23
Q

What is significant about lele Se H genes being present, (Le a-b-)?

A

will make antibodies unless it is a baby

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24
Q

Le(a) —-> seen in secretions

If Lewis b, what do they still have in secretions?

A

Le a

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25
Q

What immunoglobulin type are Lewis antibodies?

A

IgM

naturally occuring

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26
Q

What immunoglobulin type are Lewis antibodies?

A

IgM

naturally occurring

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27
Q

Pregnant women will frequently have Lewis _________ in serum.

A

antibodies

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28
Q

Are Lewis antibodies clinically significant?

________ compatible RBCs

A

No

-XM compatible RBC (no antigen testing required)

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29
Q

What phases can Lewis antigens agglutinate at?

A

can occur at immediate-spin (IS), 37°C, and AHG

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30
Q

Lewis RBCs treated with Enzymes enhance anti-Leb
reactivity and may cause…

A

hemolysis

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31
Q

Anti-Le(__) binds complement; may cause hemolysis in vitro, especially with enzyme treated cells

A

a

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32
Q

What is neutralization used for with Lewis antibody?

A

can confirm the presence or eliminate reactions with Lewis antibody

(add liquid Lewis substance to mask the presence, *this is not done often)

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33
Q

Antigen typing of donors for what antigen type does not have to be done?

What type of antigens do have to be typed on the donor?

A

IgM

IgG

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34
Q

Where are P1 antigens detected?

A

In plasma and hydatid cyst fluid*

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35
Q

___________blood group system: P antigen.

A

Globoside

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36
Q

Globoside blood group collection: _______ and ________ antigens.

A

Luke (LKE), PX2

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37
Q

High frequency antigens in the P blood group system?

A

P, P(K), and LKE

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38
Q

True or false, P blood group is effected by enzymes.

A

False. Resistant to enzymes.

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39
Q

How are the P blood group system antigens synthesized?

A

By adding sugar to precursor substances

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40
Q

Where are P blood group antigens found?

A

On RBC membrane and in secretions and other cells and tissues

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41
Q

What population expresses the P1 antigen stronger?

How is it expressed at birth?

A

blacks

poorly expressed at birth

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42
Q

____ % of people express the P1 antigen.

A

80

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43
Q

What is the first and second most common phenotype of the P blood system?

A

-P1 is most common (red cells express P, P1, and P(K)

-P2 second most common (lacks P1 antigen but expresses P and P(K))

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44
Q

What are the possible antibodies for P1? P2?

A

P1- none

P2- anti-P1 (not clinically significant, IgM, enhanced by enzymes)

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45
Q

What antibody is associated with parasitic infections?

A

anti-P1

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46
Q

What can anti-P1 be neutralized by?

A

by P1 substance (from hydatid cyst fluid)

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47
Q

True or false,

anti-P1 is non-RBC stimulated?

A

true (born with it or just have it)

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48
Q

Anti-P1 is not implicated in _______ and rarely HTRS.

A

HDFN

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49
Q

What is associated with paroxysmal cold hemoglobinuria?*

A

Autoanti-P

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50
Q

What may appear in children after a viral infection?

A

Autoanti-P

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51
Q

a biphasic hemolysin that binds with P1 or P2 cells at low temperatures before the complement is activated

-binds in cold and lyses in hot

A

IgG (Donath-Landsteiner antibody)

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52
Q

Anti-PP1Pk (aka anti-Tja) appear in what individuals?

A

individuals with the null phenotype

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53
Q

Why is Anti-PP1Pk (aka anti-Tja) clinically significant? What type of antibody is this

A
  • potential to cause severe HTRs and HDFN, and spontaneous abortions
  • IgM and IgG
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54
Q

Anti-PP1Pk (aka anti-Tja):

Binds __________ and causes hemolysis in vitro

A

complement

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55
Q

although Anti-PP1Pk (aka anti-Tja) is clinically significant, why is it never tested for?

A

because it is rare

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56
Q

What is done if Worton’s jelly is present?

A

get two sticks to remove it from the sample

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57
Q

Are I and i antithetical antigens?

A

no

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58
Q

How do I antigens from?

A

on the precursor A, B, and H chains of RBCs

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59
Q

I blood group system:

Newborns have ___ antigen. On baby cords.

Adults have ____ antigen. Found on every adult cell.*

A

i, I

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60
Q

i antigen (linear) converts to I antigen (branched)
as a child matures (about ___ years of age)

A

2

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61
Q

I antibodies:

Cold-reacting, IgM.
Does it bind compliment?

A

yes

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62
Q

Are I antibodies clinically significant?

A

No, it is common

not much, autoanti-I -Low titer

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63
Q

I antibodies are usually what?

A

Usually autoantibody
(autoanti-I)

Alloanti-I is rare

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64
Q

What can be used to verify that I is an issue when testing?

A

Use cord cells, if negative, then the patient has anti-I

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65
Q

I antibodies are usually __________.
What is unique about it?

A

autoanti-I (high-titer)

broad thermal amplitude, common in autoimmune hemolytic anemia

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66
Q

Is alloanti-I rare or common?

A

rare

-stimulated from exposure from someone else (some people who do not fully convert to I —> may be alloanti)

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67
Q

What is the issue with I antibodies and polyspecific?

A

Finds anti-I every time

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68
Q

How are I antibody reactions avoided?

A

by prewarming, and
using anti-IgG instead
of polyspecific AHG*
(starting to stop using this at some places)

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69
Q

What is meant by I antibodies react as compound antibodies?

A

*Often found as an anti-IH
*Stronger agglutination with
RBCs having many H sites
(O and A2)

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70
Q

What are the diseases associated with autoanti-I?

A

-Mycoplamsa pneumoniae
-Cold hemagglutinin disease

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71
Q

What are the diseases associated with Anti-i?

A

-Infectious mononucleosis
-Lymphoproliferative disease
-Cold hemagglutinin disease (occasionally)
-alcoholic cirrhosis

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72
Q

What are alphabetical pairs in the MNS system?

A

M and N

S and s

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73
Q

MNS system —> chromosome ____.

A

4

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74
Q

Is the MNSs system clinically significant?

A

yes

75
Q

What is the frequency of the phenotype M+N+?

A

Whites - 50%
Blacks - 44%

76
Q

What is the frequency of the phenotype S-s+?

A

Whites - 45%
Blacks - 69%

77
Q

M and N is coded by….

What is the membrane structure called?

A

GLYCOPHORIN A

SIALOGLYCOPHORIN A

78
Q

Does M and N show dosage?

A

***Yes. Homozygous inheritance enhances agglutination (M+N-) or M- N+)

79
Q

Is M and N effected by enzymes?

A

***Yes. Destroyed by enzymes.

80
Q

Is S and s easily destroyed?

A

S = usually destroyed
s = usually not destroyed

81
Q

S, s, and U is coded by…..

Membrane structure is called?

A

GLYCOPHORIN B

SIALOGLYCOPHORIN B

82
Q

S has __________; s has ________.

A

methionine

threonine

83
Q

True or false:

S, s, and U can be destroyed by some enzymes.

A

True

84
Q

Where is the U antigen loacted?

A

near membrane

85
Q

What is present when S or s is inherited?

A

U antigen

86
Q

ABSENCE OF GLYCOPHORIN B (GPB) WOULD RESULT IN…

A

S–s–U–

87
Q

What must be done anytime there is a positive antibody screen?

A

Coomb’s test***

88
Q

Anti-M is what immunoglobulin type?

A

Mostly IgM, IgG

-rarely encountered in HDFN

89
Q

Variable reactions of Anti-M antibodies depends on what?

A

reagent pH (like it slightly acidic)

90
Q

Which would you antigen type for:

Anti-M-
Anti-N-
Anti-S, s, U-

A

Anti-M- might antigen type
Anti-N- usually antigen type
Anti-S, s, U- have to antigen type

91
Q

Who are N-like antibodies typically found in?

A

dialysis patients from
formaldehydesterilized
instruments

92
Q

What immunoglobulin class are N antibodies?

A

Mostly IgG, Rare IgM

93
Q

Is the Kell System (K and k) clinically significant?

A

Yes

94
Q

Anti-S, s, and U are clinically significant Ig__ antibodies.

A

G

95
Q

What blood group system is similar to the Rh system?

A

Kell

96
Q

The 2 major antigens in the Kell system:

K (K1): ____% of the population

K (K2/cellano): ____ of the population

A

less than 9%

more than 90%

97
Q

The K and k antigens are ___________.

A

antithetical

98
Q

Ture or false:

The Kell antigens are well developed at birth.

A

True

99
Q

What antigen is very immunogenic (second to the D antigen) in stimulating antibody production?

A

K (K1) antigen

100
Q

What are other Kell antigens?

A

-analogous to the Rh system: C/c and E/e
-Kp antigens
-Js antigens

101
Q

Which are low-frequency antigens and which are high-frequency antigens in the Kell system?

A

*Kpa is a low-frequency antigen (only 2%)
*Kpb is a high-frequency antigen (99.9%)

*Jsa (20% in blacks, 0.1% in Caucasians)
*Jsb is a high-frequency antigen (80% to 100%)

102
Q

What regents are used on Kell antigens to see if there is an underlying antigen?

A

sulfhydryl reagents***

103
Q

What makes Kell antigens sensitive to sulfhydryl reagents?

A

Kell antigens have disulfide-bonded regions on the glycoproteins***

104
Q

Lacks all Kell system antigens (K0K0)

A

K0 or Kell(null) phenotype

105
Q

As a result of red blood cell (RBC) immune stimulation, K0 individuals can develop…

A

anti-Ku (Ku is on RBCs
that have Kell antigens)

106
Q

What kind of blood must be given to Kell(null) people?

A

Kell(null) blood

107
Q

K0 or Kell(null) —> _________ expression related Kx antigen.

A

increased

108
Q

K(null) is autosomal __________.

A

recessive

109
Q

What are the high-incidence Kell alleles? (99% of people)

A

k, Kp^b, Js^b, KEL 11

110
Q

What are the low-incidence Kell alleles?

A

K, Kp^a, Js^a, KEL 17

111
Q

Set of Kell alleles:

Kel 11 and Kel ____

A

17

112
Q

Why is it not usual to test for K antigen before transfusion?

A

low-incidence (9%) but still
super important ( 3rd immunogenic antigen)

113
Q

What is the frequency of K- k+?

A

white- 91%
black- 98%

114
Q

What is the frequency of K+ k-?

A

white- 0.2%
black- rare

115
Q

Kell antibodies:

Immunoglobulin ____

A

IgG

116
Q

Kell antibodies agglutinate best in _________ test

A

IAT

117
Q

Do Kell antibodies bind compliment?

A

usually not

118
Q

Are Kell antibodies associated with hemolytic transfusion reactions
(HTRs) and hemolytic disease of the fetus and newborn (HDFN)?

A

Yes

119
Q

Are Kell antibodies effected by enzymes (not reagents*)?

A

No

120
Q

What is the most common Kell antibody?

A

Anti-K (K1)

121
Q

____ ANTIGEN IS PHENOTYPICALLY RELATED TO THE KELL SYSTEM BUT IS NOT GENETICALLY SIMILAR

A

K(x)

122
Q

INDIVIDUALS WHO LACK KX
ANTIGEN MAY DEMONSTRATE
RBC ABNORMALITIES
(______________ PHENOTYPE)

A

McLeod

123
Q

McLeod phenotype is seen in….

A

Males because it is inherited on the X chromosome.
-associated with reduced expression of all Kell antigens

124
Q

MCLEOD PHENOTYPE IS
ATTRIBUTED TO MCLEOD _________

A

syndrome

125
Q

Symptoms of McLeod syndrome?

A
  • RBC ABNORMALITIES
  • MUSCULAR AND NEUROLOGIC
    DEFECTS
  • INCREASED CREATINE KINASE
126
Q

What disease is McLeod syndrome associated with?

A

CHRONIC
GRANULOMATOUS DISEASE

  • IMPAIRED PHAGOCYTOSIS
    (WHITE BLOOD CELLS [WBCS] ENGULF BUT CANNOT KILL)
127
Q

What are the Duffy system alleles?

A

Fya and Fyb

-codominant alleles

128
Q

Duffy system:

Most important for transfusion purposes?

A

Fya and Fyb

129
Q

Are Duffy antigens well developed at birth?

A

Yes

130
Q

Are Duffy antigens effected by enzymes?

A

Yes, destroyed by enzymes (along with NMS)

131
Q

Do Duffy antibodies bind compliment?

A

No

132
Q

How are Duffy antibodies stimulated?

A

BY TRANSFUSION OR
PREGNANCY

133
Q

Do Duffy antibodies cause HDFN? HTRs?

A

HDFN-not common

IMPLICATED IN ACUTE AND DELAYED HTRS

134
Q

Are Duffy antibodies effected by enzymes?

A

Does not react with enzyme treated RBCs

135
Q

Do Duffy antibodies show dosage?

A

Yes

136
Q

Anti-_____ MADE BY FY(A-B-) BUT NOT BY BLACKS WITH THIS PHENOTYPE

A

ANTI-FY3 –

137
Q

Is Anti-Fy3 effected by enzymes?

A

Not destroyed by enzymes

138
Q

THOSE THAT ARE _______ OR _______ DO NOT MAKE THE FY5 ANTIGEN.

A

FY(A-B-) OR RH
NULL

139
Q

Are Fy5 antigens effected by enzymes?

A

Not destroyed by enzymes

140
Q

Most African Americans are Fy(_____)

A

a-b-

141
Q

What is the advantage of Fy(a-b-)?

A

Certain malarial parasites (Plasmodium knowlesi and Plasmodium vivax) will not
invade Fy(a–) and Fy(b–) negative cells

142
Q

____ or ____ acts as a receptor for the merozoite to attach to the RBC

A

Fy(a) or Fy(b)

143
Q

The Fy(a–b–) phenotype is found frequently in people from…

A

west and central Africa,
supporting the theory of selective evolution

144
Q

What are the clinically significant KIDD system antigens?

A

JKA, JKB

145
Q

KIDD prevalence chart

A

*

146
Q

The KIDD system is well developed in….

A

neonates

147
Q

Do KIDD antibodies cause HDFN?

A

ONLY RARELY RESPONSIBLE FOR SEVERE HDFN

148
Q

What are the three antigens in the KIDD system?

A

JKA, JKB, AND JK3

149
Q

IN THE UNITED STATES, MOST BLACKS (51.1%) ARE JK(____)

A

Jk(a+B-)

150
Q

IN THE UNITED STATES, MOST CAUCASIANS (50.3%) ARE JK(_____)

A

JK(a+B+)

151
Q
  • JK3 IS PRESENT WHENEVER what is present?
A

JKA AND JKB ARE PRESENT

152
Q

KIDD NULL PHENOTYPES: JK(A–B–) USUALLY SEEN IN INDIVIDUALS FROM…

A

THE FAR EAST OR PACIFIC
ISLANDS (RARE)

153
Q

KIDD NULL PHENOTYPES: JK(A–B–) may produce what antibody?

A

anti-JK3

154
Q

KIDD null phenotype RBCs are resistant to…

A

2M urea

155
Q

Two important things to remember about KIDD system?

A

*shows dosage
*enhanced by enzymes

156
Q

If someone is ever positive for KIDD antibodies, what must happen?

A

always get negative blood

157
Q

What is the cause of the most common delayed severe HTRs?

A

KIDD antibodies

158
Q

Do KIDD antibodies bind complement?

A

May bind complement
-causing intra and extravascular hemolysis

159
Q

Kidd antibodies are implicated in…

A

HTRs and HDFN

160
Q

What usually appears with KIDD antibodies?

A

other antibodies

161
Q

What aids the detection of KIDD antibodies?

A

enzymes, low-ionic strength solution (LISS), and polyethylene glycol (PEG)

162
Q

KIDD antibodies can become ______________ in a few week or months.

A

undetectable

163
Q

Is the Lutheran blood group system expressed on cord blood cells?

A

weakly expressed

164
Q

Most Lutheran antigens are ____-incidence antigens.

A

high

antibodies are rare

165
Q

What are the primary antigens of the Lutheran system?

A

Lu(a) and Lu(b)

166
Q

How is Lu(null) phenotype inherited?

A

recessively, rare

167
Q

______ % Lu(a–b+)
_______% Lu(a+b+)
_______% Lu(a+b–)

A

92.4
7.4
0.2

168
Q

Is Lutheran effected by enzymes?

A

No

169
Q

Anti-Lu(a) is what immunoglobin type?
Anti-Lu(b)?

A

IgM with some IgG

IgG

170
Q

Lutheran antibodies:

Which may occur without RBC stimulation?

A

Anti-Lu(a)

171
Q

What temperature does anti-Lu(a) react best at?

A

room temp

172
Q

Both anti-Lu(a) and anti-Lu(b) show what agglutination pattern?

A

Mixed-field pattern

173
Q

Which Lutheran antibody is not clinically significant?

Which Lutheran antibody is associated with transfusion reactions (clinically significant but rare)?

A

anti-Lu(a)

anti-Lu(b)

174
Q

What are the three different inheritance types for Lutheran antibodies?

A

-Dominate type Lu (A- B-)
-Recessive type Lu (a- b-)
-X-Linked inhibitor type

175
Q

Recessive X-Linked
Inhibitor Type:

X linked inhibitor to
Lutheran due to _______

A

GATA-1

176
Q

Anti-Lu3 reacts with…

A

all RBCs except Lu (a- b-)

177
Q

Dominate type Lu (A- B-) carries….

A

trace amounts of Lutheran antigens

178
Q

Dominate type Lu (A- B-) does not make….

A

Anti-Lu3***

179
Q

***Dominate type Lu (A- B-) has reduced expression of…

A

-CD44
-P1
-I (start making anti-I)
-AnWj
-MER2
-INB

180
Q

-inherit two rare silent alleles LuLu
-lack Lutheran antigens

A

Recessive type Lu (a- b-)

181
Q

A type 1 chain has:

A

The terminal galactose in a 1-3 linkage to subterminal N-acetylglucosamine.

182
Q

MN antigens and antibodies are well developed at birth, susceptible to enzymes, and generally __________ reactive.

A

saline

183
Q

What autoantibody specificity is found in patients with paroxysmal cold hemoglobinuria?

A

Anti-P

184
Q

What is the most common antibody in blood bank after ABO and Rh antibodies?

A

Anti-K

Immunohematology - 4444 (17 decks)

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