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IMHM > other blood group 2 > Flashcards

other blood group 2 Flashcards

1
Q

what is almost undetectable in infant?

A

Anti-I

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2
Q

At what month the quantity of “i”
slowly decreases?

A

18 months

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3
Q

expressed in a reciprocal relationship that is developmentally regulated

A

I and i antigens

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4
Q

individuals who do not change their “i” status after birth

A

Rare i adult or negative phenotype

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5
Q

Common autoantibody that can be benign or
pathologic.

A

Anti-I

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6
Q

Found in serum of normal individual.

A

Benign Anti-I

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7
Q

Potent IgM agglutinins, reacting up to 30°C or 32°C

A

Pathologic Anti-I

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8
Q

Demonstrates strong reactions with adult cells and weak reactions with cord cells.

A

Anti-I

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9
Q

Not associated with HDN

A

Anti-I

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9
Q

Weak, naturally occurring saline reactive IgM agglutin that reacts at 4C.

A

Pathologic Anti-I

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9
Q

causes interfering factors when performing reverse typing

A

Benign Anti-I

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10
Q

Not associated with in vivo red cell destruction

A

Benign Anti-I

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11
Q

Pathologic Anti-I is associated with what diseases?

A

o Cold Agglutinin Disease (CAD)
o Cold Hemagglutinin Disease (CHD)
o Primary Atypical Pneumonia (PAP)

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12
Q

Pathologic Anti-I attach in vivo and causes

A

autoagglutination and vascular occlusion or intravascular hemolysis

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13
Q

This patient has walking pneumonia or Mycoplasma pneumonia

A

Autoanti-I

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14
Q

Immunoglobulin nature of Anti-I

A

IgM

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15
Q

Anti-I and autoanti-I are seen in

A

Infectious mononucleosis
Alcoholic Cirrhosis
Myeloid Leukemia
Reticuloses

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16
Q

Production of autoanti-I is also associated with

A

infectious mononucleosis (IM) (caused by EBV),
reticuloses, myeloid leukemias and alcoholic cirrhosis

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17
Q

This bacteria is reported from a patient with
cold autoimmune hemolytic anemia to absorb anti- I and stimulate its production in rabbits

A

Listeria monocytogenes

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17
Q

It was identified in 1946

A

Anti-K (Anti capital K)

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18
Q

Who described anti-k and in what year it was?

A

Levine et al ; 1949

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19
Q

It was discovered in 1957 and 1958

A

discovery of the antithetical antigens Kpa and Kpb

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20
Q

Who discovered discovered Jsa

A

Giblett

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21
Q

Who discovered Jsb

A

Walker et al

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22
Q

discovered K0

A

null phenotype

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23
Q

In 1961, Allen et al described

A

McLeod phenotype

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24
Q

rare phenotype of kell blood group system

A

McLeod phenotype

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25
Q

Second most immunogenic

A

K antigen

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26
Q

The K antigen can be detected on fetal RBCs

A

10 weeks

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27
Q

Antigens that are well developed at birth:

A
  • Kell
  • MNSs
  • Duffy
  • Kidd
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28
Q

The k antigen can be detected on fetal RBCs

A

7 weeks

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29
Q

These enzymes can destroy K antigen when used in combination.

A

trypsin and chymotrypsin

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30
Q

K
k
Kpa
Kpb
Jsa
Jsb

A
  • Kell
  • Cellano
  • Penney
  • Rautenberg
  • Sutter
  • Matthews
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31
Q

considered as the most common antibody seen in blood bank.

A

Anti- K

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32
Q

Anti- K is associated in

A

Severe hemolytic transfusion reaction
severe hemolytic disease of the newborn

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33
Q

Kx is present on all RBCs except

A

rare McLeod phenotype.

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34
Q

Anti-k phases in crossmatching

A
  • Immediate spin
  • 37 C phase
  • AHG phase/Coomb’s phase
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35
Q

Kx Antigen genes are located on what chromosome

A

X chromosome

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36
Q

It has an inverse relationship with K antigen.

A

Kx antigen

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37
Q

It is called McLeod because of

A

donor

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38
Q

weak expression of k, Kpb and Jsb is detectable by

A

adsorption-elution methods

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39
Q

McLeod phenotype also appears in

A

Kell null

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40
Q

Example of adsorption elution methods

A

washing of red cell

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41
Q

Abnormal red cell morphology seen in McLeod phenotype

A

Acanthocytes

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42
Q

Patient with Mcleod phenotype have a
chronic but well compensated hemolytic
anemia characterized by

A

reticulocytosis, bilirubinemia, splenomegaly and reduced serum haptoglobin levels.

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43
Q

McLeod phenotype is associated with

A

X-Linked CGD - (Chronic
Granulomatous Disease)

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44
Q

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

A

X-Linked CGD (Chronic Granulomatous Disease)

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45
Q

coagulation disorder wherein the blood that used in transfusion is anti-hemophilic factor or cryoprecipitated AHF

A

hemophiliac

46
Q

Fy(a–b–) RBCs resist infection in vitro by the monkey malaria organism

A

Plasmodium knowlesi
plasmodium vivax

47
Q

a marker for African black race

A

Fy(a-b-)

48
Q

Destroyed by common proteolytic enzymes

A

Fya and Fyb

49
Q

Usually IgG and react best at the antiglobulin phase

A

Anti-Fya & Anti-Fyb

50
Q

Anti-Fya & Anti-Fyb is enhanced using what enhancement medium

A

low ionic strength medium
22% Bovine albumin
and PEG

51
Q

Discovered in the serum of a pregnant patient whose infant had HDN.

A

KIDD BLOOD GROUP SYSTEM

52
Q

Null phenotype of kidd blood group system

A

Jk (a- b-)

52
Q

Associated with hemolytic transfusion reactions,
although hemolysis is not often severe

A

Anti-Fya & Anti-Fyb

53
Q

Do not react with enzyme-treated red cells

A

Anti-Fya & Anti-Fyb

54
Q

antithetical antibody of kidd blood group system

A

Anti-Jka and Anti-Jkb

55
Q

antithetical antigens of kell blood group system

A

K antigen and k antigen

56
Q

Jka can be detected on fetal RBCs

A

11 weeks

57
Q

These are not very immunogenic

A

Jka and Jkb Antigens

58
Q

Jka and Jkb Antigens are enhanced by the use of

A

proteolytic enzyme

59
Q

Have notorious reputation in the blood bank

A

Anti-Jka and Anti-Jkb

60
Q

anti-Jka and anti-Jkb
react more strongly
with RBCs that carry

A

double dose of the
respective antigen

61
Q

anti-Jka and anti-Jkb may not react with

A

Jk (a+b+) RBCs

62
Q

Anti-Jka and Anti-Jkb is enhanced by

A

LISS or PEG

63
Q

drugs that cause DIHA

A

methyldopa
Chlorpropamide dependent

64
Q

Associated with severe HDN & delayed type of HTR

A

Anti-Jka and Anti-Jkb

65
Q

First recognized antibody was
discovered in the serum of a patient with Lupus Erythematosus

A

anti-Lua

66
Q

antithetical antigen of lutheran blood group system

A

Lua and Lub

67
Q

Crawford et al discovered the first

A

Lu (a-b-) phenotype.

68
Q

major blood group system in blood banking

A

ABO, Rh, Kell, Kidd, Duffy, MNSs, P, Lewis, and
Lutheran

69
Q

poorly developed at birth and do not reach adult levels until age 15 years

A

Lua and Lub Antigens

70
Q

Lua and Lub Antigens can be detected on fetal RBCs

A

10-12 weeks

71
Q

Anti-Lua ig in nature

A

IgG
IgA
IgM

72
Q

associated with mild cases of HDN

A

Anti-Lua
Anti-Lub

73
Q

Diego system is composed of two sets of
independent pairs of antithetical antigens

A

Dia/Dib and Wra/Wrb

74
Q

useful tool in anthropologic studies
of Mongolian ancestry

A

Dia antigen

75
Q

located on the anion exchange
protein (AE-1)

A

Dia and Dib

76
Q

The gene is located on the Short arm of the X
chromosome.

A

Xga antigen

77
Q

phenotype of Xg blood group system is expressed in

A

Xg(a+) or Xg(a-)

78
Q

does not appear to be a good immunogen.

A

xga

79
Q

blood group system that has x-linked system

A
  • Xga antigen
  • kx antigen
  • McLeod phenotype
80
Q

antithetical antigens of Scianna blood group system

A

Sc1 and Sc2
Sc3 and Radin
(Rd) antigen

81
Q

The Scianna antigens are shown to be expressed by
the RBC adhesion protein

A

ERMAP (Erythroblast membrane Associated protein)

82
Q

The null phenotype in the Dombrock system
demonstrates an absence of

A

Doa, Dob, Gya, Hy, and Joa antigens.

83
Q

This is where antigen resides that anchors them to the RBC membrane.

A

glycosylphosphatidylinositol
(GPI)-linked glycoprotein

84
Q

deficient in dombrock, cromer, and john milton hagen

A
  • GPI
  • CD55
  • CDw108
85
Q

Associated with PNH

A

o Dombrock
o Cromer
o JMH (JOHN MILTON HAGEN)

86
Q

Associated in Cromer null phenotype

A

DOMBROCK BLOOD GROUP SYSTEM

87
Q

Coa, Cob, and Co3 located

A

Aquaporin-1
(AQP1)

88
Q

Nine antigens of chido/rodgers

A

6 chido antigens
2 rodgers
WH antigen

89
Q

described as high-incidence antigens in chido/rodgers

A

CH1, CH2, CH3, RG1, and RG2

90
Q

Antibody reactions of chido/rodgers

A
  • transfusion of plasma
  • transfusion of platelets
91
Q

Null CH and RG phenotypes seen in patient with

A

C4 deletion

92
Q

autoimmune diseases associated with chido/rodgers

A

systemic lupus erythematosus,
Graves’ disease,
and rheumatoid arthritis

93
Q

Expressed on RBC membrane sialoglycoproteins
glycophorins C (GPC) and/or glycophorin D (GPD)

A

gerbich blood group system

94
Q

associated with the RBC
membrane band 4.1, which is integral for
maintaining normal erythrocyte skeleton and
shape.

A

GPC and GPD

95
Q

Null phenotypes of cromer blood group system

A

Inab(-)”

96
Q

Composed of eight antigens.

A

knops blood group system

97
Q

antithetical antigens of indian blood group system

A
  • Ina
  • Inb
98
Q

antithetical antigen that is low-incidence antigen

A

Ina

99
Q

antithetical antigen that is high-incidence antigen

A

Inb

100
Q

depressed expression of Inb
in individual presenting with

A

Lu (a-b-) phenotype

101
Q

colton blood group system resides or located on

A

Aquaporin 1 (AQP1)

102
Q

The IN antigens are found in the

A

CD44 glycoprotein

103
Q

Blood Group System That Exhibits Dosage in
Serological Reactions

A

 Rh (except D antigen)
 Kidd
 Duffy
 MNSs

104
Q

Effect of Antigen-Antibody Reactions to
Proteolytic Enzymes

Enhanced:
Inactivated:
Not affected:

A

Enhanced:
Kidd
Lewis
P1
I
ABO

Inactivated:
Duffy
MNSs
Xga

Not affected:
Kell

105
Q

Phenotype that resists infection in vitro by the monkey malaria organism

A

Fy(a-b-)

106
Q

Phenotype that resists infection in vitro by the monkey malaria organism

A

Fy(a-b-)

107
Q

What kidd phenotype are most common in Asian

A

Jk (a+b+)

108
Q

Rare phenotype of lutheran

A

Lu(a-b-)

109
Q

Lutheran phenotype associated with indian bgs

A

Lu (a-b-)

110
Q

Mutation in AE1 can result in

A

Hereditary spherocytosis
Congenital acanthocytosis
Southeast asian ovalocytosis

111
Q

What are the familial bgs

A

Kell
Duffy
Lutheran
Lewis
Diego

112
Q

What are the familial bgs

A

Kell
Duffy
Lutheran
Lewis
Diego

113
Q

Chido/rodgers resides on

A

C4 complement component

114
Q

Not an integral red cell membrane

A

Chido/rodgers bgs

IMHM (10 decks)

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