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[Immunohematology] Lec > OTHER BLOOD GROUP SYSTEMS PART 2 (I TO KIDD) > Flashcards

OTHER BLOOD GROUP SYSTEMS PART 2 (I TO KIDD) Flashcards

1
Q

are structurally related to the ABO antigens

A

I blood group antigens

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2
Q

are found on RBC membranes as well as in plasma, milk, and amniotic fluid

A

I blood group antigens

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3
Q

are found on all RBCs.

A

Both I and i antigens

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4
Q

are poorly developed at birth

A

I antigens

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5
Q

As the I antigenic strength [?], i antigen strength [?].

A

increases

decreases

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6
Q

have strong I antigen expression and weak i antigen expression.

A

Most adults

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7
Q

are naturally occurring, cold-reacting IgM anti-bodies

A

Anti-l antibodies

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8
Q

They fail to react with cord RBCs.

A

Anti-l antibodies

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9
Q

react in a broader temperature range and can cause cold-agglutinin disease (CAD).

A

Some anti-l antibodies

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10
Q

may be Idlopathic or may be associated with diseases, such as Mycoplasma pneumoniae Infections.

A

CAD

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11
Q

are not associated with HDN

A

Anti-l antibodies

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12
Q

are rare

A

Anti-i antibodies

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13
Q

Like anti-l, they are cold-reacting antibodles

A

Anti-l antibodies

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14
Q

They may be seen In cases of Infectious mononucleosis

A

Anti-i antibodies

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15
Q

may cause an associated hemolytic anemia that disappears as the infection resolves

A

Anti-l antibodies

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16
Q

Testing for anti-l or anti-i antibodies is done at [?] using [?]

A

4°C

group O RBCs or cord RBCs

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17
Q

are associated with cold agglutinin syndrome and Mycoplasma pneumoniae infections.

A

Anti-l antibodies

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18
Q

are linked to infectious mononucleosis.

A

• Anti-i antibodies

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19
Q

are associated with Hodgkin’s lymphoma.

A

• Anti-IT antibodies

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20
Q

have also been reported in influenza infections.

A

• Cold autoantibodies

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21
Q

Conditions associated with increased i antigen expression on red blood cells (RBCs) include:

A

• Shortened marrow maturation time dyserythropolesis

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22
Q

• Shortened marrow maturation time dyserythropolesis, seen in:

A

• Acute leukemia.
• Hypoplastic anemia.
• Megaloblastic anemia.
• Sideroblastic anemia.
• Thalassemia.
• Sickle cell disease.
• Paroxysmal nocturnal hemoglobinuria (PNH).
• Chronic hemolytic anemia.

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23
Q

Reactive lymphocytes in infectious mononucleosis have

A

increased i antigen

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24
Q

while those in chronic lymphocytic leukemia have

A

decreased i antigen

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25
Q

is associated with Increased i activity on RBCs

A

• Chronic dyserythropoietic anemia type ll or hereditary erythroblastic multinuclearity with a positive acidified serum test
(HEMPAS)

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26
Q

are susceptible to lysis by both anti-i and anti-l antibodies.

A

HEMPAS RBCs

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27
Q

may be involved in binding immune complexes formed by certain drugs and drug antibodies, leading to complement activation and hemolysis.

A

• I antigen

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28
Q

• In Asians, the [?] has been associated with congenital cataracts, with mutations at the [?] identified In some cases, suggesting a genetic mechanism for this condition.

A

adult i phenotype

I locus

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29
Q

The MNS antigens are determined by the

A

MN and Ss loci

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30
Q

is associated with glycophorin A

A

MN

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31
Q

is associated with glycophorin B

A

Ss

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32
Q

There are five principal antigens in the MNS system:

A

M, N, S, s, and U.

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33
Q

RBCs with the S or s antigen also have the

A

U antigen.

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34
Q

are important markers in paternity studies.

A

MNS antigens

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35
Q

are relatively common

A

Anti-M antibodies

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36
Q

They are usually naturally occurring and may be both IgM and IgG

A

Anti-M antibodies

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37
Q

do not bind complement

A

Anti-M antibodies

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38
Q

react optimally at room temperature or below

A

Anti-M antibodies

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39
Q

They are only rarely associated with HDN or HTR

A

Anti-M antibodies

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40
Q

are rare

A

Anti-i

Anti-N antibodies

Anti-S, anti-s, and anti-U antibodies

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41
Q

They are weak, naturally occurring IgM antibodies that react best at room temperature or below

A

Anti-N antibodies

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42
Q

They are not usually associated with HDN or HTR

A

Anti-N antibodies

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43
Q

These IgG antibodies usually develop following RBC stimulation

A

Anti-S, anti-s, and anti-U antibodies

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44
Q

have been associated with severe HDN and HTR

A

Anti-S, anti-s, and anti-U antibodies

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45
Q

Although usually reactive in the antiglobulin phase of testing, some saline reactive antibodies have been reported.

A

Anti-S, anti-s, and anti-U antibodies

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46
Q

In addition to human, rabbit, and monoclonal serum-typing reagents, lectin reagents are also used to test for

A

M and N antigens

47
Q

Examples include Vicia graminia and several Bauhinia species for [?], and several Iberis species for [?].

A

anti-N

anti-M

48
Q

demonstrate a dosage effect

A

Many M, N, and S antibodies

49
Q

they react more strongly with homozygous than heterozygous cells.

A

M, N, and S antibodies

50
Q

are destroyed by enzyme treatment

A

M and N antigens

51
Q

are not as easily destroyed or have no effect

A

S, s, and U

52
Q

The Kell (K) system is comprised of 21 high- and low-incidence antigens, the most significant of which are [?].

A

K and k

53
Q

lack all Kell antigens

A

K, or Knull phenotype

54
Q

An antigen associated with the Kell system, [?], Is located on the X chromosome.

A

Kx

55
Q

RBCs that lack the [?] also have greatly weakened expression of the other Kell system antigens.

A

Kx antigen

56
Q

These RBCs are morphologically acanthocytes, have decreased survival, and are less permeable to water.

A

Kx antigen

57
Q

This syndrome, known as [?], is also characterized by splenomegaly, reticulocytosis, and occasional association with chronic granulomatous disease (CGD).

A

MacLeod syndrome

58
Q

are destroyed or inactivated by sulfhydryl reagents.

A

Kell antigens

59
Q

The two most important antibodies of the Kell system are

A

anti-K and anti-k (Cellano)

60
Q

is second only to the D antigen in Immunogenicity, and the resulting antibody is relatively common in transfusion practice.

A

K antigen

61
Q

Finding donor units is rarely a problem, however, because more than 90% of the population is

A

K-negative

62
Q

are usually IgG antibodies that react best at 37C

A

Anti-K antibodies

63
Q

may occasionally bind complement

A

Anti-K antibodies

64
Q

They can cause both HDN and HTR

A

Anti-K antibodies

65
Q

are rare but can cause both HDN and HTR

A

Anti-k antibodies

66
Q

Antibodies to Ko (Knull) antigens are called [?]

A

anti-Ku or anti-KEL5 antibodies

67
Q

are considered clinically significant

A

Anti-Ku

Anti-KEL5

68
Q

Ko patients should be transfused with

A

K° cells.

69
Q

In testing, K, cells can be made by treating normal RBCs with

A

2- aminoethylisothiouronium (AET) bromide or dithiothreitol (DTT) plus cysteine- activated papain (ZZAP)

70
Q

is a rare condition occurring exclusively in males, inherited through an X-linked pattern from carrier mothers.

A

Mcleod phenotype

71
Q

• Individuals with the Mcleod phenotype lack the [?] and have reduced expression of other Kell antigens.

A

Kx and Km antigens

72
Q

• RBCs from individuals with the [?] often exhibit acanthocytosis, reduced deformability, and decreased survival, leading to chronic hemolytic anemia.

A

McLeod phenotype

73
Q

includes neurological and muscular disorders such as progressive muscular dystrophy, cardiomyopathy, areflexia, choreiform movements, and elevated serum enzyme levels

A

McLeod syndrome

74
Q

has been associated with X-linked chronic granulomatous disease (CGD), characterized by severe infections due to phagocytes’ inability to produce NADH-oxidase

A

McLeod phenotype

75
Q

explains the variable expression of Kx in carrier females, resulting in RBC populations with normal Kx expression and others exhibiting the McLeod phenotype characteristics.

A

Lyon hypothesis

76
Q

Duffy system (FY) has four alleles that are responsible for the major antigens and resulting phenotypes:

A

Fya, Fyb Fy, and Fyx

77
Q

are produced by codominant alleles.

A

Fya and Fyb antigens

78
Q

is a weakened form of Fyb

A

Fyx

79
Q

allele produces no gene product.

A

Fy

80
Q

There are four phenotypes:

A

a. Fy (a+b-)
b. b. Fy (a-b+)
c. c. Fy (a+b+)
d. d. Fy (a-b-)

81
Q

There is a high incidence of this phenotype among blacks.

A

Fy (a-b-)

82
Q

The RBCs of individuals with this phenotype are resistant to infection by Plasmodium vivax.

A

Fy (a-b-)

83
Q

The most common FY antibodies are [?], which are both commonly encountered in blood banks.

A

Fya and Fyb

84
Q

are very rare

A

Other Duffy antibodies

85
Q

are usually IgG

A

Anti-Fya and anti-Fyb antibodies

86
Q

often bind complement

A

Anti-Fya and anti-Fyb antibodies

87
Q

generally react only at the antiglobulin phase of testing

A

Anti-Fya and anti-Fyb antibodies

88
Q

Both are destroyed by proteolytic enzyme treatment and heating to 56°C

A

Anti-Fya and anti-Fyb antibodies

89
Q

[?] are seen more frequently than [?], and both occur more commonly in combination with other RBC antibodies than alone.

A

Anti-Fya antibodies

Fyb antibodies

90
Q

Although both can cause delayed HTR, only [?] has occasionally been implicated in HDN.

A

Fya

91
Q

There is a long-standing correlation between Duffy blood group antigens and [?].

A

malaria Infection

92
Q

Africans and black Americans, who typically lack the Duffy antigens Fy a and Fyb, have been found to be resistant to infection by [?], a malaria parasite.

A

Plasmodium vivax

93
Q

Studies conducted by Miller et al in 1955 demonstrated that [?] only invade red blood cells (RBCs) carrying normal Fya or Fyb antigens. Blocking these antigen sites with antibodies or denaturing enzymes rendered RBCs resistant to invasion,

A

malaria merozoites

94
Q

Based on in-vivo epidemiologic data and parallel resistance factors for [?] (a simian malaria parasite) and P. vivax in West African populations, it was suggested that Fya and Fyb might serve as the invasion receptors for P. vivax.

A

P. knowlesi

95
Q

The invasion process involves two receptor sites:

A

one for initial attachment and another for invasion.

96
Q

While [?] occurs irrespective of Duffy type, the subsequent junction and [?] are Duffy antigen-dependent.

A

initial attachment

invasion

97
Q

Studies indicate that [?], a component of the Duffy glycoprotein, is important for invasion by P. vivax.

A

Fy6

98
Q

Monoclonal antibodies targeting [?] have been shown to block invasion of RBCs by P. vivax,

A

Fy6

99
Q

There are two major antigens in the Kidd (JK) system, Jka and Jkb, which allows for four phenotypes:

A

(1) Jk (a+b-)
(2) Jk (a+b+)
(3) Jk (a-b+)
(4) Jk (a-b-)

100
Q

A third antigen, [?], is present on both Jka- and Jkb-positive RBCs.

A

Jk3

101
Q

may exhibit dosage effect

A

Jka and Jkb

102
Q

reactivity may be enhanced by enzyme treatment

A

Jka and Jkb

103
Q

poorly immunogenic

A

Jka and Jkb antigens

104
Q

resulting antibodies can cause severe HTR

A

Jka and Jkb antigens

105
Q

are especially noted for causing delayed reactions

A

Jka and Jkb antigens

106
Q

can occasionally cause mild HDN

A

Jka and Jkb antigens

107
Q

are IgG1 or IgG3

A

Jka and Jkb antibodies

108
Q

bind complement very efficiently

A

Jka and Jkb antibodies

109
Q

Both react best at 37•C in the antiglobulin phase of testing, but saline-reactive antibodies may be seen

A

Jka and Jkb antibodies

110
Q

can be difficult to detect

A

Jka and Jkb antibodies

111
Q

enhancement techniques, such as enzymes, low ionic strength saline (LISS), or polyethylene glycol (PEG), can help identify them.

A

Jka and Jkb antibodies

112
Q

: These organisms have been associated with Jkb-like specificity

A

Enterococcus faecium and Micrococcus

113
Q

They are capable of converting Jk(b) cells to Jk(b), indicating a potential interaction with the Jkb antigen.

A

Enterococcus faecium and Micrococcus

114
Q

: This organism may have triggered the production of an autoanti-Jkb, suggesting a possible autoimmune response induced by exposure to

A

Proteus mirabilis

[Immunohematology] Lec (35 decks)

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