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Transfusion Medicine Fellowship > Blood groups > Flashcards

Blood groups Flashcards

1
Q

What drives hyperacute solid organ rejection?

A

Major ABO incompatibility resulting in thrombosis due to recipient anti-A/anti-B.

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2
Q

When is ABO detectable in development? When do the antibodies form?

A

Detectable at 5wks in diminished quantity (due to non-branching i chains). Antibodies develop at 3-6mo and increase until 5-10yrs.

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3
Q

What factors can drive higher anti-ABO titers in donors?

A

Multiparity, probiotic use

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4
Q

What is the difference between the A and B glycosyltransferases?

A

Only 3 amino acids differ. Hybrids between the two may have specificity for both sugars (cis-AB)

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5
Q

What is the O glycosyltransferase?

A

Actually loss of the A/B sugar transferase, usually due to frameshift or nonsense mutations.

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6
Q

How does A1 subgroup differ from A2 subgroup?

A

A1 has about 5x as much A antigen, also qualitative differences probably reflecting contributions to T3 and T4 chains.

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7
Q

What is B(A) phenotype?

A

An autosomal dominant trait that results in weak expression of A antigen in predominantly group B patients (ie, a B transferase that can transfer NAcGlc)

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8
Q

What causes acquired B? How can it be avoided from the lab’s perspective?

A

Bacterial deacetylation of GlcNAc to Glc. Can be affected by reagent pH and specific anti-B clones (ES-4), so avoid those and use acidified reagent.

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9
Q

What is the order of blood groups by decreasing H antigen expression?

A

O > A2 > B > A2B > A1 > A1B

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10
Q

How do Bombay phenotype patients present on lab workup? What causes it? Associations?

A

“O” patients that show panagglutination to reagent O cells and no Ulex agglutination. Caused by loss of both FUT1 (missense) and FUT2 (deletion). Associated with leukocyte adhesion deficiency.

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11
Q

What is para-bombay phenotype?

A

Expression of FUT2 but not FUT1 (only secreted H antigen). Some soluble H antigen can adsorb onto red cells, resulting in “Ah/Bh/ABh/Oh” phenotype, but they still don’t really react with Ulex and can express anti-H.

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12
Q

Where is anti-H seen?

A

In Bombay, para-bombay, but also randomly in healthy A1 and A1B people (not significant in these cases)

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13
Q

On what chains are Lewis antigens expressed?

A

Type 1 chains

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14
Q

Who may express both Lewis A and B antigens?

A

Infants (during development, secretor enzyme is weak) and asians (FUT2 variant “SeW”).

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15
Q

When does lewis antigen expression mature?

A

5-6 years of age.

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16
Q

What condition is associated with Le(a-b-) phenotype in African American patients?

A

Leukocyte adhesion deficiency. (E and P selectins bind CD15, or sialyl-lewis X)

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17
Q

What is the difference between I and i?

A

The degree of branching in the type 2 chain backbone sugar; I is branched, i isn’t. I is adult, i is pediatric (mostly).

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18
Q

i(adult)

A

Results from autosomal recessive GCNT2 mutations, mostly in asians. Associated with HEMPAS, congenital dyserythropoietic anemia, and cataracts (not in all forms).

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19
Q

Anti-I

A

Auto: Strong cold-reacting IgM
Allo: Only seen in i(adult), insignificant

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20
Q

Cold agglutinin syndrome

A

Autoanti-I/i seen in cancer or mycoplasma infection. Can cause hemolysis if thermal amplitude is broad.

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21
Q

How are P, Pk, and P1 made?

A

Pk is synthesized from lactosylceramide.
P (globoside) is synthesized from Pk
P1 is synthesized from Paragloboside.

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22
Q

How many P phenotypes are there? What are they?

A 
P1 (common) - P+/Pk+u/P1+
P2 (uncommon) - P+/Pk+u/P1-
p (rare) - No antigens
P1k (rare) - P-/Pk+/P1+
P2k (rare) - P-/Pk+/P1-
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23
Q

What anti-P group antibodies are significant?

A

Anti-PP1Pk (seen in p phenotype).

Anti-P (allo in Pk, auto in PCH)

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24
Q

What is FORS?

A

A single low-prevalence antigen attached to P antigen which resembles A (may react with anti-A). Encoded by GBGT1 (Forssman synthase).

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25
Q

Racial distribution of P phenotypes

A

P1: Black > White > Asian
P2: Asian > White > Black
All others rare

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26
Q

What are the relationship of RHD and RHCE?

A

They have 97% structural homology and are inverted from one another. Likely arose from a duplicationh event.

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27
Q

What are the different mechanisms of RHD negative phenotype?

A

White: Deletion of whole gene from nonsister chromatic exchange.
Black: Nonfunctional pseudogene with early stop codon (psi)
Asian: Silencing gene mutation or Del

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28
Q

What is the Ceppellini effect?

A

Less D antigen is expressed when C is expressed.

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29
Q

Weak D

A

Abnormal localization of D because of a SNP resulting in less surface D. Some may form anti-D.

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30
Q

Partial D

A

Partial replacement of RHD with RHCE&raquo_space; loss of some D epitopes. Apparently D+ patient can develop anti-D.

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31
Q

Del

A

Extremely low D expression, only detectible by adsorption/elution.

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32
Q

Elevated D

A

Replacement of RHCE by RHD.

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33
Q

What percentage of D-negative patience will alloimmunize following exposure?

A

30%

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34
Q

G antigen

A

Epitope common to C and D, antibodies are reactive with both and must be eluted with D-/C+ and D+/C-

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35
Q

Altered C

A

Whites: Expression of Cw (Gln41Arg) or Cx (Ala36Thr)
Blacks: Novel antigens JAKH (122) and JAL (114), but also V-VS+ phenotype

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36
Q

Partial e

A

Seen in *ce alleles in black pateince. Loss of high prevalence hr(b), hr(s).

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37
Q

Compound antigens

A 
Epitopes resulting from specific haplotypes...
f - ce
Rhi - Ce
Rh22 - CE
Rh27 - cE
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38
Q

What are the utilities for Rh genotyping?

A

To check zygosity
Fetal testing
Resolves typing discrepancies

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39
Q

What is RHAG?

A

A gene on chromosome 6 with limited homology with RHD and RHCE. Plays a role in stabilizing Rh proteins.

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40
Q

Rh null phenotype

A

Rhnull (“regulator”) phenotype causes loss of all RH antigens. Associated with stomatocytosis nad mild anemia.

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41
Q

What anti-Rh antibody other than D most often causes HDFN?

A

Anti-c

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42
Q

What are some causes of false-positive Rh typing?

A

Agglutinins, rouleaux, contamination/wrong reagent, gel/diluent antibody.

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43
Q

What are some causes of false-negative Rh typing?

A

Bad suspension, wrong reagent, failure to detect weak D (on IS), strongly positive DAT blocking antigen sites

44
Q

What proteins comprise the Rh complex?

A

RHD, RHCE, RHAG, CD47, protein 4-2, ankyrin 3, duffy, glycophorins B & C

45
Q

What is the main structural difference between glycophorins A and B? How do they react to enzymes?

A

Glycophorin A is N-glycosylated, Glycophorin B isn’t. Both are degraded by ficin/papin. Glycophorin A is trypsin sensitive, while glycophorin B is chymotrypsin sensitive.

46
Q

What antigens result from the “B-A-B” hybrid glycophorin?

A

Mur, MINY, Hil, Mi(a)

47
Q

Is there any racial distribution of MNS antigens and antibodies?

A

Not for M/N, but S is more common in whites, so blacks more often express anti-S as well as anti-S-s-U-.

48
Q

In what tissues are glycophorins A & B expressed? Are they pathogenic binding sites?

A

Glycophorin A is restricted to erythroid lineages, but glycophorin B is not. Both are binding receptors for Plasmodium Falciparum

49
Q

What is the structure and function of the Lutheran blood group?

A

Laminin (but with no known ligand).

50
Q

How is Lutheran blood group affected by enzyme treatment?

A

Resistant to ficin/papin, but degraded by trypsin/chymotrypsin.

51
Q

Summarize Lutheran antibodies.

A

Usually IgG but insignificant. Watch for LuA, LuB, and Lu3 (from null homozygotes). Classically causes MIXED FIELD AGGLUTINATION

52
Q

In(Lu)

A

Asymptomatic phenotype resulting from heterozygous EKLF/KLF1 muation, with reduced expression of Lu, P1, and i.

53
Q

What is the antigen prevalence of KEL1 in different races?

A

9% in whites
2% in blacks
<1% in asians

54
Q

Kp(a) (KEL3)

A

Found in 2% of whites, this antigen causes reduced expression of all other Kell antigens.

55
Q

Js(a)

A

Found in 20% of black patients, vanishingly rare in all other races.

56
Q

What are the features of HDFN due to anti-K?

A

Less amniotic and postnatal hyperbilirubinemia; presents instead as erythrosuppression with decreased reticulocytes.

57
Q

Ko

A

Kell null phenotype; Kx is preserved but all other antigens are lost. Patients are asymptomatic but can develop an anti-Ku that reacts to all Kell antigens other than Kx.

58
Q

Kmod

A

Reduced but not absent Kell antigen expression, can manifest Anti-Ku-like antibody.

59
Q

Expression of what non-Kell antigens can express Kell expression?

A

Gerbich (absence of Ge2/Ge3 lowers Kell expression)

60
Q

McLeod phenotype

A

Kx deletion, associated with muscular and neural dystrophies and acanthocytosis. May be associated with CGD (these patients also produce anti-Kx and anti-Km and are nearly impossible to transfuse).

61
Q

What is the structure and function of Duffy?

A

Chemokine receptor (scavenger?) that is widely expressed.

62
Q

What is the basis of duffy null phenotype in Africans?

A

Homozygous GATA promoter binding site mutation of FY*B abrogates expression in erythrocytes.

63
Q

What is the basis of duffy null phenotype in whites?

A

True duffy null due to inactivating mutations. These patients can produce anti-Fy3, anti-Fy5.

64
Q

What is the basis of duffy null phenotype in pacific islanders and in Brazil?

A

Homozygous GATA promoter binding site mutation of FY*A abrogates expression in erythrocytes.

65
Q

What is the binding receptor for plasmodium vivax?

A

Duffy

66
Q

What are the three relevant Kidd antigens?

A

JkA (more common in blacks than B)
JkB
Jk3 (antibodies seen in null patients)

67
Q

In(Jk)

A

Seen in some Japanese patients due to presence of an inhibitor. Very weak kidd expression.

68
Q

Summarize Kidd antibodies.

A

Half can bind complement, as they are often mixtures of IgG and IgM. Often weak and anamnestic on pre-transfusion testing. Rarely causes HDFN.

69
Q

Kidd null phenotype

A

Cells resist lysis in 2M urea

Patients can express anti-Jk3

70
Q

What is the diego antigen?

A

Band 3 (SLCA1), a major cytoskeletal protein that complexes with ankyrin, protein 4.1/4.2; also an ion transporter and gas channel.

71
Q

Di(a)

A

Low-prevalence diego antigen antithetical to Di(b). Seen in asians and native americans. Antibodies cause HDFN, but not HTR.

72
Q

Wr(a)

A

Low-prevalence diego antigen antithetical to Wr(b). Common antibody that can cause severe HTRs and HDFN.

73
Q

Yt(a) and Yt(b)

A

Yt(a) high prevalence and Yt(b) low prevalence antigens of Cartwright system. Acetylcholinesterase.

74
Q

What is unique about the XG blood group system?

A

Despite being on the X chromosome, this gene does not undergo lyonization.

75
Q

What are the two antigens of the XG blood group system?

A

Xg(a): Found on 66% of males and 89% of females.

XG2 (CD99): Also expressed on Y chromosomes.

76
Q

Scianna blood group system

A

“ERMAP”, a pretty insignificant blood group system with 7 (“sceven”) antigens

77
Q

What are the significant antigens of the Dombrock blood group system?

A

Do(a) < Do(b).
>Gy(a) in rare dombrock-null patients.
Antibodies here cause HTR but not HDFN.

78
Q

What are the significant antigens of the Colton blood group system?

A

Co(a)&raquo_space; Co(b)
>Co3 in rare Colton-null patients.
Antibodies can cause HTR but not HDFN.

79
Q

What are the significant minor blood group systems?

A

Dombrock, Colton, VEL, Diego

80
Q

In what contexts can anti-Lw antibodies be seen?

A

Lw(a) and Lw(b) homozygotes, rare LW-null and Rh-null patients (LW expression depends on Rh).

81
Q

How can anti-Lw antibodies be distinguished from Anti-D?

A

LW is degraded by DTT.

82
Q

Chido/Rodgers blood group

A

C4D.

9 antigens, insignificant.

83
Q

What abnormal red cell morphology can be seen in Gerbich-null patients? What antibodies do they form?

A

Elliptocytes. Can form anti-Ge2, -Ge3, -Ge4.

84
Q

What is the Gerbich blood group system?

A

Glycophorins C and D

Receptor for plasmodium falciparum (also true of glycphorins A and B).

85
Q

Cromer blood group system

A

CD55 (DAF)
Falciparum binding receptor. Insignificant in blood banking.
(absence does not result in PNH, need to lose CD59 too)

86
Q

Knops blood group system

A

CD35 (complement receptor)

Insignificant blood group system, falciparum binding receptor.

87
Q

Indian blood group

A

In(a)&raquo_space; In(b). In(Lu) cells useful for testing for >AnWj?

88
Q

OK blood group

A

CD147

3 antigens: All high prevalence, all insignificant.

89
Q

Raph blood group

A

CD151 (absence a/w deafness and renal failure)

Insignificant.

90
Q

JMH blood group

A

CD108; loss of expression with age causes accumulation of auto-anti-JMH. Insignificant.

91
Q

GIL blood group

A

AQP3. Insignificant.

92
Q

RHAG blood group

A 
4 antigens (Duclos, DSLK, Ola, RHAG4).
Abnormalities result in Rh-regulator phenotype.
93
Q

FORS blood group

A

Terminal sugar on GLOBOSIDE (P). Encoded by GBGT1. Low frequency.

94
Q

JR blood group

A

One antigen, associated with drug resistance. Negative in Japanese.

95
Q

LAN blood group

A

High prevalence, insignificant

96
Q

VEL blood group

A

High prevalence, significant (severe HTR)

97
Q

CD59

A

One case report, insignificant.

98
Q

Augustine

A

ENT1/At(a), nulls have bone malformations. Insignificant.

99
Q

AnWj

A

Haemophilus influenzae receptor, carried on CD44/UIn

100
Q

What are the Bg antigens?

A

HLA antigens. Some have known specificities:
Bg(a) = HLA-B7
Bg(b) = HLA-B17
Bg(c) = HLA-A28

101
Q

What erythroid phenotypes are caused by KLF1 mutations?

A

Heterozygosity in KLF1 causes In(Lu) phenotype, resulting in lowered expression of antigens on CD44 (In, AnWj) and P1. Also results in abnormal beta-globin expression resulting in persistence of fetal hemoglobin.Some mutations cause a severe congenital dyserythropoietic anemia.

102
Q

Where is the Landsteiner-Wiener antigen located? In what settings can LW-null phenotypes be seen?

A

It is associated with the Rh system; expression of LW is higher in D+ patients. Some cases of LW-null phenotype occur with Rh-null phenotype.

103
Q

How can anti-D be distinguished from anti-LW?

A

Use DTT-treated cells (degrades LW antigen, but not D). Or, just use molecular testing.

104
Q

How many A antigens per RBC are seen in A1 subgroup? A2?

A

A1: About 10^6 (one million).
A2: About 2 x 10^5 (200,000).

105
Q

What non-ABO antibodies may be naturally occurring?

A

> E
Lu(a)
Di(a)
M. >N (mostly IgM)

106
Q

What is the most common autoantibody specificity other than broad?

A

Anti-E

107
Q

What is the human RBC binding site of C3b?

A

Glycophorin B (may not be only binding site)

Transfusion Medicine Fellowship (34 decks)

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