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Immunohematology > ABO > Flashcards

ABO Flashcards

1
Q

Landsteiner’s rule

A

normal healthy individuals possess ABO antibodies to the ABO blood group antigens absent from their RBCs

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2
Q

Location of ABO antigens

A

RBCs, lymphs, platelets, epithelial cells, endothelial cells, & organs

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3
Q

Soluble antigens are detected in :

A

secretions, body fluids

NOT in spinal fluid

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4
Q

ABO statistics:

A 
white: 
A-40% B- 11% AB -4% O-45%
black: 
A-27% B-20% AB-4% O-49%
native americans:
almost exclusively O
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5
Q

Hemostasis effect on type O persons

A

Von Wildebrand Factor is decreased up to 25% –> factor 8 is also decreased 25%

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6
Q

ABO precursor

A

H antigen is the precursor for A & B antigens
type I linkages: found only in fluids
type II: found on RBCs and secretions

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7
Q

H antigen

A

inherited independently of ABO (chromosome 19 vs 9)
H allele is dominant >99.99%
h is amorph
enzymatic linkage of a fucose residue creates H antigen

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8
Q

Interaction between ABO & H antigens on RBC

A

Type A & B RBCs have low levels of H antigen

O - very high levels of H antigen

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9
Q

A allele produces:

A

N-acetylgalactosaminyltransferase

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10
Q

B allele produces:

A

D-galactosyltransferase

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11
Q

Bombay phenotype

A

hh genotype
types like O forward
cannot produce precursor for ABO antigens & can only receive blood from another bombay

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12
Q

H antigen presence with each ABO type:

A

most H antigen : O>A2>B>A2B>A1>A1B least H antigen

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13
Q

A subgroups

A

A1 (80%)& A2(20%)
A1 is dominant over A2
distinguished w/ use of Anti-A1 lectin Dolichos biflorus

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14
Q

amount of A antigen present in A subgroups:

A

most A antigen: A1> A2> A3> Ax

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15
Q

Subgroup A2

A

less effective enzyme & causes a lower number of A antigens & they are not branched - leads to a specificity in A1 lectin binding

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16
Q

Subgroup A3

A

phenotype is a mixed field
anti-A,B gives a stronger reaction to weak subgroups than anti-A
no reaction with anti-A lectin; strong anti-H lectin reaction

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17
Q

Transfusion for patients with type A2

A

must transfuse with type O blood

patients have a potential to produce an anti-A1 antibody

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18
Q

A1 vs A2 testing

A

both will agglutinate w/ anti-A strongly
anti-A1 lectin will only aggluinate w/ A1 not A2
H lectin will react stronger with A2 cellls > A1

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19
Q

ABO antibodies

A

‘naturally occuring’ non-red cell stimulated antibodies
predominantly IgM
react best at room temp in saline
can activate complement-capable of causing an acute intravascular transfusion reaction

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20
Q

Anti-A,B antibody

A

group O individuals
single crossreactive antibody that will react w/ both A antigen & B antigen
primarily IgG
clinically significant bc of an O mother w/ a B or A type child

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21
Q

Anti-H antibody

A

made by only bombay phenotypes
reacts with all RBCs except other bombay
weak anti-H produced by A1 or A1B people

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22
Q

How to type a Bombay

A

initial type as an O
antibody screen results are 4+ against all the O type in the screen cells
further testing would show a 0 agglutination reaction against Anti-H

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23
Q

Forward typing

A

agglutination should be at least 2+, any weaker may indicate a discrepancy
performed at room temperature

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24
Q

Reverse grouping

A

detects presence or absence of ABO antibodies
performed at room temp
should be at least a 2+

25
Q

Selection of ABO-compatible products for transfusion

A

1st choice: identical phenotypes
2nd: ABO compatible
persons w/ O type are universal donors
persons w/ AB type are universal recipients

26
Q

recipient: A type
donor:

A

whole blood: group A
RBC: A & O
plasma: A, AB

27
Q

recipient: B type
donor:

A

whole blood: group B
RBC: B & O
plasma: B, AB

28
Q

recipient: AB type
donor:

A

whole blood: group AB
RBC: AB, A, B, O
plasma: AB

29
Q

recipient: O type
donor:

A

whole blood: group O
RBC: O
plasma: O, A, B, AB

30
Q

type I chains precursors

A

found in secretions
precursor substance is modified by FUT-2
FUT-2 is expressed only in secretory epithelial cells
results in secreted H substance + A or B antigens if A/B type

31
Q

type II chains precursors

A

found on RBC
precursor substance is modified by FUT-1
FUT-1 is expressed in cells of erythroid lineage
results in H antigen + A/B antigens on tissues & RBC

32
Q

Secretor status

A

two alleles of FUT2: Se & se
Se: functional gene = secretor
se: an amorph = no gene product
Se is responsible for soluble H substance
80% secretors (SeSe/ Sese); 20% non-secretor (sese)

33
Q

FUT1 & FUT2 gene relation

A

FUT1 & FUT2 are linked & inherited as haplotypes
FUT1- H allele
FUT2- Se allele
Bombay phenotype - occurs when 2 mutant copies of FUT1 & FUT2 are inherited

34
Q

Parabombay

A

low levels of H antigen
1. complete loss of FUT1 activity ( hh) but still have FUT2 intact (SeSe/Sese)
2. harbor one h allele & one mutant H allele that has low activity
will product an anti-H antibody

35
Q

Saliva neutralization studies

A

determine a person’s ABO type based on secreted A or B substance
A or B substance acts as a competitive inhibitor
no agglutination can be positive- antiA will bind to ‘free antigen’s on the saliva 1st & not on the RBC so no agglutination

36
Q

A1 expected reaction

A 
antiA: 4+
antiB: 0
anti-A,B: 4+
H lectin: weak
A1 lectin: 4+
A1 cells: 0
A2 cells: 0
B cells: 4+
37
Q

A2 expected reactions

A 
antiA: 3-4+
antiB: 0
antiA,B: 3-4+
H lectin: 2-3+ (!)
A1 lectin: 0 (!)
A1 cells: 0-1+ 
A2 cells: 0
B cells: 3+
38
Q

A3 expected reactions

A 
antiA: 2+ mf
antiB: 0
antiA,B: 2+ mf
H lectin: 3+
A1 lectin: 0 
A1 cells: 1-2+
A2 cells: 0
B cells: 3+
39
Q

B expected reactions

A 
antiA: 0
antiB: 4+ 
antiA,B: 4+
H lectin: 0
A1 lectin: 0
A1 cells: 4+
A2 cells: 4+
B cells: 0
40
Q

B(A) expected reactions

A 
antiA: weak-2+
antiB: 4+
antiA,B: 4+
H lectin: 0
A1 lectin: 0
A1 cells: 4+
A2 cells: 4+
B cells: 0
41
Q

Acquired B expected reactions

A 
antiA: 4+
antiB: 1+
antiA,B: 4+
H lectin: 0
A1 lectin: 4+
A1 cells: 0
A2 cells: 0
B cells: 4+
42
Q

B(A) phenotype

A

person is actually B phenotype & normal
sensitive antiA reagent just recognizes small amounts of A substances on cells
infrequently observed today due to reagent optimization

43
Q

Acquired B phenotype

A

person is actually an A
by disease or bacterial infection (especially intestinal infection) the terminal N-acetylgalactosamine is converted to galactosasmine
this will disappear upon clearing the infection

44
Q

Resolving ABO discrepancies

A
  1. repeat typing
  2. consider other errors:
    misID of patient, mislabeling of test tubes, recording improper results, failure to follow SOP, failure to add patient’s serum, over reading, failure to add correct antisera etc
  3. consider sample-related discrepancies:
    patient history- transfusions
    specimen RBC issues
    specimen plasma issues
45
Q

Reasons for extra antigens on RBC

A

group A w/ acquired B
B(A) phenotype-rare
polyagglutination-rbcs
transplantation

46
Q

reasons for weak/absent antigens on RBC

A

ABO subgroups
disease related
age related
transplantation

47
Q

reasons for extra antibodies in serum

A

ABO subgroups
cold allo/auto antibodies
rouleaux
intravenous injected IgG

48
Q

reasons for weak/absent antibodies in plasma

A

age
disease
transfusion
low levels of immunglobulins

49
Q 
patient:
antiA: 4+
antiB: 1+
A1 cells: 0
B cells: 0
A
  1. wash cells to remove possibility of rouleaux or a polyagglutination
  2. try a different source of antiB sera
  3. likely an acquired B phenotype- check patient history
50
Q 
patient:
antiA: 1+
antiB: 4+
A1 cells: 4+
B cells: 0
A
  1. wash patient RBCs-replace w/ saline
  2. use a second source of anti-A
  3. likely a B(A) phenotype
51
Q 
patient:
antiA: 0
antiB: 0
A1 cells: 0
B cells: 3+
A
  1. try to see antiA antigen w/ more sensitive reagent (antiA,B)
  2. can incubate forward typing for longer/ colder temp
  3. likely a subgroup of A if the antiA,B gives a positive reaction
52
Q 
Patient: 
antiA: 0
antiB: 2+mf
A1 cells: 4+
B cells: 0
A
  1. look up transfusion history
  2. what is person’s ABO type?
  3. what type were they transfused with
53
Q 
patient: 4+
antiA: 4+
antiB: 0
A1 cells: 2+
B cells:
A
  1. test patient RBC for an A subgroup w/ A1 lectin
  2. is the extra antibody an A1 antibody?
  3. test patient plasma against multiple A2 & A1 cells
54
Q 
patient: 
antiA: 4+
antiB: 4+
A1 cells: 0
B cells: 1+
A

possible explanations: cold auto/allo antibody (know its cold bc tests are done at immediate spin & no incubation (IgM)
perform screening tests w/ auto controls
if auto control 1+ that means its an autoantibody

55
Q 
patient:
antiA: 4+
antiB: 2+
antiD: 2+
Rh control: 2+
A1 cells: 2+
B cells: 2+
A

testing not valid due to Rh control

could be rouleaux- perform saline replacement & check patient history

56
Q 
patient:
antiA: 0
antiB: 0
antiD: 0
Rh control: 0
A1 cells: 0
B cells: 0
A

expect O typing w/ missing antibodies
present in neonatal, elderly immunocompromised
1. check patient history
2. repeat w/ longer incubation times @ colder temperatures

57
Q 
patient: 
antiA: 2+ mf
antiB: 0
antiD: 2+
Rh control: 0
A1 cells: 0
B cell: 3+
A
  1. check patient history- possible transfusion

2. test w/ antiA1 lectin

58
Q 
patient: 
antiA: 4+
antiB: 0
A1 cells: 2+
B cells: 4+
A
  1. test patient for A subgroup w/ A1 lectin
  2. is extra antibody an A1 antibody?
  3. test patient plasma against multiple A1 & A2 cells
  4. if not it may be a cold allo/auto antibody

Immunohematology (16 decks)

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