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Immunohematology > ABO > Flashcards

ABO Flashcards

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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

Study These Flashcards
A

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

25
Selection of ABO-compatible products for transfusion
1st choice: identical phenotypes 2nd: ABO compatible persons w/ O type are universal donors persons w/ AB type are universal recipients
26
recipient: A type donor:
whole blood: group A RBC: A & O plasma: A, AB
27
recipient: B type donor:
whole blood: group B RBC: B & O plasma: B, AB
28
recipient: AB type donor:
whole blood: group AB RBC: AB, A, B, O plasma: AB
29
recipient: O type donor:
whole blood: group O RBC: O plasma: O, A, B, AB
30
type I chains precursors
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
type II chains precursors
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
Secretor status
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
FUT1 & FUT2 gene relation
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
Parabombay
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
Saliva neutralization studies
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
A1 expected reaction
``` antiA: 4+ antiB: 0 anti-A,B: 4+ H lectin: weak A1 lectin: 4+ A1 cells: 0 A2 cells: 0 B cells: 4+ ```
37
A2 expected reactions
``` 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
A3 expected reactions
``` 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
B expected reactions
``` antiA: 0 antiB: 4+ antiA,B: 4+ H lectin: 0 A1 lectin: 0 A1 cells: 4+ A2 cells: 4+ B cells: 0 ```
40
B(A) expected reactions
``` antiA: weak-2+ antiB: 4+ antiA,B: 4+ H lectin: 0 A1 lectin: 0 A1 cells: 4+ A2 cells: 4+ B cells: 0 ```
41
Acquired B expected reactions
``` antiA: 4+ antiB: 1+ antiA,B: 4+ H lectin: 0 A1 lectin: 4+ A1 cells: 0 A2 cells: 0 B cells: 4+ ```
42
B(A) phenotype
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
Acquired B phenotype
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
Resolving ABO discrepancies
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
Reasons for extra antigens on RBC
group A w/ acquired B B(A) phenotype-rare polyagglutination-rbcs transplantation
46
reasons for weak/absent antigens on RBC
ABO subgroups disease related age related transplantation
47
reasons for extra antibodies in serum
ABO subgroups cold allo/auto antibodies rouleaux intravenous injected IgG
48
reasons for weak/absent antibodies in plasma
age disease transfusion low levels of immunglobulins
49
``` patient: antiA: 4+ antiB: 1+ A1 cells: 0 B cells: 0 ```
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
``` patient: antiA: 1+ antiB: 4+ A1 cells: 4+ B cells: 0 ```
1. wash patient RBCs-replace w/ saline 2. use a second source of anti-A 3. likely a B(A) phenotype
51
``` patient: antiA: 0 antiB: 0 A1 cells: 0 B cells: 3+ ```
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
``` Patient: antiA: 0 antiB: 2+mf A1 cells: 4+ B cells: 0 ```
1. look up transfusion history 2. what is person's ABO type? 3. what type were they transfused with
53
``` patient: 4+ antiA: 4+ antiB: 0 A1 cells: 2+ B cells: ```
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
``` patient: antiA: 4+ antiB: 4+ A1 cells: 0 B cells: 1+ ```
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
``` patient: antiA: 4+ antiB: 2+ antiD: 2+ Rh control: 2+ A1 cells: 2+ B cells: 2+ ```
testing not valid due to Rh control | could be rouleaux- perform saline replacement & check patient history
56
``` patient: antiA: 0 antiB: 0 antiD: 0 Rh control: 0 A1 cells: 0 B cells: 0 ```
expect O typing w/ missing antibodies present in neonatal, elderly immunocompromised 1. check patient history 2. repeat w/ longer incubation times @ colder temperatures
57
``` patient: antiA: 2+ mf antiB: 0 antiD: 2+ Rh control: 0 A1 cells: 0 B cell: 3+ ```
1. check patient history- possible transfusion | 2. test w/ antiA1 lectin
58
``` patient: antiA: 4+ antiB: 0 A1 cells: 2+ B cells: 4+ ```
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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