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AP0509 Component 2 Exam > ABO Blood Group > Flashcards

ABO Blood Group Flashcards

1
Q

What is a blood group?

A
  • inherited character of red cell surface detected by a specific alloantibody
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2
Q

Blood group system

A
  • one or more antigens controlled at a single gene locus
  • or 2 or more very closely linked homologous genes w/little or no observable recombination
  • some are biochemically linked but genetically independent
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3
Q

ABO blood group percentages in UK

A
  • O 47%
  • A 42%
  • B 8%
  • AB 3%
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4
Q

ABO genotypes

A
  • A –> AA and AO
  • B –> BB and BO
  • AB –> AB
  • O –> OO
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5
Q

Biological role of blood groups

A
  • linked with anomalies of antigen expression with diseases/malignancy/coagulation/infection
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6
Q

Possible functions of blood groups

A
  • recognition of self and non-self
  • maintenance of cellular integrity
  • involvement in cell maturation
  • susceptibility or resistance to disease
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7
Q

ABO genes

A
  • presence of A+B blood groups is governed by 3 genes which code for glycosyltransferase enzymes
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8
Q

What are the 3 ABO genes and what chromosome are they located?

A
  • H gene on chromosome 19

- A+B genes on chromosome 9 (co-dominant alleles)

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9
Q

ABO system

A
  • terminal carbohydrate added to H substance depends on enzyme
  • H gene codes for H enzyme
  • A+B genes code for A or B enzymes
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10
Q

ABO subgroups and main subdivisions

A
  • there are no. of variations of ABO groups especially A antigen
  • A1 - 80%, A2 - 20%
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11
Q

A subgroup and genotype

A
  • A1 - A1A1, A1A2, A1O
  • A2 - A2A2, A2O
  • A2B - A2B
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12
Q

Precursor substance to H substance (ABO genetics)

A
  • H gene codes for transferase enzyme, which adds fucose residue to precursor
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13
Q

H substance to A substance (ABO genetics)

A
  • A gene codes for enzyme which adds N-acetylgalactosamine residue to H substance
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14
Q

H substance to B substance (ABO genetics)

A
  • B gene codes for enzyme which adds galactose residue to H substance
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15
Q

Alloantibodies production

A
  • can be found in 0.3-38% of population, variation depends on people tested and type of test used
  • sometimes no immunising event can be identified
  • immunisation may occur following: pregnancy, transfusion, transplantation
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16
Q

Red cell destruction

A
  • antibody-antigen binding on RC surface DOESN’T affect cell’s life span
  • immune destruction of RCs by 2 mechanisms which may be activated secondarily to antibody-antigen interaction
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17
Q

What 2 mechanisms are involved in immune destruction of RCs?

A
  • activation of complement and/or adherence to Fc

- compliment receptors on cells of monocyte/macrophage system

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18
Q

Other antibody identification techniques

A
  • PEG IAT, 2-stage IAT, enzyme IAT
  • capture R, albumin displacement, polybrene
  • NISS, LISS, BLISS, adsorptions, elutions, neutralisation
  • 37oC saline, 31oC saline, 4oC saline
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19
Q

Indirect Antiglobulin Technique

A
  • detects 37oC active antibodies
  • detects IgG antibodies
  • detects complement fixing antibodies
  • detects all Rh antibodies
  • antigen-antibody complex formed; AHG added, agglutination
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20
Q

20oC saline technique

A
  • good for resolving mixtures
  • detects antibodies which may give unclear IAT
  • detects IgM antibodies e.g. anti-M, N, PI, Lea, Leb, H, I and ABO
  • detects antibodies which are usually clinically insignificant
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21
Q

Enzyme treated cell techniques (Papain)

A
  • excellent in resolving mixtures
  • good for all Rh antibodies and anti-Jka, Jkb, Lea, Leb, PI
  • doesn’t affect anti-Fya, Fyb, M, N, S; these antigens destroyed by papain treatment
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22
Q

Panel cells

A
  • usually cell samples from 10 selected donors

- stored liquid in preservative solution

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23
Q

Specification of panel cells

A
  • all group O
  • include R1R1 (Cde) and R1wR1
  • include R2R2 (cDE), r’r (Cde) and r”r (cdE)
  • 3 rr (cde) homozygous expression of K, Fya, Fyb, Jka, Jkb, S, s and k
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24
Q

RCI - Molecular RBC typing

A
  • can provide full genetic type for highly prevalent antigens
  • simple 3 step procedure w/minimal ‘hands-on’ time, results in 3 hours
  • most technology (PCR cyclers) already present in H+I labs
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25
Q

Clinical value of molecular RBC typing

A
  • DAT +ve patients
  • multi-transfused patients
  • patients w/weak antigen expression
  • patients w/multiple antibodies
  • patients w/pan-reactive autoantibody that resists absorption procedures
26
Q

RBC genotyping

A
  • extract DNA (30mins)
  • prepare tests-microplate (10-30mins)
  • amplify DNA-thermocyclers (~2hours)
  • analysis (10mins)
27
Q

Workflow of TaqMan probe PCR-SSP

A
  • samples processed in a single day
  • 3 samples per run, 8 runs a day
  • results in 2.5hours approx
  • good reliability w/low failure rate
28
Q

Advantages of TaqMan probe PCR-SSP

A
  • most useful in multi-transfused cases
  • results can be obtained same day
  • reproducible, low fail rate
  • good concordance w/serological typing results
  • simple to use and not labour intensive
  • direct download of results
  • no significant wastage
29
Q

Disadvantages of TaqMan probe PCR-SSP

A
  • not suitable for urgent cases
  • not as fast as serological typing
  • not suitable for rare genotypes - require sequencing
  • ABO - simple serologically but complex genetically
30
Q

What did Levine and Stetson (1939) report?

A
  • agglutinating factor in blood of women w/jaundiced and anaemic babies
  • reacted w/ABO compatible husbands red cells
  • thought it could be a new blood group + cause of jaundice in infant
31
Q

What did Levine and Stetson (1939) discover?

A
  • all of their women were Rhesus -ve and husbands were Rhesus +ve
  • proposed that Rhesus -ve people should be transfused Rhesus -ve blood
32
Q

What was Landsteiner and Wiener (1941)?

A
  • immune serum in guinea pigs immunised w/blood from Rhesus monkeys reacted w/RCs from 85% from NY population
  • named this Rhesus factor
  • 85% Rh +ve, 15% Rh -ve
33
Q

Rh system

A
  • most important is D
  • RhD gene found on chromosome 1
  • unlinked RhAG gene on chromo 6 incorporates antigen into cell membrane
  • D +ve people have RhD gene
  • most D -ve people have RhD gene deletion
34
Q

The 5 commonly occurring antigens

A
  • D, C, c, E, e
  • inherited as group of 3
  • E and e; alleles on RHCE gene
  • C and c; alleles on RHCE gene
  • no d antigen, most RhD -ve individuals lack D antigen
35
Q

RhD antigen frequencies in UK

A
  • 85% Rh +ve

- 15% Rh -ve

36
Q

Rh antibodies

A
  • Anti D
  • Anti-c
  • Anti-E
  • Anti-C
37
Q

Anti-D

A
  • may be produced in males as result of transfusion w/D +ve blood
  • most potent + major cause of Haemolytic Disease of Foetus and Newborn (HDFN)
  • produced in women as result of sensitisation by RCs from D +ve foetus
38
Q

Anti-c

A
  • clinically significant
  • relatively common
  • may cause HDFN or Haemolytic Transfusion Reaction (HTR)
  • often found together w/anti-E
39
Q

Anti-E

A
  • clinically significant; less than anti-c
  • relatively common
  • may cause HDFN or HTR
  • often found w/anti-c in those who lack c and E antigens
40
Q

Anti-C

A
  • clinically significant
  • HDFN rare on its own
  • relatively common; often seen w/anti-D
  • may cause HTR
41
Q

Anti-e

A
  • clinically significant

- may cause HTR

42
Q

Rh combinations (antigen+short)

A
  • CdE-ry (extremely rare)
  • CDE-Rz (rare)
  • cde-r (1st order)
  • CDE-R1 (1st order)
  • cDE-R2 (1st order)
  • Cde-r1 (2nd order)
  • cdE-r” (2nd order)
  • cDe-Ro (1st order in black people, rare in white)
43
Q

Variations of RhD groups

A
  • Weak D

- Partial D

44
Q

Weak D

A
  • possesses all normal D antigens, but has quantitatively less
  • RhD +ve as a donor, patient and antenatal patient
  • can’t produce anti-D
45
Q

Partial D

A
  • lacks part of normal D antigen
  • can produce anti-D
  • can cause production of anti-D in D -ve recipient
  • regarded as RhD as a donor
  • RhD -ve as recipient
  • antenatal patients require anti-D prophylaxis
46
Q

IgM antibodies

A
  • 10 antigen binding sites
  • RCs repel one another and don’t come closer than within 12nm
  • a single one can bridge gap and cause agglutination of RCs
  • may find complement
  • don’t cross placenta
  • ABO blood group antibodies are IgM
  • generally minor clinical significance
  • work best at <37oC
  • pentameric structure
47
Q

IgG antibodies

A
  • 2 antigen binding sites
  • works best at 37oC
  • clinically significant
  • don’t usually bind complement
  • able to cross placenta
  • cause RC removal by extravascular haemolysis
  • single IgG can’t cause RC agglutination
  • binding site can only reach 10nm apart
  • monomeric structure
48
Q

ABO antibodies

A
  • not present at birth; develop over 1st 4 months
  • ‘naturally’ occurring
  • present in general population
49
Q

Where do ABO antibodies come from?

A
  • some immunoglobulin just happens to ‘fit’
  • via maternal milk
  • environmental factors
  • genetic basis
50
Q

Antigen and antibody development

A
  • Antigens; not fully developed at birth, development over 1st 1-2 years
  • Antibodies; not present at birth, 1st 4 months, reach max strength at 5 yrs
51
Q

ABO RC antibody in plasma and antigen status

A
  • AB; none, A+B
  • B; anti-A, B
  • A; anti-B, A
  • O; anti-A and B, none
52
Q

Clinical significance of ABO antibodies

A
  • highly clinically significant
  • IgM antibodies
  • work best at low temps
  • cause intravascular haemolysis (complement activation)
  • may cause fatal reaction in cases of incompatible transfusion
53
Q

Haemolytic Disease of Foetus and Newborn (HDFN)

A
  • condition affecting foetuses and newborn infants
  • most potent form results from RhD -ve mother + RhD +ve infant
  • blood group antibody in mother attacking RCs in infant which carry corresponding antigen inherited from father
54
Q

Main causes of HDFN

A
  • anti-D (or D+C)
  • ABO
  • other IgG antibodies
  • anti-Kell
  • anti-c
  • anti-E
  • anti-Fya
55
Q

Diagnosis of HDFN

A
  • direct antiglobulin test on cord blood, detects antibody bound to infants RC surface
  • positive result is diagnostic of HDFN
56
Q

Positive result of HDFN

A
  • mild: phototherapy under UV light
  • moderate: top-up or exchange transfusion
  • severe: exchange transfusion at birth or Intra-Uterine Transfusion (IUT) during pregnancy
57
Q

Relationship between antibody strength and HDFN outcome

A
  • moderate anti-D and anti-c
  • variable other specificities
  • useless ABO
  • poor anti-K and anti-E
  • theoretically: more IgG antibody in maternal circulation = more crosses placenta = more severe HDFN
58
Q

First pregnancy with natural history of HDFN

A
  • mother-foetus; nutrients, O2 and passive immunity

- fetus-mother; waste products and CO2

59
Q

First pregnancy delivery with HDFN

A
  • foetus-mother; small quantity of red cells
60
Q

First pregnancy post delivery with HDFN

A
  • mother is sensitised against foreign RC antigens on foetal RCs
  • antigens which are more fully developed on foetal cells are more likely to cause sensitisation
61
Q

Subsequent pregnancy with HDFN

A
  • mother-foetus; IgG directed against foetal RCs, nutrients and O2
  • foetus-mother; waste products and CO2
62
Q

Treatment - requirements for IUT/exchange transfusion red cells

A
  • Hct 0.5-0.6 for ET up to 0.7 for IUT
  • gamma irradiated
  • low level of anti-A and anti-B
  • 5 days old or less, CPD RCs
  • CMV negative
  • sickle cell negative
  • negative for any RC antibodies

AP0509 Component 2 Exam (21 decks)

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