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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
Clinical value of molecular RBC typing
- 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
RBC genotyping
- extract DNA (30mins) - prepare tests-microplate (10-30mins) - amplify DNA-thermocyclers (~2hours) - analysis (10mins)
27
Workflow of TaqMan probe PCR-SSP
- 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
Advantages of TaqMan probe PCR-SSP
- 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
Disadvantages of TaqMan probe PCR-SSP
- 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
What did Levine and Stetson (1939) report?
- 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
What did Levine and Stetson (1939) discover?
- all of their women were Rhesus -ve and husbands were Rhesus +ve - proposed that Rhesus -ve people should be transfused Rhesus -ve blood
32
What was Landsteiner and Wiener (1941)?
- 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
Rh system
- 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
The 5 commonly occurring antigens
- 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
RhD antigen frequencies in UK
- 85% Rh +ve | - 15% Rh -ve
36
Rh antibodies
- Anti D - Anti-c - Anti-E - Anti-C
37
Anti-D
- 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
Anti-c
- clinically significant - relatively common - may cause HDFN or Haemolytic Transfusion Reaction (HTR) - often found together w/anti-E
39
Anti-E
- 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
Anti-C
- clinically significant - HDFN rare on its own - relatively common; often seen w/anti-D - may cause HTR
41
Anti-e
- clinically significant | - may cause HTR
42
Rh combinations (antigen+short)
- 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
Variations of RhD groups
- Weak D | - Partial D
44
Weak D
- possesses all normal D antigens, but has quantitatively less - RhD +ve as a donor, patient and antenatal patient - can't produce anti-D
45
Partial D
- 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
IgM antibodies
- 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
IgG antibodies
- 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
ABO antibodies
- not present at birth; develop over 1st 4 months - 'naturally' occurring - present in general population
49
Where do ABO antibodies come from?
- some immunoglobulin just happens to 'fit' - via maternal milk - environmental factors - genetic basis
50
Antigen and antibody development
- 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
ABO RC antibody in plasma and antigen status
- AB; none, A+B - B; anti-A, B - A; anti-B, A - O; anti-A and B, none
52
Clinical significance of ABO antibodies
- 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
Haemolytic Disease of Foetus and Newborn (HDFN)
- 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
Main causes of HDFN
- anti-D (or D+C) - ABO - other IgG antibodies - anti-Kell - anti-c - anti-E - anti-Fya
55
Diagnosis of HDFN
- direct antiglobulin test on cord blood, detects antibody bound to infants RC surface - positive result is diagnostic of HDFN
56
Positive result of HDFN
- mild: phototherapy under UV light - moderate: top-up or exchange transfusion - severe: exchange transfusion at birth or Intra-Uterine Transfusion (IUT) during pregnancy
57
Relationship between antibody strength and HDFN outcome
- 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
First pregnancy with natural history of HDFN
- mother-foetus; nutrients, O2 and passive immunity | - fetus-mother; waste products and CO2
59
First pregnancy delivery with HDFN
- foetus-mother; small quantity of red cells
60
First pregnancy post delivery with HDFN
- 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
Subsequent pregnancy with HDFN
- mother-foetus; IgG directed against foetal RCs, nutrients and O2 - foetus-mother; waste products and CO2
62
Treatment - requirements for IUT/exchange transfusion red cells
- 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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