Blood Group Systems Flashcards

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1
Q

When was circulation of blood discovered?

A

17th century

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2
Q

What type of blood did early transfusion involve?

A

Animal

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3
Q

When was the first transfusion give, who was it given by and what was it used to treat?

A

1818
Dr James Bundell
Treated Post-partum haemorrhage.

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4
Q

Why were blood transfusions so risky from 1818-1845?

A

The ABO blood systems were not properly understood.

Transfusions were also open vein and did consider anti-coagulation.

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5
Q

When and by who were the ABO blood groups first discovered?

A

1901 by Karl Landsteiner.

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6
Q

How did Karl Landsteiner contribute to blood grouping?

A

He made compatibility studies which lead to safer blood transfusions. He also discovered the ABO blood grouping system.

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7
Q

What is the difference in transfusion time between the 1940s and now and why?

A

Blood transfusions were often lengthy in the 1940s but now only last up to 4 hour to prevent bacterial build up.

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8
Q

What were the issues with blood transfusions in the 1940s and why did these occur?

A

Bacterial build up often occurred because the transfusions were carried out over such a Long period of time.

Transfusions often lead to clotting because the blood wasn’t anti-coagulated very well.

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9
Q

In the 1940s, what were blood transfusions mainly used to treat?

A

Gastrointestinal problems, especially in men.

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10
Q

Define antigen.

A

Any substance, which in appropriate biological circumstances, can stimulate an immune response.

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11
Q

What are the antigens when on the topic of blood grouping systems?

A

Antigens on the surface of the membranes of red blood cells.

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12
Q

Define antibody

A

Proteins occurring in body fluids which are produced in response to the introduction of a foreign antigen.

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13
Q

Define agglutination.

A

When Erythrocytes are joined by cross-linking of antibody molecules.

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14
Q

How is agglutination different from clotting?

A

Agglutination does not activate a clotting cascade.

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15
Q

How is agglutination helpful in blood grouping?

A

It is used to determine what blood group antigens are present in the red blood cells and what red cell antibodies are present in the blood plasma.

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16
Q

What is Landsteiner’s law?

A

Antibodies are always preset in a healthy person’s plasma against antigens not present on their red cells.

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17
Q

What % of the population are blood type A, B or AB?

A

55%

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18
Q

Why are most fatal transfusion caused by ABO incompatibility?

A

ABO antibodies are capable of producing intravascular haemolysis.

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19
Q

Where do we get A or B blood genes from?

A

Inherited from out parents.

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20
Q

How does a precursor substance become an A or B antigen?

A

The precursor substance which coats all red blood cells produces H transferase which causes the precursor substance to convert to a H antigen. Depending on the A or B gene present, the A or B transferase enzyme will convert the H antigen to a A or B antigen.

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21
Q

What causes the OO genotype?

A

The OO genotype produces non-functional transferases and therefore the H antigen is left unchanged and doesn’t become A or B.

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22
Q

What are Immunodominant sugars in terms of blood grouping?

A

The different A, B or H transferases which determine the antigen type produced.

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23
Q

Why are the different transferases with determine the antigen type immunodominant?

A

They form the antigenic part of the molecules.

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24
Q

How do A and B gene alleles work together when they are inherited?

A

They are Codominant.

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25
Q

How does the O allele for together with other alleles when inherited?

A

It is recessive.

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26
Q

Why do different ethnic groups express different antigens and antibodies more frequently?

A

Natural selection has forced different ethnic groups to select different antigenic makeup due to their different environment and different diseases in these environments.

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27
Q

In terms of COVID-19, which blood group is most likely to need to be hospitalised?

A

A

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28
Q

How do ABO antibodies cause intravascular lysis?

A

Anti-A, Anti-B and Anti A,B antigens can bind to A or B antigens and become haemolytic in vivo. This is caused by activation of the complement pathway to completion.

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29
Q

What is the universal red cell donor?

A

Group O

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30
Q

What is the universal red cell recipient?

A

Group AB

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31
Q

What is the universal plasma donor group?

A

Group AB

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32
Q

What is the universal plasma recipient group?

A

Group O

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33
Q

By what age are full strength ABO antibodies achieved?

A

Age 5

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34
Q

When may ABO antigens be in low numbers?

A

Below 5 years of age and in old age.

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35
Q

What is meant by a ‘high titre’ when referring to blood grouping?

A

People with a very high level of their specific antibody type.

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36
Q

Why do people often have a ‘high titre’?

A

High antibody strength of the mother due to giving birth to multiple babies of different blood types. This increases the antibody strength of the children.

Often has no explanation.

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37
Q

How is ABO Haemolytic disease of the foetus and new-born often caused?

A

Mothers who have had many babies of blood types A, B or AB often produce IGG antibodies which can pass through the placenta and cause haemolytic diseases of the new-born.

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38
Q

Why are group AB the universal plasma donor?

A

They have no antibodies.

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39
Q

What is the main use of group AB plasma donation?

A

It is sent to the military for emergency situations.

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40
Q

Why is group O the universal plasma recipient?

A

Because they have both A and B antibodies.

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41
Q

What is forward cell grouping to find someones blood type?

A

Using patients red blood cells reacted against monoclonal A or B antigens to identify the antigens present on a patients cell.

42
Q

What is reverse cell groping to find someones blood type?

A

Using the patients plasma reacted against A1 and B reagent red cells to identify the ABO antibodies that are present.

43
Q

What are the issues with identifying a blood group via the tiling method?

A

Issues with writing down results - transcription errors.

Easy to misinterpret results.

44
Q

Outline the column method of blood grouping.

A
  1. Patients cell suspension is added to the column.
  2. Anti-serum is contained in the gel matrix.
  3. Red cells carrying the antigen are trapped in the gel matrix.
  4. Red cells lacking the antigen travel to the bottom of the column.
  5. Reaction strengths are graded from (-) negative to strong positive (++++).
45
Q

Revise table showing what column results indicate what blood type.

A

-

46
Q

What should you do if you experience ABO blood grouping anomalies that don’t make sense?

A
  • Check the patients record to check the sample has come from the right person and hasn’t been mixed up.
  • Have they recently received a non-ABO transfusion which could alter the results.
  • Have they had a transplant (sometimes bone marrow transplants change blood type).
  • What are their clinical details ? (some diseases can alter and cause false positive results).
  • Age of the patient can cause ABO antibodies to act differently than expected.
47
Q

How does Cold Agglutinin Disease effect ABO grouping?

A

These people have auto antibodies where they form antibodies against their own red blood cells. This can give false positive results.

48
Q

What are the subgroups of blood type A?

A

A1, A2, A3, Ax

49
Q

What % of people of blood type A are A1?

A

78%

50
Q

How do people with the blood type A, subgroup A2 defy Lansteiner’s law?

A

They have the ability to form Anti-A1 antibodies.

51
Q

Can blood type A2 form anti A antibodies?

A

Yes

52
Q

What would a faint line in the A column of a blood grouping column test indicate?

A

An A subtype is present.

53
Q

What is an ‘acquired B’ blood type?

A

Group A individuals who produce a ‘B like’ antigen.

54
Q

Why does the blood type ‘acquired B’ often occur?

A

Associated with gastrointestinal bacterial diseases and colon cancer patients due to the action of bacterial enzymes.

55
Q

Why does loss of ABO antigens often occur?

A

Often occurs due to malignancy especially with myeloid Leukaemia.

56
Q

How can ABO antigens be used to determine the level of malignancy in a patient?

A

The population of red cells lacking A or B antigens correspond to the proportion of malignant stem cells a person has.

57
Q

Why is the prognosis of people with loss of ABO antigens due to malignant cells poor?

A

There has been a total loss of normal red blood cells due to haemopoeisis.

58
Q

Why does the blood type Oh occur?

A

hh group people lack the gene to convert the precursor substance on red blood cells to into H antigens so are unable to make A or B antigens.

59
Q

How many people per million have an Oh blood type?

A

4

60
Q

Where was the Oh blood type discovered and when?

A

Bombay, Mumbai in 1952

61
Q

To what blood groups can Oh individuals donate?

A

Any

62
Q

Which organs can Oh blood groups donate?

A

None

63
Q

Which blood groups will Oh blood types react to and why?

A

All blood types other than Oh because they have naturally occurring strong Anti-H antibodies.

64
Q

What are the 5 common antigens when discussing rhesus?

A
D
C
c
E
e
65
Q

On which chromosomes do the Rh genes D and CE lie?

A

1

66
Q

Which Rhesus genes lie on chromosome 1?

A

D and CE

67
Q

What antigen does D gene produce?

A

D

68
Q

What antigens does CE gene produce?

A

ce
Ce
cE
CE

69
Q

Why is the D antigen most clinically significant in the Rh system?

A

It is the most antigenic

It is the most immunogenic

70
Q

What is meant by the D antigen being the most antigenic?

A

It gives the strongest reactions with its antibody.

71
Q

What is meant by the D antigen being most immunogenic?

A

It is capable of readily stimulating antibody production

72
Q

In the UK, what % of people are RhD positive ?

A

85%

73
Q

Why and when do RhD negative individuals produce anti-D-allo-antibodies?

A

They are large membrane proteins so even a small amount of RhD positive blood will lead to these antibodies being produced.

74
Q

How many times should a patient be tested for the D antigen?

A

2

75
Q

What is the nomenclature for having a rhesus positive gene?

A

D

76
Q

What is the nomenclature for having a rhesus negative gene?

A

d

77
Q

What is a weak D gene?

A

Quantitative difference in number of antigen sites on red blood cells. They do not form Anti-A-allo-antibodies.

78
Q

Describe the reaction of weak D antigens to antiserum?

A

Weak

79
Q

What causes weak D genes?

A

A mutation in the interior of the D molecule.

80
Q

What antibodies can’t a weak D gene form?

A

Anti-A-allo-antibodies

D antibodies

81
Q

What are partial D genes?

A

They have a qualitative difference in antigens but can still form all-antibodies to the missing section of the antigen.

82
Q

What causes partial D genes?

A

Mutations of the outside of the D molecule.

83
Q

Describe whether partial d types are RhD positive or negative as donors and recipients.

A

RhD positive donors

RhD negative recipients

84
Q

What are the issues when treating Rh matched blood.

A

ccDee phenotype is not found in the white population.

Ro prevent stimulation of anti-C or anti-E antibodies so they must use RhD negative blood. This then puts pressure on the RhD negative donation supply.

85
Q

What % of the population are red negative?

A

15

86
Q

What is Lewis blood grouping?

A

Antigens are adsorbed onto red cell membranes rather than integral.

87
Q

What is Kell blood grouping used for?

A

Anti-K causes foetal anaemia so the presence of anti-K in the blood should mean that people with child bearing potential should be treated with K-blood.

88
Q

What is the selective advantage of being blood group Fy(a-b-) in terms of Duffy blood grouping?

A

This confers resistance to malaria.

89
Q

What are the issues with having Kidd antibodies?

A

Kidd antibodies are notorious for causing delayed transfusion reactions that can be fatal.

90
Q

In what type of people is the S-s gene of MNS blood grouping found?

A

Not in white people.

91
Q

What is the reagent used to carry out blood grouping called?

A

Antisera

92
Q

What is antisera?

A

The liquid reagent used to determine good group antigens present on the red cell surface.

93
Q

What is contained in antisera?

A

A liquid solution of monoclonal antibodies.

94
Q

Outline how ‘front grouping’ works in terms of identifying a blood group

A

It takes red cells from the patient and mixes them with antisera (Anti-A or Anti-B).

95
Q

How is a positive reacting shown in front group blood grouping and how does this occur?

A

Positive result is agglutination as the antibodies in the antisera finds the corresponding antigens on the red cells

96
Q

How is a negative front grouping blood grouping result shown and why does this occur?

A

There is no agglutination because the antisera contains antibodies, but the corresponding antigens arn’t present on the red cells.

97
Q

State the red blood cell type, antibody type in the plasma and antigens in the red blood cells of a person with blood group A

A

Red blood cell type = A
Antibodies in plasma = B
Antigens in Red Blood Cell = A

98
Q

State the red blood cell type, antibody type in the plasma and antigens in the red blood cells of a person with blood group B

A

Red blood cell type = B
Antibodies in plasma = A
Antigens in Red Blood Cell = B

99
Q

State the red blood cell type, antibody type in the plasma and antigens in the red blood cells of a person with blood group AB

A

Red Blood cell type = AB
Antibodies in plasma = None
Antigens in Red blood cells = A and B

100
Q

State the red blood cell type, antibody type in the plasma and antigens in the red blood cells of a person with blood group O

A

Red blood cell type = O
Antibodies in plasma = A and B
Antigens in red blood cell = None

101
Q

Outline what ‘back group’ blood grouping is

A

Using known A and B red cells but reacting them against a patients plasma.