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HLB > Blood Groups and Blood Transfusion > Flashcards

Blood Groups and Blood Transfusion Flashcards

1
Q

Antigen definition

A

a protein which can stimulate an immune response

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2
Q

Antibody definition

A

proteins that are produced by the body in response to the introduction of a foreign antigen

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3
Q

Blood groups definition

A

a system of antigens in which the antigen specificity is controlled by specific genes

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4
Q

Agglutinate definition

A

to clump

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5
Q

Agglutinin definition

A

something that causes clumping

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6
Q

Monoclonal Antibody definition

A

lab produced and cloned molecules that bind specifically to one epitope (part of the antigen which an antibody recognises)

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7
Q

Patient is blood group A. Will they contain anti-A antibodies in plasma?

A

No
You don’t produce antibodies to antigens that you have

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8
Q

Blood Group antigens are present on the surface of

A
  • red blood cells
  • sometimes platelets and other
    body tissues (ABO)
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9
Q

Blood Group Antigens are —– characteristics

A

inherited

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10
Q

The blood group genes (via mRNA) either (2):

A
  • code for red cell membrane
    proteins directly

OR

  • code for enzymes which cause the
    production of specific red cell
    membrane carbohydrate sugars
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11
Q

2 examples of why blood group systems are so important (2)

A
  • sensitising events
  • after a blood transfusion when
    exposed to antigens you lack
  • during pregnancy, when fetal RBCs
    expressing antigens mother doesnt
    have (fathers) cross into maternal
    circulation
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12
Q

Blood group (allo) antibodies: sensitising events result in (4):

A
  • immediate catastrophic
    intravascular haemolysis via
    complement activation (ABO
    incompatability)
  • delayed haemolytic transfusion
    reactions
  • haemolytic disease of the foetus
    and newborn (HDFN)
  • problems in selecting blood for
    regularly transfused patients
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13
Q

The ABO System

A
  • ABO antigens are the most
    important blood group in relation
    to transfusion
  • also expressed on most endothelial
    and epithelial membranes
  • 4 main groups: A, B, AB, O with
    racial variation in population
    frequency
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14
Q

The structure of ABO blood antigens

A
  • RBC glycoproteins/lipids have a
    terminal sugar fucose
  • in addition, one of 2 enzymes can
    add another sugar, either galactose
    or N acetylgalactoasmine to the
    antigen making B antingen or A
    antigen
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15
Q

What type of gene control over blood groups?

A

Autosomal Co-dominance for A and B alleles

O is recessive

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16
Q

Autosomal co-dominance of A and B alleles

A

no antibodies for O because not an antigen

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17
Q

Allo antibodies vs auto antibodies

A

made in response to something foreign vs in response to a self antigen

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18
Q

Which enzyme makes antigen A, which blood group?

A
  • galactose
  • makes A antigen found in blood
    groups A and AB
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19
Q

Which enzyme makes antigen B, which blood group?

A
  • N-acetylgalactosamine
  • makes B antigen found in groups B
    and AB
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20
Q

Which enzyme makes antigen H, which blood group?

A
  • no further sugar added to terminal
    sugar fucose so no enzyme
  • makes antigen H
  • found in blood group O
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21
Q

Establishing the blood group based on the Antigen: a.k.a”Forward Grouping”

A
  • use a sample of patients RBC (eg
    antigen) and react test against
    monoclonal anti- A and anti-B
    grouping anti-sera
  • IgM antibodies causes
    haemagglutination of the RBCs
  • appears as clumping and formation
    of an aggregate where antigen and
    antibody react
22
Q

Which group is it?

A

insert table
1,2,3 = O
4,11,12 = A
5,8 = B

23
Q

Universal Blood Group Donor

A
  • O-
  • no antigens to react with
    antibodies in the patient’s blood
24
Q

Universal Blood Group recipient

A
  • AB
  • no antibodies in the patients blood
    to react with any blood given
25
Q

ABO blood group

A
26
Q

Why do we develop ABO antibodies?

A
  • in the absence of corresponding
    antigens, ABO antibodies form
    during the first few months after
    birth
  • probably as a result of exposure to
    ABH antigen like substance
    (diet, environment)***
  • antibodies are naturally occurring,
    rather than immune
  • mainly IgM antibodies
27
Q

Antibodies to blood group antigens are mainly

A
  • IgM or igG
  • IgM antibodies agglutinate blood
    cells and cause intravascular
    haemolysis because complement
    system activated
  • IgG typically binds to incompatible
    RBCs but do not directly agglutinate
    them - reactions are delayed
28
Q

Establishing the blood group (2) methods:

A
  • via antigen in serum
  • via antibody in serum
29
Q

Establishing the blood group based on the antibody in the serum: a.k.a “Reverse Grouping”

A
  • employs methods to detect the
    antibodies in serum to confirm the
    blood phenotype ie double check
    the blood group indirectly
30
Q

70 year old man called John Smith needs a blood transfusion
He is blood group A
What antibodies does he have?
What blood could he be given?

A
  • he has B antibodies
  • he can be given blood group A, and
    blood group O
31
Q

Another 70 year old man called James Smith also needs a blood transfusion
He is blood group B
What antibodies does he have?
What blood could he be given

A
  • he has antibodies for antigen A
  • he can be given blood group B and
    O
32
Q

Acute Haemolytic Transfusion Reactions due to ABO incompatibility:

A
  • RBC destruction - intravascular
    haemolysis
  • extreme cases lead to:
    - cardiovascular collapse/shock
    - renal failure
    - DIC (disseminated
    intravvascular coagulation)
  • 1/180,000 red cell units transfused
    may be ABOi:
    - major morbidity in 30%
    - 5-10% death
33
Q

Other blood group systems:

A
34
Q

The Rh blood Group System

A
  • Rh antigens are a component of
    RBC transmembrane protein
  • two genes RhD and RhCE are
    responsible for the anitgens
  • The RhD encodes for the
    membrane protein with the D
    antigen and RhCE encodes for
    membrane proteins with c or C and
    e or E antigens
35
Q

How many gene or haplotype combinations are there in the Rh blood group system?

A

8 possible gene or haplotype combinations

36
Q

What antigen is the most clinically important fo rthe Rh system?

A
  • D antigen
  • you either have the D antigen or
    not
  • the D antigen is a dominant trait
    (not DD and dd not gene?)
  • predominantly IgG anitbodies
37
Q

Variation of Rh blood group system

A
  • approx 85% of European
    population is Rh+
  • approx 15% of the population are
    Rh- and can therefore make
    antibodies to the D antibodies if
    exposed to it via transfusion or
    pregnancy
  • antibodies are predominantly IgG
38
Q

D antigen is —– and ——.

A
  • antigenic (strong reactions with
    antibody)
  • very immunogenic (good at
    stimulating the production of anti D
    antibody in D negative people who
    are exposed to the D antigen
39
Q

Sensitisation to Rhesus D antigen

A

in first pregnancy not rapid agglutination in the baby (antbodies for mum pass to baby and cause lysis of RBC) to cause a problem

40
Q

HDFN

A

haemolytic disease of the foetus and newborn

41
Q

Haemolytic Disease of the Foetus and Newborn:

A

in the second pregnancy, mum already has some antibodies, so more antibodies produced quickly, more pass to baby, more agglutination and lysis of RBC of baby

42
Q

How can prevent sensitisation (Rhesus) ?

A

Booking (10-12 weeks gestation) maternal blood samples for ABO and Rh group and red cell alloantibody screen
Give Routine Antenatal Anti D Prophylaxis (RAADP) for RhD-, non-sensitised women
Administration of anti-D IgG to a Rh- mother can protect against sensitisation of a Rh- mother from a Rh+ foetus, by destroying any foetal Rh+ red blood cells in maternal circulation.

  • prevents mum making her own anti
    D antibodies, product that has been
    manufactured hence doesnt cause
    haemolysis or cross the placenta in
    the same way

28 and 34 weeks or single larger dose at 28-30 weeks
Further doses of Anti-D immunoglobulin after ‘sensitising’ events to ‘mop up’ D antigen that has come over the placenta from mum to baby
Delivery, miscarriage, CVS, amnio, fall, trauma, APH

43
Q

If a patient has had a sensitising event, what do we do to stop the risk of developing anti- D antibodies?

A
  • Kleihauer test
  • Flow cytometry
44
Q

Kleihaur Test

A
  • sample of mum
  • look for foetal cells
  • estimate volume
  • red cells are foetal blood cells
  • pale cells are maternal blood cells
45
Q

Flow cytometry

A
  • more sensitive test
  • checks how much D antigen
    present
  • confirms volume present and gives
    more anti-D if needed
46
Q

Compatibility testing pre-transfusion

A
  • minimum requirement for all
    patients: check ABO
  • women of childbearing potential:
    RhD neg for RhD neg patients, Kell
    neg for Kell neg patients
  • frequently transfused patients:
    extended match
  • in patients who are found to have clinically significant antibodies, capable of causing transfusion reactions, units that are negative and safe are developed
47
Q

What can we transufe?

A

we rarely transufe whole blood
rather blood component therapy makes clinical sense as post patients require a specific element of blood (FFP, cyroprecipitate and buffy coats)

plasma derivatives

48
Q

Donor Selection and minimising infection transmission

A
  • donor eligibility questionnaire: health, lifestyle, travel, meds
  • specific precautions to reduced trnasmission of prio-associated diseases including vCJD
  • routine screening: Hep B, HIV, Hep C, syphillis, HTLV

special circumstances: malarial antibodies, west nile virus antibodies

49
Q

insert diagram

A

insert

50
Q

insert diagram

A

insert

51
Q

Transufsion process:

A
  • need for transufsion identified
  • blood prescribed
  • pt cannulated and blood sent for cross match
  • 2 samples required at different times
  • lab approves suitable unit
  • transport to clinical area
  • nurse checks
  • transfusion begins, with monitoring

HLB (49 decks)

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