Blood Groups Flashcards
Identify the main blood group systems.
ABO
Rhesus
How many blood group systems are there ?
26
What property distinguishes different blood groups ?
Antigens on Surface of Red Blood Cells
Describe Antibody-Antigen reactions.
Antibody from B cells in response to non-self antigens presented to T cells
• IgG antibodies occur mainly after exposure to blood transfusions or foeto-maternal transmission
(after exposure to blood group antigens which we do not have, for instance kKell negative person transfused Kell positive blood)
• IgM antibodies (naturally occurring) occur due to components in food which mimic A and B antigens
(for instance, O has naturally occurring anti A and anti B, not formed as a result of exposure to other blood groups, formed naturally early on in life)
Describe the structures of antibodies.
2 heavy chains with N terminal and C terminal end of proteins
2 Light chains attached to each heavy chain
FC portion (the first portion of the 2 heavy chains together) FAB portion (2 of them, the second portion of each of a heavy and light chain together)
What are the functions of the Fc and Fab portions of an antibody ?
Fab portion: binds antigen
Fc portion: binds phagocyte, complement activation
Are antibodies specific for particular antigens ?
Yes
Describe the structure of IgM.
IgM antibody normally circulates as 5 antigen recognising sites (pentamer)
Has J chain linking all 5 single antibodies
Describe the transfusion reactions which may arise following the recognition of an antigen on a blood cell by IgM and IgG respectively.
In both cases, immune haemolysis (
IgG
As a result of binding with IgG antibodies, red cells have shortened survival but are at least not destroyed in circulation (Fc receptors on splenic macrophages bind Ig-G coated red cells, which may then gradually be destroyed)
IgM
IgM antibodies agglutinate red cell, then activates complement and the membrane attack complex rapidly destroys red cells
Describe the main features of the ABO blood group system.
- FUT1 and FUT2 genes (chromosome 19) code for H substance
- H antigen is a precursor to each of the ABO blood group antigens
- Virtually everyone will produce this H substance
- Some people will, in addition, have genes for blood group A or B or one of each.
- Naturally occurring anti-A and/or B IgM antibodies in individuals lacking these antigens
- A and B genes (chromosome 9) code for glucosyl transferases which add further sugar groups
How may ABO antigens be distinguished ?
- ABO antigens differ in their sugars
- FUT1 and FUT2 genes will code for string of 5 sugars (lipid tail then glucose, galactose, N-Acetylglucosamine, galactose, fucose) which virtually everyone has. Lipid tail attached to red cell membrane whilst sugars sick out into plasma.
- O antigen is just an H antigen (5 sugar chain) without additional A or B antigens
- People who also have genes for A or B antigen, that codes for one more sugar (galactose for B antigen, and N-acetylgalactosamine for A antigen)
State the naturally occurring antibodies produced for each of the existing blood antigens (as part of the ABO system), and the frequency of each antigens.
O antigen - anti-A and anti-B - 46% frequency
A antigen - anti-B - 42% frequency
B antigen - anti-A - 9% frequency
AB (A and B antigens) - no naturally occurring antibodies - 3% frequency
What is the shelf life of RBCs, platelets, and plasma ?
RBCs: 35 days
Platelets: 7 days
Plasma: 2 years
Describe the main features of the Rhesus system.
- Antigens c C D e E
- coded for on chromosome 1 and inherited as a triplet eg cDe (inherit a triplet of those from each parent, those two together will determine Rhesus type)
- ‘Rhesus negative’ implies D negative (negative for Rhesus D antigen)
- No naturally occurring antibodies but can develop in response to pregnancy or transfusion
Define haemolytic disease of the newborn.
- Foetal red cells carrying antigens from the father transferring to maternal circulation (not meant to but always small number of foetal cells which escape during childbirth, abortion, trauma)
- Mother produces IgG antibodies to eg D, c, E, Kell
- Antibodies cross the placenta and attack foetal cells possessing said antigens causing anaemia and jaundice due to haemolysis. Bilirubin may then get into the brain causing brain damage. Foetal death is also possible.
- Usually, the antibodies develop as a result of exposure to the antigen from an initial pregnancy in childbirth or abortion or trauma, but only affect a foetus from a subsequent pregnancy (assuming same antigens are present on the second foetus to which the mother has developed antibodies)
What are treatment/prevention options against haemolytic disease of the newborn ?
- PREVENTION OF RHESUS D, IMMUNISATION
• Anti-D prophylaxis given to D negative mothers (15% of women will be Rhesus D negative) at 28 weeks and delivery (40 weeks), to prevent women getting sensitised to D antigen that their child may carry. Anti D helps mop up any foetal cell transmitted into maternal circulation
• Kleihauer test looks for foetal cells in maternal circulation (calculates how much anti D needed to mop up foetal cells into maternal circulation before they get a chance to do significant harm) )
• Foetal monitoring by ultrasound
• Can receive intra-uterine transfusion (Foetal transfusions possible )
What has the effect of Rhesus Prophylaxis on foetal deaths ?
Caused a reduction in the number of foetal deaths, since Rhesus babies were major health issues, causing foetal death (cerebral palsy etc).
Define cross-matching blood.
- Donor blood is checked for ABO, rhesus D and often other antigens and the bag is labelled
- Recipient’s blood is checked for ABO and rhesus D group and the plasma screened for antibodies against a panel of red cell antigens
- Recipient’s plasma is mixed with donor red cells to check for agglutination (in case possible antibody not detected in test above)
INVOLVES ONLY RED CELLS, PLATELETS AND PLASMA NOT CROSS-MATCHED
What is the significance of cross-matching blood ?
Avoiding transfusion reactions
What are transfusion reactions ?
1) Acute haemolytic reactions (pre-existing antibodies) usually due to mis-matched blood, ABO most serious
2) Delayed haemolytic reactions (new antibodies formed following transfusion, to red cell antigens that they do not share)
- Much more minor than acute haemolytic reactions. May cause jaundice and more anaemia.
3) Urticaria or anaphylaxis (drugs or plasma proteins)
4) Febrile (rise in temperature) reactions (HLA antibodies reacting to HLA antigens on few WBC still in the bag)
What are the majority of transfusion-related problems ?
What are the main concerns of patients concerning transfusions ? Are these concerns valid ?
- Transfusion-associated circulatory overload (=overloads circulation, maybe pulmonary oedema etc)
- Acute Transfusion Reactions (from pre-existing antibodies in the blood)
- Incorrect blood component transfused
- Anti-D (Rhesus negative mother not given anti-D delivery)
HIV and hepatitis. Not really valid (only 3 infections in one year)
What is the pattern of deaths definitely attributed to transfusions, over the years ?
Deaths definitely attributed to transfusions decreased
What are common sources of errors in transfusions ?
- Failure to establish patient identity and/or label tube incorrectly when taking blood
- Lab errors (eg incorrect sample used or antibodies not working)
- Failure to perform bedside check of patient identity when administering blood
