blood groups and transfusion Flashcards

1
Q

antibody-antigen reaction:
1. when are antibodies produced and by what?

  1. what are two main types of antibodies?
  2. when do antibodies A or B develop?
  3. when do other antigens develop?
A
  1. antibodies are produced by B cells in response to non-self antigens presented to T cells by “antigen presenting cells” - monocytes or macrophages
    • two types of antibodies:
    • IgG antibodies are produced mainly after exposure to blood transfusions or foeto-maternal transmission
    • naturally occurring IgM antibodies present at/soon after birth against antigens that the individual lacks (either group a or group b antigens, see later)
  2. Antibodies to A or B antigens develop in infants in response to exposure in food or environment.
  3. Other antibodies develop after exposure to “non-self” antigens from transfusion or pregnancy.
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2
Q

what is the antibody structure, of an antibody such as IgG?

what is the antibody structure of an IgM antibody?

A
  1. An IgG antibody consists of four polypeptides — two heavy chains and two light chains, with a FAB - variable region which the antigen attaches and is recognised, held together by sulpher sulphur bonds
  2. An IgM antibody is a pentamer (same subunits, just 5 subunits joined together, this structure has an impact on the behaviour of the antibody)
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3
Q

what do IgM antibodies do to red blood cells?

what do IgG antibodies do to red blood cells?

A
  • IgM antibodies: - can agglutinate red cells and IgM activates complement and the membrane attack complex rapidly destroys cells (immediate breakdown on cells)
  • IgG antibodies do not damage circulating red cells: Fc receptors on splenic macrophages bind IgG-coated red cells, which may then be gradually destroyed (slower and within the liver rather than circulation)
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4
Q

HBO system:

  1. explain simply, the pathology behind the ABO system
  2. state what antigens and antibodies each blood type has (A, B, O, AB)
A
    • there are FUT1 and FUT2 genes (on chromosome 19) code for H substance
      - a string of sugars which projects from red cell surfaces
      - A and B genes (chromosome 9) code for glucosyl transferases which add further sugar groups to the H substance backbone
      - naturally occurring anti-A and/or B IgM antibodies in individuals lacking these antigens
  1. blood group A – has A antigens on the red blood cells with anti-B antibodies in the plasma

blood group B – has B antigens with anti-A antibodies in the plasma

blood group O – has no antigens, but both anti-A and anti-B antibodies in the plasma

blood group AB – has both A and B antigens, but no antibodies

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5
Q

Rhesus system:

  1. explain simply, the Rhesus system
  2. explain the pathology behind it?
  3. how do you develop antibodies for the RhD antigen?
  4. there are other Rhesus antigens, when can they be an issue?
A
  1. Red blood cells sometimes have another antigen, a protein known as the RhD antigen. If this is present, your blood group is RhD positive. If it’s absent, your blood group is RhD negative.
  2. coded for on chromosome 1 and inherited as a triplet eg cDe - one triplet from mother, one triplet from father
  3. no naturally occuring antibodies but can develop in response to pregnancy or transfusion
  4. The other Rhesus antigens eg c, C, e, E are less clinically important than D but can be an issue in haemolytic disease of the newborn or develop post-transfusion.
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6
Q

describe the steps of haemolytic disease of a newborn?

A
  1. a rhesus negative mother conceived a rhesus positive fetus and foetal red cells carrying antigens from the father transfer to the maternal circulation during labour
    1. mother produces IgG antibodies to the rhesus antigens eg. D, c, E, Kell
  2. in the second pregnancy, the maternal antibodies cross the placenta and attack the fetal red cells causing anaemia, jaundice, brain damage or foetal death
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7
Q

what are the 4 ways of prevention of rhesus D?

A
  1. anti-D prophylaxis offered to D negative mothers at 28 weeks and delivery and after obstetric “events”
    - this mops up foetal cells which are moving into the mother’s body and are destroyed before they have a chance to induce an immune response
  2. kleihauer test (blood test at birth)
    - looks for foetal cells in maternal circulation (acid elutuion of Hb - fetal Hb is more resistant)
  3. foetal monitoring
    - foetus of mother with significant red cell antibodies can be monitored for anaemia
    e.g.
    • flow in middle cerebral artery
    • ascites - abnormal build up of fluid in abdomen
    • liver and spleen size
    • umbilical cord sampling for blood count/blood group and antibody level
  4. treatment of RhD immunisation
    - the foetus can receive intra-uterine transfusion (baby recieves transfusions during pregnancy)
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8
Q

what are the neonatal management methods of newborns?

A
  • clinical assessment
  • blood count and reticulocytes/group/red cell antibodies/bilirubin/direct Coombes test looking for membrane-bound antibody on the baby’s red blood cell surface
  • phototherapy to increase bilirubin conjugation, bilirubin levels drop when babies are placed under UV light and therefore prevents brain damage
  • top-up or exchange transfusion
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9
Q

what is the process of cross-matching blood?

what is checked in both the donor and recipients blood?

A
  • donor blood is checked for ABO, rhesus D and often other antigens and the bag is labelled, also microbiology screening: HIV, hepatitis etc
  • 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 (clumping together, coagulation)
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10
Q

what are 4 transfusion reactions?

A
  1. acute haemolyic reactions (pre-existing antibodies) usually due to miss-matched blood between donar blood and recipient blood, ABO most serious
  2. delayed haemolytic reactions (new antibodies formed following transfusion)
  3. *urticaria or anaphylaxis** (drugs or plasma proteins within the blood) - rashes
  4. debrile reactions (fever develops) (HLA antibodies)
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11
Q

why is blood transfusion much less of a problem unlike organ rejection?

A

Blood transfusion is much less of a problem for “organ rejection” than say kidney, liver etc. mainly because the latter are affected by HLA antibodies - which are not an issue for red cells as they do not express HLA antigens.

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12
Q

what are 3 possible errors to occur in transfusion?

A
  1. failure to establish patient identity and/or label tube incorrectly when taking blood
  2. failure to perform bedside check of patient identity when administrating blood
  3. lab errors for example, incorrect sample used or antibodies not working
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