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Blood Groups - Coggle Diagram

- - - - All group O
      - 1 R\(_1\)R\(_1\) (CDe) and R\(_1^w\)R\(_1\)
      - 1 R\(_2\)R\(_2\) (cDE), r'r (Cde) + r"r (cdE)
      - 3 rr (cde), homozygous expression of k, Fya, Fyb, Jka, Jkb, S, s and also express K
  - - - IgG Abs
      - 37\(^o\) active Abs
      - Complement fixing Abs
      - All Rh Abs
    - - Ag-Ab complex forms
        
        AHG (anti-human globulin) added
        
        Agglutination seen
  - - - All Rh Abs
      - Anti-Jka, -Jkb, -Lea, -Leb, -P1
    - - Anti-Fy\(^a\), -Fy\(^b\), -M, -N, -S
      - Destroyed by papain treatment
  - - - IgM Abs e.g. anti-M, -N, -P1, -Lea, Leb, -H, -I and ABO
      - Clincally signifcant Abs (except ABO)
      - Abs which may give unclear IAT
  - - - It is reactive with at least 2 examples of reagent cels carrying Ag
      - Non reactive with at least 2 samples lacking the Ag
  - - - Helps to resolve mixtures
- - - - Prepare tests - microplate
        
        Amplify DNA - thermocyclers
        
        Analysis
        
        64 cycles
  - - - If DNA region is present, primer binds + quencher molecule releases fluore
        
        Fluorescence seen
        
        Excites laser to detect fluorescence
  - - - ~8 runs a day
    - - Low failure rate
  - - - All resolved on repeat
    - - 4 resolved on repeat
  - - - Not as fast as serological typing
    - - Too genetically complex
- - - - Monomeric structure
      - 2 Ag binding sites
      - Binding site only reaches 10nm - single IgG cannot cause agglutinations of RBCs
      - Work best at 37\(^o\)
      - Do not usually bind complement
      - Able to cross placenta
      - Primarily cause removal of red cells by extravascular haemolysis
        
        Fc regions of red cell bound IgG interacts with Fc receptors on M\(\phi\) of reticuloendothelial system
    - - Pentameric
      - 10 Ag binding sites
      - Single IgM can bridge gap between 2 RBC's
        
        Causing agglutination
      - Work best below 37\(^o\)
      - Generally minor clinical significance
      - May bind complement
      - Do not cross placenta
      - ABO Ab's are mainly IgM
  - - - 47%
    - - 42%
    - - 8%
    - - 3%
  - - - Encode glycosyltransferase enzymes
    - - Chromosome 19
      - Codes for H enzyme
        
        H substance = O
    - - Chromosome 9
    - - Chromsome 9
    - - Code for A or B enzymes
    - - H substance
        
        A substance
        
        A gene \(\Rightarrow\)
        
        B substance
        
        \(\Leftarrow\) B gene
      - Under influence of H gene
    - - Blood groups
        
        A
        
        B
        
        O
        
        AB
      - AA or AO
        
        BO or BB
        
        OO
        
        AB
  - - - 80%
    - - 20%
    - - Genotype
        
        A1A1, A1A2, A1O
        
        A2A2, A2O
        
        A2B
      - A1
        
        A2
        
        A2B
    - - May be qualitative if anti-A1 is produced
  - - - Some IgG just 'fits'
        
        e.g. lectins
      - via maternal milk
      - Environmental factors
      - Genetic basis
  - - - ABO Abs are found in the plasma against the ABO Ags an individual lacks
      - Blood group
        
        Ag on red cells
        
        Ab in plasma
        
        Anti-A + B
        
        Anti-B
        
        Anti-A
        
        1 more item...
        
        None
        
        A
        
        B
        
        A and B
        
        O
        
        A
        
        B
        
        AB
  - - - Not present at birth
      - Development in first 4 months
      - Reach max strength at 5 yrs
    - - Not fully developed at birth
      - Development over first 1-2 years
  - - - Work best at low temps
      - Highly clinically signifcant
        
        Cause intravascular haemolysis
        
        Activation of complement
        
        May cause fatal reaction in cases of incompatible transfusion
- - - - RhD gene is on chromosome 1
      - Defines Rh status us donors and patients
      - Unlinked RhAG gene on chromosome 6 incorporates Ag into cell membrane
      - D positive individuals have the RhD gene
      - Most D negative individuals have an RhD gene deletion
      - UK frequencies
        
        RhD positive
        
        85%
        
        RhD negative
        
        15%
        
        Frequencies vary across the world
  - - - Possesses all normal D Ags
        
        Quantitatively less
      - RhD positive as donor, patient + antenatal patient
      - Cannot produce anti-D
    - - Lacks part of a normal D Ag
      - Can produce anti-D
      - Can cause production of anti-D in a D negative recipient
      - RhD positive as a donor
      - RhD negative as a recipient
      - Antenatal patients require anti-D prophylaxis
  - - - No RHD gene
  - - - Most potent
        
        Major cause of haemolytic disease of fetus + newborn (HDFN)
      - Produced in women as a result of sensitisation by red cells from D positive fetus
      - May be produced in males as result of transfusion with D positive blood
    - - Clinically significant
      - Relatively common
      - May cause HDFN or haemolytic transfusion reaction (HTR)
      - Often found together with anti-E
        
        In individuals who lack c and E Ags
    - - Clinically significant
        
        Less than anti-c
      - Relatively common
      - May cause HDFN or HTR
    - - Clinically significant
      - Relatively common
      - Often seen with anti-D
      - May cause HTR
      - HDFN rare when on its own
    - - Clinically significant
      - May cause HTR
  - - - All female patients under 60yrs
      - Patients needing regular transfusions e.g. sickle cell disease
      - Patients who have already produced other Abs - 'responders'
  - - - Abs attack red cells in the infant which carry corresponding antigen inherited from the father
    - - Mother is RhD negative and fetus is RhD positive
    - - Mother
        
        Nutrients and O\(_2\)
        
        Fetus
      - Fetus
        
        Waste products + CO\(_2\)
        
        Mother
      - First pregnancy - delivery
        
        Fetus
        
        Small quantity red cells
        
        Mother
        
        First pregnancy - post delivery
        
        Mother sensitised against foreign red cell Ags on fetus
        
        More fully developed Ags on fetal cells are more likely to cause sensitisation
        
        HDFN: Subsequent pregnancy
        
        Mother
        
        Antibodies (IgG), nutrients + O\(_2\)
        
        Fetus
        
        Fetus
        
        Waste products, CO\(_2\)
        
        Mother
    - - Direct antiglobulin test (DAT) on cord blood
      - Detects IgG Ab bound to surface of infants red cells
      - Positive result is diagnostic of HDFN
      - Early diagnosis enables successful treatment
    - - Main management is to prevent production of anti-D in RhD negative mothers
      - Phototherapy under UV light helps to degrade bilirubin
      - Exchange transfusion at birth or Intra-Uterine Transfusion (IUT) during pregnancy
      - Top-up or exchange transfusion
      - Requirements for IUT
        
        \(\leq\)5 days old, CPD red cells
        
        CMV negative
        
        Sickle cell negative
        
        NEgative for any red cell Abs
        
        Low level of anti-A and anti-B
        
        Gamma irradiated
        
        Haematocrit 0.5-0.6 for ET up to 0.7 for IUT