haemostasis Flashcards
blood transfusion: list the major blood groups, explain their clinical importance, explain the screening of blood donors, list the blood components used clinically and recall the potential side effects of blood and plasma transfusions
where is blood from and significance
human source (no synthetics yet), not risk free
why is blood used carefully
scarce resource (1 donor gives 1 pint every 4 months, and has shelf life of 5 weeks)
when is blood used and whose decision is it
balance between benefits and risk, so when no safer alternative is available; doctor’s decision and must prescribe
2 situations when no safer alternatives are not available to blood
if massive bleeding, if “plain fluids” are not sufficient; if anaemic, if iron/B12/folate are not appropriate
what is the most important of all blood groups in use for transfusion, and significance
ABO (cross match between donor and patient); should not die of ABO incompatible blood transfusion (human error still does)
physiology of ABO blood groups
A and B antigens on red cell formed by adding one or other sugar residue onto common glycoprotein and fucose stem on red cell membrane; group O has neither A or B sugars (stem only), group AB has both A and B sugars
how are ABO antigens determined
by corresponding genes
what does A gene code for
enzyme which N-acetyl galactosamine to common glycoprotein and fucose stem
what does B gene code for
enzyme which adds galactose to common glycoprotein and fucose stem
what are A and B genes
codominant (e.g. for blood group A, could be AA or AO)
what is O gene
recessive (e.g. for blood group A, could be AA or AO)
what antibodies exist in humans concerning red cells
IgM, which are against any antigen not present on own red cells
what type of antibody is IgM, and what it activates
naturally occurring (nearly from birth), and is “complete” antibody so fully activates complement cascade to cause haemolysis of red cells (forms membrane attack complex)
when is antibody/antigen interaction often fatal
in patient who has received an ABO incompatible transfusion, where patient has corresonding antibody -> Hb (toxic to kidney), bilirubin (jaundice), cytokine storm (hypotension and shock)
what do IgM antibodies do to corresponding antigens (e.g. when anti-A antibodies from group B patient are added to group of A cells), and what does it show
cause agglutination, showing cells are incompatible
what blood group has no antigens on red cells, and consequently has 2 sets of anti-antibodies in blood
O (agglutinate to any transfusion except O; red cell blood transfusion can be given to anyone)
what blood group has 2 antigens on red cells, and consequently has no anti-antibodies in blood
AB (so safe with any blood transfusion)
how is ABO group known
test patient blood sample (plasma and cells) with known anti-A and anti-B reagents and see if it clumps;
how is a cross match conducted to ensure compatibility
donor unit of same group selected, and patient’s serum mixed with donor red cells (should not react - if it agglutinates, it is incompatible)
of the RH antigen groups, what is the most important and why
RhD, as next most immunogenic
RhD positive vs RhD negative
RhD (DD or Dd) positive is if you have antigen, RhD negative (dd) if not
genes for RhD groups
D codes for D antigen on red cell membrane, d codes for no antigen and is recessive
naming combination of ABO and RhD groups
usually shortened, e.g. O positive means ABO group O and RH D positive
when can RhD negative people make anti-D antibodies
after exposed to RhD antigen, either by transfusion of RhD positive blood, or in women if pregnant with RhD positive foetus
what type of antibodies are anti-D antibodies
IgG
anti-D antibodies implications for future transfusions
must have RhD negative blood, otherwise anti-D would react with RhD positive blood, causing delayed (5-10 days as IgG attach to red cells but can’t activate complement system as quickly - only when macrophages in spleen detect) haemolytic transfusion reaction (anaemia, high bilirubin, janudice etc.)
anti-D antibodies implications for haemolytic disease of newborn (HDN)
if RhD negative mother has anti-D and in next pregnancy, foetus is RhD positive, mother’s IgG anti-D antibodies can cross placenta, causing haemolysis of foetal red cells (if severe, hydrops fetalis as foetus as anaemic so heart failure; death by brain damage due to bilirubin staining); prevent sensitisation by giving anti-D injections during delivery so doesn’t mount anti-D response against foetus