Lecture 17 - Introduction to Blood Serology Flashcards Preview

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Blood group antigens?

glycoproteins and glycolipids present on surface of red cells, sometimes one endothelial surfaces (e.g. ABO), genetically determined


Genetic control of blood groups?

protein determinants (Rh Kell), glycolipid determinants (ABO, lewis group)


Functional aspects of blood group antigens

duffy blood group and malaria (some africans have Fya - Fyb -, indicating resistance to malaria infection), Mcleod phenotype (Kx null phenotype associated wih Chronic Granulomatous Disease)


Blood groups and populations?

genetic drift, no biological advantage but clinical implications; fuck all polys but some whites hve RhD negative, 1% polys but essentially none whites have Kidd, U phenotype only occurs in african heritage


Antibodies of blood groups?

IgM, IgG, IgA


Naturally occuring antibodies?

IgM, glycolipid antigens, can activate compliment and destroys RBC intravascularly (first year of life, often bacterial trigger)


Immune response antibodies?

IgG, glycoprotein, no complement or early phase only, extravascular RBC destruction


ABO antigens?

phenotype determined by series of Glycosyltransferase enzymes, and H antigen for expression


Biochemical structure of ABO antigens?

A - presence of N-acetylgalactosoamine; B - presence of extra D galactose; O - absence


ABO mismatch?

can be fatal, intravascular haemolysis, renal failure, DIC



important as highly immunogenic, genotype is autisomal dominant, dd is amorph (makes no changes, just absence)



fomed by Rh(D) negative individuals who are exposed, IgG antibody causing extravascular destruction of RBC, most common cause of haemolytic disease of the newborn


Importance of minor blood group systems?

frequency of antigen in population, frequency of antibody production following antigen containing blood transfusion, ability of antibody to destroy transfused RBC


Zeta potential?

RBC are negatively charged; IgM molecule larger than zeta poential therefore cause cross-linking leading to agglutination, IgG too small to produce cross linking, requires Anti-Human globulin


Haemolytic Disease of the Newborn?

when maternal antibody crosses placenta resuling in destruction of foetal RBC, IgG, caused by anti-D, anti-c and anti-kell, reduced by immunoprophylaxis


HFDN pathophysiology?

first pregnancy little antibodies are produced, however in second the antibodies ready to attack antigen of fetus, can cause stillbirth of post-partum jaundice and kernicterus


Prevention of Rh(D) HDN?

anti-D immunoglobulin given following birth of RhD positive baby to negative mother, given during pregnancy following potentially sensitising event (abortion, termination, amniocentesis)


ABO fetal mismatch?

antigens weakly expressed on fetus and widely distributed on placental tissue and absorb antibodies before reaching fetus