Transfusion Immunology Flashcards
what macromolecules are ABO antigens found? what enzyme adds them?
ABO antigens are terminal carbohydrate moieties on large glycoproteins and glycolipids on cell membranes
(core glycan + terminal sugar)
added via glycosyltranferase
what allele determines blood type?
glycosyltranferase, enzyme which adds terminal sugar of blood antigen to core glycan, has 3 alleles and is codominant:
- A allele adds N-acetylgalactosamine
- B allele adds terminal galactose
- O allele has no activity
isoagglutinins
natural antibodies - preformed antibodies produced by an individual that cause agglutination of RBC in another person
cross-react with ABO antigens
*remember that ABO mismatch causes Type II hypersensitivity reaction
Bombay-O blood type
appear as Type O on routine typing - produce both anti-A and anti-B antibodies (contain neither A or B antigens)
but ALSO produce anti-H —> will react with Type O blood (which has H antigen) and cause agglutination
what are 4 types of transfusion (what is transfused) and their “rules”
- whole blood: antibodies and antigens (should be exact match)
- washed erythrocytes: RBC must lack antigens that would bind recipient’s antibodies (depends on blood type)
- plasma: must lack antibodies that bind recipient’s RBC
- platelets
in emergencies, what kind of whole blood can be transfused?
Type O, Rh- erythrocytes can be used as universal donor
(remember O lacks both A and B antigens)
what happens during acute hemolytic transfusion reaction?
intravascular lysis - antibodies coat RBC, complement activated (IgM!)
hemoglobin released to renal toxic amounts
DIC (disseminated intravascular coagulation) may follow - clotting in circulation
what causes ABO Incompatibility Disease?
caused by IgG crossing placenta when fetus’ blood type is different than mother’s
rare because most anti-A and anti-B Ab are IgM type, which doesn’t cross placenta, and neonatal RBCs poorly express blood group antigens
what is the importance of Rh antigen?
non-glycosylated cell surface protein on RBC
~15% of population have deletion in RhD —> will make antibodies if exposed
*if Rh- mother is sensitized via first Rh+ child during birth, IgG anti-Rh can cross placenta during next Rh+ pregnancy —> hemolytic disease of the newborn
erythroblastosis fetalis = hydrops fetalis =
hemolytic disease of the newborn: Rh incompatibility disease
Rh- mother is first sensitized by Rh+ fetus during birth, then during next Rh+ pregnancy anti-Rh Ab can cross placenta (IgG type)
how is hemolytic disease of the newborn (Rh incompatibility) treated?
Rhogam given during 3rd trimester and within 72 hours of first birth to destroy fetal RBCs before they can initiate immune response
contrast features/ effects of anti-ABO to anti-Rh antibodies
anti-ABO: abundant, IgM (activate complement well), destroy RBC in blood stream (intravascular hemolysis)
anti-Rh: sparse, IgG (does not activate complement well), Ab-coated RBC destroyed by macrophage in liver and spleen (extravascular hemolysis)
antibodies against minor blood groups are usually what type?
IgG
require exposure to antigen
explain why it makes sense that IgM but not IgG can cause agglutination of RBC (during ABO mismatch)
IgM are pentamers - large, can bind many RBC
IgG are monomers - can bind one RBC, not big enough to pull them together
(RBC also have negative charge and there is repulsion between then that IgG is not big enough to bridge)
Direct Coomb’s (DAT) Test - how does it work and what is it used for?
detects cell-bound antibodies by adding anti-IgG or anti-C3 (Coomb’s reagent) —> causes RBC to agglutinate (since IgG cannot do it on its own)
uses: test patient’s RBC for bound IgG, diagnosis autoimmune hemolytic anemia, look for bound antibodies in transfusion reactions
