transfusion Flashcards
ABO blood group antigens - what class of molecules?
carbs. antibodies naturally occuring predominantly IgM. clinically significant - bind complement (membrane attack complex formes) cause intravascular hemolysis
intravascular hemolysis
agglutination & complement fixation = membrane attack to destroy rbc.
rh blood group
Antigen = protein
d-type most immunogenic.
Ab = not naturally occuring. primary and secondary response needed.
IgG
clinically significant. extravascular hemolysis
extravascular hemolysis
destroy rbc by macrophage englufing.
other clinically significant blood groups
kell kidd MNS duffy - IgG, react at body temp, cause extravascular hemolyssis
clinically insignificant blood groups
lewis
P
MNS
react at low temp, IgM. no hemolysis
type and screen
ABO RH screen - type the blood. then check antibodies for RH, Kell, Kidd, MNS, Duffy
* screen only valid for 3 days because Ab may have formed.
acute hemolytic transfusion reaction - what blood groups? effects? cause? symptoms?
immediate
anti-A/B Ab present in pateint plasma bind donor cells - fix complement = IVH
cause: mis-ID when collecting, infusing.
symptoms = fever, chills, hemoglobinuriea, decrease bp, renal failure.
indicators of IVH
- increase plasma Hb
- decrease haptoglobin (binds free Hb)
increase lactate dehydrogenase (comes from inside of lysed rbc)
hemoglobinuriea
delayed hemolytic transfusion reaction
-what blood groups
symptoms
delayed.
Ab formed removed in spleen (EVH)
rh, kell, kidd, duffy
symptoms: fever, chill, jaundice (due to bilirubin increase from rbc breakdown)
indicators of EVH
increase bilirubin decrease Hb increase lactate dehydrogenase positivity antibody screen positive direct antiglobulin test = detect antibody coating rbc
immune response in IgG vs IgM
IgG = larger secondary response than IgG primary and IgM secondary.
hemolytic disease of fetus and newborn
maternal rbc cross placenta and attach to fetal cells causing hemolysis.
- anemia & erythropoiesis
mild to severe.
first pregnancy unaffected. Rh (-) mom delivering Rh (+) baby.
HDFN - in utero
severe case
treatment
severe case - profound anemia, hepatosplenomegaly (increase size of liver & spleen because removing coated red cells
hypoproteinemia - less proein because liver focusing on making new rbc’s
cardiovascular failure - enlarged heart
hydrops fetalis - severe edema
treat: intrauterine transfusion (IUT) - transfuse blood that has antigens negative to moms blood into umbilical cord.
HDFN - post partum
severe cases: anemia, hyperbilirubinemia, hemolysis
treatment: exchange transfucion (swap 5 mL with “good blood” slowly exchange all the blood.
prevention - screen pregnant women for RBC antibodies. Rh (-) greatest risk. Rh Ig (anti-d) if mother delivers positive baby. high dose will quickly bind to any D+ cells from baby, remove before immune system can react.