random facts about transfusion medicine- Martin Flashcards
what diseases will result in an altered A Ag
leukemia = dec Ag on each RBC
gastric/pancreatic carcinoma= increased serum BGSS–> neutralize any Anti-A Ab –>makes the blood look like “O type” on forward and backward testing
intestinal obstructions: acquired B Ag on previously A cells
–> forward typing shows AB, back typing shows only anti-B Ab
forward vs backwards typing of ABO
forward: put commerical anti-sera Ab into pt’s RBC –> will it bind pt?
bach/reverse: add pts sera into type of known At (A/B/anti-D) –> will pt attack?
is Rh Ab naturally occurring
no
McLeod Phenotype
abn Kell Ag –> acanthocytes (spur cell) with chronic compensated hemolytic anemia
chronic granulomatous ds of childhood (x NADH-oxidase on Nø)
Kell vs Kidd vs Duffy vs MNS vs Lewis systems
Kells= K and k Ags= IgG
–> HDN +hemolytic transfusion rxn
Kidd= Jk(a) and jk(b)
NO Ab detected bc its so transient and weak binding, but then causes rapid hemolysis post transfusion
dosage phenomenon= stronger rxn to homozygous cells
Duffy: Fya and Fyb
IgG Ab, cause HDN and hemolytic transfusion rxn
Fy(a-,b-) seen in AA, resistance to P. xivax
MNS system: M, N, S, s
anti-M IgM, NON HEMOLYTIC usually
dosage phenomenon
Lewis system
IgM warm Abs, naturally occuring
Le Ag –> lewis lives
shelf life of RBC
plts
plasma
RBC= 42 days plt= 5 days plasma= 1 yr frozen
antibody screen, direct vs indirect Coomb’s test
DAT= detect autoimmune hemolytic anemia
pt’s washed RBCs incubated w Ab against self Af
use RBCs
IAT= for pretransfusion ad pre-natal preg tests
recipient Ig target donor Ab= complex
use serum
bombay phenotype is what
Oh/ h/h phenotype
no H, anti-H Ab need transfusion with another of the same phenotype
given autoimmune hermolytiv anemia, which type is most problematic for Ab screening
cold can give a false (+) ABO, but if you just warm up the serum you can avoid it
oft= auto-anti-I
warm= more problematic for Rh, Kell, Kidd, Duff, no affect ABO
what infections are associated with causing cold agglutinin ds
mycoplasma pnuemoniae infectious mono (EBV)
steps of IAT
- room temp = detect cold IgM
- 37C= detect warm Ab= IgG, Rh, Kell, Kidd, Duffy
- AHG= detect warm, IgG that coat RBC
- CC: verify the AHG findigns
acute hemolytic transfusion reaction
etiology
sx
trx
prevention
preformed IgM Ab, induce complement and intravasc hemolysis
sx= HYPOtension, Hgb-emia+uria, DIC, flank pain, dyspnea, fever, –>late=renal failure
trx= discontinue and verify
Na-bicard to maintain pH
prevent: proper ID pt
delayed hemolytic transfusion reaction
etiology
sx
trx
prevention
> 24 hrs post, = IgG
(DAT), common causes= Rh, Kell, Kidd
extravasc hemolysis
labs= inc LDH+bili, dec haptoglobin
trx= IVIG, prevent renal/sickle crisis w fluids
prevention: serologic detection of RBC Ab is key!! (abo, etc)
febrile hemolytic transfusion reaction
etiology
sx
trx
prevention
MOST COMMON RXN
can be delayed up to an hour post transfusion
sx= fever, chills, HYPERtension,
trx= r/u lifethreatning ds, fever self resolve in 2-3 hrs
antipyretic (acetominophen), meperidine
NO ASA
p: prophylactic antipyretic, pre-storage leukocytes and plasma reduction
allergic urticarial transfusion reaction
etiology
sx
trx
prevention
recipient IgE against donor Ag
in IgA deficient recipeint= anti-IgA IgGs
can look like TRALI if have dyspnea = pruritis, urticaria, cut flushing, laryngeal edema and bronchoconstrictions (wheeze, CP)
trx: antihistamine (diphenhydramine)
intubate, O2 prn
p: check for IgA deficiency, prophylactic antihistamine