1/13 Blood Products - Corbett Flashcards
ABO groups
basics
H antigen is precursor onto which terminal sugars are added to yield
- A antigen (GalNac)
- B antigen (Gal)
when individuals LACK a carbohydrate antigen, they form an IgM antibody against it
- important bc IgM can fix complement → intravascular hemolysis
front typing vs back typing
front typing: pt blood + known antibody
back typing: pt serum + known cells
what happens if A, B, and O clot during a typing test?
rare phenotype: BOMBAY - lacks H antigen
- lack fucosyl transferase which adds fucose, which has to be added before A or B sugars can be added
Rh system
- protien antigens expressed by RBCs
- D antigens are VERY IMMUNOGENIC → considered most imp Rh antigen in transfusion practice
- Rh+ : D antigen present, no anti-D
- Rh- : D antigen absent, no anti-D UNLESS EXPOSED (ex. childbirth)
***both types lack anti-D antibodies at default state
antiD antibodies
IgG : too small to engage antigen AND fix complement at the same time
- instead, just bind to antigen surface and opsonize them → cause extravascular hemolysis (RES system in liver and spleen, where Fc portion of ab is recognized)
CAN CROSS PLACENTA
hemolytic disease of newborn
1st pregnancy
mom Rh-
baby Rh+
fetal-maternal blood transfer during labor → mom is sensitized to RhD antigen
- can try to prevent with Ig therapy
- can check for sensitization with Coombs test
NOW, mom has antiD antibodies in her circulation just waiting to pour through the placenta during her next pregnancy!
- issue: next Rb+ baby will have problems
hemolytic disease of newborn
second pregnancy
sensitized mother and Rh+ baby
- next contact with fetal RhD antigen
FETAL OR NEWBORN HEMOLYTIC ANEMIA
- mild: mild anemia, jaundice
- severe: incr bilirubin, CNS damage, death → erythroblastosis fetalis
hydrops fetalis
fluid in two or more fetal compartments
immune and non-immune causes, but root cause is fetal RBC destruction, leading to:
- extramedullary hematopoiesis → liver failure → low plasma oncotic pressure
- low O2 delivery triggering higher CO → heart failure → contributes to liver failure and also high central venous pressure
overall: high interstitial fluid
tx to prevent hemolytic disease of newborn
RHOGAM is IgG antiD
- antibody given close to birth to prevent mom from being sensitized
- mom wont react to Rh+ kid, no B cell activation and memory cell formation takes place
ABO hemolytic disease
mom O
baby A or B
- in very small group, some antiA, antiB, and antiAB antibodies of IgG class can develop
more common and more severe in African American infants
HDN can occur in first pregnancy bc prior sensitization not necessary
less severe than Rh HDN bc…
- amount of cross passing antibody is less than Rh
- ABO antigens are in low number
- retal RBCs less developed at birth
- presence of ABO antigens in tissues and secretions
ABO vs Rh incompatibility
blood component therapy
four main derivatives
why collected in citrate?
a unit of whole blood is processed through a series of centrifugations into four main derivatives for transfusion into recipient:
-
packed red cells
- 3-6 week shelf life: lose 2,3BPG, pH drop, K rise
- platelet concentrate
- fresh frozen plasma (FFP): coag factors II, VII, IX, X, XII, protein C, protein S
- cryoprecipitate: fibrinogen, vWF
why collected in citrate?
citrate binds Ca in blood → prevents Ca from triggering coag
treatment for packed RBCs
- refrigerate
- leukodepletion: filter granulocytes and lymphocytes
- irradiation: kill all leukocytes (esp T cells) to prevent graft vs host disease
fresh frozen plasma
contains all coagulation factors and other proteins present in original unit of blood (including antiA, antiB, antiD antibodies)
i.e MUST BE ABO COMPATIBLE
- frozen: good for 1yr
- thawed: use in 24hr
- after 24hr, F VIII level drops
cryoprecipitate
all ABO acceptable
contains proteins:
- F VIII (12h halflife)
- fibrinogen (4-7d halflife)
- vWF (24h halflife)
- F XIII (1-2wk halflife)