DSA- Transfusion Medicine (martin) Flashcards
RBC membrane contains:
proteins - Rhesus (Rh) system
carbs- ABO system
**note: there are >400 RBC blood group antigens
what are the mechanisms of immunization to RBC antigens?
primary and secondary (amnestic) response
primary response vs secondary response
primary- seen after first immune exposure to foreign protein Ag (days or weeks after exposure)
secondary- seen upon REPEAT exposure to foreign protein Ag (noticed much quicker)
typical primary response for most blood group antigens:
sustained HIGH [IgM]
some formation of IgG
typical secondary response for most blood group antigens:
sustained HIGH [IgG]
transient rise in IgM
ABO system components
3 antigens expressed: H, A, B
terminal sugar units
“O” blood type
H Ag only
A blood type
H+ A
B blood type
H+B
AB blood type
H+ (A+B)
describe a secretor
someone who is capable of making ABO antigens in their secretions and plasma
- about 80% population carries at least one allele called “Se” –> encodes enzyme that allows that individual to make the H antigen on long carbohydrate-rich chains (type 1 chains) which are found in secretions and plasma
- once H antigen is made: then person can make either A or b antigens (or both) on type 1 chains
naturally occurring antibodies seen in serum of each group
O –> anti-A, anti-B, anti-A,B
A–> anti-B
B–> anti-A
AB–> none
What can cause compatibility issues when transfusing a patient?
subtypes (ex. A is subdivide into A1 and A2)
leukemia can alter expression of ABO Ag, how?
decrease Ag on individual RBCs
how can you get “Acquired B” ag
intestinal obstruction–> increases bowel permeability, leading to bacterial polysaccharides into circulation being absorbed by grp A cells
bacterial enzymes will remove some of the acetyl groups from the A Ag–> produces B specific sugar
Mariya’s interpretation: so basically you have a person that has blood group A get infected by bacteria that will then get into their blood which will cause the person to react to B weakly also (since that person is acquiring the group B enzymes of galactose)
What is the Bombay phenotype
absence of H Ag (Oh; h/h) which is typically found on virtually all RBCs and is the building block for pdtion of antigens within the ABO blood group
Bombay: RBC has NO antigen
(anti-A, Anti-B, AntiA,B, and AntiH)
*anti-H IgM binds complement and lyses cells
what blood does a person with a bombay phenotype need to receive in a transfusion?
can ONLY receive Bombay blood
Which Ig is more common in someone w/ a Bombay phenotype
IgM > IgG
why is it impt to know if someone has the bombay phenotype?
bc of anti-H reactivity–> capable of hemolysis (can activate complement cascade which lyses RBCs while theyre still in circulation)–> intravascular hemolysis
Are there transfusion reactions in someone with bombay phenotype
YES- can cause an acute hemolytic transfusion rxn
What could arise in mothers with the Bombay phenotype?
Hemolytic Dz of the newborn(HDN) is possible
universal donor vs recipient
donor = blood group O- recipient = blood group AB+
Rh (rhesus) system most important antigens:
multiple antigens (2 genes- one for D and one for CcEe)
D- Rhesus factor/Ag
d= absence of D ): (he smol so he gone)
C= codominant w/ c (vice versa)
E= codominant w/ e (vice verse)
are antibodies naturally occurring in the rhesus system
NO (unlike ABO)
you need exposure to Ags in order to produce ABs (pregnancy or transfusion)
indication for RhoGAM
used in preventing Rh immunization for pregnancy and other obstetric conditions in Rh- women unless baby father is conclusively Rh-
other usage:
transfusion of Rh+ blood to Rh neg individual
treatment of ITP
when is RhoGAM contraindicated
in Rh+ individuals and in pts w/ known history of anaphylactic or severe systemic rxns to the administration of human immune globulin pdts
why is RhoGAM risky?
products from human blood may carry risk of transmitting infectious agents (viruses, vCJD awhen usingnd CJD agent)
What will yield positive serologic testing results after administration of Rho(D) immune globulin (rhogam)?
transitory increase of various passively transferred antibodies in pts blood
what system ranks second in immunogenicity after D (Rh)
Kell system
what are the most impt antigens and phenotypes in the kell system
Ags: K= Kell, k= Cellano
phenotypes observed: kk>Kk>KK
are alloantibodies to K common
YES
IgG and rxn at 37C
–> HDN + hemolytic transfusion rxn
what is more common in the Kell system: anti-K or anti-k
anti-K (since kk is the more common phenotype in caucasians and african americans)
antigens involved in the Kidd system
Jk^a or Kidd (a)
Jk^b or Kidd (b)
both seen commonly, but low titer and weak avidity–> disappear rapidly
what reactions are common with the Kidd system?
3/4 delayed hemolytic transfusion rxns (IgG)
activates complement–> rapid hemolysis due to synergistic activation of complement and cell-bound Ab
during initial Ab screen and Xmatch what is seen with the Kidd antibodies?
antibodies disappear–> no Abs detected (but addition of complement enhances detection)
it reappears upon transfusion w/ Kidd + unit–> hemolytic rxn):
in vitro, what do Kidd antibodies exhibit
DOSAGE phenomenon - cell w/ 2 copies of same gene (homoz) has a strong rxn than a cell w/ heterozygous genes on it
antigens involved in the Duffy system
Fy^a or Duffy (a)
Fy^b or Duffy (b)
Most common antigens among african-americans; what is it resistent to ?
Fy (a-,b-)
resistant to Plasmodium vivax infection
what is the Ab of Duffy system and what is it associated w/ ?
Ab: IgG
associated w/ HDN and hemolytic transfusion rxns
Most impt antigens of MNS system? antibody?
M+ N
S+ s
Ab: IgM (occasionally IgG)
what makes the Ab of the MNS system stand out
non-hemolytic usually
also has dosage effect–> react more strongly w/ homozygous cell than heterozygous cell
what Ab does the Lewis system use? Ags?
IgM (Warm Abs)
Le Ag= found in secretions and plasma, then Ag adsorbed onto RBC membrane; need secretor and Hh genes also
most common complication of transfusion
FEBRILE NONHEMOLYTIC rxn (fever and chills, mild dyspnea) WITHIN 6 hours of transfusion of RBCs or platelets
caused by inflammatory mediators derived from donor leukos
RESPONDS to antipyretics + are short-lived
the frequency of febrile nonhemolytic rxns varies with what?
increases- w/ storage age of product
decreases - by measures that limit donor leuko contamination
allergic rxns from transfusion
potentially fatal when blood pdts containing Ags are given to previously SENSITIZED recipients
increased in ppl w/ IgA deficiency (IgG antibodies recognize IgA)
Urticarial allergic rxns from transfusion
rxns triggered by presence of allergen in donated blood product that is recognized by IgE antibodies in the recipient
respond to ANTIHISTAMINES, do not require discontinuation of transfusion (most instances)
What causes an acute hemolytic rxn
preformed IgM Abs against donor RBCs that fix complement–> rapidly induce complement mediated lysis, intravasc hemolysis and hemoglobinuria
from: error in pt identification or tube labeling
syx: fever, shaking chills, and flank pain; may rapidly progress to DIC, shock, acute renal failure, and death
+DIRECT COOMBS
what causes delayed hemolytic rxns
ABs that recognize RBC ags that recipient was sensitized to previously (prior blood transfusion)
IgG Abs
+ DIRECT COOMBS and lab fxs of hemolysis
(Abs to Ags such as Rh, Kell, and Kidd often induce sufficient complement activation to cause severe and potentially fatal rxns)
lab features of hemolysis
low haptoglobin
elevated LDH
what cells are activated in Transfusion related acute lung injury (TRALI?
NEUTROPHILS
how does TRALI happen?
severe, frequently fatal complication - factors in transfused blood (donor leukocyte antibodies) trigger activation of neutros in lung microvasculature; occur frequently in pts with preexisting lung dz
TWO hit hypothesis; 1) priming event 2) ABs in the transfused blood product that recognize Ags expressed on neutrophils
mc antibodies associated w/ TRALI bind what? in whom?
MHC 1 antigens
these antibodies are especially found in MULTIPAROUS women
more likely occur w/ pdts containing high levels of donor ABs such as FFP and platelets
clinical px of TRALI
sudden onset respiratory failure, during or soon after transfusion
diffuse bilateral pulm infiltrates that DO NOT response to diuretics (on chest imaging)
other: fever, hypotension, hypoxemia
infectious complications of transfusions
most bacterial are of skin flora
much more common in platelet preps than RBC preps (bc platelet preps stored in room temp- favorable to bacterial growth)
syx: fever, chills, hypotension
viral infections seen w/ transfusions
-dramatically decreased w/ advances but rarely cannot detect
- HIV, hep C, hep B
- West Nile Virus, Trypanosomes, babesia, and Zika virus
Blood bank donation info:
16+ y/o; must meet weight and Hb level requirement
NOT IF:
- traveling to certain countries
- medical procedures: receipt of dura mater graft, transfusion of blood/blood components w/in previous 12 mo or human derived clotting factors
- HIV+
- hepatiitis since 11th bday
- Babesiosis or Chagas dz (trypanosoma cruzi antibodies are tested)
- needle usage for drugs (not prescirbed)
- incarceration
- piercing or tattoo using nonsterile materials w/in last 12 mo
- pregnancy
- CJD or vCJD risk factors
how do you know that a patient has a true AB or just an acquired B making it seem like they have an AB blood type?
get a WEAK interaction with anti-B –> producing AB blood type
but know its not truly an AB bc when test the serum, you get a strong anti-B response–> showing its an A blood type
how does gastric or pancreatic carcinoma alter expression of ABO ag
serum contains excessive bld grp specific soluble substances (BGSS) which neutralize antisera used in forward grouping
get neg rxns so everyone look like group O!!!
