Lecture - Transfusion medicine (martin) Flashcards
what does agglutination represent in blood typing
detecting presence of Ag corresponding to Anti-sera
ex. A+ pt
Forward/front typing
mix pt RBC w/ commercially made anti-sera
agglutination–> detecting presence of Ag corresponding to Anti-sera
if you have an A+ pt, what would you expect on their front/fwd typing to show?
would expect agglutination in anti-A, anti A,B, and Anti-D
neg on anti-B and D cont
Back/reverse typing
mix pt sera with commercially prepared cells
agglutination–> reveals presence of Ab to corresponding cells
if you have an A+ pt, what would you expect on their back/reverse typing to show?
+anti-B
Ab screen (Indirect antiglobulin test- IAT)
mix pt sera with screening cells
what does a + Ab screen result indicate?
detection of an immunoglobulin in pt sera against a foreign RBC antigen (pt must’ve been transfused at one point or exposed during a pregnancy)
if you are Rh+, what will you typically see when reacting your blood cells to anti-D sera
STRONG D expression response (one big agglutination)
can have WEAK D (Du)- weakly positive where may or may not be visible, might need to add reagent or incubation time for it to show up
if you are a weak D patient and you are donating blood, what are you considered as?
considered as Rh+ (bc have some form of D antigen there)
and a recipient could develop anti-D
if you are a weak D patient and you are receiving blood, what are you considered as?
some places may consider you as Rh- (espec in childbearing years), bc of possibility of developing anti_D
85% treat as Rh+ tho
ranked first in immunogenicity
Rhesus system (D)
ranked second in immunogenicity
Kell system
What dzs can the McLeod phenotype be associated with?
Chronic compensated hemolytic anemia
Chronic granulomatous dz
what would you see on peripheral blood smear in someone w/ chronic compensated hemolytic anemia
many acanthocytes (spur cells) - spiky, irregular cells close to normal size
special features of chronic granulomatous dz
lack Kx Ag on membrane of neutrophils and monocytes
deficiency of NADH-oxidase –> no H202 to destroy microbes (aka LOTS OF Infections)
What is impt to know about specimen collection
-specimen MUST be labeled at bedside (w/ time, date and initial of phlebotomist); permanent and unique ID of each pt
what is one of the biggest issues when have lethal transfusion rxns
misidentification
when a type and screen (T&S) is done, what is performed
only ABO, Rh, and Ab screen (no xmatch)
-usually when have surgical procedure or time needing blood
If have a positive Ab screen/indirect antiglobulin test (IAT)/indirect coombs…what do you do
Ab identification and look for units negative for that antigen that the alloantibody is against
then… Crossmatch (actually testing of pts serum compatibility w/ donor cells)
what does a positive Ab screen/indirect antiglobulin test (IAT)/indirect coombs detect
Ig in pts serum against Ag on RBCs (NOT pts RBCs)
Ab must NOT be bound to RBCs (either pts own RBCs or transfused RBCs) to enable detection
Direct vs. Indirect Coombs
Direct- Abs attached to own RBCs
[detect autoimmune hemolytic anemia and transfusion rxn workups]
Indirect- alloAbs in pts serums that will react to foreign RBCs’
[used prior to blood transfusion and in prenatal testing of pregnant women]
adding Coombs reagent (anti-human Igs) - makes it more visible to detection w/ test
what does an antibody work up screen for
UNEXPECTED allo-Abs
identify Ab in pt serum, not formed by pt (ex. maternal Ab in infant/fetal circulation)
antigen detection test
used after identifying Ab in pt serum
how: commercial anti-sera mixed w/ pt cells
confirmation pt +/- Ag on own cells
usually done in conjunction w/ Ag typing/screening donor cells for compatibility
Indirect Antiglobulin test/indirect coombs checks for what?
hemolysis + agglutination against “screening cells”
do at 3 diff phases (room temp, 37C, antihemoglobulin (AHG) )
@Room temp, IAT detects:
initial combination of pt sera w/ commercial suspension of RBCs
detect COLD Abs- IgM
(not rlly clinically significant)
@37 C, IAT detects:
“warm” Abs - Igm- IgG mixture + IgG
Warm Ab: Rh, Kell, Kidd, and Duffy
In the antihemoglobulin phase, IAT detects
“warm” Abs; IgG that coat the RBC membrane
when performing an IAT, what does adding a check cell (CC) do?
verify AHG was added and working
Rule out method
for every cell with negative rxn, go and cross out all the antigens that are positive on that cell
then find the only manufactured cell that is + for one antigen and negative in all the other cells
can take a while! why theres a delay typically; then have to antigen check them once find
what is an autoAb
Ab directed against individual own RBC ags
–> can cause RBC destruction
Autoimmune hemolytic anemia
when have intravascular hemolysis–> hemoglobinemia/uria
+/- anemia, incr reticulocytes, incr unconj bilirubin, decr haptoglobin
Confirm w/ DAT (coombs) and characterization of autoAbs as cold or warm reactive
what is the most common autoAb entity
cold autoantibodies (benign cold agglutinin) - 4 Celcius
IgM
usually low titer but often agglutinate at room temp; can activate complement in vitro
how can you get a false + rxn with cold autoAbs; how prevent this?
if self RBCs heavily coated w/ AB, may spontaneously agglutinate and cause a false +
Ab detection: can do a prewarm or autoabsorbed serum so cold Ab dont obscure alloAbs
when trying to test for compatibility of cold autoantibodies, what is most common and how do you do it?
auto-anti-I = MC (found on most donor units)
you also prewarm or use autoabsorption
What autoAbs react with an antihemoglobulin phase (autoimmune hemolytic anemia- AIHA)? what Ag group are they specific to?
warm Abs–> IgG
specific to Rh group Ags (high incidence)
how can the warm autoantibodies be induced?
idiopathic or SLE-assoc or drug-induced
need pt med hx and transfusion rxn
should you transfuse a patient with warm autoAbs
many patients dont require transfusions
can use steroids and splenectomy
Cold Agglutinin Dz
varies from none to life threatening hemolytic anemia (intravascular hemolysis- increases as pt is exposed to COLD and complement gets activated)
what should a person w/ cold agglutinin dz avoid?
COLD WEATHER (and walk in freezers lol)
infections assoc with cold agglutinin dz
mycoplasma pneumoniae pneumonia
or
infectious mononucleosis
how do you perform a crossmatch (compatibility testing)
first recheck the recipients ABO Rh type (forward and reverse typing + weak D)
if positive..AB ID
if negative (no unexpected antibodies)–>
CROSSMATCH:
utilizing pt sera and mixing it with donor RBC to make sure dont have any bad reactions and is compatible
detect agglutination: if no agglutination/hemolysis = COMPATIBLE
ex. donor PC A (compatible recipient = A and AB)
Adverse effects of transfusion include:
Shock, respiratory distress, fever, acute hemolyic or septic rxns, and TRALI
Mgmt of acute transfusion rxns
- STOP TRANSFUSION
- Keep IV open w/ 0.9% NaCl
- verify correct unit was given to correct pt
- notify attending physicians and blood bank
ADVERSE RXN: stop transfusion, report rxn to blood bank IMMEDIATELY, return bag w/ attached tubing, return all paperwork, send post-transfusional blood sample
Transfusion-related GVHD
infusion of immunocompetent donor lymphs to immunocompromised recipient
what is the circulatory overload transfusion rxn
either too large a volume or too fast infusion