Blood Bank Flashcards
In the United States, the volume of blood collected during routine phlebotomy is …
In the United States, the volume of blood collected during routine phlebotomy is either 450 mL ± 10% (405 to 495 mL) or 500 mL ± 10% (450 to 550 mL).
What volumes necessitate a new label of RBC low volume?
If 300 to 404 mL of whole blood is collected into an anticoagulant volume intended for 450 ± 10%
**333 to 449 mL of whole blood is collected into an anticoagulant volume intended for 500 mL ± 10%,
***RBCs prepared from the unit should be labeled “Red Blood Cells Low Volume.”
What happens if the blood volume collected is less than 300mL?
If the collection volume is less than 300 mL, the amount of anticoagulant must be proportionally decreased.
What platelet count is needed for platelet donation?
To prevent a post-donation platelet count below 100,000/μL, a plateletpheresis donor is deferred from future donations until a platelet count of 150,000/μL is achieved.
Deferral period for warfarin
Donors who have been taking warfarin are eligible to donate 7 days after their last dose.
Reasons for FOREVER deferral from donation
Reasons for indefinite deferral:
-History of viral hepatitis after the 11th birthday
-Repeatedly reactive test for anti-HBc on more than one occasion
-Repeatedly reactive test for HTLV on more than one occasion
-Present or past clinical laboratory evidence of infection with HIV, hepatitis C virus, or HTLV
-History of babesiosis or Chagas disease
-Evidence or obvious signs of parenteral drug abuse
-Administration of nonprescription drugs using a needle
-Risk of variant Creutzfeldt-Jakob disease (as defined in most recent FDA guidance)
Reasons for a 3 year deferral from donation
Reasons for a 3-year deferral include (think malaria)
* diagnosis of malaria (3 years after becoming asymptomatic)
*living for at least 5 years in a malaria-endemic area (3 years after departure from area).
Reasons for a 12 month deferral
Reasons for a 12-month deferral:
-Travel to an area where malaria is endemic
-Exposure to blood via mucous membranes
-Penetration of skin with instrument/object contaminated with blood or body fluids that is not from the donor (includes tattoos or permanent make-up unless applied by a state-regulated entity with sterile needles and ink that has not been reused)
-Sexual contact or lived with an individual who has acute or chronic hepatitis B; has symptomatic hepatitis C; or is symptomatic for any other viral hepatitis
-Sexual contact with an individual with HIV infection or who is at high risk of HIV infection
-Incarceration in a correctional institution for more than 72 consecutive hours
-Diagnosis of syphilis or gonorrhea (must have completed treatment)
-Reactive screening test positive for syphilis and no confirmatory test was performed
-Confirmed positive test for syphilis
How long does incarceration need to occur before deferral
72 hours
*overnight is fine
Whole blood donation interval
The whole blood (WB) donation interval is 8 weeks (56 days)
How often can you donate platelets?
After 2 days (but certain number per week overall)
*WB donors need only wait 2 days after plateletpheresis
*but WB donation is 8 weeks, no matter what you want to donate
you do NOT need to defer for which vaccines?
toxoids; synthetic or killed viral, bacterial, or rickettsial vaccines (includes hepatitis B vaccine); recombinant vaccines; and intranasal live attenuated flu vaccine.
deferral period after receipt of live attenuated viral and bacterial vaccines for measles (rubeola), mumps, polio (Sabin/oral), typhoid (oral), and yellow fever is…
2 weeks
defer for two weeks after…
deferral period after receipt of live attenuated viral and bacterial vaccines for measles (rubeola), mumps, polio (Sabin/oral), typhoid (oral), and yellow fever is 2 weeks.
Which vaccines require a 4 week deferral
The deferral period after receipt of live attenuated viral and bacterial vaccines for German measles (rubella) and chickenpox (varicella zoster) is 4 weeks.
How many days before a surgery is autologous donation needed?
Three days
*this is the anticipated time of transfusion for autologous donation as defined by the AABB standards.
*The autologous donor should have hemoglobin 11 g/dL or greater or hematocrit 33% or greater.
*An autologous donor should be deferred if he or she has a medical condition for which there is a risk of bacteremia.
deferral period following 2-U RBC apheresis donation
112 days
Infectious disease testing for blood components
All allogeneic blood donations are tested for:
*HBV surface antigen (HBsAg), anti-hepatitis B virus core (HBc) antibody, HBV DNA,
*anti-hepatitis C virus antibody, hepatitis C virus RNA,
*anti-HIV-1/2, HIV-1 RNA,
*anti-human T lymphocyte virus (HTLV) I/II antibody,
*a serologic test for syphilis
*West Nile virus RNA.
Is product testing for babesia required?
*no, but it’s common in regions like ours
*There is an FDA-approved test to detect Babesia in blood donors. Current FDA recommendations call for regional testing or pathogen reduction (for those products where licensed devices are available) in the 15 recognized Babesia-risk states. Potential blood donors who have a history of Babesia infection are indefinitely deferred from blood donation.
What’s the homozygous rule out exception?
Kell (you can rule out a heterozygous)
Most common haplotypes White
R1,r,R2,Ro
Most common haplotypes Black
Ro,r,R1,R2
Dolichos Biflorus
Dolichos Biflorus: A1
Plant thing that will kill A1
Dolichos Biflorus: A1
Ulex europaeus:
Ulex europaeus: H
Plant thing that kills H antigen
Ulex europaeus: H
Vicia graminea:
Vicia graminea: N
Plant thing that kills N antigen
Vicia graminea: N
three most important lectins
Dolichos Biflorus: A1
Ulex europaeus: H
Vicia graminea: N
Proteolytic enzymes
Proteolytic enzymes (ficin, papain, trypsin, bromelin)
samples treated with proteolytic enzymes means you can’t rule out which antigens?
MNSs and Duffy
Cannot rule out these antibodies on panels treated with these enzymes
*they are killed by ficin, papain, trypsin, bromelin
Ficin, papain, tyrpsin, bromelin all INCREASE reactivity for what antigens?
Increase reactivity for the other antibodies (Rh, P, I, Kidd, and Lewis)
Ficin, papain, trypsin, bromelin (proteolytic enzymes), do NOT affect which major antigen?
Kell
Inhibition of red blood cell antigens and antibodies through adding random stuff:
Lewis: saliva
P1: hydatid cyst fluid, pigeon egg whites
Sda: human urine
Ch/Rg: plasma from Ch+, Rg+ individuals
Inhibit lewis antigen
Saliva (amylase)
Inhibit P1 antigen
hydatid cyst fluid
pigeon egg whites
Inhibit Sda antigen
human urine
Inhibit Ch/Rg antigen
plasma from Ch/Rg + individuals
N-acetylgalactosamine is added to H antigen to give you…
A antigen
Galactose is added to H antigen to give you…
B antigen
H antigen is…
building block for A and B
*bombay phenotype doesn’t have H, which is one of the highest frequency antigens out there
Differential amount of H antigen on red cells in ABO
O>A2>B>A2B>A1>A1B
You see a reverse type discrepancy, where it looks like patient is AB+, but their reverse type has reactivity to A
Reverse type discrepant, not forward
*probably that patient is A2B (rh+)
*give them O+ blood emergently
*if not in a pinch, give B since you know they don’t have Ab to B
what is the acquired B phenotype?
They have a historical A- history
*now they weakly look like a B expressor (react with anti-B)
*very strong backtype anti-A antibody in their plasma
*Caused by result of deacetylation of the A antigen’s N-acetyl-galactosamine
Think of enteric bacteria, colon or rectal cancer
To resolve:
Use a different monoclonal anti-B or acidified human anti-B
A patient has colon cancer and now a weird ABO discrepancy
probably an acquired B phenotype
What are the highlights of the Bombay phenotype?
Total lack of H, A and B antigens due to lack of H and Se genes
Genotype: hh, sese
Naturally occurring strong anti-H, anti-A, anti-B
ABO testing: type as O forward, O reverse,
**But antibody screen is broadly and strongly positive
***No units are compatible
What can destroy the Kell antigen?
not the proteolytic enzymes…
*Destroyed by Diothiothreitol (DTT) and 2-aminoethylisothiouronium bromide (AET)
Kell causes an extra ‘hit’ in HDFN
IgG antibody, so it CAN cause HDFN
*also decreases reticulocytes and erythropoiesis
*less overall hemolysis (compared to Rh) but supression
what does McLeod phenotype have to do with Kell antigen?
X-linked rare disorder
*ACANTHOCYTES (lots of them)
*Kx is gone, so kell antigen is gone (people can make antibodies against little k, which is a high prevalence antigen)
what does x-linked granulomatous disease have to do with Kell antigen?
it’s another Kx deletion problem
*people can make antibodies to high frequency antigens (little k)
*can’t find blood after that
What antigen is a classic caused of delayed hemolytic transfusion reactions?
Kidd antigens
*antibodies drop to low levels after initial formation
*memory B cells are still there
*come back in a fury after transfusion and BAM (dhtr)
Which antigen is 0% C and 67% AA
Fy(a-b-) 0% C and 67% AA
*still NOT common for AA to have Ab against Fy3 (which is duffy a and b -) because GATA mutation is what gives them the duffy a-b- phenotype, but other tissues/cells still make duffy b, so they are at little risk of making Fyb
*exceptionally rare for a white person to have ab against Fy3
GATA mutation and duffy
GATA mutation kinda common in AA
why do so many AA not have duffy?
receptor for binding of plasmodium (malaria), specifically vivax
what antigens are located on glycophorin A & glycophorin B
Located on glycophorin A & glycophorin B
M and N on GPA
S, s, and U on GPB
Can a white person have an ab against U?
U=universal
*S-s- phenotype is super rare, only in AA
*can’t find blood because they make an anti-U antibody
MNS system with HDFN
Anti-M
Often naturally occurring
Usually not active at 37C and not clinically significant
But if present at IAT then assume clinically significant
Anti-N
Rare
Anti-S and s:
IgG and active at 37C
Implicated in HTRs and HDFN
Donath Landsteiner test
finding a paroxysmal cold hemoglobinuria antibody
*The Donath-Landsteiner (DL) test is a serologic test used to detect the presence of a biphasic hemolysin. This autoantibody is seen in patients with paroxysmal cold hemoglobinuria. The test relies on the characteristic cold binding of an IgG autoantibody with specificity to the P blood group antigen.
What antigen is implicated in Cold Agglutinin Syndrome?
Autoanti-I and autoanti-i
Pathologically significant in CAS and mixed type hemolytic anemia
Complement binding antibody with high titer and wide thermal range
***Seen in lymphoproliferative diseases, infection (esp. Mycoplasma pneum.)
You are given the results of a KB test and told to make a dose for Rhogam
Fetal cells X maternal blood volume/ total cells counted = fetal hemorrhage (mL)
Another way to think about it is:
KB% multiplied by TBV= fetal blood
Fetal blood/ 30= number of vials needed
If number after decimal is < 5, round up
If >5, round up twice (extra vial after rounded up)
Rh, K, Fy, Jk, MNSs, and i antigens
all strongly expressed on baby red cells
Most common antigens you think of in HDFN
D, c , and K
Other Rh, Duffy, and Kidd are usually mild
Anti-S, -s, -U: are uncommon but can be severe
BUUUUUT, what is the MOST common cause of HDFN
ABO
Group O mother and usually a group A baby
*pretty much everyone has ABO, so there’s more likeliehood that this will be the cause
what does the clinical team have to do with a HDFN antibody?
If identified antibody is associated with HDFN, antibody titration is performed at regular intervals
Titers are read macroscopically in the blood bank
Critical titer is 16 for D
Critical titer for Kell is 8
If a critical titer is reached, then further monitoring is needed (amniocentesis, MCA-peak systolic velocity, or direct fetal blood sampling)
Critical titre for D
16
Critical titre for Kell
8
*lower titre than D, because of hematopoiesis inhibition
