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Flashcards in Blood Bank Deck (151):

How do the following potentiating agents work:


2) 22% albumin

3) PEG

1) decreases repulsive charges between RBCs (zeta potential) allowing them to get closer together for greater antibody bridging (drawbacks are that it tends to enhance expression of cold antibodies and autoantibodies

2) also deceases zeta potential but used less commonly than LISS

3) excludes H2O and allows RBCs to get closer during centrifugation. Tends to enhance expression of warm antibodies and autoantibodies. Greater sensitivity than LISS or albumin (drawback is may lead to false positive reactions at 37C from nonspecific agglutination).


What are the most common antibodies that show dosage?

Kidd, Duffy, Rh, MNS

*Duffy and Kidd are very similar in that they both show marked dosage, variable expression and delayed HTRs


What blood groups are enhanced by proteolytic enzymes (ie ficin, papain)?

  • ABO related groups:

ABO, H systems

Lewis System

I System

P1PK/GLOB Systems

  • Rh System
  • Kidd System


What blood groups are decreased by proteolytic enzymes (ie ficin, papain)?

MNS System

Duffy System

Lutheran System


What blood groups are unaffected by proteolytic enzymes (ie ficin, papain)?

Kell System

Diego System

Colton System


What is the neutralizing substance for ABO group?

Saliva (secretor)


What is the neutralizing substance for Lewis group?

Saliva (secretor for Leb)


What is the neutralizing substance for P1?

Hydatid cyst fluid and pigeon egg whites


What is the neutralizing substance for Sda?

Human urine


What is the neutralizing substance for Chido and Rodgers group?



What lectin has specificity for:

1) A1

2) H

3) N

4) B

1) Dolichos biflorus--used to distinguish A1 from subgroups

2) Ulex europaeus--agglutinates group O cells; useful in determination of secretor status

3) Vicia graminea

4) Bandeiraea simplicifolia


What are the biochemical components of Type 1 and Type 2 chain in the ABO and H Systems?

Type 1) glycoPROTEINS in secretions and glycoLIPIDS in plasma carrying free-floating antigens

Type 2) glycoLIPIDS and glycoPROTEINS bounds to RBCs


What is the secretor (Se) gene?

FUT2; “fucosyltransferase”
1) Required to make A or B antigens in secretions
2) FUT enzyme adds fucose to type 1 chains at
terminal galactose; product is type 1 H antigen
3) 80% gene frequency


What is the H gene?


1) Closely linked to Se on chrom 19
2) FUT enzyme adds fucose to type 2 chains at
terminal galactose; product is type 2 H antigen.
3) Virtually 100% gene frequency (Bombay = hh).


Explain how A and B antigens are made and what are the respective sugars that are added to the terminal galactose?

H antigen required before A and/or B can be made on
RBCs (type 2 H) or in secretions (type 1 H).
Single sugar added to a type 1 or 2 H antigen chain
makes A or B antigens and eliminates H antigen.
Group A sugar: N-acetylgalactosamine
Group B sugar: Galactose

As more A or B is made, less H remains.
H amount: O > A2 > B > A2B > A1 > A1B


What chromosome contains the alleles for the ABO antigens and what do they code for?

Genotype determined by three alleles on long arm of chromosome 9: A, B and O
A and B alleles code for transferase enzymes, not directly for antigens (O makes nonfunctional enzyme)
ABO antigens begin to appear on fetal RBCs at 6 weeks gestation; reach adult levels by age 4.
Also platelets, endothelium, kidney, heart, lung, bowel, pancreas tissue

This is slightly different for ABO ANTIBODIES that appear at 4 months of age and reach adult levels by age 10


Which antigen does H. pylori and Norwalk virus attach to?

Leand H (important is Leb)


What two infections are Le(a-b-) people at risk for?

Candida and E. coli infections


1) What are the associations with auto-anti-I?

2) What is the association with auto-anti-i?

1) Cold agglutinin disease and Mycoplasma pneumoniae infection

2) infectious mononucleosis


What antigen is the receptor for binding shiga toxin and toxins from some E.coli strains in renal epithelium?

Pk antigen

*according to BB guy, Pk antigen inhibits HIV infection


What is the disorder in patient's who make an auto-anti-P and what is the test used to diagnose it?

Paroxymal Cold Hemoglobinuria

They make an IgG biphasic antibody with unique features. It binds in cold temps but then hemolyzes when warmed to 37C (this is demonstrated in vitro for diagnosis)

Donath-Landsteiner biphasic hemolysin test--three test tubes, when starting at 4C and heating to 37C, you see hemolysis in tube. At 4C or 37C alone, no hemolysis

Seen historically in people with syphilis but now seen mostly in kids following viral infection


What chromosome has the Rh genes?

Chromosome 1


1) Of the Wiener haplotypes, which 4 account for 97% of people?

2) What is the order of frequency for blacks and whites?

1) R1, R2, R0, and r

2) Whites: R1>r>R2>R0 and Blacks: R0>r>R1>R2

*way to remember, R0 is most common in blacks and least common in whites, r is always second in frequency, and R1 always comes before R2


What phenotype will cause patients to have stomatocytic hemolytic anemia?

Rhnull phenotype

These patients lack RhAG (Rh-associated glyocoprotein) which is needed for expression of all Rh antigens.

Altered S, s, and U antigens possible due to associations with glycophorin B


What is the receptor for P. falciparum?

MNS System:

Glycophorin A carries M or N antigens

Glycophorin B carries S or s and U antigens

Glycophorin A AND Glycophorin B are both receptors for P. falciparum!


What phentype is resistant to P. VIVAX and why?

Fy(a-b-) are resistant to P. vivax

68% of blacks have this phenotype due to inheritance of two copies of the Fy gene which gives no functioning DARC glycoprotein (which carries the Duffy antigens)

P. vivax merozoites attach to RBCs via this DARC glycoprotein so if you don't make it, organism can't attach

Because of differing mechanisms of Duffy negativity in whites and blacks, most Fy(a-b-) blacks do not form anti-Fy Abs but Fy(a-b-) whites do


What is seen clinically in pts with McLeod Syndrome?

 Acanthocytic Anemia

Neuro/Muscular Disorders

Psych Disorders

X-linked CGD association



What is the difference between McLeod syndrome and McLeoud phenotype?

Both are caused by sex-linked deletion of portion of X chromosome where Xk gene for Kx Ag resides. Kx antigen is a non-Kell system antigen that is adjacent to Kell structure on RBC membrane and is required for Kell antigen expression

*If transfused, either syndrome or phenotype patients can form anti-Kx and anti-Km; only McLeod RBCs compatible

McLeod Phenotype: Kx and Km are absent, all other Kell antigens markedly decreased but not absent like K0

McLeod Syndrome: Hemolytic anemia with acanthocytes, neuromuscular disorders, psych disorders, X-linked CGD association


What history elicits a permanent deferral for blood donation?

Infectious Risks
-High-risk behavior for AIDS
(IVDA, male-male sexual contact since 1977)
-Receiving money or drugs for sex
-Serologic positive for HIV, HBV, HCV, HTLV
-Viral hepatitis after 11th birthday
-Transfusion of clotting factor concentrates (in hemophilia)
-History of Babesiosis or Chagas’ disease
-Growth hormone from human sources (pre-1985)
-Insulin from bovine sources
-Dura mater graft
-Leukemia or lymphoma

-Tegison (Psoriasis med that hangs around a long time)


What history elicits a 3 year deferral for blood donation?

Infectious Risks
-Recovered from malaria
-Immigrants from malaria-endemic countries
(after 5 consecutive years of living there)
-Soriatane (Psoriasis med that doesn't hang around as long as Tegison)


What history elicits a one year deferral for blood donation?

Infectious Risks
-Needle sticks or other contact with blood
-Sex contact with person with HIV or hepatitis
-Sex contact with person who used needles for drugs
-Rape victims
-Incarcerated > 72 consecutive hours
-Paying money/drugs for sex
-Blood transfusion (Allogeneic); including plasma/clotting
factors in nonhemophiliacs
-Allogeneic transplant of organ/skin/bone
-Living with person with active hepatitis
(exception: Asymptomatic Hepatitis C)
-Receiving HBIG
-Tattoos/piercings (unless by regulated entity)
-Travel to malaria-endemic areas for residents of non-endemic
countries (>24 hrs, < 5 years)
-Syphilis or gonorrhea
-Non-prophylactic rabies vaccination
-“Travel” to Iraq


What immunizations get 4 week deferral?

Rubella and Varicella


What immunizations get 2 week deferral?


Oral polio
Yellow fever
Oral typhoid


What immunzations get NO deferral?

Hepatitis A
Hepatitis B

Lyme disease
Polio (injection)
Typhoid (injection)


*Definite Board Q!

What are the hemoglobin and hemocrit requirements for autologous and allogeneic blood donation?

Autologous: >11 or 33%

Allogeneic: >12.5 or 38%

Other allogeneic parameters: temp < 37.5C (99.5F), HR 50-100, BP no higher than 180/100


How long are products good for in the following solutions:

1) Acid Citrate Dextrose (ACD)

2) Citrate Phosphate Dextrose (CPD)

3) Citrate Phosphate Dextrose Dextrose (CP2D)

21 days for all

ACD is used for apheresis platelets and formerly for RBCs

CPD and CP2D are for RBCs


How long are products good for in the following solutions:

1) Citrate Phosphate Dextrose Adenine (CPDA-1)

2) Adenine Saline additives

1) 35 days

2) 42 days

more adenine=more ATP for cells



What are the storage details for RBCs/whole blood?

21 days (CPD/2D)
35 days (CPDA-1)
42 days (AS)
All @ 1-6 C



What are the storage details for frozen RBCs?

10 years @ –65 C
24 hours @ 1-6 C
after thaw



What are the storage details for washed RBCs?

24 hours @ 1-6 C



What are the storage details for platelets?

5 days @ 20-24 C
(gentle agitation);
4 hours if pooled in open system



What are the storage details for granulocytes?

24 hrs @ 20-24 C
(no agitation)



What are the storage details for frozen plasma (FFP, PF2A etc)?

1 year @ –18 C
7 years @ –65 C;
24 hours at 1-6 C
after thawing at 30-37C

*must be separated and placed in -18C within 8 hours of collection



What are the storage details for cryo?

1 year @ –18 C
6 hours @ 20-24 C
after thaw (4 hrs if pooled in open system)



What are the QC parameters for RBCs?

HCT < 80% (all);
> 50 g HGB in 95%
(apheresis RBCs)



What are the QC parameters for RBCs leukoreduced?

≤ 5 x 106 WBCs in 95%, retain 85% of RBCs



What are the QC parameters for platelets?

≥ 5.5 x 1010 and pH ≥ 6.2 in 90%



What are the QC parameters for platelets leukoreduced?

≥ 5.5 x 1010 in 75%,

pH ≥ 6.2 in 90%,

AND <8.3 x 105 WBCs in 95%



What are the QC parameters for apheresis platelets?

≥ 3.0 x 1011 and pH ≥ 6.2 in 90%



What are the QC parameters for apheresis platelets leukoreducted?

≥ 3.0 x 1011 and pH ≥ 6.2 in 90%

AND < 5.0 x 10residual WBCs in 95%



What are the QC parameters for cryo?

Factor VIII ≥ 80 IU (all)
Fibrinogen ≥ 150 mg (all)



What are the QC parameters for granulocyte concentrate?

≥ 1.0 x 1010 in 75%


What is the shipping temperature for RBCs?

1-10 C


What are the volume contents of cryoprecipate?


>150mg fibrinogen

>80 IU Factor VIII

80-120 IU vWF

40-60 IU Factor XIII




What are the established benefits of the leukoreduction of red cells?

Prevention of febrile nonhemolytic transfusion reactions, prevention of HLA immunization, prevention of CMV transmission (both CMV neg and safe have 1-4% chance of transmission), reduction of reperfusion injury post cardiac bypass


What are some indications to freezing products?

Storage of rare, autologous or O negative units, plasma hypersensitivities (as with washed) and repeated febrile reactions (as with washed)

Red cell: 10 years at -65C (40% glycerol), 24 hours at 1-6C after thawing/deglycerolizing

Platelets: At least two years at -80C after thawing/deglycerolizing


What are the Weiner Haplotypes and what are the "rules" for remembering?


“R” = D, “r” = d
“1” or “prime” = C
“2” or “double prime” = E
“0” or “blank” = ce
Any sub- or superscript letter = CE

R1: DCe          r’ : dCe
R2: DcE          r”: dcE
R0: Dce          r : dce
Rz: DCE          ry : dCE


What is the main indication for irradiating cellular components and what is the dose of radiation required?

To prevent transfusion associated graft vs host disease

2500 cGy dose required targeted to center of bag, with at least 1500 cGy in all parts of the bag

Maximum storage: 28 days after irradiation or regular expiration date, whichever comes first


Regarding transfusion therapy considerations in bone marrow, stem cell or cord blood transplants, there are 3 phases: Phase I (pre-transplant), Phase II (peri-transplant) and Phase III (post-transplant). 

1) What is the definititon of Phase II (peri-transplant)?

2) What are the rules for giving transfusion products in each phase?

1) Begins at time of treatment and ends when full engraftment has occurred. In ABO-incompatible transplants, phase II ends when recipient’s blood type has converted to donor’s type.

2) Transfusion in different phases:

  • Phase I--it's pre transplant so give patient usual compatible products
  • Phase II--tricky stage
    • ​In major mismatch (NON-O donor to O recipient or AB donor to A or B recipient), transfuse the recipient’s red
      cell type and donor’s FFP/platelet type
      (of course, you can always use AB FFP).
    • In minor mismatch (O donor to NON-O recipient or A or B donor to AB recipient), transfuse the donor’s red
      cell type and recipient’s FFP/platelet type
      c) For both major and minor mismatches (giving A to B or B to A), give O red cells and AB plasma.
  • Phase III--post transplant so they have converted to donor's blood type so use the transplant DONORs type to make decisions


Of the Weiner's haplotypes, what are the frequencies in whites, blacks and asians?

--R0 most common in blacks, least common in whites.
--r is always second in frequency.
--R1 always comes before R2.
                                     “The Big Four”
                              Whites: R1 > r > R2 > R0
                                Blacks: R0 > r > R1 > R2

--Asians usually D+; order is R1 > R2 > r = R0.


What is the blood bank guy's easy shortcut for calculating amount of RhIg vials needed for maternal-fetal exposure?

KB% x 5/3 = number of vials
In above example, (2 x 5)/3 = 3.33

Remember, the 5 is if you are assuming a BV of 5000mL because the test did not give you amount. Otherwise, if they tell you the weight of the mother, then you can calculate actual BV by using 70mL/kg conversion. If it is 6 liters, you would multiply by 6 in the above example.

Rounding rules: If number after decimal is < 5, round up once. If > 5, round up twice. So, “3.4” would mean give 4 vials, while “3.5” would mean to give 5 vials


If you are asked on test how many units will be compatible with a patient who has two or more antibodies, how do you calculate that?

Calculate the % compatible units by using frequency like usual. Then you divide the number of units the stem wants by the %.

For example, how many units would you have to test to find 2 compatible units with someone who has anti-K1 and anti-Jka?

Frequency is 21% compatible so 2/.21 = 9.5 or 10 units


What is the formula for calculating corrected count increment?

Body Surface Area (Pltpost - Pltpre) x 1011/

Number of platelets transfused x 1011

*The 1011 is irrelevant and you can ignore it because it is on top and bottom so they cancel out. The stem should give you the amount of platelets transfused because each apheresis bag gets an exact number.

7500 or above defines "adequate" response and two consecutive counts below 5000 defines refractoriness


How to do calculate the numbers of units of cryo needed for hypofibrinogenemia?

Critical Data Needed: Weight in Kg, Hct, and current fibrinogen leveltarget fibrinogen level

If they do not give target level, 100mg/dL is "adequate" and 150 mg/dL is "optimal". 


1. Calculate Blood Volume
Body weight x 70 ml/Kg
2. Calculate Plasma Volume (PV)
Blood volume x (1 - hematocrit)

Divide by 100 to convert to dL
3. Calculate mg fibrinogen needed
Plasma volume x concentration change desired
*Subtract desired level from current
(ie, 150 mg/dl – 50 mg/dl)
*Multiply level change by PV
(ie, 100 mg/dl x 36 ml)
4. Calculate bags of cryo needed
Fibrinogen needed / 250 mg per bag



How do you calculate amount of FVIII to give?

*BB guy has a more complicated way of doing this than the CP Board review book. According to that, all you need is patient weight and desired factor level. For example, if a 30kg patient has a Factor VIII activity of 1% and you have a desired activity of 50% the formula is:

%Change in activity desired x body wt (kg) x 0.5 IU/kg = Factor VIII dose

%Change in activity desired x body wt (kg) x 1.0 IU/kg = Factor IX dose

Trust BB guy because I get weird numbers when I use the above

Almost identical to fibrinogen cryo calculation

Critical data: body weight in Kg, Hct, current and target VIII level

If not given a target level, use 50% (remember FVIII is measured in percent present) for hemarthrosis, minor bleed or minor surgery and use 100% for major surgery or life threatening hemorrhage.


1. Calculate Blood Volume
Body weight x 70 ml/Kg
2. Calculate Plasma Volume (PV)
Blood volume x (1 - hematocrit)

3. Calculate FVIII units needed
Plasma volume x increase desired = FVIII units needed
4. Only if asked, calculate bags of CRYO needed
FVIII units needed / 80 units per bag





What are the 4 most common antibodies in immediate HTR?

Anti A


Anti Jka

Anti Fya


What are the 4 most common antibodies in delayed HTR?

Anti Jka

Anti E

Anti D

Anti C


What are the 4 most common antibodies in HDFN?

Anti A,B

Anti D


Anti C


What 3 antibodies commonly produce intravascular hemolysis?



P (Paroxysmal Cold Hemoglobinuria)


Which antibody targets red cell precursors in addition to mature red cells therefore suppressing erythropoiesis?



What are the rejuvenation and storage conditions for

1) CPD

2) AS-1

1) RBCs collected in CPD or CPDA-1 may be rejuvenated up to 3 days after expiration and then frozen for 10 years

2) RBCs stored in AS-1 may be rejuvenated up to the original 42 day expiration date and then frozen for up to 3 years


Kell antigens are destroyed by sulfhydryl reagents such as DTT, ZZAP and ME. What is the mechanism by which this happens?

Sulfhydryl reagents reduce disulfide bonds to produce free sulfhydryl groups. There are multiple disulfide bonds between cysteine residues in the extracellular domains of the Kell antigen.


What is the first line agent to improve hemostasis in uremic patients by inducing the release of endogenous von Willebrand factor from endothelial cells?

Desmopressin acetate (DDAVP)


Which of the following statements is correct regarding platelet specific antigens?
A) Approximately 80% of the population is HPA-1a positive.
B) Nearly 100% of patients who are HPA-1a negative will develop HPA-1a antibodies following exposure to the antigen.
C) Patients who are HPA-1a negative and who have the HLADRB*0101 are more likely to develop HPA-1a antibodies following exposure to the antigen.
D) HPA-5b is the most common cause of neonatal alloimmune thrombocytopenia (NAIT) among Caucasians.
E) HPA-1a is found on glycoprotein Ia

Patients who are HPA-1a negative and who have the HLADRB*0101 are more likely to develop HPA-1a antibodies following exposure to the antigen.

Although 98% of the population is HPA-1a positive, not all of the remaining 2% of HPA-1a negative population will make antibody when exposed to the antigen. This is due to genetic restriction associated with HLA type DRw52a (DRB3* 0101). HPA-5b is the second most common cause of NAIT (10%) after HPA -1a. HPA-1a is found on glycoprotein IIIa.


Name in decreasing the order the amount of H antigen present in the different ABO groups.

H amount: O>A2>B>A2B>A1>A1B

*A1 antigen has 5x more antigen than A2 which makes sense based on A1 having the least amount of H present


Are the antibodies made by the different ABO groups, IgM or IgG?

Group A and B: Anti-A or Anti-B is predominately IgM but each reacts strongly at body temp

Group O: Anti-A and B are predominately IgG and react best at body temp. Anti A,B is IgG


BQ! What color are the reagents used to test for Anti-A and Anti-B?

Reagent Anti-A = BLUE

Reagent Anti-B = YELLOW

so if you see a test tube with clumping with blue fluid, it's Type A blood group

This is backwards of what you would think but they love to ask this on boards for some reason!


What is the biochemistry behind the Lewis antigens?

Type I chains only, one gene: Le (FUT3)
FUT enzyme adds fucose to subterminal GlcNAc. This makes Lea (Lewis A) antigen. In a non-secretor, Lea is the only Lewis antigen possible.
Lea antigens cannot be further modified to make Leb . In secretors, Se product adds fucose, then Le product adds fucose; this makes Leb (Lewis B).
In secretors, this interaction occurs preferentially over Leformation.
As a result, the vast majority the chains of secretors who carry Le are Leb rather than Lea. In non-secretors, the Lea is the only possible Lewis antigen.

Le(a-b+) HAVE Lewis A; just undectable routinely.


What are some weird things about the Lewis antigens?

  • 22% of blacks are Le(a-b-) vs ony 6% of whites
  • 10-40% of Asians are Le(a+b+) due to "weak secretor" gene so Se and Le compete equally
  • Lewis antigens decrease during pregnancy (increased plasma volume dilutes antigens and increased plasma lipoproteins bind the antigens) so they may appear Le(a-b-) and have transient insignificant Lewis Abs
  • Le(a-b+) don't make anti-Lea 
  • H. pylori attaches to gastric mucosa via Leb antigen
  • Norwalk virus also attaches via Leb
  • Le(a-b-) are at risk for Candida and E.coli infection



On a standard blood panel, what are the low frequency and high frequency antigens represented?

Low frequency: Cw, Kpa, Jsa, Lua

High frequency: Kpb, Jsb


What is significant about the Anti-PP1Pk and how common is it?

This is a VERY rare antibody that can be seen in people that are P1-Pk-P- 

It causes SEVERE HTRs with P1 or P2 phenotype blood and patients can have spontaneous abortions from placental P/Pk attack


What antigens are MOST affected by Rhnull phenotype?

Fy5, Lw, S, s, and U


What is the weak D phenotype?

A quantitative defect in the D antigen (less D than normal)

Possible reasons: mutated form of RHD (most common by far)--point mutations cause altered amino acids in membrane or inner part of RHD. Another reason is RHCe on opposite chromosome to RHD inhibits D expression (C in trans)

Testing requirements: weak D test for all D neg DONORS but not required for D neg recipients

Only non-donors who definitely need weak D testing: D neg babies born to D neg moms

Weak D moms do NOT need RhIg


What is the partial D phenotype?

qualitiative defect (abnormal forms, missing part of the antigen)

Some also have a quantitative defect (so called partial weak D)

Cause: RHD gene mutations leading to alteration of the EXTERIOR part of the RHD antigen

Antibodies form against absent parts of RHD and this Ab appears to be Anti-D at first glance

Classic scenario is Anti-D in a D positive person

Most common: DVI (D six) in whites, DIIIa in blacks


What does partial D and weak D phenotypes matter?

  • Partial D moms need RhIg while weak D's do not
  • Partial D recipients may make Anti-D when receiving D+ RBCs, weak D recipients generally do not
  • Partial D OR weak D donor RBCs may induct anti-D in a D neg recipient
  • The distinction may be impossible without molecular testing so when in doubt, just give D neg blood


What is the G antigen?

An Rh antigen that is present when EITHER C or D is present

Anti-G reacts against (D+C-), (D-C+), or (D+C+) RBCs (rarely against (D-C-G+)

Common presentation: D neg person forms Anti-D and anti-C despite no exposure to D

Important because if D neg mom has anti-G, she DOES still need RhIg to prevent anti-D


What is the f antigen?

An Rh antigen that is present when RHce is inherited (r and R0

Anti-f is often seen with anti-e or anti-c

Can cause mild HDFN and HTR

Most common alloAb directed against compoud Rh antigens

It is found primarily in persons with DCe/DcE (R1R2)


What is the most famous association with the Kidd antibodies?

Delayed HTRs, anamnestic response, intravascular and often severe

Jka, Jkb, Jk3 (VERY high frequency)

Antigens reside on urea transport protein--Jk(a-b-) RBCs are RESISTANT to hemolysis in high conc 2M urea because there is no urea transport so no resultant osmotic lysis)

Abs require exposure, are warm reacting IgG (many with IgM component as well)

Can fix complement (with IgM component, 50%)

Marked dosage effect, variable antibody expression (Ab often dissapears with time, >3 months)--"kids like to play hide and seek"


When blood group phenotype can be confirmed by exposing RBCs to 2M urea?

Kidd negative phenotype

Jk(a-b-) RBCs are RESISTANT to hemolysis in high conc 2M urea because there is no urea transport so no resultant osmotic lysis)

Kidd antigens reside on urea transport protein so if no Kidd antigens, no urea transport


What rare autoantibody was historically induced by hemodialysis from formaldehyde sterilization of machine?



Anti-N is seen almost exclusively in what group?


Glycophorin B always has terminal amino acid sequence that matches the N version of glycophorin A

Not really a TRUE N antigen but close enough that most M+N- people won't form Anti-N

Present in all cases except those lacking glycophorn B (

Anti-N almost exclusive to blacks and presence suggest possibility of patient lacking glycophorin B and at risk for anti-U


Do Fy(a-b-) people make anti-Fyb?

Probably not

Fy (no a or b) is a Fyb variant that doesn't make Fyb on RBCs but it DOES make it on non-RBC tissues so they won't make antibody.

Usually from mutation in the GATA box


What reagent can destroy Kell antigens?

Thiol reagents (2-ME, DTT, ZZAP) but are unaffected by enzymes alone

Kell antigens are carried on a large glycoprotein held together by disulfide bonds and thiol reagents break those bonds, enzymes do not


What is unique about the type of HDFN that Kell causes?

Damages early RBC precursors so may be suppressive as well as hemolytic

Lower bilirubin and fewer reticulocytes compared to anti-D HDFN (early precursors = less hemoglobin for bilirubin formation)

Significant at lower titers (1:8 is critical)


Blood donor deferral for malaria is very confusing but must know. What are the deferral periods for the following situations:

Endemic area = CDC recommends prophylaxis to travelers; Endemic country = has at least one endemic area

1) history of malaria

2) living in endemic country for more than 5 consecutive years

3) resident of non-endemic country travels to endemic AREA for more than 24 hours and less than 5 years

4) resident of non-endemic country travels to endemic COUNTRY but not endemic AREA for more than 24 hours

5) previous resident of endemic country travel to endemic area

6) previous resident of endemic country travel to endemic area >3 years after leaving endemic country

1) history of malaria = 3 years (if asymptomatic)

2) living in endemic country for more than 5 consecutive years = 3 years (if asymptomatic)

3) resident of non-endemic country travels to endemic AREA for more than 24 hours and less than 5 years = 1 year (if asymptomatic)

4) resident of non-endemic country travels to endemic COUNTRY but not endemic AREA for more than 24 hours = no deferral

5) previous resident of endemic country travel to endemic area less than 3 years after leaving endemic country  = 3 years (if asymptomatic)

6) previous resident of endemic country travel to endemic area more than 3 years after leaving endemic country = 1 year (if asymptomatic)


What is the dose for neonates for plts, RBCs and FFP?

10-15 mL/kg


What is the half life of Factor VII?

~4 hours

Most FFP transfusions are given for elevated INR/PT (factor VII most responsible) but this is not really good practice because the INR of a unit of FFP is 1.2-1.5!



When a unit of RBCs is appraching the expiration date, what substances are increased?

Potassium triples and free hemoglobin increases in plasma indicative of mild RBC membrane damage

Storage lesion:

  • Glucose decreased
  • 2,3 DPG decreased
  • ATP decreased
  • pH decreased (acidosis)
  • Lactate increased
  • Potassium increased


What is the pathophysiology behind TRALI?

The neutrophil is the villiain!

Good PMNs behaving badly (they are doing normal functions but in the wrong time and place). About 30% of PMNs are in the lungs at all times

Anti-HLA or HNA from DONOR bind to recipient PMNs and the Ab-Ag complexes deposit in pulmonary vasculature and activate PMN bactericidal response

Damage to pulmonary endothelial cells lining capillaries with resultant leakage of fluids into the alveolar spaces (pulm edema)

Another theory: because this doesn't explain all TRALI reactions or why TRALI doesn't occur in some situations where it should, there is the two event pathway. 1) pre-existing condition activates lung endothelial cells and primes PMNs (sepsis, major surgery, massive transfusion) and then 2) transfusion of stored products prime the PMNs to secrete toxic substances


What is the culprit in anaphylactic transfusion reactions?

IgE anti-IgA

Usually in IgA deficient patients, can also be seen in Asians with haptoglobin deficiency

WASH products


What antibodies typically show delayed hemolytic transfusion reactions?

Definition: hemolysis occuring at least 24 hours but less than 28 days after transfusion

Kidd, Duffy and Kell

Anamnestic rapid production of IgG antibody

Classically leads to extravascular hemolysis

NOTE due to Kidd antibodies may be intravascular and severe

DAT usually shows MIXED FIELD


What is the mechanism of TAGVHD in an immunocompetent patient?

This is usually due to getting product from relative or similiar HLA type

The recipient is heterozygous for HLA type and donor is homozygous.

The donor WBCs attack the recipient because it recognizes the heterozygous part that it DOESN'T have whereas the donor doesn't mount a counterattack because it recognizes the HLA type as "self" since it has one copy too


What is post transfusion purpura?

A transfusion reaction that is rare and caused marked thrombocytopenia and increased risk of bleeding about 10 days after transfusion

Multiparous females at risk (5:1 female to male ratio)

Caused by antibody vs common PLT antigen

Anti-HPA-1A 70-80%

HPA1A POSITIVE transfused plts and HPA1A NEGATIVE platelets are BOTH destroyed

IVIG normalizes plt count in about 3-5 days

Mortality about 10% without tx and 0% with tx


What are the allowable minimum donor intervals for:

1) Single unit whole blood donation

2) 2 unit red cell donation by apheresis

3) Plasma by pheresis

4) Platelets by pheresis

1) single unit whole blood> 8 weeks

2) 2 unit red cell donation by apheresis>16 weeks

3) Plasma by apheresis: "frequent" donor programs: 2 donations/week at least 2 days apart

others: 4 weeks apart

4) Platelets by apheresis 2 donations/week at least 2 days apart and 24 in a 12 month period

plt count > 150,000 is required

*if there is whole blood donation or if red cells cannot be returned to a donor during apheresis then 8 weeks must elapse before repeat apheresis


What are recommended blood products for patients in emergencies?

Type O RBCs

Type AB plts and plasma

Match Rh if possible

*not necessary to cross match products for pts less than 4 months if there are no significant materal allantibodies


What size filter is in the standard blood infusion set? What size is a microaggregate filter?

170 um filter (standard blood infusion)

*RBCs, platelets, FFP ALL must be ran through a 170 filter

40 um (microaggregate filter)--not required

The same filter can be reused for multiple transfusions for up to 4 hours

Neonatal transfusions may be filtered by the blood bank staff prior to release


What rate of infusion should happen at the beginning of transfusion and how long?

2mL/min for 15 minutes

*do not transfuse with other fluids other than normal saline and certain FDA approved crystalloids

(LRs have a lot of calcium and bind all citrate so blood clots, half normal saline or other hypotonic solns may cause hemolysis)

All units released at one time must be transfused in 4 hours!


What does polyagglutination in transfusion testing refer to?

Adult plasma contains naturally occuring IgM Abs to T, Tn, Tk and Cad

These are normally cryptic antigens that are expressed only when bacterial neuraminidase enzymatically alter red cell antigens (T activation)

In adults, this phenomenon is primarily a factor in pretransfusion testing

In infants, it can be clinically significant in two instances:

1. Necrotizing enterocolitis (NEC)--T activation occurs in up to 25% caused be neuraminidase of Clostridia

2. Atypical HUS--neuraminidase of Strep pneumoniae

Testing: The lectin Arachis hypogaea can detect T activation. Polyagglutinable red cells are agglutinated by adult, not cord, serum.

Adult plasma contains naturally occuring anti-T Abs and therefore infants with T activation can develop intravascular hemolysis when transfused and such infants should receive RBCs with minimal plasma or washed RBCs

The effect is transient and abates following resolution of the infection


What is the antigen frequency of D?



What is the antigen frequency of C?



What is the antigen frequency of c?



What is the antigen frequency of E?



What is the antigen frequency of e?



What is the antigen frequency of G (CD)?



What is the antigen frequency of f (ce)?



What is the antigen frequency of K? k? Kpa?

K = 10%

k = 98%

Kpa = 2%


What is the antigen frequency of Jka? Jkb?

Both 75%

*Jk(a-b-) rare except in Pacific Islanders


What is the antigen frequency of Fya? Fyb?

Fya = 65% in whites, 10% in blacks

Fyb = 83% in whites, 20% in blacks

Fy(a-b-) rare in whites, 68% in blacks


What is the antigen frequency of M? N? S? s? U?

M = 80%

N = 72%

S = 55%

s = 90%

U = 99.9% whites, 99% blacks


What is the antigen frequency of P1?



What type of cancer can cause weakened expression of A or B antigens with mixed field agglutination?

Hematolymphoid neoplasms


What type of cancer can cause excess free A or B antigens to be present in serum which may have the effect in vitro of binding anti A or B reagents thereby neutralizing them and thus givign the false impression that the patient has type O red cells?

Gastric adenoCA


What is the rate of allommunization?

With nonphenotypically matched blood, rate of alloimmunization per transfusion is 3%, overall rate is between 19-47%

The most common alloAbs are anti K, C, E, Fya, Jkb

With blood matched for Cc, Ee, D and Kell, rate of alloimmunization rate per transfusion is 0.5%


What percentage of individuals are HPA 1A negative and how is NAIT managed?

2% of individuals are HPA1A neg

It can affect the first pregnancy

There is a 20% incidence of intracranial hemorrhage overall; about half of hemorrhages occur in utero

Tx should begin as soon as diagnosis is suspected (high dose IVIG and/or steroids)

Intrauterine platelet transfusion may begin at 18-20 weeks with antigen negative platelets (maternal platelets may be used if washed and irradiated)

Deliver by C section if possible; after birth the risk of hemorrhage is greatest during the first 24-36 hours so expedient plt transfusion is desirable


Without RhIg, what is the incidence of sensitization in an Rh- woman bearing an Rh+ fetus?


The incidence is LOWER if the mom and fetus are also ABO incompatible


What is FP24?

Plasma not frozen within 8 hours may be frozen within 24 hours and labeled "plasma frozen within 24 hours after phlebotomy" or FP24

*relatively deplete of Factors V and VIII

Useful for all indications for FFP EXCEPT DIC


How much can you expect one unit of FFP to increase factor activities?



What antigen is the epitope for CA 19-9?



Increased postnatal i antigen expression is characteristic of what two diseases?

1) Congenital dyserythropoietic anemia (CDA) type II

2) Blackfan-Diamond syndrome


What percentage of blood group A2 and blood group A2B have anti-A1?

A2 = 5%

A2B = 35%

Usually clinically insignificant


What happens if you give a Rh null person Rh negative blood?

They will form an anti total Rh antibody (anti Rh29)


When Rh+ blood is transfused to Rh- recipients, what is the rate of sensitization?



What is the Kell null phenotype?

Results from homozygous inheritance of the amorph K0 such that red cells have no Kell antigen but an abundance of Kx

Different from McLeod which is from mutations in Kx gene so no Kx with depressed Kell antigens


1) This antigen negative phenotype causes some cases of hereditary spherocytosis, acanthocytosis and hereditary elliptocytosis because it lacks this antigen which is an epitope on band 3 protein

2) This antigen negative phenotype is a cause of herediatry elliptocytosis because it lacks this antigen which is an epitope on glycophorin C

1) Diego negative

2) Gerbich negative (Leach phenotype)


1) What are the 4 most common Abs in immediate HTR?

2) What are the 4 most common Abs in delayed HTR?

3) What are the 4 most common Abs in HDN?

4) What Abs cause a mixed field reaction?

5) What are the Abs that commonly produce intravascular hemolysis?

1) 4 MC Abs in immediated HTR: anti A, anti Kell, anti Jka, anti Fya

2) 4 MC Abs in delayed HTR: anti Jka, anti E, anti D, anti C

3) 4 MC Abs in HDN: anti AB, anti D, anti Kell, anti C

4) Abs causing mixed field rxn: Lutheran, Sid, A3 (and post bone marrow transplant)

Kidd, Duffy and Kell cause a mixed field DAT due to delayed hemolytic transfusion reaction

5) Abs commonly produce intravascular hemolysis: ABO, Kidd, P (PCH)


Bacterial contamination of RBCs by what organism is known to cause hemolysis of the red cells?



What is the maximum amount of whole blood that can be donated in a single donation (including samples) in mL per kg body weight?

10.5 mL/kg


How long should you defer someone from donating if they have had West Nile virus?

120 days (4 months)

from onset of symptoms or diagnosis, whichever is more recent


All of the following are potential mechanisms for a drug induced positive DAT EXCEPT:

a) immune complex

b) nonimmune protein adsorption

c) true autoimmune hemolytic anemia

d) cold autoantibody

e) drug hapten mechanism

d) cold autoantibody

A number of drugs are associated with each mechanism and it's helpful to remember 1 or 2 for each.

Immune complex mediated: quinidine, cephalosporins

Nonimmune protein adsorption: cephalothin (a first gen cephalosporin)

True autoimmune hemolytic anemia: procainamide and aldomet (methyldopa)

Hapten associated: penicillin


What drugs are associated with the following mechanisms for a positive DAT?

a) Immune complex mediated

b) Nonimmune protein adsorption

c) True autoimmune hemolytic anemia

d) Hapten associated

a) Immune complex mediated: quinidine, cephalosporins

b) Nonimmune protein adsorption: cephalothin (a first gen cephalosporin)

c) True autoimmune hemolytic anemia: procainamide and aldomet (methyldopa)

d) Hapten associated: penicillin


All of the following antibody classes are capable of causing hemolytic disease of the newborn EXCEPT:

a) IgG1

b) IgG2

c) IgG3

d) IgG4

e) all of the above can cause HDN

b) IgG2

In addition to dimeric IgA and pentameric IgM, IgG2 is unable to cause HDN. Like IgA and IgM, IgG2 is unable to cross the placental membrane and therefore unable to initiate hemolysis


What is the approximate amount of iron in a single red blood cell unit?


Each red cell unit contains ~200mL of RBCs with each mL of red blood cells containing 1mg of iron. This means that each RBC unit has 200mg iron


Regarding centrifugation, how is a unit of whole blood separated into its components?

First it goes through a soft slow spin to separate into red blood cells and platelet rich plasma

Then the PRP undergoes a hard fast spin to separate into platelets and plasma


What are the main indications for FFP?

  • DIC (loss of multiple coagulation factors)
  • TTP to replace ADAMTS13
  • Hereditary angioedema to replace C1q
  • Antithrombin deficiency
  • Massive transfusion
  • Reversal of warfarin therapy


All of the following products would be useful in the treatment of symptomatic anemia in a patient that you wish to remain CMV negative EXCEPT:

a) RBCs, CMV negative by serology

b) frozen, thawed, and deglycerolized RBCs

c) washed RBCs

d) RBCs leukoreduced to 8 WBCs

e) all of the above are acceptable

d) RBCs leukoreduced to 8 WBCs

Leukoreduced red cells: ≤ 5 x 106 WBCs in 95%, retain 85% of RBCs

CMV negative = CMV "safe" which is leukoreduced

Washed RBCs are considered leukoreduced


All of the following genes are encoded within the MHC EXCEPT:
a) HFE

b) TNF

c) PKHD1

d) complement proteins

e) 21-hydroxylase

c) PKHD1

While this is located on Chr 6, it is not within the MHC like the rest are


Class II HLA gene encode proteins on all the following cell types EXCEPT:

a) macrophages

b) megakaryocytes

c) activated T cells

d) B cells

e) all of the above express class II HLA antigens

b) megakaryocytes

Class I HLA antigens are expressed on virtually all nucleated cells while Class II is much more restricted and facilitates humoral and cell mediated immunity



Given a donor with the minimal amount of Hb allowable,
weighing 60kg, how much Hb is in a 450ml donation?

12.5 g/dL * 4.5 dL (450 ml) = 56.25g Hb

*minimal allowable Hgb for donating is 12.5


What are some causes of false negative DAT?

Undercentrifugation, delay in adding antiglobulin agent, failure to adequately wash cells


What diagnosis should be considered in a pt with stomatocytes and hemolytic anemia?

Rh Null

LACK Lw antigen!!​

*they could phrase it like this on exam (instead of saying Rh null, say lack Lw antigen--this is actually a Rh LIKE antigen but Rh null pts lack this)


What is the storage lesion of RBC?

The storage lesion refers to changes in red cells during storage. Over time, glucose in stored blood is consumed, levels of 2,3-diphosphoglycerate (DPG) and ATP decrease, while potassium levels increase.

  • Glucose decreased
  • 2,3 DPG decreased
  • ATP decreased
  • pH decreased (acidosis)
  • Lactate increased
  • Potassium increased