Blood Bank Flashcards Preview

Pathology > Blood Bank > Flashcards

Flashcards in Blood Bank Deck (151)
Loading flashcards...

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)