Transfusion Blood Systems

Front 1

Steric Hindrance (Rh)

Back 1

Position effect (Weak D hindered by r' in trans position)

Front 2

Fisher-Race Nomenclature haplotypes (RHD/RHCE genes)

Back 2

DCE/dCE

DCe/dCe

DcE/dcE

Dce/dce

Front 3

Rosenfeld nomenclature (Rh system)

Back 3

1,2,3,4,5 (-) indicates lacking

D,C,E,c,e

Front 4

Weiner Nomenclature

Back 4

R0=Dce

R1=DCe

R2=DcE

Rz=DCE

r=dce

r'=dCe

r''=dcE

ry=dCE

Front 5

Weak D (Rh)

Back 5

Low expression of D on RBC (Hereditary or trans inheretance of C) must test in adults, Infants of Rh-neg moms, Prenatal screen (for mom)

Front 6

Partial D (Rh)

Back 6

Altered D antigen, missing or modified epitopes, must transfuse D-negative

Front 7

Prevalence (Rh)

Back 7

D (85%) c (80%)

C (68%) e (98%)

E (29%)

Front 8

Secretor gene

Back 8

Se (se) Medelian pattern

Front 9

Antigens (ABH)

Back 9

A=40%

B=11%

H=100% (O phenotype 45%)

AB= combination of A and B antigen

Front 10

Acquired B

Back 10

Bacterial exposure modifies A antigens

Front 11

Acquired A

Back 11

B enzyme non-specifically makes A antigens, resolve by using less sensitive anti-A

Front 12

Rh system antigen chemistry

Back 12

All protein, transmembrane

Front 13

ABH system chemistry

Back 13

Glycolipids

Front 14

ABO gene products

Back 14

A=N-alpha-acytylgalactosyltransferase

B=N-alpha-galactosyltransferase

O=Amorph (None)

H=L-fucosyltrasferase

h=amorph (none)

Front 15

Kell System Antigens (Significance)

Back 15

K (yes)

k (yes)

Kp^a (yes)

Kp^b (yes)

Js^a (yes)

Js^b (yes)

Front 16

Kell System antitheticals (dosage)

Back 16

K/k (yes, but K is often excepted)

Kp^a/Kp^b (yes, but Kp^a excepted)

Js^a/Js^b (yes, but Js^a often excepted)

Front 17

Kell system frequencies (white)/(Black)

Back 17

K (9%)/(rare)

k (99.8%)/(100%)

Kp^a (2%)/(rare)

Kp^b (>99.9%)/(>99.9%)

Js^a (<.1%)/(20%)

Js^b (>99.9%)/(99%)

Front 18

Kell system status at age

Back 18

Well developed at birth

Front 19

Kell system Chemistry

Back 19

Transmembrane Protein (mostly outside cell)

Front 20

Kell system Unique points

Back 20

Dependent on Kx antigen for proper expression (Failure of Kx results in McLeod Phenotype) can cause Acanthocytes

Front 21

Kell system Enzyme reactivity

Back 21

Enzymes have no effect, Thiol-reducing agents destroy them

Front 22

Kell system antibodies

Back 22

Mostly IgG, AHG phase, Do not activate complement

Front 23

Duffy blood group system antigens (signficance)

Back 23

Fya (yes)

Fyb (yes)

Fy3 (yes)

Front 24

Duffy system antitheticals (dosage)

Back 24

Fya/Fyb (yes)

Front 25

Duffy system Phenotype frequency (white)/(black)

Back 25

Fy (a+b-) 17/9

Fy (a-b+) 34/22

Fy (a+b+) 49/1 (most common in white)

Fy (a-b-) rare/68 (Most common in black)

Front 26

Duffy system expression (age)

Back 26

Strong expression in fetus/adult

Front 27

Duffy system Chemistry

Back 27

Transmembrane proteins, Urea pump

Front 28

Duffy system Unique points

Back 28

Fya/Fyb receptor for P. vivax, probably a chemokine receptor

Front 29

Duffy system enzyme reactivity

Back 29

Enzymes destroy reactivity

Front 30

Duffy system antibodies

Back 30

IgG, AHG, some do bind complement, anti-Fya more common than anti-Fyb

Front 31

MNS antigens (significance)

Back 31

M (no)

N (no)

S (yes)

s (yes)

U (possible)

Front 32

MNS antigens frequency white/black

Back 32

M: 78/74

N: 72/75

S: 55/31

s: 89/93

U: 99.9/99

Front 33

MNS antitheticals (dosage)

Back 33

M/N (yes)

S/s (yes)

Front 34

MNS enzyme reactivity

Back 34

MN destroyed, S/s often destroyed but depends on dosage.

U: resistant to blood bank enzymes

Front 35

MNS expression (age)

Back 35

Strongly expressed at birth

Front 36

MNS unique points

Back 36

U always expressed with S or s

Receptors for cytokines and receptors for P. falciparum and E. coli

Front 37

MNS chemistry

Back 37

Single pass membrane proteins, Glycophorin A (MN) and Glycophorin B (Ss)

Front 38

MNS antibodies

Back 38

MN: IgM common in children, 4C reacting

Ss: IgG, AHG, some complement binding (S>s)

U: IgG, AHG, no complement binding (only found in S-s- phenotype)

Front 39

P1Pk/GLOBOSIDE antigens (significant)

Back 39

P1 (yes)

Pk (no)

P (yes)

Front 40

P1Pk/GLOBOSIDE phenotypes (antigens) Frequency White/Black

Back 40

P1 (P1, Pk, P) 94/79

P2 (Pk, P) 6/21

P1k (P1, Pk) rare/rare

P2k (Pk) rare/rare

p (none) rare/rare

Front 41

P1Pk/GLOBOSIDE antitheticals (dosage)

Back 41

NOPE!

Front 42

P1Pk/GLOBOSIDE chemistry

Back 42

Lipid linked Carbohydrates, adds sugars to type 2 precursor chain

Front 43

P1Pk/GLOBOSIDE unique points

Back 43

Antigen degraded by storage, detectable in hydatid cyst fluid. P1 antigen can be soluble

Front 44

P1Pk/GLOBOSIDE expression (age)

Back 44

poorly developed at birth, detect as adult

Front 45

P1Pk/GLOBOSIDE antibodies

Back 45

Anti-PP1Pk (only pnull phenotype) IgG/IgM, AHG, wide range of thermal activity binds complement well.

Front 46

P1Pk/GLOBOSIDE enzyme activity

Back 46

Enhances detection of P1, no effect for other antigens

Front 47

Group I antigens (significance)

Back 47

I (mostly no)

Front 48

Group I frequency

Back 48

High frequency

Front 49

Group I chemistry

Back 49

Glycolipids (RBC), reside as residues on water soluble proteins and glycoproteins in secretions

Front 50

Group I deveopment (age)

Back 50

find unrelated i antigen in newborns, see I antigen in >18 months

Front 51

Group I unique chracateristics

Back 51

Both anti-I and anti-i are found in cold agglutinin disease. I and i are not antithetical and are not part of the same group (i has no group)

Anti-i associated with cataracts in adult asian population

Front 52

Group I antitheticals (dosage)

Back 52

NOPE

Front 53

Group I enzyme activity

Back 53

Varies

Front 54

Group I antibodies

Back 54

Usually IgM, anti-I reacts to complexed I and H as an anti-IH

Front 55

Lewis System Antigens (significant)

Back 55

Lea (yes, but only sometimes)

Leb (no)

Front 56

Lewis System Phenotype prevalence white/black

Back 56

Le (a+b-) 22/23

Le (a-b+) 72/55

Le (a-b-) 6/22

Le (a+b+) rare/rare

Front 57

Lewis System Antitheticals (dosage)

Back 57

NONE

Front 58

Lewis System Development (age)

Back 58

Poor at birth

Front 59

Lewis System Chemistry

Back 59

Galactosetransferase (antigen is the modified glycolipid that comes from the same stuff as the ABO system)

Front 60

Lewis System Unique Characteristics

Back 60

Naturally Occur, called FUT3. Lea converts precursor substance, Leb is converted type 1 (secreteor) H substance. Will have Leb if also have Se gene. Antigen mostly found in secretions and doesn't attach well to red cell

Front 61

Lewis System Antibodies

Back 61

Naturally occuring IgM, mostly found in Le(a-b-), antibodies have low avidity and are often neutralized by Le antigens in plasma before ever reaching cells

Front 62

Lewis System Enzyme Activity

Back 62

INCREASED by enzymes

Front 63

Lutheran System antigens (significant)

Back 63

Lua (no)

Lub (yes)

Front 64

Lutheran System phenotype prevalence white/black

Back 64

Lu (a+b-) .2%

Lu (a-b+) 92.4%

Lu (a+b+) 7.4 %

Lu (a-b-) rare

Front 65

Lutheran System antithetical (dosage)

Back 65

Lua/Lub (yes, but Lu^a often excepted)

Front 66

Lutheran System enzyme activity

Back 66

Varies, usually not

Front 67

Lutheran System antibodies

Back 67

Anti-Lua is IgM and naturally occurring (stringy agglutinates, most often found in XM because screening cells are usually negative), anti-Lub is IgG and IAT.

Front 68

Lutheran System chemistry

Back 68

Single-pass membrane glycoprotein, related to cell adhesion. Only found on RBC's

Front 69

Lutheran System unique characteristics

Back 69

3 reasons for null phenotype: No Lu gene, have In(Lu) inhibitor gene (DOM), X linked supressor XS2 (RECESSIVE).

Front 70

Lutheran System development (age)

Back 70

Adults (poorly expressed on fetus, but can lead to HDFN)

Front 71

Kidd System antigens (significant)

Back 71

JKa (yes)

JKb (yes)

Jk3 (yes, but only in a-b-)

Front 72

Kidd System antitheticals (dosage)

Back 72

Jka/Jkb (yes)

Front 73

Kidd System phenotype prevalence white/black

Back 73

Jk (a+b-) 26.3/51.1

Jk (a-b+) 23.4/8.1

Jk (a+b+) 50.3/40.8

Jk (a-b-) rare/rare

Front 74

Kidd System enzyme activity

Back 74

Enhanced

Front 75

Kidd System chemistry

Back 75

Multipass membrane protein, Urea transport protein.

Front 76

Kidd System antibodies

Back 76

Always IgG, AHG, do bind complement, don't store well, titers drop to undetectable after initial development

Front 77

Kidd System unique characteristics

Back 77

2 Molar urea solution destroys all RBC's but Jk(a-b-) cells.

Front 78

Kidd System expression (age)

Back 78

Strongly expressed at birth

Front 79

Antigen systems that have significant antigens

Back 79

Rh Kidd (all)

ABO

Kell (all)

Duffy (all)

MNS (Only S/s/U)

P1Pk (Only P/P1)

Lewis (Only Lea)

Lutheran (Only Lub)

Front 80

Antigen systems that express dosage

Back 80

Rh (Cc/Ee)

Kell (all, but K/Ksa/Jsa excepted in rule-outs)

Duffy

MNS (MN, Ss)

Lutheran (Lua excepted in rule-outs sometimes)

Kidd

Front 81

Antigen systems that are enhanced by enzyme reactivity

Back 81

Kidd

Lewis

Rh

P1Pk/Globoside (Only P1, destroys others)

Front 82

Antigen systems unaffected by enzymes

Back 82

MNS (only U and S/s)

P1Pk/Globoside

Lutheran (usually no)

I (varies)

Kell (Thiol-reducers destroy)

Front 83

Antigen systems destroyed by Enzymes

Back 83

Duffy

MNS (M/N)

P1Pk/Globoside (P, Pk)

Front 84

Antigen systems expressed strongly at birth

Back 84

ABO

Rh

Kell

Duffy

MNS

i (not a system, but fetal antigen)