Other Blood Group Systems - IgM and IgG

Question 1

Red cell blood groups classified as IgM

Answer 1

Lewis, MN, ABO, P, Ii

Question 2

Red cell blood groups classified as IgG

Answer 2

Rh, Kell, Duffy, Kidd, SsU

Question 3

7 characterisitics of IgM Abs

Answer 3

• Large molecule (pentamer)
• Binds C’ efficiently
• Direct agglutination at immediate spin
• Room temperature (in vitro) or colder is optimal (enhances reactivity)
• Naturally occurring
• Does not cross placenta
• Not clinically significant

Question 4

7 characteristics of IgG Abs

Answer 4

• Red cell stimulated (unexpected Abs)
• Small in size
• Warm temperature (37C)
• Does not bind C’
• Agglutination at AHG phase
• Cross placenta (HDFN)
• Cause delayed HTR

Question 5

How do Lewis “soluble” Ags differ from all other red cell Ags?

Answer 5

Ags are mfg’d by tissues and released into body fluids instead of being produced by RBCs and incorporated into the RBC membrane
- Adsorbed onto membrane (works like Velcro)

Question 6

How do Se, Hh, and Lewis system genes interact to influence and individual’s Lewis RBC phenotype?

Answer 6

?

Question 7

Genes present: Le, Se, H, ABO
Ags in secretions: ↓Le(a), Le(b), ABH
Ags on RBCs: Le(b), ABH
Lewis phenotype: ?

Answer 7

Le(a-b+)

Question 8

Genes present: Le, sese, H, ABO
Ags in secretions: Le(a) only
Ags on RBCs: Le(a), ABH
Lewis phenotype: ?

Answer 8

Le(a+b-)

Question 9

Genes present: Le, sese or Se, hh, ABO
Ags in secretions: Le(a) only
Ags on RBCs: Le(a) only
Lewis phenotype: ?

Answer 9

Le(a+b-)

Question 10

Genes present: lele, Se, H, ABH
Ags in secretions: ABH
Ags on RBCs: ABH
Lewis phenotype: ?

Answer 10

Le(a-b-)

Question 11

Genes present: lele, sese, H, ABO
Ags in secretions: None
Ags on RBCs: ABH
Lewis phenotype: ?

Answer 11

Le(a-b-)

Question 12

Genes present: lele, sese or Se, hh, ABO
Ags in secretions: None
Ags on RBCs: None
Lewis phenotype: ?

Answer 12

Le(a-b-)

Question 13

Lewis Neutralization Test

- If reactivity is ____ in neutralize serum, Lewis Abs are ____

Answer 13

Eliminated; present

Question 14

Lewis Neutralization Test

- If reactivity ____ in neutralized aliquot, Lewis Abs are ____

Answer 14

Remains; not present

Question 15

2 reasons why Lewis Abs are not implicated in HDFN

Answer 15

• Lewis Abs are IgM

- Lewis Abs aren’t developed at birth (nothing for Abs to attach to on infant’s cells)

Question 16

Main pathological disease states associated w/ anti-I

Answer 16

Infectious mononucleosis

Question 17

Main pathological disease states associated w/ anti-i

Answer 17

M. pneumoniae; Cold hemagglutinin disease (CHD)

Question 18

Describe I, i, and H Ag content on A1, O, oH adult RBCs and cord RBCs

Answer 18

?

Question 19

Use of P1 neutralizing substances in serological investigations of P1 Abs to include interpretation of results

Answer 19

?

Question 20

P1 phenotype produces ____ Ags and ____ Abs

Answer 20

P1, P, Pk Ags

No Abs

Question 21

P2 phenotype produces ____ Ags and ____ Abs

Answer 21

P, Pk Ags

anti-P1 Ab

Question 22

Ab responsible for paroxysmal cold hemoglobinurea (PCH)

Answer 22

Autoanti-P

Question 23

Describe inheritance of MNSs blood group system

Answer 23

Close linkage in genes for MN and Ss

Question 24

Name the only common RBC Ab that is enhanced in acidic conditions

Answer 24

Anti-M

Question 25

Anti-Le(a) is never made by individuals w/ Le(a-b+) phenotype b/c...

Answer 25

Le(a) won't be seen as foreign b/c it's a subgroup of Le(b)

Question 26

Are you a secretor w/ the Lewis phenotype Le(a+b-)?

Answer 26

No

Question 27

Are you a secretor w/ the Lewis phenotype Le(a-b+)?

Answer 27

Yes

Question 28

Both I and i Abs are considered to be ____

Answer 28

Autoantibodies

Question 29

I and i Abs are naturally occurring found in 100% of people at ____ and ____

Answer 29

Low titer; low thermal amplitude (detected at limited cold temps 4-6C)

Question 30

Where are P Ags found?

Answer 30

RBCs, WBCs, tissues, plasma, and some secretions

Question 31

Where are M and N Ags located?

Answer 31

Glycophorin A (GPA)

Question 32

M and N Ags are ____ at birth

Answer 32

Fully developed

Question 33

When MM or NN has a stronger reaction than MN

Answer 33

Marked dosage

Question 34

Most common phenotype in Kell blood group system

Answer 34

Kpb (> 99.0%)

Question 35

3 common allelic pairs in Kell blood group system

Answer 35

K and k Kpa and Kpb Jsa and Jsb

Question 36

In allelic pairs in Kell system, 1st Ag is ____ frequency

Answer 36

Low

Question 37

In allelic pairs in Kell system, 2nd Ag is ____ frequency

Answer 37

High

Question 38

State Ag frequencies of Kell system

Answer 38

``` Kpb → > 99% Jsb → > 99% k → 98.8% K → 9% Kpa → 2% (Caucasian) Jsa → ```

Question 39

McLeod phenotype | - Kell system Ag expression

Answer 39

-K genes inherited but no K precursor present → weakened expression of all K Ags (look like Knull)

Question 40

McLeod phenotype | - Inheritance

Answer 40

X-linked carrier of mother

Question 41

McLeod phenotype | - Lifespan of Kell Ag

Answer 41

Shortened lifespan b/c K precursor is an integral protein on the RBC membrane

Question 42

McLeod phenotype | - Associated w/ what disease?

Answer 42

Chronic Granulomatous disease

Question 43

Most immunogenic Ag of Kell system

Answer 43

?

Question 44

Abs in Kell system other than anti-K are uncommon, why?

Answer 44

B/c they're directed against high frequency Ags

Question 45

Transfusion practices w/ Kell Abs

Answer 45

All Abs of Kell system are clinically significant (IgG) and MUST "honor" in Xm w/ Ag-neg donors

Question 46

Frequency of Fy(a+b-) in Caucasians and AA

Answer 46

Caucasians: 17% AA: 9%

Question 47

Frequency of Fy(a+b+) in Caucasians and AA

Answer 47

Caucasians: 49% AA: 1%

Question 48

Frequency of Fy(a-b+) in Caucasians and AA

Answer 48

Caucasians: 34% AA: 22%

Question 49

Frequency of Fy(a-b-) in Caucasians and AA

Answer 49

Caucasians: very rare AA: 68%

Question 50

Correlation b/w AA Fy(a-b-) phenotype and its resistance to malaria

Answer 50

Fy(a-b-) is an amorph not located on RBC membrane but gene is still in the tissues, therefore not recognized as foreign

Question 51

Why are Kidd Abs referred to as "Bad Kidds"?

Answer 51

Notorious for causing HTR - Binds C' in vitro - Detected in fresh serum (red tube) not in plasma (EDTA) b/c of Ca2+ being chelated - Not detected in stored serum b/c C' died

Question 52

Why are Kidd Abs notorious for causing delayed HTR?

Answer 52

?

Question 53

Correlation of U Ag to S and s Ags of MNSs system

Answer 53

S and s are allelic; U is universal found on all cells except on S-s-

Question 54

Anti-S, anti-s, and anti-U | - Transfusion practices

Answer 54

SsU Abs are clinically significant, so you MUST "honor" Ags in donor cells and give Ag-neg blood