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Liz's Blood Bank Module 1 > Other Blood Group Systems - IgM and IgG > Flashcards

Other Blood Group Systems - IgM and IgG Flashcards

1
Q

Red cell blood groups classified as IgM

A

Lewis, MN, ABO, P, Ii

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2
Q

Red cell blood groups classified as IgG

A

Rh, Kell, Duffy, Kidd, SsU

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3
Q

7 characterisitics of IgM Abs

A
  • 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
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4
Q

7 characteristics of IgG Abs

A
  • 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
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5
Q

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

A

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)

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6
Q

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

A

?

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7
Q

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

A

Le(a-b+)

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8
Q

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

A

Le(a+b-)

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9
Q

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

A

Le(a+b-)

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10
Q

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

A

Le(a-b-)

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11
Q

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

A

Le(a-b-)

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12
Q

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

A

Le(a-b-)

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13
Q

Lewis Neutralization Test

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

A

Eliminated; present

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14
Q

Lewis Neutralization Test

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

A

Remains; not present

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15
Q

2 reasons why Lewis Abs are not implicated in HDFN

A
  • Lewis Abs are IgM

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

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16
Q

Main pathological disease states associated w/ anti-I

A

Infectious mononucleosis

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17
Q

Main pathological disease states associated w/ anti-i

A

M. pneumoniae; Cold hemagglutinin disease (CHD)

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18
Q

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

A

?

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19
Q

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

A

?

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20
Q

P1 phenotype produces ____ Ags and ____ Abs

A

P1, P, Pk Ags

No Abs

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21
Q

P2 phenotype produces ____ Ags and ____ Abs

A

P, Pk Ags

anti-P1 Ab

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22
Q

Ab responsible for paroxysmal cold hemoglobinurea (PCH)

A

Autoanti-P

23
Q

Describe inheritance of MNSs blood group system

A

Close linkage in genes for MN and Ss

24
Q

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

A

Anti-M

25
Q

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

A

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

26
Q

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

A

No

27
Q

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

A

Yes

28
Q

Both I and i Abs are considered to be ____

A

Autoantibodies

29
Q

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

A

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

30
Q

Where are P Ags found?

A

RBCs, WBCs, tissues, plasma, and some secretions

31
Q

Where are M and N Ags located?

A

Glycophorin A (GPA)

32
Q

M and N Ags are ____ at birth

A

Fully developed

33
Q

When MM or NN has a stronger reaction than MN

A

Marked dosage

34
Q

Most common phenotype in Kell blood group system

A

Kpb (> 99.0%)

35
Q

3 common allelic pairs in Kell blood group system

A

K and k
Kpa and Kpb
Jsa and Jsb

36
Q

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

A

Low

37
Q

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

A

High

38
Q

State Ag frequencies of Kell system

A 
Kpb → > 99%
Jsb → > 99%
k → 98.8%
K → 9%
Kpa → 2% (Caucasian)
Jsa →
39
Q

McLeod phenotype

- Kell system Ag expression

A

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

40
Q

McLeod phenotype

- Inheritance

A

X-linked carrier of mother

41
Q

McLeod phenotype

- Lifespan of Kell Ag

A

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

42
Q

McLeod phenotype

- Associated w/ what disease?

A

Chronic Granulomatous disease

43
Q

Most immunogenic Ag of Kell system

A

?

44
Q

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

A

B/c they’re directed against high frequency Ags

45
Q

Transfusion practices w/ Kell Abs

A

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

46
Q

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

A

Caucasians: 17%
AA: 9%

47
Q

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

A

Caucasians: 49%
AA: 1%

48
Q

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

A

Caucasians: 34%
AA: 22%

49
Q

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

A

Caucasians: very rare
AA: 68%

50
Q

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

A

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

51
Q

Why are Kidd Abs referred to as “Bad Kidds”?

A

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
52
Q

Why are Kidd Abs notorious for causing delayed HTR?

A

?

53
Q

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

A

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

54
Q

Anti-S, anti-s, and anti-U

- Transfusion practices

A

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

Liz's Blood Bank Module 1 (10 decks)

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