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Immunohematology > Other Blood Groups > Flashcards

Other Blood Groups Flashcards

1
Q

I/i Antigens

A

Subterminal portions of oligosaccharides that form A, B, and H antigens

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2
Q

i

A

Minimally-branched oligosaccharide
Abundant on fetal cells
Cord blood

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3
Q

I

A

Highly-branched oligosaccharide
Built from “i” antigen
Abundant on Adult Cells

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4
Q

I/i Found

A

on WBCs
Platelets
Secretions

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5
Q

Anti-I

A

Autoantibody
IgM antibody
Narrow thermal range & low titer
“Naturally Occurring”
Mycoplasma pneumoniae gives cross reaction

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6
Q

Anti-I Conditions

A

Cold Agglutinin Syndrome (Raynaud Syndrome)
Wider thermal range & higher titer
Binds complement

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7
Q

Anti-i

A

Very rare
Autoantibody IgM
Strongest reacting with cord cells
Infectious mononuceleosis

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8
Q

Anti-IH

A

Antibody common in A1 and A1B blood types
Anti IH reacts strongest with O and A2
Does not agglutinate Group O cord cells
Requires patient to form both Anti-I and Anti-H

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9
Q

Anti-IA

A

Antibody may be found in Group B blood types
Requires both Anti-I and Anti-A to bind

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10
Q

Anti-H

A

Common in A1 and A1B
Reacts strongly with Group O and Group A2B

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11
Q

Anti-H vs Bombay Anti-H

A

Bombay: Strong ALLOantibody (IgG) upon exposure
Anti-H: “Cold” Autoantibody (IgM) no exposure required

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12
Q

Cold Auto Antibodies (Transfusion)

A

Do not usually cause RBC Destruction
May mask significant antibodies

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13
Q

Cold Auto Antibodies ABO/Rh Typing

A

Discrepancies in Reverse Group
Interfere with Rh control (+ DAT)

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14
Q

Cold Auto Antibodies Testing

A

Can result in all positive reactions
Masking can occur at RT and AHG (very strong antibodies)

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15
Q

Cold Auto Antibodies Compatibility Testing

A

Antibodies may react with donor cells

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16
Q

Cold Auto Antibodies Reaction

A

Screening Cells I (SCI) IS pos, 37 C neg
Screening Cells II (SCII) IS pos, 37 C neg
Screening Cells III (SCIII) IS pos, 37 C neg
Auto Control (Self) IS pos, 37 C neg

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17
Q

Cold Allo Antibodies Reaction

A

Screening Cells I (SCI) IS pos, 37 C neg
Screening Cells II (SCII) IS neg, 37 C neg
Screening Cells III (SCIII) IS neg, 37 C neg
Auto Control (Self) IS neg, 37 C neg

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18
Q

Cold Screen

A

Screening Cells
Auto Control (Patient Cells + Patient Serum)
Type “O” Cord Cells - I vs i
A1c - small amount of H
A2c - more amount of H compared to A1c
Bc - more amount of H compared to A2c

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19
Q

Pre-Warming technique

A

IAT at 37 C and AHG only testing
Used to remove cold autoantibody interference
Allows tech to check for significant antibodies
Identify Warm Antibody (IgG)
May need to prewarm blood for transfusion

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20
Q

P Blood Group

A

Discovered by Landseinter & Levine
Antigen production similar to ABO

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21
Q

P Group Antigens

A

Present on all human RBCs

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22
Q

P1 Antigen

A

Most common
Varies in strength
Poorly developed at birth
Deteriorates with storage

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23
Q

pK Antigen

A

Converted to P antigen

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24
Q

P1 Phenotype

A

Has P and P1 antigen
79% Caucasians
94% African Americans

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25
Q

P2 Phenotype

A

Has P antigen
Lacks P1
Can Make Anti-P1

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26
Q

p Phenotype

A

Rare
No detectable Antigens
Can Make Anti PP1 pk
Originally called Anti-Tja

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27
Q

p1k Phenotype

A

Very Rare
Has P1 & pk antigens
Lacks P antigen (Can make Anti P)

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28
Q

p2k Phenotype

A

Very Rare
Has pk Antigen
Lacks P & P1 Antigens (Can make Anti P & Anti P1)

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29
Q

Anti-P1

A

Most Common
Naturally Occurring (IgM)
Weak - usually not hemolytic, no HDN
Optimal Activity at 4 C
P1 substance - neutralizes Anti P1 Activity

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30
Q

Anti-P

A

Strong Antibody
pk phenotypes can produce
Naturally occurring (IgM)
Rarely seen

31
Q

PCH

A

IgG
Biphasic hemolysin - binds complement
Donath-Landsteiner Test

32
Q

Anti-PP1pk

A

p phenotype can produce
Naturally occurring (most IgM, some IgG)
Binds complement
Strong hemolysin
HTR & HDN

33
Q

Lewis Blood Group

A

Lea and Leb
Poorly developed at birth
Does NOT show dosage

34
Q

Le gene

A

Codes Lewis Blood Group
Produced by glycosyl transferases

35
Q

Le/Le or Le/le

A

Fucosyl transferase that adds fucose to subterminal sugar
Type I chains in plasma
Produces Lea activity

36
Q

Type II chains on RBCs

A

no Le activity

37
Q

Type I chains

A

Reversibly adsorbed onto RBC membrane

38
Q

Se/Se or Se/se AND Le/Le or Le/le

A

Se gene codes for fucosyl transferase - Leb
Attaches fucose to terminal galactose
H gene must have added fucose to IH chain
Leb adsorbed preferentially over Lea

39
Q

Lea-b+

A

Most common phenotype

40
Q

Lea+b+

A

Rare
Asian population

41
Q

le/le

A

No Lewis antigens produced
Rare
Lea-b-

42
Q

Lewis antigens

A

Poorly developed at birth
Detectable in plasma at 10 days after birth
Accurate type at ~ 6 yrs

43
Q

Lewis Antibodies

A

Occur in Lea-b- persons
IgM and binds complement
Not usually clinically significant
Enhanced by enzyme treatment
Lacy agglutination - easily dispersed

44
Q

MNSsU Blood Group

A

MNSs are genetically linked
Most popular are: M+, N+, s+
Anti S most common antibody

45
Q

M & N Antigens

A

Co-dominant alleles
Shows dosage
Well developed at birth
Primarily RBC antigen
Built on glycophorin A
Destroyed by enzymes

46
Q

Anti M

A

Naturally occurring
IgM
Do not bind complement
Shows dosage
Rare cause of HTR or HDNA

47
Q

Anti N

A

Same as Anti M (less common)
Lectin - extracted from Vicia graminea
Found in dialysis patients when equipment sterilized with formaldehyde

48
Q

S and s antigen

A

Codominant alleles
Shows dosage
Well developed at birth
RBC antigen
Built on glycophorin B
Destroyed by enzymes

49
Q

U antigen

A

High incidence antigen
>99% of population is U+
<1% of African Americans are U-

50
Q

Anti S, Anti s, and Anti U

A

Warm reacting
37 C and AHG
IgG (Immune production)
May bind complement
Associated with HTR and HDN
Must provide antigen negative blood

51
Q

Lutheran Blood Group

A

Lua and Lub
Ag have high or low frequencies
Co-dominant alleles
Poorly developed at birth
Show dosage

52
Q

Lu gene

A

Chromosome 19
Linked to Se gene

53
Q

Lutheran phenotypes

A

Lua+b- <1%
Lua+b+ 5-7%
Lua-b+ >90%
Lua-b- very rare

54
Q

Anti Lua

A

Naturally occurring saline agglutinin
Reacts best at RT
IgM, IgG, IgA
Agglutination is mf, lacy
May cause mild HDN

55
Q

Anti Lub

A

Most are immune mediated, some naturally occurring
IgG - Reacts at 37 C and AHG
Associated with mild HDN

56
Q

KELL Blood Group

A

K, k, Kpa, Kpb, Jsa, Jsb
Glycoproteins
Well developed at birth
Show dosage
Antigens denatured by DDT, ZZAP, 2ME

57
Q

KELL Antigens

A

K (KEL1) Present in 9% Caucasians, 2% African Americans
k (KEL2 - cellano) Present in 98-100% of population

58
Q

KELL Antibodies

A

Warm reacting - 37 C & AHG
IgG
Immune mediated
Can show dosage

59
Q

Anti K

A

Frequently seen
Clinically significant - HTR & HDN
Must give Ag negative blood
Some IgM Anti K due to bacterial identification

60
Q

Anti k

A

Rarely seen
Clinically significant - HTR & HDN
Must give Ag negative blood

61
Q

Kpa & Jsa

A

Low frequency antigens
Antibodies behave like anti K
Easy to find Ag negative blood

62
Q

Kpb & Jsb

A

High frequency antigens
Antibodies behave like anti K
Hard to find Ag negative blood

63
Q

Kx

A

Previously thought to be K precursor
Now in own system (XK)

64
Q

Ko

A

Silent allele
Ko/Ko = K null phenotype
Have only Kx on RBCs

65
Q

McLeod Phenotype

A

Appears like K null
- weak expression of k, Kpb, and Jsb
Acanthocytes
Patients have abnormal neuromuscular activity
Associated with CGD

66
Q

Duffy Blood Group

A

Gene located on chromosome 1
Antigens well developed at birth
Antigens moderately immunogenic
Antigens destroyed by enzymes & ZZAP

67
Q

Duffy Antigens

A

Fya and Fyb
Codominate alleles

68
Q

Fy

A

3rd allele
High incidence in African Americans

69
Q

Fyx

A

Weakened Fyb antigen

70
Q

Duffy Antibodies

A

Warm reacting - 37 C, AHG
Rarely bind complemet
Enhanced by LISS
May show dosage
HTR, HDN
Ag negative blood required

71
Q

Fya-b-

A

Resistant to P. vivax
Helps to avoid malaria

72
Q

Fy glycoprotein

A

Recept for P. vivax

73
Q

KIDD Blood Group

A

2 antigens
Jka and Jkb
Co-dominate alleles
Well developed at birth
Show dosage
Weakly immunogenic

74
Q

KIDD Antibodies

A

Immune Production
Warm Reacting - 37 C and AHG
IgG
Bind Complement Well
HDN (mild) and HTR (can be severe)

Immunohematology (17 decks)

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