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Immunohematology > Other Blood Groups > Flashcards

Other Blood Groups Flashcards

(74 cards)

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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
P2 Phenotype
Has P antigen Lacks P1 Can Make Anti-P1
26
p Phenotype
Rare No detectable Antigens Can Make Anti PP1 pk Originally called Anti-Tja
27
p1k Phenotype
Very Rare Has P1 & pk antigens Lacks P antigen (Can make Anti P)
28
p2k Phenotype
Very Rare Has pk Antigen Lacks P & P1 Antigens (Can make Anti P & Anti P1)
29
Anti-P1
Most Common Naturally Occurring (IgM) Weak - usually not hemolytic, no HDN Optimal Activity at 4 C P1 substance - neutralizes Anti P1 Activity
30
Anti-P
Strong Antibody pk phenotypes can produce Naturally occurring (IgM) Rarely seen
31
PCH
IgG Biphasic hemolysin - binds complement Donath-Landsteiner Test
32
Anti-PP1pk
p phenotype can produce Naturally occurring (most IgM, some IgG) Binds complement Strong hemolysin HTR & HDN
33
Lewis Blood Group
Lea and Leb Poorly developed at birth Does NOT show dosage
34
Le gene
Codes Lewis Blood Group Produced by glycosyl transferases
35
Le/Le or Le/le
Fucosyl transferase that adds fucose to subterminal sugar Type I chains in plasma Produces Lea activity
36
Type II chains on RBCs
no Le activity
37
Type I chains
Reversibly adsorbed onto RBC membrane
38
Se/Se or Se/se AND Le/Le or Le/le
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
Lea-b+
Most common phenotype
40
Lea+b+
Rare Asian population
41
le/le
No Lewis antigens produced Rare Lea-b-
42
Lewis antigens
Poorly developed at birth Detectable in plasma at 10 days after birth Accurate type at ~ 6 yrs
43
Lewis Antibodies
Occur in Lea-b- persons IgM and binds complement Not usually clinically significant Enhanced by enzyme treatment Lacy agglutination - easily dispersed
44
MNSsU Blood Group
MNSs are genetically linked Most popular are: M+, N+, s+ Anti S most common antibody
45
M & N Antigens
Co-dominant alleles Shows dosage Well developed at birth Primarily RBC antigen Built on glycophorin A Destroyed by enzymes
46
Anti M
Naturally occurring IgM Do not bind complement Shows dosage Rare cause of HTR or HDNA
47
Anti N
Same as Anti M (less common) Lectin - extracted from Vicia graminea Found in dialysis patients when equipment sterilized with formaldehyde
48
S and s antigen
Codominant alleles Shows dosage Well developed at birth RBC antigen Built on glycophorin B Destroyed by enzymes
49
U antigen
High incidence antigen >99% of population is U+ <1% of African Americans are U-
50
Anti S, Anti s, and Anti U
Warm reacting 37 C and AHG IgG (Immune production) May bind complement Associated with HTR and HDN Must provide antigen negative blood
51
Lutheran Blood Group
Lua and Lub Ag have high or low frequencies Co-dominant alleles Poorly developed at birth Show dosage
52
Lu gene
Chromosome 19 Linked to Se gene
53
Lutheran phenotypes
Lua+b- <1% Lua+b+ 5-7% Lua-b+ >90% Lua-b- very rare
54
Anti Lua
Naturally occurring saline agglutinin Reacts best at RT IgM, IgG, IgA Agglutination is mf, lacy May cause mild HDN
55
Anti Lub
Most are immune mediated, some naturally occurring IgG - Reacts at 37 C and AHG Associated with mild HDN
56
KELL Blood Group
K, k, Kpa, Kpb, Jsa, Jsb Glycoproteins Well developed at birth Show dosage Antigens denatured by DDT, ZZAP, 2ME
57
KELL Antigens
K (KEL1) Present in 9% Caucasians, 2% African Americans k (KEL2 - cellano) Present in 98-100% of population
58
KELL Antibodies
Warm reacting - 37 C & AHG IgG Immune mediated Can show dosage
59
Anti K
Frequently seen Clinically significant - HTR & HDN Must give Ag negative blood Some IgM Anti K due to bacterial identification
60
Anti k
Rarely seen Clinically significant - HTR & HDN Must give Ag negative blood
61
Kpa & Jsa
Low frequency antigens Antibodies behave like anti K Easy to find Ag negative blood
62
Kpb & Jsb
High frequency antigens Antibodies behave like anti K Hard to find Ag negative blood
63
Kx
Previously thought to be K precursor Now in own system (XK)
64
Ko
Silent allele Ko/Ko = K null phenotype Have only Kx on RBCs
65
McLeod Phenotype
Appears like K null - weak expression of k, Kpb, and Jsb Acanthocytes Patients have abnormal neuromuscular activity Associated with CGD
66
Duffy Blood Group
Gene located on chromosome 1 Antigens well developed at birth Antigens moderately immunogenic Antigens destroyed by enzymes & ZZAP
67
Duffy Antigens
Fya and Fyb Codominate alleles
68
Fy
3rd allele High incidence in African Americans
69
Fyx
Weakened Fyb antigen
70
Duffy Antibodies
Warm reacting - 37 C, AHG Rarely bind complemet Enhanced by LISS May show dosage HTR, HDN Ag negative blood required
71
Fya-b-
Resistant to P. vivax Helps to avoid malaria
72
Fy glycoprotein
Recept for P. vivax
73
KIDD Blood Group
2 antigens Jka and Jkb Co-dominate alleles Well developed at birth Show dosage Weakly immunogenic
74
KIDD Antibodies
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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