Antigen/Antibodies other an ABO Flashcards
1
Q
Antibodies that react at the RT phase
A
P, I, H, Lewis
M, N,
Lutheran(a)
2
Q
Antibodies that react at AHG phase
A
S, s, U, Kell
Duff, Kidd
Lutheran (b), Xga
Rh, rarely lewis
3
Q
5 phenotypes of P system
A
P1, P2, p, P1k, P2k
4
Q
Detectable antigens for P1
A
P1P
5
Q
Detectable antigens for P2
A
PP
6
Q
Detectable antigens for p
A
None
7
Q
Detectable antigens for P1k
A
P1Pk
8
Q
Detectable antigens for P2k
A
PkPk
9
Q
Antibody that can be inhibited by hydatid cyst fluid
A
Anti-P1
10
Q
Antibody/antibody class associated with paroxysmal cold hemoglobinuria
A
Auto anti-P
IgG biphasic
ID by Donath-Landsteiner test
11
Q
What antigen in the P system deteriorates rapidly during storage?
A
P1 antigen
12
Q
What is the Donath-Lansteiner test used for?
A
Anti-P autoantibody
13
Q
- No gene for I or i but the presence or absence of many glycosyl transferases results in different sequences added to the original structure
- I and i antigens are the subterminal portions of the molecules that are eventually converted to H, A, or B
A
Transition of i to I antigen
14
Q
Antibody characteristics of Ii system
A
IgM - only significant if it is masking the presence of another antibody. Not RBC stimulated, usually autoantibody
15
Q
Transient antibody associated with infectious mononucleosis
A
Anti-i
16
Q
Anti-I thermal activity
A
usually weak IgM
17
Q
Potent anti-I thermal activity
A
Can occur with an IgM molecule that has a wide thermal range - reacting at 30 C or warmer.
18
Q
Anti-i
A
Usually IgM and react best at 4 C
19
Q
Antibody associated with Mycoplasma infections
A
Anti-I (cold agglutinin disease)
20
Q
Anti-I cord blood activity
A
Does NOT agglutinate with cord cells
21
Q
Anti-i cord blood activity
A
Agglutinates with cord blood
22
Q
How can you differentiate pathogenic anti-I and non pathogenic anti-I?
A
Pathogenic anti-I will react equally with adult or cord cells (ii)
23
Q
Which blood group is most likely to make anti-H?
A
A1B combination because they have the least amount of H on the surface
24
Q
Acquisition of Le (a)
A
Substance is produced if the individual has inherited the Le gene. This substance will absorb onto the surface of the RBC & become an RBC surface antigen & is a glycolipid Le (a+b-)
25
Acquisition of Le (b)
Substance is interaction of the Le gene, the H gene, & the Se gene. If all three are present, the Le (b) soluble antigen is produced in addition to Le (a) when both are in secretions.
- More successful at absorbing onto the surface of RBC
- Le (a-b+)
26
Is Le (a+b-) a secretor?
No
27
Is Le (a-b+) a secretor?
Yes
28
Is Le (a-b-) a secretor?
Unkown
29
Do enzymes affect the Lewis antigen?
Yes, by enhancing the activity
30
Where are the Lewis antigens produced?
Tissue
31
Significance of anti-Le(a), anti-Le(b)
Considered insignificant because of their neutralization by Lewis substances, poor attachment to RBC, IgM class
32
Do the Lewis antigens show dosage and are the reactions changed with enzymes?
No dosage, reactions are enhanced by enzymes
33
Who is most likely to make anti-Le(a) or Le(b)?
Pregnant women sometimes change to Le(a-b-) no matter what Lewis genes they have inherited.
34
Chromosome MNSsU is on
4
35
Does MNSsU show dosage?
Yes
36
Enzyme reaction of MNSsU system
All decrease with enzymes
37
When MNSsU system is developed
At birth
38
Precursor to MN
Glycophorin A
39
Precursor to SsU
Glycophorin B
40
Anti-M antibody Class
Naturally occurring IgM or rarely immune IgG
41
Anti-M complement fixation
Does not fix complement
42
Anti-M temp of reactivity
Not reaction above or at 30 C - not clinically significant
43
Anti-M cause of HDN/HTR
Should be concerned about HDN
44
Is anti-M RBC stimulated?
No
45
Anti-N antibody class
IgM or occasional IgG
46
Does anti-N fix complement?
Does not fix complement
47
Anti-N temp of reactivity
Only significant if reacting at or above 30 degrees
48
Does anti-N have the ability to cause HDN/HTR?
No
49
Is anti-N RBC stimulated?
No
50
En(a-) pheotype
Individuals make anti-En(a)
| Appears to be antibody to various portions of glycophorin A
51
M(k) phenotype
Silent gene, no M, N, S or s
52
Anti-S antibody class
IgG, occasionally IgM
53
Does anti-S fix complement?
Poorly
54
Anti-S temp of reactivity
usually 37 degrees and AHG phase
55
Does anti-S have the ability to cause HDN/HTR?
Yes
56
Is anti-S RBC stimulated?
yes
57
Anti-s antibody class
IgG
58
Can anti-s fix complement?
poorly
59
Anti-s temp of reactivity
Usually 37 degrees and at AHG phase
60
Does anti-s have the ability to cause HDN/HTR?
Yes
61
Is anti-s RBC stimulated?
yes
62
What is the prevalence of the U antigen if S and s antigen is negative?
U is part of the S structure, so if no S or s, then no U
63
Kell system dosage
Occasional
64
When is the Kell system developed?
It is well developed at birth
65
How do enzymes affect the Kell system?
No change, but will decrease with AET & ZZAP
66
McLeod phenotype & syndrome
Rare, lacks K(x) & K(m), x-linked
| Patients have a variety of muscle and nerve disorders
67
Anti-K antibody class
IgG
68
Can anti-K fix complement?
Yes, sometimes
69
Anti-K temp of reactivity
AHG phase
70
Does anti-K have the ability to cause HDN/HTR?
yes
71
Is anti-K RBC stimulated?
Yes
72
Rare antibodies of the Kell system
Kp(a), Js(a), k, Kp(b), Js(b)
73
How antigenic are the Kell antigens?
Very antigenic
74
Why don't we see anything other than anti-K very much in the Kell system?
Antigens are either very high frequency or very low frequency so exposure to an antigen that is foreign would be rare
75
Does the Duffy system have dosage?
Yes
76
When is the Duffy system developed?
At birth
77
How does enzymes affect the Duffy system?
It decreases the reactivity
78
Which antigen has a relationship to the Rh blood group?
Fy(6)
79
Duffy system antibody clas
IgG
80
Can duffy system antibodies fix complement?
Can bind compliment but not usually to lysis
81
Duffy system antibody temp of reactivity
AHG phase
82
Does the Duffy system antibodies have the ability to cause HDN/HTR?
yes
83
Are the Duffy system antibodies RBC stimulated?
yes
84
What is the antigen inheritance and significance of Fy(a-b-) in the black population?
68% of blacks will inherit. This allows them to resist Plasmodium vivax.
85
Describe Fy(x) antigen and antibody
Antigen: weak form of Fy(b)
Antibody: none
86
Describe Fy3 antigen and antibody
Antigen: probably part of the Fya and/or Fyb structure
Antibody: Seen most often in blacks that are Fy(a-b-)
87
Describe Fy5 antigen and antibody
Antigen: not entire understood but different than Fy3. There is interaction between Rh and Duffy glycoprotein
Antibody: Reacts with Fy(a-b-)Fy3- cells
88
Kidd System antibody class
IgG
89
Can the Kidd system fix complement?
It binds compliment well
90
Kidd system temp of reactivity
AHG phase
91
Does the Kidd system have the ability to cause HDN/HTR?
Yes
92
Is the Kidd system RBC stimulated?
Yes
93
Why are the kidd antibodies particularly problematic?
Anti-Jk(a) and anti-Jk(b) quantity fade quickly from circulation and if stimulated, may make an anamnestic response with delayed intravascular & extravascular hemolysis
94
Do Kidd antigens have dosage?
Yes
95
When are Kidd antigens developed?
By birth
96
What affect does enzymes have on Kidd antigens?
Increased activity
97
Does Lutheran antigens have dosage?
Yes
98
When are Lutherans antigens developed?
Poor at birth
99
How are Lutheran antigens affected by enzymes?
No effect
100
Anti-Lu(a) antibody class
IgM, and rare IgG
101
Does Anti-Lu(a) fix complement?
Will bind compliment but not to lysis
102
Anti-Lu(a) temp of reactivity
RT
103
Does Anti-Lu(a) have the ability to cause HDN/HTR?
Not usually but can be mild
104
Is Anti-Lu(a) RBC stimulated
No
105
Anti-Lu(b) antibody class
IgM/IgG
106
Does Anti-Lu(b) fix complement?
Occasionally
107
Anti-Lu(b) temp of reactivity
37/AGH phase
108
Does Anti-Lu(b) have the ability to cause HDN/HTR?
Yes but very mild
109
Is Anti-Lu(b) RBC stimulated?
Yes
110
2 non-RBC stimulated antibodies that may occur in Rh group
Anti-Cw
| Anti-E
111
Xg(a) chromosome location
X chromosome
112
Xg(a) antigen genetics
Only blood group that is produced from a gene on the X chromosome
113
Anti-Xg(a) antibody charactersitics
```
IgG - AHG phase reactivity
Can bind complement but not to hemolysis
Not implicated in HDN/HTR
Destroyed by enzymes
Rare
```
114
What is the Bg antigen
Residual MHC I on RBC surface
115
Define High Titer Low Avidity Antibodies (HTLA)
High titer (>64) reactivity but low avidity for agglutination when binding to its antigen (weak reactions)
116
Characteristics of HTLA antibodies
```
IgG
AHG phase
Usual titer > 64
Poor agglutination response with corresponding antigen
Clinically insignificant
React poorly with LISS
```
117
Antigens that are defined as HTLA
Chido, Rodgers, Knops, McCoy, York, Cost
118
What is unique about Chido and Rodgers antibodies?
Can be neutralized or inhibited by plasma containing C4d
