Rush Other Majors Flashcards
(78 cards)
1
Q
Other groups
A
MNS
P
I
Kell
Duffy
Kidd
Lutheran
2
Q
43 Antigens
Landsteiner and Levine rabbits with human RBC
A
MNS
3
Q
Antithetical antigens of MNS
A
M and N Antigens
(Only one can be expressed)
4
Q
Antibodies reproted in 1927 by Lands. and Lev.
A
Anti-M and N
5
Q
Walsh and Montgomery found what?
A
S antigen
6
Q
In 1951, what antigen was found
A
s antigen
7
Q
Weiner found this antigen in 1953
A
U antigen or Universal Antigen
8
Q
Major sialic acid-rich glycoprotein or sialoglycoprotein
A
Glycophorin A of the M and N Antigen
(Responsible for gene expression of M and N)
9
Q
These are found in GPA, well developed at birth, easilty destroyed by enzymes.
A
M and N Antigens
10
Q
Located at glycoprotein GPB, less degen by enzymes
A
S and s
11
Q
S and s is differentiated by amino acid
A
29th position
S methionine
s threonine
12
Q
Naturally occ saline agglu
Reacts at >37
50-80% IgG
Do not bind compl regardlss of anti class
A
Anti-M
13
Q
Not react with enz treat cell
reacts better with MM genotype than MN genotype
aka dosing effect on the MM
A
Anti-M
MM (+3)
MN (+1 or 0)
14
Q
Anti-M is enhanced by
A
serum:cell ratio
more incub time
less incub temp
use of agents
15
Q
rx best 6,5
reacts to rbc exposed to glu
insignificant as long as not in 37
rare HTR or HDN
A
Anti-M
16
Q
Cold reac saline agglu IgM or IgG
dosage effect
not bind to compl
not react to enz treat cell
see in renal dialysis patients sterilized by formaldehyde***
A
Anti-N
Anti-Nf (Renal Patients)
17
Q
Assoc. with rej. of chilled transplanted kidneys
A
Anti-Nf
18
Q
IgG reactive to 37 and AHG
Dosage eff
clinically significatn **
HTR and HDN
A
Anti S and s
19
Q
MNS chromosome, gene, and expression
A
4
GYPA and GYPB (Mutation = MNS mutation)
Codominant
20
Q
Anti-M lectin
A
Iberis amara
21
Q
Anti-N lectin
A
Bauhinia variegata
Bauhina purpurea
Vicea graminea
22
Q
GPB
high incidence ag
A
U phenotype
23
Q
produced by lack of GPB
IgG
can cause HTR and HDN
A
Anti-U
24
Q
may serve as recep for E coli
A
GPA
25
may serve receptr as P. falciparum
GPA,B,C
26
comp. of P antigens
P - Globoside Group
P1 - Main
Pk and Luke - Globoside Collection
27
Lands. and Lev 1927 inj. rabbits
Anti-P
P+ and P-
28
Levine 1951 found in P null individuals
Anti-Tja (Anti-PP1Pk)
Individuals who lack all P antigens
29
new names for P antigens
Anti P to Anti-P1
P+ to P1
P- toP2
Pnull to p
30
described Pk1 and Pk2 found in RBC excpt p phenotype
Matson et al 1959
31
summary of P phenotypes
P1 - P1, P
P2 - P
p - None
P1k - P1 Pk
P2k - Pk
32
found on fetal rbc 12 weaks
poorly expressed at brith
fully expressed at 7 years
deteriorates rapidly at stoage
P1 antigen
33
P1 antigens in the environment
Lumbricoided terrestris
Ascaris suum
34
P1 and Pk antigens in the environment
Echinoccocus granulosus hydatid cyst (fluid of the cyst)
35
P1-like antigen in the environment
RBC
Plasma
turtledove fluids
36
IgM
nat. occuring
weak and cold reactive at 4C
can sometimes be reactive at 37C and AHG
neutralized y P1 soluble subs
Anti-P1
37
Anti-P1 associated inf.
Fascioliasis
Clonorchis sinensis
Opisthrochis viverrini
38
Originally called anti-Tj²
First described on serum of Mrs. Jay (p phenotype w/ adenocarcinoma of stomach)
Tumors contained P system antigens and the antibody has cytotoxic properties that may have helped prevent metastatic growth post-surgery
T = tumor; j = Mrs. Jay
Anti-PP, Pk
39
Produced by all p individuals w/o exposure
Reacts with all RBCs except from p individuals
Components are separable through adsorption
Have IgM and IgG component
Have wide thermal range and binds complement (potent hemolysin)
Can cause HTR and HDN
Associated with spontaneous abortion in early pregnancy
Anti-PP, Pk
40
naturally occurring alloantibody found in all pk individuals.
Alloanti-P
41
Its reactivity is similar to Anti-PP₁pk (a potent hemolysin).
Alloanti-P
42
Alloanti-P reacts with all RBCs except:
Autocontrol (self-RBCs)
p phenotype RBCs.
43
It is a cold-reactive antibody of the IgG class with biphasic properties.
Autoanti-P
44
Associated with Paroxysmal Cold Hemoglobinuria (PCH).
Diagnosed using the Donath-Landsteiner test.
Autoanti-P
45
Defines I as representing individuality.
Wiener et al., 1956
46
It is not antithenitcal and only 1 antigen is present.
I antigen
47
High incidence antigens (commonly found in population)
I and i Antigens
48
I/i Antigen:
Predominant in fetal RBCs
Gradually decreases during first 18 months of life
i antigen
49
I/i Antigen:
Increases until reaching adult proportions
I antigen
50
____________ RBCs enhances detection of both I and i antigens
Enzyme treatment
51
Some individuals do not change their i status after birth.
Adult i
52
Antibody class: Weak, naturally occurring IgM autoantibody.
Enzyme-treated RBCs may enhance detection
Anti I
53
Reactivity of Anti-I
_________ agglutination with adult RBCs (I antigen-positive)
__________ agglutination with cord RBCs (i antigen-positive)
Strong; Weak/No
54
Antibody associated with Mycoplasma pneumoniae.
Anti-A
55
Pathologic Anti-I is associated with __________ disease, which involves strong IgM with a broad thermal range of activity.
Pathologic Anti-I can cause __________, vascular occlusion, or hemolytic anemia.
The production of Pathologic Anti-I may be stimulated by __________ infection, which has an I-like antigen.
Unlike some other antibodies, Pathologic Anti-I is not associated with __________.
cold agglutinin
autoagglutination
Mycoplasma pneumoniae
HDN (Hemolytic Disease of the Newborn)
56
Anti-i is a (frequency) antibody that shows strong reactions with (cell type) and adult i RBCs, but weaker reactions with (cell type).
Anti-i is of the (antibody class) class and reacts optimally at (temperature) with (preparation method) RBCs.
Clinically, Anti-i is associated with three conditions: (condition 1), (condition 2), and (condition 3).
rare; cord RBCs; adult I RBCs
IgM; 4°C; saline suspended
infectious mononucleosis; myeloid leukemia; alcoholic cirrhosis
57
The IT antigen represents a ______ state in the transition from i to I antigens.
Anti-IT is a(n) ______ class antibody that is frequently found in ______ and ______ populations.
Anti-IT shows a clinical association with ______.
transition
IgM; Melanesians; Yanomama Indians (in Venezuela)
Hodgkin’s lymphoma
58
The Kell system contains __________ high and low incidence antigens.
It was the first blood group system discovered after the introduction of __________ testing.
Anti-K was first discovered in 1946 from the serum of __________.
__________ discovered anti-k in 1949, which is the high incidence antithetical partner of K.
24
AHG (Anti-Human Globulin)
Mrs. Kelleher
Levine et al
59
The K antigen is a __________ incidence antigen, while k is a __________ incidence antigen.
In terms of immunogenicity, the K antigen is second only to the __________ antigen.
K antigens first appear on fetal RBCs at __________ weeks gestation.
low, high
D
7
60
K antigens are __________ (well/poorly) developed at birth.
K antigens are NOT destroyed by __________ or __________ enzyme treatments.
K antigens are destroyed by the combination of __________ and __________ enzymes.
well
ficin, papain
trypsin, chymotrypsin
61
Other names for K and k
K is Kell
k is Cellano
62
After ABO and Rh, Anti-K is the _____ antibody seen in blood banks.
Anti-K is an _____ class antibody that reacts at _____ phase.
Anti-K can _____ complement but rarely causes lysis.
Anti-K is associated with infections like _____, _____, and Campylobacter species.
most common
IgG, AHG
bind
mycobacteria, Enterococcus faecalis (or Morganella morganii)
63
_____ enhances Anti-K reactivity in blood bank testing.
Anti-K is strongly implicated in severe _____ (type of transfusion reaction).
Unlike many other antibodies, Anti-K can cause _____ (serious pregnancy complication).
PEG
extravascular HTR (Hemolytic Transfusion Reaction)
HDN (Hemolytic Disease of the Newborn)
64
Antibodies to low-incidence Kell antigens are _____ because few people are exposed to these antigens.
These antibodies are typically detected through _____ or cases of _____, since routine screening cells lack these antigens.
Their clinical significance parallels that of _____.
rare
unexpected incompatible crossmatch, HDN (Hemolytic Disease of the Newborn)
anti-K
65
Antibodies to high-incidence Kell antigens are _____ because most people _____ these antigens.
They are easy to _____ but difficult to work with since most blood banks lack _____ screening cells.
_____ or _____ treated cells are used for testing, which also destroys _____ other blood group systems.
rare, possess
detect, antigen-negative
DTT, AET, JMH/LW/Lutheran/Dombrock/Cromer/Knops (any 1-2 acceptable)
66
The Kx antigen is present on all RBCs except those with _____ phenotype.
The gene encoding Kx antigen is located on the _____ chromosome.
Kx antigen now belongs to the _____ blood group system.
McLeod
X
XK
67
The McLeod phenotype initially appears as _____ but shows weak expression of some Kell antigens.
McLeod syndrome is _____ (inheritance pattern) and characterized by acanthocytic RBCs.
Patients with McLeod phenotype lack both _____ and _____ antigens.
Kell null
X-linked
Kx, Km (accept either order)
68
The Duffy blood group was named after _____, a hemophiliac who produced the first anti-Fyᵃ antibody in _____.
The antibody anti-Fyᵇ was first described by _____ in a woman with _____.
Sanger et al discovered in 1953 that _____ individuals were Fy(a-b-).
Miller et al demonstrated in 1975 that Fy(a-b-) phenotype provides resistance to _____ and _____ malarial parasites.
Mr. Duffy, 1950
Ikin et al, 3 pregnancies
African-Americans
Plasmodium knowlesi, Plasmodium vivax
69
Fyᵃ and Fyᵇ antigens appear on fetal RBCs as early as _____ weeks gestational age and are _____ at birth.
These antigens are destroyed by common enzymes including _____, _____, and ZZAP (accept any 2).
Unlike many other blood group antigens, Fyᵃ/Fyᵇ are NOT affected by _____ or _____ treatments.
6 (or early), well-developed
ficin, papain, bromelin, chymotrypsin (any 2)
AET, glycine-acid EDTA
70
Anti-Fyᵃ is _____ times more common than Anti-Fyᵇ.
Both antibodies are typically _____ class and may _____ complement.
Their reactivity is enhanced by _____ medium.
A key distinguishing feature: they do NOT react with _____ cells.
20
IgG, bind
low ionic strength
enzyme-treated
71
Some Anti-Fy² and Anti-Fy³ antibodies may demonstrate _____ effect in testing.
These antibodies are clinically significant as they can cause both _____ and _____ transfusion reactions.
They are also associated with _____ in newborns.
dosage
acute HTR, delayed HTR (either order)
HDN (Hemolytic Disease of the Newborn)
72
The Kidd blood group was discovered when Allen et al (_____) identified an antibody in the serum of _____ whose infant had HDN.
The first Kidd antibody discovered was _____.
The antithetical antigen Jkᵇ was later described by _____.
Kidd antibodies are particularly dangerous because they're a common cause of _____.
1951, Mrs. Kidd
anti-Jkᵃ
Plaut et al
hemolytic transfusion reaction (HTR)
73
Jk² and Jk⁰ antigens are _____ in fetal RBCs, appearing at _____ and _____ weeks gestation respectively.
These antigens are considered _____ (immunogenic property).
Unlike many blood group antigens, Jk²/Jk⁰ are resistant to:
Common enzymes: _____ and _____
Chemical treatments: _____, _____, and glycine-acid EDTA
well-developed, 11, 7
not very immunogenic
papain, ficin, AET, DTT, chloroquine-2-phosphate (any 2 enzymes + any 2 chemicals)
74
Anti-Jk² and Anti-Jk⁵ have a _____ reputation in blood banks due to their challenging characteristics.
These antibodies often demonstrate _____ effect, showing stronger reactions with _____ RBCs.
They are frequently found in _____ with other antibodies, making identification difficult.
Between the two, _____ is more commonly encountered.
While primarily _____, they may also have a _____ component.
"notorious"
dosage, homozygous
combination
Anti-Jk²
IgG, IgM
75
The Lutheran blood group system was first recognized in _____.
Anti-Lu² was discovered in a patient with _____ who received blood containing a _____ antigen.
The antibody _____ was described later in 1956 by _____ and _____.
1945
lupus erythematosus diffusus, low-incidence
anti-Lu⁵, Cutbush, Chanarin
76
The most common Lutheran phenotype is _____(+).
Lu(a-b-) phenotype is _____.
Lutheran antigens appear at _____ weeks gestation but reach adult levels only by _____ years.
Lu(b)
very rare
10-12, 15
77
Anti-Luᵃ is typically _____ (Ig class) and may bind _____.
It's often missed in testing because most screening cells are _____.
Anti-Luᵃ is destroyed by _____ but not by _____.
IgM, complement
Lu(a-)
trypsin/pronase/AET/DTT (any), ficin/papain (any)
78
Anti-Luᵇ is mostly _____ (Ig class) and reacts at _____ phase.
Like Anti-Luᵃ, it's destroyed by _____ and _____.
Both antibodies are associated with _____ HDN cases.
IgG, AHG
AET, DTT
mild
