OTHER BLOOD GROUPS P2 Flashcards
1
Q
found in glycophorin A (GPA) (major RBC sialic acid- rich glycoprotein)
A
M & N Antigens
2
Q
(M & N Antigens)
antithetical and differ in their amino acid residues at positions 1 and 5
___: serine at position 1
___: glycine at position 5
A
M ; N
3
Q
(M & N Antigens)
antigens are well developed at birth
A
yes
4
Q
(M & N Antigens)
easily destroyed by _____, ____, ___ and by the less common enzymes ______ and _____
A
ficin, papain, and bromelin ; trypsin and pronase
5
Q
also destroyed by ZZAP (combination of DTT and papain or ficin) BUT not affected by DTT alone,
2-aminoethyliso-thiouronium bromide (AET), α-chymotrypsin, chloroquine, or glycineacid EDTA
treatment.
A
(M & N Antigens)
6
Q
M and N antibodies are _________
A
heterogeneous
7
Q
found in glycophorin B (GPB)
differentiated by the amino acid at position 29
A
S & s Antigens
8
Q
________ defines S, whereas ______ defines s
A
Methionine ; threonine
9
Q
S and s also are well developed at birth.
A
yes
10
Q
(S & s Antigens)
easily degraded by _____
A
enzymes
11
Q
(S & s Antigens)
destroyed by ____, ______. ______, ______, and _______ ( amount of degradation may depend on the strength of the enzyme solution, the length of treatment, and the enzyme-to-cell ratio)
A
Ficin, papain, bromelin, pronase, and α-chymotrypsin
12
Q
(S & s Antigens)
_________ by Trypsin , DTT, AET, chloroquine, or glycine-acid EDTA treatment
A
NOT destroyed
13
Q
____: associates with protein band 3, which affects the expression of the antigen Wr(b) of the Diego blood
group system (located on protein band 3)
A
GPA
14
Q
_____: associated with the Rh protein and Rh-associated glycoprotein complex as evidenced by the greatly
reduced S and s expression on Rhnull RBCs.
A
GPB
15
Q
-naturally occurring saline agglutinins that react below 37°C
- 50% to 80% are IgG or have an IgG component
A
Anti- M
16
Q
Anti- M do not bind _________ & do not react with ___________
A
complement ; enzyme-treated RBC
17
Q
more common in children (especially patients with bacterial infections)
A
Anti- M
18
Q
(Anti- M) Exhibits dosage: anti-M may react better with ______ RBCs (genotype MM) than with ______ RBCs
(genotype MN).
A
M+N– ; M+N+
19
Q
(Anti- M)
Antibody reactivity can be enhanced by increasing the ________ or ________, or both, by decreasing incubation temperature or by adding a potentiating medium.
A
serum-to-cell ratio or incubation time
20
Q
(Anti- M)
pH-dependent, reacting best at pH _____
A
6.5.
21
Q
Anti-M does not react at ____ it is not clinically significant for transfusion
A
37°C,
22
Q
- Anti-M rarely causes ____, decreased red blood cell survival, or ____
A
HTRs ; HDFN
23
Q
(Anti- M)
Some: react only with _____ exposed to glucose solutions
A
RBCs
24
Q
made by individuals whose RBCs type M+N– and S+ or s+
A
Anti- N
25
(Anti- N)
- cold-reactive IgM or IgG saline agglutinin
YES
26
not clinically significant unless it reacts at 37°C. (does not bind complement or react with enzyme-
treated RBCs.)
Anti- N
27
(Anti-N)
reacting better with _______ RBCs than with _______ RBCs
M–N+ (NN) ; M+N+ (MN)
28
Anti-N is seen in rare cases of ______
mild HDFN
29
less common than anti-M.
Anti- N
30
Also seen in renal patients who were dialyzed on equipment sterilized with formaldehyde.
Anti-N
31
(Anti-N)
Dialysis-associated anti-N reacts with any _______ RBCs treated with ________ (called anti-Nf )
anti-Nf does not react at ____, it is clinically insignificant for transfusion
N+ or N– ; formaldehyde ; 37°C
32
IgG, reactive at 37°C and the antiglobulin phase of testing
Anti- S & Anti- s
33
(Anti- S & Anti- s)
optimal reactivity between _____ and ______ by saline indirect antiglobulin test.
10°C and 22°C
34
may or may not react with enzyme-treated RBCs, depending on the extent of treatment and the
efficiency of the enzyme
Anti- S & Anti- s
35
seen less often than anti-M
Anti- S & Anti- s
36
(Anti- S & Anti- s)
clinically significant:
may bind _______
seen in severe HTRs with ______
also caused _____
complement ; hemoglobinuria ; HDFN
37
RBCs of three rare phenotypes lack GPA or GPB or both GPA and GPB; consequently, they lack all _______
MNS antigens
38
3 MNS PHENOTYPES
1. U- Phenotype
2. En(a-) Phenotype
3. M(k) Phenotype
39
- located on GPB very close to the RBC membrane between amino acids 33 and 39
- have type S–s–U–
- can make anti-U in response to transfusion or pregnancy
U- Phenotype
40
found on RBCs of all individuals except about 1% of African Americans (and 1% to35% of
Africans) who lack GPB because of a partial or complete deletion of GYPB
U antigen
41
IgG ; reported to cause severe and fatal HTRs and HDFN.
Anti-U
42
altered GPB that does not express S or s.
U variant (Uvar):
43
RBCs, although weakly, by adsorption and elution
Anti-U react with apparent U–
44
1969, they described an antibody to the same high prevalence antigen, called Ena (for envelope)
Darnborough and coworkers and Furuhjelm and colleagues
45
1969: Darnborough and coworkers and Furuhjelm and colleagues described an antibody to the same high prevalence antigen, called Ena (for envelope)
En(a–) Phenotype
46
En(a–) individuals appeared to be
M–N–
47
produce anti-Ena
En(a–) Phenotype
48
En(a–) Phenotype results from homozygosity for a rare gene deletion at the _______
Cause: no ____ is produced, but ____ is not affected
GYPA locus ; GPA ; GPB
49
En(a–) Phenotype caused severe _____ and ______
HTRs and HDFN.
50
1964; they Named a rare silent gene M(k)
Metaxas and Metaxas-Buhler
51
single, near-complete deletion of both GYPA and GYPB
M(k) Phenotype
52
null phenotype in the MNS system
MkMk genotype
53
MkMk genotype is associated with decreased ________ content
but increased ________ of RBC membrane band 3.
RBC sialic acid ; glycosylation
54
- Autoantibodies to U and Ena: ________
- associated with warm-type __________
more common ; autoimmune hemolytic anemia
55
(Disease Associations in MNS)
- ______ may serve as the receptor by which certain pyelonephritogenic strains of E. coli gain entry to
the urinary tract
- ___________ appears to use alternative receptors, including GPA and GPB for cell invasion
GPA(M) ; Plasmodium falciparum
56
ano na next group teh
The Kell (006) and Kx (019) Systems
57
- consists of 36 high-prevalence and low-prevalence antigens
- first blood group system discovered after the introduction of antiglobulin testing
Kell (006) & Kx (019) System
58
1946 ;
Anti-K was identified in the serum of ________
________ was described
Mrs. Kelleher ; anti-k
59
high-prevalence antithetical partner to K, was described
_____: was describe in 1957
Anti-K ; Kpa
60
Kpa was describe
discovery of the null phenotype designated Ko
1957
61
Kpb was describe
1958
62
Other antigens: ____ (described in 1958) and ____ (described in 1963)
Jsa ; Jsb
63
Kell blood group antigens are found only on _____
RBCs
64
K antigen can be detected on fetal RBCs as early as ______ ; well developed at birth
k antigen has been detected at _______
10 weeks ; 7 weeks
65
(Kell (006) & Kx (019) System)
- not denatured by the routine blood bank enzymes (______ & ______)
- destroyed by _______ & ________ (used in combination)
ficin & papain ; trypsin & chymotrypsin
66
(Kell (006) & Kx (019) System)
- Thiol-reducing agents, such as ___________, __________, ______, and ______ (which contains DTT in addition to enzyme), destroy Kell antigens but not Kx.
- _________ (an IgG-removal agent) also destroys Kell antigens.
100 to 200 mM DTT ; 2-mercaptoethanol (2-ME) ; AET ; ZZAP ; Glycine-acid EDTA
67
- K is rated ______ only to D in immunogenicity
second ; (ABO> D> K)
68
Anti-K appear to be induced by ________ and ________
pregnancy and transfusion
69
Alleles ____ and _____ are low-prevalence mutations of their high-prevalence partner Kpb
Kpa and Kpc
70
Kpa antigen found in about ___ of whites.
2%
71
associated with suppression of other Kell antigens on the same molecule, including k and Jsb.
Kpa gene
72
result from a reduced amount of the Kell glycoprotein inserted in the RBC membrane.
Kpa gene
73
rarer Kpa, Kpb, and Kpc antigen
Kpc antigen
74
_______, antithetical to the high-prevalence antigen Jsb
Jsa antigen
75
The prevalence of Jsa in ______ is almost 10 times greater than the prevalence of the K antigen in blacks.
blacks
76
Jsa and Jsb were linked to the _________ when it was discovered that Ko RBCs were Js(a–b–).
Kell system
77
most common antibody seen in the blood bank
Anti-K
78
Anti-K is:
- usually ___ and reactive in the ______ phase
- usually made in response to antigen exposure through ________ and ________
IgG ; antiglobulin ; pregnancy and transfusion
79
________________ examples of anti-K are rare and have been associated with bacterial infections.
Naturally occurring IgM
80
studied an IgM anti-K in an untransfused 20-day-old infant with an E. coli infection whose mother did not
make anti-K.
Marsh and colleagues
81
(IgM anti-K)
- react poorly in methods incorporating low-ionic media, such as ______, and in some automated systems.
- most reliable method of detection is the ____________
- Increase reactivity by _________, _____
- seen in severe _______.
- associated with severe ______.
- Fetal anemia in anti-K HDFN is associated with suppression of __________ due to destruction of erythroid precursor cells.
- LISS
- indirect antiglobulin test.
- potentiating medium, PEG
- HTRs
- HDFN
- erythropoiesis
82
(Antibodies to Kpa, Jsa, and Other Low-Prevalence Kell Antigens)
- _____ because so few people are exposed to these antigens.
- routine antibody detection RBCs do not carry ____________, the antibodies are most often detected through unexpected incompatible crossmatches or cases of HDFN.
rare ; low-prevalence antigens
83
(Antibodies to Kpa, Jsa, and Other Low-Prevalence Kell Antigens)
- The serologic characteristics and clinical significance of these antibodies parallel anti-K.
- The original anti-Kpa was naturally occurring, but most antibodies result from _______ or _______
transfusion or pregnancy.transfusion or pregnancy.
84
(Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens)
- rare because so few people ____ these antigens.
- They also _____ anti-K in serologic characteristics and clinical significance.
lack ; parallel
85
(Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens)
- ___________ are easy to detect but difficult to work with because most blood banks do not have the antigen-negative panel cells needed to exclude other alloantibodies
- Testing an unidentified high-prevalence antibody against _______ or _______-treated RBCs is a helpful
technique
High-prevalence antibodies ; DTT- or AET
86
(Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens)
- Caution is needed before assigning Kell system specificity until antigen-negative RBCs are tested because DTT also denatures JMH and high-prevalence antigens in the LW, Lutheran, Dombrock,
Cromer, and Knops systems.
- Finding compatible units for transfusion can be difficult; siblings and rare-donor inventories are the
most likely sources.
yes
87
located on chromosome 7 at position 7q33
KEL gene
88
(KEL gene)
- Several different mutations have been found that result in the rare null phenotype ____
-People who tested _____ for two low-prevalence Kell antigens had always been found to carry the
encoding alleles on opposite chromosomes.
Ko ; positive
89
In 2009, report, two unrelated individuals with very weak K antigens were found to be heterozygous for _______ and ________
KKpa and kKpb
90
- encodes the Kx antigen
- independent of KEL
- located on the short arm of the X chromosome at position Xp21.
gene XK
91
present on all RBCs except those of the rare McLeod phenotype
Kx
92
have increased Kx antigen.
Ko and Kmod phenotype:
93
When Kell antigens are denatured with AET or DTT, the expression of Kx _______
increases
94
(Ko Phenotype & Anti-Ku)
_____ RBCs lack expression of all Kell antigens.
- no membrane abnormality and survive normally in circulation.
- phenotype is rare
ko
95
(Ko Phenotype & Anti-Ku)
_______: single specificity and cannot be separated into components.
- caused both HDFN and HTRs.
Anti-Ku
96
- described a young male medical student who initially appeared to be Kell null but who demonstrated weak
expression of k, Kpb, and Jsb detectable by adsorption-elution methods
Named after the student
1961: Allen and coworkers
97
- very rare. All are male, inheritance is X-linked
- RBCs lack Kx and another high prevalence antigen, Km, and have marked depressionof all other Kell antigens.
McLeod Phenotype & Syndrome
98
(McLeod Phenotype & Syndrome)
- __________ (having irregular shapes and protrusions) with decreased _______ and reduced in vivo
______
acanthocytic ; deformability ; survival
99
(McLeod Phenotype & Syndrome)
have a variety of muscle and nerve disorders that, together with the serologic and hematologic picture, are
collectively known as the __________
McLeod syndrome
100
(McLeod Phenotype & Syndrome)
develop a slow, progressive form of muscular _______ between ages 40 and 50 years and _________
(leading to cardiomyopathy)
dystrophy ; cardiomegaly
101
