Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Blood Bank > Uncommon Blood Groups > Flashcards

Uncommon Blood Groups Flashcards

1
Q

When was The Lutheran System antibody anti-Lu(a) discovered?

A

In the serum of a Lupus patient in 1945.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When was The Lutheran System antibody anti-Lu(b) discovered?

A

In 1956 Lu(b) was described.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How many antigens are in the Lutheran System?

A

Consists of 20 antigens, 4 of which are antithetical pairs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the four antithetical pairs of the Lutheran System and which pair is low incidence?

A
  1. Lu(a) & Lu(b)
  2. Lu6 & Lu9
  3. Lu8 & Lu14
  4. Au(a) & Au(b)—-> low incidence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When are Lutheran antibodies first detectable?

A

In a ten week old fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What tissues are Lutheran antigens not found on?

A

Lymphocytes, granulocytes, monocytes, or platlets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What as tissues are Lutheran antigens found on?

A

Blood vessels, brain kidney heart liver, lung, pancreas, placenta.,muscle, skin,etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When maternal Lutheran ab is absorbed out, what happens?

A

Likelihood of HDFN increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are Lutheran antigens affected by enzymes?

A

They are destroyed destroyed by trypsin and alpha-chymotrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which enzymes don’t affect Lutheran antigens?

A

Ricin and papain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Do Lutheran antibodies react with DTT or AET treated RBCs?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lutheran antibodies are produced by what type of genes?

A

Allelic codominant genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are Lutheran antigens expressed expressed on cord blood cells?

A

Weakly expressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Are Lutheran antibodies clinically significant?

A

Not usually a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Are Lutheran antibodies clinically significant?

A

Not usually a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Are Lutheran antibodies clinically significant?

A

Not usually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What isotope are Lutheran antibodies?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What chromosome contains Gene’s for the Lutheran system?

A

Chromosome 19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do the Lutheran antigens hold up in storage?

A

Fragile when stored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

The Lutheran genes have a link to which other gene?

A

Se gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What percentage of RBCs express Lu (a)?

A

5-8%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What percentage of RBCs express Lu (b)?

A

99%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the antibodies of the Lutheran system?

A

Anti-Lu(a), Anti-Lu(b), and Anti-Lu3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What isotype is anti-Lu(a)?

A

May be IgG, IgM, or IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What isotype is anti-Lu(b)?

A

Mostly IgG (IgG1), some IgM, IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which Lutheran antibody can be naturally occurring?

A

Anti-Lu(a)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Will any of the three Lutheran antibodies bind complement?

A

They rarely bind complement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Anti-Lu(a) causes what clinical issues?

A

No immediate HTR, mild delayed HTR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which Lutheran antibody demonstrates mixed field agglutination reactions?

A

Anti-Lu(a)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Anti-Lu(b) causes what clinical problems?

A

Causes mild to moderate HTR; placenta can absorb it out and leads to mild HDFN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the most common cause of Anti-Lu(b) in a patient’s serum?

A

Transfusion or Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the prevalence of Anti-Lu3?

A

rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What enzymes is Anti-Lu3 sensitive to?

A

DTT, trypsin and chymotrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What Lutheran genotype most commonly produces

Anti-Lu3?

A

Lu(a-b-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What isotype is Anti-Lu3?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What antigens will Anti-Lu3 bind to?

A

Lu(a) and Lu(b) on red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Is Anti-Lu3 clinically significant?

A

No. It is not reported to cause HDFN or HTR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Blood Group System Definition

A

one or more antigens produced by alleles at a single locus or loci so closely linked that crossing over does not occur or is very rare.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Alloantibodies can detect

A

Antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Most blood group alleles have this relationship:

A

Codominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the conventions for writing the names of alleles?

A

Genes are underlined; allele number is a superscript

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the conventions for writing the names of antigens?

A

Antigens are written in regular type with a superscript.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the conventions for writing the names of phenotypes?

A

Described by the antigen present or absent; ex: M+, K-, Jk(a-), Fy(b+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the conventions for writing the names of antibodies?

A

decribed by placing anti- in front of the antigen; ex: anti-D is the antibody to D antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Who discovered anti-M and anti-N and when?

A

Landsteiner and Levine in 1927

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Who discovered S antigen and when?

A

Walsh and Montgomery in 1947

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

little s was discovered in?

A

1951

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

U became part of the MNS system in

A

1953

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

The highly complex MNS Blood Group System consists of how many antigens?

A

46 antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the most common MNS antigens?

A

M, N, S, s, and U

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

MNS antigens are found on…

A

On glycoproteins glycoporin A and/or glycoporin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

M and N antigens attach to…

A

glycoporin A (GPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

S and s antigens attach to…

A

glycoporin B (GPB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

MNS are inherited as the four haplotypes…

A

MS, Ms, NS, Ns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which MNS haplotype exhibits linkage disequilibrium?

A

MS; S is found with M twice as often as with N.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How do M and N antigens react to enzyme treatment of RBCs?

A

They are destroyed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

M and N antigens are resistant to treatment with what enzymes?

A

chymotrypsin and DTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How do S and s antigens react to enzyme treatment of RBCs?

A

Destruction can be variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How S and s antigens are react to treatment with enzymes?

A

They are destroyed by chymotrypsin, but resist treatment with DTT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which MNS genotype is often deficient in GPB?

A

S-s- U-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which MNS antigen is high prevalence?

A

U

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

U- RBCS are almost always…

A

S-s-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

S-s- genotype often goes with what antigen?

A

U+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How does U antigen react to enzyme treatment?

A

It is generally resistant to enzyme treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What isotype is anti-M?

A

IgM and/or IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Does anti-M show dosage?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How common is anti-M and how is it stimulated?

A

It is common and naturally occurring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What special environmental condition do some anti-M prefer?

A

Some react best in an acid environment; pH 6.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Is anti-M clinically significant?

A

Not always. It is rarely implicated in both acute and delayed HTR, but it may cause rare and severe HDFN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Anti-N prevalence?

A

Rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How does anti-N react?

A

It reacts at room temperature and below.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Is anti-N clinically significant?

A

No. It is rarely implicated in acute and delayed transfusion reaction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Does ant-N show dosage?

A

Yes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Autoanti-N has been reported to cause….

A

a few cases of AIHA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Anti-N occurred in a group of dialysis patients after…

A

the dialysis machine was cleaned with formaldehyde.

75
Q

Anti-S and anti-s are what isotype?

A

IgG

76
Q

Anti-S and anti-s react when?

A

at 37 degrees and at AHG

77
Q

Do anti-S and anti-s show dosage?

A

They may.

78
Q

Are anti-S and anti-s clinically significant?

A

Yes. They have been implicated in HTR and have caused severe and fatal HDFN.

79
Q

Autoanti-S has been implicated in…

A

AIHA

80
Q

Anti-U is what isotype?

A

IgG

81
Q

Anti-U is most commonly produced in what phenotypes individuals?

A

S-s-

82
Q

Autoanti has been reported in a case(s) of…

A

AIHA

83
Q

Is anti-U clinically significant?

A

It has been reported in mild to severe HTR and HDFN.

And delayed transfusion reactions.

84
Q

What diseases are associated with the MNS system?

A

E. coli infection and malaria

85
Q

How does the MNS system interact with E. coli?

A

GPA acts as a receptor for certain strains of E.coli.

86
Q

How does the MNS system interact with Plasmodium falciparum?

A

GPA and GPB act as receptor sites for the malarial parasite.

87
Q

Who discovered the Kell System and when?

A

Coombs discovered just after the development of AHG in 1946.

88
Q

How many antigens are associated with the Kell System?

A

36

89
Q

What are most important Kell antigens?

A

K, k, Kp(a), Kp(b), Js(a), Js(b)

90
Q

Where are Kell antigens found?

A

mostly on RBCs, but also on bone marrow, fetal liver, testes, brain, lymphoid, heart, skeletal muscle

91
Q

During what part of the life cycle are kell antigens present?

A

They are well-developed at birth.

92
Q

How do Kell antigens react to enzyme treatment?

A

They are not denatured by routine blood bank enzymes.

93
Q

What combination of reducing agent and enzymes will it take to denature a Kell antigen?

A

They are sensitive to a mix of trypsin, alpha chymotrypsin, and reducing agents(DTT, EZAP, EEGA).

94
Q

What genes are responsible for normal Kell antigen production?

A

KEL and Xk

95
Q

What does KEL encode for?

A

Kell glycoprotein

96
Q

What does Xk encode for?

A

—–protein

97
Q

The FDA requires that K and k antigens . . .

A

must be included on all antigen profiles.

98
Q

What is the prevalence of K or KEL 1 antigens?

A

Prevalent in about 9% of people of European origin and 1.5% in people of African origin and rare in people of East Asian origin.

99
Q

What is the prevalence of k or KEL 2 antigens?

A

High incidence in all populations

100
Q

What is the prevalence of Kp(a) or KEL 3 antigens?

A

Low incidence; <2% European only

101
Q

What is the prevalence of Kp(b) or KEL 4 antigens?

A

High incidence in all populations, >99%

102
Q

What is the prevalence of Js(a) or KEL 6 antigens?

A

20% among those of African origin.

103
Q

What is the prevalence of Js(b) or KEL 7 antigens?

A

High incidence in all populations

104
Q

How do Kell antigens rate in clinical significance among the other blood groups?

A

Excluding ABO, Kell is second only to D antigen in creating antibodies; Kell antigens are strongly immunogenic.

105
Q

How many antigens are in the Kell System?

A

36 antigens

106
Q

What are the three allelic pairs of the Kell system?

A

K and k
Kp(a) and Kp(b)
Js(a) and Js(b)

107
Q

What isotype are Kell antibodies?

A

IgG

108
Q

How are Kell antibodies stimulated?

A

by pregnancy or transfusion

109
Q

Are Kell antibodies clinically significant and why?

A

Yes. Can cause severe HDFN and HTR. It suppresses erythropoiesis in a newborn in addition to causing hemolysis.

110
Q

Can patients with anti-K have K+ blood for transfusion?

A

No. They always need K- blood.

111
Q

What is the most common antibody seen in the blood bank, outside of ABO and Rh?

A

Anti-K

112
Q

When are Kell antibodies detected?

A

at AHG of the antibody screen

113
Q

What isotype is anti-K?

A

IgG, specifically IgG1

114
Q

What stimulates anti-K?

A

Pregnancy or transfusion

115
Q

What isotype is anti-k?

A

IgG, specifically IgG1

116
Q

When is anti-k detected?

A

Most often at AHG

117
Q

What is the prevalence of anti-Kp(a), Js(a)?

A

Rare because few people are exposed to these antigens (only by pregnancy and transfusion)

118
Q

How are anti-Kp(a), Js(a) detected most commonly?

A

Detected through unexpected incompatible crossmatches or HDFN

119
Q

What other Kell antibody is similar to anti-Kp(a), anti-Js(a), Anti-Kp(b), and Anti-Js(b)serologically?

A

Anti-K

120
Q

What is the prevalence of Anti-Kp(b) and Anti-Js(b)?

A

Rare because few people are exposed to these antigens.

121
Q

Is anti-k clinically significant?

A

Yes. It can cause HTR and HDFN. And Intravascular hemolysis.

122
Q

K(null) phenotype is expressed as

A

no Kell antigens are expressed; antigens may somehow be involved in membrane integrity

123
Q

K (mod) phenotype is expressed as

A

very weak expression of Kell antigens

124
Q

K(x) phenotype is expressed as

A

a part of its own blood group system, but is linked to the Kell glycoprotein by a single disulfide bond

125
Q

What is the McLeod phenotype?

A

It occurs because of the absence of K(x) antigen and reduced expression of Kell; It is rare and leads to decreased RBC survival.

126
Q

What is McLeod syndrome?

A

It is an X-linked genotype of absent K(x) and reduced Kell expression.

127
Q

What are the diseases associated with McLeod syndrome?

A

Acanthocytosis
Neuromuscular disease
Psychiatric involvement
Chronic Granulomatous Disease

128
Q

Are transfusions a good treatment for a pt with McLeod Syndrome?

A

No. Transfusions should be avoided.

129
Q

What are characteristics of Kell autoantibodies?

A

Most are directed against high prevalence antigens.

Mimicking specificities have been reported

130
Q

Where did The Duffy System get its name?

A

It was named for Mr. Duffy, a multiple transfused hemophiliac, with anti-Fy(a); Anti-Fy(b) was discovered a year later.

131
Q

What year was Fy(a-b-) phenotype described?

A

1955

132
Q

Fy (a-b-) phenotype resists what infections?

A

P. knowlesi and P. vivax

133
Q

How many Duffy antigens?

A

5 antigens

134
Q

What is the biochemical structure of the Duffy antigens?

A

antigens reside on a glycoprotein known as the Duffy antigen receptor for chemokines or DARC

135
Q

People of African ancestry produce a third Duffy allele, Fy, that…

A

Has no glycoprotein on their RBCs

136
Q

What are the two antigen common among European and Asian populations?

A

Fy(a) and Fy(b)

137
Q

Fy=

A

Duffy

138
Q

What are the four Duffy phenotypes?

A

Fy(a+b-)
Fy(a+b+)
Fy(a-b+)
Fy(a-b-)

139
Q

How do antigens Fy(a) and Fy(b) hold up in storage?

A

may deteriorate

140
Q

How do antigens Fy(a) and Fy(b) react to enzymes?

A

destroyed by proteolytic enzymes and by ZZAP

141
Q

When are Fy(a) and Fy(b) antigens begin to be expressed?

A

well developed at birth, found in umbilical cord RBCs

142
Q

Where are antigens Fy(a) and Fy(b) found?

A

endothelial cells, brain, lung alveoli, renal epithelium

143
Q

What isotype are Anti-Fy(a) and Anti-Fy(b)?

A

Mostly IgG, specifically IgG1

144
Q

Do an Anti-Fy(a) and Anti-Fy(b) show dosage?

A

Yes

145
Q

How do Anti-Fy(a) and Anti-Fy(b) react to enzymes?

A

destroyed by enzymes

146
Q

What is the prevalence of Anti-Fy(a) and Anti-Fy(b)?

A

anti-Fy(a) is 20x more common than anti-Fy(b)

147
Q

Are Anti-Fy(a) and Anti-Fy(b) clinically significant?

A

Yes. Both can cause HTR and HDFN–acute and delayed

148
Q

How do Anti-Fy(a) and Anti-Fy(b react best?

A

at AHG phase

149
Q

Are there Anti-Fy(a) and Anti-Fy(b) autoantibodies?

A

yes. rare autoantibodies have been reported

150
Q

Fy3 antigen prevalence

A

present in about 100% whites, 32% of blacks

151
Q

What is Fy3 antigen’s reaction to enzymes?

A

not destroyed by proteolytic enzymes

152
Q

What antigens must be present for Fy3 to be expressed?

A

Fy(a) and Fy(b)

153
Q

When is Fy3 antigen first expressed?

A

Expressed on cord RBCS, and expression increases after birth.

154
Q

What is the isotype of anti-Fy3 antibody and does it bind complement?

A

IgG, rarely binds complement

155
Q

When does anti-Fy3 antibody react best?

A

detected at AHG

156
Q

What is the prevalence of anti-Fy3?

A

rare

157
Q

What is the prevalence of Fy5 antigen?

A

32% in black pop, 99.9% in everybody else

only present when either Fy(a) or Fy(b) is present and also requires a normal Rh (not Rh null)

158
Q

How does Fy5 antigen react to enzymes?

A

resists treatment with ficin and papain, and DTT

159
Q

What isotype is anti-Fy5?

A

IgG

160
Q

How does anti-Fy5 react to enzymes?

A

reacts best at AHG phase

161
Q

Is anti-Fy5 clinically significant?

A

can cause mild transfusion reactions; HDFN is unknown

162
Q

How are Duffy antibodies summarized?

A

by pregnancy and transfusion

163
Q

Do Duffy antibodies bind complement?

A

No

164
Q

Do Duffy antibodies show dosage?

A

Yes

165
Q

Are Duffy antibodies clinically significant?

A

Yes. Cause HTR, but do not commonly cause HDFN.

Patients with the antibody should receive antigen negative RBCs for transfusion and AHG crossmatch.

166
Q

The genotype Fy(a-b-) confers resistance to what disease?

A

Malaria, it confers a selective advantage.

167
Q

Explain how the Duffy glycoprotein interacts with the malarial parasite.

A

It is a receptor for Plasmodium vivax.

168
Q

The Duffy blood group is a possible receptor for…

A

chemokines. It removes excess, cleans up excess.

169
Q

Who discovered The Kidd System and when?

A

Discovered in 1951 in Mrs. Kidd whose infant suffered from HDFN.

170
Q

What are The Kidd System Antigens?

A

Jk(a), Jk(b), Jk3

171
Q

What is the composition of the Kidd antigens?

A

glycoprotein

172
Q

Which Kid antigens are products of antithetical alleles?

A

Jk(a) and Jk(b)

173
Q

What is the prevalence of the Kidd antigens?

A

Jk(a) and Jk(b) are common in most people. Jk(a) is more common than Jk(b) in people of African descent.

174
Q

When are the Kidd antigens detectable?

A

Detected at 7-11 weeks gestation. They are well-developed at birth.

175
Q

Are The Kidd antigens clinically significant?

A

No. Cause rare HDFN. Not very immunogenic.

176
Q

How do Kidd antigens react to enzymes?

A

Not denatured by enzymes.

177
Q

What function are Kidd antigens thought to have for RBCs?

A

Urea transporter in RBCs, across membrane as RBCs pass though the kidneys.

178
Q

Where are Kidd antigens found?

A

RBCs. Not on plts, monocytes, granulocytes, or lymphocytes

179
Q

What is the prevalence of anti-Jk(a) and anti-Jk(b)?

A

Not common.

180
Q

What are the Kidd antibodies?

A

anti-Jk(a) and anti-Jk(b)

181
Q

When do anti-Jk(a) and anti-Jk(b) react?

A

AHG

182
Q

Do anti-Jk(a) and anti-Jk(b) demonstrate dosage?

A

Yes

183
Q

Are anti-Jk(a) and anti-Jk(b) clinically significant?

A

Can cause severe, acute HTR.
**Common cause of delayed HTR
Very rarely cause HDFN
Have been implicated in acute renal transplant rejection.

184
Q

Do anti-Jk(a) and anti-Jk(b) bind complement?

A

Approximately 50% antibody binds complement.
titers drop quickly and can go undetected, thus previous records are useful.
Amanestic response.

Blood Bank (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions