Brainscape's Knowledge GenomeTM

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


See full index

Human Genetics > human genetics test final > Flashcards

human genetics test final Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

how do you figure out an incest child having the disease?

A

pathway tracingg

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

what is pathway tracing?

A

following the allele away from the known location and moving away from the reference point and toward the point in question

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

what is a primary relative?

A

immediate relative (just one position away along a descent line)

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

what is a secondary relative?

A

slightly removed ( two positions away)

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

what is a tertiary relative?

A

more distant relative (3 positions away)

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

are there fourth degree relatives?

A

yes, but we donﾒt go out that far

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

def of multifactorial inheritance

A

genetics is due to many factors, some genetic some not

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

two fundamental forms of multifactorial inheritance?

A

multiple genes determine trait (polygenic inheritance), and a single gene and enviromental factors

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

what are the early cases of multifactorial inheritance?

A

penetrance, variable expressivity

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

what is the example of polygenic inheritance used?

A

wheat grain color

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

what do you begin to see if one begins to put the phenotypes on a graph?

A

normal distribution (bell curve)

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

what color of wheat is most common?

A

pink (amber as he says it)

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

what else seems to work in the same way as wheat color?

A

human skin color

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

what determines the higher continuous variation?

A

the greater the number of genes involved in the polygenic system

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

what happens if you add in chances for additional enviromental variables to a polygenic system?

A

the variation becomes very smooth and continuous, and therefore it becomes very difficult to dissect out the genetic component

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

what is the genetics of obesity?

A

complex multifactorial trait

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

what are the factors of obesity?

A

a trait where you wont get saitity, and the enviromental is where you over eat and not exercise

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

what is the genetics of intelligence?

A

complex multifactorial trait

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

what did the Bach pedigree look like?

A

it LOOKED like musical genius was a autosominal dominant trait

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

is the use of a pedigree a good way to be used as convincing evidence for a complex mulifactorial trait?

A

it may be problematic

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

what should you use instead?

A

comparing specific genotypes placed in differing or same enviroments

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

what is an example of genotypes living in different enviroments?

A

monozygous twins that have lived in different enviroments

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

what are the results of the monozygous twin studies?

A

the twins yeild substantial evidence for a GENETIC basis to intelligence

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

what university has an ongoing monozygous twin study?

A

university of minnesota

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

what is the final conclusion of the twin studies?

A

merely confirm that both genetic and enviromental factors are important, although many would argue that its evidence for genetic factors

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

what is another way to approach mulitfactorial inheritence? (other than pedigree or genetic cohort)

A

heritability

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

def of heritability

A

an estimate of the population phenotypic VARIATION that is due to genotype

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

another def of heritabilityﾅ.

A

the fraction of the phenotypic variability in the population which is determined entirely by genotype

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

heritability = 1

A

the population phenotypic variance is likely due entirely to genotype

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

heritability = 0

A

the population phenotypic variance is likely due entirely to enviroment

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

what does heritability a measure of?

A

correlation between genotype and phenotype

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

what does inheritance tell us?

A

the HOW of a trait

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

what does heritability tell us?

A

how MUCH (genetic predisposition)

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

how is heritability looked at in the final analysis?

A

abstraction of limited value for routine inheritance prediction or understanding specific genetic factors

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

what is the newest way to approach multifactorial inheritance?

A

find the correlation b/t some specific DNA marker sequence found in 2 populations, one with trait one w/o

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

what have single nucleotide polymorphisms done?

A

proven to be helpful to identify genes for a susceptibility to the development of a disease

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

what are empirical risk figures?

A

a gathering of observational studies that might be used to predict the future based on the past

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

what do empirical risk figures give you?

A

only provide data based on similar prior situations, not anything b/t genetic or enviromental

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

what are the common ways to approach multifactorial inheritance?

A

pedigrees, twin studies, heritability, DNA associated studies, empirical risk tables

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

pro/ con pedigree

A

attemping to model the disease- but not good except for finding broad patterns

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

pro/con twin studies

A

difficult to use in practical way

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

pro/con heritability

A

complex mathematical derivation and of limited practical use

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

pro/con DNA associated studies

A

requiring difficult laboratory testing and only susceptibilities

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

pro/con empirical risk table

A

requires large statistical databases and do not explain mechanisms

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

familial risk compared to gen pub?

A

considerably higher

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

familial risk over generations?

A

drops sharply with increasing distance to index case

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

what is the risk of a first degree relative?

A

roughly a square root of the population risk

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

what is higher when more than one family member is affected?

A

recurrent risk

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

what are the two basic ways to look at human multifactorial traits?

A

1)model the disease 2)develop empirical risk figures

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

how do you model the human multifactorial trait?

A

look for a basic pattern of inheritance using a pedigree, then develop rules, as needed, for deviation from simple predictions

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

how do you use the empirical risk figures to look at a human multifactorial trait?

A

rely on PRIOR OBSERVATIONS to est statistical tools of prediction

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

def of adolescent idiopathic scoliosis (AIS)

A

multifactorial condition of spinal curvature laterally >10 degrees

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

how common is AIS

A

1 in 30 in persons 10-16 years of age

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

how does the pedigree of AIS look?

A

autosomal dominant with reduced penetrance

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

what is the penetrance of AIS?

A

~60%

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

how do you find the penetrance of AIS?

A

from one parent, a simple autosomal dominant model would have to have generated a recurrent risk of 50% and yet the statistic is 29% so 0.5x0.6=0.3 so 60% penetrance

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

def of spondylolysis/ spondylolisthesis

A

multifactorial conditions of spinal pars interacticularis and a common source of low back pain

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

spondylolysis=

A

a stress fracture of the pars of the vertebral body

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

spondylolithesis=

A

a slippage of vertebral bodies which may happen due to spondylolsis or degenerative changes with age

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

how common are spondylolysis?

A

~5% of pop

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

how common are spondylolithesis?

A

~2.5%

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

what is the general pedigree look of spondys?

A

autosomal dominant with reduced penetrance

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

what is the penetrance of spondys?

A

~40%

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

def of congental dislocation of the hip?

A

(acetabular dysplasia) multifactorial anomaly characterized by displacement of the femoral head outside of acetabulum prior to birth

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

how common is hip dislocation?

A

1 in 1000 births

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

what model does hip dislocation follow?

A

autosomal dominant with reduced penetrance

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

what is the recurrence risk for sibs in congenital dislocation of the hip?

A

about 5%

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

what is ankylosing spondylitis?

A

multifactorial autoimmune “spondyloarthropathy” condition. Chronic painful progressive inflammatory arthritis primarily affecting spine and si jts

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

what antigen is ankylosing spondylitis correlated to?

A

HLA- B27

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

how common is AS

A

1 in 400

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

neural tube defects (including spina bifida)

A

multifactorial condition characterized as an embryonic failure to fully close the developing neural tube

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

what chomosomes are neural tube defects linked to?

A

17q11 and 6q27

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

how common are neural tube defects?

A

1 in 1000

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

what is the recurrence risk for sibs in neural tube defects?

A

~4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

pyloric stenosis?

A

multifactorial anomaly of substantial narrowing of the stomach pylorus, where there is hypertrophy and hyperplasia of the pylorus

76
Q

incidence of pyloric stenosis?

A

1/400 m>f so SEX INFLUENCED

77
Q

what pattern does pyloric stenosis follow?

A

autosomal dominant with reduced penetrance with some sort of sex influence

78
Q

cleft lip and palate?

A

multifactorial anomalies with a development failure of fusion of the frontal process with the maxillary process during embryonic development

79
Q

incidence of cleft lip/palate?

A

1 in 700

80
Q

pattern does cleft lip/palate follow?

A

autsomal dominant with variable expressivity/ severity

81
Q

club foot?

A

multifactorial collection of congenital anomalies characterized by a foot that is twisted in and down

82
Q

what are the skeletal deformities with club foot?

A

TALIPES EQUINAVARUS, talipes calcaneovalgus, metatarsus varus

83
Q

def of talepes equinavarus?

A

adduction of the forefoot, inversion of the heel and plantar flexion of the forefoot and ankle

84
Q

incidence of club foot

A

3 in 1000

85
Q

pedigree pattern of club foot>

A

autosomal dominant with reduced penetrance

86
Q

pentrance of club foot?

A

40.00%

87
Q

diabetes

A

multifactorial condition of abnormal glucose metabolism/ utilization characterized by hyperglycemia, due to altered insulin secretion from the pancreatic beta cells or receptivity to insulin

88
Q

what types of diabetes are clinically similar to diabetes with hyperglycemia?

A

glucosuria, polyuria, and polydispsia

89
Q

which of the two diabetes has a higher genetic link?

A

type 2

90
Q

what is the sibship risk of diabetes?

A

~40%

91
Q

what is the risk of a child of a parent with type 2 diabetes?

A

33.00%

92
Q

hypertension?

A

multifactorial condition characterized by high systemic arterial blood pressure, which is a physial finding which may have many causes

93
Q

what are the 3 genetic characteristics that all biological populations have?

A

1)a gene pool 2) allelic frequencies 3) genotypic and phenotypic frequencies

94
Q

what is a gene pool?

A

the sum total of all the alleles in the reproductive gametes from members of a mendelian population; the raw material used to build a subsequent generations

95
Q

what is a mendelian population?

A

a group of diploid, sexually interbreeding (or potentially interbreeding) individuals possessing a common gene pool

96
Q

what does gene pool mathematical modeling require?

A

the hardy-weinberg equilibrium

97
Q

what is the hardy-weinberg equilibrium?

A

that a pool be in a special balanced state wherein allelic frequencies remain constant

98
Q

what are the 5 conditions that must be constant to get a H-W equilibrium

A

1) no mutation 2)no migration 3) no assortive mating 4) no selection 5) no genetic drift

99
Q

what is the “A” FREQUENCY?

A

p

100
Q

what is the “a” FREQUENCY?

A

q

101
Q

what does p+q= ?

A

1 (or 100% of the variation of the gene in question)

102
Q

what are the letters for 3 allelic forms?

A

p+q+r= 1

103
Q

what are the letters for 4 allelic forms?

A

p+q+r+s=1

104
Q

what are the letters for homozygous dominants (AA)

A

p^2

105
Q

what are the letters for heterozygotes (Aa)

A

2pq

106
Q

what are the letters for homozygous recessives (aa)

A

q^2

107
Q

in a 2-allelic system, what is the formula for the frequency of genotypes in this population?

A

p^2 + 2pq + q^2 = 1

108
Q

what is the formula for a 3 allelic system?

A

(p+q+r)^2 = 1

109
Q

what is the formula for a 4 allelic system?

A

(p+q+r+s)^2 = 1

110
Q

what are the blood types caused by?

A

glycosphinglolipids produding from the plasma membrane of the RBC

111
Q

what the ABO systema an example of?

A

a multi-allelic gene on chromosome 9

112
Q

what is erythroblastosis fetalis?

A

incompatibility b/t maternal and fetal blood leading to fetal loss

113
Q

what is the major histocompatibility complex?

A

larger cluster of genes on chromosome 6 that determine whether or not transplanted tissues will be rejected

114
Q

what does the major histocompatibiliy complex code for?

A

the production of human leukocyte antigen (HLA)

115
Q

what are the functions of HLA type 1?

A

important on all cells in establishing one’s self

116
Q

what are the functions of HLA type 2?

A

know to be imporant in the presentation of foreign antigens to the immune system

117
Q

def of haplotypes

A

a combination of alleles (for different genes) that are located closely together on the same chromosome and that tend to be inherited together

118
Q

do HLA allelic formations cause disease?

A

particular HLA allelic forms have been correlated with particular diseases

119
Q

what is the risk for anylosing spondylitis with people that have HLA antigen B27?

A

over 90 times greater than the normal population

120
Q

what is an antibody?

A

a protein coded for by a gene, though it is a rather complex example of gene expression

121
Q

what is severe combined immunodeficiency (SCID)

A

a collection of disorders characterized by a loss of immunoglobulin production, both t and b lymphocytes are crippled

122
Q

what is agammaglobulinemia?

A

Heterozygous collection of disorders involving a lack of plasma cells and no immunoglobulin production

123
Q

how do infectous agents gain “access” to the human body/ cells?

A

by having evolved to bind to specific cell surface molecules, coded for by genes

124
Q

can some cancer types run in families?

A

yes

125
Q

what is cancer ultimately a disease of?

A

genes

126
Q

what are proto-oncogenes?

A

promote cell division in many forms

127
Q

what are the forms that proto-oncogenes can promote cell division?

A

1)growth hormone r/c 2) G- protein transducers 3) transcription promoters

128
Q

what are the mutated proto-oncogenes called?

A

oncogenes

129
Q

what do oncogenes do?

A

promote uncontrolled cell division

130
Q

what are most ongenic mutations considered as?

A

dominant (bacause a single copy being inappropriately switched on will create a problem)

131
Q

what is burkitts lymphoma?

A

rare cx of the lymph organs most often due to a TRANSLOCATION b/t chromosomes 8 and 14

132
Q

what is chronic myelogenous leukemia?

A

rare cx, though a common form of leukemia that is due to TRANSLOCATION b/t chromosomes 9 and 22

133
Q

what is the Philedelphia chromosome?

A

translocation of 9 and 22

134
Q

what are tumor suppressor genes?

A

inhibit cell division

135
Q

what are the best described tumor suppressor genes?

A

Rb for retinoblastoma; BRCA1 and p53

136
Q

how common is p53?

A

active in ~50% of all cx

137
Q

what was the gene on the year in 1995?

A

p53

138
Q

where is p53 found?

A

chromosome 17

139
Q

what does the knudson hypothesis state?

A

carcinogenesis requires multiple mutations

140
Q

what is kundsons other model?

A

the two hit model

141
Q

what is the two hit model?

A

a model that may explain many cxs that mainly involve tumor-suppressor genes

142
Q

what needs to happen in the two step model?

A

1)both copies of a tumor-suppressor need to be mutated (sporadic cx) 2) if only one mutant gene is inherited, then it would only take a single hit to lose tumor-suppression (familial cx)

143
Q

what makes the cx cell exceed the normal number of mitotic cycles?

A

activation of the gene for telomerase seems to make this possible

144
Q

what is the function of telomerase?

A

enzyme lengthens the chromosomal telomeres

145
Q

how are most cxs classified as? Classically inherited or not?

A

most are not classically inherited (sporatic) but some can be considered classic

146
Q

what type (sporatic or classic) are most breast and colon cxs?

A

most are sporatic (hereditary makes up 5%)

147
Q

a person with BRCA1 or 2 have what risk of getting breast cx?

A

~60-80% risk

148
Q

carcinogenesis requires what?

A

multiple damages to cell cycle controlling genes

149
Q

what ways can oncogenes cause cx?

A

1)direct mutation 2) virus promotion (15%) 3) chromosome rearragement

150
Q

what ways can switching off tumor-suppressor gene cause cx?

A

direct mutation

151
Q

why is cx a multifactorial condition?

A

because there are genes and enviromental agents involved as well as cx is a collection of diseases, there is no simple risk assessment for all forms

152
Q

how many base pairs does mitochondria have?

A

~17000 base pairs which codes for 40 genes

153
Q

what makes the mitochondria cx predictions so difficult?

A

reproduction of mitochondria is unpredicable and there can be hundreds of them in a given cell (all with different mutations)

154
Q

what gamete passes on the mitochondria?

A

ONLY the mitochondria of the OOCYTE are thought to be transferred to the next generation

155
Q

what diseases have been confirmed to be mitochondrial in origin?

A

1) leber’s Optic Neuropathy 2)kearns-sayre 3)Leighs syndrome 4) myoclonic epilepsy with ragged red fibers 5)NARP

156
Q

what is Lebers hereditary optic neuropathy?

A

mitochondrial disorder characterized by mid-life onset of acute or subacute, painless, CENTRAL vision loss

157
Q

what is Kearns-Sayre Syndrome?

A

Mitochondrial disorder characterized by opthalmoplegia, retinal pigment degeneration, and cardiomyopathy

158
Q

what is leighs syndrome?

A

mitochondrial disorder, with early onset of neuropathy consisting of focal, bilateral lesions in one or more areas of the CNS

159
Q

*myoclonic epilepsy with ragged red fibers?

A

*Mitochondrial disorder, with multisystem weakness, and myoclonus as first symptom, then epilepsy, then weakness and dementia

160
Q

what is NARP?

A

Neurogenic weakness, Ataxia, and Retinitis Pigmentosa; mitochondrial disorder, with variable combination of developemental delay,

161
Q

how did scientists trace back to a “kind of eve” or a mother to all living people?

A

with looking at mitochondrial DNA and how it mutates in a sort of molecular clock

162
Q

is there diversity in the ability of a person to process or metabolize nutrients?

A

yes

163
Q

is there evidence that nutrients can alter gene expression?

A

yes

164
Q

can nutrients take away functions that genes would otherwise have to do?

A

yes nutrition can affect other metabolic pathways

165
Q

do nutrients represent nature or nurture?

A

nurture

166
Q

what is genetic counseling?

A

process by which patients at risk for a genetic disease are advised of the nature, risk and consquences of having or producing an affected child/relative

167
Q

what does genetic counseling involve?

A

a collaborated effort b/t health professionals

168
Q

how does almost all of the genetic counsiling start?

A

with a pedigree

169
Q

what is duputytrens contracture?

A

a Fascia closure of the hand that is not always evident until mid-life.

170
Q

how is deuputytrens contracture passed?

A

autosomal dominant

171
Q

what is Cystic Fibrosis?

A

a metabolic failure of chloride ion transport across membranes

172
Q

how is cystic fibrosis passed?

A

autsomal recessive

173
Q

what is congenital dislocation of the hip syndrome?

A

relatively benign skeletal anomaly

174
Q

hos is Congenital dislocation of the hip passed?

A

multifactorial

175
Q

what is the most common quesiton in genetic counseling scenarios?

A

what is the chance that we might have another affected child? (recurrent risk)

176
Q

what is the recurrent risk for an autosomal recessive disorder?

A

25.00%

177
Q

what is the recurrent risk for an autosomal dominanit disorder?

A

50.00%

178
Q

what is the recurrent risk for a rare, sex linked recessive?

A

25% overall (50% for male 0% female)

179
Q

what is the recurrent risk for trisomies of autosomes?

A

slight increase over the normal population of the same age

180
Q

what is the recurrent risk for a multifactorial inheritance?

A

usually less than 10% but often requires use of an empirical risk table

181
Q

what are the two bolded questions that we need to know for genetic counseling for information?

A

1) what is the exact diagnosis 2) what aare the known facts and results of an examination of a family history

182
Q

what is considered convential practice when it comes to genetic counseling?

A

refer

183
Q

what are the red flags that should prompt a consideration of a genetic causality?

A

Family GENES

184
Q

what does F GENES stand for?

A

Family history; Groups of congenital abnormalities; Extreme/ exceptional presentation, Neurodevelopemental delay, Extreme or exceptional pathology, Surprising lab values

185
Q

what is the leading indication for prenatal diagnosis?

A

late maternal age

186
Q

what are the other reasons for prenatal diagnosis and counseling?

A

1)prior child with it 2) prior history of miscarriage 3) known chromosomal defects in one of the parents 4) Family history 5)specific ethnic high-risk

187
Q

what are some of the therapies that might be able to help get rid of many genetic dzs in the womb?

A

blocking or enhancing cellular function at transcription, translation or post-translation

Human Genetics (2 decks)

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