Development and Teratogenesis Flashcards

1
Q

Teratogens

A

Come from the outside

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2
Q

4 classes of teratogens and examples

A
Maternal illness (PKU, diabetes)
INfectious agents (TORCH) 
Physical agents (radiation or heat exposure)
Drugs (thalidomide, antiepileptic drugs)
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3
Q

Response ot teratogens

A

Highly individual and could have to do with a lot of different things such as route, timing, dose

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4
Q

All or nothing theory

A

In enough cells die, spontaneous abortion

If only a few cells die, others can compensate

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5
Q

Significant exposure to teratogens during days ________ post-conception may result in cell death

A

10-14

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6
Q

Day 27

A

Closure of neural tube

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7
Q

Day 30

A

Appearance of limb buds

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8
Q

Weeks 4 and 5

A

Branchial arches, clefts, piuches, and optic vesicle

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9
Q

Week 5 to 7

A

HEart and kidneys

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10
Q

Week 8

A

Mature limb architecture

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11
Q

Weeks 7 to 10

A

Internal and external genitalia

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12
Q

Week 10

A

Rotation into abdominal cavity

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13
Q

Teratogenesis occurs _______

A

After fertilization

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14
Q

Toxic mutagenesis

A

Exposure prior to conception causing mutations

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15
Q

Toxic mutagenesis females vs. males

A

Females - DNA replication occurs during oogenesis years before ovulation
Males - continous spermatogensis makes males more susceptible

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16
Q

Infectious agents mechanisms

A

Usually direct invasion of fetal tissues…lead to inflammation and cell death

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17
Q

Infectious teratogenic agents

A

TORCH, varicella, and parvovirus B19

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18
Q

TORCH infection

A

Toxoplasmosis, rubella, cytomegalovirus, herpes, and syphilis

19
Q

Maternal illnesses mech

A

Diffusion of teratogenic metabolite or antibody across the placenta

20
Q

Insulin-dependent diabetes mellitus birth defect

A

2-3 fold increase…hyperglycema can cause diabetic embryopathy resulting in major birth defects and spon abortions…glucose acts as teratogen

21
Q

PKU (in short)

A

Inability ot make tyrosin from Phe…microceph, intellectual, cong heart disease

Causes phenylalanine embryopathy

Treat using low Phe diet

22
Q

Androgen-producing tumors effect

A

In adrenals or ovaries…can lead to viriliation of female fetuses

23
Q

MG can lead to

A

Transient neonatal myasthenia

24
Q

Maternal illness antibody diseases

A

Transient neonatal myasthenia and systemic lupus erythematosus

25
Maternal antibodies can
Cross placenta into the fetus
26
Systemic lupus erythematosus can lead to
Fetal heart block
27
Elevation in maternal core temperature can lead to
Neural tube defects
28
ACE inhibitors can cause
Miscarriage Oligohydramnios Renal failure Hypotension
29
Antiepileptics can cause
Cardiovascular Orofacial clefts Neural tube malformations GU defects
30
Teratogenic meds
``` Thalidomide Retinoic Acid Statins ACE inhibitors Antiepileptics ```
31
FASD includes
FAS, pFAS, Neurobehavrioal disorder with prenatal alcohol exposure (ND-PAE)
32
Alcohol can affect
CNS abnormalities, growth retardation, facial dysmorphism and abnormalities
33
First trimester alcohol
Facial anomalies/structural anomalies/including brain size
34
Second trimester alcohol
Increased spontaneous abortion
35
Third trimester - alcohol
Predominantly effects weight, length, and brain growth
36
How are FAS and pFAS different than ND-PAE
No facial dysmorphology or growth retardation
37
Clinical features at birth - alcohol
Facial dysmorphism
38
Facial dysmorphism of FAS
Short palpebral fissure Thin vermillion border Smooth philtrum
39
Structural CNS impairment - alcohol
Decreased head size
40
Neurologic CNS impairment - alcohol
Hard - reflexes, tone, cranial nerve defects | Soft - poor coordination or balance
41
FAS diagnosis
3 facial dysmorphology, growth retardation AND CNS involvement...does NOT require prenatal alc exposure confirmation
42
pFAS diagnosis
Confirmation of alc exposure...2/3 facial dysmorphologies, growth retardation, OR CNS involvement
43
NDPAE diagnosis
Requires confirmation | Imapaired cog function, self-regulation, and adaptive function