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embryo/fetal development Flashcards

1
Q

True/False: The leading cause of infant mortality in the US is birth defects - this is due to a higher prevalence of birth defects in the US mainly because of overexposure to chemicals.

A

False. The main reason birth defects has become the number one cause is because improved obstetrical care has reduced other causes/complications.
*however: the increase of medications/drug use/environmental toxins could also play a role.

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2
Q

How might the maternal physiological state cause teratogenesis? (5)

A
  • illness (infection, metabolic disorder, malabsorption)
  • deficiencies
  • drugs/chemical intake (drugs, alcohol, environmental toxins)
  • genetics (susceptibility to toxins, genetic makeup)
  • radiation exposure
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3
Q

An anomaly present at birth is a ____ anomaly.

A

Congenital

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4
Q

What is the leading cause of newborn/infant mortality in the US?

A

Birth Defects

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5
Q

Define “teratogenesis”

A

Production of birth defects/malformations - can be internal or external, or microscopic

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6
Q

List the causes of teratogenesis. (7)

A
  • Genetic
  • Chromosomal aberrations
  • Metabolic
  • Radiation
  • Infection
  • Drugs/Chemicals
  • Unknown???
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7
Q

The prevalence of birth defects per live births is about ___%

A

2-3%

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8
Q

True/False: The incidence of mortality due to birth defects increases for the 2 yr old age group in comparison to newborns. Why?

A

True; some defects may be symptomless at birth and may be discovered or manifest later.

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9
Q

Of the known causes of defects in humans, the largest percentage is due to ____ and _____.

A

Genetics and chromosomal aberrations

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10
Q

Defects in the ____ make up the largest proportion of causes of death due to birth defects in US infants.

A

Heart

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11
Q

True/False: the leading cause of developmental defects is due to drugs/chemicals.

A

False; 65-70% of defects have UNKNOWN causes.

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12
Q

True/False: less than 50% of fertilized eggs will result in a healthy infant

A

True

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13
Q

define “post-implantation loss”

A

A fertilized egg is shed due to the uterus lining being unprepared for pregnancy.

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14
Q

When is the fetus at its most vulnerable point?

A

Organogenic period 3-8 weeks

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15
Q

True/False: some birth defects may not manifest until adulthood.

A

True.

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16
Q

Most pregnancy failures are due to ______.

A

Post implantation losses (31%)

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17
Q

Why is the organogenic period so critical?

A

It is the period of maximum cell division and differentiation.

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18
Q

What does the organogenesis stage include?

A

Conception (zygote forming)
Implantation
Ovum dividing/differentiating

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19
Q

Why might folate supplementation be suggested for women who are trying to become pregnant?

A

The neural tube closes within 28 days, before the woman may even know she is pregnant. Folate is essential to ensure proper neural tube development, so she should ensure her levels are adequate.

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20
Q

True/False: the Neural Tube should close in the late first trimester.

A

False. The neural tube should close in the early first trimester, by 28 days.

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21
Q

True/False: Adequate folate is extremely important as soon as a woman knows she is pregnant.

A

False; adequate folate levels are especially important for any woman capable of becoming pregnant. But folate is also important for any other individual.

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22
Q

List the stages of development from fertilization to fetus:

A

zygote, morula, blastocyst, embryo, fetus

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23
Q

List the stages of cell growth during pregnancy.

A

Hyperplasia
Hyperplasia + Hypertrophy
Hypertrophy

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24
Q

How might the effects of deficiencies during the hyperplasia stage vs the hypertrophic stage differ?

A

Hyperplasia is max period of cell division; if impacted, causes a permanent reduction in cell number.
Hypertrophy is the period of cell size increase and differentiation; if affected, there is risk of biochemical or organ malfunction.

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25
True/False: Hyperplasia describes an increase in cell size, while hypertrophy is an increase in cell number.
False. Hyperplasia is the increase in cell number (division) while hypertrophy is an increase in cell size.
26
True/False: exposure to toxicants during the zygote/blastocyst phase (<1 week) has extremely severe consequences.
False. Cells are still in hyperplasia, and are pleuripotent (large restorative capacity). The blastocyst is not yet implanted, so there is less exposure to toxins. So: there is low susceptibility/incidence of abnormalities (either causes lethality or no effect)
27
Cavity formed in the center of the developing zygote:
Blastocele
28
In what period of growth during pregnancy does the cell number increase at a maximum rate, but not the cell size?
Hyperplasia
29
What are the 3 germ layers formed during gastrulation?
Ectoderm Mesoderm Endoderm
30
The developing embryo is more at risk of teratogenic effects at 8 days or 16 days after fertilization?
16 days; during gastrulation period (cell differentiation)
31
Before the placenta forms, how does the early blastocyst derive its nutrients? What is this stage called?
Phagocytosis; histiotrophic nutritional phase
32
What systems form from the mesoderm?
cardiovascular, muscles, excretory
33
What step does gastrulation begin with?
Invagination in the future cranial area, forms HENSON'S NODE -> form primitive streak
34
Why is the organogenic period so susceptible to teratogenic effects?
It is the period of cell proliferation/migration/interactions, tissue remodelling. Key organs/structures are being established.
35
What are the cell types in a blastocyst, and what are their purposes?
embryoblast: pleuripotent cells on the inside, forms the embryo trophoblast: will secrete proteolytic enzymes to erode lining of uterus for implantation, and will form the endometrium to start forming placenta
36
Which of the germ layers goes on to form the nervous system? What is this process known as?
Ectoderm (forms brain, CNS) | neurulation
37
What systems form from the endoderm?
respiratory, digestive, glandular
38
Why is it essential for the closing of the neural tube by day 27?
If it does not close, the precursor cells are exposed to amniotic fluid and will be damaged, leading to serious defects in the CNS.
39
What happens during neurulation?
1. The ectoderm differentiates into the NEURAL PLATE 2. The edges rise, to form the NEURAL GROOVE 3. The NEURAL CREST CELLS fold in and fuse, and segregate to form the NEURAL TUBE (precursor of CNS), and also the future face/skull
40
What differentiates a fetus from an embryo?
Placenta is developed | All essential internal/external structures are developed
41
True/False: the stage at which the fetus is exposed to teratogens will affect what organs systems are impacted
True; different organs systems develop at varying times. Each has their own critical period of growth.
42
Exposure to toxins after the 8th week will cause abnormalities in ____ and _____ rather than morphological defects. Why?
``` growth function Organs are mostly finished differentiating (except genitalia), but still require growth and maturation. ```
43
What is the teratogen most associated with fetal abnormalities? What does it cause?
Alcohol | Fetal Alcohol Syndrome
44
What are the classes of teratogens?
``` Medications Drugs Environmental toxins High temperature Infectious disease Chronic disease Nutrient excess/deficiency ```
45
The characteristic defects associated with a particular agent are classified as a _____.
syndrome
46
True/False: hot tubs can potentially be teratogenic
True. prolonged raising of the body core temp can have teratogenic effects.
47
Pesticides and alcohol fall under the ____ and ____ classes of teratogens
environmental toxins | drugs
48
True/False: The placenta acts as a barrier and will protect the fetus from most medications.
False. Most medications are able to cross the placenta.
49
True/False: Extra vitamin A supplementation is recommended for pregnant women, to ensure proper development of the eyes and brain in the fetus.
False. Excess vitamin A will cause defects in the CNS!
50
What are the causes of nutrient excesses/deficiencies?
Diet or drug induced
51
What is the cause of cretinism? What are its symptoms?
Iodine deficiency | Potbelly, facial abnormalities, mental/physical retardation
52
What nutrient is essential for the closing of the neural tube?
Folate
53
What nutrient excesses are of particular concern?
Vit A, Vit D, Iodine, Fluorides
54
A deficiency in vitamin ___ causes eye abnormalities and microcephaly
A
55
What are the effects of excess vit A on the fetus?
CNS abnormalities
56
Besides, folate, a period of deficiency in ____ can also lead to neural tube defects.
Zinc
57
What is microcephaly? What deficiencies might cause microcephaly?
Microcephaly = small head | Severe protein deficiency, or vit A deficiency
58
What nutrient deficiencies are of particular concern?
Protein Vit A, Vit D, Vit E, Vit K, Folate Iodine, K, Cu, Zn
59
What are the effects of excess vit D on the fetus?
Facial abnormalities | Mental retardation
60
What are the effects of excess iodine on the fetus?
Congenital goitre | Mental and physical retardation
61
What is coumadin syndrome caused by?
Vitamin K deficiency | consumption of anticoagulants during pregnancy
62
True/False: Excess vitamin A intake from food has a higher risk of causing birth defects than excess intake from supplements.
False. Excess intake from supplements has higher incidence rate.
63
What is the effect of excess Fluorides on the fetus?
Spina Bifida Occulta
64
Fetal rickets is characterized by: ____, _____, and _____. Why?
tooth enamel hypoplasia, decreased bone density, growth failure. This is caused by vitamin D deficiency, which would impair absorption of Calcium
65
What could cause a Cu deficiency in the mother? What outcomes in the infant could this cause?
severe deficiency in diet, metabolic disorder (Menkes kinky hair), or Cu chelating drugs Abnormalities in blood vessels, bones, brain
66
Would a mild-moderate protein deficiency result in microcephaly in the infant? Why or why not?
No, microcephaly is caused by severe protein deficiency. In less severe cases, the fetus can draw from maternal stores.
67
The use of what drug in particular is known to decrease vit E stores?
Smoking (nicotine)
68
The deficiency of vitamin D can cause _____.
Fetal rickets
69
When is the fetal brain most sensitive to the effects of alcohol?
3rd trimester, and the weeks following birth
70
True/False: the body can mobilize Zinc to the infant, so in the case of deficiency in the diet, the fetus will draw on maternal stores.
False; zinc is not well mobilized. Short periods of deficiency can cause NTD.
71
The deficiency of vitamin ____ causes nonspecific birth defects/abnormalities.
E
72
A deficiency in potassium can cause _____.
kidney abnormalities
73
The Alcohol Related Birth Defects include:
Microcephaly Heart/lung malformations Minor physical abnormalities
74
What are the differences between "small for gestational age" vs "premature?"
Small for gest. age: less than expected size/weight for development time (retarded growth) Premature: appropriate age-for-size but born early
75
True/False: regardless of dose, any alcohol will have the same damaging effects on the developing fetus.
False: dose-response effect. Greater consumption = greater risk of abnormalities/damage
76
What are some key characteristics of FAS?
Facial abnormalities (long face, short upper lip, underdeveloped jaw) motor and mental retardation low fat stores growth retardation (small head, low weight/height percentile)
77
What metabolic factors make a dose of alcohol more harmful to the fetus than the mother?
1. Freely crosses the placenta 2. Developing CNS and brain much more susceptible than adult tissue 3. detoxification mechanisms not fully developed in fetus 4. Fetus is smaller body weight, recieves much higher dose per weight
78
What are the toxic effects of alcohol? (list 6)
1. displaces other nutrients 2. interferes with metabolism/absorption of nutrients/minerals (Folate, Zn, K) 3. metabolism produces more toxic byproducts 4. Inflammation (free radicals, causes damage) 5. Placental toxicity (damage placenta) 6. cell death
79
How might the metabolism of alcohol make it more dangerous? | How does the body deal with this?
Alcohol is initially broken down to ACETALDEHYDE, which is more toxic. aldehyde dehydrogenase is needed to convert this to acetic acid.
80
What enzyme breaks down alcohol?
Alcohol dehydrogenase
81
What are the most severe forms of NTDs? Define them.
Anencephaly - no skull | Exencephaly - brain protrudes from skull
82
True/False: genetics play a role in NTDs
True. about 12% cases have identifiable cause, and mothers with previous instances of NTDs are more at risk for another NTD pregnancy
83
In addition to deficiencies, NTDs can also be cause by?
Genetics (chromosomal aberrations, genetic mutations) Raised core temperature during early pregnancy Maternal obesity Maternal type II diabetes Abnormalities in folate metabolism
84
What study was key in proving the essential role of folate in preventing NTDs?
the MRC vitamin study
85
If the spine does not close properly and the cord protrudes, this is known as ____ ____. What can this cause?
Spina Bifida | Can cause paralysis, impaired motor control, impaired bladder/bowel control, fatality
86
What did the MRC study show?
Folate supplementation is effective in preventing NTDs, while only a multivitamin supplement did not have such benefits
87
What converts SAM to SAH? How?
Methyltransferase | translocates a methyl group from SAM to a substrate
88
What vitamin is needed for conversion of homocysteine to cysteine?
B6
89
Vitamin B12 and Folate are needed for the _____ pathway.
Homocysteine/methionine
90
What is the homocysteine cycle used to produce?
Cysteine
91
What converts homocysteine to methionine?
Methionine synthase catalyzes the transfer to create methionine.
92
What is the role of 5-methyl-TH4-folate in the homocysteine cycle?
Contributes the methyl group to homocysteine.
93
What is required to regenerate methionine synthase?
B12 (cobalamin)
94
If there are high levels of homocysteine, then ___ levels (precursor) will increase. Why?
SAH | due to equilibrium dynamics; reaction forward will not proceed
95
DNA expression can be regulated through _____.
methylation
96
What enzyme regenerates the methyl donor for the conversion of homocysteine to methionine?
5-Methylene TH4-Folate reductase
97
What are the teratogenic effects of high homocysteine? (2)
- buildup of SAH -> decreased methylation | - oxidative stress
98
True/False: high homocysteine levels and SAH buildup will lead to DNA hypermethylation.
False. It will inhibit methylation (hypomethylation).
99
True/False: homocysteine levels are usually expected to rise slightly during pregnancy due to increased synthesis rates in the body.
False. Homocysteine levels should decrease 30-60% due to hemodilution.
100
oxidative stress caused by high homocysteine will lower enzyme activity of ____ ____, and limit availability of vitamin ___.
methionine synthase, B12
101
True/False: Folate supplementation can lower homocysteine levels
True
102
High homocysteine can lead to a potentially fatal condition known as:
pre-eclampsia (dangerously high BP)
103
Families with history of NTDs may have a shortage in the _____ enzyme.
Methyl TH4-folate reductase
104
Why is folate supplementation considered more important than B12 or B6 supplementation, when all are vital for the homocysteine cycle?
folate is low in food and poorly absorbed. Deficiencies in B12 and B6 are rare.
105
True/False: high homocysteine can cause miscarriages, spontaneous abortions, and newborn obesity.
False; higher homocysteine correlated with lower birth weight.
106
Is the monoglutamate or polyglutamate form of folate better absorbed? What are the sources of each?
Monoglutamate | mono is from supplements, poly is from food.
107
Why might natural sources (food) not be sufficient? (3)
Variability in sources Absorption is less, also variable Losses from cooking

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