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Nutrition through life > Embryo > Flashcards

Embryo Flashcards

1
Q

what is teratogenesis

A

Production of birth defects Malformations: non-reversible morphological defects present at birth Could be exterior or internally located or only microscopically visible Congenital anomalies = present at birth. >200 different congenital anomalies

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2
Q

What is the prevalence of birth defects

A

2-3%

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3
Q

What is the leading cause if infant mortality and why

A

1/4 of deaths up to the age of 15 is due to birth defects due to structural and functional defects in vital organs and for the same reason 1/3 of children younger than 1 year Because: -Improvements in obstetrical (during and after delivery) care -↑ Medications and social drug use - Environmental contaminants?

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4
Q

Can you observe birth defects at birth?

A

No sometimes they do not show themselves until later ( like heart defects)

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5
Q

what are the causes of developemental defects

A

20-25% of the causes of birth defects due to known genetic causes and chromosomal aberrations. -Maternal illnesses (infections, metabolic disturbances) Drugs & chemicals

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6
Q

Is susceptibility is influenced by some factor

A

Susceptibility to teratogenesis heavily influenced by genetics of mother and infant.

Nutritional deficiencies play a significant role + genetic susceptibilities.

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7
Q

How many pregnancies end up with healthy outspring

A

15%

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8
Q

For optimal pregnancy outcome what parameters you should have

A
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9
Q

Low birth weight can predict

A

Can be a prognostic of cognitive development , can prognose obesity, lung problems, cardiac problems, diabetes

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10
Q

What is the largest contributor to unsuccessful pregnancy

A

post implantation losses

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11
Q

what is the most vulnerable time of fetal development

A

Conception (formation of zygote) -: Implantation ->Ovum divide & differentiate= organogenesis (3-8 weeks of pregnancy)

Organogenic period = teratogenic period (max. vulnerability for fetus is 17 – 57 days post-fertilization)

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12
Q

why women need to take adequate folate at all times and how neural tube is connected to it

A

Neural tube closes within 28 days of gestation, where most women do not know they are pregnant => adequate nutrition (folate) is essential for women capable of becoming pregnant

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13
Q

Why organogenic period is the most critical period of life

A
  • Cell organization, cell differentiation, and organogenesis all take place
  • Maximal cell division and differentiation
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14
Q

what is hyperplasia and when does it occur

A
  • ↑ cell number
  • Time of maximum vulnerability for teratogenic effects
  • Day 17 to 8 wks after fertilization
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15
Q

what will happen if some factors interfere with the process of hyperplasia

A

Permanent reduction in cell number

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16
Q

hypertrophy and hyperplasia during pregnancy will lead to

A

Increase in cell size + cellular division

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17
Q

After hyperplasia ceases what period begins

A

Hypertrophy

  • Risk for development of organ or biochemical malfunctions
  • ~ after 8 wks gestation
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18
Q

What is happening after ovulation until the blastocyte

A

Ovulation: ovum expelled by ovary into Fallopian tubes à ovulation and menstrual cycle must be normal.

Fertilization: sperm penetrated oocyte -> zygote.

Blastogenesis: zygote beings to cleave -> increase in cell number à morula.

-Cavity forms in center: blastocele. The entire structure is now called a blastocyst. (4th day)

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19
Q

2 cell types in blastocyst

A

-Blastocyst: 2 cell types: embryoblast (inside) and trophoblast (outside)

Trophoblast cells secrete proteolytic enzymes -> erode epithelial uterine lining.

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20
Q

How nutrients aand fluid are absorbed at this stage?

A

Fluid and nutrients absorbed by phagocytosis = histiotrophic nutritional phase (20-25 days).

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21
Q

What will rise from embryoblast and trophoblast

A

Trophoblast forms a cord of cells -> endometrium -> start forming the placenta

Embryoblast-> cells for the fetus

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22
Q

When entry to uterine occurs of blastocyst

A

4-5 days

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23
Q

What is pre-implantation period, when and what is happening

A

Pre-Implantation (Zygote, Blastocyst)

  • < 1 week
  • Increase in cell number but no increase in cell size
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24
Q

Is there any consequences if there are any toxicants are in mother’s body

A
  • Exposure to toxicants: no effect, slight decrease in growth or lethality
  • Fate of cells not determined -> great restorative capacity
  • Low susceptibility to teratogens and few developmental abnormalities

Pleuropotency of cells à exposure to toxic conditions causes either lethality or no effect

Also: decreased exposure to toxins due to poorer accessibility of the conceptus.

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25
Q

What period is 16 days post-ovulation and how does it occur

A

gastrulation - embryo development.

Day 14: inner cell mass starts to differentiate into different cell types.

Starts with the formartion of invagination (Henson’s node) in the future cranial area of the ectoderm -> moves caudally -> primitive streak (important role in nervous system).

starts at the head region

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26
Q

What is happening at 2-3 weeks of gestation

A

Gastrulation (2 – 3 Weeks)

  1. Primitive streak = future axis of the embryo => 3 layers of the embryo
  2. Then, neurulation: ectoderm differentiates into neural plate à neural tube
  3. Mesoderm & endoderm cells migrate internally to form organs and tissues

•Cell migration through primitive streak

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27
Q

What 3 layers are fomed furing gastrulation (2-3 weeks)

A
  • Ectoderm (Brain, CNS, Skin)
  • Mesoderm (Voluntary muscles, CV and excretory systems)
  • Endoderm (Digestive and respiratory systems, glandular organs)
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28
Q

Is fetus ssuspeptible to toxicants at 2-3 weeks

A

Yes, because rapidly developing

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29
Q

Neural plate rise, forming edges, this will contribute to->

Lateral edges will form

A

Neural groove

Lateral edges: neural crest cells, precursors of CNS and contribute to face & skull.

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30
Q

What happens 27-29 days post-ovulation

A
  • General shape of embryo established, heart starts beating
  • Embryo < 1 inch and < 1oz
  • Neural folds fused -> neural tube has segregated into head region + postcranial region

If neural tube not closed by day 27-> spinal bifida

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31
Q

What happens at 3-8 weeks and is it susceptible to teratogenesis

A

Organogenesis (3 – 8 Weeks)

  • Organs and body structures established
  • Cell proliferation, cell migration, cell-cell interactions and tissue re-modeling
  • Extremely susceptible to teratogenesis
  • Periods of maximum susceptibility for each forming structure
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32
Q

At 8 th week the embryo becomes

A

fetus

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33
Q

at 8th week what is formed and who supplies nutrients

A
  • All essential external and internal structures are present.
  • Placenta has developed and accounts for most nutrient needs.
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34
Q

How vitamin A plays a role in organogenesis

A

It plays a major role in remodeling and apoptosis ( finger developement)

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35
Q

When overall size and metabolism of the fetus will be most affected

A

last trimester

very susceptible to alcohol and food

36
Q

what is the name of th eperiod form 8 weeks to birth and what abnormalities can happen

A

Fetal/Neonatal (8 Weeks to Birth)

>8 weeks = fetal growth period. Little differentiation of organs takes place except external genitalia.

  • Functional and growth abnormalities can occur rather than morphological defects.
37
Q

explain the diagram

A
  • Dark shading: greatest susceptibility to a morphological defect
  • Light shading: physiological or functional defect
  • Each organ/tissue has its own critical period of growth à spectrum of defects dependent on timing of teratogenic influence
38
Q

3 classes of teratogens

A
  • Medications
  • social drugs
  • environmental agents
39
Q

what medications are teratogens

A

•Seizure medications, Accutane (Vitamin A derivative that is stored in fat, used for cystic acne, but need to stop for several month before conceiving to prevent defects), Thalidomide, Lithium, Chemotherapy drugs (limit cell division)

40
Q

What are social drug of teratogens

A

If there is high cannabis exposure during pregnancy and it can have impact on kidneys and liver, potential cognitive development, avoid any drugs and medications during pregnancy, alcohol no safe level of exposure

Alcohol - the most frequent cause of deffects

cocaine, cigarettes

41
Q

What are environment teratogens

A

•Organic solvents, heavy metals, pesticides,

PCBs : Potential problems in cognitive even in adults, most exposure in the north regions

42
Q

Dilantin will cause

A

Fetal hydantoin syndrome

10%

43
Q

What defects will thalidomide cause

A

Limb and ear abnormalities

20%

44
Q

Antoneoplastic drugs will cause what during pregnancy

A

Congential abnormalities )17% risk

45
Q

diethylstill bestrol will cause what

A

uterine and cervical defects

22-53% risk of defect

46
Q

dextromethorphan will cause what in fetus

A

CNS abnormalities

47
Q

What is best to do with drug intake during pregnancy

A

Best: no drug exposure even for drugs with no known teratogenic history; large population studies needed to detect very low incidences

48
Q

Can drugs cross placenta and what factors influence that

A
  • Almost all medications cross the placenta.
  • Factors:
  • Type of medication
  • Time of exposure
  • Length of time of exposure
49
Q

what are other types of teratogens (not drugs and environment toxins)

A
  • High temperature or fever (hot tubs, jacuzzis)
  • Infectious diseases

Rubella, cytomegalovirus, toxoplasmosis

•Chronic diseases

Diabetes, severe overweight

•Nutrient deficiencies and excesses

50
Q

What will happen with iodine, F, vitamin D and vitamin A excess intake

A
51
Q

What is the correlation between excess vitaminA and birth defects

A
  • >10,000 IU vitamin A => x4.8 higher risk of NTD
  • Increased risk closely associated with timing of intake during pregnancy
  • 1.4% of women consume >10,000 IU; 1/57 babies with birth defects are attributable to excessive vitamin A
52
Q

Effects on pro, vitamin A, vitamin D,E,K deficiencies

A

Extreme protein deficiency -> microcephaly

Vitamin D deficiency -> hypoplasia of tooth enamel, decreased bone density, growth failure (Vitamin D is an essential hormone for calcium gut absorption)

Smoking à decrease body vitamin E stores -> nonspecific birth defects and spontaneous abortions

Vitamin K deficiency -> Coumadin syndrome (anticoagulants, e.g. dicumarol)

53
Q

results of folate,iodine, potassium, copper and zinc deficiencies

A

Folate deficiency: caused by poor diet, maternal drug intake as well as a genetic susceptibility to abnormalities in folate metabolism

Cretinism: syndrome of mental and physical retardation – potbelly, large tongue, facial characteristics of Down’s syndrome

Genetic inborn errors of Cu metabolism (Menkes kinky hair syndrome) à major developmental abnormalities in brain, bones and blood vessels.

Animal studies: short periods of Zn deficiency can cause NTD (cannot mobilize Zn to meet embryonic needs).

Acrodermatitis enteropathica = inability to absorb Zn; rashes, hair loss, diarrhea and poor growth. Increased risk of birth defects and pregnancy complications

54
Q

name folate antagonist (drug-induced deficiencies)

A
  • Folate antagonists (methotrexate)
  • 30% risk of NTD
55
Q

vitamin K drug deficiency

A
  • Vitamin K antagonists (Coumadin-Warfarin)
  • 7% risk of congenital heart disease
  • Coumadin syndrome (low birth weight, slower growth, mental retardation, deafness, small head size, and malformed bones, cartilage, and joints)
56
Q

anticonvulsant can cause what nutrient deficiencies

A

folate and Zn

57
Q

-Leading cause of birth defects & intellectual handicap in North America is

A

Fetal alcohol syndrome

58
Q

characteristics of FAS

A
  • Craniofacial dimorphism
  • Growth retardation
  • Head circumference, weight, height < 10th percentile
  • Decreased fat stores
  • Retarded psychomotor and intellectual development

-Neurological abnormalities, developmental delay, behavioral dysfunction/deficit, intellectual impairment and/or structural abnormalities (microcephaly or brain malformation)

59
Q

Fetal brain is the most susceptible in what semester

A

3rd

60
Q

Facial abnormalities in FAS

A
  • Short palpebral (re: eyelids) fissures,
  • Elongated mid-face,
  • Thin upper lip
  • Retrognathia; receding jaw
61
Q

Dose of alcohol and relationship of the outcome

A
  • 1 oz. absolute alcohol consumed in late pregnancy Þ 160 g decrease in birth weight
  • High risk – 3 oz. alcohol/day or 4 drinks/day
  • Increased risk with binge drinking
62
Q

Is there a level of alcohol that is not toxic?

A

Not known

63
Q

how many children will born with FAS if mother is an alcoholic

A

30-50%

64
Q

Diagnosis of FAS require

A

the diagnosis of FAS requires (a) confirmed maternal exposure, (b) the presence of a characteristic pattern of facial anomalies, (c) growth retardation, and (d) central nervous system neurodevelopmental abnormalities

65
Q

Apart from FAS what other effects alcohol might have in to the fetus

A
  1. Alcohol related birth defects (ABRD)
  • Microcephaly
  • Heart and lung malformations
  • Minor physical abnormalities
  1. CNS disturbances

•Decreased attention span, decreased I.Q., hyperactivity

66
Q

Why alcohol has such a dramatic impact on the fetus

A
  • ~ 95% of alcohol is metabolized by alcohol dehydrogenase
  • Alcohol crosses placenta freely
  • Mother may not experience alcohol-related symptoms while embryo/fetus may be affected adversely
  • ½ life of alcohol is increased in embryo/fetus
  • Detoxification and clearance less developed in embryo/fetus
  • After absorption, alcohol is evenly distributed to all body fluids, crosses blood-brain and placental barriers until equilibrium with mother’s blood.
  • Fetus and embryo developing CNS more susceptible to alcohol related effects than adult brain
    1. Free radicals as the side effect of alcohol, but fetus have poor antioxidant system-> leading to more problems in fetus than in the mother
67
Q

Per drink how much more alcohol reaches women blood comparing to men

A
68
Q

Mechanisms of development toxicity of alcohol (what nutrient deficiencies might result, what organs and systems may suffer)

A
  1. •Alcohol has caloric value and replaces calories from other sources
  2. •Effect on folic acid and Zn metabolism (Protein and Zn malnutrition enhance deleterious effects of alcohol.)
  3. •Acetaldehyde and free radical toxicity (-Metabolized into acetaldehyde (toxic at uM concentrations vs. mM for alcohol) Acetaldehyde converted to acetic acid by aldehyde dehydrogenase.); Chronic consumption prolongs the inflammatory process à free radicals
  4. •Excessive cell death (apoptosis) in sensitive cell populations
  5. •Placental toxicity (impaired oxygen aand nutrition delivery)
  6. •Fetal hypoxia (alcohol metabolsim uses a lot of O2)
  7. Depletion of certain minerals & vitamins. E.g. Hypokalemia
69
Q

what is the result of NTD

A

•Brain and spinal cord develop from the NT and NTD cause various CNS disorders

Most severe forms: anencephaly (absence of a major portion of the brain, skull, and scalp) and exencephaly ( the brain is located outside of the skull). Infants severely impaired and die shortly after birth.

70
Q

Most common NTD is

A
  • Most common NTD.
  • Lack of bone encasement of the spine à permanent spinal cord and spinal nerve damage.
  • Inability to walk, abnormal bladder & bowel function, fatality.
  • Not severe cases can be repaired with surgery
71
Q

Why Zn cna get depleted during prolonged alcohol consumption

A
72
Q

Etiology of NTDs (9 causes)

A
  • Multifactorial inheritance (Genetics: much greater risk when mother previously had an offspring with NTD.)
  • Single gene (autosomal recessive) disorders ( only 12% of the cases)
  • Chromosomal aneuploidy (Trisomy 13)
  • Teratogens (Valproic Acid, Thalidomide)
  • Maternal IDDM (T1DM)
  • Severe overweight
  • Family history or prior NTD-affected pregnancy
  • Hot tub use or fever in early pregnancy
  • Folate deficiency or inborn error of folate metabolism ( 50-75% of the cases)
73
Q

What is the principle and key outcomes of MRC sutdy

A

Pregnant women and women planning a pregnancy were given capsules for 12 weeks.

Folate dose: 4mg

Multivitamins did not affect the incidence of NTD. (without folic acid, multivitamins were useless)

  • Trial stopped early due to success of folate supplementation
  • 71% reduction in NTD => recommendation of 4 mg folate for women with previous NTD
74
Q

why folic food fortification was established

A

poor compliance with regular vitamin intake

75
Q

Increased homocysteine during pregnancy will lead to

A

Increased level for neural tube defects, but also heart defects and pregnancy complications (still birth)

risk factor for preeclampsia, spontaneous abortion, recurrent early miscarriages

76
Q

what acid is the indicator of vitamin B12

A

methylmalonic acid

77
Q

how folic metabolsim in mother cna be impaired

A

if 5-methylene tetrahydrofolate reductase is not functional-> folate from foods (that is depleted during cooking) is not activated

supplementation with folic acid will overcome the inactivity of this enzyme, SNPs

78
Q

Why it is important this cycle functions properly during pregnancy?

A
  1. Accumulation of homocysteine and decreased in methionine

Methionine is responsible for methylation of DNA (activation of genes) and proteins (cellular replication), lipids

  1. homocysteine
  2. High folic acid supplementation of B12 deficiency -> because of RBCs anemia mimication, B 12 is responsible Myelination of nerves, but this 2 vitamins work together, so folate trap can occcur, folate can overcome B12 deficiency for RBC
79
Q

Mechanism of teratogenicity of homocysteine

A
  1. Secondary accumulation of SAH

•-> inhibition of DNA methyltransferase reactions, DNA hypomethylation, altered gene expression

  1. Oxidative stress
  • -> damage to mitochondrial and nuclear DNA, protein structure and function, membrane lipids and signal transduction pathways
  • Decrease the functional activity of methionine synthase through limiting the availability of vitamin B12
80
Q

what can lead to increassed homocysteine

A
  • Mothers with NTD infants: ↓ plasma folate, ↑ homocysteine levels -> defects in folate-dependent homocysteine pathway
  • Families with NTDs tend to have in-born error of metabolism (shortage of mehyltetrahydrofolate reductase)
81
Q

What will be the role of folic acid supplementation

A

Folic acid supplementation

  • Normalizes RBC [folate]
  • Decreases blood homocysteine
82
Q

apart from diseases how homocysteine can influence the fetus

A
  • Maternal homocysteine at preconception, at 8 weeks & at birth: inversely related to birth weight
  • Strong correlation between preconceptional homocysteine and homocysteine during pregnancy
  • à Possibility that preconceptional homocysteine may predict homocysteine-associated pregnancy complications
83
Q

if the mother is vegetarian why it is importnat to have optimal status of folic acid and vit B12

A

Usually vegetarian have higher folic acid status

when B 12 is lower-> can cause obesity and T2DM in later life, die to epigenetic changes

84
Q

What is the best source of folate intake

A

Fortification tends to be efficient, but supplementation is the better guarantee

85
Q

is folate status is still an issue, if there is fortification

A
  • 71% of non-pregnant women do not take daily folic acid supplements
  • Typical non-pregnant female (19-49 y.o.) dietary folate intake: 137 μg/1000 kcal or ~ 230 μg
  • Fortification thought to increase intake by only 100 μg/day
  • Only 10% of these women take in 400 μg/day

Nutrition through life (7 decks)

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