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Nutrition Through Life > Embryology and Teratology > Flashcards

Embryology and Teratology Flashcards

1
Q

What is teratogenesis?

A

Production of birth defects

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2
Q

What are malformations? Where could they be located? Are they always visible?

A

non-reversible morphological defects present at birth. Could be exterior/internally located or only microscopically visible

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3
Q

What is a congenital anomalies and when is it present?

A

It is birth defects, congenital disorders or congenital malformations. Present at birth

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4
Q

How many congenital anomalies are present?

A

More than 200

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5
Q

Birth defects are present in __-__% of all live births

A

2-3%

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6
Q

Birth defects are the leading cause infant death in North America for what 3 reasons?

A
  1. improvements in obstetrical care
  2. increased medications and social drug use
  3. environmental contaminants?
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7
Q

In 1996, birth defects were what % of of infant deaths in UP?

A

22.4

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8
Q

Why does the incidence of birth defects increase by ___-___% when kids turn 2 y.o.?

A

4-6%

due to discovery of internal organ defects

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9
Q

Birth defects account for _____ of all deaths in infants < 1 y.o and ____ of all deaths in children <15 y.o.

A

> 1/3

< 15 y.o.

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10
Q

Why aren’t defects noticed at birth a lot of the times?

A

because they are symptomless

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11
Q

What make up for 20-25% of the causes of birth defects?

A

known genetic causes and chromosomal abbreviations

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12
Q

Maternal illnesses are responsible for what 2 developmental defects?

A
  1. Infections (2-3%)

2. Metabolic disturbances (1-2%)

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13
Q

Drugs and chemicals are the cause of that % of developmental defects?

A

4-5%

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14
Q

Susceptibility of teratogenesis heavily influenced by ______ of mother and infant. Nutritional deficiencies play a significant role + genetic susceptibilities.

A

genetics

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15
Q

Less than ___ % of all human pregnancies result in healthy normal infants.

A

50

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16
Q

What is the largest contributor to unsuccessful pregnancy?

A

post-implantation losses (31%)

implantation: the attachment of the fertilized egg or blastocyst to the wall of the uterus at the start of pregnancy, often delayed in some mammals by several months.

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17
Q

What is the organogenic period? What is it synonymous with? When does the organogenic period take place?

A

when ovum divides and differentiates. Teratogenic period - max vulnerability period of the fetus - 15-57 days / 3-8 weeks

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18
Q

When does the neural tube close?

A

within 28 days of gestation - most women don’t know they are pregnant - folate is essential for women CAPABLE of becoming pregnant

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19
Q

What 3 things take place during the organogenic period (a CRITICAL period)?

A
  1. cell organization
  2. cell differentiation
  3. organogenesis
  • Maximal cell division and differentiation
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20
Q

What are the two main ways that the body grows during pregnancy?

A
  1. hyperplasia:
    - Increase in cell number
    - Time of maximum vulnerability for teratogenic effects
    - Day 17-56 after fertilixation
  2. hypertrophy
    - hyperplasia ceases
    - Risk of development of organ or biochemical malfunctions
    - after 8 weeks
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21
Q

What happens if there is an interference with hyperplasia?

A

PERMANENT reduction in cell number

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22
Q

What is ovulation?

A

ovum expelled by ovary into Fallopian tubes

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23
Q

What happens during fertilization?

A

Sperm penetrates oocyte and becomes zygote

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24
Q

What is blastogenesis? What does it result in?

A

zygote begins to cleave and increase in cell number. Creation of morula: a solid ball of cells resulting from division of a fertilized ovum, and from which a blastula is formed – a cavity (blastocele) then forms in the centre of the morula and the entire structure is now called a blastocyst!

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25
Q

What are the two different cell types within blastocysts?

A
  1. embryo blast (inside)

2. trophoblast (outside)

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26
Q

What do trophoblast cells secrete and what does this do?

A

They secrete proteolytic enzymes which erode epithelial uterine lining (in order to create an implantation site for the blastocyst)

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27
Q

During the first 20-25 days after conception, how are the nutrients of the blastocyst absorbed? What is this phase called?

A

Phagocytosis because nothing connecting embryo and mom (no placenta, no fetal circulation yet)

Histiotrophic nutritional phase

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28
Q

What do trophoblasts form after the historic nutritional phase (20-25 days)?

A

a cord of cells called endometrium which starts forming the placenta

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29
Q

Pre-implatnation stage:

  1. time period?
  2. Increase in cell _____ but no increase in cell _____.
  3. what is the baby called during this stage?
  4. What happens to baby upon exposure to toxicants during this stage?
A

number, size

  1. < 1 week (pre-implantation period)
  2. number, size
  3. zygote, blastocyst
  4. no effect (because cells can be replaced by other ones easily) or lethality (pleuropotency: fate of cells is not determined therefore capable of giving rise to several different cell types and great restorative capacity)
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30
Q

What stage follows the pre-implantation stage?

  1. Time frame?
  2. What starts forming, where?
A

Gastrulation - embryo development

  1. 16 days - at day 14: inner cell mass starts to differentiate into different cell types
  2. formation of invagination (Henson’s node) in the future cranial area of ectoderm – moves caudally (from the back) - forms primitive streak (faint streak that is the earliest trace of the embryo in the fertilized ovum)
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31
Q

Gastrulation:

  1. time period
  2. What 3 things form?
  3. Teratogen susceptibility?
A

Cell migration through primitive streak

  1. week 2-3
  2. formation of 3 germ layers: ectoderm, mesoderm, endoderm
  3. very susceptible to teratogens
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32
Q

What is each germ layer going to become:

  1. Endoderm
  2. Mesoderm
  3. Endoderm
A
  1. Brain, CNS, skin
  2. voluntary muscles, CV and excretory systems
  3. Digestive and respiratory systems, glandular organs (exocrine/endocrine)
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33
Q

What 3 main events make up the gastrulation phase?

A
  1. Primitive streak = future axis of the embryo –> 3 layers of the embryo
  2. Neurulation: ectoderm differentiates into neural plate –> neural tube
  3. Mesoderm and endoderm cells migrate internally to form organs and tissues
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34
Q

What stage occurs after gastrulation - time period?

A

Post ovulation – days 27-29

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35
Q

Post-Ovulation:

  1. What is established? What vital organ becomes active?
  2. Size & weight of embryo?
  3. What is the status of the neural tube?
  4. What day must neural tube close?
A
  1. general shape of embryo established - heart starts beating
  2. < 1 inche & < 1 oz
  3. Neural folds fused –> neural tube has segregated into head region and post cranial region
  4. day 27 to prevent nerve degeneration
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36
Q

What stage occurs after Post-Ovulation?

A

Organogenesis

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37
Q

Organogenesis:

  1. Time period?
  2. What is established?
  3. What 4 things are characteristic of this stage?
  4. teratogen susceptibility?
  5. Periods of ______ susceptibility for each forming structure.
A
  1. 3-8 weeks
  2. organs and body structures established
  3. cell proliferation, cell migration, cell-cell interactions & tissue remodelling
  4. extremely susceptible to teratogens
  5. Maximum
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38
Q

What happens at the 8th week of gestation?

What does the fetus get its nutrients from at this point?

A

FETUS :) All essential and external&internal structures are present

  • Placenta has developed and accounts for most nutrient needs
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39
Q

What stage occurs after organogenesis?

A

Fetal/neonatal

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40
Q

Fetal/neonatal:

  1. Time frame?
  2. What happens at this stage?
  3. teratogen susceptibility?
A
  1. 8 weeks - birth
  2. growth & physical maturation – little differentiation of organs takes place except external genitalia
  3. effects growth and functional maturation: CNS and reproductive abnormalities, behavioural and motor deficits. More functional and growth abnormalities rather than morphological defects
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41
Q

What are the 3 classes of teratogens?

A
  1. medications
  2. social drugs
  3. environmental agents
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42
Q

What are 5 examples of medication teratogens?

A
  1. seizure medications
  2. Accutane
  3. thalidomide
  4. lithium
  5. chemotherapy drugs
43
Q

What are 4 examples of environmental agent teratogens?

A
  1. organic solvents
  2. heavy metals
  3. pesticides
  4. PCBs (polychlorinated biphenyls)
44
Q

How can teratogenic exposure to certain medications/drugs be diagnosed?

A

syndrome of the baby

45
Q

What teratogen is responsible for most fetal abnormalities?

A

alcohol

46
Q

For each drug: associated defects, risk of defect.

  1. Dilantin
  2. Thalidomide
  3. Antineoplastic drugs
  4. Diethylstilbestrol
  5. Dextromethorphan
A
  1. Fetal hydantoin syndrome (10%)
  2. Limb and ear abnormalities (20%)
  3. congenital abnormalities (17%)
  4. Uterine and cervical defects (22-53%)
  5. CNS abnormalities
47
Q

What factors affect severity of tetranogens?

A
  1. type of medication
  2. time of exposure
  3. length of time of exposure
48
Q

What are the 4 classes of tetratogens?

A
  1. High temperature or fever (sustained exposure to hot tubes - raises core body temp)
  2. Infection diseases
  3. Chronic diseases
  4. Nutrient deficiencies and excesses via dietary intake and through drug intake
49
Q

What are 3 examples of infectious diseases that are classified as teratogens?

A
  1. Rubella
  2. cytomegalovirus
  3. toxoplasmosis
50
Q

What happens if you intake excess:

  1. iodides during pregnancy?
  2. fluoride?
  3. Vitamin D?
  4. Vitamin A?
A
  1. congenital goitre, Mental and physical retardation
  2. Spina Bifida Occulta
  3. Facial abnormalities, mental retardation
  4. CNS abnormalities
51
Q

What is the % of incidence of birth defects according to each daily retinol intake?

  1. 0-5000 I.U. (international unites)
  2. 5,001-8,000 I.U.
  3. 8,001 - 10,000 I.U.
  4. > or = to 10,001 I.U.
A
  1. 1.3%
  2. 1.6%
  3. 2.7%
  4. 3.2%
52
Q

In a study conducted, women who took in >10,000 I.U. vitamin A / day saw what increase in risk of neural tube defects?

A

4.8 times - increased risk closely associated with timing of intake during pregnancy

53
Q

What % of women consume >10,000 I.U. of vitamin A today? As a result, what fraction of babies have birth defects associated with Vitamin A intake?

A

1.4%

1/57

54
Q

What is the effect of each nutrient deficiency?

  1. Protein
  2. Vitamin A
  3. Vitamin D
  4. Vitamin E
  5. Vitamin K
A
  1. Microcephaly
  2. Eye abnormalities, microcephaly
  3. Fetal rickets, hypoplasia of tooth enamel, decreased bone density, growth failure
  4. Congenital abnormalities.
  5. Coumadin syndrome (anticoagulant, e.g. dicoumarol)
55
Q

Smoking decreases vitamin __ stores - non-specific birth defects and spontaneous abortions

A

E

56
Q

What is the effect of each nutrient deficiency?

  1. Folate
  2. Iodine
  3. Potassium
  4. Copper
  5. Zinc
A
  1. neural tube defect - caused by poor diet, maternal drug intake & genetic susceptibility to abnormalities in folate metabolism
  2. Cretinism - mental and physical retardation: potbelly, large tongue, facial characteristics of Down’s syndrome
  3. Kidney abnormalities
  4. Connective tissue defects, brain and bone abnormalities.
  5. Neural tube defects - cannot mobilize Zn to meet embryonic needs
57
Q

What is the result of genetic inborn errors of Copper metabolism?

A

Menkes kinky hair syndrome –> major developmental abnormalities in brain, bones, blood vessels

58
Q

What is acrodermatitis enteropathica?

A

inability to absorb Zn - causes rashes, hair loss, diarrhea & poor growth. Increased risk of birth defects and pregnancy complications

59
Q

_______ is a folate antagonist and causes a __% risk of NTD.

A

Methotrexate, 30%

60
Q

_____ is a vitamin K antagonist and causes __% risk of congenital heart disease.

A

Coumadin, 7%

61
Q

Anticonvulsants induce ____ & ____ deficiencies.

A

Folate, Zinc

62
Q

What are 4 characteristics of Fetal Alcohol Syndrome?

A
  1. Craniofacial dimorphism
  2. Growth retardation (head circumference, weight, height < 10th percentile)
  3. Decreased fat stores
  4. Retarded psychomotor and intellectual development

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

63
Q

What is the leading cause of birth defects and intellectual handicap in North America?

A

Fetal Alcohol Syndrome

64
Q

The ___ trimester is the greatest sensitivity of the fetal brain.

A

3rd

65
Q

What are the 4 major facial abnormalities of Fetal Alcohol Syndrome?

A
  1. Short palpebral (re: eyelids) fissures
  2. Elongated mid-face
  3. Thin upper lip
  4. Retrognathia; receding jaw
66
Q

What does it mean by “dose-response relationship” in FAS?

A

The more you consume the higher the effect

67
Q

If a mother consumes __ oz. absolute alcohol in late pregnancy –> ___ g decrease in birth weight

A

1 oz.

160 g

68
Q

What alcohol consumption from mother puts kid at a high risk of getting fetal alcohol syndrome?

A

3 oz.
4 drinks / day

or just binge drinking

69
Q

Fetal alcohol syndrom is present in __-__% of children born to alcoholic mother.

A

30-50%

70
Q

1 dose of ___ drinks very early in pregnancy or av. ___ drinks/day in later pregnancy is associated with learning difficulties.

A
  1. > 5

2. 2 drinks/day

71
Q

Heavier drinkers have ___%risk of child with FAS & __-__% risk of fetal damage

A
  1. 45%

2. 50-95%

72
Q

How many diagnostic criteria (symptoms) of FAS must a baby possess in order to diagnose it as that?

A

2-3

73
Q

What are 3 alcohol related birth defects? (ABRD)

A
  1. Microcephaly
  2. Heart and lung malformations
  3. Minor physical abnormalities
74
Q

What are 3 alcohol related CNS disturbances?

A
  1. decreased attention span
  2. decreased IQ
  3. hyperactivity
75
Q

~ ___% of alcohol is metabolized by the enzyme:

A

95%

alcohol dehydrogenase

76
Q

Alcohol crosses placenta ______.

A

freely

77
Q

Is the half life of alcohol increased of decreased in embryo/fetus?

A

increased

78
Q

Is detoxification and clearance more or less developed in embryo/fetus?

A

less

79
Q

After absorption, alcohol is ______ distributed to all body fluids. It crosses the ________ and ________ barriers until at _______ with mother’s blood.

A
  1. evenly
  2. blood-brain
  3. placental
  4. equilibrium
80
Q

The fetus and embryo developing CNS is ____ susceptible to alcohol related effects than adult brain.

A

more

81
Q

Why does alcohol replace calories from other sources?

A

Because it has a higher caloric value but no nutritional value - displacement of nutrient rich foods from diet

82
Q

How does alcohol affect folic acid and zinc metabolism? What kind of vicious cycle does this cause?

A

It impairs absorption. Protein and zinc malnutrition enhance effects of alcohol so its a vicious cycle with zinc and alcohol

83
Q

What is alcohol metabolized into?

A

acetaldehyde which gets converted to acetic acid via aldehyde dehydrogenase

84
Q

why is acetaldehyde even more toxic than alcohol?

A

it is toxic at uM concentrations vs. mM for alcohol

85
Q

What process does chronic consumption of alcohol prolong?

A

inflammatory process

86
Q

Depletion of vitamin K via alcohol leads to what?

A

hypokalemia

87
Q

What are neural tube defects?

A

congenital abnormalities of the fetal spine and central nervous system - include neural tube defects

88
Q

What develops from the neural tube?

A

brain and spinal cord

89
Q

What type of disorders do neural tube defects cause?

A

central nervous system disorders

90
Q

How many people are born with neural tube defects per year?

A

0.5 million

91
Q

What is anencephaly?

A

the absence of a major portion of the brain, skull, and scalp that occurs during embryonic development. Results from a neural tube defect that occurs when the rostral (head) end of the neural tube fails to close, usually between the 23rd and 26th day following conception.

92
Q

What is the difference between exencephaly and anencephaly?

A

Exencephaly: brain is located outside the skull

Anencephaly: large part of the skull is absent along with the cerebral hemispheres of the brain

93
Q

What happens to babies born with anencephaly or exencephaly?

A

die shortly after death

94
Q

What is the most common neural tube defect?

A

Spina bifida

95
Q

What is spina bifida? What are the side effects?

A

lack of bone encasement of the spine –> permanent spinal cord and spinal nerve damage.

Effects: can’t walk, abnormal bladder & bowel function, facility.

96
Q

What are the 9 different etiologies of neural tube defects?

A
  1. multifactorial inheritance (both genetic and envr)
  2. single gene (autosomal recessive) disorders
  3. chromosomal aneuploidy (Trisomy 13)
  4. Teratogens (Valproic Acid, Thalidomide)
  5. Maternal IDDM (insulin dependent diabetes)
  6. severe overweight
  7. family history or prior NTD-affected pregnancy
  8. Hot tub/fever in early pregnancy
  9. folate deficiency or inborn error of folate metabolism
97
Q

Only __% of NTDs have an identifiable genetic cause.

A

12%

98
Q

What % of NTDs are related to folate deficiency or abnormal folate metabolism?

A

50-75%

99
Q

Folate supplements reduce risk of NTD by ___%

A

71%

100
Q

What is the supplement recommendation of folate for women who previously gave birth to a child with a neural tube defect?

A

4 mg

101
Q

What & of non-pregnant women don’t take folic acid supplements?

A

71%

102
Q

Fortification is thought to increase intake of folate by how much?

A

100 ug/day

103
Q

Typical non-pregnant women 19-50 yrs old intake how much folate on average?

A

137 ug/1000 kcal or ~230 ug

Nutrition Through Life (5 decks)

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