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Nutrition through life Part 1 > PART 2 - Embryology and Teratology > Flashcards

PART 2 - Embryology and Teratology Flashcards

1
Q

What is teratogenesis?

A

production of birth defects

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2
Q

What is a malformation? What are the 3 types?

A

non-reversible morphological defect present at birth.
exterior: visible
Interior: organs
Microscopic: tiny

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3
Q

What is a congenital abnormality?

A

present at birth regardless of cause

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4
Q

TRUE OR FALSE. All defects lead to death of baby.

A

FALSE. Some can be cured surgically or early in life, some are fatal

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5
Q

TRUE OR FALSE. defects may be symptom-less at birth

A

TRUE

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6
Q

TRUE OR FALSE. Susceptibility to teratogenesis is heavily influenced be the genetics of mother and infant

A

TRUE

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7
Q

What is the most susceptible period of the fetus to teratogenesis?

A

Organogenesis (organogenic period) at 3-8 weeks of pregnancy. dangerous since they don’t know that they are pregnant and the ovum is dividing and differentiating. By the end of this period, the major fetal structures are complete

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8
Q

Why is folate important for those CAPABLE of becoming pregnant?

A

The neural tube closes within 28 days of gestation where most people don’t know they are pregnant

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9
Q

From when do we count the weeks of pregnancy?

A

first day of last menstrual period

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10
Q

What is Hyperplasia and when does it occur?

A

increase cell number (cell division), 17 days to 8 weeks

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11
Q

What is Hypertrophy?

A

increase in cell size

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12
Q

What are the 3 phases of growth?

A

1: Hyperplasia (teratogenic vulnerability)
2: Hypertrophy + Hyperplasia
3: Hypertrophy (risk of organ or biochemical malfunctions)

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13
Q

What is happens when interfering with the hyperplasia phase?

A

Permanent reduction in cell number

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14
Q

Describe the implantation process starting from ovulation

A

Ovulation: Ovum expelled from ovaries into Fallopian tubes
Fertilization: Sperm penetrate oocyte to make zygote
Blastogenesis: zygote begins to cleave and increase cell number (not size) to form the morula
Cavity called blastocele then forms in cell. Now called blastocyst
Blastocyst: -embryoblast: inner cell mass
-trophoblast: outside
Trophoblast cells secrete proteolytic enzymes that erode epithelial uterine lining to create implantation site
Histiotrophic nutritional phase: fluid and nutrients absorbed by phagocytosis
Trophoblast forms a cord of cells –> endometrium and start forming the placenta

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15
Q

The effect of toxicants depend on what?

A

type, dose and length

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16
Q

TRUE OR FALSE. During the blastogenesis phase the zygote does not increase in size.

A

TRUE only in cell number

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17
Q

TRUE OR FALSE. Before implantation there is a decreased exposure to toxins.

A

TRUE, question of accessibility

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18
Q

What is the first step of embryo development?

A

gastrulation. 2-3 weeks

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19
Q

What is Henson’s node?

A

invagination in the future cranial area of the ectoderm (moves caudally)

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20
Q

What are the 3 germ layers formed in gastrulation?

A

ectoderm, Mesoderm, Endoderm

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21
Q

What does the ectoderm become?

A

Brain, CNS, Skin

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22
Q

What does the mesoderm become?

A

Voluntary muscles, CV and excretory systems

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23
Q

What does the Endoderm become?

A

digestive and respiratory systems, glandular organs

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24
Q

Is the gastrulation phase susceptable to teratogenesis?

A

Yes, very.

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25
Q

What is the primitive streak?

A

Henson’s node before it forms the CNS. The cells migrate using this to get where they have to be.

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26
Q

What happens to each of the germ layers during and after migration through the primitive streak?

A

Mesoderm and endoderm migrate internally to make organs and tissues.
Then neurulation: ectoderm differentiates into neural plate, the neural tube

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27
Q

What happens during neurulation?

A

Neural plate folds to make neural groove. Then the neural crest cells fuse then separate to make the spinal cord and face/skull

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28
Q

When does the heart start beating and the general shape of the embryo is established?

A

27-29 days post-ovulation (before organogenesis)

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29
Q

When is the embryo officially considered a fetus?

A

When all essential external and internal structures are present, the placenta has developed
8th week of gestation.

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30
Q

What is the fetal/neonatal period?

A

8 weeks to birth
tissue differentiation, growth and physical maturation
little differentiation of organs except external genatalia

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31
Q

What happens when the fetus is exposed to toxins in the fetal/neonatal period?

A

affects growth and functional maturation
CNS and reproductive abnormalities
behavioral and motor deficits

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32
Q

TRUE OR FALSE. All organs are equally susceptible to teratogenesis during pregnancy.

A

FALSE. each organ and tissue has its own critical period of growth. that is why timing of exposure is important.

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33
Q

What are the 7 classes of teratogens?

A

Medications, social drugs, environmental agents, temperature (or fever), infectious diseases, chronic disease, nutrient deficiencies and excesses

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34
Q

TRUE OR FALSE. Almost all medications cross the placenta.

A

TRUE

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35
Q

What effects does an excess of iodides have on the baby?

A

congenital goiter, mental/physical retardation

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36
Q

What effects does an excess of fluoride have on the baby?

A

spina bifida occulta

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37
Q

What does an excess of vitamin D have on the baby?

A

facial abnormalities, mental retardation

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38
Q

what does an excess of vitamin A have on the baby?

A

CNS abnormalities (NTD)

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39
Q

An excess of vitamin A has negative effects on the baby, but depends highly on the timing of the intake? At what time during the pregnancy is there the most effect?

A

First 8 weeks, later not much effect shown

40
Q

What effect on the baby does a deficiency of protein have? (extreme)

A

Microcephaly (small head and brain)

41
Q

What effect on the baby does a deficiency of vitamin A have?

A

eye abnormalities, microcephaly

42
Q

What effect on the baby does a deficiency of vitamin D have?

A

Fetal rickets

43
Q

A vitamin D deficiency can cause hypoplasia of the tooth enamel, decreased bone density and growth failure, why?

A

Not enough calcium available to fetus

44
Q

What effect on the baby does a deficiency of vitamin E have?

A

a variety of congenital abnormalities

45
Q

What effect on the baby does a deficiency of vitamin K have?

A

Coumadin syndrome

46
Q

Vitamin K is easily obtained from the diet, in what situation would there be a deficiency?

A

When the mother takes anticoagulants

47
Q 
Smoking can decrease the body stores of which vitamin?
A-vitamin D
B-vitamin E
C- vitamin C
D- vitaminK
A

B-vitamin E

48
Q

What effect on the baby does a deficiency of folate have?

A

neural tube defects

49
Q

What effect on the baby does a deficiency of iodine have?

A

Cretinism (mental/physical retardation)

50
Q

What effect on the baby does a deficiency of potassium have?

A

kidney abnormalities

51
Q

What effect on the baby does a deficiency of copper have?

A

connective tissue defects, brain and bone abnormalities

52
Q

What effect on the baby does a deficiency of Zinc have?

A

neural tube defects

53
Q

In what situation can there be a copper deficiency?

A

genetic: Menkes kinky hair syndrome, errors in copper metabolism
drug that kellates copper and makes it unavailable to fetus

54
Q

What disorder is characterized by an inability to absorb zinc? What are its symptoms?

A

Acrodermatitis enteropathica, rashes hair loss, diarrhea and poor growth

55
Q

Since its unethical to experiment with deficiencies on pregnant women, how do we know the effects of zinc deficiency?

A

Acrodermatitis enteropathica

56
Q

The intake of drugs that act as antagonists to certain nutrients can lead to deficiency. Which nutrients are at risk by what type of drug?

A

folate: folate antagonists
Vitamin K: coumadin (coagulant)
folate+zinc: anti-convulsant

57
Q

What does FAS stand for?

A

Fetal alcohol syndrome

58
Q

What are the effects of FAS?

A

neurological abnormalities, development delay, behavior dysfunction/deficit, intellectual impairment, structural abnormalities

59
Q

What facial abnormalities doe babies with FAS have?

A

short eye lids, elongated mid-face, thin upper lip, receding jaw

60
Q

TRUE or FALSE. drinking alcohol during pregnancy leads to same result regardless of dose.

A

FALSE. dose-response relationship

61
Q

TRUE or FALSE. The equivalent of 1 shot glass of pure alcohol spread out during the pregnancy is enough to lead to the early symptoms of FAS.

A

FALSE. the nontoxic level of alcohol is not known

62
Q

What does ARBD stand for and when is this used?

A

alcohol related birth defects. used when there is no neural disorder

63
Q

Why does alcohol have such a powerful effect on the fetus?

A
  • women have less gastric alcohol dehydrogenase. so alcohol has greater effect.
  • alcohol crosses placenta freely
  • the embryo has small body weight but equal alcohol concentration as the mother
  • detoxification process not fully developed in embryo
  • embryo still developing CNS
64
Q

Why is alcohol so toxic?

A
  • has caloric value and replaces calories from other sources
  • effect on folic acid and zinc metabolism
  • turns into acetaldehyde (toxic at even lower concentration)
  • free radicals
65
Q

What does the type of NTD depend on?

A

depends on the location on the neural tube where the defect occurs

66
Q

What is Anencephaly?

A

brain is exposed, no skull

67
Q

What is exencephaly?

A

brain is outside the skull

68
Q

Which is the most common NTD?

A

Spina Bifida, spine doesn’t close

69
Q

TRUE or FALSE. Survival is possible with spina bifida.

A

TRUE. but permanent damage

70
Q

TRUE or FALSE. NTD are related to a genetic susceptibility.

A

TRUE

71
Q

What are the possible causes of NTD?

A
  • genetics
  • teratogens
  • maternal IDDM (insulin dependent diabetes mellitus)
  • overweight
  • high temp
  • folate deficiency or problem with folate metabolism
72
Q

What is the most prevalent cause of NTD?

A

Folate related

73
Q

What is homocysteine?

A

an AA, not used in protein synthesis. is an intermediate in the metabolism of methionine

74
Q

Methionine is transformed into what?

A

S-adenosyl-methionine (SAM) by a transferase

75
Q

What is the use of SAM (S-adenosyl-methionine)?

A

Used by the enzyme methyltransferase to methylate different molecules.

76
Q

What is the use of methylation?

A
  • Can silence or activate genes in epigenetic modification processes (change how genes are expressed through methylation)
  • protein modification (change protein function)
77
Q

What happens to SAM (S-adenosyl-methionine) after it looses its methyl group?

A

Turns into S-adenosyl-homocysteine (SAH)

78
Q

How do you make homocysteine?

A

Remove adenosine from SAH (S-adenosyl-homocysteine)

79
Q

What does high levels of homocysteine mean?

A

homocysteine levels are usually low so high levels means there is a problem

80
Q

What nutrients are needed to replenish methionine?

A

B12 and folate (through a B12 and folate dependent pathway)

81
Q

What vitamin is needed to make Cysteine?

A

B6

82
Q

What can homocysteine be used for?

A

replenish methionine or make cysteine

83
Q

What is the most common cause of having increased homocysteine?

A

Usually because the system to remethylate homocysteine back to methionine is impaired due to a folate deficiency

84
Q

How does high vitamin A affect the homocysteine pathway?

A

May suppress the enzyme 5-methylenetetrahydrofolate reductase, which regenerates the methyl donor for homocysteine, so less capacity of regenerating methionine

85
Q

Describe the folate pathway

A

TH4-Folate –> 5-methylene-TH4-Folate –> [5-methylenetetrahydrofolate reductase]
5-Me-TH4-Folate –>back to beginning after donating methyl to homocysteine with enzyme methionine synthase

86
Q

B12 is a cofactor to which enzyme?

A

Methionine synthase

87
Q

B6 is the cofactor to which enzyme?

A

cystathionase in cysteine pathway

88
Q

Describe the cysteine pathway.

A

Homocysteine –>Cystathionine –> [cystathionase] Cysteine

89
Q

In what context could there be an accumulation of SAH (S-adenosyl-homocysteine)?

A

a huge rate of gene expression meaning a big rate of methyl transfers. the cycle gets backed up

90
Q

Oxidative stress can lead to limiting the availability of which vitamin? This in turn limits the functional activity of which enzyme?

A

B12, methionine synthase

91
Q

Pregnant women with NTD babies tend to have characteristic levels of folate and homocysteine i nthe blood. Compare to regular levels.

A

HIGH homocysteine and LOW folate

92
Q

What complications can happen with high homocysteine levels?

A

risk factor for preeclampsia, spontaneous abortion, recurrent early miscarriages

93
Q

What is preeclampsia?

A

High homocysteine–> high BP, damage to certain organs

94
Q

TRUE or FALSE. Maternal homocysteine levels are inversely related to birth weight.

A

TRUE

95
Q

TRUE or FALSE. There is no correlation between homocysteine levels before and during pregnancy.

A

FALSE. high before=high during. pre-conceptional may predict homocysteine related pregnancy complications

96
Q

TRUE or FALSE. The synthetic form of folate is more stable and more easily absorbed than the natural form.

A

TRUE. the synthetic form is already as monoglutamate. no need to transform from natural polyglutamate

Nutrition through life Part 1 (6 decks)

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