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Exposure During Development Flashcards

1
Q

How many children have some developmental disability? Severe ones?
Autism?

A

17%

2%

7-12/1000 children are on autism spectrum

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2
Q

What is concept of environmental justice?

A

Do not occur in a vacuum.

Communities that are entrapped (poverty)

Genetic predisposition and social circumstances.
Access to medical care lacking.
Access to healthy diets

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3
Q

What are poor diets deficient in?

A 
Calories
Protein
Iron
Iodine
Folates(vitb9) and vitB12

Sea salt does not have iodine!

Folate is most important (methylating agents to make nucleic acids)

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4
Q

What does methotrexate do?

A

Knocks out folate.

But fetus needs folate!

Mothers should be exposed to folate now! Takes time for it to build up in your system.

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5
Q

What are the principals of teratology?

A

•  Suscep6bility depends on genotype of conceptus.
•  Suscep6bility depends on developmental stage at exposure
•  Malforma6on is caused by specific pathogenic mechanisms
•  Rela6ve teratogenicity is influenced by maternal factors
•  Abnormali6es by developmental stages:
–  Func6onal deficit
–  Growth retarda6ons
–  Malforma6ons
–  Adult disease may develop long aYer fetal exposure
•  Developmental defects increase with frequency & degree as a func6on of fetal
dose

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6
Q

What is DES?

A

Diethylstilbestrol

Did not show vaginal lesions in f1 offspring.

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7
Q

Can animal studies predict congenital rubella syndrome?

A

No

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8
Q

Did animal studies predict thalidomide toxicity?

A

Some but not all. Big thing here is that animal studies cannot predict everything.

Tests never done for reproductive effects afterwards saw the phocomelia.

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9
Q

What are TORCH infections?

A 
T-Toxoplasmosis
O-Other (Zika, chicken pox, varicella, syphyllis, parvovirus)
R-Rubella
C=Cytomegalovirus
H=Herpes

Mild maternal morbidity, but with serious fetal consequences.

Treatment of maternal infection does not have a corresponding impact on fetal outcome

MICROCEPHALY and metal retardation are big ones.

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10
Q

What is critical window for Rubella/Zika in fetal development?

A

3-16 weeks.

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11
Q

What is Rubella (German Measles/Congenital rubella syndrome?)

A

Patho: Togovirus
Mild flu like sympotoms

Incubation period = 2-3 weeks.

1st trimester: 50-95% cases
2nd: 25% cases
3rd:

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12
Q

When was rubella vaccine developed?

A

1970

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13
Q

What are critical days for ear and eye development?
Upper limbs?
Lower limbs?

A

Ears/Eyes: Days20-25
Upper limbs: 26-30th
Lower limb:31-36th

Twins show remarkable differences in response. (Both monozygotic and dizygotic twins)

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14
Q

What is classic triad of Congenital Rubella syndrome (CRS)?

Other manifestations?

A

Classic Triad

  • Sensorineural deafness: 60%
  • Congenital heart diz: 50%
  • Ocular abnormalities: 45%
  • ->1. Cataracts
    2. Microophthalmia
    3. Retinopathies.
Mental retardation
LBW
Thrombocytopenia purpura
Hepaomegaly
Facial deformities
Microcephaly
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15
Q

Is MMR vaccine indicated in pregnancy?

A

NO. Live vaccine!

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16
Q

What is Zika virus?

A

Flavivirus spread primarily by A.aegypti + albopictus.

58 countries and territories have active Zika.

Adults are asymptomatic/mild.

> 30,000 cases in Brazil.

17
Q

What is congenital Zika syndrome?

A 
Fetal Death
Still birth
Neonatal death
Developmental impairment
->motor/visual/microcephaly/cognitive impairment

Thinning of normal cortex. Occurs between 16-20weeks.

18
Q

Folate (VitB9) Deficiency? Pathogenesis?

A

Folate needed for DNA syn (methyl-transferase) and b12 deficiency

Wont have any methylated DNA adducts.

Neural tube defects: spina bifida, large RBCs,

19
Q

How does folate deficiency occur?

A

Metabolic dysfunction in mother.

Diet.
(Lack animal protein and green veggies)

Maternal smoking, alcohol, and kidney dialysis
->inhibit interactions

20
Q

What are some drugs that interact with B9 receptor?

A
  1. Anticonvulsants (dec. levels)
  2. Metformin (dec. levels)
  3. MTX - Chemotx
  4. Sulfasalazine (chrons/UC)
21
Q

What are s/sx of folic acid deficiency?

A

Neural tube closed at end of 1 month.

Defects range from anencephaly (lack of brain) to spina bifida.

Supplement with Folic acid 400mg QD

22
Q

What is most common cause of preventable mental retardation in US?

A

Fetal alcohol syndrome (Pintar)

23
Q

What are clinical features?

A

Decreased growth rate.
Facial abnormalities
Microcephaly
Microophthalmia

Hyperactivity
Delayed motor skills
Delayed language and learning

4-5drinks/day

Recommend zero alcohol!

24
Q

What is thalidomide toxicity?

A

Neuropathy-adult
Gi stasis-adults
Dizziness and disorientation-adult

Teratogenesis:
-Phocomelia
Amelia
Syndactyly
Ear/eye defects.
25
Q

What is MOA of pathogenesis of Thalidomide?

A
  • Direct toxicity of affected tissues
  • Arrested development of neural tissues
  • altered permeability of blood vessels
  • arrested development of critical blood vessels ***

Now being used as multiple myeloma, leprosy, difficult dermatological case

26
Q

What was DEs first defined as?

A

1st non-steroidal estrogen

Clinical use for threatened miscarriage.

Mothers would develop clear-cell adenocarcinoma of the vagina.

Learned that placenta is not a complete barrier.

27
Q

When does IUGR occur?

A

Weeks 16-38 of development.

Placental abnormaliOes •  Pre-eclampsia or Diabetes •  Chromosomal syndromes •  Smoking •  Alcohol •  XenobioOcs (chemicals, drugs) •  TORCH infecOons •  Maternal undernutriOon

28
Q

Dutch famine hypothesis:

A

Famine in 3rd trimester: glucose intolerance issues
1st trimester exposure: no such effect.

Big point is that babies are born that are “small for gestational age”

29
Q

What are Barker studies?

A

Women give birth at early age-> obese quicker.

HYpertension
CV diz
Glucose intolerance
Dyslipidemias

Women who are heavy smokers look like this too.

30
Q

What are endocrine disruptors?

A

DES was 1st.

Interfere with normal hormones functions.

Endocrine disruption is important, but controversy over which ones are significant.

31
Q

What are main environmental chemical that we see?

A

Mercury
Polychlorinated biphenyls (PCBs_
Lead
Organophosphate pesticides (OP)

32
Q

Why is mercury so useful?

A 
Toxic to all organisms
-antiseptic
Biocide on plants and on crops
As an antimicrobial preservative in vaccines
Diuretic to poison
33
Q

Where do we see methylmercury poisoning?

A

People who eat fish high on the food chain (shark/sword/tuna) multiple times a week.

Methylmercury poisoning from dumping into ocean.

Seychelle island- have complimentary diet of fruits and veggies.

34
Q

Why are fish beneficial to nervous development?

A

Omega 3 for nervous system development

Protein quality

1 fish meal/week

Salmon low in mercury and high in omega-3s

Canned tuna is fairly high in mercury.

White tuna has much higher levels of mercury.

35
Q

Where are there fish high in PCB?

A

Great lakes.

Decrease in cognitive function.
10% decrease in gestation growth.

36
Q

What is current blood lead standard to prompt public health action?

A

> = 5ug/dL

NO SAFE LEVEL

IQ deficits

Translated to at least 3 pt drop in IQ

37
Q

What is mechanism of OP pesticides?

A

Inhibit ACHe, ACH builds up at neuronal junctions

38
Q

What kind of studies do FDA use do determine exposure to pesticides?

A

Animal studies based on “no observable dverse effect level”

Applies 3 10fold uncertainties

Really not based on anything

OP short half life. Cant get chronic picture unless you have multiple blood draws.

39
Q

What did Columbia cohort show us about OP exposure?

CHAMACOS/Mt.Sinai

A

HIghest exposure of OPs -> lowest birth weight

Maternal urine associated with abnormal reflexes and decreased Bayley mental development scores at 24 months.
Pregnancy exposure is prob most important

7 IQ points lower!

FIFRA->advisory panel.

BMS-II (9 decks)

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