Flashcards in Teratogens Deck (13):
Describe folic acid deficiency
Problems occur during fetal development, fetus is primarily vulnerable during the first month (critical period)
Caused by: lack of animal protein and green veggies, maternal smoking, alcohol with a metabolic dysfunciton in the mother.
It is associated with spina bifida, microcephaly, megaloblastic anemia, and anencephaly.
A sign is a dimpling of the coccygeal region showing incomplete closure.
Folates: are methylating agents of nucleic acid.
Totally preventable with supplements.
What are the weeks per trimester?
What are critical periods?
First trimester: weeks 1-12
Second trimester: weeks 13-26
Third trimester: weeks 27 to end of pregnancy.
Teratogens are most damaging for up to week 6
Critical periods: points in development where an insult may have a profound impact on certain targets.
Describe the effects of mercury
Prenatal & Postnatal exposure - Post natal defects
You can have elemental mercury - quicksilver, liquid
Inorganic mercury compounds: salts
Organic compound: methylmercury - greatest concern, targets the nervous system.
-we get methylmercury from eating fish, particularly high in predatory fish like shark and tuna.
-causes Minamata Disease
-affects development of the nervous system before and after birth.
Shifts the normal distribution of intelligence down 3 points.
Describe Lead and development.
What are current blood lead standards?
Post natal exposure - Post natal defects.
Interferes with cognitive and psycho-motor functioning.
Equal to or More than 5 micrograms/dl blood lead needs health action
Less than 5 micrograms/dl leads to cognitive defects
What are PCBs
- Post natal defects
They are compounds that accumulate in fish.
Cause developmental delay and lowered cognitive performance.
Like mercury but unlike lead, the damage is mostly pre-natal.
Effect of alcohol on development.
Most harmful during the first 3 months of pregnancy.
Poor growth in the womb and after birth, decreased muscle tone, poor coordination, delayed development and functional problems in the brain, heart defects,
Face: narrow small eyes, small head, small upper jaw, smooth groove in upper lip, smooth and thin upper lip.
The most common cause of preventable mental retardation.
FAS2: marked hyperactivity, delayed gross and fine motor skills, learning, lanugage skills, and hearing loss. No drinks!
What does TORCH stand for?
(infectious agents that cause serious fetal damage and congenital defects or death)
T = Toxoplasma
O = other (varicella, Zika, syphilis, mumps)
R = rubella
C =cytomegalic virus
H = herpes
Microcephaly and mental retardation are the outcomes.
What is the impact of rubella on development.
Prenatal exposure - defect apparent at birth.
Vulnerable: first trimester of pregnancy: week 1-12
During first trimester, high likelihood of congenital rubella syndrome: characterized by the classic triad
1. congenital heart disease
3. eye deformity - cataracts, microophthalmia, retinopathies.
Describe Zika virus impact on development.
A kind of Flavivirus: found in tears, saliva. and especially semen
-blocks development of the brain in the fetus. Fluid filled ventricles enlarge and skull stops enlarging. Leads to microcephaly.
-fetal death, severe motor impairment, visual impairment, microcephaly due to reduced brain size.
Mostly male to female transmission but it goes both ways.
Thalidomide effect on development
Prenatal exposure - defect apparent at birth
Lead to phocomelia: Shortened or absent arms and legs. It was a drug used to treat morning sickness.
Other symptoms: amelia, syndactyly, ear and eye defects.
It is a clear example of point source epidemic.
Mechanism: primarily thought to arrest development of neural tissue, critical blood vessels. If developing tissue isn't innervated with these, then it won't form.
Describe DES and its effect on development
Prenatal exposure and Post natal defects.
This is a drug to prevent miscarriage, when contractions began in the second trimester and death was imminent.
This lead to a super rare cancer known as clear cell vaginal cancer in adolescent girls. (they have so much estrogen it prevents tissue from being shed) then when they hit puberty a wave of estrogen causes tumors.
In utero toxicity can occur in the F2 generation
Organophosphate pesticides and their effects on development.
Derived from maternal exposure.
Affects the fetus and early child where there is rapid development of the brain.
Organophosphates inhibit acetylcholinesterase which allows acetylcholine to build up at neural junction.
This leads to acute toxicity and also disrupts cell replication, differentiation, synaptogenesis which all lead to fewer connections in the brain.