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risk-benefit analysis (pregnancy)
a clinical decision-making approach that compares risk to the fetus vs. risk of not treating the mother
teratogenic effects
drug effects that cause physical malformations in the developing fetus
neonatal / perinatal effects
drug effects that occur around the time of birth, such as withdrawal symptoms and low birth weight
behavioral teratogenesis
long-term effects on the child’s IQ, learning, and behavior
→ due to drug exposure during pregnancy
placenta not a barrier
concept that psychotropic drugs can cross the placenta and affect the fetus
first trimester vulnerability
the period of highest risk (weeks 2=8) for developmental abnormalities
maternal toxicity vs fetal toxicity
toxic effects in the mother do not reliably predict effects in the fetus
FDA pregnancy categories
A → no risk (controlled studies)
B → no evidence of risk in humans
C → risk unknown (most SSRIs)
D → evidence of risk
X → contraindicated (do not use)
untreated maternal depression
depression during pregnancy that is not treated, which can cause hormonal changes (high cortisol), developmental delays, poor prenatal care
postpartum depression (‘baby blues’)
depression occurring after childbirth, often within the first few weeks
brexanolone
a medication for postpartum depression that modulates GABA-A receptors and is given as an infusion
mood stabilizers in pregnancy
valproate = WORST
neural tube defects
autism
carbamazepine = BAD
lithium = risk (heart defects)
lamotrigine = safer
ethnopyschopharmacology
culture + genetics influence drug response
genetic polymorphisms
affect drug levels, response, and side effects
CYP450 enzymes
liver enzymes that control drug metabolism
leads to:
poor metabolizers → increase side effects
rapid metabolizers → decrease effectiveness
race & ethnicity
no sharp genetic boundaries
both are social constructs
not biological categories