Reproductive and Developmental Toxicology Flashcards
6 cards from real ABT practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 Reproductive and Developmental Toxicology flashcards as text
The benchmark dose (BMD) approach for developmental toxicants offers an advantage over the NOAEL because it:
Answer: Uses all dose-response data to fit a model and is not limited to tested doses
The BMD approach fits a dose-response model to all experimental data, interpolates to a specific response level (e.g., BMD10), and provides confidence intervals unlike the NOAEL which is limited to tested doses.
Which anti-acne drug is required to be dispensed through the iPLEDGE REMS program because of severe teratogenicity?
Answer: Isotretinoin (Accutane)
Isotretinoin (a vitamin A analog) causes retinoic acid embryopathy (craniofacial, CNS, cardiac defects) and requires the iPLEDGE risk management program including mandatory pregnancy testing.
DEHP (di-2-ethylhexyl phthalate) exerts reproductive toxicity in male rodents primarily by disrupting:
Answer: Testosterone biosynthesis via Leydig cell PPAR-α activation affecting steroidogenesis
DEHP and its metabolite MEHP activate PPAR-α in Leydig cells, disrupting testosterone biosynthesis and causing antiandrogenic effects, particularly in the masculinization programming window.
Cyclophosphamide is an alkylating agent used in cancer chemotherapy that is also an established reproductive toxicant because it:
Answer: Cross-links DNA in gametes and developing embryo, causing gonadotoxicity and teratogenicity
Cyclophosphamide alkylates and cross-links DNA in rapidly dividing cells including germ cells and embryonic cells, causing gonadotoxicity (premature ovarian failure) and teratogenicity.
Which type of study design provides the strongest epidemiological evidence of teratogenicity in humans?
Answer: Prospective cohort study with exposure assessment before outcome
A prospective cohort study with exposure assessment before outcome determination provides the strongest epidemiological evidence by minimizing recall bias and allowing temporal inference.
Which hormonal mechanism explains why fetal exposure to androgens (or androgen-mimicking chemicals) causes virilization of female fetuses?
Answer: Androgens bind fetal androgen receptors during external genitalia differentiation, causing masculinization
During the critical window of external genital differentiation (weeks 8–12), androgens binding to androgen receptors in fetal genital tissue cause virilization (clitoral hypertrophy, labial fusion) of female fetuses.