Contraception, prolactin, ectopic pregnancy, amenorrhea Flashcards
Main hormone producing contraceptive effect
Progesterone
How do OCPs decrease androgenic signs?
Estrogen increases SHBG, which binds more free testosterone
Age cut off for not giving a smoker OCPs
35 y/o
How long to wait for combined methods after delivery?
21 days (or longer if breastfeeding)
Meds that stimulate hepatic metabolism of sex hormones (and thus can make OCPs fail)
Rifampin, phenobarbital, phenytoin, cabamazepine, primidone
Mean time of return to menses after stopping OCPs
32 days
Time frame for emergency contraception
3 days for levonorgestrel (Plan B)
5 days for ulipristal (Ella) or IUD
Site of prolactin production
Anterior pituitary
Effect of dopamine on prolactin
Decreases
Ddx for galactorrhea
- Medications
- Pituitary tumors
- Hypothalamic lesions, stalk lesions, compression
- Estrogen (from OCPs, rare)
- Prolonged suckling
- Stress
- Non-pituitary sources of prolactin (lung or renal tumor)
What meds can cause galactorrhea?
Dopamine receptor blockers: antipsychotics, metoclopramide, SSRIs, TCAs
Dopamine depleting agents: methyldopa, reserpine
Dopamine release inhibitors: opiates, cimetidine
Effect of hyperprolactinemia on the menstrual cycle
Inhibits pulsatile secretion of GnRH -> often amenorrhea, low estrogen (and its complications like osteoporosis)
Micro vs macroadenoma
1 cm
Treatment for hyperprolactinemia
Dopamine agonists: bromocriptine (safe in pregnancy if symptomatic) or cabergoline
Discriminatory zone
Beta hcg 3500
Progesterone levels and use in PUL
< 5 almost always nonviable
> 20 almost always normal IUP
Relative contraindications to MTX
GS > 3.5 cm
Embryonic cardiac activity
Beta hcg > 5000
Primary amenorrhea definition
No menstruation…
By 15 y/o with normal secondary sex characteristics
By 13 y/o without normal secondary sex characteristics
Secondary amenorrhea
At least 3 months / cycles without menses
Mullerian agenesis vs androgen sensitivity on exam
Pubic hair
What does a positive progestin challenge (bleeding within 2-7 days) prove?
Estrogen and functional outflow tract
What FSH tells you about amenorrhea
> 20 suggests ovarian failure
< 5 suggests hypogonadotrophic state
Low-normal with low estradiol suggests hypothalamic dysfunction
High FSH and low estradiol
Hypergonadotrophic hypogonadism - ovarian failure (gonadal dysgenesis if primary)
Low FSH and low estradiol
Hypogonadotrophic hypogonadism - hypothalamic amenorrhea, pituitary or CNS tumor
Normal FSH and estradiol
Anovulation (PCOS), anatomic defect (Asherman)
Causes of primary ovarian insufficiency
Chromosomal, autoimmune, radiation, chemotherapy
Autoimmune associations with POI
Adrenal disease (test for anti-CYP21 antibodies), thyroid disease (test for thyroid peroxidase and anti-thyroglobulin)
Chemo most associated with POI
Alkylating agents and procarbazine
Treatment for POI
HRT, include progesterone if has a uterus
How to achieve pregnancy with hypothalamic dysfunction
May try ovulation induction agents, may need LH + FSH
Anosmia plus delayed puberty and sexual development, normal pubic hair
Kallman syndrome (congenital GnRH deficiency)
DHEAS is produced exclusively by…
Adrenals
DHEA is made mostly by, and also by…
Adrenals (90%) and ovary (10%)
Criteria for PCOS
2 of 3:
- Hyperandrogenism
- Ovarian dysfunction
- Polycystic ovaries on ultrasound
Molecular cause of hirsutism
DHT (converted from testosterone by 5 alpha reductase)
Definition of polycystic ovary on ultrasound
20 more follicles 2-9 mm
Ovarian volume > 10 mL
Hirsutism causes in pregnancy
Pregnancy luteoma (can cause female infants to be virilized), rapidly regresses after delivery Theca-lutein cysts (can cause maternal but not fetal virilization)
Ovulation induction in PCOS
Letrozole
Mechanism of spironolactone
Aldosterone antagonist diuretic, inhibits androgen synthesis, competes for androgen receptor, inhibits 5 alpha reductase
Treatment for hirsutism
Flutamide - nonsteroidal anti-androgen
Finasteride - 5 alpha reductase inhibitor
Eflonithine cream - blocks ornithine decarboxylase
What is ovarian drilling?
Destroys theca cells and lowers androgen production, can help restore ovulatory cycles but not clearly supported by evidence
Enzyme most commonly deficient in congenital adrenal hyperplasia
21-hydroxylase (95% of cases)
Lab findings for 21-hydroxylase deficiency
Low aldosterone, low cortisol, [most important] elevated 17OHP (which leads to higher androgens)
Treatment for congenital adrenal hyperplasia
Supply deficient cortisol and aldosterone
Treatment prenatally for suspected congenital adrenal hyperplasia
Diagnosed by CVS or amnio
High-dose steroids
Non-classical CAH presentation
Puberty or later, similar to PCOS
Differential diagnosis for hirsutism
PCOS Idiopathic hirsutism CAH HAIR-AN syndrome Androgen-secreting neoplasm Androgen use Cushing syndrome (rarely)
Initial work-up for hirsutism
Total testosterone, SHBG, DHEAS, 17-OH progesterone
