Female Reproductive System — Active Recall

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Built from Repro Lecture 03 (LOs 1–4). Close notes. Fill from memory. Reveal only after a genuine attempt.

📖 Use alongside: Repro Lecture 03 — Female Reproductive System (HoyaDocs) Focus on: ovary zones + oocyte timeline, 6 follicle stages + meiotic arrests, two-cell/two-gonadotropin theory, corpus luteum → progesterone, oviduct 4 segments (ampulla = fertilization + ectopic, isthmus = tubal ligation), endometrium functionalis vs basalis, HPO axis feedback rules (sustained E → LH surge, GnRH pulsatility), 3 phases of the cycle, cervix transformation zone + HPV, vagina glycogen-lactobacillus-pH, Bartholin ↔ Cowper's vs Skene ↔ prostate, breast TDLU + prolactin (synthesis) vs oxytocin (let-down).
FOLLICLE PROGRESSION — fill in all 6 stages in order (with meiotic state) before starting:
1. Dormant pool (since fetal life)
2. FSH begins; squamous → cuboidal
3. First antrum + theca
4. Dominant follicle, mid-cycle
5. Post-ovulation; yellow; progesterone
6. Final white fibrous scar
Plus: name the oocyte's TWO meiotic arrests and when each resumes.
Ovarian Follicles
Oviduct
Uterus & Menstrual Cycle
Cervix, Vagina & Breast
Practice Qs
LO 1
ON EXAM — 3 ovary zones + surface epithelium origin of most ovarian cancers, oocyte timeline (7M→1-2M→400K→0), 6 follicle stages, ZP3 = sperm receptor, two-cell theory (theca LH → androstenedione; granulosa FSH → aromatase → estradiol), LH surge → meiosis I completes, corpus luteum progesterone + hCG rescue, Call-Exner bodies = granulosa-cell tumor
Three ovary zones — fill histology + clinical point (LO1)
ZoneHistologyClinical / HY
Germinal epithelium (surface)
Cortex
Medulla
Oocyte count across the lifespan (LO1)
Follicle stage master table — fill each row (LO1)
StageFollicular cell morphologyOocyte meiotic stateKey feature / hormones
Primordial
Unilaminar primary
Multilaminar primary
Secondary / antral
Graafian / tertiary
Ovulation
Corpus luteum
Corpus albicans
Zona pellucida & fertilization (LO1)
Two-cell / two-gonadotropin theory — fill the relay (LO1)
KEY: Neither cell type can make estrogen alone. Theca makes ANDROGENS (needs LH); Granulosa AROMATIZES them to estradiol (needs FSH).
FeatureTheca internaGranulosa cells
Receptor (always present)
Starting substrate
Key enzyme
End product
Tumor produces...
Graafian follicle anatomy — layers outer → inner (LO1)
Ovulation & meiotic arrests (LO1)
Corpus luteum lifecycle (LO1)
Ovarian tumor clinical correlates (LO1)
LO 2
ON EXAM — 4 segments lateral→medial (I-A-I-I), ampulla = fertilization + ~70–80% of ectopics, isthmus = tubal ligation, ciliated + peg cells both ESTROGEN-dependent, PID (GC/Chlamydia) → scarred cilia → ectopic/infertility/hydrosalpinx, Fitz-Hugh-Curtis = violin-string perihepatic adhesions, methotrexate for stable early ectopic
Four oviduct segments — lateral to medial (LO2)
SegmentShape / featureClinical / HY point
Infundibulum
Ampulla
Isthmus
Pars interstitialis (intramural)
Histologic layers (LO2)
Two tubal epithelial cell types (LO2)
Cell typeFunctionHormonal regulation
Ciliated cells
Peg (secretory) cells
Timeline from ovulation → implantation (LO2)
Ectopic pregnancy (LO2)
Salpingitis / PID / hydrosalpinx (LO2)
LO 3
ON EXAM — endometrium (functionalis/spiral arteries vs basalis/straight arteries), Asherman syndrome, HPO axis feedback rules (sustained E → POSITIVE LH surge; P = always negative), GnRH pulsatility (leuprolide flare then shutdown), straight vs coiled glands on histology (proliferative vs secretory), luteal phase always ~14 days, hCG rescues corpus luteum, luteal-placental shift week 8–10
Three uterine layers (LO3)
LayerHistologyClinical / HY
Endometrium (innermost)
Myometrium (middle)
Perimetrium (outermost)
Endometrium: functionalis vs basalis (LO3)
FeatureFunctionalisBasalis
Location
Blood supply
Hormone responsiveness
Fate in the cycle
HPO axis cascade (LO3)
Feedback rules — fill each (LO3)
EXAM TRAP: Estrogen is USUALLY negative feedback — EXCEPT when sustained >200 pg/mL for ≥48 h, which flips to POSITIVE feedback → LH surge.
GnRH pulsatility (LO3)
Menstrual cycle — 3 phases (LO3)
Phase (days)Dominant hormonesOvarian eventEndometrial appearance
Menses (0–5)
Proliferative (6–14)
Ovulation (~14)
Secretory (15–28)
If fertilization occurs — hCG rescue (LO3)
LO 4
ON EXAM — ecto vs endocervix epithelium, transformation zone = HPV dysplasia site, HPV 16/18 + E6 (p53) + E7 (Rb), koilocytes, cervical mucus (E thin vs P thick), vagina NO glands + glycogen-lactobacillus-pH 3.8–4.5, atrophic vaginitis, Bartholin ↔ Cowper's / Skene ↔ prostate, breast TDLU = cancer origin, myoepithelial cells lost in invasive (not DCIS), prolactin (synthesis) + oxytocin (ejection)
Cervix — two epithelia + transformation zone (LO4)
RegionEpitheliumFunction / Clinical
Ectocervix
Endocervix
Transformation zone (TZ)
HPV & cervical cancer (LO4)
Cervical mucus pattern (LO4)
Mnemonic: Estrogen mucus WELCOMES sperm; Progesterone mucus BLOCKS sperm (mechanism of progestin-only contraceptives).
Vagina (LO4)
External genitalia — keratinization + homologue (LO4)
StructureEpithelium / key contentsMale homologue
Clitoris
Labia minora
Labia majora
Vestibule
Vestibular glands (LO4)
FeatureBartholin's (greater)Skene's (lesser / paraurethral)
Location
Epithelium
Male homologue
Classic clinical
Mammary glands (LO4)
Male/female homologues — master review (LO4)
FemaleMaleCommon origin
Ovary
Clitoris
Labia minora
Labia majora
Bartholin's gland
Skene's gland
Round ligament of uterus
LO 1–4 · USMLE Step 1 Style
8 questions — cover all 4 LOs. Use these after finishing all tabs.
Q1. A 29-year-old woman undergoing infertility workup is found to have homozygous loss-of-function mutations in CYP19A1 (aromatase). Which set of findings is MOST expected?
A. Low androgens, low estradiol, low FSH, normal ovulation
B. High androgens, low estradiol, high FSH, anovulation
C. High estradiol, low androgens, low FSH, menorrhagia
D. Normal estradiol, low LH, normal follicular development
E. High estradiol, high progesterone, regular cycles
B — High androgens, low estradiol, high FSH, anovulation.
Without aromatase, granulosa cells cannot convert theca-derived androstenedione → estradiol. Theca continues to make androgens under LH, so androgens accumulate, estradiol is low, positive feedback never occurs (no LH surge), and FSH rises from loss of estradiol negative feedback. The patient has anovulatory infertility. In fetal life, the absence of placental aromatase causes maternal AND fetal virilization during pregnancy.
Q2. A pathologist examines an ovarian biopsy from a postmenopausal woman with new-onset vaginal bleeding and endometrial hyperplasia on biopsy. Microscopy of the ovarian mass shows solid and tubular arrangements of cells with scattered Call–Exner bodies. Which hormone is this tumor MOST likely secreting, and from which cell of origin?
A. Progesterone — corpus luteum cell tumor
B. Testosterone — Leydig cell tumor
C. Estrogen — granulosa cell tumor
D. hCG — choriocarcinoma
E. Inhibin B — Sertoli cell tumor
C — Estrogen secreted by an adult granulosa-cell tumor.
Granulosa cells are the FSH-responsive, aromatase-containing cells of the follicle. Tumors retain estrogen production; the pathognomonic finding is Call–Exner bodies (small follicle-like rosettes around eosinophilic fluid). Postmenopausal estrogen drives endometrial hyperplasia and bleeding; in children the same tumor causes precocious puberty.
Q3. A 24-year-old woman with two prior episodes of gonococcal cervicitis presents with unilateral pelvic pain and a positive β-hCG. Transvaginal ultrasound shows an empty uterus and a 2-cm right adnexal mass. Which segment of the fallopian tube is the MOST likely site of implantation?
A. Fimbriae of the infundibulum
B. Ampulla
C. Isthmus
D. Pars interstitialis (intramural segment)
E. Ovarian surface
B — Ampulla.
The ampulla is the longest, widest, most convoluted segment and the normal site of fertilization — so an embryo with impaired tubal transport (from PID-scarred cilia) implants here in ~70–80% of ectopic pregnancies. The pars interstitialis is a much rarer site but far more dangerous due to hemorrhage risk from uterine vessels when it ruptures.
Q4. A 22-year-old woman presents with 6 months of secondary amenorrhea after a D&C for retained products of conception. FSH, LH, estradiol, and progesterone are all normal for cycle phase. A progesterone withdrawal challenge fails to produce bleeding. What is the MOST likely cause?
A. Premature ovarian insufficiency
B. Sheehan syndrome (postpartum pituitary necrosis)
C. Asherman syndrome — damage to the endometrial basalis
D. Prolactinoma
E. Polycystic ovary syndrome
C — Asherman syndrome.
The endometrial basalis is normally retained and regenerates the functionalis each cycle. Aggressive curettage or endometritis can scar the basalis with intrauterine adhesions; without it, no functionalis can be built to shed — so progesterone withdrawal can't cause bleeding (no substrate). The hormonal axis is intact, which rules out POI, Sheehan, prolactinoma, and PCOS. Tx: hysteroscopic adhesiolysis + estrogen to stimulate regrowth.
Q5. A 27-year-old patient undergoing IVF is given daily leuprolide for 2 weeks prior to egg retrieval to prevent a premature LH surge. What BEST explains how a GnRH agonist ends up SUPPRESSING LH/FSH when endogenous GnRH normally stimulates them?
A. Competitive antagonism at pituitary GnRH receptors
B. Direct suppression of hypothalamic GnRH neurons
C. Continuous (non-pulsatile) GnRH receptor occupation → receptor down-regulation + desensitization
D. Negative feedback from increased testosterone
E. Inhibition of aromatase in granulosa cells
C — Continuous receptor occupation desensitizes pituitary gonadotrophs.
Physiologic GnRH is pulsatile. Constant GnRH-agonist exposure causes an initial 24–72 h flare (↑ LH/FSH), followed by receptor internalization, downregulation, and signaling uncoupling → near-complete suppression after 1–2 weeks ("medical castration"). Uses: IVF (prevent premature LH surge), prostate cancer, endometriosis, fibroids, precocious puberty. GnRH antagonists (ganirelix, degarelix) block receptors immediately with no flare.
Q6. A 34-year-old G3P0 with two prior complete hydatidiform moles presents with bilaterally enlarged cystic ovaries on ultrasound. β-hCG is markedly elevated. Which structure accounts for the ovarian finding?
A. Endometrioma
B. Granulosa-cell tumor
C. Theca-lutein cysts
D. Corpus luteum cyst
E. Mature cystic teratoma
C — Bilateral theca-lutein cysts.
Very high β-hCG (as in complete mole, choriocarcinoma, multiple gestations) chronically stimulates theca cells → bilaterally enlarged cystic ovaries. The cysts regress as hCG normalizes after mole evacuation. Key stem: "bilateral cystic ovaries + massively elevated β-hCG."
Q7. A 54-year-old postmenopausal woman presents with vaginal itching, burning, and dyspareunia. On exam, the vaginal epithelium is thin, pale, and friable; vaginal pH is 6.5. Which single physiologic change MOST directly explains the pH shift?
A. Increased Candida colonization
B. Estrogen withdrawal → ↓ glycogen in superficial squamous cells → ↓ Lactobacillus fermentation
C. Progesterone excess thickening cervical mucus
D. Increased prolactin suppressing vaginal secretions
E. Androgen excess altering vaginal flora
B — Estrogen withdrawal → ↓ glycogen → ↓ lactobacilli → pH rises.
In reproductive years, estrogen drives glycogen accumulation in superficial squamous cells. When these cells desquamate, lactobacilli ferment glycogen into lactic acid → pH 3.8–4.5. Post-menopause, estrogen withdrawal thins the epithelium, minimizes glycogen, and allows non-lactobacillus flora to dominate → pH rises >5 → atrophic vaginitis + susceptibility to BV/candida. Treatment: topical vaginal estrogen.
Q8. A new mother experiences a warm rush and milk flow when her infant latches. Which pair of hormones and actions BEST explains the "let-down reflex" and milk production?
A. Prolactin drives ejection; oxytocin drives synthesis
B. Prolactin drives synthesis in alveolar luminal cells; oxytocin drives ejection via myoepithelial contraction
C. Estrogen drives both synthesis and ejection
D. Dopamine drives synthesis; prolactin drives ejection
E. hPL drives synthesis; hCG drives ejection
B — Prolactin (anterior pituitary) synthesis; Oxytocin (posterior pituitary) ejection.
Prolactin acts on the luminal secretory epithelium of the alveoli to synthesize milk components; dopamine tonically inhibits prolactin, so suckling (which suppresses dopamine) raises prolactin. Oxytocin acts on the myoepithelial cells surrounding alveoli and ducts to contract them and eject milk. The let-down reflex: suckling → afferent nerves → PVN/SON in hypothalamus → posterior pituitary → oxytocin release.