Memory tricks for reproductive anatomy, hormones, and development

GnRH (gonadotropin-releasing hormone) from hypothalamus is released in PULSES — pulsatile release is essential. Continuous GnRH paradoxically suppresses the axis by downregulating receptors — used clinically (GnRH agonists) to treat endometriosis, prostate cancer, precocious puberty. GnRH → anterior pituitary releases FSH and LH. FSH: follicle development (female) and spermatogenesis/Sertoli cells (male). LH: ovulation trigger + corpus luteum (female) and testosterone production via Leydig cells (male). Sex hormones feed back NEGATIVELY to suppress GnRH/FSH/LH — except at mid-cycle when high estrogen creates positive feedback → LH surge → ovulation. Inhibin (from Sertoli cells/granulosa cells) selectively inhibits FSH.

Sperm produced in seminiferous tubules (testes) → mature in epididymis (20 days, gain motility) → vas deferens → ejaculatory duct → urethra → outside. Accessory glands add to semen: seminal vesicles (60% of semen volume — fructose for energy, prostaglandins, alkaline fluid), prostate gland (25% — citric acid, enzymes, PSA, alkaline — neutralizes vaginal acidity), bulbourethral glands (Cowper's glands — pre-ejaculatory mucus, lubrication, neutralizes urethral acidity). Testes: in scrotum 2-4°C cooler than body temperature — essential for spermatogenesis (heat sensitive). Cryptorchidism (undescended testes) → impaired spermatogenesis → infertility.

Spermatogenesis occurs continuously in seminiferous tubules from puberty. Takes ~64 days total. Spermatogonia (2n): mitosis → maintain stem cell pool AND produce primary spermatocytes. Primary spermatocyte (2n): Meiosis I → two secondary spermatocytes (n). Secondary spermatocyte (n): Meiosis II → four spermatids (n). Spermatids: spermiogenesis — differentiation into spermatozoa (develop head, midpiece, tail). Final maturation in epididymis. Sertoli cells: essential support — blood-testis barrier (immune privilege), nutrient supply, phagocytose excess cytoplasm, secrete inhibin and androgen-binding protein. Testosterone from Leydig cells maintains spermatogenesis locally at very high concentrations.

Ovaries: produce oocytes and hormones (estrogen, progesterone). Ovarian cycle occurs here. Fallopian (uterine) tubes: fimbriae sweep oocyte in after ovulation. Site of fertilization (usually ampulla — outer third). Cilia and peristalsis transport zygote to uterus (~3-4 days). Uterus: three layers — perimetrium (serosal outer), myometrium (thick smooth muscle — contracts during labor), endometrium (functional layer shed in menstruation, basal layer regenerates). Cervix: lower uterus → mucus plug (progesterone-thickened), dilates during labor. Vagina: birth canal, copulatory organ. Mammary glands: modified sweat glands — produce milk. Alveoli (milk production) → lactiferous ducts → nipple. Developed under estrogen (duct growth) and progesterone (alveolar development).

Follicular phase (days 1-13): FSH rises → recruits primordial follicles → dominant follicle emerges → estrogen rises → endometrium proliferates. Estrogen peak → positive feedback → LH surge. Ovulation (day 14): LH surge → dominant follicle ruptures → secondary oocyte released (completes meiosis II only if fertilized). Luteal phase (days 15-28): empty follicle → corpus luteum → progesterone dominant (+ estrogen) → endometrium secretory (prepares for implantation). No fertilization: corpus luteum degenerates → progesterone/estrogen fall → endometrium shed = menstruation. Fertilization: trophoblast secretes hCG → maintains corpus luteum → progesterone continues → no menstruation.

Oogenesis begins in fetal life. Oogonia (2n) undergo mitosis in fetus → become primary oocytes → arrested in Prophase I of Meiosis I — remain arrested from fetal life until puberty. At puberty, each cycle: one primary oocyte completes Meiosis I just before ovulation → secondary oocyte (n) + first polar body. The secondary oocyte is arrested in Metaphase II of Meiosis II at ovulation. Meiosis II completed ONLY if fertilization occurs → ovum + second polar body. Unequal division: one large egg gets most cytoplasm, small polar bodies get discarded. Contrast with spermatogenesis: males produce 300 million/day continuously, females ovulate ~1/month, and females are born with all eggs they will ever have.

Fertilization: sperm capacitated in female tract (6-8 hours) → acrosome reaction releases enzymes → penetrates zona pellucida → sperm fuses with secondary oocyte → cortical reaction (cortical granules released → zona hardens → polyspermy prevented) → Meiosis II completed → pronuclei fuse → zygote (2n). Cleavage: mitotic divisions without growth → morula (16-cell solid ball, day 3). Blastocyst forms (day 4-5): inner cell mass (embryoblast → embryo) + trophoblast (→ placenta). Implantation (days 6-10): blastocyst implants in endometrium (usually posterior wall of uterine body) → trophoblast invades → hCG secreted immediately → detectable in urine by day 8-10.

First trimester: hCG (from trophoblast) → maintains corpus luteum → corpus luteum makes progesterone + estrogen → maintains endometrium + suppresses new cycles. hCG peaks week 8-10 (morning sickness correlates). Luteoplacental shift (week 10-12): placenta takes over progesterone and estrogen production → corpus luteum can degenerate. Second and third trimester: placenta makes estrogen (from fetal adrenal DHEA via placental aromatase) + progesterone → levels rise throughout. Progesterone: suppresses myometrial contractions (essential for pregnancy). Relaxin: loosens pelvic ligaments and softens cervix (from corpus luteum and placenta). Human placental lactogen (hPL): from placenta → promotes fetal growth + prepares mammary glands + insulin resistance (diabetogenic).

Labor initiation: late pregnancy → ↓ progesterone (relative), ↑ estrogen → uterine oxytocin receptors upregulate → fetal cortisol triggers labor. Ferguson reflex (positive feedback): cervical stretch → oxytocin release → contractions → more stretch → more oxytocin — escalates until delivery. Three stages: dilation (0-10 cm), expulsion (delivery), placental (delivery of placenta). Lactation: during pregnancy — prolactin rises but milk suppressed by high estrogen/progesterone. After delivery — estrogen/progesterone fall → prolactin uninhibited → colostrum then milk. Suckling → inhibits dopamine → ↑ prolactin (synthesis) + ↑ oxytocin (letdown). High prolactin → suppresses GnRH → lactational amenorrhea. Breastfeeding provides passive immunity via IgA in milk.