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๐Ÿงฌ Physiology ยท Reproductive Physiology

Memory tricks for reproductive hormones and cycles

The HPG axis, menstrual cycle phases, gametogenesis, fertilization, pregnancy hormones, and lactation โ€” reproductive physiology ties together endocrinology, cell biology, and development. These memory tricks make the mechanisms stick.

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๐Ÿงฌ Reproductive Physiology

Memory Tricks

Proven Mnemonics & Acronyms โ€” fast to learn, hard to forget.

HPG Axis
GnRH โ†’ FSH + LH โ†’ Gonads โ†’ Sex hormones โ†’ Negative feedback
Hypothalamus โ†’ Pituitary โ†’ Gonads โ€” three-level hormonal control
The HPG axis โ€” how the brain controls reproductive function
GnRH (gonadotropin-releasing hormone) from the hypothalamus is released in pulses โ€” pulsatile release is essential. Continuous GnRH (as with GnRH agonists) paradoxically suppresses the axis by downregulating receptors โ€” used to treat endometriosis, prostate cancer, and precocious puberty. GnRH โ†’ anterior pituitary releases FSH and LH. FSH: follicle development (F) and spermatogenesis (M). LH: ovulation trigger (F) and testosterone production (M via Leydig cells). Sex hormones feed back negatively to suppress GnRH and FSH/LH โ€” except at mid-cycle when high estrogen creates a positive feedback LH surge โ†’ ovulation.
Pulsatile GnRH
Required for normal reproduction. Continuous โ†’ downregulation โ†’ suppression.
FSH
Follicle development + Sertoli cells (spermatogenesis). Controlled by inhibin.
LH surge
Day 14 โ€” high estrogen switches to positive feedback โ†’ LH surge โ†’ ovulation.
Inhibin
From Sertoli cells and granulosa cells โ€” specifically inhibits FSH (not LH).
Difficulty: Intermediate
Menstrual Cycle Hormones
Follicular = Estrogen rises ยท Luteal = Progesterone dominates
Follicular phase: FSH โ†’ follicle โ†’ estrogen ยท Luteal phase: LH โ†’ corpus luteum โ†’ progesterone
Hormone changes across the menstrual cycle โ€” phase by phase
Follicular phase (days 1-13): FSH rises โ†’ recruits follicles โ†’ dominant follicle produces estrogen โ†’ estrogen rises โ†’ endometrium proliferates โ†’ at peak estrogen, LH surge triggered (positive feedback). Ovulation: day 14 โ€” LH surge โ†’ dominant follicle ruptures โ†’ oocyte released. Luteal phase (days 15-28): empty follicle โ†’ corpus luteum โ†’ progesterone dominant (+ some estrogen) โ†’ endometrium secretory phase (prepares for implantation). If no fertilization: corpus luteum degenerates โ†’ progesterone/estrogen fall โ†’ endometrium shed (menstruation). If fertilization: hCG from trophoblast maintains corpus luteum โ†’ progesterone continues.
Days 1-5
Menstruation โ€” low estrogen and progesterone. FSH begins to rise.
Days 6-13
Proliferative โ€” estrogen rises, endometrium rebuilds, follicle matures.
Day 14
LH surge โ†’ ovulation. Most fertile window 12-24 hours after surge.
Days 15-28
Secretory โ€” progesterone dominant. Corpus luteum. Endometrium thickens.
Difficulty: Intermediate
Estrogen Physiology
Estrogen = Estriol ยท Estradiol ยท Estrone โ€” E3 ยท E2 ยท E1
Estradiol (E2) most potent ยท Estriol (E3) dominant in pregnancy ยท Estrone (E1) postmenopause
Three forms of estrogen โ€” when each dominates and what estrogen does
Estradiol (E2): most potent estrogen โ€” dominant during reproductive years. Produced by granulosa cells (ovary). Effects: female secondary sex characteristics, endometrial proliferation, LH surge trigger, breast development, bone density maintenance, HDL increase (cardioprotective). Estriol (E3): weak estrogen โ€” dominant in pregnancy, produced by placenta using fetal adrenal precursors. Estrone (E1): weak estrogen โ€” dominant after menopause, produced by adipose tissue from adrenal androgens. Low estrogen at menopause: hot flashes, vaginal atrophy, bone loss (osteoporosis), cardiovascular risk increase.
Estradiol (E2)
Most potent. Reproductive years. Granulosa cells. Bone, heart, endometrium.
Estriol (E3)
Pregnancy dominant. Placenta + fetal adrenals. Measured in triple screen.
Estrone (E1)
Post-menopause. Adipose tissue converts adrenal androgens โ†’ estrone.
Menopause
Low E2 โ†’ hot flashes, osteoporosis, vaginal atrophy, โ†‘CVD risk.
Difficulty: Advanced
Progesterone Physiology
Progesterone = Pro-gestation โ€” maintains pregnancy and prepares uterus
Secretory endometrium ยท Suppresses contractions ยท Raises basal body temperature
What progesterone does โ€” seven key physiological effects
Progesterone is the "pro-gestation" hormone โ€” everything it does supports pregnancy. Converts endometrium from proliferative to secretory (glandular, vascular โ€” ready for implantation). Suppresses myometrial contractions (prevents premature labor). Raises basal body temperature 0.5ยฐC after ovulation โ€” used to confirm ovulation. Thickens cervical mucus โ€” forms plug, blocks sperm and pathogens. Suppresses LH and FSH (prevents new ovulation during luteal phase). Mild immunosuppressive โ€” protects fetus from maternal immune rejection. Low progesterone in luteal phase = luteal phase defect โ†’ infertility or early miscarriage.
Secretory endometrium
Glands and vessels develop โ€” prepares implantation site for blastocyst.
BBT rise
+0.5ยฐC after ovulation โ€” confirms ovulation occurred. Stays elevated in pregnancy.
Cervical mucus
Thick, impenetrable โ€” blocks sperm (prevents double ovulation fertilization).
Immunosuppression
Prevents maternal rejection of fetal antigens โ€” protects pregnancy.
Difficulty: Intermediate
Testosterone Physiology
Leydig cells make testosterone ยท Sertoli cells support sperm ยท 5ฮฑ-reductase makes DHT
Testosterone โ†’ DHT (5ฮฑ-reductase) ยท Testosterone โ†’ Estradiol (aromatase)
Testosterone โ€” where it is made, converted, and what it controls
Testosterone is produced by Leydig cells in the testes under LH stimulation. Effects: spermatogenesis, male secondary sex characteristics, libido, muscle mass, bone density, erythropoiesis (increases EPO). Testosterone is converted by 5ฮฑ-reductase to DHT (dihydrotestosterone) โ€” more potent, responsible for prostate growth, male pattern baldness, and virilization of external genitalia in fetal development. 5ฮฑ-reductase inhibitors (finasteride) treat BPH and male pattern baldness. Testosterone is also aromatized to estradiol in peripheral tissues โ€” important for bone density and libido in males. High estrogen in males can cause gynecomastia.
Leydig cells
LH โ†’ testosterone production. Located in interstitium between tubules.
Sertoli cells
FSH โ†’ support spermatogenesis. Blood-testis barrier. Inhibin secretion.
DHT
5ฮฑ-reductase converts T โ†’ DHT. Prostate, hair follicles, external genitalia.
Aromatase
Converts T โ†’ estradiol. Adipose, liver, brain, bone. Gynecomastia from excess.
Difficulty: Intermediate
hCG Physiology
hCG = Pregnancy hormone โ€” rescues corpus luteum ยท peaks week 10
Human chorionic gonadotropin โ€” trophoblast produced, LH-like, maintains progesterone
hCG โ€” the first hormone of pregnancy and how pregnancy tests work
After fertilization and implantation (days 6-10), the trophoblast immediately secretes hCG. hCG is structurally similar to LH โ€” binds LH receptors on corpus luteum โ†’ prevents corpus luteum regression โ†’ corpus luteum continues producing progesterone โ†’ endometrium maintained โ†’ pregnancy continues. Without hCG, corpus luteum would degenerate at day 23-24 โ†’ progesterone falls โ†’ menstruation. hCG peaks at week 8-10, then placenta takes over progesterone production (luteoplacental shift). Pregnancy tests detect ฮฒ-hCG subunit in urine/blood. Detectable as early as 8-10 days post-fertilization. Highest in multiple pregnancy and hydatidiform mole.
hCG function
Rescues corpus luteum โ†’ maintains progesterone โ†’ prevents menstruation.
Peak timing
Peaks weeks 8-10, then falls as placenta takes over. Morning sickness correlates.
Pregnancy test
Detects ฮฒ-hCG. Positive 8-10 days post-fertilization. Quantitative for monitoring.
Molar pregnancy
Hydatidiform mole โ†’ very high hCG. Treated with methotrexate or surgery.
Difficulty: Intermediate
Oxytocin and Labor
Positive feedback โ€” more contractions โ†’ more oxytocin โ†’ more contractions
Oxytocin from posterior pituitary ยท Ferguson reflex ยท Also controls milk letdown
Oxytocin's role in labor โ€” one of the only positive feedback loops in physiology
Oxytocin is produced in the hypothalamus and released from the posterior pituitary. During labor: baby's head presses on cervix โ†’ stretches cervical receptors โ†’ signals hypothalamus โ†’ more oxytocin released โ†’ stronger uterine contractions โ†’ more cervical pressure โ†’ more oxytocin (Ferguson reflex). This positive feedback escalates until delivery. Pitocin (synthetic oxytocin) is used to induce or augment labor. Milk letdown: infant suckling โ†’ sensory signals โ†’ hypothalamus โ†’ oxytocin โ†’ myoepithelial cells around alveoli contract โ†’ milk ejected. Also promotes bonding โ€” the "love hormone."
Ferguson reflex
Cervical stretch โ†’ oxytocin โ†’ contractions โ†’ more stretch โ†’ positive feedback.
Milk letdown
Suckling โ†’ oxytocin โ†’ myoepithelial contraction โ†’ milk ejected into ducts.
Pitocin
Synthetic oxytocin โ€” labor induction or augmentation. Monitor for hyperstimulation.
Bonding
Oxytocin released during touch, sex, breastfeeding โ€” reinforces social bonding.
Difficulty: Intermediate
Prolactin and Lactation
Prolactin makes milk ยท Oxytocin ejects milk ยท Suckling maintains both
Prolactin = milk synthesis ยท Oxytocin = milk ejection ยท Dopamine inhibits prolactin
How lactation works โ€” and why breastfeeding suppresses ovulation
Prolactin from anterior pituitary stimulates milk synthesis in mammary glands. During pregnancy, prolactin rises but milk production is suppressed by high estrogen and progesterone. After delivery, estrogen and progesterone fall โ†’ prolactin uninhibited โ†’ lactation begins. Suckling โ†’ inhibits dopamine (prolactin-inhibiting factor) โ†’ prolactin rises โ†’ milk production. Suckling also triggers oxytocin โ†’ milk letdown. High prolactin suppresses GnRH โ†’ suppresses LH and FSH โ†’ suppresses ovulation โ€” "lactational amenorrhea" (not reliable contraception but reduces fertility). Hyperprolactinemia from pituitary adenoma โ†’ galactorrhea + amenorrhea + infertility.
Dopamine
Prolactin-inhibiting factor. Suckling โ†’ less dopamine โ†’ more prolactin.
Lactational amenorrhea
High prolactin โ†’ suppresses GnRH โ†’ no ovulation. Not reliable contraception.
Hyperprolactinemia
Pituitary adenoma โ†’ galactorrhea + amenorrhea. Treat with bromocriptine (dopamine agonist).
Colostrum
First milk โ€” high in IgA, protein, immune factors. Transitions to mature milk in days 3-5.
Difficulty: Intermediate
Contraception Mechanisms
COC = Stop ovulation ยท IUD = Prevent implantation ยท Barrier = Block sperm
Combined oral contraceptive ยท Intrauterine device ยท Barrier methods
How different contraceptives work โ€” the physiology behind each method
Combined oral contraceptives (estrogen + progestin): suppress GnRH pulsatility โ†’ suppress LH surge โ†’ prevent ovulation. Also thicken cervical mucus. Progestin-only (mini-pill, implant, DMPA): primarily thickens cervical mucus, some suppress ovulation. IUD (copper): copper ions toxic to sperm โ€” prevent fertilization. Also prevents implantation if fertilization occurs. Hormonal IUD (levonorgestrel): thickens mucus, thins endometrium. Emergency contraception (Plan B): high-dose progestin โ†’ delays or prevents ovulation. Does NOT terminate established pregnancy. GnRH agonists: continuous use paradoxically suppresses HPG axis โ€” used for endometriosis, prostate cancer.
COC
Estrogen + progestin โ†’ suppress LH surge โ†’ no ovulation. 99%+ effective.
Copper IUD
Copper toxic to sperm. Most effective emergency contraception (โ‰ค5 days post-intercourse).
Plan B
High-dose levonorgestrel โ†’ delays ovulation. Less effective if already ovulated.
GnRH agonists
Leuprolide โ€” continuous use suppresses HPG. Treat endometriosis, PCa, precocious puberty.
Difficulty: Intermediate