Note: The DC Dutta Textbook of Gynecology is not in this library's collection. The closest authoritative gynecology textbook available is Berek & Novak's Gynecology, which covers the same material at the same depth and is widely used alongside DC Dutta. The content below is drawn from Berek & Novak's Gynecology and Guyton & Hall Textbook of Medical Physiology, and matches the DC Dutta chapter structure closely.

The Menstrual Cycle

Overview

1. Hypothalamus - secretes GnRH (pulsatile)
2. Anterior pituitary - secretes FSH and LH
3. Ovary - produces follicles, ovulates, forms corpus luteum; secretes estrogen and progesterone
4. Uterus (endometrium) - responds to ovarian hormones cyclically

The Menstrual Cycle Diagram

Hormonal Cycle

1. Neuroendocrine Control (Hypothalamo-Pituitary Axis)

Hypothalamus

• Secretes GnRH (Gonadotropin-Releasing Hormone) in a pulsatile fashion from the arcuate nucleus
• GnRH simultaneously controls both LH and FSH secretion from the pituitary
• The pulse frequency determines the relative amounts of LH vs FSH secreted
• Feedback loops operate at three levels:
  • Long loop: Circulating ovarian hormones (estrogen, progesterone) feed back to the hypothalamus
  • Short loop: Pituitary hormones feed back to the hypothalamus
  • Ultrashort loop: Hypothalamic secretions feed back to the hypothalamus itself

Pituitary Gonadotropins

• FSH (Follicle-Stimulating Hormone): A glycoprotein. Rises early in the follicular phase; stimulates follicular growth and estrogen production. A secondary mid-cycle FSH surge occurs at ovulation.
• LH (Luteinizing Hormone): A glycoprotein. Low in the follicular phase; the dramatic mid-cycle LH surge (peaking ~Day 13-14) triggers ovulation 24-36 hours later and then stimulates corpus luteum formation.

2. Ovarian Cycle

A. Follicular Phase (Days 1-14)

• Low estrogen, low inhibin at the end of the previous cycle allows FSH to rise
• FSH recruits a cohort of primordial/primary follicles to grow
• Follicles undergo: primordial -> primary -> secondary -> antral (Graafian) follicle
• Granulosa cells (FSH-responsive) produce estradiol via the two-cell, two-gonadotropin model:
  • LH acts on theca cells to produce androgens (androstenedione, testosterone)
  • FSH acts on granulosa cells to aromatize androgens into estradiol

• One follicle becomes dominant (the others undergo atresia)
• The dominant follicle produces increasing estradiol
• Rising estradiol exerts negative feedback on FSH (reducing FSH for other follicles) but positive feedback on LH once estradiol exceeds ~200 pg/mL for 48 hours

• Estradiol peaks just before ovulation (Day 12-13)
• This triggers the LH surge (positive feedback) - LH levels spike 10-fold

B. Ovulation (Day 14 in a 28-day cycle)

• The LH surge is the proximate cause of ovulation, occurring 24-36 hours after the surge begins
• LH causes resumption of meiosis I in the oocyte (which was arrested in prophase I since fetal life)
• The follicle ruptures and releases the secondary oocyte (arrested in metaphase II, awaiting fertilization)
• Ovulation is accompanied by a mid-cycle FSH peak and a small secondary estradiol peak

C. Luteal Phase (Days 14-28)

• After ovulation, the ruptured follicle undergoes luteinization to form the corpus luteum
• The corpus luteum secretes progesterone (primary) and estradiol (secondary)
• Progesterone peaks ~Day 21 (midluteal phase)
• Both progesterone and estrogen (plus inhibin A) act centrally to suppress FSH and LH, preventing new follicular recruitment
• The corpus luteum has a fixed lifespan of 14 days
• If no pregnancy: the corpus luteum involutes -> progesterone and estrogen fall -> menstruation
• If pregnancy: hCG from the trophoblast rescues the corpus luteum (luteotrophic effect)

3. Endometrial (Uterine) Cycle

• Stratum compactum (superficial compact zone)
• Stratum spongiosum (intermediate zone)
• Stratum basalis (deep basal layer - not shed; source of regeneration)

A. Menstrual Phase (Days 1-4)

• Fall in progesterone and estrogen causes vasospasm of spiral arteries (prostaglandin-mediated) -> ischemia -> necrosis -> shedding of the functionalis
• Normal menstrual blood loss: 30-80 mL over 3-7 days
• Menstrual blood is largely defibrinated (due to fibrinolysis in the endometrium) and does not clot normally

B. Proliferative Phase (Days 5-13) - Estrogen-Dominant

• Driven by rising estradiol from the developing follicle
• Endometrium regenerates from the basalis; surface reepithelialized within 4-7 days of menstruation
• Glands: straight, tubular, narrow, lined by columnar epithelium with mitoses
• Stroma: compact, mitotically active
• Blood vessels: straight
• Endometrial thickness increases from ~2 mm post-menses to 3-5 mm at ovulation
• Cervical mucus: thin, watery, forms ferning pattern; shows spinnbarkeit (stretchability up to 6-8 cm)
• Vaginal epithelium: proliferates under estrogen influence

C. Secretory Phase (Days 15-28) - Progesterone-Dominant

• Days 16-17: Subnuclear vacuoles appear in glandular cells (first sign of progesterone effect)
• Days 18-19: Vacuoles move to supranuclear position; secretion into gland lumen
• Days 20-22: Peak secretory activity; glands become tortuous (saw-tooth/corkscrew), filled with glycogen and mucin - "uterine milk" for nourishing the pre-implantation embryo
• Days 22-24: Stromal edema peaks; stromal predecidual change begins around spiral arteries
• Days 25-26: Predecidual reaction spreads throughout stroma
• Days 26-28: Stromal breakdown begins; infiltration by neutrophils
• At peak secretory phase (~Day 21): endometrium is 5-6 mm thick

D. Ischemic Phase (just before Day 1 - sometimes listed separately)

• Corpus luteum degenerates -> progesterone and estrogen fall
• Spiral arteries go into intermittent vasospasm
• Prostaglandins (PGF2α especially) cause vasoconstriction and myometrial contractions
• Endometrium becomes ischemic -> necrosis -> menstruation begins

4. Cervical Cycle (Cyclic Changes of Cervix)

5. Vaginal Cycle

• Proliferative (follicular) phase: Estrogen causes proliferation and superficial cell maturation; cells are large, acidophilic, with pyknotic nuclei; karyopyknotic index rises
• Secretory (luteal) phase: Progesterone causes folding and clumping of cells; intermediate cells predominate; navicular cells appear
• Vaginal cytology (Papanicolaou smear) can be used to estimate hormonal status

6. Summary of Hormonal Events - Berek & Novak's 8-Point Summary

1. FSH rises in early follicular phase (due to low inhibin/estrogen from previous cycle) and stimulates follicular development
2. Developing follicles produce increasing estradiol via the two-cell/two-gonadotropin model
3. Rising estradiol initially exerts negative feedback on FSH, causing only the dominant follicle (most FSH-sensitive) to survive
4. High sustained estradiol switches to positive feedback, triggering the LH surge at Day 13
5. The LH surge causes ovulation 24-36 hours later, and progesterone begins to rise
6. After ovulation, estradiol dips briefly then rises again from the corpus luteum; inhibin A rises
7. Progesterone rises steeply after ovulation (confirmatory of ovulation if >3 ng/mL on Day 21)
8. Progesterone + estrogen + inhibin A suppress FSH and LH through the luteal phase; their decline with corpus luteum regression triggers the next cycle

Normal Parameters of Menstruation (DC Dutta values)

Key Points (Exam-Relevant)

• The LH surge occurs 24-36 hours before ovulation and is the most reliable marker of impending ovulation
• Progesterone causes a 0.2-0.5°C rise in basal body temperature (BBT) after ovulation - used in natural family planning
• The luteal phase is fixed at 14 days; variability in cycle length is due to variation in the follicular phase
• Progesterone causes: secretory endometrium, thick cervical mucus, raised BBT, breast tenderness, and inhibition of smooth muscle (uterotonic)
• Inhibin B is a marker of ovarian reserve (high early follicular phase)
• The endometrial glands of the secretory phase contain glycogen vacuoles - first subnuclear (Days 16-17), then supranuclear (Days 18-19)