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Estrogen is secreted mainly by the dominant follicle during the follicular phase, not by the corpus luteum. The follicular phase precedes ovulation, and the corpus luteum forms after ovulation.

The ovum is released by the ruptured follicle due to the LH surge, not by the corpus luteum. The corpus luteum forms after ovulation and plays no direct role in ovum release.

GnRH is secreted by the hypothalamus and regulated by sex steroid feedback. The corpus luteum does not stimulate GnRH; in fact, progesterone from the corpus luteum inhibits it.

The follicular phase follows menstruation and involves regeneration of the endometrium under the influence of rising estrogen levels from developing follicles.

Ovulation is the release of an ovum due to the LH surge, around day 14. The endometrium is not shed during this phase; it continues to thicken in preparation for implantation.

The luteal phase occurs after ovulation and is marked by progesterone secretion from the corpus luteum to maintain the endometrium. Shedding occurs only if implantation does not happen.

Ovulation is triggered by a surge in LH, not directly by estrogen. Estrogen contributes indirectly by reaching a threshold that induces the LH surge, but it does not trigger ovulation by itself.

Maintenance of the corpus luteum is supported by LH and, if pregnancy occurs, human chorionic gonadotropin (hCG). Estrogen does not sustain corpus luteum function.

Estrogen initially inhibits FSH secretion via negative feedback, but this is not its primary role. Its main function is endometrial proliferation and preparing the body for ovulation.

Progesterone secretion continues only if fertilization occurs and hCG is produced by the trophoblast. Without hCG, the corpus luteum involutes and stops secreting hormones.

The corpus luteum forms after ovulation; it does not trigger it. Ovulation is triggered by the LH surge prior to corpus luteum formation.

The corpus luteum secretes some estrogen, but its primary function is progesterone production. After degeneration, it no longer produces either hormone in significant amounts.

The menstrual phase coincides with the early follicular phase, not the luteal phase. It involves shedding of the functional layer of the endometrium due to hormone withdrawal.

The proliferative phase occurs during the follicular phase of the ovarian cycle. It is estrogen-driven and involves rebuilding the endometrium after menstruation.

The regenerative phase is not a standard term in the clinical classification of the endometrial cycle. The correct phases are menstrual, proliferative, and secretory.

A duration of 1–3 days is shorter than the normal range and may indicate hypomenorrhea or hormonal insufficiency, though still considered normal if consistent and asymptomatic.

Bleeding for 7–10 days exceeds the upper normal limit and may suggest menorrhagia or coagulation abnormalities, requiring evaluation.

A menstrual duration of 10–14 days is abnormal and often pathological. It may suggest hormonal imbalance, fibroids, endometrial hyperplasia, or bleeding disorders.

Estrogen plays a primary role in the proliferative phase, promoting regeneration of the endometrium but not in its secretory transformation. It works before ovulation, not after.

FSH stimulates follicular development and estrogen secretion during the follicular phase, but it does not act on the endometrium directly and is not dominant in the luteal/secretory phase.

LH triggers ovulation and supports the formation of the corpus luteum, which secretes progesterone, but LH itself does not directly act on the endometrium during the secretory phase.

Ovulation typically occurs around day 14 of a 28-day cycle, not at the beginning. It is a mid-cycle event and not used as the starting point for cycle calculation.

The last day of menstruation varies among individuals and does not consistently mark the start of a new hormonal cycle, making it an unreliable reference point.

The LH surge precedes ovulation by 24–36 hours and occurs around day 13–14, mid-cycle. It is not the beginning of the menstrual cycle and occurs much later than day 1.

hCG does not stimulate new follicle development. In fact, high progesterone and estrogen levels maintained by the corpus luteum inhibit FSH, preventing new folliculogenesis during early pregnancy.

hCG prevents menstruation by maintaining the corpus luteum and its hormone output. Menstruation is triggered by progesterone withdrawal, which hCG directly prevents.

hCG supports the continued production of progesterone, not its inhibition. It ensures the endometrial lining remains intact until the placenta takes over hormone production around week 10–12.

Progesterone exerts only negative feedback on GnRH, FSH, and LH throughout the cycle, especially during the luteal phase. It does not cause the LH surge and actually prevents further ovulation.

FSH is regulated by negative feedback via estrogen and inhibin. It does not trigger the LH surge and is not part of the positive feedback loop leading to ovulation.

Inhibin is secreted by granulosa cells and specifically suppresses FSH release via negative feedback. It plays no role in triggering the LH surge or stimulating GnRH.