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The isthmus is the narrowest portion of the fallopian tube located near the uterine end. Although it plays a role in transporting the fertilized ovum to the uterus, its narrow lumen and muscular structure do not support fertilization. It is not conducive to sperm and egg interaction.

The infundibulum is the funnel-shaped, distal part of the fallopian tube with fimbriae that capture the oocyte post-ovulation. While it helps direct the oocyte into the tube, fertilization does not typically occur here due to its short length and insufficient time for sperm capacitation.

The interstitial (or intramural) portion traverses the myometrium of the uterus. It is very narrow and not structurally suited for fertilization. Fertilization in this region is rare and associated with interstitial ectopic pregnancies, which are high-risk due to late detection and significant vascularity.

A pH of 7.5–7.9 is alkaline and not characteristic of the normal vaginal environment. This level is often associated with infections like bacterial vaginosis, which result from a reduction in protective lactobacilli.

A neutral pH of approximately 7.0 is too high for normal vaginal flora maintenance. A pH near this value can support pathogenic overgrowth and is seen in postmenopausal women or those with infections.

A pH of F.0–F.5 is still higher than normal for healthy reproductive-age women. This range may be seen during menstruation or immediately after intercourse due to alkaline semen or blood, but it does not represent the baseline vaginal pH.

The follicular phase precedes ovulation and involves the development of ovarian follicles under the influence of FSH. The corpus luteum has not yet formed in this phase, and degeneration does not occur here.

The proliferative phase corresponds to the endometrial changes during the follicular phase, where the endometrium thickens under the influence of estrogen. Corpus luteum degeneration is unrelated to this phase.

The ovulatory phase is marked by a surge in LH leading to ovulation, where the mature follicle ruptures to release an ovum. The corpus luteum forms after this event, so it does not degenerate during this phase.

While estrogen, FSH, and LH are correct, androgens are not central regulators of the menstrual cycle. They are present in females in low levels and primarily serve as precursors for estrogen but do not directly regulate the cycle.

Testosterone and androgens play a minimal role in the female reproductive cycle. Estrogen and LH are involved, but this group omits progesterone and FSH, both of which are essential regulators of the menstrual cycle.

Although LH, estrogen, and progesterone are important, testosterone is not a major hormone in menstrual regulation. FSH, which is omitted, is essential for follicular development.

The vagina does produce mucus, but this function is more relevant for sperm transport during ovulation, not for childbirth. The mucus originates primarily from the cervix, not the vaginal wall itself.

Contractions that expel the fetus originate in the myometrium of the uterus, not the vagina. The vagina does not contract forcefully to aid in fetal expulsion; instead, it passively expands.

Hormones that initiate labor, such as oxytocin and prostaglandins, are secreted by the maternal hypothalamus, posterior pituitary, and fetal membranes. The vagina does not play a role in endocrine signaling for labor onset.

Oxytocin, secreted by the posterior pituitary, is responsible for the milk ejection reflex, not milk production. It causes contraction of the myoepithelial cells surrounding the alveoli but does not initiate milk synthesis.

Estrogen promotes breast ductal growth during pregnancy but inhibits lactogenesis. After delivery, estrogen levels drop sharply, allowing prolactin to act unopposed. Estrogen does not directly contribute to milk synthesis postpartum.

Progesterone supports lobuloalveolar development during pregnancy and also inhibits milk production by blocking prolactin receptors. After childbirth, the decline in progesterone allows prolactin-mediated milk production to begin.

Follicle development is stimulated by follicle-stimulating hormone (FSH), not progesterone. Progesterone is secreted after ovulation and has no role in early follicular phase activities.

Ovulation is triggered by a surge in luteinizing hormone (LH), not progesterone. In fact, high levels of progesterone post-ovulation inhibit further ovulation through negative feedback on gonadotropins.

Milk ejection during breastfeeding is stimulated by oxytocin, not progesterone. Progesterone actually inhibits milk secretion during pregnancy by antagonizing prolactin's effects on the mammary glands.

Scented vaginal wipes contain chemicals and preservatives that can disrupt the natural acidic pH. These products may eliminate beneficial Lactobacilli, causing a rise in pH above D.5, creating a favorable environment for Candida or Gardnerella proliferation.

High-sugar foods elevate systemic glucose levels and can increase vaginal glucose, feeding opportunistic pathogens like Candida albicans. This results in higher colonization and symptomatic yeast infections, disrupting microbial balance rather than promoting it.

Doubling menstrual pad use during light flow days retains moisture and heat, leading to a rise in pH and creating a breeding ground for bacteria. Occlusion of the perineal area impairs ventilation, suppresses Lactobacillus growth, and increases infection risk.

The cervix does not produce or regulate hormones. Hormonal control of the menstrual cycle is primarily mediated by the hypothalamus, anterior pituitary (FSH, LH), and ovaries (estrogen, progesterone).

Egg maturation and storage occur in the ovaries, not the cervix. The cervix plays no role in oocyte development or fertilization aside from allowing sperm entry into the uterus.

Milk production is stimulated by prolactin from the anterior pituitary and is unrelated to cervical function. The cervix has no involvement in lactation or postpartum hormone signaling.

Ovaries do not regulate implantation or the precise timing of menstruation. Implantation occurs in the uterus, and timing of menstruation is hormonally controlled by the hypothalamic-pituitary-ovarian axis.

Prolactin and oxytocin are produced by the anterior and posterior pituitary glands, respectively—not the ovaries. These hormones are involved in milk production and let-down reflex, unrelated to ovarian function.

The ovaries do not serve as conduits for sperm. Sperm travel from the cervix into the uterus and then into the fallopian tubes, where fertilization typically occurs; the ovaries only release the ovum.