The consequences of estrogen loss affect all estrogen target organs, including the genitalia, bladder, and brain.
Longer-term consequences of estrogen loss include impaired cognitive function, wound healing, and immune system function.
Hormone replacement therapy is widely used to manage both short- and longer-term consequences of menopause.
Estrogen is a potent anti-inflammatory agent, and its loss can impair the immune system.
Short-term consequences of estrogen loss include vasomotor symptoms such as hot flashes and night sweats, which are attributed to fluctuations in estrogen levels.
Exogenous control of the HPO axis allows for timed ovulation and egg collection in preparation for procedures such as IVF.
Bone density decreases with age and is pronounced in post-menopausal women.
A range of pharmacological approaches are used to manage female fertility, depending on the diagnosed/suspected causes of fertility.
Coagulation factors control blood loss locally.
Exogenous estrogen and progesterone inhibit HPO (higher doses of progesterone alone can also inhibit HPO).
Withdrawal of sex steroids at the end of the luteal phase leads to the release of prostaglandins, vasoconstriction, tissue hypoxia, connective tissue breakdown, and fragmentation.
These lesions continue to cycle under hormonal control, but are not lost at menstruation.
In males, negative feedback only by androgens occurs on GnRH, FSH, and LH.
GnRH agonists and antagonists are both used in ART to shut down ovary, in advance of controlled cycle.
Female infertility/subfertility can be caused by anovulation, endocrine disorders (PCOS), uterine receptivity, and reduced oocyte quality.
Progesterone counters the proliferative effects of estrogen during the secretory phase.
Exogenous progesterone in ART has multiple actions in preventing pregnancy, including thickening of cervical mucus, thinning of endometrial lining, and inhibiting ovulation.
Ectopic growth of endometriosis occurs due to 'reflux menstruation', where endometrial tissue fragments shed at menses pass through the Fallopian tube, then become established in ectopic sites.
Some endometriosis cannot be explained by reflux menstruation, and may arise de novo from progenitor cells in ectopic tissues.
In females, positive and negative feedback by estrogen occurs on GnRH, FSH, and LH.
The secretory phase is characterized by continued growth of glands and blood vessels and secretion of glycogen-rich fluids, in preparation for potential embryo implantation, primarily promoted by progesterone.
Menstruation is the shedding of the superficial layer (functionalis) of the endometrium.
Endometriosis is the establishment and growth of endometrial tissue outside the uterus.
Proliferation is the growth of endometrial glands and blood vessels in response to the increase in estrogen.
Suppression of HPO in ART can be achieved by GnRH agonists and antagonists, or by inhibiting the hypothalamic-pituitary feedback systems.
Family history is a risk factor for endometriosis.
Contraception via HPO inhibition in ART can be achieved by exogenous estrogen and progesterone, or by disrupting the endometrium.
Menstruation is the shedding of the uterine lining due to the decrease in estrogen and progesterone.
The hypothalamic-pituitary feedback systems are regulated differently in males and females.
Ovaries are connected to the uterus by Fallopian tubes.
Fimbriae, at the end of the Fallopian tube, capture the oocytes.
The ampulla is where the oocyte gets fertilised in the Fallopian tube.
The menstrual cycle involves differences between anterior pituitary hormones FSH and LH, as well as cyclical variations in oestrogen, progesterone, and ovarian cycle.
Each month, the development of a mature follicle undergoes ovulation, releasing an oocyte for potential fertilisation and pregnancy.
The uterine cycle changes in the uterine endometrium lining across the course of the menstrual cycle.
Follicular phase in the ovarian cycle is followed by luteal phase, after ovulation.
In the developing follicles, cells proliferate and differentiate into granulosa cells that surround the oocyte.
Secretion of non-cellular material from granulosa cells forms the zona pellucida.
Ovarian stromal cells are recruited in response to factors secreted by primary follicle to become theca cells.
Dominant follicle is selected by day 7 to complete maturation, containing the oocyte that will be released at ovulation.