Summary of Polycystic ovary syndrome
Transcript for Polycystic ovary syndrome
Polycystic ovary syndrome
In polycystic ovary syndrome, “poly” means many, and “cystic” refers to cysts.
So you might think that having many ovarian cysts is a crucial part of polycystic ovary syndrome.
But while some people with polycystic ovarian syndrome do have ovarian cysts, ovarian cysts are no longer a necessary characteristic of the condition.
Instead, polycystic ovary syndrome is a dysfunction in the hypothalamic-pituitary-ovarian axis, which are the hormones that regulate the menstrual cycle.
During the follicular phase, the hypothalamus secretes gonadotropin-releasing hormone, or GnRH.
GnRH makes the anterior pituitary gland secrete two other hormones, called gonadotropins, in roughly equal amounts, which it releases in pulses.
One of these gonadotropins is the luteinizing hormone, or LH.
The other is the follicle-stimulating hormone, or FSH.
LH and FSH travel to the follicles in the ovaries.
The follicles are small clusters of theca and granulosa cells that protect the developing oocyte, or egg.
The theca cells develop LH receptors which allow them to bind LH, and in response they secrete a hormone called androstenedione.
Granulosa cells develop FSH receptors, which allow them to bind to FSH and produce an enzyme called aromatase, which converts the androstenedione into 17β-estradiol - a member of the estrogen family.
As follicles grow, the level of 17β-estradiol in the blood increases, and it acts as a negative feedback signal – that is, it tells the pituitary to secrete less FSH.
Less FSH in the blood means there’s only enough to stimulate one follicle.
The follicle that has the most FSH receptors grows the quickest, and becomes the dominant follicle.
At this point, about midway through the follicular phase, the granulosa cells also begin to develop LH receptors.
As that happens, the dominant follicle keeps secreting estrogen, and the rising estrogen levels make the pituitary more sensitive to the pulsatile action of GnRH from the hypothalamus.
Blood estrogen levels start to climb, and now the estrogen from the dominant follicle becomes a positive feedback signal – that is, it makes the pituitary secrete a whole lot of FSH and LH in response to GnRH.
This happens a day or two before ovulation, and the massive surge of FSH and LH binds to the granulosa and theca cells which help facilitate rupture of the ovarian follicle and release of the oocyte.
While the rest theca and granulosa cells degenerate and die off, a now fully-matured oocyte breaks away from the dominant follicle, and pops out of the ovary.
The egg begins its journey down the fallopian tube to the uterus. The luteal phase has begun.
While polycystic ovary syndrome affects the whole menstrual cycle, it really starts with a breakdown in this follicular phase.
In polycystic ovarian syndrome, the anterior pituitary makes too much LH, at least double the amount as FSH.
Excessive LH causes the theca cells to produce excess amounts of androstenedione, way too much for those granulosa cells to convert.