Female Physiology
Erection
erection takes more time than in males
a more complex process that involves psychological, emotional, and social factors in addition to physiological events
does not require a refactory period
sexual arousal leads to increased blood flow
engorgement of clitoral cavernosa and labia
increased interacavernous pressure causes tumenscence, protusion of glans clitoris, and eversion of labia minora
arousal causes vestibular glands to produce lubricating mucus and antimircobial fluids
also causes vaginal smooth muscle to relax
regulated by both the PNS and CNS
coordination of brain activity, spinal cord reflexes, and PNS neurotransmitter release
nitric oxide plays a role as in male erection
relaxes smooth muscles to increase blood flow, lubrication, and sensitivity; helps release oxytocin
lack of NO linked to menopause/vascular dysfunction
decreased lubrication, increased discomfort, and/or difficulty achieving orgasm
vasoactive intestinal peptide (VIP) enhances vaginal blood flow, lubrication and secretions
sacral segments of the spinal cord serve as reflex centers for erection
pudendal nerve sends sensory feedback from the clitoris and vagina to the brain
hypothalamus, visual cortex, olfactory cortex, and other regions of the brain process stimuli and send signals down the spinal cord
parasympathetics from pelvic nerve cause vasodilation allowing lubrication and clitoral engorgement (arousal)
sympathetics from hypogastric nerve involved in initial arousal and in orgasm
response manifests as engorgement and swelling of genital tissues (especially the clitoris), increased vaginal wall compliance, and production of secretions
results from increases in blood flow to the clitoris, vagnia, and labia
regulated by vascular smooth muscle tone of erectile tissues and assiociated blood vessels
emissary veins and a subtunical venous plexus as in males
relaxation of the tunica albuginea allows blood to drain via these vein networks
Sex Hormones
gonadotropin-releasing hormone
stimulates secretion of LH and FSH
luteninizing hormone
triggers ovulation and supports pregnancy
follicle-stimulating hormone
stimulates ovarian follicles to secrete estrogens, progesterones, and androgens
suppressed by inhibin
progesterone
prepares uterus for possible pregnancy
androgens (DHEAS, DHEA, DHT, androstenedione, and testosterone)
low levels until after menopause, then ovaries primarily secrete androgens
estrogens (primarily estradiol)
comes from androstenedione
triggers many changes during puberty
involved in development and function of reproduction system - vital in ovarian cycle
Oogenesis
female germ cells arise from the yolk sac
colonize gonadal ridges in 5-6 weeks od embryonic development → differentiate and multiply → become primary oocytes
development arrests until adolescence
divide into secondary oocytes and polar body
secondary oocyte proceeds to metaphase II, then arrests until after ovulation
completes meiosis II (if fertilized) or dies
polar bodies cast off/disintegrate
Folliculogenesis
primordial follicles contain the primary oocyte
features a single layer of squamous granulosa cells and is a dormant stage prior to birth
primary follicles form during ovarian follicle activation as granulosa cells become cuboidal in shape and oocytes are activated
develop receptors for FSH and the zona pellucida (surrounds oocyte; separates from the granulosa cells)
secondary follicles have muliple layers of granulosa cells and feature theca cells
theca cells surrounds the outer most layer and differentiate into the theca externa and theca interna and capillaries form between them
tertiary follicles feature fluid-filled cavities called antra (sing. antrum) and grow in size dependent upon the availablity of FSH
granulosa cells differentiate into subtypes that behave differently in response to FSH
theca cells developreceptors for luteinizing hormone (LH) and start producing androgens in response to LH
follicle burst to release oocytes during ovulation
ruptured follicles transform into the corpus luteum, which secretes progesterone and some estrogen
if the egg is fertilized, corpus luteum becomes corpus luteum gravidiatis to support implantation and early embryogenesis
if egg isnt fertilized, the corpus luteum degenerates after ~10 days and becomes the corpus albicans (scar tissue)
Ovarian Cycle
occurs monthly unless pregnant
averages 28 days (varies from 20-45 days)
occurs in the ovaries (3 phases)
follicular phase, ovulation, and luteal phase
follicular phase (~2 weeks)
mentruation during the first 3-5 days
shedding of uterine lining
uterus replaces lost tissue via mitosis
FSH stimulates follicles to grow
follicles secrete estradil
dominant follicle becomes increasingly senstive to FSH, LH, and estradiol
becomes the preovulatory follicle
other antral follicle degenerate (atresia)
later in the phase, LH spikes
induces primary oocyte to complete meiosis I
causes follicular fluids to rapidly build up
triggers WBCs to weaken follicle wall
follicle detaches and releases chemicals that encourage the uterine tube to move closer and surround the follicle
ovulation (around day 14)
mature follicle swells, then ruptures ad releases egg into the abdominal cavoty
fimbriae sweep over burst follicle to pick up secondary oocyte and move into the uterine tube
muscle contractions of the tube push the secondary oocyte towards the uterus
if encounters sperm → fertilization
if doesnt encounter sperm → reabsorbed
luteal phase (~ 2 weeks; day 15-28)
starts after ovulation and ends when mentruation begins (unless pregnant)
remainder of the dominant follicle becomes the corpus luteum
produces progesterone and some estrogen
prepares the uterus for pregnancy
thickens uterine linging (progesterone)
thickens cervical mucus to prevent bacteria
if a fertilized ovum impants, it will start secreting human chorioonic gonadotropin (HCG) to keep the corpus luteum functioning
if not pregnant:
hormone levels decline
negative feedback on pituitary
corpus luteum shrinks around day 22-26
ceases functioning and becomes known as the corpus albicans
uterine lining shed during mentrual cycle
marks the end of the luteal phase
Mentrual Cycle
occurs in the uterus concurrently with the ovarian cycle
involves menstuation, which occurs during the follicular phase (following the luteal phase)
buildup, breakdown, and vaginal discharge of the endometrium (4 phases)
begins during puberty and lasts until menopause
four phases of the mentrual cycle:
proliferative phase → rebuilding of the endometrium stimulated by estrogen
secretory phase → progesterone stimulates thickening of the endometrium
premenstrual phase → endometrial degeneration
menstual phase → discharge of endometrium and menstrual fluids
fibrinolysin prevents clotting in this phase
Puberty
puberty - period in which adolescents reach sexual maturity
secondary sex characteristics develop externally as the breasts, ovaries, uterus, and vagina mature
enlarging breasts, widening hips, growth of pubic and axillary hair, and general growth spurt
regulated by LH and FSH
levels increase in early puberty
regulate GH secretion
starts earlier and peaks sooner in girls
occurs in the same stages as males
onset influenced by:
genetics/epigenetics
mother’s onset is a strong predictor
smoking while pregnant can lead to early onset
nutrition/general health
better nutrition/health typically earlier onset
leptin stimulates GnRH
obese onset earlier
underweight onset later
stress suc as a family conflicts tied to earlier onset
Menopause
typically occurs around age 51 or 52
5% of women with early menopause between ages of 40 and 45
1% of women experience premature menopause before age 40
perimenopause occurs prior to the onset of menopause (often between 40 and 44)
ovaries gradually begin producing less estrogen, but kepp releasing oocytes until menopause begins
typically lasts about 4 years
some women continue experiencing symptoms post-menopause
loss of function in the ovarian follicles and subsequent decline in estrogen levels
diminished number of primary follicles leaves nothing to respond to FSH
LH surges cease → no ovulation → less estrogen produced → cessation of menes
less estradiol and inhibn disrupts negative feedback to the hypothalamus → increase in production of FSH and LH
loss of estrogen affects many systems:
ovaries, breasts, and mucosal layer of the vagina may being to atrophy
dry/itchy vagina, stress incontinence or increased frequency/urgency with urination, dyspareunia (painful intercourse), dysuria (painful urination)
increased osteoclastic activity → loss of bone mass and decrease in height
induces vasoconstriction, increased rigidity for arteries, and increases LDL levels
hot flashes, night sweats, heart palpitations, elevated bp, weight gain, migraines, and mood/sleep disturbances
various supports treatments
short term hormone therapies such as combination estrogen/progestin (if uterus is healthy) or estrogen alone (if no uterus because may incluce cancer)
selective estrogen receptors modulators (“SERMs”) to moduate estrogen without stimulating endometrial growth (cancer risk)
non-hormone short-term treatments such as SSRIs or gabapentin
treatments for osteoporosis, such as osteoclastic activity disrupters, ca/vitamin D supplements, and increasing intake of estrogen-related foods (e.g soy)
treatments for vasomotor symptoms, such as vitamin E and olmega-3 fatty acid supplements