Female Reproductive Function Flashcards
(32 cards)
1
Q
ovarian cycle
A
- series of hormone mediated changes in the ovaries
- culminates in the monthly production of a viable ovum in women of reproductive age
- release ova and produce hormones
2
Q
follicular phase
A
- FSH stimulates development of follicles
- also rising estradiol
- estrogen is in a positive feedback loop that causes more FSH, which leads to true maturation of the follicle
3
Q
ovulatory phase
A
-LH surge causes rupture of Graafian follicle
4
Q
luteal phase
A
- LH converts the ruptured follicle to a corpus luteum
- progesterone (from corpus luteum) and some estradiol
5
Q
corpus luteum
A
-becomes corpus albicans if no fertilization
6
Q
primordial follicle
A
- increases in size during the ovarian cycle
- contains the ovum
- thecal and granulosa cells
- thecal cells feed granulosa cells and are vascularized
- granulosa cells produce estrogen
- other follicles regress
- the antrum has high levels of hormone that sustain the follicle
- graafian follicle gets to 20-33 mm
7
Q
uterine phases
A
- prepare uterus for implantation
- estrogen promotes proliferation of the endometrium and primes uterus for progesterone actions
- progesterone converts the proliferative uterus to a secretory uterus
8
Q
proliferative phase
A
- thickness of endometrium increases from 1-2 mm to 8-10
- comparable to the follicular phase
- dominated by estrogens and is variable in length
9
Q
secretory phase
A
- dominated by progesterone and has a fixed length of 14 days following ovulation
- progesterone promotes accumulation of glycogen, increased glandular secretions, and increased vascularity
- comparable to the luteal phase
10
Q
menstrual phase
A
- associated with prostaglandin mediated vasoconstriction of spiral arteries and local ischemic injury/ inflammation
- associated with the regression of the corpus luteum
11
Q
positive feedback
A
- in late follicular phase
- blood estradiol reaches a high level that initiates positive feedback and a surge in LH and FSH release, provoking ovulation
12
Q
negative feedback
A
- luteal phase
- estradiol, progesterone and inhibin produced by the corpus luteum have negative feedback on gonadotropin release
- no more FSH/LH- no ovulation again
- inhibin from granulosa cell
13
Q
LH
A
- secretion is pulsatile and increases in amplitude in the follicular phase
- high levels of estradiol (late follicular) enhance the sensitivity of the gonadotrophs to GnRH by increasing the number of receptors on gonadotrophs (ant pit)- surge in LH and FSH
14
Q
hypothalamic-pituitary-gonadal axis
A
- small bodied neurons in the arcuate nucleus and pre-optic are of the hypothal secrete GnRH
- increases secretion of FSH and LH
- FSH to granulosa cells-gene transcription and synthesis of relevant enzymes, activins and inhibins
- LH binds to receptors on ovarian thecal cells, stimulates biosynthesis of progestins and androgens
- androgens enter granulosa cells and are converted to estrogens
- granulosa cells also have LH receptors
15
Q
activins and inhibins
A
- negative feedback only on ant pit
- estogens and progestins on both
16
Q
regulation of gonadotropin secretion
A
- binding of GnRH to G protein linked receptor activates the PLC pathway and the release of Ca+ from internal stores
- activated PLC leads to formation of DAG
- DAG stimulates PKC
- PKC phosphorylates targets that indirectly stimulate gene transcription
- FSH and LH are ab dimers the a subunits are identical. the beta subunit determines specificity
- gonadotropins are synthesized, dimerized, and glycosylated in the secretory pathway, regulated by the rhythm of GnRH
- Ca released from internal stores activates CA channels leading to sustained increased CA
- the increased Ca triggers exocytosis and release of gonadotropin
**follicular phase estrogen and activin increase PKC activity, inhibin and luteal phase estrogen and progesterone decrease it
17
Q
estrogens and progesterone
A
- derived from cholesterol
- estradiol and progesterone are the primary forms
- bind loosely to albumin and sex hormone binding globulins (SHBGs)
- exert effects on many tissues in the body including breast, bone, vagina, cervix, fallopian tubes, uterus
- estrogens are inactivated in the liver through conjugation with glucuronic or sulfuric acids and excreted in the urine
- progesterone is rapidly degraded in the liver to steroids with no progestational effect and excreted in the urine
18
Q
two cell, two gonadotropin model
A
- theca cell doesn’t have aromatase activity
- granulosa cell doesn’t have 17a-hydroxylase and 17,20 desmolase activity
- progesterone made in both cells
- turned to androstenedione in theca cell
- then to testosterone and estradiol in granulosa cell
- to estrogen stimulated by FSH (Gs)
- LH increases synthesis of progesterone in granulosa cell in luteal phase (Gs) (estrogen still substantial in luteal phase even though major increase in progesterone)
19
Q
effects of estrogens
A
- proliferation of the uterine endometrial stroma and development of endometrial glands
- proliferation and development of mucosal lining of the fallopian tubes
- stimulation of bone growth by inhibition of osteoclastic activity
- increased fat in the subcutaneous tissue
20
Q
progesterone effects
A
- secretory changes in the uterine endometrium
- decreased frequency and intensity of uterine contractions
- increased fallopian tube secretions
21
Q
puberty
A
-transition to cyclic female reproductive function
22
Q
thelarche
A
breast development
23
Q
adrenarche
A
increased secretions of adrenal androgens
24
Q
menarche
A
menstrual cycles begin
25
estrogens in puberty
- inhibit osteoclasts in bone, promoting rapid growth, followed by uniting of epiphysis with the shaft of a long bones to stop growth
- promote deposition of fate, development of stromal tissue and ductile growth in breasts
- promote deposition of fat in subQ tissue
- progesterone promotes development of lobules and alveoli in breasts
26
before puberty
- release of gonadotropins is inhibited by low amounts of sex steroids
- negative feedback sensitivity is high
- lose sensitivity as you become an adult
- higher levels of steroid hormones in an adult
- GnRH pulses first at night and then during the day
27
menopause
- cyclic reproductive function and menstruation cease
- average age is 51-52 years but can occur earlier
- virtually no remaining ovarian follicles
- levels of circulating sex steroids decrease (some peripheral conversion- adrenal)
- levels of circulating gonadotrophins rise
- a variety of physical and mental changes occur
28
changes during menopause
- vasomotor instability
- hot flashes
- night sweats
- mood changes
- short term memory loss
- sleep disturbances
- headaches
- loss of libido
- atrophy of the vaginal epithelium
- changes in vaginal pH
- decrease in vaginal secretions
- decrease in circulation of vagina and uterus
- pelvic relaxation
- loss of vaginal tone
- cardiovascular disease, osteoporosis, alzheimers
29
menopause 2
- no remaining ovarian follicles to respond to FSH and LH
- decline in steroid hormone production
- 6-7 million germ cells to 1-2 to 400,000
- 400 released during reproductive life
- ongoing atresia of cells-loss of follicles
30
reduced estrogen production
- leads to increased gonadotropin production in menopausal women
- no inhibition of GnRH, high LH and FSH, but no estrogen
- loss of negative feedback
31
estrone
- muscle and adipose tissue
- derived primarily from androstenedione in the adrenal gland provides a postmenopausal source of estrogen-estrone
- 15-25% as potent estradiol
- since many of the symptoms of menopause due to estrogen deficiency, the functionally of system accounts in the part for the observation that some women are less disturbed by menopause
32
estrogens and menopause
- prevent bone resorption
- decreased circulating estrogens after menopause places many woman at increased risk for osteoporosis and fractures
- compression fractures in the vertebrae lead to a loss of height, spinal deformity, and back pain
- healthy diet, vitamin D, weight bearing exercise
