KEY NOTES WK 1 Flashcards
round ligament attachment
ovarian ligament and down to mons pubis and labia major
broad ligament
double layer peritoneum surrounding most other ligaments (cardinal, uterosacral, round, ovarian)
uterus position
anteverted (lie over bladder)h and ante flexed (angle at cervix)
ligaments to maintain anteverted and ante flexed uterus
cardinal and uterosacral ligaments
function for cortex and medulla of ovaries
cortex= follicles found
medulla= CT and blood vessels
opening of uterine tube to ovary is called and is lined with
and opening of uterine tube to uterus
infundibulum lined by fimbriae (fingers to draw oocytes in)
isthmus
where does fertilization occur
ampulla of uterine tube
cells of fallopian tube
cilia
peg cells (secrete glycoproteins to nourish and protect sperm and oocyte)
2 mucosal layers of the uterus
basal layer: not shed during menses, gives rise to functional layer
functional layer: shed, has spiral arteries and tortuous glands
spiral arteries in uterus are sensitive to
progesterone
progesterone withdrawal at end of cycle –> constrict and ischemia of functional layer or endometrium
transformation zone of the cervix
columnar –> stratified squamous (mouth of external os)
cervix differs from uterus
no spiral arteries or myometrium
vagina lacks
glands (moisture via cervical glands)
thickness of vaginal epithelium via
estrogen
external part of clitoris with nerve endings
glans clitoris (union of both corpora caverns)
body of clitoris (corpora caverns) is surrounded by what muscle
ischiocavernous muscle
enhance blood flow to clit and engorge
muscle surrounding vestibular organs and secrete fluid from vestibular gland for engorgement of bulboclitoral erectile organ
bulbosponguisum muscle
vestibular glands aka and function
bartholin glands (in labia minora)
release mucus to lubricate vestibule during sex
mechanisms behind PCOS
- Inappropriate gonadotropin secretion
- Insulin resistance with hyperinsulinemia
- Excessive androgen production
GhRH pulsatility and LH:FSH ratio in PCOS
increase puslatility leads to high LH:FSH ratio
LH stimulates androgen production
in PCOS the altered gonadotropic prevents a ____ from devleoping
pdominant follicle (bc premature LH secretion)
no luteal phase and no progesterone; estrogen is unopposed
more androgens and estrogen in periphery in PCOS
decrease SHBG that bind androgens (from insulin resistance)
adipose tissue makes estrogen (chronically high throughout cycle)
anovulation in PCOS (infertility)
from GnRH altered pulsatility
androgens make many antral follicles (that aren’t maturing for ovulation- would do follicular atresia if dominant follicle developed)
metformin can help oligoovulation (insulin resistance)
altered menses in PCOS
amenorrhea, oligomenorrhea and heavy menstrual bleeding (leading to iron-deficiency anemia)
chronic unopposed estrogen thickens endometrium (too much?) and leads to unpredictable bleeding
oligo vs amenorrhea
oligo: <9 menses/year
amen: no menses for 3+ months
menstural intervals
Menstrual intervals <20 or >45 days > 2 years after menarche or an interval >90 days at any time warrants further evaluation
signs of hyperandrogenism and signs that are not in PCOS and would be in androgen secreting tumor
PCOS: hirsutism, acne, alopecia
rapid increase in androgen: increase muscle mass, deep voice, cliteromegaly (NOT IN PCOS)
hirsutism; testosterone into ____ via ______ and turns ____ hair into _____ hair
testosterone is converted by 5 alpha reductase to dihydrotestosterone (DHT)
vellus –> terminal hair (in androgen sensitive follicles ie. chin)
alopecia in PCOS
excess 5 alpha reductase activity turning testosterone to DHT
for terminal hairs that dont need androgens they transform to vellus and fall out
4 factors in pathogenesis of acne in PCOS
- Blockage of the follicular opening by hyperkeratosis
- Sebum overproduction
- Proliferation of commensal bacteria (Propionibacterium acnes)
- Inflammation
testosterone –> DHT in sebaceous glands
acanthosis nigrigans in PCOS
hyperisulinemia –> keratinocyte growth
cancer risk in PCOS
endometrial hyperplasia/ neoplasia from anovulation and unopposed estrogen, hyperandrogenism, hyperinsulineamis, obesity, decreased SHBG
pregnancy complications in PCOS
miscarriage, hypertensive disorders, gestational diabetes (GDM), and preterm birth
use fertility interventions can cause multi fetal gestations
ovulation to menses is __ days because of lifespan of _____
14 days, bc corpus luteum
menstruation to ovulation can vary
GnRH released from where in hypothalamus
pre optic and arcuate nuclei
pulsatility of GnRH for LH and FSH
rapid= LH
slower= FSH
2 cells in ovary and what hormones stimulate them and what hormones they make
theca cells (via LH and cholesterol): steroidogenesis; progesterone and androgens
granulosa cells (via FSH, and some LH): convert androgens to estrogens (activins, inhibins, follistatin)
negative and positive feedback in menstrual cycle
negative: progesterone and estrogen inhibit GnRH
positive: late follicular phase, estradiol promotes GnRH to create LH surge
what enzyme in granulosa cell to create the hormones
testosterone –> estradiole
androstenedione –> estrone
via aromatase enzyme
Estrone converted into estradiol via 17Beta-hydroxysteroid dehydrogenase
if too much androgens they will get converted into what in the grnaulosa cell
dihydrotestrone –> apoptosis of grnaulosa cell and follicular atresia
what phase does primary oocyte arrest in until ovulation during puberty
prophase
what do primary follciles develop into after puberty and due to exposure of what
into secondary follicles via LH and FSH
Just before ovulation, the antral follicle(s) will develop into
Graafian follicle(s)
dominant follicle gets selected at ovulation via how much growth factors, oxytocin, steroids, peptides it has
dominant follicles releases _____ to trigger ____
estradiol ; LH surge (ovulation)
what does secondary oocyte arrest in until fertilization
metaphase
LH surge promotes release of ____ so follicle swells and basement membrane disintegrates
then granulosa cells activate _____ so the rupture follicle ovum is released
release of histamine, prostaglandins and bradykinins, which cause vasodilation
prostaglandins activate lysosomal enzymes to degrade ovarian wall
Granulosa cells (FSH stimulation) release plasminogen activator→ get activated plasmin and with collagenases (LH stimulation) will digest the connective tissue matrix
when Graafian follicle collapses at ovulation if fills with blood and becomes ____ which releases ____.
if not fertilized it apoptosis and necrosis and becomes ____
corpus luteum ; progesterone
corpus albicans
if fertilized, maintain corpus luteum via
hCG and progesterone (reduce contractility)
follicular phase hormone levels
low LH, estrogen, progesterone, inhibin
high FSH (stimulate granulosa cells, increase aromatase to make estradiol increase, increase LH receptors on growing follicle)
day 5-7 pick dominant follicle via size and streoidogenic activity
late follicular phase
increase estradiol to cause LH surge
reduce FSH
luteal phase
corpus luteum secretes progesterone (some estradiol), FSH and LH decline
endometrial cycle
- proliferative phase [mid-late follicular phase] (estrogen causing hyperplasia, vascularize with spiral arteries)
- secretory phase [ovulation and early-mid luteal phase] (coiled glands with glycogen, tortuous spiral arteries, thickest 1 week after ovulation, progesterone decreases and causes myometrial contraction to prep for implantation)
cervical mucus in follicular vs ovulation vs luteal
follicular: alkaline, viscose, elastic
ovulation: most elastic for sperm to pass
luteal: progesterone decreases amount and elasticity so sperm and infection cant enter
body temp increases
after ovulation bc of progesterone
mensturation
low progesterone and estradiol cause vasospasm of spiral arteries –> ishemia of endometrail layer –> necrosis and apoptosis –> macrophage and WBC invade to phagocytose ischemic tissue
autonomic nervous sytem for arousal
- Cerebral sympathetic stimulation→promotes desire
- Peripheral parasympathetic stimulation→clitoral vasocongestion and vaginal secretions; both processes depend on nitric oxide
ovarian cyst
follicular cysts (if follicle doesnt rupture in ovulation)
luteal cyst (if corpus luteum doesnt dissolve)
endometriosis
endometrial tissue in ectopic location
endometrial hyperplasia
Increase in endometrial gland to stroma ratio
could be typical or atypical (cancer risk)
endometrial hyperplasia caused by
excess estrogen stimulation
(anovulation, exogenous estrogen, PCOS, obesity)
fibroids- leiomyomas
benign tumor of myometrium
sx: menorrhagia (heavy bleed)
