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describle the hypothalamic pitutary acsess
hypothalamus has arcuate nuculus that release gonadotropin releaseing hormotone to anterior pitutary through hypothalamic hypopheseal portal circulation for pit to release gonadotropin hormones (fsh and lh)
gonadortopin releasing hormone characters
deca peptide (10 aa)
what are gonadotropins
released from pitutary
fsh and lh
are glycoprotiens
2 polypeptide chains connected by carbohydrate links
function of gonadotropins
sent to ovary to make steroidogenisis and ovulation
describe steroidogenis
ovary forming hormones (esctrogen and progesteron and androgens )
what is the needed criteria for ovary to have 2 functions
the gonadorophins need to be in correct level and rythm (irregular)
if one only is correct then only one function can be done
what are 2 examples of only steroidogenis function of ovary without ovulation
early menarche at 9 years
pco
due to amount but no rythm
end product of female genital system cyclic changes
menstruation
pregnancy
asherman syndrome c/p and pathology
uterus dont perform cyclic changes result in
infertility
recurrent preg loss
ammenoreha , hypomenohrrea
what are inhibitory and arucate nuclues of hypothalamus
increase dopamine
beta endorphin
melatonine
inhibitory
chatecolamin and chatecolestrogen
what is effect of melatonin on menarche
released from pineal body in large amount before menarche and inhibit gonadrotropin releaseing hormone
at puberty is released less from pineal body in irregular way so the hypo thalamus release in irregular way so result in irregular release of gonadotrophins causing only telarche no ovulation
what is the regular way GNRL
pulsatile manner every 90-120 mins
very short lived
function can be assesed by level of LH and FSH
how is pitutary gonadotrophin effect on ovary controled
by positive and negative feed back mechanism
1ry oocyte in prophase lag of 1st miotic division (perimordial follicle ) affected by FSH and LH (in correct amount to be fully matured ) and low levels of estrogen have positive feedback released from ovary
estrogen stimulate formation of estrogen receptor on ova so it stimulate multiple layers of granulosa cells and have theca interna and theca externa and form fluid spaces (filled with estrogen) forming preantral follicle
preantral follicle relaase estrogen and cause negative feed back mechanism and this result in FSH decrease and develop in to antral follicle theca interna and theca externa and granulosa and zona pellucida to become preovulatory follicle (mature grafian follicle)
development of preovulatory follice to ovulator follicle
need LH surge to ovulate stimulated by e2 >200picogram for 50 hours (2 days and 2 hr) negative feedback turn into positive feedback to release LH SURGE and lower FSH SURGE leading to ovulation
what is the function of FSH surge along with LH surge
to inc LH receptors
and finalise maturation of follicle
effect after LH surge
ovulation
corpus luteum
make it proliferation and leutinization (deposit of cholesterol and leutin)
and vascularisation
detailes of ovulation due to LH surge
stimulate release prostaglantin and porteases so ovulation occur
corpus leuteum
release progesterone that increase till 10ng for 7 days after ovulation : 3 days in tube and 7 in uterus
progesterone form sercretory endometrium
what is the
10 ng above this it is negative feed back so FSH and LH are decreased so corpus leutem degenerate and is nor called corpus albicans (hyaline degeneration) to be corpus fibrosum
overian cycle duration
21-35 days
1) follicular phase (1-growth 2- selection )from 1-3 weeks (according to fsh receptor)
2) ovulation phase 1day
3)leuteal phase 14 days ( 7 inc 7 dec )
leutealleuteal phase insufficency duration
<14 days
curves GTH
fsh low then inc then dec then surge(14) decrease (2 peaks 2nd peak at day 14)
lH all time normal then 1 surge(day 14)
steroid hormones (1 peak)
steroid hormones curve
estrogen: low then inc till 200ng decrease and inc again (2nd peak at day 21)with proges (2 peaks )
progesterone:increase after lH surge and does SURGE (day 21) and then dec (1peak)
premenuposal bleeding curve
weak follicles that dont stay until it release enough estrogen for 50 hours (only 10 for ex) and no lh surge
effect of hormones on endometrium during overian cycle
in follicular phase estrogen inc (proliferation and vascularziation) so endometrium thickness inc from 0.5 ml to become 5-8 ml(0.5-1 cm) and columnar cells become psuedostratifeid
in ovulation inc progesterone (stimulate secretory activity and inhibit proliferative activity of estrogen) endometrial gland is distended with secreations and become tortous
2 cenarios in test hormonal release from ovary by giving 5 day progesterone and stoping it
if bleed so means ovary release estrogen and no prog
if no bleeding then there is no estrogen
what are the 3 secretory phases
1-early subluminlar vacule
2-mid increase
3-late nutbuch layer and spongosium and basalis and compact form
when does bleeding occur in end of cycle (menstruation)
corpus fibrosum doesnt release hormones so mestruation occur
do both ovaries work simultaneously
one month on
one ovary temporary off for 1 month
can both work at same time to get 2 ovas and twins
how to measure the time of ovulation
ask if regular cycle
it is the LMP (1st day of overian cycle )
add length of cycle
minus 14
add it to LMP
mechanism of menstruation
when corpus leuteum degenerate destruction of secretory cells release lysosymes contatin prostaglandin synthtase that work onarachidonic acid turn it into prostag f2 alpha (that cause vasoconstriction in endometrium) then in the cascade of prostag release of pgi2 (ccause VD) that disrupt the bV and explode causing separating heamatoma (that devide spongy layer to basal layer)(between separated spongy and basal layers are bv torn that cause bleeding ) with fibrinolytic system break down clots
what is heavy menstraul bleeding and its cause
clots more than >3mm
severe bleed and pain
cervixs cause bleed and form it self blood clots
how does menstruation decrease
some enzymes that release PGi2 are consumed so the upper hand went to PGf2 alpha that cause VC to stop menstruation a blod clot forms above and stops
when does menstruation stop
when reepithelization occur
what can stop heavy menstrual bleeding
anti prostaglandin
antifibrinolytic
how to predict and diagnose ovulation
predict by calender method , uriniray LH kits , basal body temp(dt progesterone) and cervical muscus ( dryer)
diagnose by Trans vag folicometry and mid leuteal estrogen
cervical cycle
proliferative (dt estrogen) prolif and vascularity and bl supply inc so release watery cervical mucus
criteria of cervical muscus
profuse mucus
low viscosity
highly elastic (by shpin parke test
how to test cervicas mucus in proliferative phase
by spin parke test
and positive fern test ( acellular)
secretory phase of cervical
secreation become heavieer
with leukocytes and mucus bemoce thicker
and amount little
and viscosity high
elasticity low
how to test cervical mucus in secretory phase
negative spin parke
negative fern ( cellular )
what is the physiology of cervical cylcle
ealry watery and more desire and easy fertilization peak at e2 >200
then after ovulation progesterone become thick dry and many leukocytes
describe proliferative phase in vaginal cycle
more proliferation and vascularisation and forms basasl and parabasal cells and an intermediate layer (proliferate away from blood supply ) which has picnotic nuculus and with ratio 70:30:0(superfacial: 30 intermediate) in this area more glycoprotien that break down to become acidic 3.5
secretory phase in vaginal cycle
progesterone causes less proliferation and superfacial layer fall and not regenerate having a ratio 30:70:0 and ph with increase to 4.5
diffrence between effect of GRTH pulsatileand continious manner
GTRH is pulsatile from hypothalamus stimulate pit (for induction)
if continuous causes downgrade the receptors in pitutary (to treat fibroid )
aa in GRHs
alpha 92
beta in LH 118 in FSH 101
anerior pit cells and functions
chromopohbe (reserve cell)
basophil ( GRH,ACTH,TSH)
acidophil (GH ,Prolaction)
estrogen types and origin and transport and strongest
e1 (estrone) (never stops) (from adipose)
e2 (esterdiol) (from ovaries) (strongest)
e3 (estertriol) (from placenta)
on sex hormone binding protien
systemic effect of estrogen
-bone stimulate osteoblast and inhibit osteoclast ( inc growth in puberty)
-breast form fats and BV and ducts
-inc prolactin but not its effect
-periphral VD
-salt and water retention
- anti insulin
- inc HDL and dec LDL
- anabolic
-2ry sex characters
types of progesterol and origin
progesterol mincronised (ovary and placenta)
17oh progesterone (adrenal)
effect of progesterone
-basal body temprature
-salt and water retention
-smooth muscle relax
-increase resp deapth
-secabeous secreateion