the granulosa cels become leutanised as in senstiive to LH after ovulation
estrogen has to prep the endometrum for it to be receptive to porgesterone ..it needs to be done to provide norishment to the early impanting mebyro
luteal phase is fixed...so ovulation happens 14 days before mentruation = because the CL lives for 10-12 days.
normal clotting mechanism works at the level of the endometrium. but menstraul blood has fibronolysin
primordial follicles take 70 days plus to be ready. Many primordial follicles get ready but only a few reach grafian follicle status and only 1 ovulate.
The primordial follicles arent dependant on fsh or lh but on local growth factors
the text for ovuclation can use the progesterone peak
Vlaues above correct or nah?
MAx activity of Cl = day of highest progesterone = progesterone peak when
In ocp, the dose of oestrogen is less so no positive feed back just supression.....but in PCOS dose high and can cause LH to remain continiously high but with no surge so no ovulation
how does the pirritary know what to secrete fsh or lh? 1. negative and positive feedback from oestrogen and pregesterone 2. changes in the pulsatile manner of hnrh production
Primary Amenorrhea
second is like a glocal delay
gonadal dysgnesis is the mc cause of primary dysmenorreha
streak gonads in turners syndrome
risk of trisomies increases with increased maternal age
but increased maternal age doesnt increase risk of turners
height is a key difference between the two
for the above only tall height and dleayed puberty
wide carrying anglem in turners
intelligence is not impaired in turners syndrome
tumout can compress the tract
cycl ab pain to check for presence of uterus
per rectal to check for presence of uterus
if breast presence then the axis is working meaning hypo-pit-ov workinf and estrogen present
if fsh is low can do mri brain to exclude brain tumours
next investigation vs best investination. in here next is ultrasiund, but best is mri.
Karyotype is important and useful necause 1. it confirms gonadal dysgysnesis and 2. if theres y chromose have to take off gonads
kallman is more common than sweys thats why the above
Secondary amneorrhea
pcos has a classicial picture of slow onset...increased cycle duration with heavy mentrual beeding.
mc cns tumour is a secretory one here vs the obstruction one in primaryn amneoorhea
progesterone challenge test is used to test wheter the amneorrhea because of ovulation failure - because no onulations means no CL and no prgesterone released. and no stabalisation and stuff of endometrium . so the prgesterone causes withdrawal bleeding after the tablets are finished. .
menses is basically progesterone wtihdrawal bleeding
so if there is withdrawal bleeding then it means anovulation for which pcoxs is the mc cause. it doesnt prove ovarian failure since in that estrogen also defienct and there wont be withdrawal bleeding. we can then go for the rotterdam criteria.
caues of hyperprolactinemia ? Hyperthyroidism or drugs or tumourd
synechia is scarringfsh normal 5 to 20.
the endometrium has three layers. the first 2 are shed off with mentruation but the deeper one isnt shed off.
common cause of hypomenorrehea is ashermans syndrome.
all of this is a classical icture of panhypopituitarism
the first sign of sheehans syndrome is lactational failure.
Cryptomenorrhea
per rectal exam in young women instead of per vagina because can be painful cause hymen . but can do one finger per vaginal exam
MRI is needed because cant exacly see the septum in physcial and utrasound and since needs to operate on this ..need more information so take mri
Case
