Disorders of ovulation and disturbances of the menstrual cycle Flashcards
menstrual cycle split into
ovarian cycle - development of follicle and ovulation
uterine cycle
2 weeks leading up to ovulation is Called
follicular phase - menstrual and rpoliferative phase
follicular phase starts on first day of menstruation
GnRH secreted to cause pituitary to release FSH or LH
afte rpibertu GnRH is released in pulses sometimes more sometimes less
follicles have what cells
theca cells
granulose cells on primary oocyte
theca cells bind to LH in first 10 days and release
androstenedione
grnaulsoe cells do same converting armomatsase
this converted androstenedione converts into oestrogen by this which increase follicle growth - causing less FSH to be produced via negative feedback so only one follicle with develop
dominant follicule releases oestrogen more - now becomes positive feedback so more FSH and LH released - this happens a couple days before ovulation and rupture of follicle
proliferative phase - oestrogen levels rise causing
thickening of endometrium
growth of endometrial glands
emergence of spiral arteries
cervical mucus more hospital too
following ovulation remembrance of follicle becomes
corpus luteum
low lH causes grnaulosa cells secrete P450 to make pregnelone which makes more progesterone so more of this is made during this phase , oestrogen decreases
inhibit as well
progesterone spiral arteries grow longer and uterine glands secrete more mucus
after 15 days window for fertilisation loses
CL degenerates to corpus albicans docent make hormones.
cervicla mucus thickens - progesterone
corpus albican
all hormones decline
Lh receptors on
theca cells
cholesterol to progesterone to androgens then need aromatase to make oestrogen wihcih comes from the granulosa cells
FSH receptors on granulosa cells
true
ovulation breaks the basement membrane so grnaulsoa cells can take in cholesterol to make progesterone but they can’t turn that into androgens but make progesterone which goes into the blood but less oestrogen made
grnaulosa cells responsible for making oestrogen in proliferative phase
what is ovarian steroidogenesis
Ovarian steroidogenesis is the process through which ovarian cells produce hormones for the maintenance of reproductive tissues, regulation of ovarian function and ovulation, and establishment of pregnancy
hirsutism
excess hair growth in adorn dependent areas in women for example face, chest, abdomen, lower back and upper arms and thighs
virilization
deep voice, reduced breast size, increased muscle bulk and clitorial hypertrophy
commonest causes of secondary amenorrhea
ovaries - PCOS, POF/POI
uterus - adhesions
hypothalamus and pituitary - functional hyperprolactinaemia
sheehans syndrome
cushions
other is hyperthyroid , congenital adrenal hyperplasia and ovarian tumours
how do you diagnose PCOS
Rotterdam criteria
2 out of 3
oligomenorrhoea or amenorrhea
hyperandrogism - are clinical effects of that
cystic ovaries on USS - at least 20 - string or pearl on US
24yr women. 5 COCp stopped to have children still not pregnant. Cycles long and variable. Overweight, waxes her chin and has acne what is going on
she has oligomenorrhoea how many periods has she had in last month
preg negative and elevated free androgen index and high LH with normal FSH what additional result would you like to see
TSH and prolactin normal - does she have PCOS by Rotterdam criteria
6
TSH and prolactin ( can disturb these levels)
LH - increase theca cells
yes
PCOS tends to emerge after puberty and the young you are more likely , likely to have androgen problem and leading cause of infertility. what are the treatments
weight loss, lifestyle
contraceptive pill
clomifenen
metformin
Case 2
17yr , period at 13 and been erratic since
icnrease body hair on face abdomen and chest. Acne , BMI 27 Breast tanner 4 and pubic tanner 5
increased deltoids and hirsutism
(pregame test biochemistry) what Ix first
FSh and LH and oesotrgne normal , testosterone is way above limit
17alpha hydroxylase is high - ( if this docent work then you get more aldosterone and cortisol made) - steroid formation - what test now needs to be done
which enzyme is the girl low in to cause this
this is non-classical congenital adrenal hyperplasia
biochemistry
ACTH stimualtion test (short synacthen test)
21-hydroxylase - therefore less aldosterone and cortisol not made so more testosterone
COH is autosomal recessive - oligomenorrhoea, fertility problems, hyperandrogegism , enzyme deficiency causes excess of androgens and deficit of corticoids and more easily recognised in females due to abnormal hair. signs start during puberty
treamtent
steroids - as they are deficient
classical - is mild version and result in absent corticoids and early onset leading to adrenal crisis.
case 3 - 29yr woman , periods stoped 5 months , very slim , no signs of hyperandrogneism
FSH LH and oestrogen low to normal what additional test do you want
what is shown
TSH, prolactin and coeliac screen
osteopenia
case 4- inability to conceive for about 1.5years
very tired and constipated
low BP
blood test results - hb is normal and ferritin , blood glucose normal , normal coeliac screen and normal EBV screen
creatinine normal
TSH is high and freeT4 is low she has milky discharge from the nipples over the past few months. what do you want to check
prolactin levels and thyroid peroxidase levels high too - diagnosed as Hashimotos thyroidisitis and treat with L-thyroixin
hypothyroidism adn hyperprolactinoma
TRH secretion is increased by hypothalamus due to feedback mechanism in hypothyroidism, this increased TRH affects prolactin and TSH levels by increasing their secretion from the thyroid gland
primary amenorrhea
no menarche by 15 years old
secondary amenorrhea
absence of menses for over 3 months of woman previously having them
oligomenorrhoea
ireggualr menses fewer than 6-8 periods a year
commonest cause of secondary amenorrhea
PCOS POI adnehsion hyperporlactinaemia sheehans syndromen cushions congenial adernal hyperplasia
roterdarm criteria need 2 out of 3 for PCOS
oligo or amenorrhea
hyperadnrogensism - clinical or biochemistry
cystic ovaries in USS
in addition to LH and FSH what tests shield you check
TFT and prolactin
human steriodegnenesis showing the reactions
what does a deficiency in 21-hydroxylase cause
less aldosterone and cortisol made but more oestorne and testosterone
leading to irregular menstruation, decreased fertility, baldness, hirustims
