L06 - Disorders of Ovulation Flashcards
what are potent stim of GnRH
what are potent stimulators stim by and what do they drive by stim GnRH?
what does GnRH stimulate and what does this then do and what cells does it act on what are the effects.
what are the after effects
what happens when the stimulated hormones get to a critically high level?
what does LH trigger
Kisspeptin and KDNy neurones are potent stim of GnRH. they are stim by high oestrogen and drive LH production, through GnRH stim.
they are all pulsatile.
GnRH stim FSH, acts on primary follicle granulosa cells –> start producing oestrogen and inhibin.
FSH also increases LH receptors in granulosa vells
these hormones inhibit FSH - negative feedback
when oestrogen gets to critically high level, they positively act on Kisspeptin and KNDy neurones –> these stimulate the production of GnRH, this produces LH
Lh triggers ovulation, oocyte meiosis resumption and changes granulosa cells into luteal cells
How to diagnose ovulation
CLINICAL?
how long is reg cycle
what should you look out for
BIOCHEMISTRY
what tests can you do
also other tests
take hisory. reg cycle is 28 days
mid cycle pain at ovulation
vaginal discharge altered? incr mucus post ovulation?
Day 21 progesterone blood test –> 7 days before start of next menstrual period
also LH detection kits:
urinary kits OTC
also transvaginal pelvic ultrasound done from day 10
— alternate dats to demonstrate developing follicle size and corpus luteum
WHat are the causes of ovulation problems
Hypothalamus (lack of GnRH) ' Kissl gene deficiency- rare ' GnRH gene deficiency - rare ' weight loss/stress related/excessive exercise ' anorexia/bulimia
Pituitary (lack of FSH and LH)
—pituitary tumours (prolactinoma/other tumours)
‘—post pituitary surgery /radiotherapy
Ovary (lack of oestrogen/progesterone)
Premature ovarian insufficiency
— Developmental or genetic causes eg Turner’s syndrome
— Autoimmune damage and destruction of ovaries
— Cytotoxic and radiotherapy
— Surgery
Polycystic Ovarian Syndrome: commonest cause
df of
amenorrhoea (primary and secondary)
oligomenorrhoea
polymenorrhoea
hirsutism
Amenorrhoea - lack of a period for more than 6 months
‘ Primary Amenorrhoea - never had a period (never
went through menarche)
‘ Secondary Amenorrhoea -has menstruated before
Oligomenorrhoea - irregular periods
•usually occurring more than 6 weeks apart
Polymenorrhoea - periods occurring less than 3 weeks
apart
HIRSUTISM 'Androgen-dependent' hirsutism — Excess body hair in a male distribution NOT: — Androgen-independent hair growth ' Hypertrichosis — Familial / racial hair growth
PCOS
what are the clinical features
how is it related to the metabolic syndrome?
Hyperandrogenism — Hirsutism, acne Chronic oligomenorrhoea / amenorrhoea —S 9 periods / year — Subfertility Obesity (but 25% of women with PCOS are "lean")
PCOS and the metabolic syndrome
INCR Insulin resistance with INCR in insulin
— INCR androgen production by ovarian theca cells
— DECR SHBG production by the liver
Impaired glucose tolerance
— INCR risk gestational DM and T2 DM
Dyslipidaemia
Vascular dysfunction
? INCR risk cardiovascular disease ?
USS appearance of Polycystic Ovaries?
USS appearance of Polycystic Ovaries
around 10 or more subcapsular follicules 2-8 mm in diameter,
arranged around a thickened ovarian stroma
not all women with PCOS will have USS appearance
PCOS hormonal abnormalities
what are the hormonal changes
–
what `are the reproductive effects of PCOS
what about endometrial cancer - why
Raised baseline LH and normal FSH levels. Ratio LH:FSH 3:1
Raised androgens and free testosterone
Reduced Sex Hormone Binding Globin (SHBG)
Oestrogen usually low but can be normal
SHBG
what does it do how does it work
also
how do you treat PCOS
life style mod
combined oral contraceptives
anti androgens (with COCP) - CYPROTERONE ACETATE and SPIRONLACTONE
hair removal
metformin for insulin resistance
decr ovarian androgen production
PRIMARY OVARIAN INSUFFICIENCY
what does it present as
what are the possible causes of it
what would you see hormone wise in investigations. what other investigations woyld you do
turner syndrome
what is it
what does it present as
–
if someone has hirsutism, what is the differential diagnosis?
when would you worry?
congenital adrenal hyperplasia
what us it
what is most cases caused by
when and how does it present
CAH Treatment
whats given
21-hydroxylase deficiency
–cortisol and my have aldosterone defic
androgen XS
lack of aldosterone and cortisol causes lack of negative feedback, so XS adrenal andorgen produced
treat
hydrocortisone and fludrocortisone as glucorticoid and mineralocorticoid replacement. additional salt in infancy
xs glucocorticoid may be needed. but monior growth as it may be inhibited by this