L06 - Disorders of Ovulation Flashcards

1
Q

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

A

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

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2
Q

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

A

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

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3
Q

WHat are the causes of ovulation problems

A
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

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4
Q

df of

amenorrhoea (primary and secondary)

oligomenorrhoea

polymenorrhoea

hirsutism

A

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
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5
Q

PCOS

what are the clinical features

how is it related to the metabolic syndrome?

A
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 ?

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6
Q

USS appearance of Polycystic Ovaries?

A

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

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7
Q

PCOS hormonal abnormalities

what are the hormonal changes


what `are the reproductive effects of PCOS
what about endometrial cancer - why

A

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

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8
Q

SHBG

what does it do how does it work

also
how do you treat PCOS

A

life style mod

combined oral contraceptives

anti androgens (with COCP) - CYPROTERONE ACETATE and SPIRONLACTONE

hair removal

metformin for insulin resistance
decr ovarian androgen production

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9
Q

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

A
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10
Q

turner syndrome

what is it
what does it present as

A

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11
Q

if someone has hirsutism, what is the differential diagnosis?

when would you worry?

A
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12
Q

congenital adrenal hyperplasia

what us it
what is most cases caused by

when and how does it present

CAH Treatment
whats given

A

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

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