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203: Reproduction and endocrinology > T2 L6: Disorders of Ovulation > Flashcards

T2 L6: Disorders of Ovulation Flashcards

1
Q

what does GnRH stimulate FSH to do

A

Act on the primary follicle granulosa cells which start producing oestrogren & Inhibin

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2
Q

FSH increases the LH receptors but in which cells

A

granulosa cells

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3
Q

when does oestrogen act positively on Kisspeptin & (KNDy neurones )

A

At critically high levels

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4
Q

what are the 2 potent stimulators of GnRH

A

Kisspeptin-( KNDy neurones )

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5
Q

what stimulates the kisspeptin and GnRH neurons

A

High oestrogen and LH production (via stim of GnRH)

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6
Q

what is the function of LH and FSH

A

FSH causes the follicle to produce oestrogen and inhibin both of which negatively feedback to the hypothalamus and pitutary to decrease FSH.

LH triggers ovulation, resumption of oocyte meiosis and changes the granulosa cells into luteal cells

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7
Q

what is a key concept to understand with the regulation of LH and FSH

A

FSH causes the follicle to produce oestrogen and inhibin both of which negatively feedback to the hypothalamus and pitutary to decrease FSH.

However as the oestrogen levels rise there is an effect of high levels of oestrogen on the Kisspeptin and KNDy neurones that stimulates the production of GnRH which stimulates the production of LH, (due to increased frequency and amplitude of the pulse from GnRH)
.

Its release occurs in a pulsatile fashion and triggers ovulation, oocyte meiosis & changes the granulosa cells into luteal cells ( small rise in FSH at this time).

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8
Q

describe the first half of the ovulation cycle

A

First half of cycle: FSH falls as oestrogen and inhibin rises. At a critical level oestrogen positively feeds back to Kisspeptin and in turn causes an increas in freq and amplitude of GnRH which causes the LH surge.
Second half of cycle: As LH now converts the granulosa cells to luteal cells hormone production swaps from oestrogen to progesterone. Progesterone peaks at Day 21 ( 7 days before the period). Progesterone, oestrogen and inhibin inhibit FSH and LH.

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9
Q

when taking a history, what important features of the menstrual cycle must you take into account

A

Regular cycle is 28 days

Bleeding begins from day 1-5

fertility is from day 11-15

mid cycle pain at ovulation

vaginal discharge alters (increased mucus post ovulation)

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10
Q

what is ovulation pain

A

leakage of follicle fluid at the time of ovulation irritates the peritoneum and causes pain

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11
Q

how do you diagnose ovulation

A

Biochemistry :
- Day 21 progesterone blood test

LH detection kits:
-urinary kits bought over the counter

Transvaginal pelvic ultrasound (done from day 10)

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12
Q

what can’t you do to diagnose ovulation

A

not: Basal temperature, cervical mucus change, vaginal epithelium changes nor endometrial biopsies

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13
Q

what are the 2 groups and possible causes of ovulation problems

A

Hypothalamus (lack of GnRH)

  • Kiss1 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
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14
Q

Causes of ovulation problems

A

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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15
Q

Define :
Amenorrhoea

oligomenorrhoea

polymenorrhoea

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

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16
Q

Define hirsutism

A

Androgen-dependent’ hirsutism
Excess body hair in a male distribution

-NOT
-Androgen-independent hair growth
Hypertrichosis
-Familial / racial hair growth

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17
Q

what are the clinical features of PCOS Polycystic Ovarian syndrome (PCOS)

A
  • Hyperandrogenism
  • –Hirsutism, acne

Chronic oligomenorrhoea / amenorrhoea
 -9 periods / year
-Subfertility

Obesity (but 25% of women with PCOS are “lean”)

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18
Q

what are the 3 elements in the diagnosis of PCOS

A

Polycystic ovaries

Androgen excess

Oligo/anovulation

(need at least 2 of these to diagnose PCOS)

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19
Q

what is the relationship that PCOS has with the metabolic syndrome

A

Insulin resistance with + insulin

    • androgen production by ovarian theca cells
  • +SHBG production by the liver

Impaired glucose tolerance
-+ risk gestational DM and T2 DM

  • Dyslipidaemia
  • Vascular dysfunction
  • ? +risk cardiovascular disease ?
20
Q

what is the mechanism between insulin resistance and PCOS

A

Insulin resistance is the underlying problem ( genetic factors also important).

High levels of Insulin and androgens cause granulosa cells to become less functional ( less oestrogen) and the follicle to arrest=anovulation,

also causes increased LH levels which drives thecal cells to increase androgens. leading to hirsutism

21
Q

what is the USS appearance of Polycystic Ovaries

A

10 subcapsular follicules 2-8 mm in diameter,

arranged around a thickened ovarian stroma

( not all women with PCOS will have USS appearance & technically Not cysts – definition of cyst is a mass > 3cms. Wrong name for the condition! Should be poly small follicles disease!
)

22
Q

what are the hormonal abnormalities in PCOS

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

23
Q

Describe the sex hormone binding globulin SHBG

A
  • Produced by the liver
  • Binds testosterone and oestradiol
  • If testosterone bound - not converted to active component dihydrotestosterone ie not “free”
  • SHBG increased by oestrogens
  • SHBG decreased by testosterone thus releasing more free testosterone
24
Q

what are the reproductive effects of PCOS

A

PCOS is maybe associated with varying degrees of infertility

  • 15% of all causes of infertility is lack of ovulation
  • 80% of lack of ovulation due to PCOS
  • Associated with increased miscarriages
  • Increased risk of Gestational Diabetes
25
Q

what is the relationship between PCOS and endometrial cancer

A
  • Increased endometrial hyperplasia and cancer
  • Lack of progesterone on the endometrium
  • Endometrial cancer associated with type 2 diabetes & obesity
26
Q

How do you treat PCOS (1)

A

Lifestyle modifications :
-Diet & exercise
Stop smoking

27
Q

what does treatment result in

A
  • less insulin resistance
  • increased SHBG
  • decreased free testosterone
  • improved fertility
  • Improve metabolic syndrome risk factors
28
Q

How do you treat PCOS (2)

A

Combined Oral Contraceptives:

  • increases SHBG and thus decreases free testosterone
  • decreases FSH & LH and therefore ovarian stimulation
  • regulates cycle & decreases endometrial hyperplasia

(BUT may cause weight gain, venous thrombosis, adverse effects on metabolic risk factors )

29
Q

how do you treat PCOS (3)

A

-With COCP / other form of secure contraception

  • Cyproterone Acetate (oral tablet)
  • -inhibits binding of testosterone & 5 alpha dihydrotestosterone to androgen receptors
  • Spironolactone (oral tablet)
  • -anti mineralocorticoid and anti androgen properties
30
Q

how do you treat PCOS (4)

A

Photoepilation (laser) / electrolysis etc

Eflornithine cream (non-NHS)
Inhibits ornithine decarboxylase enzyme in hair follicles
31
Q

How do you treat PCOS (5)

A

Metformin (biguanide)
-+ insulin resistance,  insulin levels,  ovarian androgen production

  • May help with weight loss / diabetes prevention
  • May + ovulation (with clomifene), safe in pregnancy
  • Less helpful for hirsutism & oligomenorrhoea, but may be an option for obese PCOS women
32
Q

what is primary ovarian insufficiency

A

Presentation:

  • Primary or secondary amenorrhoea
  • –Secondary amenorrhoea may be associated with hot flushes & sweats

Other terms used:

  • Premature ovarian failure
  • Premature menopause

Aetiology:

  • Autoimmunity
  • -May be associated with other autoimmune endocrine conditions
  • X chromosomal abnormalities
  • Turner syndrome
  • Fragile X associated
  • Genetic predisposition
  • -Premature menopause
  • Iatrogenic
  • -Surgery, radiotherapy or chemotherapy
33
Q

what can you investigate in premature ovarian failure

A
  • history / examination
    • LH and FSH
  • ? Karyotype

-Consider pelvic USS
Consider screening for other autoimmune endocrine disease
—Thyroid function tests, glucose, cortisol

34
Q

how do you manage ovarian failure

A

Management:

-Psychological support

HRT
–Continue till +-52

Monitor bone density
-DEXA scan

Fertility
-IVF with donor egg

35
Q

what is turner syndrome

A

Complete / partial X monosomy in some / all cells

  • 50% of cases will be XO
  • Rest: partial absence of X or mosaicism

-1:2000 – 1:2500 live-born girls

Presentation

  • May be diagnosed in the neonate
  • May present with short stature in childhood
  • May present with primary / secondary amenorrhoea
36
Q

what are the associated problems with turner syndrome

A

Short stature
-Consider GH treatment

CV system

  • Coarctation of aorta
  • Bicuspid aortic valve
  • Aortic dissection
  • Hypertension (adults)

Renal
-Congenital abnormalities

Metabolic syndrome

Hypothyroidism

Ears / hearing
problems

Osteoporosis (lack HRT)

37
Q

look at slide 32

A

how is it

38
Q

what are the differentials of hirsutism

A

95% PCOS or ‘idiopathic hirsutism’

1% Non-classical congenital adrenal hyperplasia (CAH)

<1% Cushing’s syndrome

<1% Adrenal / ovarian tumour

Prevalence of polycystic ovarian syndrome:
5-10% women!

39
Q

what are the very worrying/serious symptoms of hirsutism

A

Sudden onset of severe symptoms

Virilisation

  • Frontal balding
  • Deepening of voice
  • Male-type muscle mass
  • Clitoromegaly

Possible Cushing’s syndrome

40
Q

describe congenital adrenal hyperplasia

CAH

A

disorders of cortisol biosynthesis
-Carrier frequency 1 : 60
-Most patients are compound heterozygotes
Different mutations on two alleles

95% CAH cases caused by 21-hydroxylase deficiency

  • Cortisol deficiency
  • May have aldosterone deficiency
  • Androgen excess
  • Depends on degree of enzyme deficiency
41
Q

what is the CAH- 21 hydroxylase deficiency

A

Defect in cortisol biosynthesis  raised CRH / ACTH (lack of negative feedback)  drives excess adrenal androgen production

Diagnosis: high concentrations of 17-hydroxyprogesterone
Can confirm with Synacthen test

42
Q

how does CAH present itself (non-specific general )

A

childhood:
- classic/severe

  • salt-losing -2/3rd
  • non-salt losing -1/3rd
  • simple virilising

Adulthood

  • Non-classic
  • Late onset
43
Q

CAH presentation specifics

A

Childhood:
Salt wasting
-Hypovolaemia, shock

Virilisation

  • Ambiguous genitalia in girls
  • Early virilisation in boys

-Precocious puberty

Abnormal growth

  • Accelerated early
  • Premature fusion

Adulthood

  • Hirsutism
  • Oligo / amenorrhoea
  • Acne
  • Subfertility

-Similar to ‘PCOS’ presentation

44
Q

CAH treatment

A

Glucorticoid & mineralocorticoid replacement

  • Hydrocortisone & fludrocortisone
  • Additional salt in infancy

Glucocorticoids suppress CRH / ACTH

Supraphysiological glucocorticoid doses may be needed to suppress adrenal androgen production
-Excess glucocorticoid treatment may inhibit growth

Surgical management for ambiguous genitalia

45
Q

Do quiz

A

how did it go

203: Reproduction and endocrinology (53 decks)

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