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203 - Theme 2 - Reproductive System, Fetal Development, Pregnancy and Birth > L6 Disorders of Ovulation > Flashcards

L6 Disorders of Ovulation Flashcards

1
Q

What stimulates GnRH?

A

Kisspeptin

KNDy neurones

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2
Q

What are kisspeptin and KNDy neurones stimulated by?

A

High oestrogen

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3
Q

What do kisspeptin and KNDy neurones drive the production of?

A

LH production through stimulation of GnRH

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4
Q

Pulsatility of kisspeptin/GnRH/LH

A

60-90 minutes

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5
Q

Normal process of ovulation

A

GnRH stimulates FSH which acts on the primary follicle granulosa cells which start producing oestrogen and inhibin

FSH also increases the LH receptors in the grannulosa cells

These hormones in turn inhibit FSH (negative feedback)

HOWEVER when oestrogen levels get to a critical high level they positively act on the Kisspeptin and KNDy neurones which stimulate the production of GnRH which in turn produces LH (due to increased frequency and amplitude of the pulse from GnRH)

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

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6
Q

First half of menstrual cycle

A

FSH falls as oestrogen and inhibin rise

At a critical level, oestrogen positively feeds back to Kisspeptin and in turn causes an increase in frequency and amplitude of GnRH which causes the LH surge

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7
Q

Second half of menstrual cycle

A

As LH now converts the granulosa cells to luteal cells, hormone production swaps from oestrogen to progesterone.

Progesterone peaks at Day 21 (7days before period).

Progesterone, oestrogen and inhibit inhibit FSH and LH

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8
Q

Diagnosis of ovulation: clinical

A

Clinical: Take a history from the woman

Regular menstruation usually 28 days (check not on hormonal contraception)

Mid cycle pain at ovulation

Vaginal discharge alters (increased mucus post ovulation)

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9
Q

Diagnosis of ovulation: biochemistry

A

Day 21 progesterone blood test (7 days before start of next menstrual period)

LH detection kits:
urinary kits bought over the counter

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10
Q

Diagnosis of ovulation: transvaginal pelvic ultrasound

A

Done from day 10, alternate days to demonstrate the developing follicle size and Corpus Luteum

NOT basal body temp, cervical mucus change, vaginal epithelium changes nor endometrial biopsies

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11
Q

Causes of ovulation problems: hypothalamus

A

Lack of GnRH

Kiss1 gene deficiency - rare

GnRH gene deficiency - rare

Weight loss/ stress related/ excessive exercise

Anorexia/bulimia

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12
Q

Causes of ovulation problems: pituitary

A

Lack of FSH and LH

Pituitary tumours (prolactinoma/ other tumours)

Post pituitary surgery/radiotherapy

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13
Q

Causes of ovulation problems: ovary

A

Lack of oestrogen/progesterone

Premature ovarian insufficiency

  • Developmental or genetic causes e.g. Turner’s syndrome
  • Autoimmune damage and destruction of ovaries
  • Cytotoxic and radiotherapy
  • Surgery
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14
Q

Causes of ovulation problems: commonest cause

A

Polycystic Ovarian Syndrome

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15
Q

Define amenorrhoea

A

Lack of a period for more than 6 months

Primary amenorrhoea - never had a period (never went through menarche)

Secondary amenorrhoea - has menstruated before

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16
Q

Define oligomenorrhoea

A

Irregular periods

Usually occurring more than 6 weeks apart

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17
Q

Define polymenorrhoea

A

Periods occurring less than 3 weeks apart

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18
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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19
Q

Clinical features of PCOS

A

Hyperandrogenism
-Hirsutism, acne

Chronic oligomenorrhoea/amenorrhoea

  • = 9 periods/year
  • subfertility

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

20
Q

Elements in the diagnosis of PCOS

A

Polycystic ovaries

Androgen excess

Oligo-anovulation

21
Q

PCOS and the metabolic syndrome

A

Insulin resistance with increased insulin

  • increased androgen production by ovarian theca cells
  • decreased SHBG production by the liver

Impaired glucose tolerance
-increased risk of gestational DM and T2 DM

Dyslipidaemia

Vascular dysfunction

? Increased risk of cardiovascular disease ?

22
Q

USS appearance of polycystic ovaries

A

> /= sub capsular follicules 2-8mm in diameter

arranged around a thickened ovarian stroma

not all women with PCOS will have USS appearance

23
Q

Hormonal abnormalities in PCOS

A

Raised baseline LH and normal FSH levels. Ratio LH:FSH 3:1

Raised androgens and free testosterone

Reduced SHBG

Oestrogen usually low but can be normal

24
Q

Sex Hormone Binding Globulin: synthesis, role, what happens when testosterone bound and what it is increased/decreased by

A

Produced by the liver

Binds testosterone and oestradiol

If testosterone bound - not converted to active component dihydrotestosterone i.e. not ‘free’

Increased by oestrogens

Decreased by testosterone thus releasing more free testosterone

25
Q

Reproductive effects of PCOS

A

PCOS is maybe associated with varying degrees of infertility

  • 15% of all causes of infertility is lack f ovulation
  • 80% of lack of ovulation due to POS

Associated with increased miscarriages

Increased risk of Gestational Diabetes

26
Q

PCOS and endometrial cancer

A

Increased endometrial hyperplasia and cancer

Lack of progesterone on the endometrium

Endometrial cancer associated with type 2 diabetes and obesity

27
Q

Treatment of PCOS: life -style modifications

A

Diet and exercise

Stop smoking

Results:

  • decreased insulin resistance
  • increased SHBG
  • improved fertility/pregnancy outcomes
  • improve metabolic syndrome risk factors

High frequency eating disorders
-Bulimia associated with PCOS

Lean women with PCOS should try not to get fat

28
Q

Treatment of PCOS: combined oral contraceptives

A

Increases SHBG and thus decreases free testosterone

Decreased FSH and LH and therefore ovarian stimulation

Regulates cycle and decreases endometrial hyperplasia

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

29
Q

Treatment of PCOS: anti-androgens

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

Treatment of PCOS: hair removal

A

Photoepilation (laser)/electrolysis etc

Elflornithine cream (non-NHS)
-inhibits ornithine decarboxylase enzyme in hair follicles
31
Q

Targeting insulin resistance in PCOS

A

Metformin (biguanide)

  • decreases insulin resistance, decreases insulin levels, decreases ovarian androgen production
  • may help with weight loss/diabetes prevention
  • may increase ovulation (with clomifene), safe in pregnancy
  • less helpful for hirsutism and oligomenorrhoea but may be an option for obese PCOS women
32
Q

Presentation of primary ovarian insufficiency

A

Primary or secondary amenorrhoea

-secondary amenorrhoea may be associated with hot flushes & sweats

33
Q

Other terms used for primary ovarian insufficiency

A

Premature ovarian failure

Premature menopause

34
Q

Aetiology of primary ovarian failure

A

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

35
Q

Investigations for premature ovarian failure

A

History/examination

Increased LH/FSH

? Karyotype

Consider pelvic USS

Consider screening for other autoimmune endocrine disease
-thyroid function tests, glucose, cortisol

36
Q

Management of premature ovarian failure

A

Psychological support

HRT
-continue till 52

Monitor bone density
-DEXA scan

Fertility
-IVF with donor egg

37
Q

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 primary/secondary amenorrhoea
38
Q

Turner syndrome: associated problems

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)

39
Q

Differential diagnosis 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 PCOS: 5-10% of women

40
Q

When to worry about Turner’s syndrome

A

Sudden onset of severe symptoms

Virilisation

  • frontal balding
  • deepening of voice
  • male-type muscle mass
  • clitoromegaly

Possible Cushing’s syndrome

41
Q

What are adrenal steroids synthesised by?

A

cholesterol

via progesterone/DHEA

42
Q

Congenital adrenal hyperplasia

A

Disorders of cortisol biosynthesis

  • carrier frequency 1:60
  • most patients are compound heterozygotes i.e. 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
43
Q

21-dehydroxylase deficiency

A

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

44
Q

CAH presentation

A

Childhood

  • ‘classic’/’severe’
  • salt-losing (2/3rd)
  • non-salt losing (1/3rd)
  • simple virilising

Adulthood

  • ‘non-classic’/’mild’
  • ‘late-onset’
45
Q

CAH presentation in childhood (detailed)

A

Salt wasting
-hypovolaemia, shock

Virilisation

  • ambiguous genitalia in girls
  • early virilisation in boys

Precocious puberty

Abnormal growth

  • accelerated early
  • premature fusion
46
Q

CAH presentation in adults (detailed)

A

Hirsutism

Oligo/amenorrhoea

Acne

Sub fertility

Similar to PCOS presentation

47
Q

CAH treatment

A

Glucocorticoid and mineralocorticoid replacement

  • hydrocortisone & fludrocortisone
  • additional salt in infancy

Glucocorticoids suppress CRH/ACTH

Supra physiological glucocorticoid doses may be needed to suppress adrenal androgen production

  • monitor [17-OH-P]/androstenedione
  • monitor growth in childhood -excess glucocorticoid treatment may inhibit growth

Surgical management for ambiguous genitalia

Non-classical CAH in adult women (mild)
-can treat as for PCOS with COCP and anti-androgen

203 - Theme 2 - Reproductive System, Fetal Development, Pregnancy and Birth (17 decks)

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