Disorders of ovulation Flashcards

1
Q

First step in ovulation

A

Starts at the hypothalamus with the supra chiasmic nucleus

Interacts with the kisspeptin neurones and the KNDy neurones

Kisspeptin neurones in the arcuate nucleus and anteroventral peri ventricular area

Kisspeptin and KNDy are potent stimulators of GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

FSH action

A

Causes the follicle to produce oestrogen and inhibin

Both negatively feedback on the hypothalamus and pituitary to decrease FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Rising oestrogen levels cause

A

Kisspeptin and KNDy neurones to stimulate GnRH to produce LH in pulsatile fashion

Triggers ovulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diagnosis of ovulation: clinical

A

Take a history from the woman

Regular menstraution usually 28 days

Mid cycle pain at ovulation

Vaginal discharge alters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
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

Transvaginal pelvic ultrasound done from day 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of ovulation problems: hypothalamus

A

Kiss1 gene deficiency- rare

GnRH deficiency- rare

Weight loss/ stress related/ excessive exercise

Anorexia/ bulimia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of ovulation: pituitary

A

Pituitary tumours (prolactinoma/ other tumours)

Post pituitary surgery/ radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of ovulation: ovary

A

Premature ovarian insufficiency

  • developmental or genetic causes e.g. Turner’s syndrome
  • autoimmune damage and destruction of ovaries
  • cytotoxic and radiotherapy
  • surgery

Polycystic ovarian syndrome: commonest cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Amenorrhoea

A

Lack of period for more than 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Primary amenorrhoea

A

Never had a period (never went through menarche)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Secondary amenorrhoea

A

Has menstruated before

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Oligomenorrhoea

A

Irregular periods

Usually occuring more than 6 weeks apart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Polymenorrhoea

A

Periods occuring less than 3 weeks apart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Androgen dependent hirsutism

A

Excess body hair in a male distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical features of POCS

A

Hyperandrogenism
- hirsutism, acne

Chronic oligomenorrhoea/ amenorrhoea

  • <9 periods/ year
  • subfertility

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Elements in the diagnosis of PCOS

A

Polycystic ovaries

Andorgen excess

Oligo/ anovulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

PCOS and the metabolic syndrome

A

Insulin resistance with increase insulin

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

Impaired glucose tolerance
- increase risk gestational DM and T2 DM

Dyslipidaemia

Vascular dysfunction

Increase risk CVD

18
Q

Hormonal abnormalities in PCOS

A

Raised baseline LH and normal FSH levels

Raised androgens and free testosterone

Reduced sex hormone binding globuln

Oestrogen usually low but can be normal

19
Q

Sex hormone binding globulin

A

Produced by the liver

Binds testosterone and oestradiol

If testosterone bound, not converted to active component dihydrotestosterone

SHBG increased by oestrogens

SHBG decreased by testosterone so released more free testosterone

20
Q

Reproductive effects of PCOS

A

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

21
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

22
Q

Treatment of PCOS: lifestyle modification

A
Diet and exercise 
Stop smoking
- decrease insulin resistance
- increase [SHBG]
- decrease [free testo]
- improved fertility
- improved metabolic syndrome 

High frequency eating disorders
- bulimia associated with PCOS

Lean women with PCOS should try not to get fat

23
Q

Combined oral contraceptive

A

Increases SHBG and thus decreases free testosterone

Decreases FSH and LH and therefore ovarian stimulation

Regulates cycle and decreases endometrial hyperplasia

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

24
Q

Anti-androgens

A

With COCOP/ other form of secure contraception

Cyproterone acetate (oral tablet)
- inhibits binding of testosterone and 5 alpha dihydrotestosterone to androgen receptors

Sprionolactone (oral tablet)
- anti mineralocorticoid and anti androgen properties

25
Q

Hair removal

A

Photoepilation (laser)/ electrolysis

Eflornithine cream (non NHS)
- inhibits ornithine decarboxylase enzyme in hair follicles
26
Q

Targeting insulin resistance in PCOS: metformin

A

Decrease insulin resistance, decrease insulin levels, decrease 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

27
Q

Primary ovarian insufficiency: presentation

A

Primary or secondary amenorrhoea

Secondary amenorrhoea may be associated with hot flushes and sweats

28
Q

Primary ovarian insufficiency: aetiology

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, chemotherapy

29
Q

Premature ovarian failure: investigations

A

History. examination

Increase LH and FSH

Karyotype

Consider pelvic USS

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

30
Q

Premature ovarian failure: management

A

Psychological support

HRT
- continue till around 52

Monitor bone density
- DEXA scan

Fertility
- IVF with donor egg

31
Q

Turner syndrome

A

Complete/ partial X monosomy in some/ all cells

  • 50% of cases will be XO
  • rest: partial absence of mosaicism

1:2000 - 1:2500 live born girls

32
Q

Turner syndrome presentation

A

May be diagnosed in the neonate

May present with short stature in childhood

May present with primary/ secondary amenorrhoea

33
Q

Turner syndrome associated problems

A

Short stature
- consider GH treatment

CV system

  • coarctation of aorta
  • bicuspid aortic valve
  • aortic dissection
  • hypertension

Renal
- congenital abnormalities

Metabolic syndrome

Hypothyroidism

Ears/ hearing problems

Osteoporosis

34
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

35
Q

When to worry

A

Sudden onset of severe symptoms

Virilisation

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

Possible Cushing’s syndrome

36
Q

Congenital adrenal hyperplasia

A

Disorders of cortisol biosynthesis

  • carrier frequency 1:60
  • most patients are compound heterozygotes

95% CAH caused by 21-hydroxylase deficiency

  • cortisol deficiency
  • may have aldosterone deficiency
  • androgen excess
  • depends on degree of enzyme deficiency
37
Q

CAH childhood

A

Classic/ severe

Salt losing (2/3rd)

Non salt losing (1/3rd)

Simple virilising

38
Q

CAH adulthood

A

Non classic/ mild

Late onset

39
Q

CAH childhood presentation

A

Salt wasting
- hypovolaemia, shock

Virilisation

  • ambiguous genitalia in girls
  • early virilisation in boys

Precocious puberty

Abnormal growth

  • accelerated early
  • premature fusion
40
Q

CAH adulthood presentation

A

Hirsutism

Oligo/ amenorrhoea

Acne

Subfertility

Similar presentation to PCOS

41
Q

CAH treatment

A

Glucorticoid and mineralocorticoid replacement

Glucocorticoid suppress CRH/ ACTH

Supraphysiological glucocorticoid doses may be needed to suppress andrenal androgen production

Surgical management for ambiguous genitalia

Non classical CAH in adult women