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Module 203, Theme 2- Reproductive System, Fetal Development, Pregnancy and Birth > T2 L6 Disorders of Ovulation > Flashcards

T2 L6 Disorders of Ovulation Flashcards

1
Q

What initiates the first step of ovulation?

A

(in the hypothalmus the) Supra chiasmic nuclei (SCN) is the master circadian clock

Interacts with the Kisspeptin neurones and the KNDy neurones ( neurokinin B and dynorphin )

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2
Q

Where are the Kisspeptin neurons located?

A

Arcuate Nucleus (ARN)

Anteroventral peri ventricular area (AVPV).

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3
Q

What is the function of the Kisspeptin and KNDy neurons?

A

Potent stimulators of the GnRH neurons which drives LH production

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4
Q

What is stimulates the Kisspeptin and KNDy neurons?

A

High oestrogen levels

When oestrogen levels are critically 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)

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5
Q

Recap the function of GnRH, FSH and LH.

A

GnRH stimulates the release of LH and FSH

FSH acts on the follicles causing them to mature. It also increases the LH receptors on granulosa cells

LH is involved in ovulation. It’s also involved in the resumption of oocyte meiosis and changes the granulosa cells into luteal cells (corpus luteum)

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6
Q

How can ovulation be diagnosed?

A

History taking from the woman

  • Regular menstruation lasts 28 days (but first check that the woman is not on hormonal contraception)
  • Pain is felt mid cycle at ovulation
  • Increased mucus release post ovulation
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7
Q

How is ovulation diagnosed?

A

Biochemistry:
- Day 21 progesterone blood test
(7 days before start of next menstrual period)
- LH detection kits : urinary kits which can be bought over the counter
NOTE: If cycle longer then take blood 7 days before expected usual period e.g. day 28 if cycle is 35 days long.

Transvaginal pelvic ultrasound
- Done from Day 10, on alternate days to demonstrate the developing follicle size and Corpus Luteum. Once the LH surge is detected ovulation occurs 24-36 hours later.

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8
Q

What are the various 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 (which could be non-functional))
  • 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
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9
Q

What is the most common cause of ovulation problems?

A

Polycystic Ovarian Syndrome (PCOS)

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10
Q

Define the following menstrual patterns terminology

  1. Amenorrhoea (primary and secondary)
  2. Oligomenorrhoea
  3. Polymenorrhoea
A
  1. 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
  2. Oligomenorrhoea - irregular periods
    usually occurring more than 6 weeks apart
  3. Polymenorrhoea - periods occurring less than 3 weeks apart
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11
Q

Define “HIRSUTISM”

A

‘Androgen-dependent’ hirsutism = excess body hair in a male distribution (on a female)

IT IS NOT:
Androgen-independent hair growth ( a.k. a hypertrichosis)

Familial / racial hair growth

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12
Q

What the clinical features of PCOS?

A

Hyperandrogenism
-hirsutism, acne

Chronic oligomenorrhoea / amenorrhoea

   - 9 (or less) periods / year
   - subfertility

Obesity (but 25% of women with PCOS are “lean”). In these patients the way to prevent it from getting worse is by avoiding weight gain.

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13
Q

How does PCOS relate to the metabolic syndrome?

A

Insulin resistance with increased insulin

  • increased androgen production by ovarian theca cells (due to increased LH)
  • granulosa cells become less functional ( = less oestrogen) and the follicles arrest
  • reduced SHBG production by the liver

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

Dyslipidaemia

Vascular dysfunction

Increased risk cardiovascular disease (scientists are still unsure as to whether this is the case)

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14
Q

What appearance do polycystic ovaries have when examined using ultrasound?

A

10 (or more) subcapsular follicules 2-8 mm in diameter,

-arranged around a thickened ovarian stroma

NOTE: not all women with PCOS will have USS appearance

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15
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
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16
Q

What is SHBG?

A

A glycoprotein that binds to androgens and oestrogens

It is produced by the liver

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17
Q

What happens if testosterone is bound to SHBG?

A

If testosterone bound it is not converted to active component dihydrotestosterone
i.e. it is not “free”

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18
Q

Which hormones increases/reduces SHBG levels?

A

Increased by oestrogens

Decreased by testosterone thus releasing more free testosterone

19
Q

What 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

20
Q

What is the association of PCOS with endometrial cancer?

A

Increased endometrial hyperplasia and cancer due to lack of progesterone on the endometrium

Endometrial cancer associated with type 2 diabetes & obesity

NOTE: There has to be at least 4 periods per year to prevent endometrial hyperplasia

21
Q

What lifestyle modifications are used to treat PCOS?

A

Diet & exercise

Stop smoking

22
Q

What are the results of these lifestyle modifications?

A

Reduced insulin resistance

Increased [SHBG]

Reduced [free testo]

Improved fertility / pregnancy outcomes

Improve metabolic syndrome risk factors

NOTE: Lean women with PCOS should NOT try to get fat.

23
Q

How do combine oral contraceptives pills help to treat PCOS?

A

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

24
Q

What are the anti-androgens used to treat PCOS and how do they work?

A 
Cyproterone Acetate (oral tablet)
-inhibits binding of testosterone & 5 alpha dihydrotestosterone to androgen receptors

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

NOTE: These drugs are used with COCP / other form of secure contraception

25
Q

What drug is used to target insulin resistance in PCOS? How does it work?

A

Metformin (biguanide)

FUNCTION

  • 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

NOTE: It is less helpful for hirsutism & oligomenorrhoea, but may be an option for obese PCOS women

26
Q

How is hirsutism treated?

A

Via hair removal methods:
Photoepilation (laser) / electrolysis etc

Eflornithine cream (non-NHS)
Inhibits ornithine decarboxylase enzyme in hair follicles
27
Q

Name the differential diagnosis for hirsutism and their %

A
  • 95% PCOS or ‘idiopathic hirsutism’
  • 1% Non-classical congenital adrenal hyperplasia (CAH)
  • <1% Cushing’s syndrome
  • <1% Adrenal / ovarian tumour
28
Q

What % of women have PCOS?

A

5 - 10 %

29
Q

What is the aetiology of Primary Ovarian Insufficiency (POI) ?

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

30
Q

What is the presentation of Primary Ovarian Insufficiency (POI)?

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

NOTE: Other terms used for POI are “Premature ovarian failure” or “Premature menopause”

31
Q

What investigations are used to diagnose Primary Ovarian Insufficiency (POI)?

A

History / examination

Increased LH and FSH

Karyotype

Consider pelvic USS

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

32
Q

How is Primary Ovarian Insufficiency (POI) managed?

A

Psychological support

HRT = continue till approx 52 years of age

Monitor bone density = use DEXA scan

Fertility treatment via IVF with donor egg

33
Q

What is Turner syndrome?

A

Complete / partial X monosomy in some / all cells

- 50% of cases will be XO
- 50% due partial absence of X or mosaicism
34
Q

What proportion of live born girls have this condition?

A

1:2000 – 1:2500

35
Q

What are the presentations of Turner syndrome?

A

Diagnosed in the neonate

Short stature in childhood

Primary / secondary amenorrhoea

36
Q

What problems are associated with Turner syndrome (according to systems)?

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

When should you be worried about POI?

A

Sudden onset of severe symptoms

Virilisation

Frontal balding

Deepening of voice

Male-type muscle mass

Clitoromegaly (abnormal enlargement of the clitoris)

NOTE: This could be due to Cushing’s syndrome

38
Q

What is Congenital Adrenal Hyperplasia (CAH)?

A

Disorders of cortisol biosynthesis

Carrier frequency 1 : 60

Most patients are compound heterozygotes (they have different mutations on two alleles)

39
Q

What causes 95% of CAH cases? What does it result in?

A

21-hydroxylase deficiency

LEADS TO

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

NOTE: This depends on degree of enzyme deficiency

40
Q

How is CAH diagnosed?

A
  • High concentrations of 17-hydroxyprogesterone

- Can confirm with Synacthen test

41
Q

How does CAH present in childhood?

A

‘Classic’ / ‘severe’

Salt wasting
-hypovolaemia, shock

Virilisation

- ambiguous genitalia in girls
- early virilisation in boys

Precocious puberty (puberty occurs at an earlier age)

Abnormal growth

- accelerated early
- premature fusion

NOTE: Salt-losing (2/3rd), Non-salt losing (1/3rd)

42
Q

How does CAH present in adulthood?

A

‘Non-classic’ / ‘mild’, ‘late onset’

Hirsutism

Oligo / amenorrhoea

Acne

Subfertility

NOTE: Its presentation is similar to ‘PCOS’ presentation

43
Q

How is CAH treated?

A

Glucorticoid & mineralocorticoid replacement

- hydrocortisone &amp; fludrocortisone
- additional salt in infancy

Glucocorticoids suppress CRH / ACTH

Supraphysiological glucocorticoid doses may be needed to suppress adrenal androgen production
-Monitor [17-OH-P] / androstenedione
-Monitor growth in childhood
NOTE: 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 with/without anti-androgen

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

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