PCOS and hyperandrogenism - GT33 and various TOGs Flashcards

1
Q

When should women with a history of PCOS be screened for GDM?

A

At 24-28/40

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2
Q

How should women with PCOS be screend for T2DM?

A

BMI >= 25 or normal but with risk factors (e.g. Age >40, GDM, FHx of T2DM) - 2 hour GTT

If impaired (fasting BM 6.1-6.9 or 2 hour BM >7.8 but <11.1) - annual GTT

HbA1C if GTT unacceptable - fasting not accurate

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3
Q

When should lipid-lowering treatment be used in PCOS?

A

If CV risk factors, but only by a specialist

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4
Q

What are the health concerns with PCOS?

A
  • Risk T2DM/insulin resistance (65-80%)
  • Cardiovascular risk
  • Obstructive sleep apnoea
  • Psychological issues
  • Risk of endometrial Ca
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5
Q

When should endometrial biopsy +/- hysteroscopy be considered in PCOS?

A

If ET >7-9mm, appears abnormal on USS or suspected polyp

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6
Q

What is first line treatment for oligo/amenorrhoea?

A

Withdrawal bleed using progestogens (12/7) every 3-4 months

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7
Q

When can bariatric surgery by considered in PCOS?

A

If BMI >= 40 or 35 with high-risk obesity-related condition and weight loss strategies have failed

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8
Q

What is the prevalence of PCOS?

A

2.2-26%

Higher in South Asian - younger, more severe

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9
Q

What are the Rotterdam criteria?

A
  1. Polycystic ovaries (>=12 follicles, volume >10cm3)
  2. Oligo-ovulation or anovulation
  3. Clinical +/- biochemical signs of hyperandrogenism
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10
Q

What is the recommended baseline blood test for hyperandrogenism and how is it calculated?

A

Free androgen index

Total testosterone
————————— x 100
SHBG

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11
Q

What differentials should be excluded if rapid hirsutism (<1yr), virilisation, +/- testosterone >5?

A

Androgen-secreting tumours

Late onset CAH (17 alpha hydroxyprogesterone raised, confirmed by ACTH stimulation test)

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12
Q

How much more frequent is GDM in PCOS compared to general population?

A

x2

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13
Q

By how much are women with PCOS at increased risk of endometrial cancer?

A

x 2.89

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14
Q

How little weight loss could improve insulin resistance and testosterone levels in PCOS?

A

5%

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15
Q

What % of PCOS have normalisation of androgens/SHBG and persistence of ovulation for up to 20 years following lap ovarian drilling?

A

> 60%

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16
Q

What is the prevalence of PCOS?

A

6-7%

17
Q

What is the biochemical profile in PCOS?

A
  • Hyperinsulinism causing raised LH - potentiates LH and IGF-1
  • Upregulate synthesis of androgens (adrenal and ovarian) testosterone and DHEA-S
  • All cause arrest of follicles
  • Overproduction of AMH antagosises FSH
18
Q

What % of women with PCOS will have insulin resistance?

A

80%

19
Q

What are the adrenal androgens?

A

DHEA (predominant)

DHEA-S (sulphuric acid ester) - useful measure of adrenal androgen production

20
Q

Which androgens are produced by the ovary?

A

20% of DHEA
50% of androstenedione
25% circulating testosterone

21
Q

How does testosterone circulate around the body?

A

80% bound to SHBG
19% bound to albumin
1% circulates freely

22
Q

Which androgens can activate androgen receptors?

A

Testosterone

DHT (active metabolite)

23
Q

How is testosterone excreted?

A

Metabolised in liver
Conjugated
Excreted in urine as 17-ketosteroids

24
Q

Where in the brain are the highest concentration of androgen receptors?

A

Preoptic area of the hypothalamus - close to oestrogenic

25
Q

What is the scoring system and limits for hirsutism?

A

Ferriman-Gallwey score
11 body areas 0-4
>=8 defines hirsutism

26
Q

What testosterone level should prompt concerns of an androgenic tumour?

A

> 5nmol/L

27
Q

What is the differential diagnosis of hyperandrogenism?

A
  • PCOS
  • Ovarian hyperthecosis
  • Congenital adrenal hyperplasia (2%)
  • Cushing’s syndrome
  • Androgen-secreting tumour (ovarian/adrenal)
  • Exogenous androgen administration
  • Gestational hyperandrogenism
28
Q

What is ovarian hyperthecosis?

A
  • Accounts for most hyperandrogenism in post-menopausal
    -Presence of luteinised theca cell nests in the ovarian
    stroma
  • Testosterone may be >7
29
Q

Which are the virilising ovarian androgenic tumours?

A
  • Sertoli Leydig cell tumours (0.5% all ovarian)
  • Granulosa cell
  • Hilar cell
  • Brenner tumours
30
Q

What are the most common causes of gestational hyperandrogenism?

A

Luteomas
Theca lutein cysts

SHBG should go up in preg - protective
Unilateral solid androgenic masses in pregnancy - increased chance of malignancy