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A4 Reproductive Physiology and Endocrinology > PCOS > Flashcards

PCOS Flashcards

1
Q

Describe the pathophysiology of PCOS

A

Androgen excess caused by rapid GnRH pulses, leading to excessive LH and insufficient FSH.

Increased LH:FSH ratio leads to excess androgen production from theca cells.

Ovulatory dysfunction: multiple preantral and antral follicles develop but failure to select a dominant follicle leading to anovulation.

Lack of corpus luteum secreted progesterone leads to infrequent menstruation.

Unopposed oestrogen causes endometrium to thicken until it destabilises and sheds, often resulting in heavy menstruation.

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2
Q

What is the prevalence of PCOS?

A

5-10% of reproductive age women depending on diagnostic criteria used

RANZCOG says 6-7%

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3
Q

Define the Rotterdam criteria for diagnosing PCOS

A

Need two out of three of the following:

  • Oligo- or amenorrhoea
  • Polycystic ovaries on ultrasound (increased ovarian volume >10 mL or >20 follicles per ovary)
  • Clinical or biochemical androgen excess
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4
Q

List the clinical features of hyperandrogenism associated with PCOS?

What are some other clinical features associated with PCO?

A
  • Hirsuitism
  • Acne
  • Alopecia

Other features:

  • Heavy periods
  • Obesity
  • Infertility
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5
Q

What is a ultrasonographic feature of polycystic ovarian morphology?

A

Increased ovarian volume >10 mL
>20 follicles in each ovary
String of pearls

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6
Q

What tests would you order to make a diagnosis of biochemical hyperandrogenism?

A

Serum testosterone, SHBG, free androgen index on day 2-5 of cycle.

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7
Q

How might concurrent use of the combined oral contraceptive pill affect testing for androgen excess?

A

The COCP inhibits ovarian and adrenal production of androgens and increases the level of SHBG, leading to falsely low levels of androgen.

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8
Q

Why might you organise serum LH and FSH levels in a woman being investigated for PCOS?

A

To exclude primary ovarian insufficiency (characterised by elevated FSH >30-40 mIU/L measured at least 4 weeks apart).

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9
Q

List the differential diagnoses for PCOS and appropriate investigations you would order to differentiate these

A
  • Pregnancy: BhCG
  • Thyroid dysfunction: TSH
  • Hyperprolactinaemia: prolactin level
  • Congenital adrenal hyperplasia: 8 am 17-OHP and synacthen (ACTH) test.
  • Androgen-secreting tumour: pelvic ultrasound and abdominal CT.
  • Functional hypothalamic amenorrhoea: diagnosis of exclusion
  • Primary ovarian insufficiency: FSH on two occasions at least 4 weeks apart.
  • Cushing’s disease: 1 mg dexamethasone suppression test; a low / suppressed cortisol level excludes Cushing’s disease.
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10
Q

Outline the long term sequelae for untreated PCOS

A
  • Increased risk of endometrial hyperplasia and malignancy
  • Increased risk of infertility
  • Increased risk of cardiovascular disease
  • Increased risk of diabetes
  • Increased risk of depression
  • Increased risk of OSA
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11
Q

Outline your approach to managing a woman with PCOS

A
  • Weight loss
  • Endometrial protection / contraception if desired
  • Fertility
  • Cardiometabolic risk
  • Hirsuitism and acne
  • Mental health
  • OSA
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12
Q

Describe what advice you would give regarding weight loss

A
  • Weight loss target 5-10%; improves ovulation rates, hirsuitism and insulin sensitivity.
  • Diet, exercise
  • Referral for bariatric surgery if appropriate (BMI > 40 or BMI > 35 with an obesity related condition)
  • Orlistat (lipase inhibitor that reduces dietary fat absoprtion)
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13
Q

Describe what advice would you give regarding endometrial protection and contraception

A
  • Unopposed oestrogen long term increases risk of endometrial hyperplasia and malignancy.
  • Options: COCP, Mirena, cyclical (12 days) oral progesterone
  • Offer endometrial sampling if abnormally thickened endometrium + other risk factors (HMB, high BMI, diabetes etc).
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14
Q

Describe what advice you would give regarding fertility

A
  • Weight loss will lead to resumption of ovulatory cycles.
  • 1st line: Ovulation induction: letrozole, clomiphene citrate
  • 2nd line: gonadotrophin injections
  • 3rd line: laparoscopic ovarian drilling
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15
Q

Describe the mechanism of action of letrozole for ovulation induction

A

Aromatase inhibitor that inhibits ovarian and adrenal conversion of androstenedione and testosterone to oestrone and oestradiol. Lower circulating oestrogen results in reduced negative feedback inhibition of GnRH leading to more FSH secretion and follicular development.

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16
Q

Describe a commonly used ovulation induction protocol with letrozole and risks associated with its use.

A

After period or induced bleeding, commence letrozole 2.5 mg po daily on days 3 to 7 of cycle. If anovulatory can increase dose in 2.5 mg increments (i.e. 2.5, 5 and 7.5 mg) up to max dose of 7.5 mg daily.

Need TVUSS monitoring to detect hyperresponse; if too many follicles are selected couple should be advised not to have sex due to risk of multiple pregnancies.

Risks associated with letrozole use: multiple pregnancies; hot flushes, nausea, fatigue, dizziness.

17
Q

Describe the mechanism of action of clomiphene citrate for ovulation induction

A

Selective estrogen receptor modulator / anti-oestrogen that competitively inhibits oestrogen binding to its receptor.Primary site of action is at hypothalamus; it blocks the negative feedback of circulating endogenous oestradiol leading to increased GnRH pulse frequency and increased serum concentrations of FSH and LH. This in turn increases ovarian follicular development

18
Q

Describe a commonly used ovulation induction protocol with clomiphene citrate and risks associated with its use.

A

After a period or induced bleed, start clomiphene at 50 mg po daily on day 5 of cycle and continue for 5 days.
Advise couple to start having sexual intercourse every second day 5 days after the last dose of clomiphene. *Rule of 5s

Need TVUSS monitoring to detect hyperresponse; if too many follicles are selected couple should be advised not to have sex due to risk of multiple pregnancies.

Risks associated with letrozole use: multiple pregnancies; hot flushes, nausea, fatigue, dizziness.

19
Q

What management options are there for acne and hirsuitism associated with PCOS?

A

1st line: COCP
2nd line: cyproterone acetate OCP (Ginet)
3rd line: conventional acne treatments e.g. antibiotics, topical retinoids, isotretinoin

20
Q

What metabolic screening should be performed?

What cardiovascular screening should be performed?

A

Metabolic:

  • OGTT; if impaired glucose tolerance, should be performed annually.
  • OGTT in pregnancy

Cardiovascular:

  • Annual: BP, BMI, waist circumference, OGTT
  • Twice a year: lipid profile
21
Q

With PCOS, what is the RR of getting GDM?

A

3

22
Q

With PCOS, what is the RR of getting T2DM?

A

2

23
Q

With PCOS, what is the RR of getting endometrial cancer?

A

2-6

24
Q

What five components make up metabolic syndrome?

A 
Elevated BP
Increased waist circumference
Elevated fasting BSLs
Reduced high density lipoprotein cholesterol levels
Elevated triglyceride levels

A4 Reproductive Physiology and Endocrinology (9 decks)

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