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General Gynaecology > PCOS > Flashcards

PCOS Flashcards

1
Q

Describe the pathophysiology of PCOS

A
  • Unclear exactly why PCOS occurs, thought to be related to insulin resistance –> increases insuin —> insulin receptors on theca cells –>cause theca cells to grow and divide —> increase in LH receptors —> GnRH increases secretion of LH
  • excess LH in comparison to FSH
  • LH->Theca cells-> androstenedione ++++ (androgen)
  • Low FSH–>can’t convert all of androstenedione to oestrogen via aromatase
  • Excess estrone converted instead
  • Estrone negatively feeds back to ant pit to decrease FSH
  • No LH surge therefore no ovulation - amenorrhoea or oligomenorrhoea
  • Remaining follicles either become cysts (hence polycystic) or degenerate
  • Relative hyperoestrogenic with low levels of progesterone due to anovulation
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2
Q

What is the prevalence of PCOS?

A

8-13% of reproductive age women depending on diagnostic criteria used

(MONASH)

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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 (without corpus luteum) 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 PCOS?

A
  • Hirsuitism
  • Acne
  • Alopecia

Other features:

  • Heavy periods
  • Obesity
  • Infertility
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5
Q

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

A

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

Women should be off hormonal contraception for >1 month as affects SHBG and androgen levels.

Free T increased
SHBG decreased
FAI increased

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6
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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7
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 twice at least 4 weeks apart).

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8
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
  • Late onset Congenital adrenal hyperplasia: 8 am 17-OHP
  • Androgen-secreting tumour: DHEA and DHEA-S; if elevated consider abdominal CT.
  • Primary ovarian insufficiency: FSH/LH on two occasions at least 4 weeks apart, consider estrogen level
  • Cushing’s disease: 1 mg overnight dexamethasone suppression test; a low / suppressed cortisol level excludes Cushing’s disease. If not suppressed, perform high dose dexamethasone suppression test to delineate between pituitary tumour vs ectopic production of ACTH.
  • Intracranial pathology (e.g. tumour, sheehans syndrome, etc); low FSH/LH and oestrogen - arrange CT or MRI head
  • Functional hypothalamic amenorrhoea: diagnosis of exclusion based on Hx and exam
  • Previous uterine surgery and concern for Ashermans; saline infused sonohysterogram or hysteroscopy
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9
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/metabolic syndrome
  • Increased risk of diabetes
  • Increased risk of OSA
  • Increased risk of depression
  • Increased risk poor body image
  • Increased risk of eating disorders (notably bullimia)
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10
Q

Outline your approach to managing a woman with PCOS

A
  • Weight loss
  • Endometrial protection / contraception if desired
  • Regulation of cycles
  • Fertility
  • Cardiometabolic risk
  • Hirsuitism and acne
  • Mental health
  • OSA
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11
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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12
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).
  • Should have a cycle at least every 3-4 months - can be induced with progesterone for 12/7
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13
Q

Describe what advice you would give regarding fertility

A
  • Even 5-10% weight loss will lead to resumption of ovulatory cycles.
  • 1st line: Ovulation induction: letrozole (first), clomiphene citrate, clomiphene citrate plus metformin (for women resistant to clomiphene)
  • 2nd line: gonadotrophin injections OR laparoscopic ovarian drilling
  • 3rd line: IVF
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14
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 on hypothalamus and anterior pituitary leading to more FSH secretion and follicular development.

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15
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.

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

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16
Q

Describe the mechanism of action of clomiphene citrate for ovulation induction

A

A selective oestrogen receptor modulator (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

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17
Q

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

A

Rule of 5s
The starting dose of clomiphene citrate is 50 mg per day for 5 days, commencing between day 2 and 5 of menses.

Menses may be induced with a progestin if required.

If this dose produces multiple follicular development, the dose can be lowered to 25 mg.

If ovulation is not achieved using 50 mg per day, the dose can be increased to maximum 150 mg per day. Maximum 6 months therapy.

Advise couple to start having sexual intercourse every second day 5 days after the last dose of clomiphene.

Risks associated with letrozole use: multiple pregnancies; hot flushes, nausea, fatigue, dizziness. Increased risk of borderline ovarian tumours if >12cycles

Success rates: 60% to 85% of patients will ovulate on CC, only about one half will conceive

18
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
- Vaniqa – eflornithine hydrocholride a cream applied twice daily to prevent new hair growth.

If unsuitable for COCP or persistence on COCP trial anti androgens :

  1. Spirinolactone 100–200mg/day. Renal function and potassium should be monitored if using with a drosperidone COCP.
  2. Cyproterone acetate 50–100mg ten days/month. Liver function tests should be monitored.
  3. Flutamide 250mg oral dosing. Liver function tests must be monitored – liver failure has been reported.
  4. Finasteride 2.5mg oral dosing may be helpful for androgenic alopecia.
19
Q

What metabolic screening should be performed?

What cardiovascular screening should be performed?

A

Metabolic:

  • OGTT and HbA1c
  • Screening every 1-3 years depending on risk factors
  • early OGTT in pregnancy and repeat at 24-28 weeks

Cardiovascular:

  • Annual: BP, BMI, waist circumference, OGTT, smoking status
  • If elevated BMI >25: fasting lipid profile
20
Q

With PCOS, what is the RR of getting GDM?

A

3

21
Q

With PCOS, what is the RR of getting T2DM?

A

2

22
Q

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

A

2-6

23
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
24
Q

Ongoing management of cardiovascular risk factors for PCOS?

A
  • Monitor for conversion to T2DM (fasting levels not as helpful for diabetes in women wit PCOS, should have OGTT)
  • Measure cholesterol/lipid profile
  • Manage BP
  • Encourage lifestyle factors/weight loss
  • Ask about sx of OSA- increased risk even when controlled for BMI with link. OSA a risk factor for CVD.
25
Q

What is the role of metformin in PCOS for reducing CVD risk?

A

Insulin sensitising agents such as metformin have a role when IGT or T2D has been diagnosed.

However, there is no current evidence indicating that these drugs lower cardiovascular risk, and their routine use in PCOS is not recommended.

Trials suggest that metformin is not superior to lifestyle intervention in improving cardio-metabolic risk or progression to T2D.

26
Q

When should bariatric surgery be considered?

A

where obesity is not controlled by lifestyle modifications.

27
Q

Risks of bariatric surgery?

A

0.1-1% mortality,
risk of bowel obstruction,
infection,
oesophagitis
nutritional abnormalities.
● perinatal risks such as small for gestational age, premature delivery, possibly
increased infant mortality
● recommendations for pregnancy avoidance during periods of rapid weight loss
and for at least 12 months after bariatric surgery with appropriate contraception.

Bariatric surgery should be performed only when standard weight loss regimes have failed in PCOS women with a BMI greater than 40 or greater then 35 with a high-risk obesity related condition

28
Q

How to differentiate CAH from PCOS?

A
  • 17-hydroxyprogesterone should be measured in the follicular phase and will be raised in CAH
  • If 17- hydroxyprogesterone is borderline, it will have to be confirmed by an ACTH stimulation test to
    diagnose CAH
29
Q

Which women with PCOS should be screened for diabetes?

A

All women should have glycemic status assessed by one of: OGTT, fasting plasma glucose or HbA1c

OGTT is recommended in high-risk women with PCOS including:

  • BMI > 25kg/m2 or in Asians > 23kg/m2,
  • history of impaired fasting glucose,
  • impaired glucose tolerance or gestational diabetes,
  • family history of diabetes mellitus type 2,
  • hypertension
  • high-risk ethnicity.
30
Q

An endometrial thickness of less than ___mm is unlikely to be endometrial hyperplasia in women with PCOS?

A

7mm

for every 1 mm increase in endometrial thickness, the odds ratio of hyperplasia increases by 1.48

31
Q

What lifestyle intervention techniques have been shown to be effective for weight loss?

A

motivational interviewing and established behaviour techniques appear more effective than traditional advice giving for changes in weight, diet and/or exercise.

Suggesting ways to access support to help with weight loss and exercise, establishing self-monitoring
(including pedometer use), time management techniques, relapse prevention techniques, individual
tailoring, engaging social support and setting goals have all been shown to be useful.

Individual, group and mixed interventions have been shown to be effective

32
Q

Role of weight loss and fertility in PCOS

A

Obese women with PCOS are more likely than thin women with PCOS to suffer from anovulation

In obese, anovulatory women with PCOS, weight loss of even 5% to 10% of body weight often restores ovulatory cycles

overweight women are also less likely to respond
to pharmacologic ovulation induction methods

Exercise increases insulin sensitivity

33
Q

Mechanism of action of metformin?

A

A biguanide insulin-sensitizing agent.

Metformin works by decreasing gluconeogenesis, lipogenesis and enhancing glucose uptake in the liver, skeletal muscle, adipose tissue and ovaries.

It is known in other populations to assist with weight loss, to prevent and manage DM2, gestational diabetes (GDM), and to reduce microvascular and cardiovascular disease in DM2

Side effects are not uncommon,
yet these are primarily gastrointestinal, appear mild and self-limiting

It does not stimulate secretion of insulin or cause hypoglycemia

34
Q

Metformin and fertility in PCOS?

A

Metformin combined with clomiphene citrate may
increase ovulation rates and pregnancy rates but does not significantly improve the live birth rate over that of
clomiphene citrate alone.

Metformin may be added to clomiphene citrate in women with clomiphene resistance who are older and who have visceral obesity

35
Q

Ovulation induction with gonadotrophins in PCOS?

A

Second line treatment

Higher risk of hyperstimulation

Method:
- Daily injections of gonadotropins combined with concurrent blood and ultrasound monitoring
- Aim is monofollicular growth and development. However, multifollicular development is not uncommon,
despite careful dose adjustment and monitoring.

  • Once the dominant follicle has reached the appropriate size, hCG is administered to trigger ovulation.

Pregnancy rates with gonadotropins are 20% to 25% per cycle.

Gonadotrophin induced ovulation is only triggered when ≤ 2 mature follicles, if 3 or more the patient advised to avoid unprotected intercourse due to risk OHSS and multiple pregnancy.

36
Q

What should be recommended to reduce risk of OHSS during IVF?

A
  • GnRH antagonist short protocol; reduce the length of exposure/stimulation
  • lowest dose HCG trigger
  • Consider using metformin before and during follicle stimulation
  • Consider electively freezing all embryos
37
Q

Compare letrozole, clomiphene and clomiphene +metformin for ovulation induction

A

Letrozole has higher ovulation, pregnancy and live birth rates than CC. Reduced rate multiple pregnancies.

Letrozole outcomes comparable to CC + metformin for women who are CC resistant.

38
Q

What is the increase in live birth rate when using letrozole vs clomiphene?

A

40-60% increased live birth rate.

39
Q

What are the risks of multiple pregnancy and OHSS with clomiphene?

A

multiple pregnancy 5-7%

OHSS <1%

40
Q

Evidence for laparoscopic ovarian surgery for ovulation induction.

A

A 15-25 year follow-up of nearly 150 women after ovarian wedge resection shows that regular menstrual patterns lasting up to 25 years after surgery were restored in 88% of patients with a cumulative pregnancy/live birth rate of 78%

(MONASH)

41
Q

Why is USS not included in diagnostic criteria within 8 years of menarche?

A

Normal to have PCOM during this timeframe, leading to false diagnosis of PCOS.

If high suspicion of PCOS - testing can be repeated after this time frame to confirm.

42
Q

What are the diagnostic values for HbA1c and OGTT for IR and diabetes mellitus?

A

insulin resistance

  • HbA1c 42-47
  • OGTT fasting = 6.0-7.0, 2hr = 7.0 - 11.1

diabetes mellitus

  • Hba1c ≥ 48
  • OGTT fasting > 7.0 and 2 hour after 75g glucose challenge >11.1

General Gynaecology (16 decks)

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