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O&G > PCOS & Subfertility (Mx) > Flashcards

PCOS & Subfertility (Mx) Flashcards

1
Q

What is the Rotterdam Criteria for PCOS?

A

At least 2:
- Oligo/anovulation (>2 years)
- Clinical or biochemical features of hyperandrogenism
- Cysts on USS

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2
Q

What are the requirements for cysts on USS for PCOS?

A

> =12 in one/both ovaries measuring 2-9mm or ovarian volume >10cm3

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3
Q

What is the approach for PCOS management outside of pregnancy/ not planning on pregnancy?

A

Lifestyle
Hormonal
Symptomatic

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4
Q

What is the lifestyle management for PCOS?

A
  • Weight reduction
  • Dietary modification (consider referral to dietician)
  • Screen for T2DM and cardiovascular disease
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5
Q

What is the hormonal management for PCOS?

A
  • COCP
  • Cyclical oral progesterone
  • Levonogestrel IUS
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6
Q

What is the mechanism of hormonal treatment in PCOS?

A

Increases sex hormone binding globulin which helps relieve androgenic symptoms

&increases progesterone (not produced by CL during anovulation) causing withdrawal bleed (regular periods) and protects against unopposed oestrogen

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7
Q

What is the management for PCOS if there are too many risk factors for COCP?

A

3 monthly progesterone to induce withdrawal bleeds (should take place every 3-4 months) & protect endometrium

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8
Q

What is the symptomatic management for PCOS?

A
  • Topical eflornithine cream (hirsuitism)
  • Co-cyprindiol
  • Cyproterone acetate
  • Metformin
  • GnRH analogues
  • Surgical treatment (laser or electrolysis)
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9
Q

When would co-cyprindiol be used for PCOS?

A

When it’s complicated by hirsutism and acne (also acts as a contraception)

Cyproterone acette + ethinyloestradiol

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10
Q

What is the mechanism of cyproterone acetate?

A

Antiandrogen

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11
Q

When are GnRH analogues used in PCOS?

A

When women are intolerant of other therapies

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12
Q

What is the managment of PCOS for subfertility?

A
  • Encourage weight loss
  • Clomiphene (1st line for women with normal BMI)
  • Gonadatrophins
  • Laprascopic ovarian drilling
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13
Q

When would metformin be added to clomiphene for PCOS subfertility?

A

After 3 failed cycles with clomiphene

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14
Q

What is the risk with gonadatrophins?

A

Ovarian hyperstimulation syndrome

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15
Q

What is laparoscopic ovarian drilling?

A

Destroys the ovarian stroma and may prompt ovulatory cycles

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16
Q

Describe the hormonal changes in the first part of the follicular phase?

A
  • LH and FSH released from the anterior pituitary
  • LH attaches to theca cells and causes androstenedione production
  • FSH attaches to the granulosa cells and causes aromatase production
  • Aromatase catalyses formation of 17beta oestradiol from androstenedione
  • 17beta oestradiol negatively feeds back to the pituitary and reduces predominantly FSH (to prevent more than one follicle developing)
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17
Q

Describe the hormonal changes midway through the follicular phase?

A
  • Granulosa cells in the dominant follicle increase LH receptors
  • Increased 17beta oestradiol produced
  • Levels of 17beta oestradiol exceed the threshold and now positively feedback onto the hypothalamus
  • Positive feedback predominantly increases LH secretion, causing an LH surge and release of the oocyte from the follicle

(Luteal phase begins)

18
Q

What are the hormonal changes in PCOS?

A
  • Anterior pituitary secretes too much LH
  • Increased circulating androstenedione
  • Travels into the blood and converted to oestrone by aromatase in peripheral tissues
  • Negative feedback to the pituitary, predominantly suppresses FSH production resulting in a 2:1 LH:FSH
  • No LH surge (high levels of baseline LH) meaning follicles don’t rupture and form cysts
19
Q

What are the symptoms of PCOS?

A

Hyperandrogenism
- Male pattern baldness
- Acne (face, back, chest)
- Hirsutism (upper lip, chin, chest)

Anovulation
- Amenorrhea
- Oligomenorrhea

Insulin resistance
- Overweight/ obese
- Acanthosis nigricans

20
Q

What is the mechanism of raised testosterone in PCOS?

A
  • Increased insulin can inhibit SHBG, increasing amount of free testosterone
  • Increased LH causes increased androstenedione which can be converted to testosterone by 17beta-hydroxysteroid dehydrogenase (produced by granulosa cells)
21
Q

What is the mechanism of clomiphene improving fertility in PCOS?

A

Selective oestrogen receptor modulator

  • Blocks oestrogen receptors in hypothalamus
  • No negative feedback, predominantly increasing FSH secretion (normalising LH:FSH ratio)
  • Normalised ratio, increases follicle development
  • Dominant follicle producing oestrogen causes positive feedback, increasing predominantly the LH secretion and leading to an LH surge causing ovulation
22
Q

What is the mechanism of cyproterone acetate?

A

Antiandrogen
- Blocks androgen receptors to reduce hirsutism and scalp hair loss

Decreased androgen production
- Progestogenic effects decrease LH secretion from pituitary (decreased androstenedione production)

23
Q

Why do progesterone treatments work for PCOS?

A

Anovulation leads to decreased progesterone from the corpus luteum –> amenorrhea, oligomenorrhea (and increased unopposed oestrogen)

Taking progesterone maintains the uterine lining and causes a withdrawal bleed (pill free interval)

Protective against unopposed oestrogen (endometrial cancer) and can increase SHBG which relieves androgenic sx

24
Q

What is the most successful biomarker for ovarian reserve?

A

Anti-mullarian hormone

Produced by granulosa cells and doesn’t change in response to gonadotrophins

25
Q

Which blood hormones should be measured when investigating subfertility?

A
  • Early follicular phase FSH, LH and oestradiol levels (day 2-3)
  • Anti-mullerian hormone
  • Mid-luteal progesterone (confirms ovulation)
  • TFTs, prolactin, testosterone
26
Q

What STI screening should be done in subfertility?

A

Chlamydia (men + women)

27
Q

What STIs should be screened for before considering assisted reproductive technology?

A
  • HIV
  • Hep C
  • Hep B
28
Q

What is the use of TVUSS in subfertility?

A
  • Pelvic anatomy
  • Cysts (PCOS)
  • Antral follicle count
  • Any pathology
29
Q

When is a tubal assessment performed in subfertility?

A

If there are risk factors for tubal damage eg. PID, endometriosis, ectopic pregnancy

30
Q

How is a tubal assessment performed?

A

Hysterosalpingography using x-ray OR

Laparoscopy and dye

31
Q

What is the conservative management of subfertility?

A
  • Regular intercourse (every 2-3 days)
  • Reduce smoking (affects semen quality)
  • Reduce alcohol intake (may affect semen quality)
  • Obesity and body weight (BMI <19 or BMI >30)
  • Drug use, occupational risks, stress, caffeine, pre-conception advice
32
Q

What is the medical management of subfertility?

A
  • Ovulation induction (clomiphene or FSH)
  • Intrauterine insemination (+-FSH)
  • Donor insemination (+-FSH)
  • IVF
  • Donor egg with IVF
33
Q

When is ovulation induction used?

A

Anovulation (idiopathic or PCOS)

34
Q

When is intrauterine insemination used?

A
  • Unexplained subfertility
  • Anovulation unresponsive to OI
  • Mild male factor
  • Minimal - mild endometriosis
35
Q

When is donor insemination used?

A
  • Azoospermia
  • Single woman
  • Same sex couples
36
Q

When is IVF used?

A
  • Tubal pathology
  • Previous fertility treatments without success
37
Q

When in donor egg with IVF used?

A
  • Poor egg quality
  • Previous surgery/ chemo where ovarian function adversely affected
38
Q

What is the surgical management of subfertility?

A
  • Operative laparoscopy to treat disease and restore anatomy
  • Myomectomy
  • Tubal surgery
  • Laparoscopic ovarian drilling
39
Q

When is operative laparoscopy used?

A
  • Adhesions
  • Endometriosis
  • Ovarian cyst
40
Q

When is myomectomy used?

A

Fibroid uterus

41
Q

When is tubal surgery used?

A

Blocked fallopian tubes amenable to repair

42
Q

When is laparoscopic ovarian drilling used?

A

PCOS unresponsive to medical treatment

O&G (11 decks)

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