oligomenorrhea and amenorrhea, menopause, urogynaecology Flashcards

1
Q

What is the definition of oligomenorrhea?

A

infrequent / irregular menstrual periods (defined variably as fewer
than 6 - 8 per year).

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2
Q

What is the definition of amenorrhea?

A

the absence of a menstrual period.
○ Primary amenorrhea: absence of a period at age 15 in the presence of normal
secondary sexual characteristics or at age 13 with no secondary sexual
characteristics.
○ Secondary amenorrhea: absence of a period for three consecutive cycles in a
woman with a previously established menstrual cycle.

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3
Q

What are the primary causes of amenorrhea?

A

○ Constitutional delay (familial)
○ Imperforate hymen
○ Hypo- / hyperthyroidism, hyperprolactinaemia, Cushing’s syndrome
○ Androgen insensitivity syndrome
○ Turner’s syndrome

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4
Q

What are the secondary causes of amenorrhea?

A

○ Functional Hypothalamic Amenorrhea - excessive exercise, weight loss,
stress, eating disorders.
○ Premature ovarian insufficiency
○ Sheehan’s syndrome, prolactinoma, hypopituitarism
○ Hypo- / hyperthyroidism

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5
Q

What is the definition of PCOS?

A

Endocrinopathy resulting in syndrome of ovarian cysts, oligomenorrhea and
hyperandrogenism.

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6
Q

What is the criteria for PCOS?

A
  • PCOS is defined by the Rotterdam Criteria - a woman must meet 2 of the 3:
    1. Hyperandrogenism
    2. Oligo- or anovulation
    3. Polycystic morphology on ultrasound.
  • Therefore PCOS can be diagnosed in the absence of ovarian cysts.
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7
Q

What is the aetiology and pathophysiology of PCOS?

A
  1. Disrupted balance between androgens, anti-Mullerian hormone and FSH levels
    leads to arrest in follicular development:
    a. Increased GnRH release frequency leads to high LH:FSH ratio.
    b. This results in high androgen:oestradiol ratio.
    c. Low oestrogen (due to reduced granulosa cell activity) prevents follicle
    selection and subsequent ovulation. Instead, multiple immature follicles
    remain and form cysts.
    d. Additionally, high androgens may inhibit sex steroid negative feedback on
    the HPG axis, leading to a ‘vicious circle’ of rising androgens.
  2. Insulin resistance and hyperinsulinaemia:
    a. Peripheral insulin resistance (skeletal muscle, adipose tissue) leads to
    hyperglycaemia and subsequent hyperinsulinaemia.
    b. High insulin levels stimulate theca cell androgen production and reduce
    sex-hormone binding globulin levels (SHBG); this means increased free
    circulating androgens.
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8
Q

What is the presentation of PCOS?

A

● Hyperandrogenism: hirsutism, acne, hyperhidrosis.
● Oligomenorrhea - due to oligo-ovulation.
● Subfertility / infertility

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9
Q

What are the risk factors of PCOS?

A
  1. Obesity
  2. Family history
  3. Premature adrenarche (pubic / axillary hair, apocrine sweat gland development).
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10
Q

What investigations are done for PCOS?

A
  1. Total serum testosterone - elevated
  2. Sex hormone-binding globulin (SHBG) - normal to low
  3. Free androgen index - elevated
  4. Rule-out tests: LH and FSH (premature ovarian failure), prolactin
    (hyperprolactinaemia), TFTs (hypothyroidism); used to eliminate other causes of
    oligomenorrhea.
  5. Imaging: ultrasound - 12 or more follicles on one ovary.
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11
Q

Management for PCOS when fertility is not desired?

A
  1. First Line: COCP plus weight loss
  2. Second Line (in event of prolonged amenorrhea)
    a. Cyclical progesterone (taken for 14 days every 3 months) to induce a
    withdrawal bleed to protect endometrium.
    b. Also offer transvaginal USS to assess endometrial thickness
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12
Q

What is the management when fertility is desired in PCOS?

A
  1. First Line: weight loss plus:
    a. Clomifene or
    b. Letrozole (aromatase inhibitor).
  2. Second Line:
    a. Metformin
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13
Q

What is the mechanism of COCP for PCOS treatment?

A

regulation of menstrual cycle through stabilisation of oestrogen & progesterone levels. Also
increases hepatic SHBG production (lowering free androgen index) and blocks some androgen receptors.

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14
Q

What is the mechanism of action for metformin for PCOS?

A
  • improves peripheral insulin sensitivity to downregulate effects of insulin resistance
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15
Q

What is the mechanism for clomifene for PCOS?

A

selective oestrogen receptor modulator; blocks hypothalamic oestrogen receptors, thereby
inhibiting HPG axis negative feedback and inducing FSH / LH secretion to lead to ovulation

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16
Q

What is the mechanism for letrozole for PCOS?

A

aromatase inhibitor, inhibits peripheral conversion of androgens into oestrogen, reducing HPG
axis negative feedback to promote ovulation.

17
Q
A