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OnG Active > Gynae presentations - 1) Amenorrhoea > Flashcards

Gynae presentations - 1) Amenorrhoea Flashcards

1
Q

What is primary and secondary amenorrhoea?

A
  • Primary: absence of menarche
    • (girls aged 16+ with secondary sexual characteristics;
    • aged 14+ without)
  • Secondary: cessation of periods for ≥6 months after menarche (excluding pregnancy)
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2
Q

What are the main causes of amenorrhoea?

A
  • hypothalamic
  • pituitary
  • ovarian
  • adrenal
  • genital tract abnormalities
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3
Q

What are the hypothalamic causes of amenorrhoea?

A
  • Eating disorders (suppress GnRH),
  • Hypo/hyperthyroidism,
  • Kallmann syndrome
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4
Q

What are the pituitary causes of amenorrhoea?

A
  • Prolactinomas (negative feedback on GnRH),
  • Other pituitary tumours (mass effect),
  • Sheehan’s syndrome,
  • Post-contraception amenorrhoea (Depot causes downregulation of pituitary hormones)
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5
Q

What are the ovarian causes of amenorrhoea?

A
  • Turner’s syndrome,
  • Gonadal dysgenesis
  • PCOS,
  • Premature ovarian insufficiency/menopause
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6
Q

What are the adrenal causes of amenorrhoea?

A
  • Mild CAH
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7
Q

What are the genital tract abnormalities causes of amenorrhoea?

A
  • Congenital obstruction to normal menses flow e.g.,
    • vaginal septum,
    • imperforate hymen,
    • Rokintansky syndrome,
  • Iatrogenic obstruction to menses flow e.g.,
    • cervical stenosis
    • Asherman’s syndrome
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8
Q

What is oligomenorrhoea?

A

Oligomenorrhoea:

  • irregular periods
  • with cycle length >35d
  • and/or <9 periods/year
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9
Q

What must be looked for on examination in a woman presenting with amenorrhoea?

A
  • BMI
    • (high ~ = PCOS, low ~ = eating disorder)
  • Assess for features of:
    • Cushing’s syndrome (striae, buffalo hump, significant central obesity, easy bruising, hypertension, and proximal muscle weakness)
    • Hypo-/hyperthyroidism
    • Excess androgens (hirsutism, acne) + features of virilization (hirsutism, acne, deep voice, temporal balding, increase in muscle bulk, breast atrophy, and clitoromegaly)
      • (~ = PCOS, CAH, androgen-producing tumour of the ovaries, adrenals, pituitary, etc.)
    • Decreased endogenous oestrogen (reddened or thin vaginal mucosa)
      • (~ = premature ovarian insufficiency, etc.)
    • Hyperprolactinaemia (galactorrhoea)
      • (~ = prolactinoma, hypothyroidism, etc.)
  • Visual field assessment
    • (~ = pituitary tumour)
  • Bimanual examination
    • (~ = genital tract abnormalities e.g., vaginal septum, imperforate hymen, etc.)
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10
Q

What are the Ix in a woman presenting with amenorrhoea?

A
  • Pregnancy test
  • Bloods:
    • TFTs,
    • Prolactin,
    • LH, FSH,
    • Testosterone, oestrogen, 17-hydroxyprogesterone
  • Progesterone challenge to elicit a withdrawal bleed (no bleed suggests low oestrogen/outflow obstruction)
  • Karyotyping
  • USS (malformations, Turner’s, PCOS)
  • Hysteroscopy
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11
Q

Suggest what might be seen on FSH and LH in different causes of amenorrhoea

A
  • High FSH and LH levels on two occasions suggest premature ovarian insufficiency (in women younger than 40 years of age)
  • Normal or low FSH levels and normal or low LH levels suggest hypothalamic causes (weight loss, excessive exercise, stress, or rarely, a hypothalamic or pituitary tumour)
  • Normal FSH levels and normal or moderately increased LH levels may be found in PCOS
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12
Q

Suggest what might be seen on testosterone in different causes of amenorrhoea

A
  • High levels of total testosterone (5.0 nanomol/L or greater) warrant investigation to exclude other causes, such as Cushing’s syndrome, late-onset congenital adrenal hyperplasia, or an androgen-secreting tumour
  • A moderately increased testosterone level (2.5–5.0 nanomol/L) may be seen in PCOS.
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13
Q

What must be seen on transvaginal/transabdominal USS to diagnose PCOS?

A

Polycystic ovaries on US =

  • presence of ≥12 follicles (measuring 2–9 mm in diameter) in one or both ovaries
  • and/or increased ovarian volume (greater than 10 cm3)
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14
Q

What is the cause of PCOS?

A

The 2 main hormonal abnormalities are:

  • Insulin resistance
    • Leads to high insulin levels
    • Insulin promotes androgen production (possibly directly or through LH) and suppresses hepatic SHBG production (leading to higher levels of free circulating androgens)
  • Excess LH
    • Due to increased GnRH pulse frequency (which may be due to excess insulin)
    • Stimulates ovarian androgen production
    • LH is increased relative to FSH
      • Despite high LH levels, the LH surge is suppressed (due to increased androgens) → anvovulation
  • Follicles develop within the ovary but are arrested at an early stage  remain visible as cysts
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15
Q

What are the RFs for PCOS?

A
  • FHx,
  • premature adrenarche,
  • obesity (exacerbates severity),
  • DM
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16
Q

What are the signs & symptoms of PCOS?

A
  • Oligomenorrhoea or amenorrhoea (75%)
    • 40% have anovulatory cycles
  • Subfertility (75%)
  • Obesity (40%)
  • Hirsutism
  • Acne
  • Acanthosis nigricans
  • HTN
17
Q

What are the criteria for diagnosing PCOS?

A
  • Rotterdam criteria for diagnosis (2 of the following):
    • Oligo- or anovulation
    • Clinical and/or biochemical signs of hyperandrogenism
    • Polycystic ovaries on imaging
18
Q

What are the Ix for PCOS?

A
  • Bloods:
    • To aid diagnosis:
      • Serum total and free testosterone, and serum dehydroepiandrosterone sulfate (DHEAS)
        • Raised
      • LH & FSH
        • Raised LH, raised LH:FSH ratio → >3:1
        • Now not essential for diagnosis
      • Day 21 progesterone (low – suggests anovulation)
      • SHBG (low)
    • To exclude other causes (PCOS is largely a diagnosis of exclusion)
      • TFTs, prolactin, 17-hydroxyprogesterone
  • OGTT and fasting lipid panel
  • TVUSS
    • ≥12 follicles in each ovary, 2-9mm in diameter, and/or increased ovarian volume (>10ml)
19
Q

What is the Mx of PCOS?

A

Tailored to the symptoms and need for fertility

Lifestyle advice (for all patients)

  • Weight management → having normal BMI can reduce symptoms/trigger menstruation
  • Promote healthy diet and exercise
  • Hair removal (e.g. laser hair removal, hair removal cream)
  • Also treat underlying conditions (DM, HTN)

Treatment of oligo/amenorrhoea:

  • Need to induce bleeds because unopposed oestrogen (without progesterone) can cause endometrial hyperplasia
  • COCP (2nd line after weight loss)
    • Also increases SHBG → helps to reduce androgenic symptoms
  • Metformin (3rd line)
    • Insulin sensitiser; improves menstrual irregularity and restores ovulation; improves insulin sensitivity
    • Also improves hyperandrogenic symptoms by decreasing testosterone and increasing SHBG
  • Cyclic oral progestogen (4th line)
    • If COCP is contra-indicated, or in refractory cases

Treatment of hyperandrogenic features (hirsutism, acne):

  • COCP (1st line)
  • Metformin (adjunct)
  • Anti-androgen (e.g. spironolactone, finasteride)
    • Avoid in pregnancy (cause ambiguous genitalia)

Treatment of infertility (if desiring fertility):

  • Metformin
    • Weight loss should be tried first; metformin added if no response
    • Lower live birth rate than clomifene but no increased risk of multiple pregnancy
  • Clomifene (1st esp in normal weight women)
    • Anti-oestrogen → blocks oestrogen receptors in hypothalamus/pituitary → increased FSH and LH
    • Given on days 2-6; stepwise dose increase  induces follicular maturation and ovulation
    • 10% risk of multiple pregnancy, risk of ovarian hyperstimulation syndrome
    • Metformin can be added if not responsive
  • Gonadotrophins (2nd line)
    • Used if clomifene has failed
    • Daily SC injections
    • Risk of multiple pregnancies and ovarian hyperstimulation syndrome
  • IVF or laparoscopic ovarian drilling (3rd line)
    • Laparoscopic ovarian drilling uses laser to reduce the amount of functional ovarian tissue to reduce androgen and inhibin production  restores FSH levels and ovulation
20
Q

What are the complications and prognosis of PCOS?

A

Complications:

  • T2DM later in life (50%) and GDM (30%)
  • Increased risk of endometrial cancer (due to unopposed oestrogen)

There is no cure for PCOS so treatment should be continued through reproductive years

  • Improves after menopause
21
Q

What is Ashmerman’s sydrome?

A

Rare condition in which scar tissue or adhesions partially or completely occlude the uterine cavity

22
Q

Aetiology of Ashmerman’s sydrome?

A

Due to damage of the basal layer of endometrium

  • Basal layer does not regenerate → fibrosis and adhesion formation inside uterine cavity
  • Occurs after trauma (from instrumentation, e.g. D&C, ERPC, myomectomy), or infection (endometritis)
23
Q

What are the signs and symptoms of Asherman’s syndrome?

A
  • Amenorrhoea or reduced menstrual bleeding
  • Dysmenorrhoea or cyclical abdominal pain
  • Subfertility
24
Q

What are the Ix for ?Asherman’s syndrome?

A
  • Ix for subfertility
  • Hysteroscopy (gold standard)
  • Other:
    • Hysterosalpingogram (HSG): dye injected into cervix; X-rays visualise uterine cavity defects
    • Saline hysterosonography (TVUSS with saline in uterus)
25
Q

What is the Mx of Asherman’s syndrome?

A

Treatment is not needed if not planning to conceive & asymptomatic

Hysteroscopic adhesionolysis

  • To manually break down adhesions
  • Risks further trauma → scarring may recur
    • Reduce risk of adhesion recurrence with copper IUD and PO oestrogens (induce endometrial proliferation)
    • Reassess cavity 2-3 months later

Fertility treatment may be needed

26
Q

What are the complications and prognosis of Asherman’s syndrome?

A

Complications:

  • Subfertility
    • If patient does conceive, increased risk of miscarriage, placenta praevia and placenta increta

Menstrual disturbance often improves after treatment; post-treatment pregnancy rates are 50%

27
Q

What is menopause?

A

Permanent cessation of menstruation, defined as 12 months after the final period

28
Q

What is difference between:

  • perimenopause
  • early menopause
  • premature ovarian insufficiency?
A

Perimenopause: time from the beginning of the first features of menopause, until 12 months after the last period

Early menopause: menopause in a woman aged 40-45yo

Premature ovarian insufficiency: menopause in a woman <40yo

29
Q

What is the aetiology of menopause? Which other symptoms may be seen and why?

A

Hormonal changes:

  • Decreased follicular activity (due to reduced quality and quantity of eggs) causes reduced oestrogen secretion from ovaries
  • LH and FSH rise due to low oestrogen and inhibin (so removal of negative feedback)
  • Irregular bleeding occurs → some bleeds are menstruation from ovulatory cycles; others are anovulatory cycles which can occur up to every fortnight

Symptoms are due to hormonal changes

  • Vasomotor symptoms: due to pulsatile LH influencing temperature control
  • Urogenital symptoms: uterus, vagina, bladder and urethra are maintained by circulating oestrogen → decreased oestrogen causes atrophy of vagina/bladder/urethra and thinning of myometrium
  • Bone density: oestrogen reduces osteoclast activity → drop causes increase bone resorption
  • Ischaemic heart disease: oestrogen is protective by reducing LDL and raising HDL
30
Q

Aetiology of premature ovarian insufficiency?

A
  • In most women no cause is found, but causes can include:
    • Primary POI: chromosomal abnormalities (Turner’s), autoimmune diseases (hypothyroid, Addison’s, myasthenia gravis), enzyme deficiencies (CAH)
    • Secondary POI: surgical following bilateral oophorectomy, chemo/radiotherapy, infections
  • It can be reversible, so is not termed an early menopause
    • May experience unpredictable spontaneous ovarian activity → irregular vaginal bleeding and small risk/chance of pregnancy
31
Q

What are the signs and symptoms of menopause/early menopause/POI?

A
  • Persistent amenorrhoea
    • Often initial oligomenorrhoea or irregular/shortened cycles
  • Vasomotor symptoms: hot flushes, night sweats, palpitations, headaches
  • Urogenital symptoms: vaginal dryness, dyspareunia, frequency, dysuria, recurrent UTIs
  • Psychological symptoms: poor concentration, lethargy, mood disturbance, reduced libido
    • Usually the first to present
32
Q

What are the Ix for menopause/early menopause/POI?

A
  • Largely clinical diagnosis
  • Pregnancy test (for everyone)
  • Bloods:
    • In women <45yo; not recommended in >45yo
    • FSH: >30Iu/L is high → indicated menopause
      • Increased levels suggest fewer oocytes remaining in the ovaries
      • Varies throughout the cycle → best measured between days 2-5
    • Oestradiol: low
    • Anti-Mullerian hormone (AMH): low
      • Direct measurement of ovarian reserve; stable throughout menstrual cycle
    • Exclude other causes of symptoms: TFTs, catecholamines and 5-hydroxyindolacetic acid (phaeo and carcinoid syndrome), progesterone (low indicates anovulation), prolactin
  • TVUSS
    • Only if uncertainty
  • DEXA scan
    • If RFs for osteoporosis (early menopause, low BMI, FHx, corticosteroids etc.)
33
Q

What is the Mx for menopause/early menopause/POI?

A

Conservative measures:

  • Stop smoking, regular exercise, healthy eating, avoid alcohol and caffeine
    • To improve symptoms and address long-term health
  • Some women try alternative therapies (acupuncture, evening primrose oil)
  • May be sufficient for some women

Hormone replacement therapy (HRT):

  • For women who cannot tolerate the symptoms; and in POI until 50yo
  • Regimens:
    • Women with a uterus: oestrogen + progestogen
      • Unopposed oestrogen increases risk of endometrial hyperplasia and carcinoma (progesterone is given to counteract this)
      • Usually given as norethisterone/oestradiol transdermal patch; changed twice weekly
        • May be given orally; oestrogens are sometimes given as implant; progestogens are sometimes given as IUS
      • Perimenopausal women are given cyclic therapy (continue to bleed); postmenopausal women are given continuous therapy
    • Women without a uterus (or IUS fitted in last 5yrs): oestrogen (as above)
    • For urogenital atrophy (without other symptoms): topical oestrogen
      • Progesterone is not needed (don’t increase systemic oestrogen)
      • Cream, ring, pessary
    • For reduced libido: methyltestosterone
      • Patch or subcutaneous implant
      • Not successful in all women → other factors may be involved
    • NB tibolone is sometimes used as an alternative → oestrogenic, progestogenic and androgenic actions

POI:

  • HRT until 50yo
  • Oocyte donation for fertility treatment
  • Supportive care and counselling
34
Q

What are the risks and benefits of HRT?

A

Benefits of HRT:

  • Menopausal symptoms: reduces hot flushes and urogenital symptoms
    • Libido may be improved by oestrogen alone or may need testosterone in addition
  • Reduces risk of osteoporosis
  • Reduces risk of colorectal cancer and may slightly reduce risk of CVD

Risks of HRT:

  • Breast cancer: combined HRT (but not oestrogen alone) increases risk
    • Effect is not seen in women who start oestrogen early for premature ovarian insufficiency (not seen below 50yrs)  suggests lifetime exposure is relevant
  • Endometrial cancer: unopposed oestrogen increases risk
  • Venous thromboembolism: oral HRT increases risk 2x
  • Gallbladder disease: risk increased by oral HRT
35
Q

What is the duration of therapy for different types of ‘menopause’?

A
  • Menopausal symptoms: 5yrs then stop to assess whether still needed
  • Premature menopause/POI until 50yo: continue until 50yo
  • Osteoporosis: treatment may need to be lifelong
36
Q

What are some other Mx options for types of ‘menopause’?

A

Other management options (considered if HRT contraindicated or insufficient):

  • SSRIs may be effective for hot flushes
  • Lubricants and moisturisers for vaginal atrophy
  • Osteoporosis treatments, e.g. vitamin D/calcium, bisphosphonates
37
Q

What are the complications and prognosis of menopause?

A

Complications:

  • CVD → same risk as men after menopause
  • Osteoporosis
  • Depression increases during perimenopausal period

Troublesome symptoms usually decrease after 5 years; may persist (esp vaginal dryness

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