Menstrual Disorders Flashcards

1
Q

Define hypomenorrhoea

A

Bleeding that is decreased in amount

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2
Q

Define oligomenorrhoea

A

Bleeding occurring at intervals more than 35d

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3
Q

Define menorrhagia/hypermenorrhoea

A

Bleeding at regular intervals that is prolonged in duration (>7d) or excessive in amount

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4
Q

Define metrorrhagia

A

Bleeding at regular intervals, particularly between expected menstrual periods

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5
Q

Define menometrorrhagia

A

Excessive bleeding at usual time of menstrual periods and at other irregular intervals

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6
Q

Define postmenopausal bleeding

A

Any bleeding that presents >1 yr after menopause; endometrial cancer until proven otherwise

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7
Q

Define primary amenorrhoea

A

No menses by age 14 in absence of secondary sexual characteristics or no menses by age 16 with secondary sexual characteristics

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8
Q

Define secondary amenorrhoea

A

No menses for >6 months or 3 cycles after documented menarche

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9
Q

How is menopause defined/diagnosed?

A

Amenorrhoea for 1 year - clinical.

Can look at FSH levels (increased) but not always predictive

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10
Q

Describe the pathophysiology of menopause

A

Theca cells degenerate and fail to react to endogenous gonadotropins (FSH/LH) –> less oestrogen is produced –> decreased negative feedback on HPA axis –> increased FSH and LH –> increased LH stimulation leads to stromal cells producing androgens

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11
Q

When does physiological menopause occur?

A

average age 51; range 45-55 (95% of women)

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12
Q

What are the clinical features of menopause? (5)

A

All due to oestrogen deficiency

  1. Vasomotor instability - hot flushes, night sweats, sleep disturbances
  2. Urogenital atrophy - dyspareunia, vaginal dryness, can cause bleeding, urinary frequency, urgency, incontinence
  3. Skeletal - osteoporosis, joint and muscle pain, back pain
  4. Skin and soft tissue - decreased breast size, skin thinning/loss of elasticity
  5. Psychological - mood disturbance, changes in cognitive function
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13
Q

Describe the menstrual cycle changes in women in their late reproductive years vs. menopausal transition

A

Late reproductive years - cycle shortens

Menopausal transition - lengthening of intermenstrual interval (25-35 –> 40-50 days)

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14
Q

Investigations for irregular menstrual cycles in women over 45?

A

No diagnostic evaluation of symptoms required if highly likely menopausal (hot flushes, mood changes, sleep disturbance as opposed to new endocrine disorder, FSH can be done

Additional endocrine testing only if there are any suggestive features of hyperprolactinaemia or thyroid disease

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15
Q

Investigations for irregular menstrual cycles in women between 40-45 yo?

A

Pregnancy - serum beta-HCG
Hyperprolactinaemia - serum prolactin
Hyperthyroidism - serum TSH

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16
Q

How is menopause treated? (4)

A
  1. HRT alleviates vasomotor instability (primary indication), mood and memory and vaginal atrophy, reduces osteoporosis risk
  2. Lubricants and local oestrogen cream for vaginal atrophy
  3. Osteoporosis prevention - calcium, vit D, weight-bearing exercise, BISPHOSPHONATES
  4. Management of cardiovascular disease
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17
Q

What is the most important health hazard associated with menopause?

A

Osteoporosis

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18
Q

What is the leading cause of death post-menopause?

A

cardiovascular disease

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19
Q

What is the primary indication for the use of HRT?

A

Treat vasomotor instability

20
Q

What are the components of HRT?

A

Oestrogen and progestin

Combination given for women with intact uterus to prevent development of endometrial hyperplasia/cancer

21
Q

List 4 side effects of HRT

A
  1. Abnormal uterine bleeding
  2. Breast tenderness
  3. Oedema, bloating
  4. Mood changes (progesterone)
22
Q

List 4 contraindications to HRT

A

ABCD

  1. Acute liver disease
  2. Undiagnosed vaginal Bleeding
  3. Cancer (breast/uterine)
  4. DVT (thromboembolic disease)
23
Q

List 7 causes of post-menopausal bleeding

A
  1. Cancer - ENDOMETRIAL CANCER UNTIL PROVEN OTHERWISE
  2. Atrophy of vaginal mucosa or endometrium - part of perimenopausal period due to decreased oestrogen
  3. Polyps
  4. Post-menopausal HRT
  5. Endometrial hyperplasia - exogenous oestrogen therapy, obesity, soy herbal and dietary supplements
  6. Disease in adjacent organs causing uterine fistulisation
  7. Uncommon: infection, fibroids
24
Q

What is endometriosis?

A

The presence of endometrial tissue outside of the uterine cavity

25
Q

What is the aetiology of endometriosis? (3)

A

(No one really knows)

  1. Retrograde menstruation - seeding of endometrial cells
  2. Metaplasia of coelomic epithelium - induction of undifferentiated peritoneal cells to turn into endometrial tissue
  3. Aberrant vascular or lymphatic dissemination of cells e.g. ovarian endometriosis may be due to direct lymphatic flow from uterus to ovaries
26
Q

What is the incidence of endometriosis?

A

15-30% of pre-menopausal women

27
Q

List three features of history often seen in endometriosis

A
  1. Menstrual symptoms - cyclic due to growth and bleeding of ectopic endometrium, usually precede menses and continues throughout and after flow
  2. Infertility
  3. Bowel and bladder symptoms - characteristically dyschezia
28
Q

What is the classic triad of symptoms seen in endometriosis?

A

Dysmenorrhoea
Dyspareunia
Dyschezia

29
Q

How is endometriosis definitvely diagnosed?

A

Although clinical features can give you high index of suspicion, direct visualisation of lesions typical of endometriosis seen on laparoscopy is definitive

30
Q

List 4 menstrual symptoms seen in endometriosis

A
  1. Secondary dysmenorrhoea
  2. Sacral backache with menses
  3. Premenstrual and postmenstrual spotting
  4. Deep dyspareunia
31
Q

How is endometriosis treated? (3)

A
  1. Pain relief - NSAIDs
  2. Improve menstrual symptoms - OCP, progestogens, GnRH agonists
  3. Surgery - laparoscopic cautery/ablation, sometimes laparotomy, rarely hysterectomy and oophorectomy
32
Q

What is adenomyosis?

A

Extension of areas of endometrial glands and stroma into the myometrium (uterine wall may be diffusely involved)

33
Q

What are the symptoms of adenomyosis?

A

Similar to endometriosis - menorrhagia, dyspareunia, dyschezia - uterus symmetrically bulky

34
Q

In which phases are oestrogen and progesterone predominantly secreted and which cells secrete them?

A

Oestrogen is secreted by the dominant ovarian follicle in response to FSH during the follicular/proliferative phase

Progesterone is secreted by the corpus luteum (remnant of dominant follicle after it releases oocyte) in response to LH during the luteal/secretory phase

35
Q

What occurs during the follicular/proliferative phase of the menstrual cycle? (3)

A
  1. (Somehow) GnRH pulse frequency is increased causing an increase in LH and FSH
  2. FSH stimulates follicular growth in 3-30 follicles causing increased oestrogen production from the granulosa cells
  3. There is one dominant follicle which secretes the majority of the oestrogen. Oestrogen acts on the endometrium to cause proliferation of glandular and stromal tissue (to get ready for potential baby)
36
Q

What occurs during the luteal/secretory phase of the menstrual cycle? (4)

A
  1. Oestrogen: Sudden switch from negative to positive feedback causing increased FSH and LH around day 14
  2. LH surge causes ovulation (i.e. release of oocyte from the dominant follicle)
  3. Dominant follicle now called the corpus luteum, produces progesterone which stabilises endometrium
  4. When there is no fertilised oocyte, corpus luteum degenerates, therefore decreased progesterone which causes shedding of the endometrium (menstruation)
37
Q

What is the reasoning behind the progesterone challenge in evaluating amenorrhoea?

A

Assessing oestrogen status by assessing for uterine bleed after progesterone challenge

If there is a withdrawal bleed after completion of the progesterone challenge (i.e. 2 week PO of MDPA/Provera) - this suggests that there is adequate oestrogen to thicken the endometrium

If there is no withdrawal bleeding, there may be either:
1. inadequate oestrogen (hypoestrogenism) or excessive androgens = suggestive of HP axis dysfunction

OR a

  1. uterine defect or Asherman’s syndrome (adhesions and/or fibrosis of the endometrium)
38
Q

What investigations should be considered in evaluating amenorrhoea? (5)

A
  1. B-HCG
  2. Hormonal work-up - TSH (hypothyroidism),prolactin (for prolactinoma), FSH, LH, androgens (PCOS), oestradiol
  3. Progesterone challenge to assess oestrogen status
  4. Karyotype if indicated
  5. U/S to confirm normal anatomy, identify PCOS
39
Q

What investigations should be considered in evaluating primary amenorrhoea and why? (2)

A
  1. In a patient with secondary sexual characteristics - karyotyping. XX suggests anatomical problem (imperforate hymen, transverse vaginal septum, cervical or Mullerian agenesis). XY suggests androgen insensitivity syndrome
  2. FSH/LH particularly in patients without secondary sexual characteristic. If high, suggests hypergonadotrophic hypogonadism (i.e. gonadal agenesis/dysgenesis that can be present in those with normal chromosomes or in Turner’s XO). If low, suggests hypogonadotrophic hypogonadism, suggests constitutional delay, pituitary failure/tumours, etc.
40
Q

What are the Rotterdam diagnostic criteria for PCOS?

A

Two of the following three criteria are required:
1. oligo/anovulation

  1. hyperandrogenism - clinical OR biochemical (raised free androgen index or free testosterone)
  2. Polycystic ovaries on ultrasound - not reliable in adolescents and young women
41
Q

How is PCOS managed? (4)

A
  1. OCP - addresses cycle control and hirsutism
  2. Metformin - addresses metabolic risk
  3. In infertility - ovulatory induction using clomiphene
  4. Lifestyle considerations - optimal weight, diet and exercise, cessation of smoking, assess for prediabetes
42
Q

Define dysmenorrhoea

A

Painful menstruation - usually sharp but may be cramping, throbbing or dull, may radiate to legs

43
Q

What is the difference between primary and secondary dysmenorrhoea? Which is more common?

A

Primary: symptoms cannot be explained by structural gynaecologic disorders - pain thought to be mediated by prostaglandins resulting in uterine contractions and ischaemia.

Secondary: due to pelvic abnormalities e.g. endometriosis, adenomyosis, uterine anomalies, PID, copper IUD

44
Q

Which is more common - primary vs secondary dysmenorrhoea?

A

Primary! Symptoms usually begin soon after menarche or during adolescence

45
Q

How is dysmenorrhoea treated?

A

If primary - PG synthetase inhibitors (e.g. naproxen) or OCP (suppresses ovulation/reduce menstrual flow

If secondary - treat underlying cause

46
Q

What investigations would be ordered in suspected PCOS? (2)

A

Labs - free testosterone, TFTs, SHBG

2. U/S - polycystic-appearing ovaries