1.01 - Menstrual Disorders Flashcards

1
Q

At what age is menarche occur for most women?

A

11 to 15

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2
Q

What is the normal duration of a single menstrual cycle?

A

21-35 days

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3
Q

What axis regulates the menstrual cycle?

A

Hypothalamic-Pituitary Gonadal (HPG) axis

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4
Q

The HPG axis.

A
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5
Q

What are the feedback systems of the HPG axis?

A
  • moderate oestrogen levels negatively feedback on the HPG axis
  • high oestrogen levels positively feedback on the HPG axis
  • oestrogen and progesterone negatively feedback on the HPG axis
  • inhibits selectively inhibits FSH at the anterior pituitary
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6
Q

What are the phases of the ovarian cycle?

A

1) Follicular phase (days 1-13)

2) Ovulation (day 14)

3) Luteal phase (days 15-28)

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7
Q

Changes in the follicular phase of the ovarian cycle.

A

Days 1-13:

1) Low steroid and inhibin levels = low negative feedback = increase in FSH and LH.

2) As oestrogen levels rise, negative feedback reduces FSH levels so only one follicle survives.

3) Follicular oestrogen rises until it initiates positive feedback on the HPG axis, causing an LH surge.

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8
Q

Changes in ovulation of the ovarian cycle.

A

Day 14:

In response to the LH surge, the follicle ruptures and the mature oocyte is assisted to the fallopian tube by fimbria, where it is viable for fertilisation for 24 hours.

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9
Q

Changes in the luteal phase of the ovarian cycle (no fertilisation).

A

Days 15-28:

1) Corpus luteum forms at site of ruptures follicle, secreting oestrogen and progesterone.

2) Oestrogen and progesterone negatively feedback on HPG axis, stalling the cycle and maintaining conditions for fertilisation and implantation.

3) In absence of fertilisation, corpus luteum regresses after 14 days - there is a fall in hormones, resetting the HPG axis.

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10
Q

Changes in the luteal phase of the ovarian cycle (fertilisation).

A

Days 15-28:

1) Corpus luteum forms at site of ruptures follicle, secreting oestrogen and progesterone.

2) Oestrogen and progesterone negatively feedback on HPG axis, stalling the cycle and maintaining conditions for fertilisation and implantation.

3) If fertilised, the syncytiotrophoblast of the embryo produces HcG, maintaining the corpus luteum. This maintains conditions for embryo development*.

*Note at 4 months gestation, placental steroid hormones are sufficient to control the HPG axis.

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11
Q

What are the phases of the uterine cycle?

A

1) Proliferative phase

2) Secretory phase

3) Menses

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12
Q

Changes in the proliferative phase of the uterine cycle (days 7-14).

A

Under the action of oestrogen, there is:

  • fallopian tube formation
  • thickening of the endometrium
  • increased growth and motility of the myometrium
  • thin, alkaline cervical mucus
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13
Q

Changes in the secretory phase of the ovarian cycle (days 15-28).

A

Under the action of progesterone, there is:

  • further thickening of the endometrium into a glandular secretory form
  • thickening of the myometrium
  • reduction in motility of the myometrium
  • thick, acidic cervical mucus
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14
Q

Changes in the menses phase of the uterine cycle (days 1-7).

A

In the absence of fertilisation, the corupus luteum regresses and oestrogen / progesterone levels fall.

The internal lining of the uterus is shed, with bleeding lasting 2-7 days with 10-80ml of blood loss.

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15
Q

What are some important details to obtain in a menstrual history?

A
  • duration of periods
  • frequency of periods
  • volume of periods
  • menstrual pain
  • last menstrual period
  • age at menarche
  • menopause (if relevant)
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16
Q

What are some physical complications of abnormal menstrual cycles?

A
  • iron deficiency anaemia (menorrhagia)
  • osteoporosis (low oestrogen in oligomenorrhoea / amenorrhoea)
  • cardiovascular disease (low oestrogen in oligomenorrhoea, amenorrhoea)
  • endometrial hyperplasia (few menses in oligomenorrhoea, amenorrhoea, increases risk of endometrial cancer)
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17
Q

What are some psychological consequences of abnormal menstruation?

A
  • depression (pain, subfertility)
  • pain
  • anxiety
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18
Q

What are some social consequences of abnormal menstruation?

A
  • relationship breakdown
  • no sexual intercourse
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19
Q

Causes of abnormal menstrual bleeding.

A
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20
Q

What is polycystic ovary syndrome (PCOS)?

A

Common endocrine disorder, characterised by excess androgen production and the presence of multiple follicles (cysts) within the ovaries.

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21
Q

What are the most common hormonal abnormalities present in PCOS?

A

1) Excess LH in response to increased GnRH pulse frequency - this stimulates ovarian production of androgens by theca cells.

2) Insulin resistance resulting in high levels of insulin secretion. Insulin suppresses SHBG, resulting in higher levels of free circulating androgens.

High levels of circulating androgens suppresses the LH surge, causing follicles to arrest and remain viable as ‘cysts’ within the ovary.

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22
Q

Risk factors for PCOS.

A
  • diabetes
  • irregular menstruation
  • family history
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23
Q

Clinical features of PCOS.

A
  • oligomenorrhoea or amenorrhoea
  • infertility
  • hirsutism
  • obesity
  • chronic pelvic pain
  • depression
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24
Q

OE of PCOS.

A
  • hirsutism (A)
  • acne
  • acanthosis nigricans (B)
  • male pattern hair-loss
  • obesity
  • hypertension
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25
Q

Differential diagnoses to PCOS.

A
  • hypothyroidism: obesity, hair loss and insulin resistance
  • hyperprolactinaemia: oligomenorrhoea, acne and hirsutism
  • Cushing’s disease: obesity, acne, hypertension, insulin resistance, depression
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26
Q

Rotterdam Criteria (2003)

A

Diagnosis of PCOS is made if two out of three criteria are met:

1) oligo- and/or anovulation

2) Clinical signs of hyperandrogenism

3) Polycystic ovaries on imaging

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27
Q

Blood tests for PCOS.

A
  • testosterone (raised)
  • SHBG (low)
  • LH (raised)
  • FSH (normal)
  • progesterone (low)

To exclude differentials:
- TSH (hypothyroidism)
- serum prolactin (hyperprolactinaemia)

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28
Q

What is the imaging of choice for PCOS?

A

Transvaginal ultrasound scan:

  • peripheral ovarian follicles
  • ovarian volume >10cm3
29
Q

Management of oligomenorrhoea / amenorrhoea as a complication of PCOS.

A

In anovulatory cycles, the effect of oestrogen is unopposed due to lower levels of progesterone. This can cause endometrial hyperplasia.

In amenorrhoeic women, it is important to protect the endometrium from hyperplasia by inducing at least 3 bleeds per year:

  • COCP
  • dydrogesterone
30
Q

Management of obesity as a complication of PCOS.

A

Achievement of BMI <30 may be enough to trigger a regular menstrual cycle.

Advise and encourage a health lifestyle, including healthy diet and exercise.

Orlistat can be prescribed.

31
Q

Management of infertility as a complication of PCOS.

A

Clomifene +/- metformin induces ovulation, and is first line treatment for women wishing to conceive.

Limited to use in 6 cycles due to risk of ovarian cancer.

32
Q

Management of hirsutism as a complication of PCOS.

A

Treated cosmetically and/or with anti-androgen medications (e.g. spironolactone, finasteride).

Avoid during pregnancy as teratogenic.

33
Q

What are uterine fibroids?

A

Leiomyomas are benign smooth muscle tumours of the uterus, with an incidence of 20-40%.

The risk of a fibroid becoming malignant is 0.1%.

34
Q

Aetiology of uterine fibroids.

A

Growth stimulated by oestrogen, arising from the myometrium of the uterus:

  • Intramural (most common) (B)
  • submucosal (C)
  • subserosal (A)
35
Q

Risk factors for uterine fibroids.

A
  • obesity
  • early menarche
  • increasing age
  • family history
  • ethnicity (African-American)
36
Q

Clinical features of uterine fibroids.

A

Majority of women are asymptomatic.

History:
- urinary frequency
- chronic urinary retention
- heavy menstrual bleeding
- subfertility
- acute pelvic pain (rare)

OE solid mass or enlarged uterus palpable on abdominal or bimanual examination.

37
Q

Differential diagnoses for uterine fibroids.

A
  • endometrial polyps
  • ovarian tumour
  • leiomyosarcoma
  • adenomyosis
38
Q

Investigations for uterine fibroids.

A

Imaging:
- pelvic ultrasound
- MRI (if sarcoma suspected)

39
Q

Outline the role of hormonal contraceptives in the treatment of uterine fibroids.

A

COCP, POP and IUS useful to control menorrhagia.

40
Q

Outline the role of GnRH analogues (Zolidex) in the treatment of uterine fibroids.

A

Suppresses ovulation, inducing a temporary menopausal state.

Useful pre-operatively to reduce fibroid size and lower operative complications.

Can be used for 6 months only, due to risk of osteoporosis.

41
Q

Outline the role of selective progesterone receptor modulators (Ulipristal) in the treatment of uterine fibroids.

A

Reduces size of fibroid and menorrhagia, so useful pre-operatively or as an alternative to surgery.

Use of Ulipristal restricted due to risk of severe liver injury.

42
Q

What are the surgical options to treat uterine fibroids?

A

Hysteroscopy and Transcervical Resection of Fibroid (TCRF) - useful for submucosal fibroids.

Myomectomy - option in women wanting to preserve their uterus.

Uterine artery embolisation (UAE) - performed by radiologist via the femoral artery, with pain and fever common post-operative complications.

Hysterectomy

43
Q

What are some complications of uterine fibroids?

A
  • iron deficiency anaemia
  • compression of pelvic organs (ie. incontinence, hydronephrosis, urinary retention)
  • subfertility
  • degeneration
  • torsion
44
Q

What is endometriosis?

A

A chronic condition in which endometrial tissue is located at sites other than the uterine cavity:

  • ovaries
  • pouch of Douglas
  • uterosacral ligaments
  • pelvic peritoneum
  • bladder
  • umbilicus
  • lungs
45
Q

What is the retrograde menstruation theory of endometriosis?

A

Endometrial cells travel backwards from the uterine cavity, through the Fallopian tubes, and deposit on pelvic organs - they can seed and grow.

46
Q

Risk factors associated with endometriosis.

A
  • early menarche
  • family history
  • short menstrual cycles
  • long duration of menstrual bleeding
  • heavy menstrual bleeding
  • defects in the uterus or fallopian tubes
47
Q

Clinical features of endometriosis.

A
  • cyclical pelvic pain*
  • dysmenorrhoea
  • dyspareunia
  • dysuria
  • dyschezia
  • subfertility

*pain is cyclical due to endometrials responsive nature to oestrogen, which fluctuates throughout the menstrual cycle.

NB pain may be constant if adhesions form due to chronic inflammation.

48
Q

On bimanual examination, findings consistent with endometriosis are:

A
  • fixed, retroverted uterus
  • uterosacral ligament nodules
  • genderal tenderness
49
Q

Differential diagnoses to endometriosis.

A

Pelvic inflammatory disease - dyspareunia, pelvic pain, heavy bleeding.

Ectopic pregnancy - dyspareunia, pelvic pain, heavy bleeding.

Fibroids - pelvic pain, long duration of menstrual bleeding, heavy menstrual bleeding, feeling of a mass.

Irritable bowel syndrome: abdominal pain, dyspareunia, bloating.

50
Q

Investigations of endometriosis.

A

Gold standard = laparoscopy

Typical findings:
- chocolate cysts
- adhesions
- peritoneal deposits

51
Q

Management of endometriosis.

A

Pain = NSAIDs / analgesic ladder

Ovulation - COCP to suppress ovulation for 6-12 months, causing atrophy of endometriosis and reduction in symptoms.

Laser ablation to surgically remove ectopic endometrial tissue.

Definitive management is hysterectomy.

52
Q

What is the aetiology of cervical polyps?

A
  • chronic inflammation
  • abnormal response to oestrogen
  • localised congestion of the cervical vasculature
53
Q

What is the pathophysiology of cervical polyps?

A

Focal hyperplasia of columnar epithelium of the endocervix.

54
Q

Clinical features of cervical polyps.

A
  • asymptomatic (most common)
  • abnormal vaginal bleeding
  • infertility

On speculum examination, may be seen as polypoid growths projecting through the external os.

55
Q

Differential diagnoses of cervical polyps.

A
  • sexually transmitted infections
  • endometrial carcinoma
56
Q

Investigations of cervical polyps.

A

Definitive diagnosis via histological examination after removal.

To exclude alternative causes:
- triple swabs (if suggestion of infection)
- cervical smear (exclude cervical intraepithelial neoplasia)

57
Q

Management of cervical polyps.

A

Removal once identified due to small risk of malignant transformation.

Polypectomy forceps can be used in primary care for small polyps.

Colposcopy clinic referral if polyps are large, for removal via diathermy loop excision.

58
Q

Complications of polypectomy.

A
  • infection
  • haemorrhage
  • uterine perforation
59
Q

What is pre-menstrual dysphoric syndrome?

A

A set of symptoms some women experience in the weeks before their menses:
- cramps
- headaches
- binge eating
- problems sleeping
- anxiety
- depression / suicidal ideation

60
Q

What self-help advice can be given to help manage pre-menstrual dysphoric syndrome?

A
  • regular exercise
  • ibuprofen / paracetamol
  • smoking cessation
  • nutritional optimisation
  • limit alcohol intake
61
Q

What are some medical treatments for pre-menstrual dysphoric syndrome?

A
  • COCP
  • cognitive behavioural therapy
  • antidepressants
62
Q

At what age is menopause most common?

A

Perimenopause begins at around age of 45, and progresses until the final menses and the end of fertility (UK average is 51).

63
Q

What are the hormonal changes that occur during menopause?

A

Reduced sensitivity of the ovary to FSH and LH causes reduced oestrogen secretion and an increase in anovulatory cycles.

Low circulating oestrogen removes positive feedback on the hypothalamus and anterior pituitary gland, so FSH and LH increase significantly.

64
Q

Symptoms of perimenopause.

A
  • hot flushes
  • dyspareunia
  • urinary incontinence
  • UTIs
  • osteoporosis
65
Q

Define ‘menopause’.

A

Amenorrhoea for 12 consecutive months.

66
Q

Biochemical changes in menopause.

A
  • oestrogen low
  • FSH raised
67
Q

Outline the role of HRT in the treatment of menopause.

A
  • oestrogen + progesterone to women with a uterus
  • oestrogen alone to women without a uterus

HRT can be used to alleviate symptoms of menopause, usually precipitated by reduced oestrogen.

68
Q

What are the long-term benefits of HRT?

A
  • reduced risk of coronary heart disease
  • risk of fragility fracture decreased
  • improve muscle mass and strength
69
Q

What are the long-term risks of HRT?

A
  • increased risk of VTE*
  • HRT with oestrogen and progesterone associated with increased risk of breast cancer

*BMI >30kg/m2 give transdermal patch