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Obstetrics and Gynaecology > Gynaecology - done > Flashcards

Gynaecology - done Flashcards

1
Q

What are some differentials for amenorrhoea?

A

Primary

  • Abnormal functioning of the hypothalamus or pituitary gland (hypogonadotrophic hypogonadism)
  • Abnormal functioning of the gonads (hypergonadotrophic hypogonadism)
  • Imperforate hymen

Secondary

  • Pregnancy
  • Menopause
  • Physiological stress: excessive exercise, low body weight, chronic disease
  • Polycystic ovarian syndrome
  • Medication e.g. hormonal contraceptives
  • Premature ovarian insufficiency (menopause before 40)
  • Thyroid hormone abnormalities (hyper or hypothyroid)
  • Excessive prolactin from a prolactinoma
  • Cushing’s syndrome
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2
Q

What are some causes of irregular mensturation?

A
  • Extremes of reproductive age
  • Polycystic ovarian syndrome
  • Physiological stress (excessive exercise, low body weight, chronic disease)
  • Medication e.g. progesterone only contraception, antidepressants / antipsychotics
  • Hormonal imbalances e.g. thyroid abnormalities, Cushing’s syndrome and high prolactin
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3
Q

What can cause intermenstrual bleeding?

A
  • Hormonal contraception
  • Cervical ectropion, polyps or cancer
  • STI
  • Endometrial polyps or cancer
  • Pregnancy
  • Ovulation (causes spotting)
  • Medication SSRIs and anticoagulants
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4
Q

What is dysmenorrhoea?

A

Painful periods

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5
Q

What are the causes of dysmenorrhoea?

A
  • Primary (no underlying cause)
  • Endometriosis / adenomyosis
  • Fibroids
  • PID
  • Copper coil
  • Cervical or ovarian cancer
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6
Q

What is menorrhagia?

A

Heavy menstural bleeds

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7
Q

What causes menorrhagia?

A
  • Dysfunctional uterine bleeding (no identifiable cause)
  • Extremes of reproductive age
  • Fibroids
  • Endometriosis / adenomyosis
  • PID
  • Copper coil
  • Bleeding disorders (Von Willebrand disease)
  • Endocrine disorders (diabetes / hypothyroidism)
  • Connective tissue disorders
  • PCOS
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8
Q

What is post coital bleeding?

A
  • Bleeding after sexual intercourse
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9
Q

What is the cause of post coital bleeding (often no cause is found)

A
  • Cervical cancer, ectropion, infection
  • Trauma
  • Atrophic vaginitis
  • Polyps
  • Endometrial cancer
  • Vaginal cancer
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10
Q

What are the differentials for pelvic pain?

A

UTI

Dysmenorrhoea (painful periods)

IBS (irritable bowel syndrome)

Ovarian cysts

Endometriosis

PID

Ectopic pregnancy

Appendicitis

Mittelschmerz (cyclical pain during ovulation)

Pelvic adhesions

Ovarian torsion

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11
Q

What are the differentials for vaginal discharge?

A
  • Bacterial vaginosis
  • Candidiasis (thrush)
  • Chlamydia
  • Gonorrhoea
  • Trichomonas vaginalis
  • Foreign body
  • Cervical ectropion
  • Polyps
  • Malignancy
  • Pregnancy
  • Ovulation
  • Hormonal contraception
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12
Q

What is pruritus vulvae?

A

Itching of the vulva and vagina

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13
Q

What can cause pruritus vulvae?

A
  • Irritants e.g. soap, detergents and barrier contraception
  • Atrophic vaginitis
  • Infections e.g. candidiasis (thrush) and pubic lice
  • Eczema
  • Vulval malignancy
  • Pregnancy related vaginal discharge
  • Urinary or faecal incontinence
  • Stress
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14
Q

What is the definition of primary amenorrhoea?

A

Not starting mensturation:

  • By 13 when there is no other evidence of pubertal development
  • By 15 if there are other signs of puberty e.g. breast bud development
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15
Q

When does puberty begin in boys and girls respectively?

A

8-14 in girls

9-15 in boys

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16
Q

How long does puberty take?

A

About 4 years

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17
Q

What is the progression of puberty in girls?

A
  • Breast bud development
  • Pubic hair development
  • Menstural periods (about 2 years from onset)
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18
Q

What is hypogonadism?

A

Lack of sex hormones (oestrogen and testosterone)

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19
Q

What are the two types of hypogonadism?

A

Hypogonadotrophic hypogonadism (deficiency of LH and FSH)

Hypergonadotrophic hypogonadism (lack of response to LH and FSH by the gonads - testes and ovaries)

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20
Q

What can cause a deficiency of LH and FSH?

A

Abnormal functioning of the hypothalamus or pituitary gland

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21
Q

What increases the release of LH and FSH from the anterior pituitary?

A

Gonadotrophin releasing hormone (GnRH)

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22
Q

What can cause hypogonadotrophic hypogonadism?

A

Hypopituitarism (under production of the pituitary hormones)

Damage to the pituitary gland (surgery or chemotherapy)

Chronic conditions (CF or IBD)

Excessive exercise or dieting

Constitutional delay in growth and development (temporary delay in growth and puberty)

Kallman syndrome

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23
Q

What can cause hypergonadotrophic hypogonadism?

A

Abnormal functioning of the testes:

  • Previous damage to the gonads (e.g. torsion, cancer or infections e.g. mumps)
  • Congenital absence of the ovaries
  • Turner’s syndrome (XO)
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24
Q

What is Kallman’s syndrome?

A

Hypogonadotrophic hypogonadism and failure to start puberty

Associated with reduced or absent sense of smell

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25
Q

What is congenital adrenal hyperplasia?

A

Congenital deficiency of the 21-hydroxylase enzyme

Causing underproduction of cortisol and aldosterone and an overprodution of androgens from birth.

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26
Q

What is the pattern of inheritance of congenital adrenal hyperplasia?

A

Autosomal recessive pattern

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27
Q

What are the possible enzyme deficiencies in congenital adrenal hyperplasia?

A

21-hydroxylase enzyme

11-beta-hydroxylase

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28
Q

How does congenital adrenal hyperplasia usually present?

A
  • Usually neonate is severely unwell after birth with electrolyte disturbances and hypoglycaemia
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29
Q

How do mild cases of congenital adrenal hyperplasia present?

A
  • Tall for age
  • Facial hair
  • Absent periods (primary amenorrhoea)
  • Deep voice
  • Early puberty
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30
Q

What happens in androgen insensitivity syndrome?

A

Tissues are unable to respond to androgen hormones (e.g. testosterone)

Causes a female phenotype (female external gentalia and breast tissue)

Internally = testes in abdomen / inguinal canel and absent uterus, upper vagina, fallopian tube and ovaries

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31
Q

What structural pathology can cause primary amenorrhoea?

A
  • Imperforate hymen
  • Transverse vaginal septae
  • Vaginal agenesis
  • Absent uterus
  • FGM
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32
Q

When should investigations for primary amenorrhoea be undertaken?

A

No evidence of pubertal changes in a girl aged 13

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33
Q

What testing is there for primary amenorrhoea?

A

FBC and ferritin for anaemia

U&E for chronic kidney disease

Anti-TTG or anti-EMA for coeliacs disease

FSH and LH

Thyroid function tests

Insulin-like growth factor I for GH deficiency

Prolactin for hyperprolactinoma

Testosterone - raised in PCOS, Androgen insensitivity syndrome and congenital adrenal hyperplasia

Genetic testing with a microassay for Turner’s syndrome

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34
Q

What imaging for primary amenorrhoea?

A

Imaging (X-ray of the wrist - assess for constitutional delay)

Pelvic ultrasound (assess the ovaries and other pelvic organs)

MRI of the brain (for pituitary pathology and olfactory bulbs in Kallman syndrome)

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35
Q

What is the management of primary amenorrhoea?

  • Constitutional delay in growth?
  • Low body weight ?
  • Hypogonadotrophic hypogonadism (e.g. hypopituitarism / Kallman syndrome)?
  • Ovarian causes?
A
  • Establish and treat the underlying cause
  • Replacement hormones where necessary
  • Patients with constitutional delay in growth and development may only require reassurance and observation
  • Patients with low body weight / stress causes require reduction in stress, CBT and healthy weight gain
  • Patients with hypogonadotropism treated with pulsatile GnRH to induce ovulation / mensturation (can induce fertility) / if pregnancy is not wanted then COOP can induce regular mensturation and prevent symptoms of oestrogen deficiency
  • Patients with ovarian causes e.g. PCOS, damage to the ovaries or absence of can have the COCP to induce regular mensturation and prevent the symptoms of oestrogen deficiency
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36
Q

What is secondary amenorrhoea?

A

No mensturation for more than three months after previous regular menstural periods

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37
Q

When should investigations be done for secondary amenorrhoea?

A

After 3-6 months after regular periods

After 6-12 months after irregular periods

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38
Q

What are the causes of secondary amenorrhoea?

A

- Pregnancy

  • Menopause and premature ovarian failure
  • Hormonal contraception (IUS or POP)
  • Hypothalamic or pituitary pathology
  • Ovarian causes e.g. polycystic ovarian syndrome
  • Uterine pathology such as Asherman’s syndrome
  • Thyroid pathology
  • Hyperprolactinaemia
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39
Q

Why and when does the hypothalamus reduce the production of GnRH?

A

Prevent pregnancy in situations where the body may not be fit for it e.g.:

  • Excessive exercise (e.g. athletes)
  • Low body weight
  • Chronic disease
  • Psychological stress
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40
Q

What are some pituitary causes of secondary amenorrhoea?

A

Pituitary tumours e.g. prolactin-secreting prolactinoma

Pituitary failure due to trauma, radiotherapy, surgery or Sheehan syndrome

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41
Q

What is hyperprolactinaemia and what does it result in?

A

High prolactin levels, this acts on the hypothalamus to prevent the release of GnRH, without GnRH there is no release of LH and FSH = hypogonadotrophic hypogonadism

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42
Q

What % of women with a high prolactin level with have galactorrhoea? (breast milk production and secretion)

A

30%

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43
Q

What is the most common cause of hyperprolactinaemia?

A

Pituitary adenoma secreting prolactin

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44
Q

How can a pituitary tumour be assessed for?

A

CT or MRI scan of the brain

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45
Q

What type of pituitary tumour will not show up on a scan?

A

Microadenoma

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46
Q

What is the treatment of hyperprolactinoma?

A

Dopamine agonists such as bromocriptine or cabergoline can be used to reduce prolactin production.

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47
Q

What are dopamine agonists used to treat?

A

Hyperprolactinaemia

Parkinson’s

Acromegaly

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48
Q

How is secondary amenorrhoea assessed?

A
  • Detailed history and examination to assess for causes
  • Hormonal blood tests
  • Ultrasound of the pelvis to diagnose polycystic ovarian syndrome
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49
Q

What are the hormone tests for secondary amenorrhoea?

A

Beta human chorionic gonadotrophin (HCG) urine or blood tests for pregnancy

Luteinising hormone and follicle-stimulating hormone

High FSH suggests primary ovarian failure

High LH or LH:FSH ratio suggests polycystic ovarian syndrome

Prolactin can be measured to assess for hyperprolactinaemia followed by an MRI to identify a pituitary tumour

Thyroid stimulating hormone (TSH) to screen for thyroid pathology, followed by T3 and T4 when the TSH is abnormal

Raised TSH and low T3 and T4 indicates hypothyroidism

Low TSH and raised T3 and T4 indicates hyperthyroidism

Raised testosterone indicates polycystic ovarian syndrome, androgen insensitivity syndrome or congenital adrenal hyperplasia

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50
Q

What does the management of secondary amenorrhoea involve?

A

Establishing and treating underlying cause

Replacement hormones can induce mensturation and improve symptoms

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51
Q

How are patients with polycystic ovarian syndrome and secondary amenorrhoea treated?

A

Require a withdrawal bleed every 3-4 months to reduce the risk of endometrial hyperplasia and endometrial cancer

Medroxyprogesterone for 14 days, or regular use of the combined oral contraceptive pill - to stimulate a withdrawal bleed

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52
Q

How to treat the osteoporosis risk in patients with amenorrhoea associated with low oestrogen?

A

When the amnorrhoea lasts more than 12 months treat with:

  • Adequate vitamin D and calcium intake
  • Hormone replacement therapy or the combined oral contraceptive pill
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53
Q

What is premenstural syndrome (PMS)?

A

Psychological, emotional and physical symptoms that occur during the luteal phase of the menstural cycle particularly in the days prior to onset of mensturation

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54
Q

When do the symptoms of PMS resolve?

A

Once mensturation begins

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55
Q

When are symptoms of PMS definitely not present for a woman?

A

Before menarche

During pregnancy

After menopause

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56
Q

What is the cause of PMS?

A

Fluctuation in oestrogen and progesterone during the menstural cycle (exact cause unknown)

May be due to increased sensitivity to progesterone or an interation between the sex hormones and the neutotransmitters serotonin and GABA

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57
Q

What are some common PMS symptoms?

A
  • Low mood
  • Anxiety
  • Mood swings
  • Irritability
  • Bloating
  • Fatigue
  • Headaches
  • Breast pain
  • Reduced confidence
  • Cognitive impairment
  • Clumsiness
  • Reduced libido
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58
Q

When can PMS occur in the absence of mensturation?

A

After a hysterectomy, endometrial ablation or on the mirena coil as the ovaries continue to function and the hormonal cycle continues

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59
Q

When can progesterone induced premenstrual disorder occur?

A

In response to the combined contraceptive pill or cyclical hormone replacement therapy

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60
Q

What is PMS called when features are severe and have a significant effect on quality of life?

A

Premenstrual dysmorphic disorder

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61
Q

How is PMS diagnosed?

A

Symptom diary spanning two menstrual cycles - demonstrating cyclical symptoms which occur just before and resolve after the onset of menstruation

Adminstering GnRH to temporarily halt the menstrual cycle and temporarily induce the menopause, to see if symptoms improve

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62
Q

What does the management of PMS in general practise involve?

A
  • Improve diet, exercise, alcohol, smoking, stress and sleep
  • COCP
  • SSRI antidepressants
  • CBT
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63
Q

What type of COCP does the RCOG recommend first line?

A

Drospirenone containing COCP (i.e. Yasmin )

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64
Q

How should the dospironone COCP be taken?

A

Continuous use of the pill as opposed to cyclical (has some antimineralocorticoid effects - similar to spironolactone)

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65
Q

What type of patches for COCP can be used?

A

Continuous transdermal oestrogen (progesterone are required for endometrial protection against endometrial hyperplasia when using oestrogen - this can be in the form of low dose cyclical progestogens e.g. norethisterone to trigger a withdrawal bleed or the minera coil)

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66
Q

What can be used to induce a menopausal state in patients with PMS?

A

GnRH analogues they are very effective however they have adverse effects (e.g. osteoporosis) HRT can be used to add back the hormones to mitigate these effects

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67
Q

What can be used for PMS symptoms where medical management has failed?

A

Hysterectomy and bilateral oophorectomy

HRT will be required particularily in women under 45 years

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68
Q

What can be used to treat breast pain associated with PMS?

A

Danazole and tamoxifen (initiated and monitored by a breast specialist)

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69
Q

What are the physical symptoms of PMS and what can be used to treat it?

A

Spironolactone to treaat breast swelling, water retention and bloating

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70
Q

What is the medical term for heavy menstrual bleeding?

A

Menorrhagia

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71
Q

How much blood do women lose on average during mensturation?

A

40mls

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72
Q

What amount of blood to lose during mensturation is excessive?

A

80ml or more

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73
Q

How is a diagnosis of menorrhagia made?

A

Symptoms:

  • Changing pads every 1-2 hours
  • Bleeding lasting more that 7 days
  • Passing large clots
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74
Q

What are the possible causes of menorrhagia?

A

Dysfunctional uterine bleeding (no identifiable cause)

Extremes of reproductive age

Fibroids

Endometriosis and adenomyosis

Pelvic inflammatory disease (infection)

Contraceptives, particularly the copper coil

Anticoagulant medications

Bleeding disorders (e.g. Von Willebrand disease)

Endocrine disorders (diabetes and hypothyroidism)

Connective tissue disorders

Endometrial hyperplasia or cancer

Polycystic ovarian syndrome

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75
Q

What are the key components to any gynaecological history?

A

Age at menarche

Cycle length, days menstruating and variation

Intermenstrual bleeding and post coital bleeding

Contraceptive history

Sexual history

Possibility of pregnancy

Plans for future pregnancies

Cervical screening history

Migraines with or without aura (for the pill)

Past medical history and past drug history

Smoking and alcohol history

Family history

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76
Q

What are the investigations for menorrhagia?

A
  • Pelvic examination with a speculum and bimanual (to assess for fibroids, ascites and cancers)
  • FBC for iron deficiency anaemia
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77
Q

When should outpatients hysteroscopy be arranged for menorrhagia?

A
  • Suspected submucosal fibroids
  • Suspected endometrial pathology such as endometrial hyperplasia or cancer
  • Persistent intermenstrual bleeding
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78
Q

When should a pelvic and transvaginal ultrasound for menorrhagia be arranged?

A
  • Possible large fibroids (palpable pelvic mass)
  • Possible adenomyosis (associated pelvic pain or tenderness on examination
  • Examination is difficult to interpret (e.g. obesity)
  • Hysteroscopy is declined
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79
Q

What additional tests can be used for menorrhagia?

A

Swabs if there is evidence of infection (e.g. abnormal discharge or suggestive sexual history)

Coagulation screen if there is a family history of clotting disorders (e.g. Von Willebrand disease) or periods that have been heavy since menarche

Ferritin if they are clinically anaemic

Thyroid function tests if there are additional features of hypothyroidism

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80
Q

What is the initial managment of menorrhagia?

A
  • Exclude underlying pathology such as anaemia, fibroids, bleeding disorders and cancer
  • Identifiable causes should be managed initially (e.g. menorrhagia caused by a copper coil should stop when the coil is removed)
  • Next step is to determine if contraception is required or acceptable
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81
Q

What treatment can a woman who declines contraception be offered?

A

Tranexamic acid when no associated pain (antifibrinolytic - reduces bleeding)

Mefenamic acid when there is associated pain (NSAID - reduces bleeding and pain)

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82
Q

What treatment can be offered to a patient with menorrhagia who accepts contraception?

A
  • Mirena coil (first line)
  • COCP
  • Cyclical oral progestogens such as norethisterone 5mg three times daily from day 5-26 (although this is associated with progestogenic side effects and an increase risk of venous thromboembolism

Progesterone only contraception may also be tried, as it can suppress menstruation (e.g. progesterone-only pill or a long-acting progesterone (e.g. depo injection or implant)

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83
Q

When is referral to secondary care needed for menorrhagia?

A

If treatment is unsuccessful, symptoms are severe or there are large fibroids (>3cm)

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84
Q

What are the final management options for menorrhagia?

A

Endometrial ablation and hysterectomy

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85
Q

What is endometrial ablation?

A

First generation technique = hysteroscopy and direct destruction of the endometrium

Second generation technique = (not using hysteroscopy) e.g. passing a specially designed balloon into the endometrial cavity and filling it with high-temperature fluid that burns the endometrial lining (ballon thermal ablation)

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86
Q

What are fibroids?

A

Benign tumours of the smooth muscle of the uterus

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87
Q

What are fibroids also called?

A

Uterine leiomyomas

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88
Q

What proportion of women do they affect in later reproductive years?

A

40-60% of women

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89
Q

What race of women are fibroids more common in?

A

Black women

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90
Q

What hormone do fibroids grow in response to?

A

Oestrogen (oestrogen sensitive)

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91
Q

What are the different types of fibroids?

A

Intramural means within the myometrium (the muscle of the uterus). As they grow, they change the shape and distort the uterus.

Subserosal means just below the outer layer of the uterus. These fibroids grow outwards and can become very large, filling the abdominal cavity.

Submucosal means just below the lining of the uterus (the endometrium).

Pedunculated means on a stalk.

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92
Q

How do fibroids present?

A

Often symptomatic, however they can present:

Heavy menstrual bleeding (menorrhagia) is the most frequent presenting symptom

Prolonged menstruation, lasting more than 7 days

Abdominal pain, worse during menstruation

Bloating or feeling full in the abdomen

Urinary or bowel symptoms due to pelvic pressure or fullness

Deep dyspareunia (pain during intercourse)

Reduced fertility

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93
Q

What may examination reveal of fibroids?

A

Abdominal examination may reveal a palpable pelvic mass or an enlarged firm non-tender uterus

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94
Q

What are the investigations for fibroids?

A

Hysteroscopy

Pelvic ultrasound is the investigation of choice for larger fibroids.

MRI scanning before surgical options, where more information is needed about the size, shape and blood supply of the fibroids.

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95
Q

What is the management of fibroids less than 3cm?

A

Less than 3cm (same as with heavy menstrual bleeding):

Mirena coil (1st line) – fibroids must be less than 3cm with no distortion of the uterus

Symptomatic management with NSAIDs and tranexamic acid

Combined oral contraceptive

Cyclical oral progestogens

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96
Q

What are the surgical options for smaller fibroids with heavy menstrual bleeding?

A

Endometrial ablation

Resection of submucosal fibroids during hysteroscopy

Hysterectomy

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97
Q

What is the medical management for fibroids more than 3cm?

A

Referral to gynaecology for investigation and management, options:

Symptomatic management with NSAIDs and tranexamic acid

Mirena coil – depending on the size and shape of the fibroids and uterus

Combined oral contraceptive

Cyclical oral progestogens

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98
Q

What are the surgical options for larger fibroids?

A

Uterine artery embolisation

Myomectomy

Hysterectomy

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99
Q

What may be used to reduce the size of the fibroid before surgery?

A

GnRH agonists e.g. goserelin (Zoladex) or leuprorelin (Prostap) - induce a menopause-like state and reduce the amount of oestrogen maintaining the fibroid - only used short term

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100
Q

What is uterine artery embolisation?

A

Performed by interventional radiologists - using a catheter into an artery (usually femoral) - passed through to the uterine artery under x-ray guidance

Once in place, particles are injected creating a blockage in the supply to the fibroid - causing it to shrink

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101
Q

What is a myomectomy?

A

Surgically removing the fibroids via laparoscopic (keyhole) surgery or laparotomy (open surgery) - only treatment to potentially improve fertility in patients with fibroids

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102
Q

What is endometrial ablation?

A

Used to destroy the endometrium

Second generation, non-hysteroscopic techniques are used e.g. balloon thermal ablation

Inserting a balloon in the uterus and filling with high temp fluid to burn the endometrial lining of the uterus

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103
Q

What does a hysterectomy involve?

A

Removing the uterus and fibroids - may be done laparoscopically or laparotomy or vaginally - ovaries may be left

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104
Q

What are the key complications of fibroids?

A

Heavy menstrual bleeding, often with iron deficiency anaemia

Reduced fertility

Pregnancy complications, such as miscarriages, premature labour and obstructive delivery

Constipation

Urinary outflow obstruction and urinary tract infections

Red degeneration of the fibroid

Torsion of the fibroid, usually affecting pedunculated fibroids

Malignant change to a leiomyosarcoma is very rare (<1%)

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105
Q

What is red degeneration of fibroids?

A

Ischaemia, infarction and necrosis of the fibroid due to disrupted blood supply

More likely in larger fibroids (above 5cm) during the second and third trimester of pregnancy

May occur to growing of fibroid during pregnancy or kinking in the blood vessel as the uterus changes shape and expands

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106
Q

How may red degeneration of fibroids present?

A

Severe abdo pain

Fever

Tachycardia

Vomiting

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107
Q

What is the treatment of red degeneration of fibroids?

A

Supportive, rest, fluids and analgesia

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108
Q

What is endometriosis?

A

Ecotopic endometerial tissue outside of the uterus (lump of tissue = endometrioma)

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109
Q

What are endometriomas in the ovaries nicknamed?

A

Chocolate cysts

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110
Q

What is adenomyosis?

A

Endometrial tissue within the myometrium (muscle layer) of the uterus

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111
Q

What causes endometriosis? What are some theories?

A

Not clear, but there is a genetic component

  • Retrograde menstruation: during menstration flow is backwards through fallopian tubes and into the pelvis and peritoneum
  • Embryonic cells destined to become endometrial tissue may remain in areas outside the uterus during the delelopment of the fetus and become ectopic tissue
  • Lymphatic system may spread the tissue
  • Metaplasia may change cells outside the uterus
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112
Q

What is the pathophysiology behind endometriosis?

A

Pelvic pain is the main symptom - cells of endometrial tissue respond to hormones in same way as endometrial tissue - causing the ectopic tissue to shed lining and bleed causing irritation and inflammation in the tissues around the sites of endometriosis.

Cyclical, dull, heavy or burning pain is the result

Deposits of endometriosis in the bladder or bowel can lead to blood in the urine or stools

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113
Q

What is a complication of endometriosis?

A

Adhesions from localised bleeding and inflammation (e.g. ovaries to the peritoneum, uterus to bowel)

Causes chronic, non-cyclical pain which can be sharp, stabbing or pulling and associated with nausea

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114
Q

Are women with endometriosis fertile?

A

Can lead to reduced fertility (maybe due to adhesions around the ovaries and fallopian tubes)

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115
Q

How may endometriosis present?

A

Cyclical abdominal or pelvic pain

Deep dyspareunia (pain on deep sexual intercourse)

Dysmenorrhoea (painful periods)

Infertility

Cyclical bleeding from other sites, such as haematuria

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116
Q

What are the other symptoms related to other aread affected by the endometriosis?

A

Urinary symptoms

Bowel symptoms

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117
Q

What may examination of endometriosis reveal?

A

Endometrial tissue visible in the vagina on speculum examination, particularly in the posterior fornix

A fixed cervix on bimanual examination

Tenderness in the vagina, cervix and adnexa

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118
Q

How is endometriosis diagnosed?

A

Pelvic ultrasound - for large endometriomas and chocolate cysts

Laparoscopic surgery - gold standard - definitiev diagnosis with biopsy of the lesion during laparoscopy (surgeon can remove deposits of endometriosis

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119
Q

What is the american society of reproductive medicine (ASRM) staging system for endometriosis?

A

Stage 1: Small superficial lesions

Stage 2: Mild, but deeper lesions than stage 1

Stage 3: Deeper lesions, with lesions on the ovaries and mild adhesions

Stage 4: Deep and large lesions affecting the ovaries with extensive adhesions

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120
Q

What does the inital management of endometriosis involve?

A

Establishing a diagnosis

Providing a clear explanation

Listening to the patient, establishing their ideas, concerns and expectations and building a partnership

Analgesia as required for pain (NSAIDs and paracetamol first line)

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121
Q

What hormonal managment can be tried before estabilshign a definitive diagnosis with laparoscopy?

A

Combined oral contractive pill, which can be used back to back without a pill-free period if helpful

Progesterone only pill

Medroxyprogesterone acetate injection (e.g. Depo-Provera)

Nexplanon implant

Mirena coil

GnRH agonists

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122
Q

What are the surgical management options for endometriosis?

A

Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis)

Hysterectomy

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123
Q

What treatment for endometriosis improved fertility?

A

Laparoscopic treament (hormonal therapies do not improve fertility)

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124
Q

What are the treatment options for endometriosis?

A

Cyclical pain - COCP, oral progesterone-only pill, progestin depot injection, progestin implant (nexplanon) stop ovulation and reduce endometrial thickening

GnRH agonists - induce menopause-like state using GnRH agonists e.g. goserelin (zoladex) or leuprorelin (prostap) (risk of osteoporosis)

Laparoscopic surgery - excise or ablate the ectopic endometrial tissue, where there is chronic pelvic pain due to adhesions surgery can dissect these

Hysterectomy and bilateral salpingo-opherectomy - final surgical option, removing ovaries induces menopause, stopping ectopic endometrial tissue responding to menstrual cycle

Infertility - treated by removing as much of the endometriosis as possible

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125
Q

What is adenomyosis?

A

Endometrial tissue inside the myometrium (muscle layer of uterus)

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126
Q

When is adenomyosis common?

A
  • Later reproductive years
  • Several pregnancies (multiparous)
  • 10% of women overall
  • Cause is not fully understood (hormone dependent)
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127
Q

How does adenomyosis present?

A

Painful periods (dysmenorrhoea)

Heavy periods (menorrhagia)

Pain during intercourse (dyspareunia)

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128
Q

What proportion of women with adenomyosis are asymptomatic?

A

1/3

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129
Q

What does examination show of adenomyosis?

A

Enlarged and tender uterus

Feels more soft than a uterus containing fibroids

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130
Q

How is adenomyosis diagnosed?

A

Transvaginal ultrasound of the pelvis (first-line)

MRI and transabdominal ultrasound alternatives where TV is nor suitable

Gold standard is to perform a histological examination of the uterus after a hysterectomy (not always suitable for obvious reasons)

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131
Q

What is the management of adenomyosis?

A

Depends on symptoms, age and plans for pregnancy:

  • Non-contraceptive: tranexamic acid (antifibrinolytic - used when no pain), mefenamic acid (NSAID - reduces bleeding and pain
  • Contraceptive: Mirena coil (first line), COCP, cyclical oral progestogens (progesterone only medication e.g. the pill, implant or depot injection may also be helpful)
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132
Q

What other treatments may be considered for adenomyosis by a specialist?

A

GnRH analogues (menopause-like state)

Endometrial ablation

Uterine atery embolisation

Hysterectomy

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133
Q

What pregnancy complications is adenomyosis associated with?

A

Infertility

Miscarriage

Preterm birth

Small for gestational age

Preterm premature rupture of membranes

Malpresentation

Need for caesarean section

Postpartum haemorrhage

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134
Q

How is menopause diagnosed?

A

Retrospectively - after woman has no periods for 12 months

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135
Q

What is the average age of menopause?

A

51 years old

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136
Q

What is postmenopause?

A

Period from 12 months after the final period

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137
Q

What is perimenopause?

A

Time around menopause, vasomotor symptoms and irregular periods

Including time leading up and 12 months after menopause

Women older that 45

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138
Q

What is premature menopause?

A

Menopause before the age of 40 - result of premature ovarian insufficiency

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139
Q

How are the sex hormones in menopause?

A

Lack of ovarian follicular function:

  • Oestrogen and progesterone levels are low
  • LH and FSH levels are high in response to an absence of negative feedback from oestrogen
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140
Q

What is the physiological process behind menopause?

A

In ovaries primordial follicles mature into primary and secondary follicles (independent of the menstrual cycle) at start of menstrual cycle FSH stimulates the development of secondary follicles - as these grow granulosa cells which surround them secrete increasing amounts of oestrogen

Menopause begins in the decline of the development of follicles - reducing oestrogen levels - increasing LH and FSH

Anovulation results and without oestrogen the endometrium doesnt develop = amenorrhoea

Low levels of oestrogen cause perimenopausal symptoms

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141
Q

What are some perimenopausal symptoms?

A

Hot flushes

Emotional lability or low mood

Premenstrual syndrome

Irregular periods

Joint pains

Heavier or lighter periods

Vaginal dryness and atrophy

Reduced libido

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142
Q

What are the risks associated with a lack of oestrogen?

A

Cardiovascular disease and stroke

Osteoporosis

Pelvic organ prolapse

Urinary incontinence

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143
Q

How is menopause diagnosed?

A

Perimenopause / menopause diagnosis can be made in women over 45 years old with typical symptoms

FSH blood test is recommended in women under 40 with premature menopause / women aged 40-45 with menopausal symptoms/ change in menstrual cycle

144
Q

How long do women need contraception for around the menopause?

A
  • Two years after LMP in women < 50
  • One year after LMP in women > 50
145
Q

Do hormonal contraceptives affect the menopause?

A

No, they may suppress and mask the symptoms

146
Q

Which contraceptives are UKMEC1 for women approaching menopause?

A

Barrier methods

Mirena or copper coil

Progesterone only pill

Progesterone implant

Progesterone depot injection (under 45 years)

Sterilisation

147
Q

What category is the COCP in women aged 40-50?

A

UKMEC2

148
Q

What COCP should be considered in women over 40 and why?

A

Those containing norethisterone or levonorgestrel due to the relatively lower risk of VTE

149
Q

What are the two side effects that are unique to the depot injection?

A

Weight gain

Osteoporosis (so, unsuitable for women over 45)

150
Q

How long do vasomotor symptoms last without any treatment?

A

2-5 years

151
Q

What are the options for management of perimenopausal symptoms?

A

No treatment

Hormone replacement therapy (HRT)

Tibolone, a synthetic steroid hormone that acts as continuous combined HRT (only after 12 months of amenorrhoea)

Clonidine, which act as agonists of alpha-adrenergic and imidazoline receptors

Cognitive behavioural therapy (CBT)

SSRI antidepressants, such as fluoxetine or citalopram

Testosterone can be used to treat reduced libido (usually as a gel or cream)

Vaginal oestrogen cream or tablets, to help with vaginal dryness and atrophy (can be used alongside systemic HRT)

Vaginal moisturisers, such as Sylk, Replens and YES

152
Q

What is menopause before 40 called?

A

Premature ovarian insufficiency

153
Q

What ‘type’ of failure is premature ovarian insufficiency?

A

Hypergonadotrophic hypogonadism - lack of negative feedback on the pituitary gland resulting in an excess or gonadotrophins:

Raised LH and FSH

Low oestradiol levels

154
Q

What are the causes of premature ovarian failure?

A

Idiopathic (the cause is unknown in more than 50% of cases)

Iatrogenic, due to interventions such as chemotherapy, radiotherapy or surgery (i.e. oophorectomy)

Autoimmune, possibly associated with coeliac disease, adrenal insufficiency, type 1 diabetes or thyroid disease

Genetic, with a positive family history or conditions such as Turner’s syndrome

Infections such as mumps, tuberculosis or cytomegalovirus

155
Q

How does premature ovarian insufficiency present?

A

Irregular menstrul periods, lack of menstrual periods (secondary amenorrhea), symptoms of low oestrogen levels such as hot flushes, night sweats and vaginal dryness

156
Q

How is premature ovarian insufficiency diagnosed?

A

Women younger than 40 years old with typical menopausal symptoms plus elevated FSH

FSH elevation needs to be on two consecutive samples separated by more than 4 weeks (results are difficult to interpret in women taking hormonal contraception)

157
Q

What are the conditions associated with premature ovarian insufficiency?

A
  • CVD
  • Stroke
  • Osteoporosis
  • Cognitive impairment
  • Dementia
  • Parkinsonism
158
Q

What is the management of premature ovarian insufficiency?

A

Hormone replacement therapy - reducing risk of CVD, osteoporosis, cognitive and psychological risks

  • Traditional HRT (associated with a lower BP compared to COCP)
  • COCP (less stigma for younger women)

Contraception - as pregnancy is still possible

159
Q

Is HRT considered to increased the risk of breast cancer?

A

Not before the age of 50 as women would produce these hormones

BUT increased risk of VTE (decreased using transdermal methods - patches)

160
Q

What is the HRT regime and when is it given?

A

Without a uterus: exogenous oestrogen

With a uterus: Oestrogen and progesterone (prevents endometrial hyperplasia and endometrial cancer due to “unopposed” oestrogen)

Still having periods: cyclical HRT, with cyclical progesterone and regular breakthrough bleeds

161
Q

What are some non-hormonal treatments for menopausal symptoms?

A

Lifestyle changes such as improving the diet, exercise, weight loss, smoking cessation, reducing alcohol, reducing caffeine and reducing stress

Cognitive behavioural therapy (CBT)

Clonidine, which is an agonist of alpha-adrenergic and imidazoline receptors

SSRI antidepressants (e.g. fluoxetine)

Venlafaxine, which is a selective serotonin-norepinephrine reuptake inhibitor (SNRI)

Gabapentin

162
Q

What is clonidine? When is it used?

A

Agonist of alpha-2 adrenic receptors and imidazoline receptors in the brain

Lower BP and reduced HR

Useful for vasomotor symptoms and hot flushes particularly when there are contraindications to HRT

163
Q

What are the side effects to clonidine?

A

Dry mouth

Headaches

Dizziness

Fatigue

(sudden withdrawal can cause rapid increase in BP and agitation)

164
Q

What are some alternative remedies for HRT? What are their side effects?

A

Black cohosh, which may be a cause of liver damage

Dong quai, which may cause bleeding disorders

Red clover, which may have oestrogenic effects that would be concerning with oestrogen sensitive cancers

Evening primrose oil, which has significant drug interactions and is linked with clotting disorders and seizures

Ginseng may be used for mood and sleep benefits

165
Q

What are the indications for HRT?

A

Replacing hormones in premature ovarian insufficiency, even without symptoms

Reducing vasomotor symptoms such as hot flushes and night sweats

Improving symptoms such as low mood, decreased libido, poor sleep and joint pain

Reducing the risk of osteoporosis in women under 60 years

166
Q

What are the risks of HRT?

A

More significant in older women and increase with longer duration of treatment:

  • Increased risk of breast/endometrial cancer
  • Increased risk of VTE (2-3 times background risk)
  • Increased risk of stroke and coronary artery disease
  • Inconclusive evidence about ovarian cancer
167
Q

When do the risks of HRT not apply?

A
  • Not increased in women under 50 years compared with other women their age
  • No risk of endometrial cancer in women without a uterus
  • No increased risk of breast cancer with oestrogen-only HRT (risk may even be reduced)
  • No increased risk of CVD with oestrogen-only HRT (risk may be reduced)
168
Q

How to reduce the risks of HRT?

A
  • Adding progesterone in women with a uterus to reduce risk of endometrial cancer
  • Using patches instead of pills to reduce the risk of VTE
  • Using local progestogens (e.g. mirena coil) to reduce the risk of breast cancer and CVD
169
Q

What are some contraindications to starting HRT?

A

Undiagnosed abnormal bleeding

Endometrial hyperplasia or cancer

Breast cancer

Uncontrolled hypertension

Venous thromboembolism

Liver disease

Active angina or myocardial infarction

Pregnancy

170
Q

What are some assessments to do before HRT?

A
  • Full history to ensure no contraindications
  • Family history (for oestrogen dependent cancers (e.g. breast cancer and VTE)

- BMI and BP

  • Ensure cervical and breast screening is up to date
  • Encourage lifestyle changes which are likely to improve symptoms
171
Q

What are the three factors to consider with HRT?

A

Local / systemic symptoms:

Local symptoms: use topical treatments such as topical oestrogen cream or tablets

Systemic symptoms: use systemic treatment – go to step 2

Step 2: Does the woman have a uterus?:

No uterus: use continuous oestrogen-only HRT

Has uterus: add progesterone (combined HRT) – go to step 3

Step 3: Have they had a period in the past 12 months?

Perimenopausal: give cyclical combined HRT

Postmenopausal (more than 12 months since last period): give continuous combined HRT

172
Q

What aare the two options for delivering systemic oestrogen?

A
  • Oral (tablets)
  • Transdermal (patches / gels)
173
Q

Who are patches most suited to for HRT?

A

Women with poor control on oral treatment

Women with higher risk of VTE, CVD, headaches

174
Q

Why is progesterone added to a HRT regime?

A

Reduces the risk of endometrial hyperplasia and endometrial cancer

Only required in women that have a uterus

175
Q

When is cyclical / vs non cyclical progesterone given?

A

Cyclical = 10 - 14 days per month - women that have had a period within 12 months allowing to have monthly breakthrough bleeds

Continuous = woman has no period in the past:

  • 24 months if under 50
  • 12 months if over 50
176
Q

What can result with continuous combined HRT before postmenopause?

A

Irregular breakthrough bleeding

177
Q

When can patients switch from cyclical to continuous HRT?

A

At least 12 months of treatment in women over 50

At least 24 months in women under 50

178
Q

What are the three options for delivering progesterone for endometrial protection?

A

Oral (tablets)

Transdermal (patches)

Intrauterine system (e.g. mirena coil)

179
Q

How long is the mirena coil licenced for use in endometrial protection?

A

4 years after which it needs replacing

Added benefit of contraception and treating heavy menstrual periods

180
Q

What are progestogens, progesterones and progestins?

A

Progestogens: any chemical which targets and stimulates progesterone receptors

Progesterone: hormone produced naturally in the body

Progestins: synthetic progestogens

181
Q

What are the two significant progestogen classes used in HRT?

A

C19 and C21 progestogens (referring to chemical structure and number of carbon atoms in molecule)

182
Q

Where are C19 progestogens derived from?

What are some examples?

When are they helpful?

A

Testosterone

Norethisterone, levonorgestrel and desogestrel

Helpful with reduced libido

183
Q

Where are C21 progestogens derived from?

What are some examples?

When are they helpful?

A

Derived from progesterone

Progesterone, dydrogesterone medroxyprogesterone

Helpful with depressed mood / acne

184
Q

What is the suggested HRT regime in women with no uterus?

A

Oestrogen-only pills, for example, Elleste Solo or Premarin

Oestrogen-only patches, for example, Evorel or Estradot

185
Q

What is the suggested HRT regime in perimenopausal women with periods?

A

Cyclical combined tablets

Cyclical combined patches

Mirena coil plus oestrogen-only pills

Mirena coil plus oestrogen-only patches

186
Q

What are the suggested HRT regimes in postmenopausal women with a uterus?

A

Continuous combined tablets

Continuous combined patches

Mirena coil plus oestrogen-only pills

Mirena coil plus oestrogen-only patches

187
Q

What is the best way of delivering oestrogen and progesterone respectively?

A

Oestrogen = with patches (reduced risk of VTE)

Progesterone = with intrauterine device (e.g. mirena - treats heavy periods and provides contraception)

188
Q

What is tibolone?

A

Synthetic steroid which stimulates oestrogen and progesterone receptors (also weakly stimulates androgen receptors - helpful in patients with reduced libido)

189
Q

What is Tibolone used as?

A

Form of continuous combined HRT (need to be more than 12 months without period / more than 24 if below 50)

Expected to not have breakthrough bleeding

Tibolone can cause irregular bleeding, resulting in futher investigations to exclude other causes

190
Q

Can treament with testosterone be given in menopause?

A

Yes, helps with low energy and reduced libido (sex drive

Given as transdermal application, applied as a gel/cream to the skin

191
Q

What are some additional management points of HRT?

A
  • Follow-up in 3 months
  • Takes 3-6 months to experience full effects
  • Problematic / irregular bleeding is an indication for referral
  • Ensure woman has contraception
  • Stop oestrogen-containing contraceptives 4 weeks before major surgery
  • Consider other diagnoses where symptoms persist (e.g. thyroid, liver disease, diabetes)
192
Q

What are common contraceptive choices in perimenopausal women on HRT?

A

Mirena coil

Progesterone only pill, given in addition to HRT

193
Q

What are the oestrogenic side effects of HRT?

A

Nausea and bloating

Breast swelling

Breast tenderness

Headaches

Leg cramps

194
Q

What are the progestogenic side effects of HRT?

A

Mood swings

Bloating

Fluid retention

Weight gain

Acne and greasy skin

195
Q

How to deal with patients with side effects from HRT?

A

Change type of HRT or route of administration (switch between patches and pills)

196
Q

How should patients with progestogenic side effects on HRT be managed?

A

Switch to different form of progesterone e.g. dyhydrogesterone for acne and mood swings

Norethisterone for reduced libido

Mirena coil for endometrial protection (avoiding progesterone all together)

197
Q

When can unscheduled bleeding occur in HRT?

A

First 3-6 months of HRT (in women with a uterus) - if it continues the consider referral for investigations

198
Q

How to stop HRT?

A

No specific regime - can be abrupt or gradual

199
Q

What are the characteristic features of polycystic ovarian syndrome?

A

Multiple ovarian cysts

Infertilify

Oligomenorrhoea

Hyperandrogenism

Insulin resistance

200
Q

What do the following terms mean:

Anovulation

Oligoovulation

Amenorrhoea

Oligomenorrhoea

Androgens

Hyperandrogenism

Hirsutism

Insulin resistance

A

Anovulation refers to the absence of ovulation

Oligoovulation refers to irregular, infrequent ovulation

Amenorrhoea refers to the absence of menstrual periods

Oligomenorrhoea refers to irregular, infrequent menstrual periods

Androgens are male sex hormones, such as testosterone

Hyperandrogenism refers to the effects of high levels of androgens

Hirsutism refers to the growth of thick dark hair, often in a male pattern, for example, male pattern facial hair

Insulin resistance refers to a lack of response to the hormone insulin, resulting in high blood sugar levels

201
Q

What criteria is used for making a diagnosis of polycystic ovarian syndrome?

A

Rotterdam criteria - At least 2 of the 3 key features:

  • Oligoovulation / anovulation - presenting with irregular / absent periods
  • Hyperandrogenism - hirsutism and acne
  • Polycystic ovaries on ultrasound (or ovarian
202
Q

How do women with polycystic ovarian syndrome present?

A

Oligomenorrhoea or amenorrhoea

Infertility

Obesity (in about 70% of patients with PCOS)

Hirsutism

Acne

Hair loss in a male pattern

203
Q

What are some other features of PCOS?

A

Insulin resistance and diabetes

Acanthosis nigricans

Cardiovascular disease

Hypercholesterolaemia

Endometrial hyperplasia and cancer

Obstructive sleep apnoea

Depression and anxiety

Sexual problems

204
Q

What is acanthosis nigricans?

A

Thickened, rough skin, typically found on the axilla and on the elbows, has a velvety texture occurs with insulin resistance

205
Q

Other than PCOS, what else can cause hirsutism?

A

Medications, such as phenytoin, ciclosporin, corticosteroids, testosterone and anabolic steroids

Ovarian or adrenal tumours that secrete androgens

Cushing’s syndrome

Congenital adrenal hyperplasia

206
Q

How is insulin resistance linked to PCOS?

A

Pancreas produces more insulin which promotes the release of androgens from the ovaries and adrenal glands - causing higher levels of testosterone

Insulin suppresses sex hormone-binding globulin (SHBG) production by the liver. SHBG normally binds to androgens, supressing them - thus less SHBG promotes hyperandrogenism in women with PCOS

Diet, exercise and weight loss help to reduce insulin resistance

207
Q

What blood tests can diagnose PCOS (and exclude other diagnoses)?

A

Testosterone

Sex hormone-binding globulin

Luteinizing hormone

Follicle-stimulating hormone

Prolactin (may be mildly elevated in PCOS)

Thyroid-stimulating hormone

208
Q

What do the blood tests reveal for PCOS?

A

Raised luteinising hormone

Raised LH to FSH ratio (high LH compared with FSH)

Raised testosterone

Raised insulin

Normal or raised oestrogen levels

209
Q

What imaging can be used for PCOS?

A

Transvaginal ultrasound (gold standard) - follicles may be arranged around the periphery of the ovary, giving a “string of pearls” appearance.

Diagnostic criteria:

  • 12/ more developing follicles
  • Ovarian volume of more than 10cm3
210
Q

What is the screening test for diabetes in patients with PCOS?

A

2-hour 75g oral glucose tolerance test (OGTT):

Morning prior to having breakfast, take baseline fasting plasma glucose, then 75g glucose drink, then measure plasma glucose 2 hours later

211
Q

What are the possible results for an OGTT?

A

Impaired fasting glucose – fasting glucose of 6.1 – 6.9 mmol/l (before the glucose drink)

Impaired glucose tolerance – plasma glucose at 2 hours of 7.8 – 11.1 mmol/l

Diabetes – plasma glucose at 2 hours above 11.1 mmol/l

212
Q

How to lower the risks associated with PCOS (obesity, T2DM, CVD)?

A

Weight loss

Low glycaemic index, calorie-controlled diet

Exercise

Smoking cessation

Antihypertensive medications where required

Statins where indicated (QRISK >10%)

213
Q

What complications should PCOS patients be screened for?

A

Endometrial hyperplasia and cancer

Infertility

Hirsutism

Acne

Obstructive sleep apnoea

Depression and anxiety

214
Q

What plays a significant part of the management of PCOS?

A

Weight loss - result in ovulation, restoration of fertility, improve insulin resistance, reduce hirsutism, reduce the risks of associated conditions.

Orlistat may be used to help in women with a BMI about 30

Orlistat is a lipase inhibitor (preventing absorption of fat in the intestines)

215
Q

What are the risk factors for endometrial cancer in PCOS?

A

Obesity

Diabetes

Insulin resistance

Amenorrhoea

216
Q

Why is there a risk of endometrial cancer in women with PCOS?

A

Normally corpus luteum releases progesterone after ovulation - women with PCOS ovulate infrequently - less progesterone

Oestrogen is “unopposed” and continues to proliferate the endometrial lining - causing endometrial hyperplasia

217
Q

How to investigate women with extended gaps between periods (more than 3 months) / abnormal bleeding?

A

Pelvic ultrasound to assess endometrial thickness

Cyclical progestogens should be used to induce a period prior to the ultrasound scan

If endometrial thickness is more than 10mm, need to be referred for a biopsy to exclude endometrial hyperplasia / cancer

218
Q

How to reduce the risk of endometrial hyperplasia and cancer?

A

Mirena coil for continuous endometrial protection

Inducing a withdrawal bleed (every 3-4 months) with:

  • Cyclical progestogens (e.g. medroxyprogesterone acetate 10mg once a day for 14 days)
  • COCP
219
Q

How to manage infertility in PCOS?

A

Weight loss, can restore regular ovulation

Clomifene

Laparoscopic ovarian drilling

In vitro fertilisation (IVF)

220
Q

What more specialist techniques can be used to restore fertility in PCOS?

A

Metformin and letrozole may also help under guidance of a specialist, evidence to support their use is not clear

Ovarian drilling involving laparoscopic surgery - surgeon punctures multiple holes in the ovaries using diathermy or laser therapy

Screening for gestational diabetes using OGTT performed before pregnancy and at 24-28 weeks gestation

221
Q

How may hirsutism be managed with PCOS?

A

Weight loss or hair removal e.g. waxing, shaving and plucking

Co-cyprindiol is a COCP liscensed for the treatment of hirsutism and acne (anti-androgenic effect) - BUT significant risk of VTE, co-cyprindiol is usually stopped after 3 months of use

Topical eflornithine - used to treat facial hirsutism - takes 6-8 weeks to see improvement (hirsutism will return in 2 months of stopping eflornithine)

222
Q

What other options may be considered by a specialist experienced in treating hirsutism?

A

Electrolysis

Laser hair removal

Spironolactone (mineralocorticoid antagonist with anti-androgen effects)

Finasteride (5α-reductase inhibitor that decreases testosterone production)

Flutamide (non-steroidal anti-androgen)

Cyproterone acetate (anti-androgen and progestin)

223
Q

How is acne with PCOS managed?

A

COCP (first line) - co-cyprindiol has anti-androgen effects (high risk of VTE)

Other standard acne treatments:

  • Topical adapalene (a retinoid)
  • Topical antibiotics (e.g. clindamycin 1% with benzoyl peroxide 5%)
  • Topical azelaic acid 20%
  • Oral tetracycline antibiotics (e.g. lymecycline)
224
Q

What are cysts and when do they occur in women?

A

Cyst = fluid filled sac

Functional ovarian cysts = related to fluctuating hormones of menstrual cycle, very common in premenopausal women (vast majority are benign)

Cysts in post menopausal women are more concerning for malignancy

225
Q

How do ovarian cysts present?

A

Pelvic pain

Bloating

Fullness in the abdomen

A palpable pelvic mass (particularly with very large cysts such as mucinous cystadenomas)

226
Q

When may ovarian cysts present with acute pain?

A

Ovarian torsion

Haemorrhage

Rupture of cyst

227
Q

What are follicular cysts?

A

Follicle fails to rupture and release egg

Most common ovarian cyst

Harmless and disappear after a few menstrual cycles

Thin walled and no internal structure (reassuring on ultrasound)

228
Q

What are corpus luteum cysts?

A

Corpus luteum fails to break down and instead fills with fluid

Cause pelvic discomfort, pain or delayed menstruation

Seen in early pregnancy

229
Q

Define other types of ovarian cysts:

Serous cystadenoma

Mucinous cystadenoma

Endometrioma

Dermoid cyst / germ cell tumour

Sex cord-stromal tumours

A

Serous cystadenoma = benign tumour of epithelial cells

Mucinous cystadenoma = benign tumour of epithelial cells, can become huge

Endometrioma = lumps of endometrial tissue within the ovary, occur in patients with endometriosis

Dermoid cyst / germ cell tumour = benign ovarian tumours, teratomas meaning they come from the germ cells and may contain various tissue types e.g. skin, teeth, hair and bone - associated with ovarian torsion

Sex cord-stromal tumours= rare tumours that can be benign or malignant - arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles) e.g. Sertoli-Leydig cell tumours and granulosa cell tumours

230
Q

What history may suggest a malignant cyst?

A

Abdominal bloating

Reduce appetite

Early satiety

Weight loss

Urinary symptoms

Pain

Ascites

Lymphadenopathy

231
Q

What are the risk factors for ovarian malignancy?

A

Age

Postmenopause

Increased number of ovulations

Obesity

Hormone replacement therapy

Smoking

Breastfeeding (protective)

Family history and BRCA1 and BRCA2 genes

232
Q

What factors reduce number of ovulations and thus risk of ovarian cancer?

A

Later onset of periods (menarche)

Early menopause

Any pregnancies

Use of the combined contraceptive pill

233
Q

What blood tests should be done to rule out malignancy for an ovarian cyst?

A

Premenopausal women with a simple ovarian cyst less than 5cm on ultrasound do not need further investigations

CA125 is the tumour market for epithelial cell ovarian cancer (forms part of the risk malignancy index)

Women under 40 years with a complex ovarian mass require tumour markers for a possible germ cell tumour:

  • Lactate dehydrogenase (LDH)
  • Alpha-fetoprotein (alpha-FP)
  • Human chorionic gonadotrophin (HCG)
234
Q

What are some non-malignant causes of a raised CA125?

A

Endometriosis

Fibroids

Adenomyosis

Pelvic infection

Liver disease

Pregnancy

235
Q

What 3 elements are there to the risk of malignancy index?

A

Estimates the risk of an ovarian mass being malignant:

  • Menopausal status
  • Ultrasound findings
  • CA125 level
236
Q

How to manage:

Possible ovarian cancer (complex cysts or raised CA125)

Possible dermoid cysts

Simple ovarian cysts in premenopausal women?

A

Possible ovarian cancer: 2WW referral to a gynae oncology specialist

Possible dermoid cysts: referral to a gynaecologist for further investigations

Simple ovarian cysts in premenopausal women:

  • Less than 5cm cysts will almost always resolve in 5 cycles
  • 5cm-7cm: resuire routine referral to gynar and yearly ultrasound
  • > 7cm consider an MRI scan or surgical evaluation (difficult to characterise with ultrasound)
237
Q

How are cysts in postmenopausal women managed?

A

Require correlation with the CA125 (2WW referral if raised)

Simple cysts under 5cm with normal CA125 may be monitored with ultrasound every 4-6 months

238
Q

How are persisting or enlarging cysts managed?

A

Surgical intervention (usually with laparoscopy)

Ovarian cystectomy (removing cyst)

Oophorectomy (removing the affected ovary)

239
Q

What are the main complications of ovarian cysts?

A

Torsion

Haemorrhage into the cyst

Rupture, with bleeding into the peritoneum

240
Q

What is Meig’s syndrome?

A

Triad:

- Ovarian fibroma (benign ovarian tumour)

- Pleural effusion

- Ascites

Typically occurs in older women - removal results in complete resolution of effusion and ascites

241
Q

What is ovarian torsion usually due to?

A

Ovarian mass larger than 5cm e.g. cyst or a tumour (usually benign) more likely in pregnancy

242
Q

When else in life can ovarian torsion occur?

A

Younger girls, who have longer infundibulopelvic ligaments that can twist more easily

243
Q

Why is ovarian torsion an emergency?

A

Twisting of blood supply leads to ischaemia and necrosis

244
Q

How does ovarian torsion present?

A

Sudden onset severe unilateral pain - constant - gets worse - associated with N&V

Pain is not always severe (can twist and untwist)

Localised tenderness (may be a palpable mass)

245
Q

How is ovarian torsion diagnosed?

A

Pelvic ultrasound - TV is ideal but transabdominal will do

“Whirlpool sign”, free fluid in pelvis and oedema of the ovary may be seen

Doppler studies may show a lack of blood flow

Definitive diagnosis = laparoscopic surgery

246
Q

What is the management of ovarian torsion?

A

Admission under gynaecology

Require laparoscopic surgery to either:

  • Untwist the ovary and fix it in place (detorsion)
  • Remove the affected ovary (oophorectomy)

Decision is made during surgery based on visual inspection

247
Q

What are some complications of ovarian torsion?

A

If only ovary - can lead to infertility and menopause

Necrotic ovary which isnt removed can become infected, develop an abscess and lead to sepsis

May rupture resulting in peritonitis and adhesions

248
Q

What is Asherman’s syndrome?

A

Adhesion (aka synechiae) form within the uterus following damage

249
Q

When does Asherman’s syndrome usually occur?

A

Pregnancy related dilatation and curettage procedure e.g. in treatment of RPOC (e.g. removing placental tissue left after birth)

Occurs after uterine surgery (e.g. myomectomy) or several pelvic infections (e.g. endometritis)

250
Q

How may endometrial curettage (scraping) damage the uterus?

A

Damages basal layer of the endometrium - tissue may heal abnormally

251
Q

What are the result of these uterine adhesions?

A

Menstration abnormalities

Infertility

Recurrent miscarriages

252
Q

Are asymptomatic adhesions classified as Asherman’s?

A

No

253
Q

How does Asherman’s syndrome present?

A

Following recent dilatation and curettage:

Secondary amenorrhoea (absent periods)

Significantly lighter periods

Dysmenorrhoea (painful periods)

254
Q

How are intrauterine adhesions diagnosed?

A

Hysteroscopy - gold standard - can dissect and treat adhesions

Hysterosalpingography - contrast is injected into the uterus and imaged with xrays

Sonohysterography - uterus is filled with fluid and pelvic ultrasound

MRI

255
Q

What is the managment of intrauterine adhesions?

A

Dissecting the adhesions during hysteroscopy (recurrence is common)

256
Q

What is cervical ectropion also known as?

A

Cervical ectopy

Cervical erosion

257
Q

What happen in cervical ectropion?

A

Columnar epithelium of the endocervix (the canal of the cervix) has extended out to the ectocervix (outer area od the cervix)

Cells of the endocervix are more fragile and prone to trauma - more likely to bleed with sexual intercourse - often presents with post-coital bleeding

258
Q

What is cervical ectropion associated with?

A

Higher oestrogen levels and therefore more common in younger women, the COCP and pregnancy

259
Q

What is the transformation zone?

A

Border between the columnar epithelium of the endocervix (the canal) and the stratified squamous epithelium of the ectocervix (the outer area of the cervix)

260
Q

How does cervical ectropion present?

A

Mainly asymptomatic - found incidentally suring speculum examination

  • Increased vaginal discharge
  • Vaginal bleeding
  • Dyspareunia (pain during sex)
  • Postcoital bleeding
261
Q

How is cervical ectropion managed?

A

Asymptomatic requires no treatment - typically resolves as patient gets older, stops the pill or is no longer pregnant (not a contraindication to the COCP)

Problematic bleeding - treated with cauterisation of the ectropion using silver nitrate or cold coagulation during colposcopy

262
Q

What are nabothian cysts?

A

Fluid filled cysts seen on surface of cervix (also called nabothian follicles or mucinous retention cysts)

Up to 1cm in size - harmless and unrelated to cancer

263
Q

How do nabothian cysts occur?

A

When the squamous epithelium of the ectocervix slightly covers the mucus-secreting columnar epithelium of the endocervix then the mucus becomes trapped and forms a cyst

Happens: after childbirth, minor trauma to the cervix or cervicitis secondary to infection

264
Q

How do nabothian cysts present?

A

Incidentally on speculum - smooth rounded bumps near the os

Whitish or yellow appearance

265
Q

What is the managment of nabothian cysts?

A

If diagnosis is clear then only reassurance

If diagnosis is uncertain then women can be reffered for colposcopy to examine in detail - excised or biopsied to exclude other pathology

266
Q

What is pelvic organ prolapse the result of?

A

Weakness and lengthening of the ligaments anf muscles surrounding the uterus, rectum and bladder

267
Q

What is uterine prolapse?

A

Uterus descends into the vagina

268
Q

What is vault prolapse?

A

Women who have had a hysterectomy

Top of vagina descends into the vagina

269
Q

What are rectocoeles?

A

Rectum prolapses into the vagina due to a defect in the posterior vaginal wall - associated with constipation

270
Q

What is the result of rectocoeles?

A

Faecal loading into the part of the rectum which has prolapsed causing constipation, urinary retention (due to compression on the urethra) and a palpable lump in the vagina

271
Q

What are cystocoeles?

A

Dur to a defect in the anterior vaginal wall allowing the bladder to prolapse backwards into the vagina (prolapse of the urethra is called a urethrocele, or both cystourethrocele)

272
Q

What are some risk factors for pelvic organ prolapse?

A

Multiple vaginal deliveries

Instrumental, prolonged or traumatic delivery

Advanced age and postmenopause status

Obesity

Chronic respiratory disease causing coughing

Chronic constipation causing straining

273
Q

How does pelvic organ prolapse present?

A

Feeling of “something coming down” in the vagina

Dragging or heavy sensation in pelvis

Urinary symptoms e.g. incontinence, urgency, frequency, weak stream, retention

Bowel symptoms e.g. constipation, incontinence and urgency

Sexual dysfunction e.g. pain, altered sensation and reduced enjoyment

274
Q

How can a prolapse be examined?

A

Patient should empty bladder and bowel before examination of prolapse

A Sim’s speculum is a U-shaped, single bladed speculum used to support the anterior wall to examine for a rectocoele and the posterior wall for a cystocele

Woman asked to cough

275
Q

What are the different gradings of uterine prolapse?

A

Grade 0: Normal

Grade 1: The lowest part is more than 1cm above the introitus

Grade 2: The lowest part is within 1cm of the introitus (above or below)

Grade 3: The lowest part is more than 1cm below the introitus, but not fully descended

Grade 4: Full descent with eversion of the vagina

276
Q

What is a prolapse extending beyone the introitus referred to as?

A

Uterine procidentia

277
Q

What are the options for managing a uterine prolapse?

A

Conservative = physio (pelvic floor exercises), weight loss, reduced coffee intake, incontinence pads, treat related symptoms e.g. stress incontinence with anticholinergic medications, vaginal oestrogen cream

Vaginal pessary = placed into vagina for support, many types (ring sit around cervix, shelf and gellhorn pessaries are a flat disc with a stem, cube are cube shaped, donut are a thick ring, hodge), oestrogen cream can help protect against irritation

Surgey = mesh repairs (now avoided entirely - over a lot of controversy)

278
Q

What are some complications of surgery for pelvic organ prolapse?

A

Pain, bleeding, infection, DVT and risk of anaesthetic

Damage to bladder

Recurrence of the prolapse

Altered experience of sex

279
Q

What are some complications of mesh repairs?

A

Chronic pain

Altered sensation

Dyspareunia (painful sex) for the woman / partner

Abnormal bleeding

Urinary / bowel problems

280
Q

What is urge incontinence?

A

Overactive bladder caused by overactivity of the detrusor muscle of the bladder

281
Q

What is stress incontinence due to?

A

Weakness of the pelvic floor and sphincter muscles causing leakage when laughing, coughing or surprised

282
Q

What is mixed incontinence ?

A

Combination of urge and stress incontinence

283
Q

What is overflow incontinence due to?

A

Obstruction to the outflow of the urine causing chronic urinary retention (incontinence occurs without the urge to pass urine)

Occurs without the urge to pass urine

284
Q

What can cause overflow incontinence?

A

Anticholinergic medications

Fibroids

Pelvic tumours

Neurological conditions e.g. MS, diabetic neuropathy, spinal cord injuries

285
Q

Who is overflow incontinence more common in?

A

More common in men than women

286
Q

What are some risk factors for urinary incontinence?

A

Increased age

Post menopausal

High BMI

Previous pregnancies and vaginal deliveries

Pelvic organ prolapse

Pelvic floor surgery

Neuro conditions e.g. MS

Cognitive impairment / dementia

287
Q

What are some modifiable lifestyle factors which can contribute to incontinence?

A

Caffeine consumption

Alcohol consumption

Medications

BMI

288
Q

How to assess the severity of urinary incontinence?

A

Frequency of Urination/ Incontinence

Nighttime urination

Use of pads and changes of clothing

289
Q

What should examination of urinary incontinence check for?

A

Pelvic organ prolapse

Atrophic vaginitis

Urethral diverticulum

Pelvic masses

Ask for patient to cough and watch for leakage from urethra

290
Q

What is the modified Oxford grading system for pelvic muscle contractions?

A

0: No contraction

1: Faint contraction

2: Weak contraction

3: Moderate contraction with some resistance

4: Good contraction with resistance

5: Strong contraction, a firm squeeze and drawing inwards

291
Q

How can urinary incontinence be investigated?

A

Bladder diary tracking fluid intake and episodes of urination and incontinence over 3 days (mix of work and leisure days)

Urine dipstick for infection, microscopic haematuria and other pathology

Post-void residual bladder volume measured using a bladder scan to assess for incomplete emptying

Urodynamic testing for urge incontinence patients not responding to first line medical treatments, difficulties urinating, urinary retention, previous surgery, unclear diagnosis

292
Q

How are urodynamic tests performed?

A

Patients stop any anticholinergic medication (and other bladder meds) 5 days before

Thin catheter (that measures pressure) is inserted into the bladder and rectum, bladder is filled with liquid and various outcome measures are taken:

Cystometry measures the detrusor muscle contraction

Uroflowmetry measures the flow rate

Leak point pressure is the point at which the bladder pressure results in leakage (after coughing - for stress incontinence)

Post void residual bladder volume for incomplete emptying of bladder

Video urodynamic testing - filling the bladder with contrast and taking x-rays images as the bladder is emptied (this is not routine)

293
Q

What is the first step in managing urinary incontinence?

A

Distinguish between urge and stress incontinence as this dictates management

294
Q

What are the management options for stress incontinence?

A

Avoid caffeine, diuretics and overfilling of the bladder

Avoid excessive / restrictive fluid intake

Weight loss (if appropriate)

Supervised pelvic floor exercise for at least 3 months before considering surgery (8 contractions 3 times daily)

Surgery

Duloxetine is a SNRI antidepressant used second line where surgery is less preferred

295
Q

What are the surgical options to treat stress incontinence?

A

Tension-free vaginal tape (TVT) - procedure involving a mesh sling looped under the urethra and up behind the pubic symphysis to abdo wall (supporting urethra)

Autologous sling procedure (similar to TVT procedure but strip of fascia from abdo wall is used rather than tape)

Colposuspension involves using stitches connecting the anterior vaginal wall and the pubic symphysis around the urethra - for support

Intramural urethral bulking - injections around the urethra to reduce diameter and add support

296
Q

What can be used to treat stress incontinence where surgical options have failed?

A

Operation to create an artificial urinary sphincter - using a pump inserted into the labia which inflates and deflates a cuff around the urethra

297
Q

How can urge incontinence and overactive bladder be managed?

A

Bladder retraining - gradually increasing time between voiding (for at least 6 weeks)

Anticholinergic medication: oxybutynin, tolterodine, solifenacin

Mirabegron: alternative to anticholinergic medication

Invasive procedures where medical treatment fails

298
Q

What are the anticholinergic side effects -

A

Dry mouth

Dry eyes

Urinary retention

Constipation

Postural hypotension

Coginitive decline

Memory problems

Worsening of dementia

299
Q

What is mirabegron?

A

Beta-3-agonist (contraindicated in uncontrolled hypertension, bp needs to be monitored)

Less of anticholinergic burden

300
Q

What are the options beyond retraining and medical management for an overactive bladder?

A

Botulinum toxin type A injection into the bladder wall

Percutaneous sacral nerve stimulation involves implanting a device in the back that stimulates the sacral nerves

Augmentation cystoplasty involves using bowel tissue to enlarge the bladder

Urinary diversion involves redirecting urinary flow to a urostomy on the abdomen

301
Q

What is atrophic vaginitis?

A

Dryness and atrophy of the vaginal mucosa due to a lack of oestorgen occuring in women entering the menopause

302
Q

How does the epithelial lining of the vagina respond to oestrogen?

A

Thickens

More elastic

Produces secretions

303
Q

What else can a lack of oestrogen in women cause?

A

Pelvic organ prolapse

Stress incontinence

304
Q

How does atrophic vaginitis present?

A

Itching

Dryness

Dyspareunia (discomfort or pain during sex)

Bleeding due to localised inflammation

305
Q

What does examination of atrophic vaginitis reveal?

A

Pale mucosa

Thin skin

Reduced skin folds

Erythma and inflammation

Dryness

Sparse pubic hair

306
Q

How can atrophic vaginitis be treated?

A

Vaginal lubricants e.g. sylk, replens and YES

Topical oestrogen

307
Q

What are the options for topical oestrogen?

A

Estriol cream, applied using an applicator (syringe) at bedtime

Estriol pessaries, inserted at bedtime

Estradiol tablets (Vagifem), once daily

Estradiol ring (Estring), replaced every three months

308
Q

What are the contraindications of topical oestrogen?

A

Breast cancer

Angina

VTE

309
Q

What are Bartholin’s glands?

A

Pair of glands located either side of the posterior part of the vaginal introitus (vaginal opening) - usually pea sized and not palpable - produce mucus for lubrication

310
Q

What is a Bartholin’s abscess?

A

When the ducts become blocked - glands swell and become tender causing a cyst (unilateral and fluid filled up to 4cm) this can then become infected forming an abscess which will be hot, red, and potentially draining pus

311
Q

How is a Bartholin cyst / abscess diagnosed?

A

Clinically

312
Q

How is a Bartholin cyst managed?

A

Good hygiene

Analgesia

Warm compresses

Biopsy (if vulval malignancy needs to be excluded)

313
Q

How is a Bartholin’s abscess treated?

A

Antibiotics

Swab of pus for organism and sensitivities (E. Coli most common, send swabs for chlamydia and gonorrhoea too)

Surgical intervention = Word catheter / Marsupilisation

314
Q

What is a Word catheter?

A

Small rubber tube with a balloon on the end

Local anaesthetic is used to numb the area - incision is made - pus is drained from abscess

Catheter in inserted in the space and inflated with saline (keeping catheter in place) - fluid can drain around catheter preventing a cyst of abscess reoccuring - tissue heals around catheter which can then be deflated and removed at a later date

315
Q

What is marsupialisation?

A

Using a GA in theatre - incision is made and the abscess is drained - sides of abscess are sutured open (allowing continuous drainage and preventing recurrence)

316
Q

What is lichen sclerosus?

A

Chronic inflammation of the skin which causes patches of white shiny areas on labia, perineum and perianal skin in women (can affect men on foreskin and glans of the penis)

317
Q

What causes lichen sclerosus?

A

Autoimmune condition associated with other sutoimmune diseases e.g. type 1 diabetes, alopecia, hypothyroid and vitiligo

318
Q

How is lichen sclerosus diagonosed?

A

Clinically

Vulval biopsy can be used to confirm the diagnosis

319
Q

What does “lichen” mean?

A

Flat eruption which spreads

320
Q

What is lichen simplex?

A

Chronic inflammation and irritation caused by repeated scratching of an area of skin

Excoriations, plaques, scaling and thickened skin

321
Q

What is lichen planus?

A

Autoimmune condition which causes chronic inflammation with shiny, purplish, flat-topped raised aread with white lines across the surface called Wicham’s striae

322
Q

How does lichen sclerosus presents?

A

45-50 year old woman with vulval itching and skin changes

Itching

Soreness and pain (worse at night)

Skin tightness

Painful sex (superficial dyspareunia)

Erosions

Fissures

323
Q

What is the Koebner phenomenon?

A

Where symptoms of lichen sclerosus is made worse with friction to the skin e.g. wearing tight underwear, scratching

324
Q

What are the skin changes with lichen sclerosus?

A

“porcelain-white” in colour

Shiny

Tight

Thin

Slightly raised

Papules / plaques

325
Q

How is lichen sclerosus treated?

A

Chronic disease, symptomatic treatment:

  • potent topical steroids clobebasol propionate (dermovate) 0.05%
  • Steroids once a day for 4 weeks until condition controlled
  • Emollients used regularly
326
Q

What are the complications of lichen sclerosus?

A

Squamous cell carcinoma of the vulva

Other complications:

  • Pain and discomfort
  • Sexual dysfuction
  • Bleeding
  • Narrowing of the vaginal / urethral openings
327
Q

What is female genital mutilation?

A

Surgically changing the genitals of a female for non medical reasons - form of child abuse and safeguarding issue

328
Q

What are the four types of female genital mutilation?

A

Type 1: Removal of part or all of the clitoris.

Type 2: Removal of part or all of the clitoris and labia minora. The labia majora may also be removed.

Type 3: Narrowing or closing the vaginal orifice (infibulation).

Type 4: All other unnecessary procedures to the female genitalia.

329
Q

Where is FGM more common ?

A

Somalia, Ethiopia, Sudan and Eritrea (data from UNICEF)

330
Q

What are the risk factors for FGM?

A

Coming from a community which practises FGM

Having relatives with FGM

331
Q

What are the immediate complications of FGM?

A

Pain

Bleeding

Infection

Swelling

Urinary retention

Urethral damage and incontinence

332
Q

What are some long term complications of FGM?

A

Vaginal infections (e.g. BV)

UTIs

Dysmenorrhoea

Dyspareunia

Infertility

Psychological issues (e.g. depression)

Reduced engagement with screening

333
Q

What is the management of FGM?

A
  • Educate that its illegal
  • Report all FGM under 18 to police (and social services, paediatrics, specialist gynae services, counselling)
  • Consider reporting in over 18s using risk assessment tool, consider relatives at risk, unborn child at risk?
  • De-infibulation - to correct narrowing or closure (re-infibulation is illegal)
334
Q

Where do the upper vagina, cervix, uterus and fallopian tubes develop from?

A

Paramesonephric ducts (Mullerian ducts)

335
Q

In men, what suppresses the growth of the paramesonephric ducts?

A

Anti-Mullerian hormone

336
Q

What is a bicornate uterus?

A

Where there are “two horns” to the uterus, giving it a heart shaped appearance (diagnosed on pelvic ultrasound)

337
Q

What is a bicornate uterus associated with?

A

Adverse pregnancy outcomes:

- Miscarriage

- Premature death

- Malpresentation

338
Q

What is an imperforate hymen?

A

Hymen is fully formed without an opening (discovered when menstration starts - menses trapped = cyclical pain and cramping, no bleeding)

Diagnosed on examination, treated with surgical incision

339
Q

What can an imperforate hymen lead to?

A

Retrograde menstruation causing endometriosis

340
Q

What is a transverse vaginal septae?

A

Error in development where a septum (wall) forms across the vagina - can either be perforate (with a hole) or imperforate (completely sealed)

Perforate = still menstruate but difficulty with intercourse/tampon

Imperforate = present similarly to an imperforate hymen with cyclical pelvic symptoms

Can cause infertility

341
Q

How is a vaginal septae diagnosed?

A

Examination

Ultrasound

MRI

Treat with surgical correction (complication = vaginal stenosis / recurrence of septae)

342
Q

What is vaginal hypoplasia?

A

Abnormally small vagina

343
Q

What is vaginal agenesis?

A

Absent vagina

344
Q

What is vaginal hypoplasia and vaginal agenesis caused by?

A

Failure of the Mullerian ducts to properly develop (may have absent uterus and cervix)

345
Q

When are the ovaries affected in structural abnormalities?

A

When there is androgen insensitivity syndrome creating testes rather than ovaries

346
Q

How is vaginal hypoplasia / agenesis treated?

A

Vaginal dilator over a prolonged period of time or vaginal surgery

347
Q

What is androgen insensitivity syndrome?

A

Condition where cells are unable to respond to androgen hormones due to a lack of androgen receptors

348
Q

What is the pattern of inheritance of androgen insensitivity syndrome?

A

X-linked recessive (caused by mutation in the androgen receptor gene on the X chromosome)

349
Q

What happens in androgen insensitivity syndrome?

A

Extra androgens are converted into oestrogen resulting in female secondary sexual characteristics - previously known as testicular feminisation syndrome

350
Q

What sex are patients with androgen insensitivity syndrome?

A

Genetically male with XY sex chromosome

Absent response to testosterone and conversion of androgens to oestrogen results in female phonetype externally - male sexual characteristics don’t develop, patients have normal female external genitalia and breast tissue

351
Q

How do the sex organs develop in patients with androgen insensitivity syndrome?

A

Testes in the abdomen or inguinal canal with absence of a uterus, upper vagina, cervix, fallopian tube and ovaries (these organs don’t develop as the testes produce anti-Mullerian hormone)

352
Q

How does androgen insensitivity syndrome affect the appearance of a patient?

A

Lack of pubic hair / facial hair and male type muscle development

Slightly taller than the average female, infertile, increased risk of testicular cancer unless testes are removed

353
Q

How does partial androgen insensitivity syndrome present?

A

Ambiguous signs cells have a partial response to androgens, micropenis, clitoromegaly, bifid scrotum, hypospadias, diminished male characteristics

354
Q

How does androgen insensitivity syndrome present?

A

Infancy with inguinal hernias containing testes

Alternatively, in puberty with primary amenorrhoea

355
Q

What are the results of hormone testing in androgen insensitivity hormone?

A

Raised LH

Normal / raised FSH

Normal / raised testosterone levels (for a male)

Raised oestrogen levels (for a male)

356
Q

What does the management of androgen insensitivity hormone involve?

A

Bilateral orchidectomy (removal of the testes) to avoid testicular tumours

Oestrogen therapy

Vaginal dilators / vaginal surgery to create length

(management involves paediatrics, gynae, urology, endocrinology, clinical psychology)

Generally patients are raised as female but this is sensitive and tailored to the individual, offered support and counselling

Obstetrics and Gynaecology (10 decks)

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