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HY OBGYN - (edited) > Gynaecology > Flashcards

Gynaecology Flashcards

1
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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2
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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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 (no secondary sexual characteristics)
  • 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
  • Menstrual periods (about 2 years from onset)
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18
Q

What is hypogonadism?

A

Lack of sex hormones (oestrogen and testosterone)

This causes a delay in puberty

2 reasons

  1. Hypogonadotropic hypogondism- deficiency of LH & FSH
  2. Hypergonadotropic hypogonadism- gonads don’t respond to LH & FSH
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19
Q

What can cause a deficiency of LH and FSH?

A

Abnormal functioning of the hypothalamus or pituitary gland

  • Hypopituitarism
  • Damage to hypothalamus/ pituitary eg RT/ surgery for cancer
  • Significant chronic conditions- CF, IBD
  • Excessive xercise or dieting
  • Constitutional delay in growth & development- no underlying physical pathology
  • Endocrine- GH deficiency, hypothyroidism, Cushing’s, hypoprolactinaemia
  • Kallman syndrome (genetic cause of hypogonadotrophic hypogonadism)
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20
Q

What can cause hypergonadotrophic hypogonadism?

A

Abnormal functioning of the gonads:

  • 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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21
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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22
Q

What is congenital adrenal hyperplasia?

What is the mode of inheritance?

How does it present?

A

Congenital deficiency of the 21-hydroxylase enzyme

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

Genetic- autosomal recessive

In severe cases, neonate is unwell shortly after birth - electrolyte disturbances, hypoglycaemia

In mild cases, females present later in childhod or at puberty- tall for age, facial hair, primary amenorrhoea, deep voice, early puberty

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23
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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24
Q

What structural pathology can cause primary amenorrhoea?

A
  • Imperforate hymen
  • Transverse vaginal septae
  • Vaginal agenesis
  • Absent uterus
  • FGM
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25
Q

When should investigations for primary amenorrhoea be undertaken?

A

No evidence of pubertal changes in a girl aged 13

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26
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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27
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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28
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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29
Q

What is secondary amenorrhoea?

A

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

  • 3-6 months in women with previously normal and regular menses
  • 6-12 months in women with previous oligomenorrhoea
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30
Q

What are the causes of secondary amenorrhoea?

A
  • Pregnancy & lactation account for most cases of amenorrhoea in the reproductive years.
  • 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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31
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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32
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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33
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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34
Q

What is the most common cause of hyperprolactinaemia?

A

Pituitary adenoma secreting prolactin

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35
Q

How can a pituitary tumour be assessed for?

A

CT or MRI scan of the brain

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36
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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37
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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38
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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39
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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40
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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41
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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42
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

Thought to be caused by fluctuation in oestrogen & progesterone levels

Exact mechanism unknown

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

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43
Q

When do the symptoms of PMS resolve?

A

Once mensturation begins

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44
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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45
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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46
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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47
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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48
Q

What does the management of PMS involve?

A
  • Improve diet, exercise, alcohol, smoking, stress and sleep
  • COCP- using drospiernone first line as recommended by RCOG - ie Yasmin. Has mineralcorticoid effects (similar to spironolactone). Continuous use rather than cyclical use of the pill may be more effective
  • SSRI antidepressants
  • CBT
  • GnRH analogues to induce a menopausal state, HRT may be required to reduce adverse effects such as osteoporosis.
  • Hysterectomy and bilateral oophorectomy to induce menopause when symptoms are really severe & medical mx has failed.
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49
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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50
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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51
Q

How much blood do women lose on average during mensturation & how much is classified as heavy menstrual bleeding- how is this quantified?

A

40ml is normal

>80 ml = HMB

  • Changing pads every 1-2 hrs
  • Passing large clots
  • Bleeding > 7 days
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52
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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53
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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54
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
  • OP hysteroscopy if suspecting submucosal fibroids, endometrial pathology eg hyperplasia/ cancer, persistent IMB
  • Pelvic/ TV USS if there is a palpable pelvic mass (possible large fibroids), pelvic pain/ tenderness o/e (possible adenomysois), examination difficult to interpret eg obesity, hysteroscopy declined
  • Swabs for infection if discharge/ suggestive sexual hx
  • Coag screen if fhx of clotting disorders
  • Ferritin if clinically anaemic
  • TFTs if additional features of hypothyroidism
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55
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
  • Pt declines contraception: tranexamic acid if no associated pain or mefenamic acid with associated pian
  • Pt happy to use contraception: mirena coil is first line, COCP, cyclical oral progestogens
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56
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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57
Q

What are fibroids?

A

Benign tumours of the smooth muscle of the uterus

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58
Q

What race of women are fibroids more common in?

A

They are thought to occur in around 20% of white and around 50% of black women in the later reproductive years.

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59
Q

What hormone do fibroids grow in response to?

A

Oestrogen (oestrogen sensitive)

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60
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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61
Q

How do fibroids present?

A

Often asymptomatic, 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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62
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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63
Q

What are the investigations for fibroids?

A

Hysteroscopy initially for submucosal fibroids presenting w/ HMB

Pelvic / TV 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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64
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 (mefenamic acid) and tranexamic acid
  • Combined oral contraceptive
  • Cyclical oral progestogens
  • Injectable progestogen
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65
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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66
Q

What is the management for fibroids more than 3cm?

A

Medical-

  • 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
  • GnRH agonists typically useful for short-term treatment

Surgical-

  • Uterine artery embolisation- blocks the blood supply to the fibroid so it shrinks
  • Myomectomy- surgical removal of fibroid via laparoscopic/ laparotomy or hysteroscopically
  • Endometrial ablation- destroying the endometrium
    • Can be done hysteroscopically
    • Or non-hydsteroscopic- balloon thermal ablation- inserting a balloon into the endometrium and filling it with high-temperature fluid that burns the endometrial lining of the uterus
  • Hysterectomy
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67
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- haemorrhage into tumour- commonly occurs during pregnancy
  • Torsion of the fibroid, usually affecting pedunculated fibroids
  • Malignant change to a leiomyosarcoma is very rare (<1%)
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68
Q

What is red degeneration of fibroids? Briefly how does it present and how is it managed?

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

Presents with severe abdo pain, low grade fever, tachycardia, vomiting

Mx- supportive, rest, fluids, analgesia

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69
Q

What is endometriosis?

A

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

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70
Q

What causes endometriosis? What are some theories?

A

Not clear, but there is a genetic component

  1. Retrograde menstruation: during menstration flow is backwards through fallopian tubes and into the pelvis and peritoneum
  2. Embryonic cells destined to become endometrial tissue may remain in areas outside the uterus during the delelopment of the fetus and become ectopic tissue
  3. Lymphatic system may spread the tissue
  4. Metaplasia may change cells outside the uterus
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71
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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72
Q

How may endometriosis present?

A
  • Cyclical abdominal or pelvic pain
  • Deep dyspareunia
  • Dysmenorrhoea
  • Infertility/ subfertility
  • Cyclical bleeding from other sites, such as haematuria
  • Non-gynaecological: urinary symptoms e.g. dysuria, urgency, haematuria. Dyschezia (painful bowel movements)
  • O/E- reduced organ mobility in pelvis, tender nodularity in the posterior vaginal fornix and visible vaginal endometriotic lesions may be seen
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73
Q

How is endometriosis diagnosed?

A

Pelvic ultrasound - for large endometriomas and chocolate cysts - if the symptoms are significant, the pt should be referred for a definitive diagnosis. USS has little role

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

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74
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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75
Q

What does the management of endometriosis involve?

A

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

If analgesia doesn’t help then hormonal treatments such as COCP or progestogens eg medroxyprogesterone acetate should be tried

If analgesia/ hormonal treatments don’t improve or fertility is a priority- refer to secondary care

  • GnRH analogues- improve symptoms due to low oestrogen, however no effect on fertility
  • Laparoscopic excision or laser treatment of endometriotic ovarian cysts may improve fertility
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76
Q

What hormonal managment can be tried before estabilishing 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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77
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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78
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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79
Q

What is adenomyosis?

A

Endometrial tissue inside the myometrium (muscle layer of uterus)

It is more common in multiparous women towards the end of their reproductive years.

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80
Q

How does adenomyosis present?

A
  • Dysmenorrhoea
  • Dyspareunia
  • Menorrhagia
  • Enlarged, boggy uterus
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81
Q

What does examination show of adenomyosis?

A

Enlarged and tender uterus

Feels more soft than a uterus containing fibroids

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82
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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83
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)
  • GnRH analogues to induce menopause-like state
  • Hysterectomy
  • Uterine artery embolisation
  • Endometrial ablation
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84
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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85
Q

How is menopause diagnosed?

A

Retrospectively - after woman has no periods for 12 months

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86
Q

What is the average age of menopause?

A

51 years old

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87
Q

What is postmenopause?

A

Period from 12 months after the final period

~51 years of age

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88
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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89
Q

What is premature menopause?

A

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

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90
Q

Describe the levels of LH, FSH, oestrogen and progesterone during 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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91
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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92
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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93
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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94
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

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95
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
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96
Q

Do hormonal contraceptives affect the menopause?

A

No, they may suppress and mask the symptoms

97
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

98
Q

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

A

UKMEC2- benefits generally outweigh the risks

99
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

100
Q

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

A

Weight gain

Osteoporosis (so, unsuitable for women over 45)

101
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

102
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

103
Q

What are the causes of premature ovarian failure?

A

Idiopathic (the cause is unknown in more than 50% of cases; may be fhx )

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

104
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

Raised FSH, LH levels

Low oestradiol

105
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)

106
Q

What are the conditions associated with premature ovarian insufficiency?

A
  • CVD
  • Stroke
  • Osteoporosis
  • Cognitive impairment
  • Dementia
  • Parkinsonism
107
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

108
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

109
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

110
Q

What are the side effects to clonidine?

A

Dry mouth

Headaches

Dizziness

Fatigue

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

111
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

112
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
113
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
114
Q

What are some contraindications to starting HRT?

A
  • Current, past, suspected breast cancer
  • Known or suspected oestrogen-dependent cancer
  • Undiagnosed vaginal bleeding
  • Untreated endometrial hyperplasia
  • Previous idiopathic or current VTE Active or recent arterial thromboembolic disease eg angina or MI
  • Active liver disease with abnormal LFTs
  • Pregnancy
  • Thrombophilic disorder
115
Q

How to choose a HRT formulation? (ie cyclical/ continuous, oestrogen only/ progestogen)

A
  • Local or systemic symptoms?
    • Local → topical oestrogen creams/ tablets
    • Systemic → Uterus or no uterus?
      • No uterus → continuous oestrogen-only HRT
      • Uterus → have they had a period in the last 12 months?
        • Yes → cyclical combined
          • Can be switched to continuous after 12 months for women > 50, after 24 months in women < 50
        • No uterus → continuous combined
116
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

117
Q

What are the characteristic features of polycystic ovarian syndrome?

A
  • Multiple ovarian cysts
  • Infertilify
  • Oligomenorrhoea
  • Hyperandrogenism (olgomenorrhoea, hirsutism, acne)
  • Insulin resistance
  • Obesity
  • Hair loss in male pattern
  • Acanthosis nigricans
  • CVD
  • Hypercholesterolaemia
  • Endometrial hyperplasia and cancer
  • OSA
  • Depression, anxiety
  • Sexual problems
118
Q

What do the following terms mean:

  1. Anovulation
  2. Oligoovulation
  3. Amenorrhoea
  4. Oligomenorrhoea
  5. Androgens
  6. Hyperandrogenism
  7. Hirsutism
  8. Insulin resistance
A
  1. Anovulation refers to the absence of ovulation
  2. Oligoovulation refers to irregular, infrequent ovulation
  3. Amenorrhoea refers to the absence of menstrual periods
  4. Oligomenorrhoea refers to irregular, infrequent menstrual periods
  5. Androgens are male sex hormones, such as testosterone
  6. Hyperandrogenism refers to the effects of high levels of androgens
  7. Hirsutism refers to the growth of thick dark hair, often in a male pattern, for example, male pattern facial hair
  8. Insulin resistance refers to a lack of response to the hormone insulin, resulting in high blood sugar levels
119
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 volume of > 10cm^3)
120
Q

What are some complications of PCOS?

A
  • Metabolic disorders, such as impaired glucose tolerance and type 2 diabetes.
  • Cardiovascular disease.
  • Infertility.
  • Pregnancy complications, such as pre-eclampsia and gestational diabetes.
  • Endometrial cancer.
  • Psychological disorders, such as anxiety and depression.
  • Obstructive sleep apnoea.
121
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

122
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
123
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
124
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
125
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
126
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
127
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

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

128
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%)
129
Q

What complications should PCOS patients be screened for?

A
  • Endometrial hyperplasia and cancer
  • Infertility
  • Hirsutism
  • Acne
  • Obstructive sleep apnoea
  • Depression and anxiety
130
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)

131
Q

What are the risk factors for endometrial cancer in PCOS?

A
  • Obesity
  • Diabetes
  • Insulin resistance
  • Amenorrhoea
132
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

133
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

134
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
135
Q

How to manage infertility in PCOS?

A

Weight loss, can restore regular ovulation

Clomifene

Laparoscopic ovarian drilling

In vitro fertilisation (IVF)

136
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)

Other options initiated by specialist- spironolactone, finasteride (reduces testosterone production), flutamide (non-steroidal anti-androgen), cyproterone acetate (anti-androgen and progestin)

137
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)
138
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

139
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)

140
Q

When may ovarian cysts present with acute pain?

A

Ovarian torsion

Haemorrhage

Rupture of cyst

141
Q

What are the types of functional cysts?

A

Follicular cysts

  • commonest type of ovarian cyst
  • due to non-rupture of the dominant follicle or failure of atresia in a non-dominant follicle
  • commonly regress after several menstrual cycles

Corpus luteum cyst

  • during the menstrual cycle if pregnancy doesn’t occur the corpus luteum usually breaks down and disappears. If this doesn’t occur the corpus luteum may fill with blood or fluid and form a corpus luteal cyst
  • more likely to present with intraperitoneal bleeding than follicular cysts
  • may occur during early pregnancy
142
Q

Define other types of ovarian cysts:

  1. Serous cystadenoma
  2. Mucinous cystadenoma
  3. Endometrioma
  4. Dermoid cyst / germ cell tumour
  5. Sex cord-stromal tumours
A
  1. Serous cystadenoma = the most common benign tumour of epithelial cells which bears a resemblance to the most common type of ovarian cancer (serous carcinoma). Bilateral in ~20%
  2. Mucinous cystadenoma = 2nd most common benign tumour of epithelial cells, can become huge, if ruptures may cause pseudomyxoma peritonei
  3. Endometrioma = lumps of endometrial tissue within the ovary, occur in patients with endometriosis
  4. Dermoid cyst / germ cell tumour = benign ovarian tumours, teratomas meaning they come from the germ cells, usually lined with epithelial tissue hence may contain various tissue types e.g. skin, teeth, hair and bone - associated with ovarian torsion. Median age of diagnosis is age 30. Bilateral in 10-20%
  5. 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
143
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
144
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

145
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)
146
Q

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

A
  • Endometriosis
  • Fibroids
  • Adenomyosis
  • Pelvic infection
  • Liver disease
  • Pregnancy
147
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
148
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 3 cycles- repeat USS for 8-12 weeks and referral considered if persists
  • 5cm-7cm: resuire routine referral to gynar and yearly ultrasound
  • > 7cm consider an MRI scan or surgical evaluation (difficult to characterise with ultrasound)
149
Q

How are cysts in postmenopausal women managed?

A

In post-menopausal women, by definition physiological cysts are unlikely

Hence refer all to gynae for assessment regardless of nature/ size

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

150
Q

How are persisting or enlarging cysts managed?

A

Surgical intervention (usually with laparoscopy)

Ovarian cystectomy (removing cyst)

Oophorectomy (removing the affected ovary)

151
Q

What are the main complications of ovarian cysts?

A

Torsion

Haemorrhage into the cyst

Rupture, with bleeding into the peritoneum

152
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

153
Q

What are the risk factors for ovarian torsion?

A
  • Ovarian mass
  • Pregnancy
  • Being of a reproductive age- younger girls before menarche as they have longer infundibulopelvic ligaments that twist easily
  • Ovarian hyperstimulation syndrome
154
Q

How does ovarian torsion present? What is seen on USS?

A

Sudden onset deep- seated severe unilateral pain - constant / colicky- gets worse - associated with N&V

Pain is not always severe (can twist and untwist)

Localised tenderness (may be a palpable mass)

Vaginal examination may reveal adnexial tenderness

Fever may be seen secondary to adnexal necrosis

USS- free fluid or whirlpool sign

155
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

156
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

157
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

158
Q

What is Asherman’s syndrome?

A

Adhesion (aka synechiae) form within the uterus following damage to the endometrium basal layer, the damaged tissue may heal abnormally creating scar tissue (adhesions) connecting areas of the uterus which are usually not connected

  • Pregnancy-related dilatation and currettage procedure- eg during treatment of retained products of conception- removal of placental tissue after birth
  • Uterine surgery eg myomectomy
  • Pelvic infection eg endometritis
159
Q

How does Asherman’s syndrome present?

A

Following recent dilatation and curettage:

Secondary amenorrhoea (absent periods)

Significantly lighter periods

Dysmenorrhoea (painful periods)

160
Q

How are intrauterine adhesions diagnosed & managed?

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

Mx- disseciton of adhesions during hysteroscopy. Reoccurance is common.

161
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

Often associated with high oestrogen levels- common in younger women, COCP, pregnancy

162
Q

What is the transformation zone of the cervix?

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)

163
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

Examination reveals well-demarcated border between the redder, velvety columnar epithelium extending from the os and the pale pink squamous epithelium of the endocervix. This border is the transformation zone.

164
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

165
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

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

166
Q

How do nabothian cysts present?

A

Incidentally on speculum - smooth rounded bumps near the os

Whitish or yellow appearance

No treatment required

If uncertain of diagnosis, refer to colposcopy for further examination

167
Q

What is vault prolapse?

A

Women who have had a hysterectomy

Top of vagina (the vault) descends into the vagina

Vaginal vault prolapse occurs when the upper portion of the vagina loses its normal shape and sags or drops down into the vaginal canal or outside of the vagina. ​

168
Q

What are rectocoeles?

A

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

169
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)

170
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
  • Spina bifida
171
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
172
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

173
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

Prolapse extending beyond the introitus = uterine procidentia

174
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)

175
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

176
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

177
Q

What are the types of urinary incontinence?

A

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

Stress: pelvic floor muscles are weak, canals (urethral/ vaginal/ rectal) become lax, weak sphincter muscles, allows urine to leak when there is increased pressure on the bladder eg when laughing, coughing or surprised

Mixed: urge and stress

Overflow: when the bladder becomes dilated or flaccid with minimal or no tone/function. Can occur with anticholinergics, fibroids, pelvic tumours, neuro conditions eg MS, diabetic neuropathy, spinal cord injury

178
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
  • FHx
179
Q

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

A

Caffeine consumption

Alcohol consumption

Medications

BMI

180
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

181
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

182
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)

183
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

  • a combined noradrenaline and serotonin reuptake inhibitor
  • mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced
184
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

185
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

186
Q

How can urge incontinence be managed?

A

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

Bladder stabilising drugs: antimuscarinics are first-line

  • NICE recommend oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation)
  • Immediate release oxybutynin should, however, be avoided in ‘frail older women’

Mirabegron (a beta-3 agonist): alternative to anticholinergic medication, may be useful if there is concern about anticholinergic side-effects in frail elderly patients

Invasive procedures where medical treatment fails

187
Q

What are the anticholinergic side effects -

A

Dry mouth

Dry eyes

Urinary retention

Constipation

Postural hypotension

Coginitive decline

Memory problems

Worsening of dementia

188
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

189
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

190
Q

How can atrophic vaginitis be treated?

A

Vaginal lubricants e.g. sylk, replens and YES

Topical oestrogen

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

191
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

192
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

193
Q

How is a Bartholin cyst managed?

A

Good hygiene

Analgesia

Warm compresses

Biopsy (if vulval malignancy needs to be excluded)

194
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

195
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)

Lichen sclerosus leads to atrophy of the epidermis with white plaques forming

Features

  • white patches that may scar
  • itch is prominent
  • may result in pain during intercourse or urination
196
Q

What causes lichen sclerosus?

A

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

197
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

198
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

199
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

200
Q

What are the skin changes with lichen sclerosus?

A

“porcelain-white” in colour

Shiny

Tight

Thin

Slightly raised

Papules / plaques

201
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
202
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
203
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

204
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.

205
Q

What are the immediate complications of FGM?

A

Pain

Bleeding

Infection

Swelling

Urinary retention

Urethral damage and incontinence

206
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

207
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)
208
Q

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

A

Paramesonephric ducts (Mullerian ducts)

209
Q

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

A

Anti-Mullerian hormone

210
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)

Typical complications- miscarriage, premature birth, malpresentation

No specific mx

211
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

212
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

213
Q

How is a vaginal septae diagnosed?

A

Examination

Ultrasound

MRI

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

214
Q

What is vaginal hypoplasia?

A

Abnormally small vagina

mx- vaginal dilator over a prolonged period of time

215
Q

What is vaginal agenesis?

A

Absent vagina

216
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)

217
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)

218
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

219
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)

220
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

221
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

222
Q

How does androgen insensitivity syndrome present?

A

Infancy with inguinal hernias containing testes

Alternatively, in puberty with primary amenorrhoea

223
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)

224
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

225
Q

Describe what hormones are used in HRT?

A
  • Systemic oestrogen
    • Natural oestrogens- conjugated oestrogen, estradiol, estrone, estriol are used
    • Synthetic oestrogens- mestranol or ethinylestradiol generally not used except in women in POI due to the greater metabolic effect
  • Progestogen
    • Almost all synthetic
    • C19 progestogens: derived from testosterone- norethisterone, levonorgestrel (good for reduced libido)
    • C21 progestogens: dydrogesterone, medroxyprogesterone (good for mood, depression, acne)
    • Given cyclically to women who have had a period in last 12 months to induce a withdrawal bleed
    • Mirena coil: LNG-IUS is an alternative route of delivery of progestogen and provides endometrial protection locally (good for contraception too)
226
Q

Describe the regimens that may be prescribed for HRT?

A
  • Combined HRT can be prescribed as a:
    • Monthly cyclical regimen- oestrogen daily and progestogen given at the end of the cycle for 10-14 days
    • 3 monthly cyclical regimen- oestrogen daily and progestogen given for 14 days every 13 weeks
    • Continuous combined regimen- oestrogen and progestogen daily
  • Peri-menopausal women: monthly or 3 monthly regimen
    • Absence of bleeding reflects atrophic endometrium
  • Post-menopausal: monthly or 3 monthly cyclical or continuous combined may be used
  • Vaginal oestrogen therapy regiments eg 1 vaginal tablet daily for 2 weeks then 1 twice weekly
227
Q

Why is progesterone added to oestrogen in HRT?

A
  • Reduce risk of endometrial hyperplasia and cancer
  • Continuous provides better protection than cyclical
228
Q

What are some adverse effects of HRT?

A
  • Oestrogen related
    • Fluid retention
    • Bloating
    • Breast tenderness or enlargement
    • Nausea
    • Headaches
    • Leg cramps
    • Dyspepsia
  • Progestogen-related
    • Fluid retention
    • Breast tenderness
    • Headaches or migraine
    • Mood swings/ PMS symptoms/ depression
    • Acne vulgaris
    • Lower abdo/ back pain
  • Vaginal bleeding
229
Q

Describe when vaginal bleeding is expected in a woman on HRT? When should this be investigated?

A
  • Vaginal bleeding
    • Unscheduled bleeding is common within first 3 months of treatment
    • Monthly cyclical regiments produce withdrawal bleeding towards end of the progestogen phase
    • Continuous combined HRT produces irregular breakthrough bleeding or spotting in first 4-6 months of treatment
      • If beyond 6 months, exclude endometrial pathology
      • If serious gynae pathology has been exclude, alter the progestogen part of the regimen and this may improve bleeding problems- eg increase duration/ dose or switch to LNG-IUS combined with oral/ transdermal oestrogen preparation
230
Q

What is tibolone?

A
  • Synthetic steroid, stimulates oestrogen, progesterone and androgen receptors
  • Used as a form of continuous combined HRT
231
Q

What is the risk of developing gestational diabetes in women with PCOS?

A

Clinicians may consider offering screening for gestational diabetes to women who have been diagnosed as having PCOS before pregnancy.

This should be performed at 24–28 weeks of gestation, with referral to a specialist obstetric diabetic service if abnormalities are detected.

232
Q

How should women with PCOS be screened for type II diabetes?

A

Women presenting with PCOS who are overweight (body mass index [BMI] ≥ 25 kg/m2 ) and women with PCOS who are not overweight (BMI < 25 kg/m2 ), but who have additional risk factors such as advanced age (> 40 years), personal history of gestational diabetes or family history of type II diabetes, should have a 2-hour post 75 g oral glucose tolerance test performed.

In women with impaired fasting glucose (fasting plasma glucose level from 6.1 mmol/l to 6.9 mmol/l) or impaired glucose tolerance (plasma glucose of 7.8 mmol/l or more but less than 11.1 mmol/l after a 2-hour oral glucose tolerance test), an oral glucose tolerance test should be performed annually

233
Q

Difference between simple and complex ovarian cyst?

A
  • Simple: unilocular, more likely to be physiological or benign
  • Complex: multilocular, more likely to be malignant
234
Q

What is an enterocele?

A

An enterocele is formed by a prolapse of the small bowel through the rectouterine pouch, i.e. the pouch of Douglas, through the upper part of the vaginal vault

235
Q

Define abnormal uterine bleeding? What are the causes?

A

AUB is any bleeding disturbance that occurs during or between menstrual periods, or that is excessive, frequent or prolonged. This is the overarching term to describe any significant disturbance of menstruation or the menstrual cycle.

Structural lesions: PALM

  • Polyps- endometrial, endocervical
  • Adenomysois
  • Leiomyoma (uterine fibroids)
  • Malignancy and hyperplasia

Non-structural causes: COEIN

  • Coagulopathies
    • Von Willebrand disease
    • Platelet dysfunctions
    • Rare clotting factor deficiencies
    • Thrombocytopenia
  • Ovulatory dysfunction
    • Anovulation
    • PCOS
    • Thyroid disease
  • Endometrial primary causes
  • Iatrogenic- eg IUDs
  • Not yet classified- rare or novel causes eg uterine arteriovenous malformations which can cause very HMB
236
Q

Define dysmenorrhoea? How to treat the different types?

A

Dysmenorrhoea is characterised by excessive pain during the menstrual period. It is traditionally divided into primary and secondary dysmenorrhoea.

Primary: no underlying pelvic pathology, usually appears within 1-2 hrs of menarche

  • Excessive endometrial prostaglandin production is thought to be partially responsible.
  • Mefenamic acid/ ibuprofen
  • COCP second line

Secondary: evelops many years after the menarche and is the result of an underlying pathology. In contrast to primary dysmenorrhoea the pain usually starts 3-4 days before the onset of the period.

Causes: endometriosis, adenomyosis, PID, IUD (copper- IUS mirena may help), fibroid

  • Refer all pts with secondary dysmenorrhoea to gynae for ix
237
Q

What signs would you look for on examination of a female patient complaining of urinary incontinence and why?

A
  • Speculum and bimanual examination whilst getting pt to cough to feel for prolapse
  • Assess pelvic tone and examine for pelvic organ prolapse, atrophic vaginitis, urethral diverticulum, pelvic masses
238
Q

What is duloxetine, what is the rational behind using it in urinary incontinence, and what are its side effects?

A
  • Combined serotonin and noradrenaline reuptake inhibitor
  • Thought to increase serotonin and noradrenaline in the pudendal motor nucleus of the sacral spinal segments leading to increased urethral muscular tone and closure pressure, improving the functions of the urethral sphincter
  • S/E: Anxiety; appetite decreased; constipation; diarrhoea; dizziness; drowsiness; dry mouth; fall; fatigue; flushing; gastrointestinal discomfort; gastrointestinal disorders; headache; muscle complaints; nausea; pain; palpitations; paraesthesia; sexual dysfunction; skin reactions; sleep disorders; sweat changes; tinnitus; tremor; urinary disorders; vision disorders; vomiting; weight changes; yawning
239
Q

Complications of surgery used for treating urinary incontinence?

A
  • Pelvic organ prolapse: more common after colposuspension that after a retropubic mesh sling
  • Mesh-related complications after retropubic mesh sling including pain and vaginal problems
  • Bleeding: needing a transfusion occurs in <1%
  • Damage to bladder: 1-10% - more likely with mesh surgery
  • Damage to bowel
  • Damage to nerves leading to loss of sensation or persistent pain
  • Problems emptying bladder fully- may require catheter for a few days or weeks or longer
  • Having to get to the toilet quickly to urinate or not getting to the toilet in time
  • Infections including wound infections, vaginal infections and UTIs
  • Persistent pain in abdomen, pelvis, or during sex

HY OBGYN - (edited) (10 decks)

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