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3A Womens health > Period Related > Flashcards

Period Related Flashcards

1
Q

What is menopause?

A

retrospective diagnosis, made after a woman has had no periods for 12 months. It is defined as a permanent end to menstruation

point at which menstruation stops.

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2
Q

Around when do women experience menopause?

A

On average, women experience the menopause around the age of 51 years, although this can vary significantly. Menopause is a normal process affecting all women reaching a suitable age.

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3
Q

What is postmenopause?

A

describes the period from 12 months after the final menstrual period onwards.

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4
Q

What is perimenopause?

A

time around the menopause, where the woman may be experiencing vasomotor symptoms and irregular periods

includes the time leading up to the last menstrual period, and the 12 months afterwards. This is typically in women older than 45 years.

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5
Q

What is premature menopause?

A

menopause before the age of 40 years. It is the result of premature ovarian insufficiency.

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6
Q

What is menopause caused by?

A

caused by a lack of ovarian follicular function, resulting in changes in the sex hormones associated with the menstrual cycle:

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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7
Q

What is the epidemiology of menopause?

A

Average age of menopause is 51 years old; it typically occurs between 40 and 60 years
old

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8
Q

What is the physiology of a period?

A
  • Processo of primordial follicles maturing into primary and secondary alway occurs
  • start of cycle FSH causes development of secondary follicles
  • follicles grow , granulose cells surrounding increase oestrogen
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9
Q

What is the aetiology and physiology of menopause?

A
  1. Declining reserves of oocytes and associated follicles leads to reduced oestrogen
    production in response to FSH and LH stimulation.
  2. Therefore serum LH and FSH rise in response (lack of negative feedback).
  3. Eventually insufficient oestrogen means the LH surge and subsequent ovulation do not
    occur, leading to anovulatory cycles.
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10
Q

How does the process of menopause occur?

A
  • decline in the amount of follicles
  • thus no follicle matures- no oestrogen is released
  • causes more FSH release to compensate
  • overtime excess FSH causes desensitisation of the follicle receptors
  • no more ovulation = no more period
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11
Q

What does the failing follicular development cause in menopause?

A
  • means ovulation does not occur (anovulation),
  • resulting in irregular menstrual cycles.
  • Without oestrogen, the endometrium does not develop, leading to a lack of menstruation (amenorrhoea).
  • Lower levels of oestrogen also cause the perimenopausal symptoms.
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12
Q

S + S of 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
○ Menstrual irregularity leading to amenorrhea
○ Vasomotor symptoms (hot flushes / night sweats
○ Mood disturbance
○ Sleep disturbance

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13
Q

What are the risks/ risk factors of menopause?

A

A lack of oestrogen increases the risk of certain conditions:

Cardiovascular disease and stroke
Osteoporosis
Pelvic organ prolapse
Urinary incontinence

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14
Q

How do we make a diagnosis for menopause?

A

A diagnosis of perimenopause and menopause can be made in women over 45 years with typical symptoms, without performing any investigations.

NICE guidelines (2015) recommend considering an FSH blood test to help with the diagnosis in:

Women under 40 years with suspected premature menopause
Women aged 40 – 45 years with menopausal symptoms or a change in the menstrual cycle

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15
Q

What are the complications for menopause?

A

● Osteoporosis - due to increased bone turnover (normal oestrogen levels inhibit
osteoclast activity).
● Increased cardiovascular risk - due to alterations in LDL:HDL ratio, raised serum
cholesterol, arterial stiffening (among many other factors that are not entirely clear).

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16
Q

What are the investigations for menopause?

A

● Typically diagnosed clinically - investigations are usually not indicated in women with
menopausal symptoms over the age of 45.
● If indicated:
○ Serum FSH - elevated
○ Serum oestradiol - reduced

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17
Q

Contraception for menopause?

A

Fertility gradually declines after 40 years of age. However, women should still consider themselves fertile. Pregnancy after 40 is associated with increased risks and complications. Women need to use effective contraception for:

Two years after the last menstrual period in women under 50
One year after the last menstrual period in women over 50

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18
Q

What are the good contraception options for menopause?

A
  • Barrier methods
  • Mirena or copper coil
  • Progesterone only pill
  • Progesterone implant
  • Progesterone depot injection (under 45 years)
  • Sterilisation
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19
Q

Combined oral contraceptive pill

A
  • The combined oral contraceptive pill is UKMEC 2 (the advantages generally outweigh the risks) after aged 40, and can be used up to age 50 years if there are no other contraindications.
  • Consider combined oral contraceptive pills containing norethisterone or levonorgestrel in women over 40, due to the relatively lower risk of venous thromboembolism compared with other options.
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20
Q

What is treatment of menopause based on?

A
  • Treatment can be beneficial for both symptomatic relief and cardiovascular / osteoporotic
    risk.
  • HRT should be prescribed in the lowest effective dose for the shortest duration of
    treatment possible
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21
Q

What is the first line management for menopause?

A

lifestyle measures:
○ Regular excess
○ Weight loss (as necessary)
○ Avoidance of triggers (smoking, alcohol, spicy food).

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22
Q

What is second line management for menopause?

A

hormone replacement therapy (HRT):
○ Women with a uterus:
■ Oral or transdermal (patch) combined oestrogen and progesterone e.g.
tibolone for systemic i.e. vasomotor symptoms, mood disturbance.
■ Note - in situ Mirena can act as progesterone component of HRT.
■ Topical oestrogen gel for local i.e. vaginal symptoms.
○ Women without a uterus:
■ Oral or transdermal oestrogen only treatment for systemic symptoms.
■ Topical oestrogen gel for local symptoms.
○ HRT is prescribed in different regimens depending on the woman’s stage of
menopause.

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23
Q

What is the management for perimenopausal women and postmenopausal women?

A

For perimenopausal women:
■ Monthly or 3 monthly cyclical regime to produce a protective bleed:
● Oestrogen daily, plus progestogen for 12 days every 4 weeks or 3
months.
○ For postmenopausal women (i.e. 12 months after LMP):
■ Cyclical or continuous combined regime:
● Cyclical (as above).
● Continuous oestrogen and progesterone daily.

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24
Q

How do we manage 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
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25
Q

What are the risks of HRT?

A

● Systemic HRT is associated with increased risk of breast cancer. The longer its duration
of use, the higher the associated risk.
○ Topical HRT is thought to have no effect on breast cancer risk due to minimal
systemic absorption.
● Systemic HRT is associated with increased risk of venous thromboembolism.

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26
Q

What are the absolute contraindications to HRT?

A
  1. History of breast cancer, any oestrogen-dependent cancer, current undiagnosed PV
    bleeding, current endometrial hyperplasia.
  2. History of idiopathic VTE (if not anticoagulated).
  3. Thromboembolic disease e.g. MI, angina
  4. Liver disease.
  5. Inherited thrombophilia.
  6. Pregnancy.
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27
Q

What is adenomyosis?

A

endometrial tissue inside the myometrium (muscle layer of the uterus).

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28
Q

When is adenomyosis most common?

A

more common in later reproductive years and those that have had several pregnancies (multiparous). It occurs in around 10% of women overall. It may occur alone, or alongside endometriosis or fibroids

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29
Q

What is adenomyosis dependent on?

A

condition is hormone-dependent, and symptoms tend to resolve after menopause, similarly to endometriosis and fibroids.

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30
Q

What is the cause of of adenomyosis?

A

cause is not fully understood, and multiple factors are involved, including sex hormones, trauma and inflammation

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31
Q

How do women with adenomyosis present?

A
  • Painful periods (dysmenorrhoea)
  • Heavy periods (menorrhagia)
  • Pain during intercourse (dyspareunia)
  • It may also present with infertility or pregnancy-related complications. Around a third of patients are asymptomatic.
  • boggy uterus

Examination can demonstrate an enlarged and tender uterus. It will feel more soft than a uterus containing fibroids.

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32
Q

Investigations for adenomyosis

A

Transvaginal ultrasound of the pelvis is the first-line investigation for suspected adenomyosis.

MRI and transabdominal ultrasound are alternative investigations where transvaginal ultrasound is not suitable.

The gold standard is to perform a histological examination of the uterus after a hysterectomy. However, this is not usually a suitable way of establishing the diagnosis for obvious reasons.

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33
Q

What does management for adenomyosis depend on?

A

symptoms, age and plans for pregnancy.

NICE recommend the same treatment for adenomyosis as for heavy menstrual bleeding.

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34
Q

What do we give women who do NOT want contraception for symptomatic relief?

A
  • Tranexamic acid when there is no associated pain (antifibrinolytic – reduces bleeding)
  • Mefenamic acid when there is associated pain (NSAID – reduces bleeding and pain)
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35
Q

What is the management when contraception is wanted or acceptable?

A
  • Mirena coil (first line)
  • Combined oral contraceptive pill
  • Cyclical oral progestogens
  • Progesterone only medications such as the pill, implant or depot injection may also be helpful.
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36
Q

What are some alternative options for adenomyosis?

A
  • GnRH analogues to induce a menopause-like state
  • Endometrial ablation
  • Uterine artery embolisation
  • Hysterectomy
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37
Q

What happens with adenomyosis and pregnancy?

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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38
Q

What is Asherman’s syndrome?

A

Asherman’s syndrome is where adhesions (sometimes called synechiae) form within the uterus, following damage to the uterus.

39
Q

When does Asherman’s usually occur?

A
  • pregnancy-related dilatation and curettage procedure, for example in the treatment of retained products of conception
  • can also occur after uterine surgery (e.g. myomectomy) or several pelvic infection (e.g. endometritis)
40
Q

What is endometrial curettage?

A

Endometrial curettage (scraping) can damage the basal layer of the endometrium. This damaged tissue may heal abnormally, creating scar tissue (adhesions) connecting areas of the uterus that are generally not connected. There may be adhesions binding the uterine walls together, or within the endocervix, sealing it shut.

41
Q

What does endometrial curettage cause?

A

These adhesions form physical obstructions and distort the pelvic organs, resulting in menstruation abnormalities, infertility and recurrent miscarriages.

42
Q

How does Asherman’s syndrome present?

A

Asherman’s syndrome typically presents following recent dilatation and curettage, uterine surgery or endometritis with:

  • Secondary amenorrhoea (absent periods)
  • Significantly lighter periods
  • Dysmenorrhoea (painful periods)
  • It may also present with infertility.
43
Q

What are the investigations for Asherman’s syndrome?

A

There are several options for establishing a diagnosis of intrauterine adhesions:

  • Hysteroscopy is the gold standard investigation, and can involve dissection and treatment of the adhesions
  • Hysterosalpingography, where contrast is injected into the uterus and imaged with xrays
  • Sonohysterography, where the uterus is filled with fluid and a pelvic ultrasound is performed
  • MRI scan
44
Q

What is the management for asherman’s syndrome?

A

Management is by dissecting the adhesions during hysteroscopy. Reoccurrence of the adhesions after treatment is common.

45
Q

What is the definition of oligomenorrhea?

A

infrequent / irregular menstrual periods (defined variably as fewer
than 6 - 8 per year).

46
Q

What is the definition of amenorrhea?

A

the absence of a menstrual period.
○ Primary amenorrhea: absence of a period at age 15 in the presence of normal
secondary sexual characteristics or at age 13 with no secondary sexual
characteristics.
○ Secondary amenorrhea: absence of a period for three consecutive cycles in a
woman with a previously established menstrual cycle.

47
Q

What are the primary causes of amenorrhea?

A

○ Constitutional delay (familial)
○ Imperforate hymen
○ Hypo- / hyperthyroidism, hyperprolactinaemia, Cushing’s syndrome
○ Androgen insensitivity syndrome
○ Turner’s syndrome

48
Q

What are the secondary causes of amenorrhea?

A

○ Functional Hypothalamic Amenorrhea - excessive exercise, weight loss,
stress, eating disorders.
○ Premature ovarian insufficiency
○ Sheehan’s syndrome, prolactinoma, hypopituitarism
○ Hypo- / hyperthyroidism

49
Q

What is the definition of PCOS?

A

Endocrinopathy resulting in syndrome of ovarian cysts, oligomenorrhea and
hyperandrogenism.

50
Q

What is the criteria for PCOS?

A
  • PCOS is defined by the Rotterdam Criteria - a woman must meet 2 of the 3:
    1. Hyperandrogenism
    2. Oligo- or anovulation
    3. Polycystic morphology on ultrasound.
  • Therefore PCOS can be diagnosed in the absence of ovarian cysts.
51
Q

What is the aetiology and pathophysiology of PCOS?

A
  1. Disrupted balance between androgens, anti-Mullerian hormone and FSH levels
    leads to arrest in follicular development:
    a. Increased GnRH release frequency leads to high LH:FSH ratio.
    b. This results in high androgen:oestradiol ratio.
    c. Low oestrogen (due to reduced granulosa cell activity) prevents follicle
    selection and subsequent ovulation. Instead, multiple immature follicles
    remain and form cysts.
    d. Additionally, high androgens may inhibit sex steroid negative feedback on
    the HPG axis, leading to a ‘vicious circle’ of rising androgens.
  2. Insulin resistance and hyperinsulinaemia:
    a. Peripheral insulin resistance (skeletal muscle, adipose tissue) leads to
    hyperglycaemia and subsequent hyperinsulinaemia.
    b. High insulin levels stimulate theca cell androgen production and reduce
    sex-hormone binding globulin levels (SHBG); this means increased free
    circulating androgens.
52
Q

What is the presentation of PCOS?

A

● Hyperandrogenism: hirsutism, acne, hyperhidrosis.
● Oligomenorrhea - due to oligo-ovulation.
● Subfertility / infertility

53
Q

What are the risk factors of PCOS?

A
  1. Obesity
  2. Family history
  3. Premature adrenarche (pubic / axillary hair, apocrine sweat gland development).
54
Q

What investigations are done for PCOS?

A
  1. Total serum testosterone - elevated
  2. Sex hormone-binding globulin (SHBG) - normal to low
  3. Free androgen index - elevated
  4. Rule-out tests: LH and FSH (premature ovarian failure), prolactin
    (hyperprolactinaemia), TFTs (hypothyroidism); used to eliminate other causes of
    oligomenorrhea.
  5. Imaging: ultrasound - 12 or more follicles on one ovary.
55
Q

Management for PCOS when fertility is not desired?

A
  1. First Line: COCP plus weight loss
  2. Second Line (in event of prolonged amenorrhea)
    a. Cyclical progesterone (taken for 14 days every 3 months) to induce a
    withdrawal bleed to protect endometrium.
    b. Also offer transvaginal USS to assess endometrial thickness
56
Q

What is the management when fertility is desired in PCOS?

A
  1. First Line: weight loss plus:
    a. Clomifene or
    b. Letrozole (aromatase inhibitor).
  2. Second Line:
    a. Metformin
57
Q

What is the mechanism of COCP for PCOS treatment?

A
  • regulation of menstrual cycle through stabilisation of oestrogen & progesterone levels.
  • Also
    increases hepatic SHBG production (lowering free androgen index) and blocks some androgen receptors.
58
Q

What is the mechanism of action for metformin for PCOS?

A
  • improves peripheral insulin sensitivity to downregulate effects of insulin resistance
59
Q

What is the mechanism for clomifene for PCOS?

A
  • selective oestrogen receptor modulator; blocks hypothalamic oestrogen receptors,
  • thereby
    inhibiting HPG axis negative feedback and inducing FSH / LH secretion to lead to ovulation
60
Q

What is the mechanism for letrozole for PCOS?

A
  • aromatase inhibitor, inhibits peripheral conversion of androgens into oestrogen,
  • reducing HPG
    axis negative feedback to promote ovulation.
61
Q

What is the definition of dysmenorrhea?

A

● Painful lower abdominal cramping that occurs before / during menstruation.

62
Q

What are the differentials for dysmenorrhea?

A

● Primary dysmenorrhea - dysmenorrhea in the absence of identifiable pelvic pathology.
● Secondary dysmenorrhea - dysmenorrhea due to identifiable pelvic pathology:
○ Endometriosis
○ Adenomyosis
○ Fibroids
○ Pelvic Inflammatory Disease (PID)
○ Endometrial polyps

63
Q

What is the pathophysiology of primary dysmenorrhea?

A

● Progesterone withdrawal leads to prostaglandin release - this sensitises to pain due to
modulation of sensory neurons.
● Progesterone release also facilitates uterine contractions.
● Spiral arteriolar vasoconstriction and rupture causes painful tissue ischaemia.

64
Q

What happens in progesterone withdrawal and spinal arteriolar vasoconstriction?

A
  • Endothelins are 3-peptide molecules which act as potent local vasoconstrictors, exerting their effect
    directly onto the smooth muscle cells found in the tunica media.
  • It has been demonstrated in vitro that progesterone withdrawal leads to increased endothelin release by
    human uterine spiral arterioles.
  • It is therefore theorised that spiral arteriolar vasoconstriction (and subsequent tissue ischaemia and
    stratum functionalis shedding) is related to increased endothelin release from upstream uterine arterial
    supply in response to progesterone withdrawal after the degeneration of the corpus luteum.
65
Q

What are the s+s / presentation of dysmenorrhea?

A

● Painful lower abdominal cramping, beginning before the onset of the menstrual bleed
and improving as the bleed goes on.
● Onset is 6-12 months after menarche - a later onset e.g. a woman in her 20s / 30s
would suggest a secondary cause.
● Can include systemic symptoms such as nausea and vomiting, fatigue, bloating etc

66
Q

What are the investigations for menorrhea?

A

● Clinically diagnosed - if a secondary cause is suspected then this must be investigated
appropriately.

67
Q

What is the management for dysmenorrhea?

A

● First Line: oral NSAID e.g. ibuprofen, naproxen +/- paracetamol
● Alternate First Line: COCP
● Second Line: NSAID / paracetamol plus COCP (or alternative hormonal contraception)

68
Q

What is the definition of endometriosis?

A

● Presence of endometrial glands and stroma outside of the uterine cavity.

69
Q

What is the prevalence of endometriosis?

A

● 10% of reproductive age women.

70
Q

What is the pathophysiology and aetiology of endometriosis?

A

● Uncertain; best current theory is retrograde menstruation:
○ Fragments of endometrial tissue pass from the uterine cavity into the pelvis via
the open-ended fallopian tubes during menstruation.
○ This ectopic tissue is responsive to the normal hormonal fluctuations of the
menstrual cycle, so undergoes painful inflammation at the end of the cycle.

71
Q

What is the pain in endometriosis thought to be caused by?

A
  • Neuroangiogenesis - development of new blood vessels and (nociceptive) peripheral nerves.
  • Pro-inflammatory and pro-neurogenetic factors are increased in women with endometriosis.
  • Increased risk of central sensitisation and related CNS changes (akin to other chronic pain) - this
    might explain treatment-resistant pain.
72
Q

What are the signs of endometriosis?

A

fixed retroverted uterus, palpable mass on examination (endometrioma).

73
Q

Symptoms of endometriosis

A

dysmenorrhea, acyclic / chronic pelvic pain, dyspareunia,
dyschezia, subfertility.

74
Q

What are the investigations for endometriosis?

A
  1. Clinical Examination - can identify endometriomas (cystic lesions) / deep nodules.
  2. Transvaginal ultrasound - endometrioma, deep pelvic endometriosis
  3. Gold Standard: Diagnostic laparoscopy - biopsy-confirmed glands / stroma outside of
    endometrial cavity.
75
Q

What is the management for endometriosis?

A

● First Line: oral NSAID e.g. ibuprofen, naproxen.
● Alternative First Line: combined contraception (e.g. COCP) or progesterone
contraception (LNG-IUS, implant, medroxyprogesterone).
● Second Line: GnRH agonist (e.g. leuprorelin) or GnRH antagonist (e.g. elagolix).
○ N.B. limited duration of treatment due to bone mineral density issues.
● Alternative Second Line: laparoscopy with ablation.

76
Q

What is the definition for menorrhagia?

A

● Excessive menstrual blood loss, interfering with a woman’s physical, social, emotional,
material quality of life (NICE).

77
Q

What are the differentials for menorrhagia?

A

● Heavy Menstrual Bleeding (HMB) - primary, no identified cause (50% of cases)
● Secondary causes:
○ Fibroids
○ Endometrial polyps
○ Gynaecological cancer
○ Endometriosis / adenomyosis
○ Systemic: hypothyroidism, inherited coagulopathy (von Willebrand’s).

78
Q

How do we investigate Heavy menstrual bleeding?

A
  1. Full blood count - anaemia
  2. Consider further investigations for a cause as guided by the history.
79
Q

What is the management of Heavy menstrual bleeding?

A

● First Line: offer LNG-IUS
● Second Line: tranexamic acid (anti-fibrinolytic) or alternative hormonal treatment e.g.
COCP, POP.

80
Q

What is the definition of Uterine Fibroids?

A

● Benign uterine tumours made of smooth muscle and connective tissue; also known as
leiomyomata.

81
Q

What is the pathophysiology of uterine fibroids?

A

● (Probably) derived from myometrial stem cells; considered to be oestrogen-dependent
tumours, they express higher than normal numbers of certain oestrogen and
progesterone receptors.
● It is uncertain how fibroids lead to HMB - proposed mechanisms include distortion of
uterine lining and abnormal humoral factors due to altered histology of the overlying
endometrium.
`

82
Q

What are the different types of fibroids?

A

○ Intramural - contained within the myometrium.
○ Submucosal - projecting inwardly.
○ Subserosal - projecting outwardly.
○ Pedunculated - attached on a stem.

83
Q

What are the risk factors for uterine fibroids?

A

● High BMI, age in 40s, black ethnicity, low serum vitamin D levels.

84
Q

What is the link between fibroids and high BMI?

A
  • Increased adiposity leads to increased peripheral aromatase levels - therefore increasing circulating
    oestrogen due to conversion of adrenal DHEA into oestradiol.
  • The increased oestrogen has an inhibitory effect on the HPG axis, leading to anovulation, decreased
    progesterone levels and thus reduced progestogenic endometrial protection (menses).
  • Fibroids are oestrogen dependent; high oestrogen and low progesterone stimulates their growth.
85
Q

What are the signs of uterine fibroids?

A

palpable mass or enlarged uterus on bimanual examination.

86
Q

What are the symptoms of uterine fibroids?

A

menorrhagia, pelvic pain / pressure, bloating, dysmenorrhea.

87
Q

What are the investigations for uterine fibroids?

A

● First Line: transabdominal and transvaginal ultrasound scan

88
Q

What is the management for uterine fibroids?

A

● First Line: offer treatment as per HMB (LNG-IUS, tranexamic acid, alternative hormonal
contraception).
● Second Line: GnRH agonist e.g. leuprorelin or antiprogesterone e.g. mifepristone
● Alternative - surgical management:
○ Myomectomy (surgical removal of fibroids) - fertility-preserving
○ Uterine artery embolisation (deliberate infarction of fibroid tissue whilst preserving
surrounding uterus; performed by interventional radiologist, via percutaneous
femoral access).
○ Hysterectomy.

89
Q

UKMEC 1 (no restrictions) contraception options for women approaching menopause are?

A

Barrier methods
Mirena or copper coil
Progesterone only pill
Progesterone implant
Progesterone depot injection (under 45 years)
Sterilisation

90
Q

Combined oral contraceptive pill (UKMEC 2) for premenopause?

A

after aged 40, and can be used up to age 50 years if there are no other contraindications. Consider combined oral contraceptive pills containing norethisterone or levonorgestrel in women over 40, due to the relatively lower risk of venous thromboembolism compared with other options.

91
Q

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

92
Q

How can we manage hot flushes

A

hormonal therapies:
oestrogen therapy is the most effective modality in reducing hot flush frequency and severity
progestogens (both oral and intramuscular formulations) have shown efficacy in management of hot flushes
two anti-hypertensive agents, clonidine and methyldopa, have shown modest efficacy in the management of hot flushes. However their use has been associated with a relatively high rate of adverse effects (2):
- only licensed option (8)
methyldopa 250-500 mg twice daily has been shown to halve the frequency of hot flushes in comparison to placebo (3)
clonidine - cant be first line

93
Q

what is androgen insensitivyt

A

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

3A Womens health (33 decks)

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