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Gynaecology > Menstruation and dysmenorrhea > Flashcards

Menstruation and dysmenorrhea Flashcards

1
Q

Stages of puberty

A

Breast bud
Pubic hair
menstrual periods

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2
Q

Age of menarche

A

11-15

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3
Q

Age of menopause

A

45-55

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4
Q

Normal duration of single cycle

A

21-35 days

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5
Q

Feedback of oestrogen on HPG axis

A

Moderate oestrogen: negative feedback
High oestrogen in absence of progesterone: positive feedback
Oestrogen in presence of progesterone: negative feedback
Inhibin selectively inhibits FSH at anterior pituitary

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6
Q

How long is the mature oocyte viable for fertilisation for in the fallopian tube?

A

24 hours

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7
Q

After how many months of gestation can placenta take over steroid hormone production?

A

4 months

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8
Q

Follicular phase of menstrual cycle

A 
No negative feedback
Increase FSH/LH
Increase Follicle growth and O
O-> low FSH
O-> high GnRH and LH (inhibin inhibits FSH)
Day 1-14
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9
Q

Luteal phase of menstrual cycle

A 
Day 14-28
LH surge
Oocyte released (ovulation)
Corpus luteum (O and P)-> low GnRH
Regresses after 14 days
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10
Q

Proliferative phase of uterine cycle

A 
Oestrogen:
Fallopian tube formation
thickens endometrium
increased growth and motility of myometrium
thins cervical mucus 
Alongside follocular phase
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11
Q

Secretory phase of uterine cycle

A 
Progesterone:
thickening of endometrium into glandular secretory form 
thickening of myometrium 
reduction in motility of myometrium
thick acidic cervical mucus
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12
Q

Menses:
Days
Blood loss

A

2-7 days

10-80ml blood loss

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13
Q

Age of puberty in girls

A

8-14

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14
Q

Primary amenorrhea causes

A 
Delayed puberty
Imperforate hymen, transverse vaginal septum
absent vagina 
mullerian agenesis
gonadal dysgensis (Turner's)
PCOS
CAH
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15
Q

Secondary amenorrhea causes

A 
Pregnancy
PCOS
premature menopause
prolactinoma
thyroid disease
cushing's 
ED
exercise-induced
asherman's syndrome
sheehan syndrome
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16
Q

Intermenstrual bleeding causes

A 
Cervical ectropion, polyps or cancer
endometrial polyps or cancer
vaginal pathology, cancer
STI
hormonal contraception
ovulation
pregnancy 
SSRI, antidepressants
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17
Q

Dysmenorrhea causes

A 
primary dysmenorrhea
copper coil
cervical/ ovarian cancer
fibroids
endometriosis
PID
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18
Q

menorrhagia cause

A 
dysfunctional uterine bleeding
extremes of reproductive age
fibroids
endometriosis
hormonal contraceptives
PID
anticoagulant medications, bleeding disorders
endocrine disorders (DM, hypothyroidism)
CT disorders
endometrial hyperplasia or cancer
PCOS
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19
Q

Post-coital bleeding causes

A 
cervical cancer, ectropion or infection
trauma 
atrophic vaginitis
polyps
endometrial cancer
vaginal cancer
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20
Q

Pelvic pain causes

A

Urinary tract infection

Dysmenorrhoea (painful periods)

Irritable bowel syndrome (IBS)

Ovarian cysts

Endometriosis

Pelvic inflammatory disease (infection)

Ectopic pregnancy

Appendicitis

Mittelschmerz (cyclical pain during ovulation)

Pelvic adhesions

Ovarian torsion

Inflammatory bowel disease (IBD)

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21
Q

vaginal discharge causes

A

Bacterial vaginosis

Candidiasis (thrush)

Chlamydia

Gonorrhoea

Trichomonas vaginalis

Foreign body

Cervical ectropion

Polyps

Malignancy

Pregnancy

Ovulation (cyclical)

Hormonal contraception

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22
Q

pruritis vulvae causes

A

Irritants such as soaps, detergents and barrier contraception

Atrophic vaginitis

Infections such as candidiasis (thrush) and pubic lice

Skin conditions such as eczema

Vulval malignancy

Pregnancy-related vaginal discharge

Urinary or faecal incontinence

Stress

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23
Q

oligomenorrhea features

A

Infrequent periods

Cycle >35 days but less than 6 months in length

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24
Q

causes of oligomenorrhea

A

Constitutional:
No pathology
Cycle takes longer to complete

Anovulation: 
PCOS 
Thyroid disease 
Prolactinoma 
CAH
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25
Q

Primary amenorrhea definition

A

By 13 years when there is no other evidence of pubertal development

By 15 years of age where there are other signs of puberty, such as breast bud development

No menarche by age 16

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26
Q

hypogonadotropic hypogonadism

hormone levels

A

deficiency of LH/FSH

deficiecny of sex hormones

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27
Q

hypogonadotrophic hypogonadism causes

A 
hypopituitarism 
damage to hypothalamus or pituitary 
CF/ IBD
excessive exerice or dieting
constitutional delay
GH deficiency, hypothyoirism, Cushings, hyperprolactinaemia
Kallman syndrome
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28
Q

hypergonadotrophic hypogonadism hormone levels

A

high LH/FSH

low oestrogen/ sex hormones

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29
Q

hypergonadotrophic hypogonadism causes

A

previous damage to gonads (torsion, cancer, mumps)
congenital absence of ovaries
Turner’s

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30
Q

Features of congenital adrenal hyperplasia

A 
neonate: unwell shortly after birth, electrolyte disturbance, hypoglycaemia
tall for age
facial hair
absent periods (primary amenorrhea)
deep voice
early puberty
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31
Q

androgen insensitivity syndrome pathophysiology

A

tissues unable to respond to androgens
male sexual characteristics dont develop
female phenotype with male genotype and internal pelvic organs

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32
Q

congenital adrenal hyperplasia pathophysiology

A

congenital deficiency of 21-hydroxylase enzyme
underproduction of cortisol and aldosterone
overproduction of androgens
autosomal recessive

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33
Q

androgen insensitivity syndrome features

A

Patients have normal female external genitalia and breast tissue.
Internally there are testes in the abdomen or inguinal canal, and an absent uterus, upper vagina, fallopian tubes and ovaries.

34
Q

Structural causes of primary amenorrhea

A

Imperforate hymen

Transverse vaginal septae

Vaginal agenesis

Absent uterus

Female genital mutilation

35
Q

cryptomenorrhea

A

Haematocolpos

Haematometra

USS: fluid collection at vagina/uterus

Blood cant get out

Imperforate hymen, transverse vaginal septum

All bloods normal

36
Q

initial investigations for underlying medical conditions causing primary amenorrhea

A

Full blood count and ferritin for anaemia

U&E for chronic kidney disease

Anti-TTG or anti-EMA antibodies for coeliac disease

37
Q

Hormonal blood tests assess for hormonal abnormalities in primary amenorrhea

A

FSH and LH will be low in hypogonadotropic hypogonadism and high in hypergonadotropic hypogonadism

Thyroid function tests

Insulin-like growth factor I is used as a screening test for GH deficiency

Prolactin is raised in hyperprolactinaemia

Testosterone is raised in polycystic ovarian syndrome, androgen insensitivity syndrome and congenital adrenal hyperplasia

38
Q

genetic testing with a microarray test to assess for underlying genetic conditions in primary amenorrhea

A

Turner’s syndrome (XO)

39
Q

imaging in primary amenorrhea

A

Xray of the wrist to assess bone age and inform a diagnosis of constitutional delay

Pelvic ultrasound to assess the ovaries and other pelvic organs

MRI of the brain to look for pituitary pathology and assess the olfactory bulbs in possible Kallman syndrome

40
Q

management of primary amenorrhea: stress/ low body weight

A

Where the cause is due to stress or low body weight secondary to diet and exercise, treatment involves a reduction in stress, cognitive behavioural therapy and healthy weight gain.

41
Q

Management of hypogonadotrophic hypogonadism

A

hypopituitarism or Kallman syndrome: treatment with pulsatile GnRH can be used to induce ovulation and menstruation. This has the potential to induce fertility.

Alternatively, where pregnancy is not wanted, replacement sex hormones in the form of the combined contraceptive pill may be used to induce regular menstruation and prevent the symptoms of oestrogen deficiency.

42
Q

management of primary amenorrhea from PCOS

A

the combined contraceptive pill may be used to induce regular menstruation and prevent the symptoms of oestrogen deficiency.

43
Q

Secondary amenorrhea definition

A

Absent periods for at least 3/12 if cycles previously regular

Absent periods for at least 6/12 if previously had oligomenorrhea

44
Q

Causes of secondary amenorrhea

A

Pregnancy is the most common cause

Menopause and premature ovarian failure

Hormonal contraception (e.g. IUS or POP)

Hypothalamic or pituitary pathology

Ovarian causes such as polycystic ovarian syndrome

Uterine pathology such as Asherman’s syndrome

Thyroid pathology

Hyperprolactinaemia

45
Q

The hypothalamus reduces the production of GnRH in response to significant physiological or psychological stress. This leads to hypogonadotropic hypogonadism and amenorrhoea. The hypothalamus responds this way to prevent pregnancy in situations where the body may not be fit for it, for example:

A

Excessive exercise (e.g. athletes)

Low body weight and eating disorders

Chronic disease

Psychological stress

46
Q

Pituitary causes of secondary amenorrhea

A

Prolactinoma

Pituitary failure: trauma, radiotherapy, surgery, Sheehan syndrome

47
Q

Investigations for secondary amenorrhea

A

Hormonal blood tests

Ultrasound of the pelvis to diagnose polycystic ovarian syndrome

48
Q

Hormone tests for secondary amenorrhea

A 
bHCG to rule out pregnancy 
High LH:FSH ratio in PCOS
Prolactin 
TSH, T3, T4
Raised testosterone in PCOS, androgen insensitivity, CaH
49
Q

Management of secondary amenorrhea (PCOS)

A

It is worth remembering that women with polycystic ovarian syndrome 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, can be used to stimulate a withdrawal bleed.

50
Q

Menorrhagia features

A

Heavy menstrual bleeding is also called menorrhagia.

On average, women lose 40 ml of blood during menstruation.

Excessive menstrual blood loss involves more than an 80 ml loss.

The volume of blood loss is
rarely measured in practice. The diagnosis is based on symptoms, such as changing pads every 1 – 2 hours, bleeding lasting more than seven days and passing large clots.

A diagnosis can be made based on a self-report of “very heavy periods”.

Heavy menstrual periods can have a significant impact on quality of life.

51
Q

causes of menorrhagia

A

es

Dysfunctional uterine bleeding (no identifiable cause)

Heavy menstrual bleeding with no recognizable pelvic pathology, pregnancy or general bleeding disorders

Extremes of reproductive age

Fibroids

Polyps

Endometriosis and adenomyosis

Pelvic inflammatory disease (infection)

Contraceptives, particularly the copper coil

Anticoagulant medications

Bleeding disorders (e.g. Von Willebrand disease, thrombocytopenia, platelet disorders, coagulation disorders, leukaemia)

Endocrine disorders (diabetes and hypothyroidism)

Liver disease

Connective tissue disorders

Endometrial hyperplasia or cancer

Polycystic ovarian syndrome

52
Q

low risk patients for menorrhagia

A

Age <45, no IMB, no risk factors for endometrial cancer

History, examination, FBC

53
Q

high risk patients for menorrhagia

A

Age >45, IMB, suspected pathology, risk factors for endometrial cancer

History, examination, FBC, USS, hysteroscopy and biopsy

54
Q

outpatient hysteroscopy should be arranged if there is:

A

Suspected submucosal fibroids

Suspected endometrial pathology, such as endometrial hyperplasia or cancer

Persistent intermenstrual bleeding

55
Q

management of menorrhagia

A

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

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

56
Q

mefenamic acid mechanism of action in menorrhagia

A

Inhibits production of PG and inhibits the binding of PGE2 to its receptor

Reduces MBL by 20-44.5%

SE: GI usually mild (50%), dizziness and headaches (20%), deranged liver function, asthma, renal

57
Q

transexamic acid mechanism for menorrhagia

A

Inhibits plasminogen activation (inhibit tPA, and uPA), thus reduce fibrinolysis

Reduces MBL by 50%

SE: nausea, dizziness, tinnitus, rash, abdominal cramp

Low incidence of thrombotic disorders

58
Q

management of menorrhagia when contraception is wanted or acceptable

A

Mirena coil (first line)

Combined oral contraceptive pill

Cyclical oral progestogens, such as norethisterone 5mg three times daily from day 5 – 26 (although this is associated with progestogenic side effects and an increased risk of venous thromboembolism)

59
Q

management of menorrhagia when medical management fails

A

Endometrial ablation involves destroying the endometrium.

The first generation of ablative techniques involved a hysteroscopy and direct destruction of the endometrium.

This has been replaced by second generation, non-hysteroscopic techniques that are safer and faster.

A typical example of one of these techniques involves passing a specially designed balloon into the endometrial cavity and filling it with high-temperature fluid that burns the endometrial lining. This is called balloon thermal ablation.

60
Q

short-term emergency control of heavy menstrual bleeding

A

norethisterone

GnRH analogues

61
Q

short-term emergency control of heavy menstrual bleeding:

norethisterone

A

5mg PO TDS for up to 7 days

Can be used in a 3 weeks on, 1 week off pattern for 3-4months to temporise

When patient is on waiting list on treatment

62
Q

short-term emergency control of heavy menstrual bleeding:

GnRH

A

Monthly injection to downregulate the cycle and induce temporary ‘medical menopause’

Often used to stop very heavy periods in the presence of fibroids, to allow for correction of anaemia and iron stores in preparation for another intervention

63
Q

Pre-menstrual dysphoric syndrome

A

Psychological, emotional and physical symptoms that occur during the luteal phase of the menstrual cycle

64
Q

causes of PMS

A

Premenstrual syndrome is though to the caused by fluctuation in oestrogen and progesterone hormones during the menstrual cycle.

The exact mechanism is not known, but it may be due to increased sensitivity to progesterone or an interaction between the sex hormones and the neurotransmitters serotonin and GABA.

65
Q

PMS symptoms

A

Low mood

Anxiety

Mood swings

Irritability

Bloating

Fatigue

Headaches

Breast pain

Reduced confidence

Cognitive impairment

Clumsiness

Reduced libido

66
Q

Diagnosis of PMS

A

Symptom diary spanning two menstrual cycles

cyclical symptoms that occur just before, and resolve after, the onset of menstruation

GnRH analogue to see if symptoms resolve

67
Q

management of PMS

A

General healthy lifestyle changes, such as improving diet, exercise, alcohol, smoking, stress and sleep

Combined contraceptive pill (COCP)

SSRI antidepressants

Cognitive behavioural therapy (CBT)

RCOG recommends COCPs containing drospirenone first line (i.e. Yasmin). Drospironone as some antimineralocortioid effects, similar to spironolactone. Continuous use of the pill, as opposed to cyclical use, may be more effective

68
Q

Severe cases of PMS management

A

continuous transdermal oestrogen (patches)

norithisterone, Mirena coil

GnRH analogues

Hysterectomy and bilateral oopherectomy to induce menopause

Danazole and tamoxifen for cyclical breast pain

spironolactone for physical symptoms

69
Q

Progesterone in PMS management

A

progestogens for endometrial protection against endometrial hyperplasia when using oestrogen

trigger withdrawla bleed

70
Q

Physiology of menopause

A

Inside the ovaries, the process of primordial follicles maturing into primary and secondary follicles is always occurring, independent of the menstrual cycle.

At the start of the menstrual cycle, FSH stimulates further development of the secondary follicles.

As the follicles grow, the granulosa cells that surround them secrete increasing amounts of oestrogen.

The process of the menopause begins with a decline in the development of the ovarian follicles. Without the growth of follicles, there is reduced production of oestrogen.

Oestrogen has a negative feedback effect on the pituitary gland, suppressing the quantity of LH and FSH produced.

As the level of oestrogen falls in the perimenopausal period, there is an absence of negative feedback on the pituitary gland, and increasing levels of LH and FSH.

The failing follicular development 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.

71
Q

Symptoms of menopause

A

Hot flushes

Emotional lability or low mood

Premenstrual syndrome

Irregular periods

Joint pains

Heavier or lighter periods

Vaginal dryness and atrophy

Reduced libido

Night sweats

Anxiety

Some women get spaced, irregular or erratic bleeding before their final period which should be investigated

72
Q

risk factors for menopause

A

Cardiovascular disease and stroke

Osteoporosis

Pelvic organ prolapse

Urinary incontinence

73
Q

diagnosis of 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

Serum FSH levels are more than 40MIU/ML at least twice 4-6weeks apart

74
Q

contraception in 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

Hormonal contraceptives do not affect the menopause, when it occurs or how long it lasts, although they may suppress and mask the symptoms. This can make diagnosing menopause in women on hormonal contraception more difficult.

75
Q

managemet of perimenopausal symptoms

A

vasomotor symptoms are likely to resolve after 2-5 years

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

76
Q

natural management of menopause

A

Exercises

Running, swimming, yoga are highly recommended

Smoking cessation

Reduced alcohol and coffee intake also helps with symptoms of hit flushes and night sweats

Mediterranean style diet

77
Q

benefits of HRT menopause

A

Symptomatic women <60 years or <10 years from their menopause

HRT is the most effective treatment for hot flushes and low mood

Decline in sexual function: due to lack of oestrogen and HRT can improve sexual desire and also it reduces vaginal dryness and pain with sex

It prevent osteoporosis, thereby reducing risk of falls and associated fractures

HRT reduces some urinary symptoms and risk of uterine infections particularly when used topical vaginal preparations

78
Q

side effects of HRT in menopause

A

Headaches

Breast tenderness

Bloating

Muscle cramps

Irregular bleeding

CVD risk

IHD risk:

stroke

breast cancer

VTE

79
Q

types of HRT in menopause

A

Sequential HRT:

Starting within 12 months of the last period to minimise the risk of irregular bleeding patterns

Continuous combined HRT:

Not had a period for 12 months

Women can experience some irregular bleeding in the first 3 months of treatment

Tibolone:

Own class of HRT

Vaginal oestrogen:

Vaginal pessaries or creams can help with vaginal and urinary symptoms

80
Q

starting HRT in menopause

A

Transdermal oestrogen including patches and gel (estrador, sandrena)

Micronised progesterone or dydrogesterone or mirena

Transdermal combined HRT like evorel conti

Oral ERT estradiol valerate (zumenon), hormonin (estradiol, estriol, esterone), or conjugated equine esterogen (premarin)

Oral combined HRT including femostan, indiving depends on progestogen component

81
Q

Non-hormonal treatment options

A

Bio-identical hormones:
Derived from soy and plant extracts
Modified to be structurally identical to natural body hormones
Not regulated or licensed in the UK

Herbal medicines:
Not regulated by medicine authority
These can react with drugs used for treatment of breast cancer, epilepsy, asthma and heart disease
Some reduce the symptoms of hot flushes and night sweats like St John’s wort, black cohosh, iso-flavones (contained in soya beans)

Vaginal lubricants and moisturiser:
Symptoms of vaginal discomforts can be treated with lubricants such as yes WB

Alternative therapy:
Acuepressure
Acupuncture
Reflexology or homeopathy is limited in managing menopausal symptoms of hot flushes
Likewise, role of aromatherapy is not proven to be beneficial

Psychological treatments:
CBT has proven to elevate the low mood or anxiety related to menopause

82
Q

medical treatments in menopause

A

Other medical treatment:

Available on prescription includes clinidine, gabapentin and SSRI for hot flushes

Androgen (testosterone) therapy:

Known reduction in rates of testosterone production from ovary leading to low blood testosterone levels might be associated with a fall in libido or sex drive

Also loss of energy and concentration

Currently this hormone is not available on NHS or treatment for menopausal symptoms

Gynaecology (10 decks)

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