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Core clinical problems > 78. Menstrual disturbance > Flashcards

78. Menstrual disturbance Flashcards

1
Q

DDX dysmennorhoea

A

primary dysmenorrhoea
endometriosis
adenomyosis
fibroids
PID
IUD

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2
Q

DDX menorrhagia

A

benign
anovulatory cycles (extremes of reproductive age)
dysfunctional uterine bleeding

gynae
fibroids
adenomyosis
PID

iatrogenic
IUD

systemic
hypothyroidism
bleeding disorders eg von willebrans

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3
Q

DDX secondary amenorrhoea

A

pregnancy
hypothalamic amenorrhoea
pituitary pathoogy
sheehans syndrome
PCOS
premature ovarian insufficiency
menopause
ashermans

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4
Q

What gynaecological conditions can cause sub fertility

A

annovulation
- priamary amenorrhoea eg hypothalamic
- secondary eg pcos

tubal
- endometriosis

uterine
- fibroids
- polyps

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5
Q

History taking menstrual disturbance

A
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6
Q

Examination menstrual disturbance

A
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7
Q

Examination findings menstrual disturbance

A
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8
Q

What is primary dysmenorrhoea

A

Primary dysmenorrhoea occurs in young females in the absence of any identifiable underlying pelvic pathology. It is thought to be caused by the production of uterine prostaglandins during menstruation, which causes uterine contractions and pain.

It affects up to 50% of menstruating women and usually appears within 1-2 years of the menarche. Excessive endometrial prostaglandin production is thought to be partially responsible.

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9
Q

pain typically starts just before or within a few hours of the period starting
suprapubic cramping pains which may radiate to the back or down the thigh
The pain starts shortly before the onset of menstruation and may last for up to 72 hours, improving as the menses progresses.

A

primary dysmenorrhoea

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10
Q

management primary dysmenorrhoea

A
  1. NSAIDs such as mefenamic acid and ibuprofen are effective in up to 80% of women. They work by inhibiting prostaglandin production
  2. combined oral contraceptive pill
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11
Q

how is the pain in secondary dysmenorrhoea different to priamry

A

In contrast to primary dysmenorrhoea the pain usually starts 3-4 days before the onset of the period.

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12
Q

what is dysfunctional uterine bleeding

A

this describes menorrhagia in the absence of underlying pathology. This accounts for approximately half of patients

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13
Q

what is primary amenorrhoea vs secondary?

A

primary -the failure to establish menstruation by 15 years of age in girls with normal secondary sexual characteristics (such as breast development), or by 13 years of age in girls with no secondary sexual characteristics

secondary - pt previously had periods, subsequently stopped, cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhea

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14
Q

what is oligomenorrhoea

A

irregular and inconsistent menstrual blood flow

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15
Q

PC: menorrhagia, prolonged menstruation (>7days), abdominal pain worse during menstruation, bloating or feeling full in the abdomen, urinary or bowel symptoms due to pelvic pressure, deep dyspareunia, reduced fertility
o/e: abdominal and bimanual exam may reveal palpable pelvic mass or an enlarged non-tender uterus

A

fibroids

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16
Q

PC: cyclical abdominal or pelvic pain, deep dysparenunia, dysmenorrhoea, infertility, cyclical bleeding from other sites eg haematuria, urinary symptoms, bowel symptoms
o/e: endometrial tissue visible in vagina, particularly in posterior fornix, fixed cervix on bimanual examination, tenderness in the vagina, cervix and adenexa

A

endometriosis

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17
Q

Usually presents in later reproductive years
PC: dysmenorrhoea, menorrhagia, dysparenunia, infertility
o/e: enlarged and tender uterus. More soft than a uterus containing fibroids

A

adenomyosis

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18
Q

PC: Cessation of menstruation for 3-6 months in women with previously normal and regular menses

A
  1. ?pregnancy
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19
Q

PC: secondary amenorrhoea
HoPC: excessive exercise, low body weight/eating disorders, chronic disease, psychological stress

A

hypothalamic amenorrhoea

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20
Q

PC: weight gain, hair loss, constipation, cold, amenorrhoea, struggled to breastfeed after birth
HoPC: recent post partum haemorrhage

A

sheehans syndrome

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21
Q

PC: oligomenorrhoea, secondary amenorrhoea, subfertility and infertility
HoPC: hirsutism, acne, obesity, acanthosis nigricans

A

PCOS

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22
Q

PC: oligomenorrhea, secondary amenorrhoea in patients <40, hot flushes, night sweats, vaginal dryness

A

premature ovrian insufficiency

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23
Q

PC: no periods for 12 months, hot flushes, night sweats, vaginal dryness, mood disturbance

A

menopause

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24
Q

PC: secondary amenorrhoea, lighter periods, dysmenorrhoea
HoPC: recent dilatation and courgette, uterine surgery or endometritis

A

ashermans syndrome

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25
Q

What are fibroids

A

Fibroids are benign smooth muscle tumours of the uterus.

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26
Q

Risk factors for fibroids

A

race, increasing age

Occur in around 20% of white women
Occur in 50% of black women

later reproductive years.

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27
Q

Typical history fibroids and examination

A

PC: menorrhagia, prolonged menstruation (>7days), abdominal pain worse during menstruation, bulk-related symptoms (lower abdominal pain, cramping pains, often during menstruation, bloating) urinary symptoms, e.g. frequency, may occur with larger fibroids, subfertility, deep dyspareunia, reduced fertility

o/e: abdominal and bimanual exam may reveal palpable pelvic mass or an enlarged non-tender uterus

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28
Q

PC: may be asymptomatic, menorrhagia (may result in iron-deficiency anaemia)
bulk-related symptoms (lower abdominal pain, cramping pains, often during menstruation, bloating) urinary symptoms, e.g. frequency, may occur with larger fibroids, subfertility

A

fibroids

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29
Q

investigation ?fibroids

A

Diagnosis
transvaginal ultrasound
hysteroscopy?

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30
Q

Management asymptomatic fibroids

A

no treatment is needed other than periodic review to monitor size and growth

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31
Q

Management of menorrhagia secondary to fibroids if fibroids <3cm

A
  1. levonorgestrel intrauterine system (LNG-IUS)
    - useful if the woman also requires contraception
    - cannot be used if there is distortion of the uterine cavity
  2. Non-hormonal : NSAIDs e.g. mefenamic acid or tranexamic acid
  3. Hormonal: combined oral contraceptive pill or oral progestogen eg norethisterone
  4. injectable progestogen
  5. try any not tried or rf for surgical consideration
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32
Q

Management of menorrhagia secondary to fibroids if fibroids >3cm

A
  1. Refer to secondary care
  2. In meantime : non-hormonal : NSAIDs e.g. mefenamic acid or tranexamic acid

Considered in secondary care:
1. levonorgestrel intrauterine system (LNG-IUS)
- useful if the woman also requires contraception
- cannot be used if there is distortion of the uterine cavity

  1. Medical treatment to shrink/remove fibroids
    - GnRH agonists may reduce the size of the fibroid but are typically used more for short-term treatment
  2. Surgical treatment to shrink/remove fibroids
    - myomectomy if wanting to preserve fertility
    - hysteroscopic endometrial ablation
    - hysterectomy
    - uterine artery embolization
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33
Q

Side effects of GnRH agonists

A

menopausal symptoms (hot flushes, vaginal dryness) and loss of bone mineral density

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34
Q

Examples of GnRH agonists

A

leuprorelin (brand name Lupron) and triptorelin (brand name Decapeptyl), goserelin (zoladex)

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35
Q

Mechanism of action GnRH agonists

A

Prolonged activation of GnRH receptors by GnRH leads to desensitization and consequently to suppressed gonadotrophin secretion. This is the primary mechanism of action of agonistic GnRH analogues.

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36
Q

Prognosis and complications of fibroids

A
  • regress after menopause as estrogen driven
  • red degeneration particularly in pregnancy
  • subfertility
  • iron deficiency anemia
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37
Q

what is endometriosis

A

Endometriosis is a condition where there is ectopic endometrial tissue outside the uterus.

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38
Q

what are chocolate cysts

A

Endometriomas in the ovaries are often called “chocolate cysts”.

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39
Q

what is an endometrioma

A

A lump of endometrial tissue outside the uterus is described as an endometrioma.

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40
Q

typical history endometriosis

A

PC: cyclical abdominal or pelvic pain, deep dyspareunia, dysmenorrhoea, infertility, cyclical bleeding from other sites eg haematuria, urinary symptoms, bowel symptoms

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41
Q

examnination endometriosis

A

o/e: endometrial tissue visible in vagina, particularly in posterior fornix, fixed cervix on bimanual examination, tenderness in the vagina, cervix and adnexa

42
Q

plan ?endometriosis

A

Plan
Investigation
Laparoscopic surgery (gold standard)
USS may show chocolate cysts

Management
Non-hormonal:
Analgesia for pain (NSAIDs and paracetamol)
Hormonal:
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
Surgical:
Laparoscopic surgery to excise or ablate the endometrial tissue and remove adhesions (adhesiolysis)
Hysterectomy
Laparoscopic treatment may improve fertility. Hormonal therapies may improve symptoms but not fertility.

43
Q

gold standard investigation endometriosis

A

laparoscopy

44
Q

what may uss show endometriosis

A

chocolate cysts

45
Q

how does the pill help endometriosis

A

by reducing endometrial thickening, the pill may slow the development of endometriomas and reduce dysmenorrhoea

The normal rise and fall of hormones causes thickening and shedding, by taking the pill, the thickening is less and therefore the shedding is less painful (and can be less frequent as you can take pill packets back to back)

46
Q

how could a GnRH agonist help endometriosis ?

A

endometriosis is estrogen driven, this is what causes the thickening, therefore by decreasing the

47
Q

what is adenomyosis

A

Adenomyosis refers to endometrial tissue within the myometrium (muscle layer) of the uterus.

48
Q

typical history adenomyosis

A

Usually presents in later reproductive years
PC: dysmenorrhoea, menorrhagia, dyspareunia, infertility
o/e: enlarged and tender uterus. More soft than a uterus containing fibroids

49
Q

Plan invetsigating adenomyosis

A

Investigation
Initial
Transvaginal USS
MRI or transabdominal USS if transvaginal USS not suitable
GOLD STANDARD
Histological examination after hysterectomy

50
Q

gold standard invetsigation adenomyosis

A

Histological examination after hysterectomy

51
Q

Management of adenomyosis

A

Management
Non-hormonal:
Tranexamic acid (antifibrinolytic) where no associated pain
Mefenamic acid (NSAID) where associated pain

Hormonal:
COCP
Cyclical oral progestogens
Progesterone only eg POP, implant, depot

Secondary care:
GnRH analogues
Ablation
Uterine artery embolisation
Hysterectomy

52
Q

what is pelvic inflammatory disease?

A

Pelvic inflammatory disease (PID) is a term used to describe infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surrounding peritoneum. It is usually the result of ascending infection from the endocervix.

53
Q

most common cause PID

A

Chlamydia trachomatis

54
Q

causes of PID

A

Chlamydia trachomatis is the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis

55
Q

features of PID

A

lower abdominal pain
fever
deep dyspareunia
dysuria and menstrual irregularities may occur
vaginal or cervical discharge
cervical excitation

56
Q

plan ?PID

A

Invetsigation
- Pregnancy test to exclude an ectopic pregnancy

  • Triple swab (NAAT for chlamydia and gonorrhoea, high vaginal charcoal swab for trichomonas, endocervical charcoal swab for gonorrhoea sensitivities)
  • Pus cells on microscopy. The absence of pus cells is useful for excluding PID.
  • Raised CRP/ESR

Management
1. Refer to GUM
2. Treat with low threshold as often swabs negative
3. 1g IM ceftriaxone (for gonorrhoea), doxycycline 100mg bd for 14 days (chlamydia and mycoplasma genitalium), metronidazole bd for 14 days (for anaerobes such as gardanella)

57
Q

Complications of PID

A

perihepatitis (Fitz-Hugh Curtis Syndrome)- occurs in around 10% of cases

infertility - the risk may be as high as 10-20% after a single episode
chronic pelvic pain
ectopic pregnancy

58
Q

RUQ pain, with features of PID

A

perihepatitis (Fitz-Hugh Curtis Syndrome)

59
Q

pharmacological management of PID

A

Ceftriaxone IM 1g (to cover gonorrhoea)

Doxycycline 100mg twice daily for 14 days (to cover chlamydia and Mycoplasma genitalium)

Metronidazole 400mg twice daily for 14 days (to cover anaerobes such as Gardnerella vaginalis)

60
Q

what is the most common cause of inherited abnormal bleeding

A

von willebrand disease

61
Q

inheritance von willebrand disease

A

usually autosomal dominant

62
Q

what is von willebrand disease

A

Inherited deficiency, absence or malfunctioning von willebrand factor (involved with platelet adhesion) causing easy and prolonged bleeding

63
Q

typical history von willebrand disease

A

PC: unusually easy, prolonged or heavy bleeding
Bleeding from gums when brushing teeth
Nose bleeds
Menorrhagia
Heavy bleeding during surgical operations
FHx: von willebrand disease

64
Q

plan ?von willebrand disease

A

Plan
Investigation
Refer to specialist for bleeding assessment

Management
Von Willebrand disease does not require day to day treatment. Management is required either in response to major bleeding or trauma (to stop bleeding) or in preparation for operations (to prevent bleeding):
Desmopressin can be used to stimulates the release of VWF
VWF can be infused
Factor VIII is often infused along with plasma-derived VWF

Management of menorrhagia
Combination of:
Tranexamic acid
Mefanamic acid
Norethisterone
Combined oral contraceptive pill
Mirena coil

Hysterectomy may be required in severe cases.

65
Q

most common cause of secondary amenorrhoea

A

pregnancy

66
Q

what is hypothalamic amenorrhoea? typical history?

A

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:

Excessive exercise (e.g. athletes)
Low body weight and eating disorders
Chronic disease
Psychological stress

67
Q

what type of pituitary adenoma may cause amenorrhoea

A
  • prolactinoma (high prolactin inhibits release of GnRH –> no release of LH and FSH) hypogonadotrophic hypogonadism
  • compressive pituiatry adenoma –> low LH and FSH
68
Q

plan ?pituitary adenoma causing secondary amenorrhoea

A

Plan
Investigation
a pituitary blood profile (including: GH, prolactin, ACTH, FH, LSH and TFTs)
formal visual field testing
MRI brain with contrast

Management
dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
surgery is performed for patients who cannot tolerate or fail to respond to medical therapy.

69
Q

“A 26-year-old woman comes to see her GP after complaining of weight gain, hair loss, constipation and feelings of being cold all the time. She is also amenorrhoeic and struggled to breastfeed after birth. She has no significant past medical history but during her daughter’s birth she suffered from a large amount of blood loss and subsequent hypovolaemic shock which required a 6 weeks hospital stay.”

A

sheehans

70
Q

pathophysiology sheehans syndrome

A

Sheehan’s syndrome (SS) is postpartum hypopituitarism caused by necrosis of the pituitary gland. It is usually the result of severe hypotension or shock caused by massive hemorrhage during or after delivery. Patients with SS have varying degrees of anterior pituitary hormone deficiency. Therefore widespread hypopituitarism which includes low FH and LSH

71
Q

how does hypothyroidism cause secondary amenorrhoea

A

Low thyroid hormones → high thyroid releasing hormone(TRH) → increased prolactin production → decreases the release of GnRH → decreases LH and FSH

72
Q

how does hyperthyroidism cause secondary amenorrhoea

A

High thyroid hormone → increases sex hormone binding globulin (SHBG) → prevents ovulation

73
Q

how are insulin and testosterone related?

A

Insulin promotes the release of androgens from the ovaries and adrenal glands. Therefore, higher levels of insulin result in higher levels of androgens (such as testosterone). Insulin also suppresses sex hormone-binding globulin (SHBG) production by the liver. SHBG normally binds to androgens and suppresses their function. Reduced SHBG further promotes hyperandrogenism

74
Q

how does insulin cause anovulation

A

Hyperinsulinemia affects granulosa cells in small follicles and theca cells. This condition induces early response to luteinizing hormones on granulosa cells of small follicles and causes premature differentiation of these cells, which eventually results in anovulation

75
Q

typical history PCOS

A

PC: oligomenorrhea, secondary amenorrhoea, subfertility and infertility
HoPC: hirsutism, acne, obesity, acanthosis nigricans, ask about snoring and daytime somnolence (increased risk of OSA), depression

o/e: overweight/obesity, acanthosis nigricans

76
Q

what is acanthosis nigricans

A

thickened, rough skin, typically found in the axilla and on the elbows. It has a velvety texture. It occurs with insulin resistance.

77
Q

What is the rotterdam criteria?

A

Rotterdam criteria for diagnosis of PCOS (2 of:)
Amenorrhoea (no or infrequent periods)
Clinical or biochemical signs of hyperandrogenism (hirsutism, acne) (raised total or free testosterone)
Polycystic ovaries on USS (defined as the presence of ≥ 12 follicles (measuring 2-9 mm in diameter) in one or both ovaries and/or increased ovarian volume > 10 cm³)

78
Q

clinical signs of hyperandrogenism?

A

hirsutism
acne

79
Q

definition of polycystic ovaries?

A

the presence of ≥ 12 follicles (measuring 2-9 mm in diameter) in one or both ovaries

and/or increased ovarian volume > 10 cm³)

80
Q

what biochemical markers are suggetsive, but not diagnostic of PCOS

A

Raised LH:FSH ratio
Raised prolactin or normal
SHBG may be normal or low

81
Q

Investigations PCOS

A

TV USS “string of pearls” polycystic ovaries as defined as the presence of ≥ 12 follicles (measuring 2-9 mm in diameter) in one or both ovaries and/or increased ovarian volume > 10 cm³)

Testosterone

FH, LH, prolactin, TSH, SHBG

OGTT if eligible, Check for impaired glucose tolerance

QRISK

82
Q

General management of PCOS

A

Weight loss, refer to dietician
Refer for specialist consideration of metformin

83
Q

Management of amenorrhoea PCOS

A

Amenorrhoea - needs to be controlled in order to prevent endometrial hyperplasia and endometrial cancer

  1. Cyclical progestogen (such as medroxyprogesterone 10 mg daily for 14 days) to induce a withdrawal bleed) then,
  2. Refer for transvaginal USS to asses thickness of endometrium
  3. If normal choose from following treatments as prevention
    - A cyclical progestogen, such as medroxyprogesterone 10 mg daily for 14 days every 1–3 months.
    - COCP
    - The levonorgestrel-releasing intrauterine system (LNG-IUS
84
Q

why does amenorrhoea need to be controlled PCOS

A

in order to prevent endometrial hyperplasia and endometrial cancer

85
Q

management acne pcos

A

+ Advise that weight loss may decrease hyperandrogenism

  1. COCP- use a lower risk one 1st line but Co-cyprindiol (Dianette) may be considered, but increased risk of VTE
  2. Normal acne treatment eg 1. a fixed combination of topical adapalene with topical benzoyl peroxide
86
Q

management hirsutism pcos

A

+ Advise that weight loss may decrease hyperandrogenism
1. COCP but not Co-cyprindiol (Dianette) 1st line as increased risk of VTE
2. Topical eflornithine

87
Q

management subfertility pcos

A

+ Weight loss
1. Specialists may use clomifene or metformin

88
Q

how does clomifene work?

A

Clomifene works by occupying hypothalamic oestrogen receptors without activating them. This interferes with the binding of oestradiol and thus prevents negative feedback inhibition of FSH secretion therefore more FSH and more

89
Q

define premature ovarian insufficiency

A

menopause before the age of 40 years. It is the result of a decline in the normal activity of the ovaries at an early age. It presents with early onset of the typical symptoms of the menopause.

90
Q

pathophysiology premature ovarian insufficieny

A

Hypergonadotropic hypogonadism. Under-activity of the gonads (hypogonadism) means there is a lack of negative feedback on the pituitary gland, resulting in an excess of the gonadotropins (hypergonadotropism).

Causes:
Idiopathic
Iatrogenic eg chemo, radiotherapy, surgical oophorectomy
Autoimmune
Genetic
Infections such as mumps, tuberculosis or CMV

91
Q

typical history premature ovarian insufficiency

A

PC: hot flushes, night sweats, vaginal dryness, mood swings, amenorrhoea, subfertility

92
Q

plan ?premature ovarian insufficiency

A

Plan
Investigations
1. FSH raised >25IU twice, separated by more than 4 weeks (difficult to interpret if on hormonal contraception
Management
1. HRT until age 51 either traditional HRT or COCP
2. Ensure adequate vitamin D and calcium intake

93
Q

what are women with premature menopause at higher risk of?

A

Cardiovascular disease
Stroke
Osteoporosis
Cognitive impairment
Dementia
Parkinsonism
Pelvic organ prolapse
urinary incontinence

94
Q

what is the menopause

A

Menopause is a retrospective diagnosis, made after a woman has had no periods for 12 months. It is defined as a permanent end to menstruation. On average, women experience the menopause around the age of 51 years, although this can vary significantly.

Menopause is 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

95
Q

what are some peri-menopausal 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

96
Q

when would peri-menopausal symptoms usually resolve

A

Likely to resolve after 2-5 years without treatment

97
Q

how long do women need contraception for?

A

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

98
Q

Management of menopause?

A
  • no treatment
  • lifestyle managemet (exercise, weight loss, sleep hygeine, relaxation)
  • non-HRT management: SSRIs, vaginal moisuriser, vaginal oestrogen, CBT
  • HRT management
99
Q

What s ashermans syndrome

A

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

100
Q

typical history ashermans

A

PC: amenorrhoea, lighter periods, dysmenorrhoea, subfertility, miscarriage

101
Q

gold standard invetsgationa dn treatment ashermans

A

hysteroscopy with dissecting adhesions

Core clinical problems (94 decks)

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