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MFSRH Part 2 (2023) > Abnormal Vaginal Bleeding > Flashcards

Abnormal Vaginal Bleeding Flashcards

1
Q

Define primary amenorrhoea

A
  • Lack of menstruation by age 16 in the presence of secondary sexual characteristics (or by age 14 in their absence)
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2
Q

If suspecting a physiological delay in onset of menstruation, what can you give to identify this / reassure the patient?

A
  • Progesterone challenge
  • Norethisterone for 5 days, and then a withdrawal bleed should occur
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3
Q

Define secondary amenorrhoea

A

Absence of menstruation for 6 months in the absence of pregnancy

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4
Q

What examination findings might ascertain a cause of amenorrhoea?

A
  • Extremes of BMI
  • Presence of secondary characteristics
  • Stigmata of endocrinopathies (e.g. thyroid)
  • Evidence of virilisation (deep voice, balding, clitoromegaly)
  • Abdominal mass (genital tract obstruction)
  • Pelvic exam - imperforate hymen, blind ending vaginal septum, absence of cervix and uterus
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5
Q

Name some physiological and iatrogenic causes of amenorrhoea

A
  • Pregnancy
  • Breastfeeding (high postpartum levels of prolactin suppress ovulation)
  • Menopause
  • Contraceptives
  • Therapeutic progestogens (such as GnRH analogues)
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6
Q

Name some hypothalamic causes of amenorrhoea

A
  • Stress
  • Anorexia
  • Excessive exercise
  • Pseudocyesis (phantom pregnancy)
  • SOL
  • Surgery
  • Radiotherapy
  • Kallman’s syndrome (primary GnRH deficiency)
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7
Q

What anterior pituitary causes would cause amenorrhoea?

A
  • Prolactinoma
  • SOL
  • Surgery
  • Sheehan’s syndrome
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8
Q

What are some ovarian causes of amenorrhoea?

A
  • PCOS
  • POI (surgery, viral infection, cytotoxic drugs, radiotherapy)
  • Ovarian dysgenesis (Turner’s syndrome 45XO)
  • Menopause
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9
Q

What are some genital tract causes of amenorrhoea?

A

Genital tract outflow obstruction
- Imperforate hymen
- Transverse vaginal septum
- Cervical stenosis
- Asherman’s syndrome

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10
Q

What are some endocrinopathies that can cause amenorrhoea?

A
  • Hyperprolactinaemia
  • Cushing’s syndrome
  • Hypo/hyperthyroidism
  • CAH
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11
Q

Why does primary hypothyroidism cause amenorrhoea?

A

TSH stimulates prolactin secretion

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12
Q

What investigations can you do for someone with amenorrhoea?

A
  • Pregnancy test
  • FSH/LH
  • Testosterone
  • Prolactin level
  • TFTs
  • Pelvic ultrasound scan
  • Karyotype (if uterus absent or Turner’s expected)
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13
Q

Treatment for amenorrhoea depends on what?

A

Desire for fertility
Those requiring ovulation usually respond well to an anti-estrogen such as clomifene

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14
Q

What is oligomenorrhoea?

A

Cycles lasting longer than 32 days (although some sources say 35 days, some say 42 days)

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15
Q

Name some causes of oligomenorrhoea

A
  • PCOS most common
  • Borderline low BMI
  • Obesity
  • Ovarian resistance leading to anovulation
  • Milder degrees of hyperprolactinaemia and mild thyroid disease
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16
Q

Once ruled out pathology, and fertility is not desired yet, what is the treatment for oligomenorrhoea?

A
  • CHC or cyclical progestogens
  • Minimum of 3 periods a year is recommended to reduce the risk of endometrial hyperplasia due to unopposed estrogen (if not on hormones)
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17
Q

Define primary dysmenorrhoea

A
  • Pain has no obvious cause
  • Begins with onset of ovulatory cycles, within first 2 years of menarche
  • Pain more severe on the day of menstruation or the day preceding it
  • Prostaglandins are involved in the aetiology
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18
Q

If no physical cause is found for primary dysmenorrhoea, what can you give to diagnose?

A
  • Ovulation suppression by tricycling COCP or GnRH analogues for 6-12 months
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19
Q

Name some causes of secondary dysmenorrhoea

A
  • Endometriosis
  • Adenomyosis
  • PID
  • Pelvic adhesions
  • Fibroids
  • Cervical stenosis
  • Asherman’s syndrome
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20
Q

What medications can be given for secondary dysmenorrhoea?

A
  • Mefenamic acid (or ibuprofen / naproxen)
  • COCP
  • DMPA
  • LNG-IUS
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21
Q

What is the cause of HMB in 60% of cases?

A

Dysfunctional uterine bleeding

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22
Q

Name some benign uterine pathology that causes HMB

A
  • Fibroids (>50% of those with HMB will have fibroids)
  • Polyps
  • Adenomyosis
  • Pelvic infection
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23
Q

What investigations should be done for heavy menstrual bleeding?

A
  • Pregnancy test
  • FBC
  • Ferritin, TFTs, clotting if clinically indicated
  • STI screen
  • If under 45, can consider treating first before further investigations
  • If over 45, TV USS, pipelle biopsy, hysteroscopy and biopsy
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24
Q

Name some medical treatments for HMB

A
  • LNG IUD (reduction in blood loss by 90%)
  • Antifibrinolytics (TXA 1g TDS for 4 days)
  • NSAIDs
  • COCP
  • Oral progestogens are of limited benefit
  • DMPA
  • GnRH analogues
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25
Q

Describe endometrial ablation

A
  • Destruction of endometrium down to basalis layer
  • Microwave (MEA), thermal balloon (thermachoice), novasure (electrical impedance)
  • 90% will be significantly improved
  • 30% will be amenorrhoeic
  • 20% will need a second procedure by 5 years
  • Small risk of bleeding, infection, uterine perforation, failed procedure
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26
Q

How does PCOS lead to insulin resistance / hyperinsulinaemia?

A
  • Reduced production of SHBG in the liver
  • Testosterone therefore unbound
  • Increased androgens stop follicular development and causes anovulation and menstrual disturbance
  • Weight gain = insulin resistance and more insulin production
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27
Q

What happens to LH levels in PCOS?

A
  • Elevated due to increased production from anterior pituitary
  • Theca cells from ovary produce excess androgens due to hyperinsulinaemia and increased serum levels of LH
  • When more LH than FSH, ovaries synthesise androgens rather than estrogens
  • Theca cells therefore produce more testosterone
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28
Q

Why do women with PCOS have more estrogen?

A
  • Follicular development stops just short of full maturation
  • No ovulation but continued estrogen production
  • Continued estrogen unopposed by progestogen causes the endometriuim to become hyperplastic
  • Testosterone is also converted to estrogen in peripheral fat tissue
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29
Q

What metabolic problems arise from PCOS?

A
  • Insulin resistance in up to 80% of women
  • Independent of obesity but exacerbated by weight gain
  • 40% of obese women with PCOS have glucose intolerance of T2DM by end of their 4th decade
  • Limited evidence to suggest higher risk of CVD
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30
Q

What pregnancy complications occur from PCOS?

A
  • Infertility
  • Gestational diabetes
  • 3-4x increased risk of PIH, PET, GDM
  • 2x increased risk of premature delivery
  • Children of women with PCOS are at increased risk of metabolic and reproductive dysfunction
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31
Q

What are the diagnostic criteria for PCOS?

A

If two or three of the following features are present
- Infrequent or no ovulation (i.e. menstrual disturbance)
- Clinical and/or biochemical signs of hyperandrogenism (i.e. hirsutism, acne, raised testo levels)
- Polycystic ovaries seen on USS (presence of 12 or more follicles) or increased volume >10mm3

In adolescents, the first two HAVE to be present

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32
Q

Who with PCOS should be offered a glucose tolerance test?

A
  • When planning a pregnancy
  • When pregnant
  • If BMI >25
  • Ethnicities at higher risk of DM
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33
Q

Who might receive insulin-sensitising drugs in PCOS (in a non-fertility setting)?

A
  • Severe oligomenorrhoea or amenorrhoea
  • Impaired glucose tolerance
  • Low SHBG

Usually not done in primary care

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34
Q

How can you manage the menstrual irregularities of PCOS if fertility is not desired?

A
  • Cyclical progestogens
  • COCP
  • LNG IUS
35
Q

A woman with PCOS presents with <1 period every 3 months and has a BMI of 38. What investigation will you do?

A
  • Prescribe a cyclical progestogen (MPA) to induce a withdrawal bleed
  • Refer for TV USS to check endometrial thickness
  • If >10mm, may need endometrial sample (certainly if <7mm it is unlikely to be hyperplasia)
36
Q

Who would you refer with hirsutism?

A
  • 2WW if possibility of underlying adrenal/ovarian neoplasm (i.e. rapid new hair growth, signs of virilisation, pelvic or abdominal mass)
  • Refer to secondary care if raised testo >4 or elevated 17-hydroxyprogesterone (CAH)
37
Q

What treatments can be given for hirsutism?

A
  • Topical vaniqua (topical eflornithine)
  • CHC containing EE (off-label)
  • CHC containing cyproterone acetate (Dianette) is licensed for moderate hirsutism
38
Q

How do COCs manage hirsutism?

A
  • Reduce hyperandrogenism by suppressing LH secretion
  • Reduces ovarian androgen secretion
  • Increases production of SHBG
  • Reduces free androgen levels
  • Cyproterone acetate and drospirenone act as a weak androgen receptor antagonist
39
Q

Which hormones are more androgenic?

A
  • COCs containing levonorgestrel and norethisterone are more androgenic, but these have less VTE risk
  • Progestogens with low androgenicity are norgestimate, desogestrel and gestodene
40
Q

Describe the treatment of hirsutism with Dianette

A
  • Co-cyprindiol (ethinylestradiol with cyproterone acetate)
  • Licensed for severe acne that has not responded to antibacterials
  • Licensed for moderate-severe hirsutism
  • Risk of VTE is higher
  • Shouldn’t be used as a sole contraceptive, but will provide contraceptive cover
  • Advise patient of signs/symptoms of VTE
  • Discontinue 3 months after acne has been controlled
41
Q

What happens to LH and FSH throughout the menstrual cycle (and how does it change in PCOS)?

A
  • At beginning of cycle, LH and FSH are usually 5-20mlU/ml
  • At LH surge, LH increases to 25-40
  • In PCOS, LH will be 2-3x higher than FSH (i.e. LH may be 18 when FSH is 6)
  • This will disrupt ovulation
42
Q

What happens to DHEA-S in PCOS?

A
  • DHEA-S (dehydroepiandrosterone) is another male hormone found in all women
  • An androgen secreted by the adrenal gland
  • Normal range between 35-430 ug/dl
  • PCOS levels will be >200
43
Q

What happens to prolactin in PCOS?

A
  • It’s usually normal, but is important to check to rule out other causes
  • Some PCOS do have a slightly higher prolactin though, between 25-40
44
Q

How is SHBG difference in PCOS?

A
  • Normal range is 18-144 nmol/L
  • May be reduced in PCOS (resulting in more free testo)
45
Q

What is free androgen index and how are these levels different in PCOS?

A
  • FAI estimates the amount of free testosterone
  • Divide total testosterone level by the SHBG = FAI
  • Normal levels are 0.18-7% (higher in women >50)
  • FAI may be elevated in PCOS
46
Q

What is the subjective and objective measurement of HMB?

A
  • Subjective: interferes with physical, emotional, social and material quality of life
  • Objective: >80ml or prolonged bleeding (>7/7)
47
Q

What is the FIGO classification of abnormal uterine bleeding?

A

PALM - COEIN

Structural
- Polyps
- Adenomyosis
- Leiomyoma
- Malignancy and hyperplasia

Nonstructural causes
- Coagulopathy
- Ovulatory dysfunction
- Endometrial
- Iatrogenic
- Not yet classified

48
Q

What lab tests are recommended by NICE for investigation of HMB?

A
  • FBC for all
  • Coagulation if HMB since periods started and personal / family history suggesting coag disorder
  • Do not routinely test for ferritin, hormone profile, TFTs (unless other symptoms)
49
Q

Who does NICE recommend should have an outpatient hysteroscopy?

A
  • Symptoms such as persistent IMB or
  • Risk factors for endometrial pathology

(recommended for women with HMB if uterine cavity abnormalities or endometrial pathologies are suspected because it is more accurate than USS and has a low risk of complications)

50
Q

Who does NICE recommend should have an endometrial biopsy?

A
  • High risk of endometrial pathology
    – Persistent IMB or irregular bleeding
    – Infrequent HMB who are obese or PCOS
    – Tamoxifen
    – HMB treatment failure

States endometrial biopsy should only be done in the context of hysteroscopy

51
Q

What considerations are there for management of HMB?

A
  • Desire for fertility
  • Severity of symptoms
  • Potential underlying cause
  • Acceptability of treatments
  • Potential contraindications to treatment
52
Q

When can LNG IUD be used first line for management of HMB (NICE)

A
  • No identified pathology
  • Fibroids <3cm
  • Suspected / diagnosed adenomyosis
53
Q

What pharmacological treatment is there for fibroids >3cm?

A

Non-hormonal
- TXA
- NSAIDs

Hormonal
- LNG IUD (if no cavity distortion)
- COCP
- Cyclical oral progestogens
- UPA

54
Q

What are the surgical options for fibroids >3cm?

A
  • Uterine artery embolisation
  • Myomectomy
  • Hysterectomy
  • Can consider endometrial ablation if no distortion of the cavity
55
Q

When can UPA be used in management of fibroids?

A
  • Intermittent tx of mod-severe symptoms of fibroids (>3cm) in premenopausal women

Only if
- Surgical options not suitable / have tried and failed / declined
- No underlying liver disease

56
Q

What risks are there with UPA used for fibroid treatment?

A
  • Serious liver injury / failure
  • LFTs will need to be done prior to starting, monthly for first 2 courses, and once before each new treatment
57
Q

What is endometrial hyperplasia?

A
  • Irregular proliferation of endometrial glands with increase in gland:stroma ratio
  • Precursor to endometerial cancer
58
Q

What causes endometrial hyperplasia?

A
  • Unopposed estrogen stimulated endometrial cell growth by binding to estrogen receptors in nuclei of endometrial cells
59
Q

Name some risk factors for endometrial hyperplasia

A
  • Increased BMI (peripheral conversion of androgens in adipose tissue to estrogen)
  • Anovulation
  • Estrogen-secreting tumours (e.g. granulosa cell tumours have 40% prevalence of endometrial hyperplasia)
  • Drug-induced (estrogen-only HRT without endometrial protection)
  • Tamoxifen (long-term)
60
Q

What is the 2014 WHO classification of endometrial hyperplasia?

A
  • Hyperplasia without atypia
  • Atypical hyperplasia
61
Q

What is the cancer progression risk of hyperplasia without atypia?

A

-5% risk over 20 years

62
Q

What is the cancer progression risk of atypical hyperplasia?

A
  • 27.5% after 19 years
  • Concomittant cancer in up to 43% undergoing hysterectomy for atypical hyperplasia
63
Q

If endometrial thickness is 3mm on TVUSS in someone with PMB, what is the probability of cancer?

A

<1%

64
Q

What are the pharmacological treatment options for hyperplasia without atypia?

A

1st line LNG IUD
- Higher regression rate, more favourable bleeding profile, less side effects

Continuous oral progestogen 2nd line
- Medroxyprogesterone 10-20mg/day
- Norethisterone 10-15mg/day

Treat for minimum of 6 months

65
Q

What is the surveillance schedule for hyperplasia without atypia?

A
  • 6 monthly intervals until 2x consecutive negative biopsies
  • If higher risk e.g. BMI >35 or treated with oral progestogens, long-term FU with annual biopsies
66
Q

When would someone with hyperplasia without atypia require a hysterectomy?

A
  • Progresses to atypical hyperplasia
  • No regression after 12 months of treatment
  • Relapse / persistent symptoms
  • Woman declines endometrial surveillance or medical treatment
67
Q

What is the management for atypical hyperplasia in someone who is not concerned re. fertility?

A
  • Total hysterectomy due to risk of underlying malignancy or progression to cancer
  • +BSO if peri- or post-menopausal
  • Consider salpingectomies in pre-menopausal as this may reduce ovarian malignancy risk
68
Q

What is the management of atypical hyperplasia in someone wishing to preserve fertility?

A
  • MDT discussion with histology, imagine (TVUSS +/- MRI) and tumour markers (Ca 125)
  • LNG IUD first line, oral progestogens 2nd line
  • 25% live birth rate - refer to fertility specialist, consider assisted reproduction
  • Endometrial biopsy every 3 months until 2x negatives, then 6-12 monthly
  • Hysterectomy once fertility no longer required
69
Q

How should you manage someone with endometrial hyperplasia on tamoxifen?

A
  • Routine use of LNG IUD cannot be recommended as uncertain risk of breast cancer recurrence
  • Reassess need for tamoxifen if endometrial hyperplasia diagnosed
  • MDT with breast team / oncologist
70
Q

What is Kallmann Syndrome?

A
  • GnRH deficiency with anosmia
  • Would present with primary amenorrhoea
  • Also low FSH, LH and estradiol
71
Q

What are streak ovaries?

A
  • Seen with abnormalities / absence of X chromosome (i.e. Turner’s 45XO or triple XXX syndrome)
  • ‘streak’ of fibrous tissue where ovaries should be
  • Form of aplasia
  • Usually removed due to malignant transformation risk
72
Q

A pregnant woman has a pituitary adenoma, which dopamine agonist can she take?

A

Bromocriptine

73
Q

Name some causes of PMB

A
  • Atrophic vaginitis
  • Trauma (e.g. pessary)
  • HRT
  • Endometrial polyp
  • Endometrial hyperplasia
  • Endometrial carcinoma
  • Rarely estrogen secreting tumours (theca and granulosa cell tumours)
74
Q

What are 75% of endometrial cancers?

A

Endometrioid adenocarcinoma

75
Q

Name some complications of having fibroids

A
  • Calcification
  • Hyaline degradation
  • Red degradation
  • Sarcoma change
  • Torsion of pedunculated fibroids
  • Prolapse of cervical fibroids
76
Q

What treatment options are there for fibroids in women who wish to conceive?

A
  • UAE
  • Myomectomy
77
Q

What happens during the follicular phase of the menstrual cycle?

A
  • Formation of dominant follicles
  • Secrete estrogen ++ which in turn stimulates LH/FSH, until rupture of dominant follicle from the LH surge
78
Q

What happens during the luteal phase of the menstrual cycle?

A
  • Remnant of ruptured dominant follicle (corpus luteum) produces progesterone
  • Negatively inhibits LH
  • Makes the endometrium go through secretory phase and growth of spiral arteries
  • When estrogen and progesterone fall, the endometrium collapses
79
Q

How does anorexia, excessive exercise and stress cause amenorrhoea?

A
  • Reduction in GnRH
  • Reduction in LH and FSH
80
Q

Why does breastfeeding cause amenorrhoea?

A
  • Raised prolactin inhibits GnRH production, thereby inhibiting LH and FSH
81
Q

Why does Asherman syndrome cause amenorrhoea?

A
  • No functional endometrium left
  • Scar tissue makes endometrium refractory to hormonal stimulation
82
Q

What is a submucosal fibroid?

A
  • Extends into the uterine cavity
83
Q

What is a submural fibroid?

A
  • Within the myometrium / muscular uterine wall
84
Q

What is a subserosal fibroid?

A
  • Project outside the uterus

MFSRH Part 2 (2023) (22 decks)

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