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Obstetrics + gynaecology > Menstrual disorders > Flashcards

Menstrual disorders Flashcards

1
Q

Describe the hypothalamic-pituitary-ovarian axis

A
  • Hypothalamus pulsatile secretion of GnRH - AP secretes FSH+LH - inhibited by high concentrations of O+P
  • FSH: acts on granulosa cells to convert testosterone to oestradiol which recruits oocytes
  • LH: acts on theca cells to make testosterone, helps determine the dominant follicle, initiates ovulation and causes luteinisation of the granulosa cells
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2
Q

What’s the role of oestrogen + progesterone?

A
  • Oestrogen: peak at ovulation, it stimulates reproductive growth, reduces vaginal pH, thins cervical mucus to allow sperm penetration, inhibits FSH, develops the primordial follicle, stimulates breast growth, promotes bone calcification + involved in female fat + hair distribution
  • Progesterone: endometrial secretory changes, myometrial growth during pregnancy, glandular activity in breast
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3
Q

Outline the steps of follicular development

A
  • Ovum enlarges, stromal cells enlarge
  • Dominant follicle selected
  • Granulosa cells collect around ovum forming zona pellucida
  • Graafian follicle assumes its mature form, cells around become theca interna + externa
  • Follicle enlarges and bulges to ovary surface, cavity often fills with blood
  • Granulosa + theca cells luteinise
  • Corpus luteum regresses unless implantation occurs
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4
Q

Outline oogenesis

A
  • W4-primordial germ cells, by W20 primary oocytes made and suspended in prophase I
  • Puberty: first dominant follicle is triggered by LH to start ovulation, at each ovulation meiosis I completes and meiosis II begins
  • Meiosis II only completed at fertilisation
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5
Q

What controls the length of the menstrual cycle?

A

The length of the follicular phase - can be affected by pregnancy, lactation, emotional stress, low body weight and pre-menopause (shorter in pre-menopause as follicles lesser quality)

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6
Q

Describe the uterine cycle

A
  • Proliferative phase: folliculogenesis + growth of follicles driven by FSH, oestradiol from granulosa cells causes endometrial proliferation
  • Ovulation: LH surge due to positive feedback from O, one oocyte released into fallopian tube
  • Secretory phase: progesterone increased so endometrium becomes more glandular, decidual cells develop which secrete prolactin (in case need to make a placenta)
  • Corpus luteum secretes progesterone then regresses
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7
Q

Describe the ovarian cycle

A
  • Follicular phase-oestrogen made. Changes in vagina, skin, hair, metabolism.
  • Pre-ovulation: rapid rise in O + inhibin, O increases GnRH sensitivity causing an LH surge, GnRH pulses get more rapid, progesterone produced
  • Ovulation: meiosis I completes, meiosis II starts, mature oocyte extruded
  • Luteal phase: progesterone causes breast, metabolic, myometrial changes and reduces motility so conceptus not expelled, thickens mucus to limit infection + prevent extra sore getting in. Follicle luteinised by LH to make the CL which secretes O, P and inhibin, LH suppressed by negative feedback ,CL regresses after 14d unless pregnant when hCG maintains the CL
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8
Q

What’s the physiology of menstruation?

A
  • 12-14d post-ovulation - spasm of endometrial spiral arterioles because of prostaglandins - tissue hypoxia + death in superficial area - shed
  • Loss controlled by platelet plugs + vasoconstriction
  • Basal layer regenerates, cycle resumes
  • Corpus luteum converted to corpus albicans as LH is reduced
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9
Q

Describe the control of the hormones

A
  • Hyp releases GnRH - stimulates AP to make FSH + LH
  • FSH stimulates granulosa cells to make oestrogen which causes follicle to grow
  • Oestrogen sends positive feedback to the H+P which causes further LH release, but FSH is inhibited by inhibin
  • Just before ovulation oestrogen is high and no longer relies on FSH for production so inhibin rises
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10
Q

Define primary amenorrhoea

A

No period by age 16y
If no secondary sex characteristics by 14y then investigate, if they are present then can leave until 18y to investigate as usually will have had menarche by then

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11
Q

What are the causes of primary amenorrhoea?

A
  • Hypothalamic (no GnRH) or hypogonadotrophic (no FSH/LH):
  • Chromosomal: Turner’s syndrome, androgen insensitivity syndrome, congenital adrenal hyperplasia
  • Congenital deformities e.g. absent hymen, absence of vagina/uterus (but ovaries usually present)
  • Cyptomenorrhoea: hidden loss due to obstructed flow e.g. a septum so may get cyclical abdo pain, masses, bluish bulge inside hymen
  • Delayed menarche: if otherwise normal and it happens by 18y usually
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12
Q

What are the features of Turner’s syndrome?

A

45, XO. They have no ovaries but they do have a uterus + vagina – poor breast development, little pubic/axillary hair, short (low GH), webbed neck (lymphedema), a/w coarctation of the aorta and bicuspid aortic valve, deafness, high arched palate, short 4th metacarpal, multiple pigmented naevi, osteopenia. M - HRT

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13
Q

What investigations are indicated in primary amenorrhoea?

A

BMI, check for secondary characteristics, measure hormones (LH, FSH, oestradiol + testosterone), USS to check for ovaries + follicle activity, karyotyping if suspect chromosomal defect

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14
Q

Define secondary amenorrhoea

A

No periods for 6 months once they have already started

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15
Q

What are the causes of secondary amenorrhoea

A
  • Physiological: pregnancy, lactation, menopause
  • Functional effects on hypothalamus: excess exercise, eating disorder, stress - suppress GnRH release
  • Pituitary: destruction by radiotherapy/tumours, Sheehan’s syndrome (severe PPH - pituitary anoxia), hyperprolactinaemia (adenoma or drugs), anorexia nervosa, post-contraception temporary downregulation (Depot)
  • Thyroid disorders: may cause amenorrhoea or menorrhagia
  • PCOS: commonest cause of anovulation, causes oligo or amenorrhoea
  • Spontaneous premature ovarian failure: no disease state, premature menopause <40y as ovary stops responding to FSH/LH, causes low O and high FSH
  • Surgical/radiation damage to ovary
  • Uterus: severe infections, endometrial ablation, curettage
  • Any general disease, including starvation or obesity
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16
Q

How would you investigate secondary amenorrhoea?

A

hCG, TFT, prolactin, FSH, LH, oestradiol, progesterone, testosterone, US for pelvic anatomy, progesterone challenge to elicit a withdrawal bleed (if positive suggests there’s enough oestrogen but they’re not ovulating e.g. PCOS, whereas lack of bleeding suggests there’s not enough oestrogen or there’s an obstruction)

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17
Q

What is androgen insensitivity syndrome?

A

46XY but phenotypically female. Breasts develop (testosterone converted to oestradiol) but no P+A hair, usually no uterus, gonads are either testes or undifferentiated and often in the inguinal canal/abdomen. Male levels of androgens, raised LH+FSH

M: remove testes due to malignancy risk, oestrogen HRT to prevent osteoporosis

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18
Q

What is congenital adrenal hyperplasia?

A

XX, autosomal recessive. Defective cortisol production - excess CRH - enlarged adrenal cortex - more androgens produced

Ambiguous genitalia due to excessive androgens, often anovulatory. Often p/w early pubic hair, irregular/absent periods, hirsutism, acne. Give O+P

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19
Q

How do thyroid disorders cause menstrual problems?

A
  • Hypothyroidism: low T3/4 - raised TSH - raised TRH - prolactin stimulated - inhibits LH/FSH
  • Hyperthyroidism: high T3/4 - raised SHBG - reduced ratio of free oestrogen - LH spike not triggered
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20
Q

Outline the pathophysiology of PCOS

A
  • Stromal hyperplasia of ovaries – multiple immature follicles in ovaries (cysts-icing sugar capsule, string of pearls descriptions)
  • Cysts make lots of oestrogens - more endometrial proliferation
  • Excess LH (stimulates ovarian androgen production) and insulin resistance (more insulin secreted) – suppresses SHBG – more free circulating androgens
  • Androgens suppress the LH surge – follicular development is arrested early
  • Androgens - acne + hirsutism
  • Ovulation is irregular
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21
Q

What are the CF of PCOS?

A
  • Oligomenorrhoea, amenorrhoea
  • Hirsutism, acne
  • Infertility/subfertility
  • Hyperinsulinaemia - predisposed to obesity + T2DM, acanthuses nigerians (insulin resistance)
  • Chronic pelvic pain
  • Hypertension
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22
Q

What are the complications of PCOS?

A
  • Miscarriage
  • Gestational diabetes
  • T2DM
  • CV disease
  • Endometrial hyperplasia - unopposed oestrogen as progesterone is low
  • Acne
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23
Q

How is PCOS managed?

A
  • Get BMI <30
  • COCP may help regulate + cause withdrawal bleeds (+contraception obv, as most do ovulate but irregularly). Aim for at least 3 bleeds per year
  • Hirsutism+acne: COCP (e.g. co-cyprindiol as has anti-androgen action), topical eflornithine, with a specialist may have spironolactone/flutamide/finasteride
  • Infertility: weight reduction, specialist management with metformin or clomifene, ovarian drilling
24
Q

What is oligomenorrhoea?

A

*Having irregular periods - intervals between cycles >35d
or
*<9 periods per year

25
Q

What is the general management for secondary amenorrhoea?

A
  • Regulate periods to reduce endometrial proliferation so reduce risk of endometrial cancer
  • HRT for premature ovarian failure + calcium + vitamin D
  • Lifestyle issues
  • Manage underlying disorders e.g. thyroid
  • Improve fertility with metformin/clomifene/assisted reproduction
  • Surgery for tumours or genital tract abnormalities
26
Q

What are the common causes of oligomenorrhoea?

A

PCOS, hormone medications, peri-menopause, thyroid disease, DM, eating disorders, excessive exercises, medications e.g. anti-epileptics/antipyschotics

27
Q

What are investigations likely to show in PCOS?

A
  • Multiple peripheral ovarian follicles and/or enlarged ovarian volume on US
  • Raised LH:FSH ratio ‘classical’ (but no longer used diagnosis). Best measured d1-3
  • Testosterone may be raised (but if very high consider ddx)
  • Progesterone often low
  • Serum prolactin - may be slightly high but if very high consider hyperprolactinaemia
  • OGTT if BMI > 30
  • TSH to r/o thyroid cause
28
Q

How is PCOS diagnosed?

A

Rotterdam criteria (2/3 met):

  • Oligo/anovulation
  • Clinical/biochemical hyperandrogenism
  • Polycystic ovaries on imaging
29
Q

Define menorrhagia

A

Loss of >80ml/cycle, or if amount lost interferes with their QoL

30
Q

What are the causes of menorrhagia?

A
  • Dysfunctional uterine bleeding - heavy w/o apparent cause
  • Uterine fibroids, polyps, cancer (more likely irregular) or endometrial hyperplasia
  • Adenomyosis (usually also dysmenorrhoea + enlarged uterus)
  • Ovulatory disorders - hypothyroidism, PCOS, menopausal transition (e.g. in PCOS unopposed oestrogen - hyper plastic endometrium that is unstable so erratic breakdown)
  • Infection - endometritis, PID
  • Iatrogenic - IUD, incorrectly controlled HRT/contraception, progesterone contraception
  • Functional ovarian tumours
  • Clotting disorders - vWD, thrombocytopenia, leukaemia
  • Medical - hypothyroidism, liver disease, SLE
31
Q

How would you assess a woman p/w heavy menstrual bleeding?

A
  • Ask about flooding, if is a recent change, pain (more likely adeno/PID), IMB/PCB (more likely structural), consider RF for cancer
  • Examine for anaemia, thyroid, pelvic + smear (masses most likely fibroid but may be cancer)
  • Ix: FBC, TFTs, clotting, TV USS, hysteroscopy + biopsy if indicated
32
Q

How do you manage menorrhagia?

A
  • Consider referral if large masses, suspected cancer, not improving
  • Counselling: discuss natural variability, range of menstrual blood loss (may be able to reassure)
  • Non-hormonal: mefenamic acid if painful as well (NSAID-inhibits PG synthesis so less blood + analgesic) or tranexamic acid (anti-fibrinolytic that inhibits plasminogen). Use whilst bleeding
  • Consider IUS, COCP, oral norethisterone (high dose progesterone), any progestogen-only contraception may suppress menstruation
  • If have fibroids and above not working consider ulipristal acetate, uterine artery embolisation, myomeectomy, local/transcervical ablation (removes basal layer so endometrium doesn’t regenerate), TAH (only in severe)
33
Q

PALM-COEIN? causes of menorrhagia

A 
Polyp
Adenomyosis
Leiomyoma (fibroid)
Malignancy
Clotting disorder 
Ovulatory disorder
Endometrial (inc DUB)
Iatrogenic
Not otherwise classified
34
Q

What advice should you give to women with menorrhagia about the various treatments?

A
  • IUS: anticipate changes in bleeding in first few cycles, wait at least 6 cycles to see benefits
  • Uterine artery embolisation: use femoral artery to find uterine vessels, impair blood supply to uterus + fibroids, may allow them to retain artery
  • Myomectomy: may retain fertility
  • Hysterectomy: may be V/A/Lap, may remove or preserve ovaries/cervix. Adv about risk of serious comps, possible loss of ovarian function (even if ovaries kept), include alternatives + psych support + expectations + comps + need for further treatment + bladder function + fertility
  • Endometrial ablation: destroy the lining and the superficial muscle of uterus, avoid pregnancy and use effective contraception if needed
35
Q

Primary dysmenorrhoea

A
  • Not a/w a physical abnormality, progesterone causes excessive uterine contractions
  • Usually severe abdo/lower back/thighs pain in first few hours-days, +/- vomiting/syncope/diarrhoea
  • RF include FH, early menarche and mother’s perception
  • M: reassure, general like exercise/heat pack, para, ibuprofen, mefenamic acid, codeine, hormonal to stop ovulation
36
Q

Secondary dysmenorrhoea

A

Painful menstruation a/w a pathology, mostly occurring >25 (tho endometriosis often starts as severe dysmenorrhoea in adolescence). Pain begins a few days before menstruation and is sometimes better once its started

  • Causes: chronic infection, endometriosis, adenomyosis, fixed retroversion of uterus, fibroids
  • Examine for abdo masses, uterine + adnexal tenderness, uterine mobility, triple swabs, pelvic US, laparoscopy if persistent/progressive
  • M: explanation + reassurance, stop smoking, general like exercise/heatpack, NSAIDs, COCP to suppress ovulation + reduce uterine PG release, POP
37
Q

Inter menstrual bleeding

A

Bleeding which may occur at the same time each cycle or be random, often a/w PCB as superficial lesions common cause
*Causes: STIs (esp new onset), cervical polyps/ectropion/cancer, uterus (endometritis, fibroids, adenomyosis, cancer, sarcoma), ovulation spotting, breakthrough bleeding from COCP/POP/IUS/implant

38
Q

Post-coital bleeding

A

Non-menstrual bleeding after sex

  • Causes: cervical ectropion (most common), surface lesions (infection, polyps), cerv/endo/vaginal cancer, trauma
  • Ix: colposcopy (as is a common PC for cervical ca)
39
Q

Pre-menstrual syndrome

A

Usually occurs in 2nd half of menstrual cycle and stops after period

  • CF: irritability, depression, lassitude, insomnia, cramps, lack of concentration, oedema of limbs/abdo, weight gain, migraine
  • M: COCP to suppress ovulation, antidepressants may help
40
Q

Post-menopausal bleeding

A
  • Check if truly menopausal, when, how heavy, fresh/old, precipitating factors, HRT/tamoxifen/anticoagulants, cervical screening, urinary symptoms
  • Causes: genital tract atrophy (most common), endometrial cancer, endometrial hyperplasia, cervical/endometrial polyps, cancer of cervix/vagina/vulva/urethra, vulval ulceration/itch, urethral caruncle
  • Ix: TV USS - uniformly thickened suggests cancer or hyperplasia, localised thickening suggests a polyp
41
Q

What hormonal changes occur at the menopause?

A
  • In peri-menopause follicular phase shortens, ovulation is early/absent, FSH + LH begin to rise) and oestradiol levels erratic
  • No more follicles to develop - dramatic fall in oestrogen, lack of inhibin means FSH + LH rise (esp FSH)
  • Some oestrogen is still made by the adrenal gland and peripheral conversion of oestrone+testosterone in adipose
42
Q

What are the CF of the menopause?

A
  • Hot flushes - typically maximal in first 12m and last up to 5y - cos of low oestrogen
  • Vaginal dryness - cos of reduced oestrogen which causes epithelial thinning, reduced vascularity, reduced muscle bulk. Can lead to dyspareunia, PCB, loss of libido
  • Uterovaginal prolapse and urinary sx - atrophic bladder epithelium
  • Thin skin/dry hair
  • Palpations - due to oestradiol levels but r/o CVS issue
  • Headache
  • Bone/joint pain
  • Tiredness
  • Tender breasts or breast involution
  • Psychological sx: anxiety, depression, impaired memory, irritability, poor concentration
43
Q

When would you investigate a woman with suspected menopause?

A

> 45y don’t investigate

<40y - two readings with FSH >40 indicates menopause

44
Q

How does the menopause affect the CVS + bones?

A
  • CVS: increased cholesterol + lipoproteins, reduced HDL:LDL ratio
  • Bones: less trabecular bone –> osteoporosis (when T score less than -2.5)
45
Q

What is the role of HRT in menopausal women?

A
  • Oestrogen for sx relief, given with progesterone if still have a uterus to prevent endometrial hyperplasia/cancer
  • Can be oral, injection, implant (IUS licensed for the progesterone component) or topical administration
  • Within 12m of LMP - sequential HRT - mimics natural cycle to reduce irregular bleeding
  • 12m of no bleeds - continuous combined HRT
46
Q

What are the side effects + risks of systemic HRT?

A

Headaches (usually go in a couple of months), tender breasts, bloating, muscle cramps, irregular bleeding

Higher risk of endometrial + breast cancer (and possibly ovarian), VTE and hypertension

47
Q

What are the contraindications to HRT?

A 
Breast/endometrial cancer
VTE
Acute liver disease
IHD
Undiagnosed vaginal bleeding
Untreated endometrial hyperplasia

Relative CI: fibroids, familial hyperlipidaemia, DM, gallbladder disease

48
Q

What non-oestrogenic treatments may be employed in menopause treatment?

A
  • Tibolone: synthetic weak androgen with a low O concentration so doesn’t cause endometrial proliferation, use >12m after last bleed, good for osteoporosis + aches but not good for vasomotor sx (due to low O)
  • Clonidine: antihypertensive (alpha agonist)
  • Adv regular weight bearing exercise to reduce osteoporosis and sunlight and stop smoking and reduce alcohol and calcium+vitD
  • SSRI or clonidine for vasomotor sx, but clonidine has more s/e like depression + dry mouth
  • Gabapentin for hot flushes - but further research being done
  • Testosterone supplements for low libido
49
Q

What is the peri-menopause?

A

From the beginning of clinical/biological/endocrinological features and ending 12m after the final menstrual period

50
Q

What is the menopause?

A

Menstrual cycles have stopped for 12m and there are no more follicles to develop

Usually occurs between ages 45-55

Premature if occurs before age 40

51
Q

What are the ‘seven dwarves of the menopause’?

A

Itchy, bitchy, sweaty, sleepy, bloated, forgetful, psycho

52
Q

What is Sheehan syndrome?

A

A rare complication of PPH where there is ischaemic necrosis of the pituitary causing hypopituitarism –> agalactorrhoea, amenorrhea, hypothyroidism, hypoadrenalism

53
Q

A 52 year old woman has had a Mirena coil in situ for 4 years and experiences an episode of bleeding. How do you proceed?

A

Refer to PMB clinic - consider endometrial biopsy in women aged 45+ using hormonal contraception who present with a change in bleeding

Could be because of coil coming to the end of its lifespan but need to exclude pathology

54
Q

How can lifestyle modifications help menopause?

A
  • Flushes - exercise, WL, stress reduction
  • Sleep disturbance - avoid late evening exercise, maintain good sleep hygiene
  • Mood - sleep, exercise, relaxation
  • Cognitive - regular exercise, good sleep hygiene
55
Q

What would you advise a woman enquiring about HRT?

A

Menopause sx last for 2-5y. HRT can be very helpful but certain risks:

  • VTE slight increase in all oral, no higher risk if transdermal
  • Stroke slightly higher risk with oral oestrogen
  • Coronary heart disease slightly higher risk with combined
  • Breast cancer higher with all combined HRT (tho risk of dying from BC not raised)
  • Ovarian cancer higher risk with all HRT
56
Q

How can non-HRT treatments help menopause?

A
  • Vasomotor sx - fluoxetine, citalopram, venlafaxine
  • Vaginal dryness - vaginal lubricant or moisturisers
  • Psychological - self help groups, CBT, antidepressants
  • Urogenital - vaginal oestrogen for atrophy (even if already taking HRT), dryness moisturisers/lubricants

Obstetrics + gynaecology (13 decks)

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