Gynae - Menstrual Disorders

Question 1

Dysmenorrhoea

Primary Dysmenorrhoea
Secondary Dysmenorrhoea
Causes of Secondary Dysmenorrhoea
Management

Answer 1

1. ) Primary Dysmenorrhoea - menstrual pain occurring without any underlying pelvic pathology
   - often occurs 6-12 months after menarche
2. ) Secondary Dysmenorrhoea - menstrual pain occurring with an associated pelvic pathology
   - often presents after several years of painless periods
   - pain may persist post-menstruation or be exacerbated by menstruation
   - pelvic exam may be abnormal or normal
3. ) Causes of Secondary Dysmenorrhoea
   - endometriosis/adenomyosis: chronic pelvic pain, menorrhagia, deep dyspareunia
   - fibroids: abdominal pain, menorrhagia, pelvic mass
   - PID: abdominal pain, AUB, dyspareunia, fever
   - ovarian/cervical cancer, IUD insertion (3-6 months)

Question 2

Primary Dysmenorrhoea

Pathophysiology
Clinical Features
Investigations
Management

Answer 2

1. ) Pathophysiology - oversensitivity of endometrial cells to decline in progesterone during menstruation leads to the excessive release of prostaglandins
   - prostaglandin functions: spiral artery vasospasm (ischaemic necrosis and shedding of the endometrium), increased myometrial contractions
   - risk factors: early menarche, long menstrual phase, heavy periods, smoking, nulliparity
2. ) Clinical Features
   - crampy lower abdo/pelvic pain, which can radiate to the lower back or anterior thigh, associated symptoms:
   - headaches, dizziness, malaise, N+V, diarrhoea
   - lasts 2-3days around menses, worse at the onset
   - normal examinations, may have uterine tenderness
3. ) Investigations
   - exclude secondary dysmenorrhoea: endometriosis, adenomyosis, PID, adhesions, IBD, IBS
   - HVS and endocervical swabs if at high risk of STI
   - transvaginal USS: if pelvic mass on examination
4. ) Management - all symptomatic improvement
   - 1°: NSAIDs (e.g. mefanamic acid) +/- paracetamol
   - 2°: hormonal contraception (COCP/IUS) can be then trialled for 3 to 6 months
   - non-pharmacological: heat application, TENS
   - lifestyle: smoking cessation

Question 3

Causes of Primary Amenorrhoea

Turner’s Syndrome
Complete Androgen Insensitivity Syndrome
Isolated GnRH Deficiency
Anatomical Causes

Answer 3

1. ) Turner’s Syndrome - genotype is 45, X0
   - ovary doesn’t complete normal development
   - high FSH and LH but low oestrogen
   - low oestrogen means no pubertal changes
2. ) Complete Androgen Insensitivity Syndrome
   - resistant to testosterone due to receptor defect
   - 46, XY but has female external genitalia
   - no female internal genitalia so no period
   - testes should be surgically excised after puberty to prevent cancer
3. ) Isolated GnRH Deficiency - idiopathic hypo-gonadotropic hypogonadism (no GnRH secretion)
   - poor development of 2° sexual characteristics
   - Kallmann syndrome if it occurs with anosmia
4. ) Anatomical Causes - produces 20% of cases
   - imperforate hymen (no vaginal opening)
   - transverse vaginal septum
   - Mayer-Rokitansky-Kuster-Hauser syndrome: Mullerian agenesis causing the congenital absence of the uterus and upper two-thirds of the vagina

Question 4

Causes of Secondary Amenorrhoea

Hypothalamic 
Pituitary 
Ovarian 
Adrenal
Anatomical Causes

Answer 4

1. ) Hypothalamic - reduced GnRH
   - functional disorders: e.g. eating disorders or high-level exercise can suppress GnRH production
   - hypothyroidism: ↓T3/T4 –> ↑TRH which stimulates the secretion of prolactin therefore LH/FSH is inhibited
   - hyperthyroidism: ↑T3/T4 –> ↑sex hormone-binding globulin (SHBG) which ↑the amount of free oestrogen required to trigger the LH spike needed for ovulation
   - severe chronic conditions: e.g psychiatric disorders, sarcoidosis
2. ) Pituitary - reduced FSH and LH
   - prolactinomas: secretes prolactin, suppressing GnRH causing anovulation, amenorrhoea and galactorrhoea
   - other pituitary tumours: mass effect of tumour +/- hyperprolactinaemia causes FSH/LH deficiency
   - Sheehan’s syndrome – postpartum pituitary necrosis secondary to massive obstetric haemorrhage.
   - destroyed pituitary gland e.g. radiation, autoimmune
   - post-contraception: prolonged use downregulates the pituitary gland causing irregular/absent periods
3. ) Ovarian
   - PCOS: hyperandrogenism and chronic anovulation
   - premature ovarian failure: menopause < 40
4. ) Adrenal Hyperplasia - due to partial deficiency of 21-hydroxylase, can be congenital (AR) or late-onset
   - present with the early development of pubic hair, irregular or absent periods, hirsutism and acne,
   - high levels of 17-hydroxyprogesterone in blood
5. ) Anatomical Causes
   - Ashermann’s syndrome: secondary to instrumentation of the uterus damaging the basal layer of the endometrium which causes intrauterine adhesions which fail to respond to oestrogen stimulus
   - scarring due to cervical stenosis

Question 5

Amenorrhoea and Oligomenorrhoea

Classification
Causes of Oligomenorrhoea
Blood Tests
Other Investigations

Answer 5

1. ) Classification
   - primary amenorrhoea: absence of menarche (>16s w/ secondary sexual characteristics (pubic hair or breast development) or >14s w/o characteristics)
   - secondary amenorrhea: cessation of periods for >6 months after the menarche (excluding pregnancy)
   - oligomenorrhoea: irregular periods with cycles > 35 days and/or less than nine periods per year
2. ) Causes of Oligomenorrhoea
   - PCOS, thyroid disease, diabetes, functional disorders
   - contraceptive/hormonal treatments, perimenopause
   - medication: e.g. anti-psychotics, anti-epileptics
3. ) Blood Tests - pregnancy test and bloods
   - GnRH/FSH/LH/oestradiol/progesterone/testosterone
   - TFTs, PRL, 17 hydroxyprogesterone (CAH)
   - hypothalamic: ↓GnRH, ↓LH/LH:FSH, ↓oestrogen
   - PCOS: ↑LH/LH:FSH, normal or ↑testosterone
   - prolactinoma: ↑PRL, ↓GnRH | POI: ↑FSH/LH, ↓oestrogen
4. ) Other Investigations
   - karyotyping: if suspecting a genetic abnormality
   - USS: to visualise ovaries and pelvic anatomy
   - progesterone challenge: to elicit a withdrawal bleed, bleed suggests anovulation w/ normal oestrogen levels, no bleed suggests low oestrogen or outflow obstruction

Question 6

Management of Amenorrhoea/Oligomenorrhoea/PCOS

Treat Underlying Disorders
Inducing Menstruation
Symptomatic Treatment (PCOS)
Primary Ovarian Insufficiency
Surgery

Answer 6

1. ) Treat Underlying Disorders
   - functional hypothalamic disorders: strict regime to ↑body fat and stimulate GnRH production
   - hypothyroidism and hyperthyroidism
   - treating diabetes and hypertension
2. ) Inducing Menstruation - amenorrhoeic women have unopposed oestrogen due to low progesterone
   - this –> endometrial hyperplasia –> ↑ risk of cancer
   - important to induce at least 3 bleeds per year:
   - COCP (low dose) or dydrogesterone (progesterone analogue if COCP contraindicated)
3. ) Symptomatic Treatment (PCOS)
   - obesity: reduce BMI <30, lifestyle advice, orlistat (pancreatic lipase inhibitor) in severe cases
   - infertility: ovulation induction with 1°letrozole or 2°clomifene +/- metformin (help weight loss), 3°gonadotropin therapy, 4°laparoscopic ovarian drilling if normal BMI, 5°IVF
   - hirsutism: particular types of the COCP eg Yasmin, cyproterone acetate (Co-cyprinidol/Dianette), eflornithine cream to reduce the growth of facial hair, spironolactone and finasteride,
   - acne: topical BPO, retinoids, antibiotics etc…
4. ) Primary Ovarian Insufficiency - cyclical HRT (oestrogen +/- progesterone (w/o uterus)) or COCP
   - treats menopausal sx, ↓risk of CVD, maintains bone density to prevent osteoporosis (consider Ca/vitD)
   - HRT does not provide contraception
   - reassess the need for HRT once they reach 51yrs old
5. ) Surgery
   - pituitary tumours and genital tract abnormalities

Question 7

Polycystic Ovarian Syndrome (PCOS)

Pathophysiology
Clinical Features
Diagnostic Criteria
Investigations

Answer 7

1. ) Pathophysiology
   - excess LH: due to ↑GnRH pulse frequency, causes overstimulation of ovaries –> androgen excess
   - insulin resistance: leads to ↑insulin secretion which ↓ SHBG production –> ↑ free circulating androgens
   - ↑ circulating androgens suppresses the LH surge, which prevents ovulation so follicles in the ovaries are arrested at an early stage, remaining as ‘cysts’
   - risk factors: DM, irregular menstruation, FH of PCOS
2. ) Clinical Features
   - oligo/amenorrhoea, infertility (anovulation), obesity
   - hirsutism, acne, male-pattern hair loss
   - acanthosis nigricans (due to insulin resistance)
   - chronic pelvic pain, depression and other psych sx
3. ) Diagnostic Criteria - Rotterdam criteria, 2/3 of:
   - oligomenorrhoea and/or anovulation
   - clinical or biochemical signs of hyperandrogenism
   - polycystic ovaries on imaging
   - differential diagnoses: hypothyroidism, Cushing’s disease, hyperprolactinaemia
4. ) Investigations
   - blood tests: ↑LH:FSH, ↑testosterone, ↓progesterone ↓sex hormone-binding globulin
   - TFTs, prolactin, HbA1c
   - USS: ‘ring of pearls sign’, ovaries contain >12 antral follicles (‘cysts’) and/or ­ovarian volume >10ml

Question 8

Heavy Menstrual Bleeding (Menorrhagia)

What is it?
PALM
COEIN
Clinical Features

Answer 8

1. ) What is it? - excessive menorrhagia affecting QoL
   - not related to pregnancy and not post-menopausal
   - risk factors: age (near menarche and menopause), obesity, previous C-section (adenomyosis)
   - majority (40-60%) have no clear pathology so are termed as dysfunctional uterine bleeding
2. ) PALM - structural causes
   - Pregnancy: must exclude in every patient, vaginal bleeding could suggest miscarriage or an ectopic
   - Polyps: not often associated w/ dysmenorrhoea
   - Adenomyosis/Endometriosis: associated w/ painful periods, bulky uterus can be present on examination
   - Leiomyoma (fibroids): hx of pressure sx (e.g. urinary frequency), bulky uterus also on examination
   - Malignancy/Hyperplasia: endometrial/cervical/vaginal
3. ) COEIN - non-structural causes
   - Coagulopathy: vWf disease most common (HMB since menarche, other clues), could also be anticoagulant use
   - Ovulatory Dysfunction: PCOS and hypothyroidism
   - Endometrial Dysfunction: diagnosis of exclusion
   - Iatrogenic: hormonal contraception, IUD
   - Not yet classified
4. ) Clinical Features
   - excessive (patient’s own definition) bleeding
   - fatigue, SOB or pallor (anaemia)
   - abdominal palpation: palpable uterus or pelvic mass
   - bi-manual: irregular uterus (fibroids), tender uterus or cervical excitation (endometriosis/adenomyosis)
   - speculum: inflamed cervix, cervical polyp/tumour, vaginal tumour

Question 9

Management of Heavy Menstrual Bleeding

Blood Tests and Imaging
Histology and Microbiology
Pharmacological Management
Surgical Management

Answer 9

1. ) Blood Tests and Imaging
   - pregnancy test and a series of blood tests:
   - FBC, TFTs, coagulation, vWF test, androgens (?PCOS)
   - imaging: pelvic US if uterine/pelvic mass, TVUS for assessing the endometrium and ovaries
2. ) Histology and Microbiology
   - cervical smear (no need to repeat if up to date)
   - HVS and endocervical swabs: suspect infection
   - pipelle endometrial biopsy: persistent intermenstrual bleeding, >45yrs, failed pharmacological treatment
   - hysteroscopy and endometrial biopsy: performed when USS identifies pathology or is inconclusive
3. ) Pharmacological Management - tranexamic acid +/- contraception
   - LNG-IUS: thins endometrium and can shrink fibroids
   - COCP: second line if not contraindicated
   - new POP: taken everyday, much fewer side effects
   - old POP: norethisterone taken for 3 wks (5-26), withdrawal bleed for 1wk
   - tranexamic acid (anti-fibrinolytic) can be taken during menses along with NSAIDs
   - Depot: better for younger women due to osteoporosis risk, can also cause weight gain
   - implant is not liscenced for HMB
4. ) Surgical Management
   - endometrial ablation: obliterate endometrial lining, causes infertility, can be done as an outpatient w/ LA
   - hysterectomy: only definitive treatment, can be partial (cervix remains) or total (removes uterus and cervix)
   - myomectomy and uterine artery embolisation: only used to treat HMB caused by fibroids