Menstrual Disorders

Overview

Menstrual disorders are among the most common gynaecological presentations in primary care and gynaecology outpatient practice — heavy menstrual bleeding alone accounts for 12 percent of all gynaecology referrals in the UK.^[7] They span four broad domains: (1) abnormalities of bleeding volume (heavy menstrual bleeding, postcoital bleeding, intermenstrual bleeding, postmenopausal bleeding); (2) abnormalities of cycle timing (amenorrhoea, oligomenorrhoea, polymenorrhoea); (3) menstrual pain (dysmenorrhoea); and (4) cyclical mood and somatic symptoms (premenstrual syndrome and premenstrual dysphoric disorder). ^[1]

The unifying framework for the commonest complaint — abnormal uterine bleeding (AUB) — is the FIGO PALM-COEIN classification, published in 2011 by Munro, Critchley and Broder, and adopted globally as the standard system for categorising AUB in non-gravid women of reproductive age.^[1] It separates structural causes (PALM — identifiable on imaging or histology) from non-structural causes (COEIN — functional, endocrine, haematological or iatrogenic, not detectable on imaging alone).

^{[7] [12] [13]}

Menstrual Physiology — The HPO Axis

A thorough understanding of the hypothalamic–pituitary–ovarian (HPO) axis is essential for classifying and managing menstrual disorders. Every amenorrhoea, oligomenorrhoea and ovulatory dysfunction question in exams ultimately tests this axis. ^[48]

The Hypothalamic Pulse Generator

The arcuate nucleus of the mediobasal hypothalamus houses kisspeptin neurons, which are the master regulators of the reproductive axis. Kisspeptin stimulates gonadotropin-releasing hormone (GnRH) neurons in the preoptic area to release GnRH in a pulsatile fashion — pulses roughly every 60–90 minutes in the early follicular phase, increasing in frequency in the late follicular phase and slowing again in the luteal phase (progesterone-dominated). ^[48]

Pulsatility matters: a fast GnRH pulse frequency favours LH synthesis, while a slow frequency favours FSH synthesis in the same gonadotrope cells of the anterior pituitary. This is why only one dominant follicle is selected. ^[48]

KNDy neurons (Kisspeptin, Neurokinin B, Dynorphin) within the arcuate nucleus form the GnRH pulse generator. Neurokinin B stimulates and dynorphin (an opioid) inhibits the pulse generator, providing fine-tuning. Loss-of-function mutations in TAC3 (neurokinin B) or TACR3 cause hypogonadotropic hypogonadism — a direct exam link. The kisspeptin-neurokinin-dynorphin (KNDy) network mediates sex-steroid feedback control of GnRH secretion. ^[48]

The Anterior Pituitary

GnRH stimulates the gonadotropes to secrete follicle-stimulating hormone (FSH) and luteinising hormone (LH) — both glycoprotein heterodimers sharing an alpha subunit. ^[48]

• FSH — recruits a cohort of follicles (days 1–5), stimulates granulosa cell proliferation and aromatase activity, converting theca-derived androstenedione to oestradiol. ^[48]
• LH — stimulates theca cells to produce androstenedione, which granulosa cells aromatise to oestradiol (the "two-cell, two-gonadotropin" model). The mid-cycle LH surge triggers ovulation and luteinisation.

The Follicular Phase (Days 1–13)

The cycle begins with the recruitment of a cohort of primordial follicles under rising FSH. Granulosa cells proliferate, and the follicle with the most FSH receptors and highest aromatase activity becomes the dominant follicle by day 6–7 — it produces exponentially more oestradiol, which exerts negative feedback on FSH, causing atresia of the subordinate follicles. This is the FSH threshold/window concept. ^[1]

The dominant follicle produces inhibin B, which further suppresses FSH. As oestradiol rises progressively (the growing follicle has ever-more granulosa cells), it eventually reaches a threshold of approximately 200 pg/mL sustained for roughly 48–50 hours, at which point oestrogen switches from negative to positive feedback on the pituitary — the positive feedback mechanism triggers the massive LH surge and a smaller FSH surge. The LH surge begins roughly 34–36 hours before ovulation, and ovulation follows about 10–12 hours after the LH peak (typically day 14). ^[48]

Ovulation (Day 14)

The LH surge causes: (1) resumption of meiosis I in the oocyte with release of the first polar body; (2) prostaglandin and proteolytic enzyme release (collagenase, plasmin) digesting the follicular wall; (3) stigma formation on the ovarian surface; (4) release of the cumulus–oocyte complex into the peritoneal cavity, captured by the fimbriae. ^[48]

The Luteal Phase (Days 15–28)

The ruptured follicle transforms into the corpus luteum under LH influence; the luteal phase lasts 14 days in most women. Luteinised granulosa cells produce progesterone (the dominant luteal hormone) and oestradiol. Progesterone: ^[48]

• Converts the proliferative endometrium to a secretory endometrium (sub-nuclear vacuoles day 16–20, then supranuclear vacuoles, stromal oedema, spiral artery development).
• Raises basal body temperature (thermogenic effect).
• Thickens cervical mucus, making it less penetrable to sperm.
• Exerts negative feedback on GnRH (slow pulse frequency) and LH/FSH. ^[1]

If pregnancy occurs, human chorionic gonadotropin (hCG) from the trophoblast rescues the corpus luteum, which maintains progesterone production until the placenta assumes this role later in pregnancy (the luteoplacental shift); exogenous LH or hCG can extend corpus luteum function by about two weeks. ^[48]

If pregnancy does not occur, the corpus luteum regresses after 14 days, progesterone and oestradiol fall abruptly, and progesterone withdrawal causes increased coiling and constriction of the spiral arterioles, tissue ischaemia and endometrial prostaglandin release — the endometrium undergoes ischaemic necrosis and sheds. This is menstruation. The fall in oestradiol and progesterone removes negative feedback, FSH rises again, and a new cycle begins. ^[48]

Steroid Feedback Summary

PALM-COEIN Classification

Enlarge

The FIGO classification is the single highest-yield framework for AUB in any gynaecology exam.^[1] It divides causes into structural (PALM) — identifiable on imaging or histology — and non-structural (COEIN) — systemic, endocrine, haematological, or functional, not detectable on ultrasound or biopsy alone.

Structural Causes — PALM (Detailed)

Polyps (P): Endometrial polyps are benign overgrowths of endometrial glands and stroma projecting into the uterine cavity. Common in women with AUB. Risk factors: nulliparity, obesity, tamoxifen use, HRT. Most are benign; the prevalence of malignant change in endometrial polyps is reported at 0.8 to 8 percent, depending on the population studied.^[38] Presentation: intermenstrual bleeding, postcoital bleeding, HMB, infertility. Diagnosis: TVS (echogenic focal lesion); saline infusion sonohysterography (SIS) improves detection; hysteroscopy is gold standard (direct visualisation and biopsy/polypectomy). Treatment: hysteroscopic polypectomy (see-and-treat); small asymptomatic polyps in premenopausal women may be managed conservatively. ^[1]

Adenomyosis (A): Endometrial glands and stroma within the myometrium, causing a diffusely enlarged, boggy, tender uterus. Classic triad: HMB, dysmenorrhoea, and enlarged uterus. Typically presents in the late reproductive years and perimenopause (parous women). Diagnosis: TVS using MUSA-criteria features (asymmetric myometrial thickening, myometrial cysts, fan-shaped shadowing, junctional-zone thickening) or MRI (junctional-zone thickening is the hallmark; T2 hyperintense foci).^[45] Treatment: LNG-IUS first-line (reduces bleeding and pain); hysterectomy is definitive for completed family. GnRH analogues and uterine-sparing procedures (adenomyomectomy) have limited efficacy. Adenomyosis is NOT the same as endometriosis — endometriosis is outside the uterus, adenomyosis is within the myometrium. ^[1]

Leiomyoma (L) — Fibroids: Benign smooth-muscle tumours, the commonest pelvic tumour. Ultrasound screening suggests a cumulative incidence of fibroids by age 50 of over 80 percent in Black women and around 70 percent in white women^[36]; reported prevalence ranges from 4.5 to 68.6 percent depending on the population and detection method. Black race is the factor most consistently associated with risk, two- to three-fold higher than white race.^[37] Classification by location:

• Submucosal (project into cavity) — most likely to cause heavy bleeding and infertility; type 0 (pedunculated intracavitary), type 1 (under 50 percent intramural), type 2 (over 50 percent intramural).
• Intramural (within wall) — commonest; cause HMB, dysmenorrhoea, bulk symptoms.
• Subserosal (project outward) — may cause pressure on bladder/bowel.
• Cervical, parasitic, intraligamentous — rarer locations. ^[1]

Malignant transformation to leiomyosarcoma is rare — the "rapid growth" sign has a low positive predictive value (rapidly growing fibroids are usually benign). Presentation: HMB, dysmenorrhoea, pressure symptoms (frequency, constipation), abdominal mass, infertility, pregnancy complications. Diagnosis: TVS (hypoechoic well-circumscribed mass); MRI for mapping before surgery. Treatment depends on symptoms, fertility wishes and fibroid size/location (see HMB management and surgical procedures). ^[1]

Malignancy and Hyperplasia (M): Endometrial hyperplasia and endometrial cancer are the critical diagnoses to not miss in any woman presenting with AUB, particularly postmenopausal bleeding. ^[1]

Endometrial hyperplasia is classified (WHO 2014) as:

• Hyperplasia without atypia — progression to carcinoma is uncommon: 1 percent of simple and 3 percent of complex hyperplasia in Kurman's classic series of untreated women; treat with progestogen (LNG-IUS or oral).^[35]
• Atypical hyperplasia — 8 percent of simple atypical and 29 percent of complex atypical hyperplasia progressed in the same series; treat with hysterectomy (or progestogen if fertility-sparing).^[35]

Endometrial cancer — commonest gynaecological malignancy in high-income countries; risk factors: obesity (unopposed oestrogen), nulliparity, late menopause, PCOS, tamoxifen, diabetes, Lynch syndrome, oestrogen-secreting tumours. Histology: endometrioid (type I, 80 percent) — oestrogen-related, good prognosis; serous/clear cell (type II) — aggressive, not oestrogen-related. Staging: surgical (FIGO 2009). Treatment: total abdominal hysterectomy + bilateral salpingo-oophorectomy ± lymphadenectomy; adjuvant radiotherapy/chemotherapy depending on stage and grade. ^[1]

Non-Structural Causes — COEIN (Detailed)

Coagulopathy (C): In 7–20 percent of menorrhagia the underlying cause is von Willebrand disease (vWD)^[22], and in women with vWD, menorrhagia from menarche occurs in 60–93 percent. Other causes add to this burden (platelet disorders, anticoagulants).^[22] Always screen for coagulopathy when HMB has been present since menarche, there is a family history of bleeding disorder, or there are other bleeding manifestations (epistaxis, gum bleeding, easy bruising, postpartum haemorrhage, post-surgical bleeding). Workup: FBC, coagulation screen (PT, APTT), von Willebrand factor antigen (vWF:Ag), ristocetin cofactor activity (vWF:RCo), factor VIII. Other causes: immune thrombocytopenia (ITP), platelet function disorders, anticoagulant therapy (warfarin, DOACs), haemophilia carrier. ^[1]

Ovulatory dysfunction (O): The commonest category of non-structural AUB. Causes include PCOS (most common — see below), thyroid dysfunction (both hypo- and hyperthyroidism cause menstrual irregularity), hyperprolactinaemia (suppresses GnRH), premature ovarian insufficiency, perimenopause, stress, weight loss, eating disorders, excessive exercise, and non-classic congenital adrenal hyperplasia. The hallmark is irregular, unpredictable cycles — anovulatory or oligo-ovulatory. Management targets the underlying cause. ^[1]

Endometrial (E): A primary disorder of endometrial haemostasis — the endometrium fails to mount the normal local vasoconstrictor (prostaglandin F2-alpha, endothelin) and platelet plug response, leading to excessive bleeding despite a structurally normal uterus and normal systemic haemostasis. Abnormal ratios of vasodilatory (PGE2, PGI2) to vasoconstrictor prostaglandins have been demonstrated. This is essentially a diagnosis of exclusion after other causes have been ruled out. ^[1]

Iatrogenic (I): Medication-induced AUB — hormonal contraception (breakthrough bleeding on COCP, POP, implant, injection, IUD), anticoagulants (warfarin, DOACs), SSRIs (platelet dysfunction), tamoxifen (endometrial stimulation and polyp formation), spironolactone (menstrual irregularity), and phenytoin/anticonvulsants. Management: address the medication if possible; if treatment must continue, add a progestogen or consider switching formulations. ^[1]

Not yet classified (N): Rare causes not fitting the above categories — uterine arteriovenous malformations (AVMs), Caesarean section scar defects (isthmoceles) causing postmenstrual spotting, non-tuberculous pelvic tuberculosis (in endemic regions), and chronic endometritis. ^[1]

Definitions

Clinical Assessment

History Taking

A structured menstrual history is the single most important diagnostic tool. The mnemonic "GOLIAD" captures the key parameters: Gravidity/parity, Onset, Length of cycle, Interval/duration, Amount, Dysmenorrhoea — but a more practical approach follows: ^[1]

Menstrual history:

• Age at menarche (delayed menarche suggests constitutional delay, eating disorder, or chromosomal abnormality; very early suggests precocious puberty)
• Cycle length (normal 21–35 days; under 21 = polymenorrhoea; over 35 = oligomenorrhoea)
• Cycle regularity (regular = likely ovulatory; irregular = anovulatory — PCOS, thyroid, perimenopause, POI)
• Duration of bleeding (average 4–6 days, normal range up to 8 days; prolonged beyond 8)
• Volume of bleeding — quantify using PBAC (Pictorial Blood Assessment Chart) score (over 100 = HMB); ask about pad/tampon count per day, passage of clots (over 1 inch), flooding, need for double protection, and interference with daily activities
• Pain — primary dysmenorrhoea: cramping suprapubic pain, day 1–2, no pathology; secondary: deep dyspareunia, cyclical bowel/bladder symptoms (endometriosis), progressive dysmenorrhoea (adenomyosis)
• IMB, PCB, PMB — each a red flag requiring specific workup ^[1]

Associated symptoms (system-directed):

• Weight change — weight loss (hypothalamic amenorrhoea, anorexia); weight gain (PCOS, hypothyroidism, Cushing syndrome)
• Hirsutism, acne, alopecia — androgen excess (PCOS, non-classic CAH, androgen-secreting tumour)
• Virilisation (clitoromegaly, deep voice, temporal balding) — androgen-secreting tumour (urgent)
• Galactorrhoea — hyperprolactinaemia (prolactinoma, drug-induced)
• Thyroid symptoms — heat/cold intolerance, palpitations, weight change, tremor
• Hot flushes, night sweats, vaginal dryness — premature ovarian insufficiency (under 40), perimenopause
• Cyclical pelvic pain, dyspareunia, dyschezia — endometriosis; dysuria haematuria — bladder endometriosis
• Pressure symptoms — urinary frequency, constipation, abdominal distension (fibroids) ^[1]

Past medical, surgical, drug and family history:

• Thyroid disease, diabetes, coagulation disorders, autoimmune disease
• Previous gynaecological surgery (LLETZ, cone biopsy — cervical stenosis/insufficiency)
• Medications: hormonal contraception, anticoagulants, SSRIs, tamoxifen, antipsychotics (hyperprolactinaemia), valproate
• Family history: endometrial/breast/ovarian/colorectal cancer (Lynch syndrome, BRCA), bleeding disorders, PCOS ^[1]

Red Flags

Other red flags requiring urgent investigation:

• Persistent postcoital bleeding — exclude cervical cancer (speculum, colposcopy, biopsy)
• Intermenstrual bleeding with weight loss or systemic symptoms — exclude endometrial/cervical malignancy
• HMB with anaemia refractory to iron — exclude coagulopathy (vWD), endometrial pathology
• Sudden change in menstrual pattern in a woman over 40 — exclude endometrial pathology
• New HMB after menopause (any bleeding) — endometrial cancer
• Virilisation (clitoromegaly, deep voice, frontal balding) — androgen-secreting tumour (urgent imaging and referral)
• Cyclical haematuria or rectal bleeding — deep infiltrating endometriosis ^[1]

Examination

General examination:

• BMI — under 18.5 (hypothalamic amenorrhoea, eating disorder, POI with weight loss); over 30 (PCOS, endometrial cancer risk, metabolic syndrome)
• Hirsutism — Ferriman-Gallwey score (the modified score is the standard visual grading tool for hirsutism; cut-offs vary with ethnicity and age); assess upper lip, chin, chest, abdomen, thighs, lower back
• Acne, acanthosis nigricans (insulin resistance in PCOS)
• Virilisation (clitoromegaly, deep voice, frontal balding, increased muscle mass — suggests androgen-secreting tumour)
• Galactorrhoea — expressible milky nipple discharge
• Thyroid — goitre, bruit, eye signs
• Stigmata of Turner syndrome — short stature, webbed neck, widely spaced nipples, low posterior hairline
• Stigmata of Cushing syndrome — moon face, buffalo hump, striae, proximal myopathy ^[1]

Abdominal examination:

• Distension, mass (fibroid uterus — smooth, firm, mobile, non-tender; 14–16 weeks size is palpable abdominally)
• Tenderness (endometriosis, PID)
• Hepatomegaly, ascites (in metastatic disease) ^[1]

Pelvic (bimanual) examination:

• Uterus — size (compare to weeks of pregnancy), mobility, contour, tenderness (enlarged/tender = adenomyosis; irregular = fibroids; fixed/retroverted = endometriosis)
• Cervix — excitation tenderness (cervical motion tenderness suggests PID/endo)
• Adnexae — masses (ovarian cyst, endometrioma), tenderness ^[1]

Speculum examination:

• Cervical appearance — ectropion, polyp, malignancy, discharge (infection)
• Take cervical screening if due (never assume abnormal bleeding is just a missed smear)
• Swabs if infection suspected (chlamydia, gonorrhoea NAAT) ^[1]

Investigation Strategy

Investigations are guided by the clinical picture, but a core panel applies to most presentations: ^[1]

^[1]

Heavy Menstrual Bleeding (HMB)

Definition and Impact

Heavy menstrual bleeding (HMB) is menstrual blood loss perceived by the woman as excessive, interfering with her physical, emotional, social and material quality of life — the current definition, which has replaced the classical objective cut-off.^[13] Classically, HMB was defined as 80 mL or more of blood loss per cycle, but women may complain of excessive bleeding even when loss is below that threshold.^[7] On the pictorial blood loss assessment chart (PBAC), a score of 100 or more identifies menorrhagia with sensitivity and specificity above 80 percent.^[12] HMB accounts for 12 percent of all UK gynaecology referrals.^[7]

^{[7] [12] [13] [22]}

NICE NG88 Management Algorithm

The NICE guideline NG88 (Heavy menstrual bleeding: assessment and management) provides a stepwise pharmacological-first approach: ^[7]

Step 1 — Levonorgestrel intrauterine system (LNG-IUS, Mirena 52 mg):

• First-line for ALL women with HMB and no identified pathology or small fibroids (under 3 cm) not distorting the cavity
• Releases 20 micrograms/day of levonorgestrel locally to the endometrium, causing endometrial atrophy and decidualisation
• Reduces menstrual blood loss by up to 90 percent^[13]
• Achieves a significant reduction in menstrual blood loss within 3 to 6 months of insertion (Mirena SPC)
• Licensed for 5 years in the HMB indication and 8 years for contraception
• Also treats dysmenorrhoea, endometriosis pain, and provides endometrial protection in women on oestrogen HRT
• Contraindications: active pelvic infection, distorted uterine cavity (large fibroids), current breast cancer, unexplained bleeding (investigate first), gestational trophoblastic disease
• Side effects: irregular spotting/bleeding for first 3–6 months (counsel and reassure — this is the main reason for early discontinuation), hormonal symptoms (headache, breast tenderness, mood change — usually mild)
• Allow 3–6 months before judging efficacy (significant reduction in blood loss is achieved within 3 to 6 months, Mirena SPC); counsel that bleeding is irregular in the first months — the commonest reason for early discontinuation

Step 2 — If LNG-IUS declined, unsuitable, or while awaiting its effect (NICE advises tranexamic acid and/or NSAIDs in the interim):^[24] Offer a non-hormonal or hormonal option based on contraceptive needs and patient preference: ^[7]

• Tranexamic acid — non-hormonal option taken during menses only: 1 g (two 500 mg tablets) three times daily for up to 4 days, maximum 4 g/day, started only once bleeding has begun (SPC); more effective at reducing blood loss than short-course (luteal-phase) cyclical progestogens.^[14]
• Mefenamic acid (or other NSAID) — non-hormonal option during menses (500 mg three times daily; SPC); inhibits prostaglandin synthesis (cyclooxygenase inhibition) and also relieves dysmenorrhoea.^[10]
• Combined oral contraceptive pill (COCP) — hormonal option that suppresses ovulation and regularises the cycle; one of the oral comparators against which the LNG-IUS achieved a greater reduction in blood loss.^[13]
• Cyclical oral progestogen — short luteal-phase courses (7–10 days; e.g. norethisterone 5 mg three times daily for 10 days, the licensed menorrhagia course) or longer 21-day-per-cycle regimens; Cochrane found short-cycle luteal progestogens inferior to other medical therapy including tranexamic acid and the LNG-IUS for reducing blood loss.^[14]

Step 3 — If pharmacological treatment fails (after 3 months of optimised therapy): Refer to specialist. Investigate for structural cause (TVS ± hysteroscopy) and consider second-line treatments: ^[7]

Surgical second-line options carry different effectiveness profiles: endometrial resection/ablation is less invasive than hysterectomy and offers an alternative, but women having it are more likely to need further surgery for treatment failure; hysterectomy is definitive.^[11]

Step 4 — Surgical management: ^[7]

If pharmacological management fails or is not appropriate, and structural causes have been identified and addressed: ^[7]

1. Endometrial ablation — for completed family, no desire for future pregnancy, normal cavity or small fibroids. See Surgical Procedures below.
2. Hysterectomy — definitive treatment; for failed medical/ablative therapy, large fibroids, coexisting pathology (prolapse, severe dysmenorrhoea), or patient preference.
3. Myomectomy — for fibroids when fertility preservation is desired.
4. Uterine artery embolisation (UAE) — minimally invasive option for symptomatic fibroids. ^[7]

HMB with Identified Structural Pathology

Fibroids (PALM-L): Treatment depends on size, location, symptoms, fertility wishes: ^[7]

Polyps (PALM-P): Hysteroscopic polypectomy (see-and-treat outpatient under local anaesthesia for small polyps; general anaesthesia for larger). Send all polyps for histology (malignancy risk higher in postmenopausal). ^[7]

Adenomyosis (PALM-A): LNG-IUS first-line; hysterectomy if completed family and refractory. GnRH analogues provide temporary relief. Adenomyomectomy (uterus-sparing) has high recurrence. ^[7]

Amenorrhoea

Definition and Classification

Amenorrhoea is the absence of menstrual periods. It is classified as: ^[9]

• Primary amenorrhoea — evaluate if menarche has not occurred by age 15 or within 3 years of thelarche; investigate delayed puberty if there is no pubertal development by age 13.^[16]
• Secondary amenorrhoea — absence of menses for 3 consecutive months in a woman with previously regular cycles, or 6 months in a woman with previously irregular cycles. ^[16]

Approach to Amenorrhoea — The Algorithm

ALWAYS do a pregnancy test (β-hCG) FIRST. Pregnancy is the commonest cause of secondary amenorrhoea — missing it is a catastrophic clinical error. ^[9]

After excluding pregnancy, the workup follows a functional/anatomical localisation approach — hypothalamus, pituitary, ovary, uterus/outflow tract — using three key hormones: FSH, prolactin, TSH. ^[9]

Step 1: β-hCG — exclude pregnancy. ^[9]

Step 2: TSH and prolactin — thyroid disease and hyperprolactinaemia are common, easily treated, and should be excluded before complex workup. ^[9]

• If TSH high → thyroid dysfunction is a recognised, treatable cause of menstrual disturbance; treat the thyroid disorder and re-assess the cycle.^[16]
• If prolactin elevated → confirm on repeat with the history reviewed for medication effects, galactorrhoea and thyroid dysfunction; pituitary imaging is individualised to the clinical picture rather than automatic.^[16]

Step 3: FSH and oestradiol — to localise the level of the defect: ^[9]

• Low or normal FSH with low oestradiol (hypogonadotropic hypogonadism) → hypothalamic or pituitary cause.
• High FSH with low oestradiol (hypergonadotropic hypogonadism) → ovarian failure (primary ovarian insufficiency).
• Normal FSH with normal oestradiol (eugonadotropic) → consider PCOS (most common), or uterine/outflow tract obstruction. ^[9]

Step 4: Targeted second-line testing — additional tests should be individualised to the clinical picture: karyotyping (e.g., primary amenorrhoea with absent uterus or short stature), serum androgen evaluation (hyperandrogenic features), and pelvic or brain imaging where indicated.^[16]

Step 5: Interpret and treat the cause — treatment should address the underlying cause: hormone replacement therapy, contraception or infertility services for POI; correction of energy deficit in functional hypothalamic amenorrhoea; screening and intervention for metabolic disease and endometrial cancer risk in PCOS.^[16]

Causes of Amenorrhoea (Comprehensive)

Hypothalamic causes (hypogonadotropic — low FSH/LH, low oestradiol):

• Functional hypothalamic amenorrhoea — stress, weight loss (BMI under 18.5), excessive exercise (the "female athlete triad" of low energy availability, menstrual dysfunction, low bone density), eating disorders (anorexia nervosa). The hypothalamic GnRH pulse generator is suppressed. Treatment: restore energy balance — increase caloric intake, reduce exercise, psychological support; HRT for bone protection if amenorrhoea persists.
• Kallmann syndrome — isolated GnRH deficiency with anosmia (absent sense of smell); X-linked or autosomal inheritance. MRI shows absent or hypoplastic olfactory bulbs. Treatment: pulsatile GnRH or gonadotropin therapy to induce ovulation; HRT for bone/cardiovascular health.
• Constitutional delay of puberty — delayed puberty in otherwise healthy adolescents (often familial); rule out organic causes first.
• Structural lesions — craniopharyngioma, glioma, tuberculosis, sarcoidosis, head trauma, cranial irradiation.
• Drugs — antipsychotics (hyperprolactinaemia), chronic opioid use, GnRH agonists. ^[9]

Pituitary causes (hypogonadotropic):

• Hyperprolactinaemia — prolactinoma (micro under 10 mm or macro over 10 mm), drug-induced (antipsychotics, metoclopramide, opiates), hypothyroidism (TRH stimulates prolactin), pregnancy/lactation, renal/hepatic failure. Presents with amenorrhoea, galactorrhoea, infertility, and (macroadenoma) headaches, visual field defects (bitemporal hemianopia from optic chiasm compression). Treatment: dopamine agonists (e.g. cabergoline) are the cornerstone of prolactinoma pharmacotherapy.^[41][40]
• Sheehan syndrome — pituitary infarction following postpartum haemorrhage (hypovolaemic shock); panhypopituitarism. Presents with failure to lactate, persistent amenorrhoea, hypothyroidism, adrenal insufficiency. Treatment: replacement of all deficient hormones (hydrocortisone, levothyroxine, sex steroids, GH).
• Other pituitary tumours — non-functioning adenoma, Cushing disease (ACTH-secreting), acromegaly (GH-secreting).
• Empty sella syndrome — herniation of subarachnoid space into sella turcica. ^[9]

Ovarian causes (hypergonadotropic — high FSH over 25 IU/L, low oestradiol):

• Premature ovarian insufficiency (POI) — loss of normal, predictable ovarian activity before age 40, characterised by amenorrhoea (primary or secondary) with raised circulating FSH.^[17] At least 1 in 100 women is affected, including 1 in 1000 before the age of 30.^[17] Causes: unknown in most patients (with a substantial genetic basis — chromosomal anomalies and gene variants), plus autoimmune disease, infections, and medical interventions such as ovarian surgery or cytotoxic cancer therapy.^[17] Diagnosis (2024 ESHRE guideline): a single elevated FSH over 25 IU/L now suffices when there is diagnostic certainty (repeat FSH and/or AMH where uncertain); the same guideline reports new prevalence data suggesting POI may affect up to 3.5 percent of women.^[18] Treatment: hormone therapy — mitigates the adverse effects on bone, cardiovascular and cognitive health; the guideline also updates recommendations on oestrogen doses and regimens, the combined oral contraceptive and testosterone therapy.^[18] Women with POI can maintain unpredictable ovarian function and may need contraception or fertility services alongside HRT.^[16]
• Turner syndrome (45,X) — streak ovaries, short stature, webbed neck, widely spaced nipples, coarctation of aorta, renal anomalies. Diagnosis: karyotype. Treatment: growth hormone in childhood, oestrogen replacement for puberty induction and bone health.
• Surgical/radiation/chemotherapy-induced ovarian failure — counsel before treatment; consider fertility preservation (egg/embryo freezing, ovarian tissue cryopreservation).
• Physiological menopause — average age 51; diagnosis clinical (over 12 months amenorrhoea with vasomotor symptoms); FSH is NOT needed routinely if over 45. ^[9]

Uterine and outflow tract causes (normal hormones):

• Asherman syndrome (intrauterine adhesions/synechiae) — scarring of the endometrium, typically after dilation and curettage (especially postpartum or post-miscarriage), endometritis, or uterine surgery. Presents with secondary amenorrhoea or hypomenorrhoea, cyclical pain (if outflow blocked), infertility, recurrent miscarriage. Diagnosis: hysteroscopy (gold standard — direct visualisation of adhesions); TVS, SIS, hysterosalpingography may suggest. Treatment: hysteroscopic adhesiolysis under direct vision, followed by oestrogen therapy (to regenerate endometrium) and IUD (to prevent re-adhesion). Recurrence rate high; pregnancy outcomes variable.
• Mullerian agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome) — congenital absence of uterus and upper two-thirds of vagina; normal ovaries, normal secondary sex characteristics, normal karyotype (46,XX). A leading cause of primary amenorrhoea after gonadal dysgenesis. Associated malformations: renal malformation in 13.1 percent and skeletal malformation in 39.2 percent of a 274-case cohort.^[44] Diagnosis: karyotype (46,XX), normal hormones, absent uterus on ultrasound/MRI. Treatment: vaginal dilators or vaginoplasty (for sexual function); fertility requires surrogacy (patient's own eggs). Psychological support essential.
• Imperforate hymen — presents at puberty with cyclical pelvic pain, primary amenorrhoea, haematocolpos (bulging bluish membrane on inspection). Treatment: cruciate incision of hymen. Transverse vaginal septum and cervical atresia are rarer obstructive causes.
• Complete androgen insensitivity syndrome (CAIS) — 46,XY karyotype, non-functional androgen receptor; phenotypic female, normal breast development (aromatised testosterone), scanty/absent pubic and axillary hair, blind-ending vagina, no uterus (Mullerian structures absent due to AMH from testes), intra-abdominal testes (high malignancy risk — gonadectomy after puberty). Presents with primary amenorrhoea. Diagnosis: karyotype (46,XY), high testosterone (male range), no uterus on imaging. Treatment: gonadectomy after completion of breast development; oestrogen replacement; vaginal dilators.
• Cervical stenosis — post-surgical (cone biopsy, LLETZ), post-radiation; causes obstructive amenorrhoea with cyclical pain. ^[9]

Primary Amenorrhoea Workup Summary

Polycystic Ovary Syndrome (PCOS)

Definition and Epidemiology

PCOS is the commonest endocrine disorder in reproductive-age women, affecting around 1 in 8 women per the 2023 International PCOS Guideline (older estimates 6–10 percent).^[46] It is the leading cause of anovulatory infertility. ^[2]

Rotterdam Diagnostic Criteria

The Rotterdam criteria (2003 consensus, revised) require 2 of 3 features after exclusion of other causes:^[2]

1. Oligo-ovulation or anovulation — menstrual irregularity: oligomenorrhoea or amenorrhoea.^[2]
2. Hyperandrogenism — clinical signs of androgen excess (hirsutism, acne, alopecia) and/or biochemical hyperandrogenism.^[2]
3. Polycystic ovarian morphology on ultrasound — no single criterion is sufficient alone; the Endocrine Society recommends the Rotterdam framework with exclusion of alternate androgen-excess disorders. ^[15]

Before diagnosing PCOS, exclude: congenital adrenal hyperplasia (17-OH progesterone), androgen-secreting tumour (very high testosterone/DHEAS), Cushing syndrome, thyroid dysfunction, hyperprolactinaemia. ^[2]

NIH criteria (1990) require hyperandrogenism plus ovulatory dysfunction; the AE-PCOS Society (2006) requires hyperandrogenism plus 1 of the 2 remaining criteria (ovulatory dysfunction or PCOM).^[15] Rotterdam is the broadest and most widely used, capturing more phenotypes. ^[2]

Pathophysiology

The pathophysiology is multifactorial and incompletely understood: ^[2]

• Insulin resistance — common in PCOS (independent of obesity); hyperinsulinaemia stimulates ovarian androgen production and reduces SHBG (raising free testosterone). This is the rationale for metformin use.^[15]
• Hypothalamic-pituitary dysfunction — increased GnRH pulse frequency favours LH over FSH, producing elevated LH:FSH ratio (often over 2:1). High LH stimulates theca cells to produce excess androstenedione and testosterone.
• Ovarian follicular arrest — high androgen and insulin environment arrests follicular development at the 2–9 mm stage, producing the characteristic "string of pearls" appearance.
• Low SHBG — from insulin resistance and androgens — raises free (bioavailable) testosterone.
• Adrenal androgen excess — DHEAS may be elevated. ^[2]

Clinical Features

Management

Management is symptom-directed — there is no cure. The approach depends on the woman's primary concern. ^[2]

1. Lifestyle (all women):

• Lifestyle intervention — beneficial in overweight/obese women with PCOS for broader health benefits, although the role of weight loss in improving PCOS per se is uncertain.^[15]
• Exercise — part of lifestyle intervention; supports weight management.
• Diet — caloric deficit for weight loss where overweight/obese. ^[15]

2. Menstrual irregularity and endometrial protection:

• Hormonal contraceptives (COCP) — first-line management for menstrual abnormalities (and for hirsutism/acne) in PCOS; regularises cycles and protects the endometrium from unopposed oestrogen.^[15]
• Cyclical progestogen — alternative for endometrial protection where hormonal contraceptives are unsuitable.
• Metformin — beneficial for metabolic/glycaemic abnormalities and improves menstrual irregularities, but has limited or no benefit for infertility.^[15]

3. Hirsutism and acne:

• Hormonal contraceptives (COCP) — first-line pharmacological management for hirsutism and acne in PCOS; allow an adequate trial before judging effect.^[15]
• Cosmetic — electrolysis, laser hair removal, waxing, bleaching (adjunctive).
• Metformin — limited or no benefit for hirsutism or acne; do not rely on it as the primary strategy for androgenic symptoms.^[15]

4. Fertility (anovulatory infertility):

• Lifestyle intervention — first step in overweight/obese women, for general health benefit (its direct effect on ovulation is uncertain).^[15]
• Letrozole — aromatase inhibitor. The PPCOS II trial (Legro et al., NEJM 2014) found letrozole superior to clomiphene for live birth (27.5 percent vs 19.1 percent) and cumulative ovulation (61.7 percent vs 48.3 percent); twin pregnancy rates were 3.4 percent (letrozole) vs 7.4 percent (clomiphene).^[3]
• Clomiphene citrate — was the first-line infertility treatment when the Endocrine Society guideline was published; PPCOS II showed letrozole achieves higher live-birth and ovulation rates.^[15][3]
• Metformin — beneficial for metabolic/glycaemic abnormalities and menstrual irregularities, but of limited or no benefit for infertility itself.^[15]

5. Long-term metabolic health:

• Evaluate for endometrial cancer risk factors, mood disorders, obstructive sleep apnoea, diabetes and cardiovascular disease (Endocrine Society)^[15] — annual BMI, blood pressure and fasting glucose/HbA1c is conventional.
• Screen for obstructive sleep apnoea (STOP-BANG questionnaire).
• Mental health screening for anxiety and depression. ^[2]

Endometriosis

Definition and Pathophysiology

Endometriosis is the presence of endometrial glands and stroma outside the uterine cavity, most commonly on the ovaries (endometriomas), peritoneum, uterosacral ligaments, pouch of Douglas, bladder, and bowel. It affects approximately 10 percent of women of reproductive age and is strongly associated with infertility and chronic pelvic pain.^[42]

Theories of pathogenesis: retrograde menstruation (Sampson, most widely accepted — menstrual tissue flows back through tubes into pelvis), coelomic metaplasia (peritoneal cells transform into endometrial cells), Mullerian remnants, lymphatic/haematogenous spread, and immune dysfunction (failure to clear ectopic endometrial cells). ^[4]

Clinical Features

• Dysmenorrhoea (secondary, progressive)
• Deep dyspareunia (from uterosacral/rectovaginal disease)
• Chronic pelvic pain (non-cyclical)
• Dyschezia (painful defecation, especially with deep infiltrating disease)
• Cyclical dysuria/haematuria (bladder endometriosis)
• Infertility (inflammatory environment, distorted anatomy, ovulatory dysfunction)
• Examination: tender nodularity in the pouch of Douglas, fixed retroverted uterus, tender adnexae, bluish lesions on cervix/vagina (rare) ^[4]

Diagnosis

• Laparoscopy with biopsy is the gold standard for definitive diagnosis (histology: endometrial glands + stroma + haemosiderin-laden macrophages).
• TVS — first-line for ovarian endometriomas (homogenous hypoechoic "ground glass" cyst with no papillations); also for deep infiltrating endometriosis (specialised technique).
• MRI — for deep infiltrating endometriosis mapping (bowel, bladder, ureter).
• CA-125 — may be elevated (non-specific; not for diagnosis or screening; useful for monitoring response).
• Empirical treatment — NICE NG73 advises offering hormonal treatment to women with suspected (as well as confirmed or recurrent) endometriosis, so treatment can start without laparoscopic confirmation when features are typical; laparoscopy is reserved for diagnostic uncertainty or treatment failure.^[26]

Management

^[4]

Pain management (NICE NG73, ESHRE guideline): ^[4]

1. Paracetamol or an NSAID — NICE NG73 advises a short trial (for example, 3 months) of paracetamol or an NSAID, alone or in combination, for first-line management of endometriosis-related pain; NSAIDs inhibit prostaglandin synthesis (cyclooxygenase inhibition).^[26][10]
2. Hormonal treatments — NG73: "Offer hormonal treatment (for example, the combined oral contraceptive pill or a progestogen) to women with suspected, confirmed or recurrent endometriosis"; hormonal treatment reduces pain without permanently harming subsequent fertility.^[26]
3. GnRH analogues — ESHRE's 83 recommendations cover treatment of pain, infertility, incidentally found disease, recurrence prevention and menopausal symptoms.^[4] GnRH agonists (e.g. goserelin 3.6 mg every 28 days) are used for endometriosis for 6 months only, with add-back HRT to reduce bone-mineral-density loss and vasomotor symptoms (Zoladex SPC); NICE 2025 technology appraisals add oral GnRH antagonists (relugolix, linzagolix) with add-back therapy.^[26]

Surgical management (laparoscopic):

• Laparoscopic excision (ablation) of endometriotic deposits — for pain refractory to medical therapy, or diagnostic laparoscopy with treatment.
• Ovarian endometrioma — laparoscopic cystectomy (excision preferred over drainage/ablation; higher recurrence with ablation); protect ovarian reserve (avoid excessive diathermy).
• Deep infiltrating endometriosis (DIE) — laparoscopic excision of bowel, bladder, ureteric involvement; multidisciplinary team (gynaecologist, colorectal surgeon, urologist).
• Presacral neurectomy / laparoscopic uterosacral nerve ablation (LUNA) — for refractory central pelvic pain; limited evidence. ^[4]

Fertility management:

• Surgical excision of mild–moderate endometriosis improves spontaneous pregnancy rates.
• Ovarian endometrioma cystectomy before IVF may improve outcomes (controversial — balance ovarian reserve loss vs improved access).
• IUI with stimulation for minimal–mild disease, unexplained infertility.
• IVF for moderate–severe disease, tubal involvement, male factor, or failed surgery/IUI. ^[4]

Endometriosis is a chronic disease — recurrence of pain and disease after surgery is common; long-term hormonal suppression is used to reduce recurrence. Provide psychological support and refer to endometriosis support groups. ^[4]

Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD)

Definition

Premenstrual syndrome (PMS) is a cluster of recurrent somatic and psychological symptoms occurring during the luteal phase of the menstrual cycle, resolving within a few days of menstruation, causing significant distress or functional impairment. ^[5]

Premenstrual dysphoric disorder (PMDD) is the severe, predominantly psychological form of PMS, formally recognised in DSM-5 (2013). It affects at least 5–8 percent of women of reproductive age.^[20]

DSM-5 Criteria for PMDD

The DSM-5 requires 5 or more of the following symptoms in the week before menses, improving within a few days after onset, with at least one being a core symptom (marked with asterisk): ^[5]

1. Marked affective lability (mood swings, sudden sadness/tearfulness, increased sensitivity to rejection)
2. Marked irritability or anger or increased interpersonal conflicts
3. Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts
4. Marked anxiety, tension, and/or feelings of being keyed up or on edge
5. Decreased interest in usual activities
6. Subjective difficulty concentrating
7. Lethargy, easy fatigability, marked lack of energy
8. Changes in appetite (food cravings, overeating)
9. Hypersomnia or insomnia
10. Sense of being overwhelmed or loss of control
11. Physical symptoms (breast tenderness, bloating, weight gain, joint/muscle aches, headache) ^[5]

Additional requirements:

• Symptoms severe enough to interfere with work, school, usual activities, or relationships
• NOT merely an exacerbation of another disorder (e.g., depression, anxiety, bipolar)
• Confirmed by prospective daily symptom ratings over at least 2 symptomatic cycles (retrospective reporting is unreliable — the symptom diary is essential) ^[5]

Pathophysiology

PMDD is thought to be due to altered CNS sensitivity to normal circulating levels of oestrogen and progesterone (and their neuroactive metabolites) — the hormones themselves are normal, but the brain's response is abnormal. Key mechanisms: ^[5]

• Allopregnanolone (a progesterone metabolite) — a positive allosteric modulator of GABA-A receptors; in PMDD, this response is paradoxical or deficient, producing irritability and anxiety.
• Serotonergic dysregulation — reduced serotonergic activity in the luteal phase.
• Calcium dysregulation — altered parathyroid hormone and calcium metabolism across the cycle (Thys-Jacobs et al.)^[8]
• Genetic component: PMDD runs in families; stress and trauma are risk factors.

Management

^{[5] [19] [21]}

SSRI protocols for PMDD: The Cochrane review (Marjoribanks et al., 2013) confirmed SSRIs are effective for PMDD, with continuous and luteal-phase-only dosing both effective.^[5]

• Sertraline symptom-onset dosing was tested in a randomised controlled trial of 252 women with PMDD (125 sertraline, 127 placebo): benefit depended on the symptom scale — some secondary scales favoured sertraline, the primary scale did not.^[21] Luteal-phase dosing of sertraline is proven effective and sertraline is FDA-approved for PMDD.^[20]
• Other SSRIs with trial evidence: fluoxetine, paroxetine, citalopram, escitalopram — continuous or luteal-phase-only dosing.^[5]
• Onset is faster in PMDD than in depression — clinical response is reported within several days of starting treatment.^[20]
• Luteal-phase-only dosing is as effective as continuous dosing, minimises adverse effects and reduces the burden of long-term daily medication.^[5][20]
• Side effects: at moderate dose, nausea (NNH 7) and asthenia/decreased energy (NNH 9) are the most common; adverse effects are dose-related.^[5]

GnRH analogues for PMDD: specialist endocrine suppression is occasionally used in refractory PMDD, but the first-line pharmacological evidence base is for SSRIs, and no specific GnRH regimen for PMDD is supported by the sources cited here. If symptoms are refractory to SSRI therapy (continuous and luteal-phase dosing), refer for specialist gynaecological and psychiatric assessment. ^[5]

Postmenopausal Bleeding (PMB)

Definition

Postmenopausal bleeding (PMB) is any vaginal bleeding occurring 12 months or more after the last menstrual period. It is always abnormal and requires urgent investigation. The pooled risk of endometrial cancer among women with PMB is 9 percent (95% CI 8–11), varying from 5 to 13 percent by region and hormone use; 91 percent of women with endometrial cancer report PMB.^[34] Risk factors (obesity, nulliparity, tamoxifen, late menopause, diabetes, unopposed oestrogen, Lynch syndrome) raise the risk further. Other causes include endometrial polyps, atrophic vaginitis, endometrial hyperplasia, cervical cancer, hormone replacement therapy, and (rarely) ovarian or fallopian tube cancer. ^[6]

Workup Algorithm

Step 1 — Clinical assessment:

• Confirm bleeding is from the uterus (not rectal, urinary, or vaginal atrophy)
• History: timing, amount, risk factors for endometrial cancer, HRT use, bleeding pattern
• Examination: speculum (exclude cervical/vaginal source), bimanual ^[6]

Step 2 — Transvaginal ultrasound (TVS):

• Measure endometrial thickness (ET) — double-layer measurement
• Accuracy of the thickness cut-off (Smith-Bindman et al., JAMA 1998): using a 5-mm threshold to define abnormal thickening, 96 percent (95% CI 94–98) of women with cancer had an abnormal EVUS result (92 percent for any endometrial disease); specificity 92 percent in women not on HRT. Action thresholds vary between units (4–5 mm); HRT and tamoxifen raise baseline thickness.^[6]

Step 3 — Hysteroscopy and endometrial biopsy:

• Gold standard for endometrial assessment — direct visualisation of cavity + targeted biopsy
• Outpatient hysteroscopy with Pipelle biopsy (or similar) is standard
• General anaesthesia if outpatient not tolerated or anticipated difficult procedure
• Biopsy all focal lesions (polyps) — send for histology ^[6]

Step 4 — Manage based on histology:

• Atrophic endometrium — reassure; consider topical oestrogen for atrophic vaginitis
• Endometrial polyp — hysteroscopic polypectomy
• Endometrial hyperplasia without atypia — LNG-IUS or oral progestogen; surveillance biopsy at 3–6 months
• Atypical hyperplasia / endometrial cancer — refer to gynaecological oncology; total hysterectomy + BSO ± staging ^[6]

Exam application bank (NEET-PG / INICET)

One-line answer

Menstrual disorders encompass abnormalities in menstrual cycle frequency, duration, volume, or associated symptoms. FIGO PALM-COEIN classification (2011/2018) categorises abnormal uterine bleeding: Polyps, Adenomyosis, Leiomyoma, Malignancy/hyperplasia (structural); Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified (non-structural). Management follows NICE NG88: LNG-IUS first-line for HMB; tranexamic acid/mefenamic acid/COCP alternatives.

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. ^[1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. ^[1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. ^[1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. ^[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. ^[1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Menstrual Disorders.

Dysmenorrhoea

Primary Dysmenorrhoea

Primary dysmenorrhoea is painful menstruation without pelvic pathology. It is due to increased prostaglandin (PGF2-alpha) production by the endometrium during menses, causing uterine hypercontractility, vasoconstriction, and ischaemia. Very common in adolescent women. Presents as cramping suprapubic pain radiating to lower back and thighs, starting just before or at onset of menses, lasting 24–72 hours, with nausea, vomiting, diarrhoea, headache, fatigue. ^[10]

Management:

1. NSAIDs — first-line; inhibit prostaglandin synthesis by blocking cyclooxygenase. Across 35 placebo-controlled RCTs, NSAIDs more than quadrupled the odds of moderate/excellent pain relief (OR 4.37) — about 45–53 percent of women achieve relief with NSAIDs versus 18 percent with placebo — at the cost of more adverse effects (notably gastrointestinal).^[10]
2. No single NSAID has been shown to be the safest or most effective — the Cochrane review found insufficient evidence to choose between individual agents.^[10]
3. If pain does not respond adequately to NSAIDs, or the history is atypical for primary dysmenorrhoea, investigate for secondary causes. ^[10]

Secondary Dysmenorrhoea

Secondary dysmenorrhoea is painful menstruation due to pelvic pathology. Typical features: onset years after menarche (after age 20), progressive, dull aching/bearing-down pain starting days before menses, persisting throughout and after menses, not relieved by NSAIDs/COCP. ^[10]

Surgical Procedures

Hysteroscopy

Hysteroscopy is the gold standard for evaluation of the uterine cavity, allowing direct visualisation and treatment of intracavitary pathology. ^[11]

Technique:

• Timing — proliferative phase (day 6–10 of cycle) for best visualisation; endometrium is thin. Exception: investigation of PMB (any time).
• Pre-procedure — pregnancy test, cervical screening up to date, vaginal swabs if infection suspected. Consider cervical priming (misoprostol or laminaria tent) in nulliparous women: misoprostol significantly eases cervical dilatation before hysteroscopy (except in postmenopausal women) at the cost of more adverse effects (systematic review).^[43]
• Anaesthesia — outpatient (no anaesthesia or paracervical block), conscious sedation, or general anaesthesia.
• Distension medium — normal saline (most modern hysteroscopes); historically glycine 1.5 percent (for monopolar diathermy — risk of hyponatraemia/TURP syndrome). Use the lowest effective distension pressure and monitor the fluid deficit to limit intravasation.
• Technique — bimanual exam, sterile prep, visualise cervix, insert hysteroscope under direct vision, advance through cervical canal into cavity, systematically inspect fundus, anterior/posterior/lateral walls, tubal ostia. Identify and treat pathology: polyps (polypectomy), submucosal fibroids (resection/morcellation), septum (metroplasty), adhesions (adhesiolysis), retained products.
• Post-procedure — mild cramping and spotting for 1–2 days; resume normal activities next day. ^[11]

Indications: abnormal uterine bleeding (especially IMB, PMB), suspected polyps/fibroids, infertility workup, recurrent miscarriage, Asherman syndrome, suspected congenital anomaly, retained products of conception, localisation/removal of lost IUD. ^[11]

Complications: uterine perforation (rare, but the most significant — if suspected, stop, observe, and consider laparoscopy), bleeding, infection (endometritis), cervical trauma, fluid intravasation (hyponatraemia with hypotonic media), vasovagal reaction. ^[11]

Endometrial Ablation

Endometrial ablation destroys the endometrial lining to reduce or eliminate menstrual flow. For women with HMB who have completed their family, have no malignancy on biopsy, and have a normal-sized or slightly enlarged uterus. ^[11]

Pre-requisites:

• Endometrial biopsy to exclude malignancy/atypia (mandatory before ablation)
• Completed family — pregnancy after ablation is high-risk (miscarriage, ectopic, abnormal placentation); contraception is essential
• Normal or small cavity (large fibroids/cavity distortion is relative contraindication)
• No active pelvic infection
• No desire for future pregnancy ^[11]

First-generation (hysteroscopic):

• Transcervical resection of endometrium (TCRE) — hysteroscopic resectoscope with electrocautery loop; removes endometrium to basalis layer. Requires hysteroscopic skill; risk of perforation, fluid overload.
• Rollerball ablation — hysteroscopic electrocautery rollerball coagulates endometrium. ^[11]

Second-generation (non-hysteroscopic, global): NICE recommends second-generation endometrial ablation (NG88), with fluid-filled thermal balloon and microwave ablation techniques appraised in TA78:

• Bipolar radiofrequency devices (e.g. NovaSure) — brief, operator-independent treatment.
• Fluid-filled thermal balloon ablation.
• Free-flow heated-saline ablation.
• Microwave endometrial ablation (MEA).^[24]

Outcomes (Cochrane 2021, EA/ER vs hysterectomy):^[11]

• Satisfaction at 1 year is similar to hysterectomy (RR 0.91 vs open hysterectomy); quality of life at 2 years similar
• Women choosing EA/ER over open hysterectomy accept a 13 percent risk of requiring further surgery for treatment failure (0 percent after hysterectomy)
• Advise avoidance of pregnancy and effective contraception after ablation (NG88)^[24]

Contraindications: pregnancy desire, malignancy/hyperplasia, active pelvic infection, large cavity (over 12 cm), submucosal fibroids over 3 cm (relative), previous classical Caesarean (thin isthmic scar). ^[11]

Hysterectomy

Hysterectomy — surgical removal of the uterus — is the definitive treatment for many benign gynaecological conditions (HMB, fibroids, adenomyosis, endometriosis, prolapse) and for gynaecological malignancy. ^[11]

Types by extent:

• Total hysterectomy — uterus and cervix removed (most common)
• Subtotal/supracervical hysterectomy — uterine body removed, cervix retained (some evidence of less sexual/urinary dysfunction; cervix needs continued screening)
• Total hysterectomy with bilateral salpingo-oophorectomy (BSO) — for endometrial/cervical/ovarian cancer, prophylactic (BRCA), or menopausal women
• Radical (Wertheim) hysterectomy — uterus, cervix, upper vagina, parametrium, and pelvic lymph nodes; for early cervical cancer ^[11]

Routes (in order of preference per NICE): ^[11]

1. Vaginal hysterectomy — preferred route where feasible; no abdominal incision, fastest recovery, lowest complication rate. Indications: prolapse, mobile uterus under 12 weeks size. Contraindications: very large uterus, restricted access, suspected malignancy, need for abdominal exploration.
2. Laparoscopic hysterectomy — total laparoscopic (TLH), laparoscopically assisted vaginal (LAVH), or subtotal laparoscopic. Minimally invasive; faster recovery than open; longer operative time; requires advanced laparoscopic skill. Preferred over abdominal where vaginal not feasible.
3. Abdominal hysterectomy — open approach (Pfannenstiel or midline incision); reserved for large masses, malignancy requiring open staging, severe adhesions, or when laparoscopic/vaginal approaches not feasible. Highest morbidity, longest recovery, most postoperative pain. ^[11]

Pre-operative: consent (must discuss ovaries, HRT, bladder/bowel/sexual function, prolapse risk, vaginal cuff dehiscence), anaesthetic assessment, VTE prophylaxis (LMWH, TEDS), antibiotic prophylaxis, bowel prep (selected cases), crossmatch if anticipated blood loss. ^[11]

Post-operative recovery: vaginal — 2–4 weeks; laparoscopic — 2–4 weeks; abdominal — 4–6 weeks. Avoid heavy lifting, intercourse, tampons for 6 weeks. ^[11]

Complications:

• Early — bleeding, infection (wound, urinary, pelvic), visceral injury (uncommon: in the Finnish national register, ureter lesions 0.3–1.1 percent after laparoscopic and bowel lesions 0.1–0.5 percent after vaginal hysterectomy)^[39], VTE (DVT/PE)
• Late — vault prolapse, possible loss of ovarian function even when ovaries are retained (warn women, NG88)^[24], sexual dysfunction, urinary incontinence, adhesions/obstruction, vault dehiscence (laparoscopic risk), pelvic pain ^[11]

Oophorectomy decision: If under 45, conserve ovaries (consider BSO for BRCA, Lynch, strong family history). If 45–51, discuss risks/benefits — conserving avoids surgical menopause. If over 51, BSO is generally offered (natural menopause age reached). Consensus varies by guideline. ^[11]

Drug Dosing Quick Reference

Complications and Follow-up

Iron-deficiency anaemia — a recognised consequence of chronic menstrual blood loss; diagnose by blood testing and treat with iron replacement therapy (oral or intravenous route), combined with investigation and treatment of the underlying cause of bleeding.^[23]

Endometrial hyperplasia/cancer — women with untreated chronic anovulation (PCOS, POI, obesity, oestrogen-secreting tumour) are at risk of unopposed oestrogen-driven endometrial proliferation. All women with over 3 months amenorrhoea due to anovulation should receive cyclical progestogen or LNG-IUS for endometrial protection. Surveillance biopsy for hyperplasia: without atypia every 3–6 months until regression; atypical — refer for hysterectomy. ^[11]

Bone health (POI, hypothalamic amenorrhoea) — long-term oestrogen deficiency adversely affects bone density (and cardiovascular and neurological health); hormone therapy mitigates these effects and is a core component of POI management.^[18] Functional hypothalamic amenorrhoea may signal disordered eating and low bone density, so bone health must be addressed there too.^[16]

Cardiovascular disease (POI) — POI has far-reaching implications for cardiovascular and cognitive health; hormone therapy mitigates some of these effects.^[18]

Infertility — PCOS (letrozole/clomiphene), POI (donor egg IVF), endometriosis (surgery/IUI/IVF), Asherman (adhesiolysis). NICE NG257: offer assessment after 12 months of unprotected intercourse without conception, and at presentation if the woman is 36 or over or there is a suspected/known cause.^[32]

Psychological impact — menstrual disorders significantly affect quality of life, mental health, sexual function, and productivity. Screen for anxiety, depression, eating disorders, and relationship strain. Offer psychological support, CBT, and support groups. ^[11]

Exam Tips and High-Yield Points

Top 10 exam points: ^[1]

1. LNG-IUS is the most effective medical treatment for HMB — users report blood-loss reductions of up to 90 percent, and it beats oral medical therapy for reducing loss and improving quality of life.^[13]
2. PMB = investigate to exclude endometrial cancer; using a 5-mm endometrial-thickness threshold on TVS detects 96 percent of endometrial cancers.^[6]
3. β-hCG FIRST in all amenorrhoea — every patient should be offered a pregnancy test plus FSH, LH, prolactin and TSH.^[16]
4. Raised FSH over 25 IU/L with amenorrhoea before age 40 = premature ovarian insufficiency (2024 ESHRE guideline: a single elevated FSH suffices); treat with hormone therapy to protect bone and cardiovascular health.^[18]
5. PCOS (Rotterdam) = 2 of 3 criteria (androgen excess, ovulatory dysfunction, polycystic ovaries); letrozole beats clomiphene for live birth (PPCOS II: 27.5 percent vs 19.1 percent).^[15][3]
6. von Willebrand disease underlies 7–20 percent of menorrhagia — consider it, especially with heavy bleeding since menarche.^[22]
7. SSRIs first-line for PMDD (sertraline, fluoxetine); luteal-phase or continuous dosing both effective.^[5]
8. Endometriosis — start empirical medical treatment (NSAIDs, COCP, LNG-IUS, progestogen) without laparoscopy if clinical picture typical (NICE NG73, ESHRE).^[4]
9. Atypical endometrial hyperplasia = 29 percent of complex atypical cases progress to carcinoma in Kurman's classic series → hysterectomy (not progestogen).^[35]
10. Kallmann syndrome = hypogonadotropic hypogonadism + anosmia; Sheehan syndrome = postpartum pituitary infarction → panhypopituitarism.

^{[1] [1]}

Summary

Menstrual disorders are common, impactful, and excellent exam topics because they test reproductive physiology, pharmacology, and clinical reasoning. The PALM-COEIN framework structures the approach to abnormal uterine bleeding; the HPO axis underpins the classification of amenorrhoea; NICE NG88 guides HMB management with LNG-IUS first-line; Rotterdam criteria diagnose PCOS with letrozole first-line for fertility; NICE NG73 guides endometriosis; DSM-5 criteria diagnose PMDD with SSRIs first-line; and PMB mandates TVS and biopsy to exclude endometrial cancer. A structured, algorithmic approach — always starting with a pregnancy test in amenorrhoea — will serve both patient and examiner well. ^[1]

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References40ShowHide

1. [1]Munro MG, Critchley HO, Broder MS, et al. FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age Int J Gynaecol Obstet, 2011.PMID 21345435
2. [2]Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome Fertil Steril, 2004.PMID 14711538
3. [3]Legro RS, Brzyski RG, Diamond MP, et al. Letrozole versus clomiphene for infertility in the polycystic ovary syndrome N Engl J Med, 2014.PMID 25006718
4. [4]Dunselman GA, Vermeulen N, Becker C, et al. ESHRE guideline: management of women with endometriosis Hum Reprod, 2014.PMID 24435778
5. [5]Marjoribanks J, Brown J, O'Brien PM, Wyatt K. Selective serotonin reuptake inhibitors for premenstrual syndrome Cochrane Database Syst Rev, 2013.PMID 23744611
6. [6]Smith-Bindman R, Kerlikowske K, Feldstein VA, et al. Endovaginal ultrasound to exclude endometrial cancer and other endometrial abnormalities JAMA, 1998.PMID 9809732
7. [7]Lethaby A, Hussain M, Rishworth JR, Rees MC. Progesterone or progestogen-releasing intrauterine systems for heavy menstrual bleeding Cochrane Database Syst Rev, 2015.PMID 25924648
8. [8]Thys-Jacobs S, McMahon D, Bilezikian JP. Cyclical changes in calcium metabolism across the menstrual cycle in women with premenstrual dysphoric disorder J Clin Endocrinol Metab, 2007.PMID 17488795
9. [9]Practice Committee of the American Society for Reproductive Medicine. Electronic address: asrm@asrm.org Current evaluation of amenorrhea: a committee opinion. Fertil Steril, 2024.PMID 38456861
10. [10]Marjoribanks J, Ayeleke RO, Farquhar C, et al. Nonsteroidal anti-inflammatory drugs for dysmenorrhoea. Cochrane Database Syst Rev, 2015.PMID 26224322
11. [11]Bofill Rodriguez M, Lethaby A, Fergusson RJ Endometrial resection and ablation versus hysterectomy for heavy menstrual bleeding. Cochrane Database Syst Rev, 2021.PMID 33619722
12. [12]Higham JM, O'Brien PM, Shaw RW. Assessment of menstrual blood loss using a pictorial chart Br J Obstet Gynaecol, 1990.PMID 2400752
13. [13]Bofill Rodriguez M, Lethaby A, Jordan V. Progestogen-releasing intrauterine systems for heavy menstrual bleeding Cochrane Database Syst Rev, 2020.PMID 32529637
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