Menstrual Cycle & Disorders of Menstruation

A high-yield gynaecology topic built around four pillars: the physiology of the normal cycle, the PALM-COEIN classification of abnormal uterine bleeding (AUB), the dysmenorrhoeas, and the stepwise workup of amenorrhoea. Post-2020 NEET PG loves single-best-answer questions on PALM-COEIN categories and the amenorrhoea algorithm, so anchor your revision here.

The normal menstrual cycle

Menstruation results from cyclical interaction of the hypothalamo-pituitary-ovarian (HPO) axis with the endometrium. The cycle has two paired phases that run in parallel in ovary and endometrium.

Day	Ovarian phase	Endometrial phase	Dominant hormone
1–14	Follicular	Proliferative	Oestradiol (FSH-driven)
14	Ovulation	—	LH surge
14–28	Luteal	Secretory	Progesterone (from corpus luteum)

Key control points:

• Follicular phase: FSH recruits a cohort of follicles; the dominant follicle secretes rising oestradiol. Below threshold, oestradiol exerts negative feedback; once it crosses ~200 pg/mL sustained for ~50 hours it flips to positive feedback → LH surge.
• Ovulation: LH surge triggers resumption of meiosis I (oocyte completes to metaphase II) and follicle rupture ~36 h after LH-surge onset / ~10–12 h after the LH peak.
• Luteal phase: the corpus luteum makes progesterone, converting proliferative endometrium to secretory. The luteal phase is the fixed 14-day part of the cycle; variability in cycle length comes from the follicular phase.
• If no implantation, the corpus luteum regresses (~day 24), progesterone and oestrogen fall, and the spiral arterioles spasm → ischaemic shedding = menstruation.

High-yield: The luteal phase length is constant (~14 days). Therefore in a 35-day cycle, ovulation occurs around day 21, not day 17.

High-yield: Progesterone is the hormone of the secretory phase; the most reliable marker of ovulation having occurred is a mid-luteal (day 21) serum progesterone > 3 ng/mL (>10 ng/mL suggests adequate luteal function).

Normal cycle parameters (FIGO 2018)

Parameter	Normal range
Frequency	24–38 days
Regularity (cycle-to-cycle variation)	≤ 7–9 days
Duration of flow	≤ 8 days
Volume of blood loss	5–80 mL (≈ "normal" ≤ 80 mL)

Older terms (menorrhagia, metrorrhagia, polymenorrhoea) are abandoned by FIGO. Use descriptive terms: heavy menstrual bleeding (HMB), intermenstrual bleeding (IMB), infrequent/frequent/irregular bleeding.

High-yield: Menorrhagia is now called Heavy Menstrual Bleeding (HMB) — blood loss > 80 mL or bleeding that interferes with quality of life. The old "metrorrhagia" = intermenstrual bleeding.

Abnormal Uterine Bleeding (AUB) and PALM-COEIN

AUB is bleeding abnormal in frequency, regularity, duration or volume in a non-pregnant reproductive-age woman. The FIGO PALM-COEIN system (2011, revised 2018) is the single most tested item here. First exclude pregnancy in any AUB.

The acronym splits causes into structural (PALM) — diagnosable by imaging/histology — and non-structural (COEIN).

Structural (PALM)	Non-structural (COEIN)
P – Polyp	C – Coagulopathy
A – Adenomyosis	O – Ovulatory dysfunction
L – Leiomyoma (sub: SM submucosal / O other)	E – Endometrial
M – Malignancy & hyperplasia	I – Iatrogenic
	N – Not otherwise classified

Notation example: AUB-L (leiomyoma) or combined AUB-P; A if multiple coexist.

Quick characterisation of each:

• Polyp (AUB-P): focal endometrial/endocervical overgrowth; typically intermenstrual bleeding; diagnosed on saline infusion sonography (SIS) or hysteroscopy.
• Adenomyosis (AUB-A): endometrial glands within myometrium → HMB + dysmenorrhoea + bulky, tender, globular uterus. Best diagnosed on MRI (junctional zone > 12 mm) or TVS; definitive on hysterectomy specimen.
• Leiomyoma (AUB-L): fibroids; submucosal ones cause the most bleeding. Subclassified by FIGO 0–8 (type 0 = entirely intracavitary pedunculated).
• Malignancy/hyperplasia (AUB-M): endometrial hyperplasia/carcinoma; suspect in age > 45, or younger with obesity/PCOS/unopposed oestrogen. Needs endometrial biopsy.
• Coagulopathy (AUB-C): ~13% of HMB; commonest is von Willebrand disease. Suspect with HMB since menarche, postpartum/surgical bleeding, family history.
• Ovulatory dysfunction (AUB-O): anovulation — adolescents (immature axis), perimenopause, PCOS, thyroid, hyperprolactinaemia. This replaces the old term "DUB."
• Endometrial (AUB-E): primary disorder of endometrial haemostasis/inflammation in a woman with regular ovulatory cycles and HMB; diagnosis of exclusion.
• Iatrogenic (AUB-I): copper IUCD, hormonal contraceptives/breakthrough bleeding, anticoagulants, tamoxifen.
• Not otherwise classified (AUB-N): arteriovenous malformation, caesarean scar niche, chronic endometritis.

High-yield: PALM = structural causes (imaging/histology). COEIN = non-structural. Memorise that DUB no longer exists — anovulatory DUB is now AUB-O.

High-yield: Commonest coagulopathy underlying AUB-C is von Willebrand disease — screen adolescents with HMB since menarche.

Mnemonic: "PALM you can feel/see (structural), COEIN you cannot (functional)."

Investigation of AUB — stepwise approach

Rule out pregnancy (urine/serum β-hCG) → CBC + ferritin (anaemia) → TSH, prolactin, coagulation screen if indicated → transvaginal ultrasound (first-line imaging) → SIS/hysteroscopy for focal lesions → endometrial biopsy if AUB-M suspected.

Endometrial sampling indications (commit these):

• Age ≥ 45 years with AUB.
• Age < 45 with risk factors: obesity, PCOS, unopposed oestrogen, tamoxifen, Lynch syndrome, or failed medical therapy / persistent bleeding.

High-yield: Office endometrial biopsy (Pipelle) is the investigation of choice to exclude hyperplasia/malignancy. TVS endometrial thickness > 4 mm in a postmenopausal woman with bleeding mandates sampling.

Management of AUB (non-structural / HMB)

Step up from least to most invasive (assuming malignancy excluded):

1. Medical (first-line):
   • LNG-IUS (levonorgestrel intrauterine system, Mirena) — most effective medical therapy for HMB; reduces loss by ~90%.
   • Tranexamic acid (antifibrinolytic) during menses — best non-hormonal option.
   • NSAIDs (mefenamic acid) — reduce loss ~25–30%, also help dysmenorrhoea.
   • Combined oral contraceptive pills; oral/cyclical progestogens for anovulatory AUB-O.
   • Acute severe bleeding: high-dose IV/oral oestrogen or COC taper; tranexamic acid.
2. Surgical: endometrial ablation (completed family), hysteroscopic resection of polyp/submucosal fibroid, hysterectomy = definitive.

High-yield: LNG-IUS is the first-line treatment for HMB when no structural/malignant cause and contraception acceptable. Tranexamic acid is the best non-hormonal agent.

Dysmenorrhoea

Painful menstruation; cramping lower-abdominal pain. Classified into primary and secondary.

Feature	Primary	Secondary
Onset	6–12 months after menarche (ovulatory cycles begin)	Years after menarche, later age
Cause	No pelvic pathology; excess PGF2α	Identifiable pathology
Timing of pain	Begins with or just before flow, lasts 1–3 days	May precede menses by days, lasts longer
Pelvic exam	Normal	Often abnormal
Common pathology	—	Endometriosis, adenomyosis, fibroids, PID, IUCD, cervical stenosis
Treatment of choice	NSAIDs ± COC	Treat the cause

Pathophysiology of primary dysmenorrhoea: progesterone withdrawal → endometrial release of prostaglandins F2α and E2 → myometrial hypercontractility, vasoconstriction, uterine ischaemia → pain. Hence it occurs only in ovulatory cycles and responds to prostaglandin synthetase inhibitors (NSAIDs).

High-yield: NSAIDs are the drug of choice for primary dysmenorrhoea (block prostaglandin synthesis). Combined OCPs are second-line/added by suppressing ovulation.

High-yield: Endometriosis is the commonest cause of secondary dysmenorrhoea. Suspect when dysmenorrhoea is progressive, with dyspareunia and infertility.

Amenorrhoea

Absence of menstruation. Two clinical categories:

• Primary amenorrhoea: no menarche by age 15 with normal secondary sexual characteristics, OR by age 13 with absent secondary sexual characteristics, OR no menarche within 5 years of breast development.
• Secondary amenorrhoea: cessation of established menses for ≥ 3 months (if previously regular) or ≥ 6 months (if oligomenorrhoeic).

High-yield: The single most important first step in evaluating secondary amenorrhoea is a pregnancy test (β-hCG) — pregnancy is the commonest cause.

Causes by compartment

A clean way to organise: think anatomically from outflow tract upward.

Compartment	Examples
Outflow tract / uterus	Imperforate hymen, transverse vaginal septum, Müllerian agenesis (MRKH), Asherman syndrome
Ovary	Gonadal dysgenesis (Turner 45,X), premature ovarian insufficiency, PCOS
Anterior pituitary	Sheehan syndrome, prolactinoma, empty sella
Hypothalamus / CNS	Functional hypothalamic amenorrhoea (stress, weight loss, exercise, anorexia), Kallmann syndrome

Classic eponyms / named entities:

• MRKH (Mayer-Rokitansky-Küster-Hauser) syndrome: Müllerian agenesis — primary amenorrhoea, absent uterus & upper vagina, normal ovaries → normal secondary sexual characters, 46,XX, normal testosterone. Often associated renal anomalies.
• Androgen Insensitivity Syndrome (AIS): 46,XY, female phenotype, absent uterus, scanty pubic/axillary hair, testosterone in male range, testes present (need removal due to malignancy risk).
• Turner syndrome (45,X): short stature, streak gonads, high FSH (hypergonadotrophic).
• Asherman syndrome: intrauterine adhesions post-curettage → secondary amenorrhoea with normal hormones.
• Sheehan syndrome: postpartum pituitary necrosis → failure of lactation, secondary amenorrhoea.
• Kallmann syndrome: GnRH deficiency + anosmia (hypogonadotrophic hypogonadism).

High-yield: MRKH (46,XX) vs AIS (46,XY) — both present with primary amenorrhoea + absent uterus. Differentiate by karyotype and serum testosterone (normal female in MRKH; male range in AIS). Pubic hair present in MRKH, sparse/absent in AIS.

Stepwise workup of secondary amenorrhoea (commit this algorithm)

Step 1 — β-hCG → exclude pregnancy. Step 2 — TSH and prolactin → exclude thyroid disease and hyperprolactinaemia (raised prolactin causes amenorrhoea-galactorrhoea). Step 3 — Progestogen challenge test (medroxyprogesterone 10 mg × 5–7 days):

• Withdrawal bleed → anovulation with adequate oestrogen (e.g., PCOS). Outflow tract patent, endometrium primed.
• No bleed → proceed to step 4. Step 4 — Oestrogen + progestogen challenge:
• Bleed → problem is upstream (no endogenous oestrogen) → check FSH/LH.
• No bleed → outflow tract/endometrial problem (Asherman) or obstruction. Step 5 — FSH/LH levels:
• High FSH (hypergonadotrophic) → ovarian failure (POI, Turner).
• Low/normal FSH (hypogonadotrophic) → hypothalamic/pituitary cause → MRI brain/sella and assess prolactin.

High-yield: A positive progestogen withdrawal bleed proves (a) endogenous oestrogen is adequate and (b) the outflow tract is patent — pointing to anovulation as the cause.

High-yield: High FSH = ovarian (hypergonadotrophic hypogonadism); Low FSH = hypothalamic/pituitary (hypogonadotrophic hypogonadism). This single distinction answers most amenorrhoea MCQs.

Primary amenorrhoea — quick branch

Assess breast development (oestrogen) and uterus (USG):

Breasts	Uterus	Likely diagnosis
Present	Absent	MRKH or AIS (differentiate by karyotype/testosterone)
Absent	Present	Gonadal failure (Turner) or hypogonadotrophic (Kallmann) — check FSH
Present	Present	Outflow obstruction (imperforate hymen), or same workup as secondary
Absent	Absent	Rare — e.g., 17,20-lyase deficiency / swyer-type variants

Premenstrual syndrome (often clubbed here)

Cyclical physical and behavioural symptoms in the luteal phase, relieved by menses. Severe form with predominant mood symptoms = premenstrual dysphoric disorder (PMDD).

High-yield: SSRIs are first-line for PMDD (can be given continuously or luteal-phase only); COCs and lifestyle measures help PMS.

Complications worth knowing

• Chronic HMB → iron-deficiency anaemia (commonest, most testable consequence).
• Untreated anovulatory AUB-O / unopposed oestrogen → endometrial hyperplasia → carcinoma.
• Severe acute AUB → haemodynamic instability needing transfusion.
• Functional hypothalamic amenorrhoea → hypo-oestrogenism → osteoporosis & infertility.
• Endometriosis-related secondary dysmenorrhoea → adhesions, infertility, chocolate cysts.

Key differentials at a glance

• HMB with bulky tender uterus + dysmenorrhoea → adenomyosis (AUB-A).
• HMB since menarche + family bleeding history → coagulopathy/vWD (AUB-C).
• Irregular infrequent cycles + hirsutism + obesity → PCOS (AUB-O).
• Intermenstrual/postcoital bleeding → polyp, cervical pathology, malignancy — examine cervix.
• Postmenopausal bleeding → endometrial carcinoma until proven otherwise (TVS + biopsy).
• Primary amenorrhoea, cyclical pain, no flow, bulging blue membrane → imperforate hymen (cryptomenorrhoea).

Recently asked / exam angle

• PALM-COEIN is the darling of post-2020 papers. Expect "which is a structural cause of AUB?" (answer among PALM) or "AUB-O corresponds to…" (anovulation/old DUB). Know that DUB terminology is obsolete.
• Adenomyosis features (globular tender uterus, MRI junctional zone) and its PALM-COEIN letter (A) are repeatedly tested.
• Investigation of choice questions: TVS (first-line imaging), SIS/hysteroscopy (focal lesions), endometrial biopsy/Pipelle (rule out malignancy), and the ≥45 years / postmenopausal ET > 4 mm sampling thresholds.
• Amenorrhoea algorithm: first test (β-hCG), interpretation of progestogen withdrawal bleed, and the high vs low FSH dichotomy are favourite single-best-answer stems.
• MRKH vs AIS differentiation by karyotype/testosterone — a classic image/clinical-vignette question.
• Drug of choice lines: NSAIDs for primary dysmenorrhoea, LNG-IUS for HMB, SSRIs for PMDD, tranexamic acid as best non-hormonal HMB agent.
• Mid-luteal day-21 progesterone as the confirmatory test of ovulation.

Rapid revision

1. Normal cycle: frequency 24–38 days, flow ≤ 8 days, loss 5–80 mL; luteal phase fixed at 14 days.
2. Ovulation occurs ~36 h after LH-surge onset; confirmed by day-21 progesterone > 3 ng/mL.
3. PALM = structural (Polyp, Adenomyosis, Leiomyoma, Malignancy); COEIN = non-structural (Coagulopathy, Ovulatory, Endometrial, Iatrogenic, Not classified).
4. DUB is obsolete → anovulatory bleeding = AUB-O; menorrhagia → HMB.
5. Commonest coagulopathy in AUB-C = von Willebrand disease; screen adolescents with HMB.
6. TVS = first-line imaging for AUB; endometrial biopsy if ≥ 45 yrs, risk factors, or failed therapy.
7. LNG-IUS = most effective medical therapy for HMB; tranexamic acid = best non-hormonal.
8. NSAIDs = drug of choice for primary dysmenorrhoea; endometriosis = commonest cause of secondary dysmenorrhoea.
9. First step in any amenorrhoea/AUB = rule out pregnancy (β-hCG).
10. Positive progestogen withdrawal bleed = adequate oestrogen + patent outflow → anovulation.
11. High FSH = ovarian failure (Turner, POI); low FSH = hypothalamic/pituitary (Kallmann, Sheehan).
12. MRKH (46,XX, normal testosterone, pubic hair present) vs AIS (46,XY, male-range testosterone, sparse hair) — both have absent uterus + breasts present; SSRIs first-line for PMDD.