Menstrual Disorders & PCOD

Menstrual complaints are the commonest reason women attend gynaecology clinics, and the subject looks like an unstructured list of conditions until one idea is applied.

The organising tool is to read the bleeding backwards to the signal. Normal menstruation requires an ordered sequence: oestrogen builds the endometrium, progesterone stabilises it, and withdrawal of progesterone sheds it cleanly.

Abnormal bleeding therefore means one of two things. Either the structure being acted on is abnormal, or the signal acting on it is abnormal.

That division is exactly what the PALM-COEIN classification formalises, and it is why anovulation causes irregular unpredictable bleeding while a fibroid causes heavy but regular bleeding.

Anovulation produces unopposed oestrogen with no progesterone and therefore no clean withdrawal, so the endometrium proliferates until it outgrows its blood supply and sheds erratically. Every consequence of anovulation, including the endometrial cancer risk, follows from that single sentence.

1. Terminology and PALM-COEIN

The older terms, menorrhagia and metrorrhagia among them, have been abandoned in favour of plain description: heavy menstrual bleeding, intermenstrual bleeding, and irregular bleeding.

Abnormal uterine bleeding is classified by cause into two groups.

The value of the split is that structural causes are found by imaging and non-structural causes are not, so a normal ultrasound does not mean nothing is wrong; it means the problem is in the right-hand column.

Coagulopathy deserves particular attention because it is under-diagnosed. Von Willebrand disease is present in a meaningful proportion of adolescents with heavy menstrual bleeding since menarche, and heavy bleeding from the very first period is the clue that distinguishes it from later-onset causes.

2. Anovulatory Bleeding

Anovulation is the commonest non-structural cause and occurs at the two ends of reproductive life, in adolescence before the axis matures and in the perimenopause as it declines, and throughout it in polycystic ovary syndrome.

Without ovulation there is no corpus luteum, so there is no progesterone. The endometrium is exposed to oestrogen alone.

Unopposed oestrogen produces continued proliferation without the structural stabilisation progesterone provides, so the endometrium becomes thick, fragile and vascular but disorganised.

Bleeding then occurs when parts of it outgrow their blood supply and break down, which happens irregularly and unpredictably, and is heavy because there is no coordinated vasoconstriction to stop it.

That mechanism explains the whole clinical picture: irregular timing, variable volume, and painless bleeding, since the prostaglandin release responsible for dysmenorrhoea depends on progesterone withdrawal.

It also explains why anovulation causes endometrial hyperplasia and eventually carcinoma, which is why persistent anovulatory bleeding in a woman over 40, or with risk factors, requires endometrial sampling.

3. Structural Causes

Fibroids are the commonest uterine tumour, are oestrogen and progesterone dependent, and therefore grow during reproductive life and regress after the menopause.

Their effect depends on position rather than size. Submucosal fibroids distort the cavity and cause heavy bleeding and implantation failure out of proportion to their size. Intramural fibroids cause bulk symptoms and bleeding if large. Subserosal fibroids cause pressure symptoms and rarely bleed.

Red degeneration occurs in pregnancy when a fibroid outgrows its blood supply, causing acute pain and tenderness, and is managed conservatively with analgesia.

Sarcomatous change is rare, and rapid growth after the menopause is the feature that raises the suspicion.

Adenomyosis is endometrial tissue within the myometrium and produces a diffusely enlarged, tender, boggy uterus with heavy and painful periods, typically in a parous woman in her forties. Magnetic resonance imaging shows a thickened junctional zone.

Endometrial polyps cause intermenstrual and postcoital bleeding and are removed hysteroscopically.

The distinction from fibroids matters because adenomyosis is diffuse and cannot be excised selectively, so hysterectomy is the definitive treatment where medical management fails.

4. Evaluation

History establishes the pattern, and the pattern points to the group. Regular heavy bleeding suggests a structural or endometrial cause; irregular unpredictable bleeding suggests anovulation; bleeding since menarche suggests a coagulopathy.

Examination and a full blood count are universal. Iron deficiency anaemia is extremely common in Indian women with heavy menstrual bleeding and is often the presenting problem rather than the bleeding itself.

Thyroid function is checked because both hypothyroidism and hyperthyroidism disturb the cycle, and hypothyroidism is a recognised and easily missed cause of heavy bleeding.

Transvaginal ultrasound is the first-line imaging study and identifies the PALM group. Saline infusion sonography or hysteroscopy defines cavity lesions more precisely.

Endometrial sampling is indicated in women over 45 with abnormal bleeding, in younger women with risk factors for hyperplasia, and in anyone whose bleeding persists despite treatment. The threshold is deliberately low because endometrial cancer is curable when caught early.

5. Managing Heavy Bleeding

Treatment depends on whether contraception is wanted, whether fertility is desired, and whether a structural cause is present.

The levonorgestrel intrauterine system is the most effective medical treatment for heavy menstrual bleeding without a large structural cause, reducing blood loss substantially and often producing amenorrhoea.

Tranexamic acid is an antifibrinolytic taken only during bleeding and is useful for women who want no hormonal treatment. Non-steroidal anti-inflammatory drugs reduce both bleeding and pain by inhibiting prostaglandin synthesis.

Combined oral contraceptives regulate the cycle and reduce loss. Cyclical progestogens are widely used but are less effective than commonly assumed unless the problem is anovulation, in which case they replace the missing signal directly.

Surgical options are endometrial ablation, which destroys the endometrium and is unsuitable for women wanting fertility, myomectomy where fibroids are the cause and fertility is desired, uterine artery embolisation, and hysterectomy as the definitive treatment.

6. Puberty and Its Disorders

Puberty proceeds in a fixed order, and knowing the order is what allows an abnormality to be recognised.

In girls the sequence is thelarche, then adrenarche, then the growth spurt, then menarche, and the growth spurt occurring before menarche is why girls have limited height gain afterwards.

Precocious puberty means secondary sexual characteristics before the age of 8. It divides into central and peripheral forms, and the distinction determines both investigation and treatment.

Central precocious puberty is gonadotropin-dependent, meaning the axis has switched on early. It is idiopathic in the great majority of girls, follows the normal sequence, and is treated with a gonadotropin-releasing hormone agonist to suppress the axis and preserve final height.

Peripheral precocious puberty is gonadotropin-independent, driven by a source of sex steroid outside the axis such as an ovarian tumour, congenital adrenal hyperplasia or McCune-Albright syndrome. Gonadotropins are suppressed, the sequence is often disordered, and treatment is directed at the source.

Delayed puberty means no secondary sexual characteristics by 13. Constitutional delay is the commonest cause, but gonadal dysgenesis and hypogonadotropic hypogonadism must be excluded, and gonadotropin measurement separates them in the same way it does in amenorrhoea.

7. Amenorrhoea

Amenorrhoea is best approached by compartment, working from the outflow tract upwards, because that structure organises an otherwise unmanageable differential.

Primary amenorrhoea is failure to menstruate by 15 with secondary sexual characteristics, or by 13 without them. Secondary amenorrhoea is cessation for three to six months in a woman who previously menstruated.

The first test in secondary amenorrhoea is always a pregnancy test, and the second is prolactin and thyroid stimulating hormone with follicle stimulating hormone.

A high follicle stimulating hormone localises the problem to the ovary, because the pituitary is shouting at a gonad that cannot respond. A low or normal level points above the ovary.

Presence or absence of breast development and of a uterus efficiently narrows primary amenorrhoea. Breasts present with no uterus suggests Mullerian agenesis or androgen insensitivity, and testosterone distinguishes them. Absent breasts with high gonadotropins suggests gonadal dysgenesis, and Turner syndrome should be considered.

Sheehan syndrome is postpartum pituitary necrosis following major obstetric haemorrhage, presenting with failure of lactation followed by amenorrhoea, and it remains relevant in India.

8. Polycystic Ovary Syndrome

Polycystic ovary syndrome is the commonest endocrine disorder in women of reproductive age and is a disorder of metabolism as much as of reproduction.

Insulin resistance drives much of it. Hyperinsulinaemia stimulates ovarian theca cells to produce androgens and suppresses hepatic sex hormone binding globulin, so both total and free androgen levels rise.

Androgen excess disrupts follicular development, so follicles arrest as small antral follicles rather than maturing, producing anovulation and the polycystic appearance simultaneously.

The 2023 international guideline updated the diagnostic criteria. In adults, two of three features are required: clinical or biochemical hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology on ultrasound or a raised anti-Mullerian hormone.

Adding anti-Mullerian hormone as an alternative to ultrasound is the substantive change, and it works because the hormone correlates closely with antral follicle count.

Crucially, neither ultrasound nor anti-Mullerian hormone should be used within eight years of menarche, because polycystic morphology is common and non-specific in that period. Diagnosing an adolescent therefore requires hyperandrogenism plus ovulatory dysfunction alone.

Other causes must be excluded, principally thyroid disease, hyperprolactinaemia and non-classical congenital adrenal hyperplasia.

9. Managing Polycystic Ovary Syndrome

Management is directed at the presenting complaint, and the same patient may need different treatment at different times of life.

Weight reduction is first line for every manifestation, because even modest loss reduces insulin resistance, restores ovulation in a proportion of women and improves androgenic features.

For irregular cycles and endometrial protection, the combined oral contraceptive is first line. It suppresses ovarian androgen production, raises sex hormone binding globulin and provides the progestogen that anovulatory women lack, which protects against hyperplasia.

Endometrial protection is not optional. Long-standing anovulation carries a genuine endometrial cancer risk, and a woman who declines contraception still needs cyclical progestogen or a levonorgestrel intrauterine system.

For hirsutism, the combined pill is combined with an antiandrogen such as spironolactone, with cosmetic measures, and treatment takes months because the hair growth cycle is slow.

For fertility, letrozole is first line, having replaced clomiphene on the basis of higher live birth rates. Metformin improves insulin resistance and menstrual regularity and is used particularly where there is impaired glucose tolerance.

The long-term risks are type 2 diabetes, dyslipidaemia, metabolic syndrome, obstructive sleep apnoea and endometrial carcinoma, so screening for glucose intolerance is part of ongoing care rather than an optional extra.

10. Contraception

Contraception belongs with this subject because the hormonal methods used to treat menstrual disorders are the same methods used to prevent pregnancy, and their non-contraceptive benefits are frequently the reason they are chosen.

Combined hormonal contraceptives work principally by suppressing ovulation through negative feedback on gonadotropin release, with secondary effects on cervical mucus and endometrium.

Their non-contraceptive benefits are substantial and examinable: reduced menstrual loss and dysmenorrhoea, improvement in acne and hirsutism, and a durable reduction in ovarian and endometrial cancer risk.

The important absolute contraindications reflect thrombotic and vascular risk: migraine with aura, a history of venous thromboembolism, uncontrolled hypertension, smoking over the age of 35, and active breast cancer.

Migraine with aura is the one candidates most often miss, and it matters because the combined pill raises ischaemic stroke risk in exactly that group.

Progestogen-only methods avoid oestrogen and are therefore usable where the combined pill is contraindicated, including during breastfeeding.

The copper intrauterine device works by a spermicidal inflammatory reaction and contains no hormone, but it increases menstrual loss, so it is a poor choice for a woman with heavy periods. The levonorgestrel system does the opposite and reduces loss, which is why it treats and prevents at the same time.

For emergency contraception, the copper device is the most effective method and can be inserted up to five days after intercourse, while oral levonorgestrel and ulipristal act by delaying ovulation and are less effective the later they are taken.

11. Dysmenorrhoea, Endometriosis and Menopause

Primary dysmenorrhoea is painful menstruation with no underlying pathology, caused by prostaglandin-mediated myometrial contraction and ischaemia. It begins with the onset of ovulatory cycles and responds to non-steroidal anti-inflammatory drugs and hormonal suppression.

Secondary dysmenorrhoea has an underlying cause, appears later, worsens over time and is often accompanied by other symptoms.

Endometriosis is endometrial tissue outside the uterus and produces cyclical pelvic pain, dysmenorrhoea, deep dyspareunia and subfertility. Laparoscopy is the diagnostic standard, and there is characteristically poor correlation between the extent of disease and the severity of symptoms.

Treatment is medical suppression with combined contraceptives, progestogens or gonadotropin-releasing hormone analogues, or surgical excision, and definitive surgery is reserved for completed families.

Premenstrual syndrome is symptoms in the luteal phase resolving with menstruation, and it is diagnosed by prospective symptom diaries rather than by recall.

The menopause is diagnosed clinically after twelve months of amenorrhoea and does not require hormone measurement in a woman of appropriate age. Vasomotor symptoms, urogenital atrophy and accelerated bone loss follow oestrogen deficiency.

Hormone therapy is effective for vasomotor symptoms, and a woman with a uterus must receive a progestogen alongside oestrogen, because unopposed oestrogen causes endometrial hyperplasia and carcinoma.

12. Worked Examples

Example 1. A 16-year-old has had heavy periods since menarche, lasting eight days, with a haemoglobin of 8.4. Cycles are regular.

Regularity argues against anovulation, which produces irregular bleeding, and heavy bleeding from the very first period is the classic clue to an inherited bleeding disorder.

Von Willebrand disease is present in a meaningful proportion of adolescents presenting this way, so coagulation studies including von Willebrand testing are indicated alongside iron replacement. Attributing it to immature cycles without testing is the common error.

Example 2. A 17-year-old, two years post-menarche, has irregular cycles and acne. Ultrasound shows multiple small follicles in both ovaries.

The ultrasound must not be used. Within eight years of menarche, polycystic ovarian morphology is common in normal girls and lacks specificity, so it cannot contribute to the diagnosis.

In an adolescent the diagnosis requires hyperandrogenism together with ovulatory dysfunction, both of which are present here clinically. Other causes such as thyroid disease, hyperprolactinaemia and non-classical congenital adrenal hyperplasia are excluded first.

Example 3. A 46-year-old with polycystic ovary syndrome has had two or three periods a year for many years and declines contraception.

She needs endometrial protection regardless of her contraceptive preference. Years of anovulation mean years of unopposed oestrogen, which carries a real risk of endometrial hyperplasia and carcinoma.

Cyclical progestogen or a levonorgestrel intrauterine system provides the missing progesterone signal. Given her age and the duration of anovulatory bleeding, endometrial sampling is also indicated before starting treatment.

Summary

• Read the bleeding backwards to the signal: oestrogen, progesterone, withdrawal.
• PALM causes are structural and found on imaging; COEIN causes are not.
• A normal scan means the problem is non-structural, not that nothing is wrong.
• Von Willebrand disease presents with heavy bleeding from the first period.
• Anovulation means no corpus luteum and therefore unopposed oestrogen.
• The endometrium proliferates, outgrows its supply and sheds irregularly.
• Anovulatory bleeding is painless because dysmenorrhoea needs progesterone withdrawal.
• Persistent anovulation causes hyperplasia and eventually carcinoma.
• Fibroid effects depend on position, not size.
• Submucosal fibroids cause heavy bleeding and implantation failure.
• Red degeneration occurs in pregnancy and is managed conservatively.
• Rapid growth after the menopause raises suspicion of sarcoma.
• Adenomyosis gives a bulky tender uterus and a thickened junctional zone.
• Adenomyosis is diffuse, so hysterectomy is definitive.
• Regular heavy bleeding suggests structure; irregular suggests anovulation.
• Check thyroid function, since hypothyroidism causes heavy bleeding.
• Sample the endometrium over 45, with risk factors, or if treatment fails.
• The levonorgestrel system is the most effective medical treatment.
• Tranexamic acid is taken only during bleeding.
• Ablation is unsuitable for women wanting fertility.
• Approach amenorrhoea by compartment from the outflow tract upwards.
• The first test in secondary amenorrhoea is a pregnancy test.
• High follicle stimulating hormone localises the problem to the ovary.
• Breasts present with no uterus suggests Mullerian agenesis or androgen insensitivity.
• Sheehan syndrome presents with failure of lactation, then amenorrhoea.
• Insulin resistance drives polycystic ovary syndrome.
• Hyperinsulinaemia raises androgens and lowers sex hormone binding globulin.
• Adults need two of three: hyperandrogenism, ovulatory dysfunction, morphology or raised anti-Mullerian hormone.
• Anti-Mullerian hormone is now an accepted alternative to ultrasound in adults.
• Neither may be used within eight years of menarche.
• Adolescents are diagnosed on hyperandrogenism plus ovulatory dysfunction alone.
• Weight loss is first line for every manifestation.
• Endometrial protection is mandatory even if contraception is declined.
• Letrozole is first line for fertility, ahead of clomiphene.
• Screen for glucose intolerance as part of routine care.
• Puberty in girls runs thelarche, adrenarche, growth spurt, menarche.
• Central precocious puberty is gonadotropin-dependent and usually idiopathic.
• Peripheral precocious puberty has an external steroid source and suppressed gonadotropins.
• Combined contraceptives reduce ovarian and endometrial cancer risk durably.
• Migraine with aura contraindicates the combined pill because of stroke risk.
• The copper device increases menstrual loss; the levonorgestrel system reduces it.
• The copper device is the most effective emergency contraceptive, up to five days.
• Primary dysmenorrhoea is prostaglandin-mediated and needs no imaging.
• Endometriosis severity correlates poorly with symptoms.
• Menopause is a clinical diagnosis after twelve months of amenorrhoea.
• A woman with a uterus needs a progestogen alongside oestrogen.