Approach absent menstruation from pregnancy and anatomy through ovarian and hypothalamic-pituitary physiology, identify urgent endocrine disease, and protect bone, endometrium and fertility while treating the cause.
Normal menstruation requires a patent outflow tract, responsive endometrium, ovarian follicles and coordinated hypothalamic-pituitary signalling. A disruption at any level can stop bleeding. Primary amenorrhoea places greater emphasis on pubertal development, anatomy and genetic conditions; secondary amenorrhoea commonly reflects pregnancy, PCOS, functional hypothalamic suppression, hyperprolactinaemia, thyroid disease or POI.
Bleeding itself does not reveal the hormone mechanism. Chronic anovulation with oestrogen exposure can place the endometrium at risk, while low-oestrogen states threaten bone and genitourinary health. A person taking a progestogen-only contraceptive may have neither problem. Treatment should therefore follow physiology rather than prescribing a withdrawal bleed as a diagnostic substitute.
The central decision is whether pregnancy or an acute pituitary, adrenal or pelvic disorder makes the presentation urgent, then whether gonadotrophins indicate ovarian or central hypogonadism, and whether androgen excess or anatomy redirects the pathway. The consultation should also identify disordered eating, coercion, pregnancy intention and psychological burden sensitively.
Pregnancy, lactation, menopause and hormonal contraception can stop bleeding without the same pathological ovarian, pituitary or endometrial mechanism.
Polycystic ovary syndrome commonly causes chronic anovulation, while premature ovarian insufficiency reduces oestrogen and raises gonadotrophins through loss of ovarian feedback.
Low energy availability, high training load, stress, pituitary disease or hyperprolactinaemia can reduce gonadotrophin drive and interrupt ovulation and endometrial cycling.
Thyroid dysfunction, androgen excess and adrenal disorders can disturb coordinated reproductive signalling, particularly when accompanied by weight change, hirsutism or systemic features.
Normal menstruation requires coordinated hypothalamic, pituitary and ovarian signalling, responsive endometrium and a patent outflow tract; interruption at any level can stop bleeding.
Failure to recruit and ovulate a follicle alters progesterone cycling, while ovarian or central failure may reduce oestrogen enough to prevent endometrial proliferation.
Chronic anovulation with continuing oestrogen can expose the endometrium, whereas prolonged low-oestrogen states impair bone and genitourinary health through a different mechanism.
Pregnancy, lactation and menopause are physiological contexts, while hormonal contraception can suppress bleeding; confirm the context before applying an endocrine disease label.
Reduced intake, high training load, stress, weight loss, bradycardia, stress fracture or eating-disorder features with low oestrogen and non-raised gonadotrophins suggests relative energy deficiency.
Irregular or absent bleeding with hirsutism, acne or biochemical androgen excess supports PCOS after pregnancy, thyroid, prolactin and adrenal mimics are excluded.
Hot flushes, vaginal dryness and repeatedly raised FSH before age 40 suggests POI; iatrogenic, genetic and autoimmune causes require assessment.
Galactorrhoea, low libido, headache or visual change with suppressed gonadotrophins suggests prolactin excess, although galactorrhoea may be absent and medicine causes are common.
Normal breast development with absent uterus suggests Müllerian agenesis or androgen insensitivity, while cyclic pain with retained blood suggests outflow obstruction requiring gynaecological assessment.
Rapid hair change, deep voice, clitoromegaly or marked testosterone abnormality suggests an ovarian or adrenal source rather than uncomplicated PCOS.
Acute headache, ophthalmoplegia, visual loss, collapse, vomiting or severe postural hypotension can indicate apoplexy or cortisol deficiency and needs immediate treatment.
Pregnancy is the immediate alternative in anyone with relevant reproductive potential; history alone does not reliably exclude it when bleeding has stopped.
Irregular cycles with hirsutism, acne or biochemical androgen excess support PCOS after pregnancy, thyroid, prolactin and severe androgen disorders are excluded.
Weight loss, restricted intake, heavy exercise, bradycardia or stress fracture with non-raised gonadotrophins suggests relative energy deficiency rather than ovarian failure.
Hot flushes, vaginal dryness and repeatedly raised gonadotrophins with low oestrogen support ovarian insufficiency rather than central suppression.
Persistent anovulation with unopposed oestrogen can cause prolonged endometrial stimulation, increasing irregular bleeding and longer-term endometrial risk.
Prolonged oestrogen deficiency reduces bone accrual or accelerates bone loss, increasing stress injury and later fragility-fracture risk.
Absent or unpredictable ovulation reduces opportunities for conception and may signal ovarian reserve or pituitary disease requiring time-sensitive assessment.
No endocrine pattern safely excludes pregnancy before beta-hCG testing. Irregular ovulation and prior infertility labels frequently create false reassurance.
Raised FSH indicates loss of ovarian feedback, while a non-raised value in low oestrogen points upstream. This simple split structures the rest of the investigation.
A progestogen withdrawal bleed demonstrates a responsive outflow tract and endometrium but does not establish spontaneous follicular ovulation or fertility.
Energy availability depends on intake relative to expenditure, not appearance alone. Athletes and people with restrictive eating can be medically compromised at many weights.
Stress, medicines, macroprolactin and renal failure can elevate a result. Repeat thoughtfully, but do not delay imaging when visual or severe pituitary features are present.
In primary amenorrhoea, distinguish Müllerian agenesis from androgen insensitivity and outflow disorders through anatomy, karyotype and hormones with supported specialist disclosure.
Oestrogen may protect some bone endpoints, but ongoing severe energy deficit harms cardiovascular, skeletal, immune and psychological health beyond amenorrhoea.
Use the person's language and never infer sexual behaviour or pregnancy possibility from gender or partner identity; explain why anatomy-specific questions affect safe testing.
Ordering a hormone panel before excluding pregnancy.
Diagnosing functional hypothalamic amenorrhoea without excluding pituitary and ovarian disease.
Using BMI alone to assess low energy availability.
Treating a single stressed prolactin result as a pituitary tumour.
Missing ectopic pregnancy because the person has PCOS or prior infertility.
Giving oestrogen without uterine progestogen protection.
Using a withdrawal bleed as proof that ovulation has returned.
Failing to protect bone during prolonged hypo-oestrogenism.
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A 24-year-old with previously regular cycles has had no bleeding for four months. She reports using contraception but has intermittent pelvic discomfort. Which investigation must come first?
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Nausea, postural hypotension, impulse-control effects and product-specific cardiac valve monitoring require counselling. Pregnancy and tumour plans are specialist led; do not stop antipsychotics abruptly.
Confirm primary versus central disease; in suspected pituitary failure assess and replace cortisol before thyroid hormone. Separate from interacting iron or calcium preparations.
It is not a treatment for restoring energy balance and standard HRT is not contraception. Investigate unscheduled bleeding and individualise for thrombosis, migraine and cancer history.
It does not treat hypo-oestrogenic bone loss, prove ovulation or reliably prevent pregnancy. Persistent abnormal bleeding requires investigation.
Multiple pregnancy and ovarian hyperstimulation are preventable treatment harms; self-directed or unmonitored use is unsafe and local access criteria vary.