Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Oligomenorrhoea and amenorrhoea assessment
Obstetrics and gynaecology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Do not miss pregnancy or physiological instability
Amenorrhoea with pelvic pain or bleeding may be ectopic pregnancy, while marked bradycardia, hypotension, electrolyte disturbance or syncope may indicate severe energy deficiency requiring acute medical care.
Action: Check pregnancy promptly, assess observations and abdominal findings, and arrange same-day early-pregnancy or acute medical review when pain, bleeding, haemodynamic change, severe nutritional compromise or neurological signs are present.
Overview
Assess absent or infrequent menstruation systematically, exclude pregnancy and urgent pathology, localise reproductive-axis dysfunction, and protect fertility, bone and endometrial health.
Menstruation requires a patent genital outflow tract, an endometrium able to respond, functioning ovarian follicles and coordinated hypothalamic-pituitary signalling. Oligomenorrhoea and amenorrhoea are therefore presentations, not diagnoses. Establish the previous cycle pattern, age at menarche, timing of breast development and whether the person has ever menstruated. Ask what outcome matters now: explaining a new change, preventing pregnancy, trying to conceive, reducing androgen symptoms or protecting long-term health.
Pregnancy is the first biological branch. Ask about sexual activity in an inclusive and private way, current and recent contraception, emergency contraception, pregnancy symptoms, pain and bleeding. A urine test is often adequate, but use serum hCG and urgent early-pregnancy assessment when timing is uncertain or symptoms suggest ectopic pregnancy. Hormonal contraception, lactation and gender-affirming treatment can alter or stop bleeding; this may be expected, yet a new symptom pattern or pregnancy possibility still requires assessment.
Practice
Two practice questions
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Obstetrics and gynaecologyOriginal SBA
First branch in amenorrhoea
A 24-year-old with previously regular cycles has had no bleeding for four months and reports mild lower abdominal discomfort. Which investigation should be performed before interpreting reproductive hormone tests?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
The history should interrogate the whole reproductive axis. Weight loss, restricted eating, food insecurity, intense training, psychological stress, sleep change and chronic illness point toward functional hypothalamic suppression. Hirsutism, acne and weight-related metabolic features suggest PCOS, while hot flushes, vaginal dryness, chemotherapy, pelvic radiotherapy or ovarian surgery suggest primary ovarian insufficiency. Galactorrhoea, headache and visual change raise prolactin or sellar causes. Ask about thyroid symptoms, uterine instrumentation, postpartum haemorrhage and medicines including antipsychotics, antiemetics, opioids and exogenous hormones.
Examination begins with dignity, consent and a chaperone where appropriate. Record pulse, blood pressure, postural change, weight trajectory and BMI without allowing BMI alone to exclude energy deficiency. Look for thyroid signs, galactorrhoea only when clinically appropriate, acne, hirsutism, virilisation, acanthosis, Cushingoid features and visual-field deficit. In primary amenorrhoea, Tanner staging, stature, dysmorphism and confirmation of uterine and vaginal anatomy guide testing. Pelvic examination is selective rather than automatic, especially in adolescents.
After pregnancy testing, targeted bloods usually include TSH, prolactin, FSH and oestradiol. Interpret the pattern rather than an isolated number and account for hormonal treatment. Add total and calculated free testosterone or free androgen index when androgen excess is possible, and 17-hydroxyprogesterone when non-classic congenital adrenal hyperplasia is plausible. Pelvic ultrasound is useful for anatomy, uterine development and selected ovarian questions. Persistent true hyperprolactinaemia or central neurological features lead to pituitary assessment; raised FSH in a person under 40 leads into the POI pathway.
Treatment should address both the cause and the consequence of not ovulating. Chronic anovulation with ongoing oestrogen exposure may leave the endometrium unopposed and require cycle regulation or progestogen protection. Oestrogen deficiency from POI or prolonged hypothalamic suppression threatens bone acquisition and maintenance, but simply producing a withdrawal bleed does not repair an energy deficit. Fertility treatment depends on the diagnosis and should not start before medical instability, nutritional deficiency or tumour risk is addressed.
Close the assessment with an explicit plan for results, referral and safety-netting. Offer prompt reproductive-medicine input when age, duration or a known cause makes delay important, and do not require a person with amenorrhoea to wait a year before fertility referral. Discuss psychological effects, eating-disorder symptoms, gender needs and safeguarding privately. Explain that recovery may be intermittent and that a bleed, a normal scan or one hormone result does not by itself prove the axis is healthy.
Key points
Oligomenorrhoea means persistently infrequent cycles; secondary amenorrhoea generally merits assessment after three months without bleeding when cycles were regular, or six months when they were previously irregular.
Primary amenorrhoea requires evaluation by age 15 or more than three years after breast development begins; absent secondary sexual development at 13 is an earlier referral trigger.
Exclude pregnancy before interpreting reproductive hormones, even when contraception is reported, fertility seems unlikely or occasional spotting has occurred.
Use history and examination to separate ovarian androgen excess, ovarian insufficiency, hypothalamic energy or stress suppression, hyperprolactinaemia, thyroid disease, uterine or outflow pathology and medicine effects.
FSH with oestradiol helps localise the axis: raised FSH with low oestradiol suggests ovarian insufficiency, while low or inappropriately normal gonadotrophins with low oestradiol suggests central suppression.
Pelvic ultrasound defines uterine anatomy, endometrial appearance and ovarian morphology but neither confirms PCOS by itself nor excludes endocrine disease.
Management is cause directed and goal specific: contraception, desired fertility, endometrial protection, oestrogen replacement and recovery of adequate energy availability are different clinical aims.
Aetiology
01
Pregnancy and physiological states
Pregnancy, lactation and the pubertal or menopausal transition alter ovulation and bleeding; hormonal contraception may intentionally suppress endometrial shedding.
02
Endocrine axis disruption
PCOS, ovarian insufficiency, hypothalamic energy suppression, pituitary disease, hyperprolactinaemia and thyroid dysfunction interrupt coordinated follicular development or ovulation.
03
Anatomical or iatrogenic causes
Congenital uterine or outflow differences, intrauterine adhesions, cervical stenosis, ovarian treatment and medicines can prevent bleeding by distinct mechanisms.
Pathophysiology
1
Central drive changes
Reduced pulsatile GnRH from energy deficit, stress or pituitary disease lowers gonadotrophin support and ovarian oestradiol production.
Low oestrogen leaves a thin inactive endometrium, while chronic anovulation with continuing oestrogen can produce prolonged unopposed proliferation.
4
Outflow prevents visible menses
A functioning endometrium may cycle behind a congenital or acquired obstruction, causing pain and retained blood despite absent external bleeding.
Clinical features and red flags
Hyperandrogenic anovulation
Infrequent bleeding with slowly progressive hirsutism or acne and biochemical androgen excess supports PCOS after pregnancy and alternative endocrine causes are excluded.
Hypergonadotrophic pattern
Vasomotor or genitourinary symptoms with low oestradiol and repeatedly raised FSH indicate loss of ovarian feedback and require age-specific POI assessment.
Hypogonadotrophic pattern
Low oestradiol with low or inappropriately normal LH and FSH fits hypothalamic, pituitary or systemic suppression, interpreted alongside nutrition, exercise and neurological findings.
Anatomical presentation
Normal breast development with primary amenorrhoea, a shortened vagina or cyclical pain suggests uterine absence or outflow obstruction rather than failed ovarian oestrogen production.
Prolactin phenotype
Amenorrhoea with galactorrhoea, infertility or low libido may reflect prolactin-mediated GnRH suppression, although breast discharge can be absent and modest elevations have many causes.
Red flags requiring action
A positive pregnancy test with unilateral pelvic pain, shoulder-tip pain, bleeding, collapse or peritoneal signs needs urgent assessment for ectopic pregnancy.
New severe headache, vomiting, visual-field change, ophthalmoplegia, polyuria or polydipsia raises concern for pituitary or hypothalamic disease and requires expedited endocrine imaging assessment.
Investigations
01Urine or serum hCGFirst step
Why
Exclude pregnancy before endocrine classification or hormonal treatment.
Interpretation and limitations
A positive result changes the pathway immediately; pain, bleeding or haemodynamic symptoms require urgent localisation because amenorrhoea may be the presenting feature of ectopic pregnancy.
02FSH, LH and oestradiol
Why
Distinguish reduced ovarian feedback from inadequate central drive and document oestrogen exposure.
Interpretation and limitations
Raised FSH with low oestradiol supports ovarian insufficiency; low or normal gonadotrophins with low oestradiol suggests central suppression, while normal-range values do not alone establish PCOS.
03Prolactin and thyroid function
Why
Identify prolactin excess and thyroid disease that can disrupt ovulation.
Interpretation and limitations
Repeat a modest prolactin under calm conditions, review medicines and request macroprolactin where relevant; interpret TSH with free T4 rather than attributing every small variation to the cycle.
04Androgen profile and 17-hydroxyprogesterone
Why
Characterise suspected androgen excess and screen for important adrenal mimics.
Interpretation and limitations
Slow mild elevation can accompany PCOS, whereas marked or rapidly changing testosterone or DHEAS with virilisation requires urgent ovarian and adrenal evaluation; raised 17-hydroxyprogesterone needs specialist confirmation.
Differential diagnosis
01
Polycystic ovary syndrome
Persistent ovulatory dysfunction with clinical or biochemical hyperandrogenism supports PCOS after pregnancy, thyroid, prolactin and important androgen disorders are excluded.
02
Functional hypothalamic amenorrhoea
Low energy availability, high exercise load, stress or illness produces low-oestrogen central suppression and may coexist with a normal BMI.
03
Primary ovarian insufficiency
Menstrual disturbance and oestrogen-deficiency symptoms before 40 with appropriately confirmed raised FSH indicate impaired ovarian function rather than central suppression.
04
Hyperprolactinaemia
True prolactin excess suppresses GnRH and can cause amenorrhoea, infertility and low libido from medicines, systemic disease, stalk pathology or prolactinoma.
05
Uterine or outflow disorder
Müllerian difference, imperforate hymen, transverse septum or acquired intrauterine adhesions prevents or reduces visible bleeding despite other axis function.
Management
01Initial assessmentExclude urgent and reversible causesFirst stepA person presents with absent or persistently infrequent menstruation.+
1Clarify primary versus secondary amenorrhoea, cycle timing, pregnancy possibility, contraception, pain, bleeding, pubertal development and the person's reproductive goal.
2EscalationCheck hCG, observations and red flags before arranging routine endocrine testing; escalate pregnancy symptoms, neurological change, virilisation or nutritional instability immediately.
3Review weight trajectory, intake, exercise, stress, chronic disease, uterine procedures and every relevant medicine, then perform a consented targeted examination.
02Axis localisationUse a hypothesis-led test setPregnancy and immediate instability have been excluded but the bleeding disturbance remains unexplained.+
1
Complications
01
Endometrial hyperplasia
Prolonged anovulation with continued oestrogen exposure can thicken the endometrium and increase hyperplasia and endometrial-cancer risk over time.
02
Low bone density
Sustained oestrogen deficiency impairs peak bone acquisition or accelerates loss, particularly with undernutrition, stress fracture and delayed recognition.
03
Subfertility
Absent or unpredictable ovulation reduces conception opportunities, while some causes also alter ovarian reserve, uterine anatomy or overall medical fitness for pregnancy.
04
Psychological harm
Diagnostic delay, unwanted androgen effects, fertility uncertainty, disordered eating and differences in sex development can cause substantial distress and stigma.
Monitoring and follow-up
Track menstrual dates and symptoms while recognising that withdrawal bleeding from hormones does not demonstrate spontaneous ovulation or correction of the underlying mechanism.
Monitor weight trajectory, pulse, blood pressure, energy intake, exercise, stress injury and psychological recovery when hypothalamic suppression is possible.
Review bleeding frequency and unexpected heavy, prolonged or intermenstrual bleeding in chronic anovulation, escalating endometrial assessment according to age and risk.
Recheck diagnosis-specific markers rather than repeating a broad hormone panel: examples include FSH confirmation for POI, prolactin after cause review and androgen trend when initially abnormal.
Revisit contraception and fertility intention at every material change because ovulation may return before cycles become predictable.
Special situations
Bleeding is not ovulation
A spontaneous or medication-induced bleed shows endometrial shedding but does not prove that ovulation occurred or that fertility timing is predictable.
Normal BMI can mislead
Low energy availability and functional hypothalamic suppression can occur at any BMI when intake does not meet physiological and exercise expenditure.
Hormones need context
Combined contraception suppresses gonadotrophins and alters androgen-binding proteins, so results obtained during treatment may not reflect the untreated reproductive axis.
An absent uterus branches early
Normal breast development with uterine absence directs assessment toward Müllerian agenesis or androgen insensitivity, which have different chromosomes, gonads and associated screening needs.
Fertility referral can be immediate
A known ovulatory disorder or amenorrhoea is a recognised fertility factor, so investigation need not wait for twelve months of unsuccessful attempts.
Common pitfalls
01
Assuming pregnancy is impossible because cycles are irregular, contraception is used or fertility was previously reduced.
02
Calling polycystic ovarian morphology on ultrasound a diagnosis of PCOS without the clinical criteria and exclusion of mimics.
03
Using BMI alone to dismiss restricted intake, excessive exercise or medical instability from low energy availability.
04
Interpreting prolactin, gonadotrophins or androgens without considering stress, medicines and current hormonal treatment.
05
Producing a progestogen withdrawal bleed and treating the underlying cause, bone risk or fertility question as resolved.
06
Applying an adult secondary-amenorrhoea algorithm to primary amenorrhoea without assessing pubertal development and genital anatomy.
Amenorrhoea is not reliable contraception; ovulation can resume unpredictably during recovery from hypothalamic suppression, prolactin treatment or intermittent ovarian function.
Rapidly progressive hirsutism, voice deepening, clitoromegaly or a new abdominal mass suggests an androgen-secreting ovarian or adrenal disorder rather than uncomplicated PCOS.
Bradycardia, hypotension, orthostasis, hypothermia, electrolyte abnormality, recurrent syncope or very low weight in a person with restricted intake or excessive exercise warrants urgent medical and eating-disorder assessment.
Primary amenorrhoea with cyclical severe pelvic pain or a palpable mass may reflect obstructed menstrual outflow and requires prompt gynaecological examination and imaging.
05Pelvic ultrasound
Why
Confirm uterine presence and anatomy, assess endometrium and answer selected ovarian or obstructive questions.
Interpretation and limitations
Polycystic morphology is only one diagnostic feature in adults and is common without PCOS; a thin endometrium may fit hypo-oestrogenism, while absent uterus requires structured differences-of-sex-development assessment.
06Pituitary MRI or genetic testing
Why
Investigate a persistent biochemical or phenotypic signal after initial localisation.
Interpretation and limitations
MRI is indicated for unexplained true hyperprolactinaemia or mass features; karyotype and FMR1 testing are specialist choices in primary amenorrhoea or non-iatrogenic POI with counselling.
Measure TSH, prolactin, FSH and oestradiol, adding androgen studies, 17-hydroxyprogesterone or systemic bloods only when history and examination support them.
2Use pelvic ultrasound for anatomy, endometrium and selected ovarian assessment, not as a standalone label for PCOS or ovarian failure.
3Route raised FSH, persistent monomeric prolactin, virilising androgens, central deficiency or structural abnormality to the relevant specialist pathway.
03Cause-directed careProtect health while pursuing the goalThe likely mechanism has been identified or specialist confirmation is underway.+
1Correct energy deficit or systemic disease, review causative medicines collaboratively and treat endocrine disease without delaying urgent tumour or eating-disorder care.
2Provide endometrial protection for chronic anovulation or physiological sex-steroid replacement for established deficiency, matching contraception and uterine protection to the individual.
3Arrange early fertility referral for anovulation, POI, amenorrhoea or another known factor rather than applying a routine twelve-month wait.
04Primary amenorrhoeaIntegrate development and anatomyMenarche has not occurred by the expected developmental threshold.+
1Document breast development, growth pattern, stature, dysmorphic features, androgen effects and cyclical symptoms with sensitive adolescent communication and safeguarding awareness.
2Confirm uterine anatomy and interpret gonadotrophins with oestradiol, then add karyotype, testosterone, renal imaging or pituitary tests according to the pattern.
3Coordinate paediatric endocrinology, adolescent gynaecology, genetics and psychology where gonadal dysgenesis, Müllerian difference or androgen insensitivity is possible.