Amenorrhea, Dysmenorrhea and Abnormal Uterine Bleeding

Foundations and mechanisms

Normal menstrual physiology: the reference framework

The menstrual cycle reflects coordinated function of the hypothalamic-pituitary-ovarian (HPO) axis and an anatomically intact outflow tract. Pulsatile hypothalamic GnRH stimulates anterior pituitary secretion of LH and FSH; continuous GnRH suppresses gonadotropins, a key pharmacologic principle. FSH promotes granulosa cell aromatase activity and follicular estradiol production; LH stimulates theca cell androgen synthesis and later luteinization. Estradiol initially exerts negative feedback, then sustained high estradiol triggers the LH surge, causing ovulation approximately 36 hours later.

A typical cycle lasts 21–35 days in adults, with menses lasting 2–7 days and average blood loss approximately 30–40 mL; blood loss >80 mL is classically considered heavy menstrual bleeding. The follicular phase is variable, whereas the luteal phase is relatively fixed at about 14 days. Progesterone from the corpus luteum converts proliferative endometrium into secretory endometrium. If implantation does not occur, corpus luteum regression decreases progesterone and estradiol, causing spiral artery vasoconstriction, endometrial ischemia, matrix metalloproteinase activation, and menstruation.

Amenorrhea: definitions and mechanistic classification

Amenorrhea is absence of menses and is best approached by asking whether the problem is anatomic, ovarian, pituitary, hypothalamic, or physiologic pregnancy. Primary amenorrhea is commonly defined as no menarche by age 15 years with normal secondary sexual characteristics, or within 3 years after thelarche; evaluation is earlier if no breast development by age 13 years. Secondary amenorrhea is absence of menses for 3 months in previously regular cycles or 6 months in previously irregular cycles.

Category	Core mechanism	High-yield examples	Typical hormone pattern
Outflow tract obstruction	Endometrium responds normally, but menstrual blood cannot exit	Imperforate hymen, transverse vaginal septum, Müllerian agenesis	Normal FSH/LH/estradiol; cyclic pain may occur
Primary ovarian insufficiency	Failed follicular estradiol production removes negative feedback	Turner syndrome, autoimmune oophoritis, chemotherapy	High FSH, low estradiol
Hypothalamic suppression	Reduced GnRH pulse frequency/amplitude	Low weight, excessive exercise, stress, chronic illness	Low/normal FSH and LH, low estradiol
Pituitary disease	Impaired gonadotropin release or prolactin-mediated GnRH inhibition	Prolactinoma, Sheehan syndrome	Low/normal FSH/LH; prolactin may be high
Chronic anovulation	No LH surge; unopposed estrogen without cyclic progesterone	Polycystic ovary syndrome, thyroid disease	Variable FSH/LH; hyperandrogenism common in PCOS

Pregnancy must be considered first in any reproductive-age patient because trophoblastic hCG maintains the corpus luteum and progesterone production. Serum hCG becomes detectable about 8–10 days after ovulation; urine pregnancy tests are often positive around the missed menses.

Dysmenorrhea: prostaglandin-driven pain versus secondary pathology

Dysmenorrhea means painful menstruation. Primary dysmenorrhea occurs without pelvic structural disease and usually begins within 6–12 months after menarche, once ovulatory cycles are established. Progesterone withdrawal increases endometrial cyclooxygenase activity and release of prostaglandin F_2α and prostaglandin E₂, producing uterine hypercontractility, vasoconstriction, ischemia, cramping pain, nausea, diarrhea, and headache. Pain typically begins shortly before or at onset of bleeding and lasts 24–72 hours.

Secondary dysmenorrhea results from identifiable pathology and is more likely with progressive pain, noncyclic pelvic pain, dyspareunia, infertility, abnormal bleeding, or onset after age 25 years. High-yield causes include endometriosis with ectopic endometrial glands/stroma causing cyclic bleeding and inflammation, adenomyosis with endometrial tissue within myometrium causing a boggy enlarged uterus, leiomyomas, pelvic inflammatory disease, and cervical stenosis.

Drug principle	Mechanism	Step 1 relevance
NSAIDs	Inhibit COX enzymes, decreasing prostaglandin synthesis	Most mechanistically direct therapy for primary dysmenorrhea; examples include ibuprofen 400–600 mg every 6 hours or naproxen 500 mg load then 250 mg every 6–8 hours
Combined hormonal contraception	Suppresses ovulation and thins endometrium	Decreases endometrial prostaglandin production and menstrual volume

Abnormal uterine bleeding: mechanisms and classification

Abnormal uterine bleeding (AUB) refers to bleeding abnormal in frequency, regularity, duration, or volume in nonpregnant reproductive-age patients. The International Federation of Gynecology and Obstetrics classifies causes using PALM-COEIN: structural causes are Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia; nonstructural causes are Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified.

Pattern	Mechanism	Classic associations
Ovulatory dysfunction	Irregular or absent progesterone exposure leads to unstable, proliferative endometrium	PCOS, adolescence, perimenopause, thyroid disease, hyperprolactinemia
Coagulopathy	Impaired hemostasis at denuded spiral arteries	von Willebrand disease; heavy bleeding since menarche
Leiomyoma	Benign smooth muscle tumor; submucosal lesions distort endometrial cavity	Estrogen-sensitive; firm, enlarged, irregular uterus
Endometrial hyperplasia	Prolonged unopposed estrogen causes glandular proliferation	Obesity, chronic anovulation, PCOS; risk of endometrioid carcinoma

The central pathophysiologic distinction is ovulatory bleeding, which is usually predictable because progesterone withdrawal is cyclic, versus anovulatory bleeding, which is irregular because estrogen-driven endometrial proliferation outpaces vascular support and sheds unpredictably. This explains why chronic anovulation causes both amenorrhea and intermittent heavy AUB.

Clinical assessment and investigations

Initial clinical framing

Evaluation of amenorrhea, dysmenorrhea, and abnormal uterine bleeding begins by determining whether the patient is pregnant, hemodynamically stable, and at risk for structural, endocrine, or systemic disease. Menstrual history should include age at menarche, cycle interval, duration, volume, pain timing, sexual activity, contraception, weight change, exercise, eating patterns, galactorrhea, hirsutism/acne, headaches/visual symptoms, medications, and prior uterine instrumentation.

Disorder	Key definition	High-yield clinical clues
Primary amenorrhea	No menses by age 15 years with normal secondary sexual characteristics, or by 13 years without secondary sexual characteristics	Absent breasts suggests estrogen deficiency; cyclic pelvic pain suggests outflow obstruction
Secondary amenorrhea	Absence of menses for ≥3 months in previously regular cycles or ≥6 months in irregular cycles	Pregnancy, hypothalamic suppression, PCOS, hyperprolactinemia, premature ovarian insufficiency
Dysmenorrhea	Painful menstruation	Primary: begins within 6–12 months of menarche; secondary: new/worsening pain, dyspareunia, infertility, abnormal bleeding
Abnormal uterine bleeding	Bleeding abnormal in frequency, regularity, duration, or volume	Heavy bleeding, intermenstrual bleeding, postcoital bleeding, postmenopausal bleeding

Pregnancy testing and urgent assessment

A urine or serum β-hCG test is the first investigation in any reproductive-age patient with amenorrhea, pelvic pain, or abnormal bleeding. β-hCG is produced by syncytiotrophoblasts and becomes detectable in serum about 8–10 days after ovulation. Most urine tests detect β-hCG at approximately 20–25 mIU/mL; quantitative serum assays detect levels as low as 1–5 mIU/mL. In early viable intrauterine pregnancy, β-hCG typically rises by at least 35–53% over 48 hours. A β-hCG above the transvaginal ultrasound discriminatory zone, approximately 1500–3500 mIU/mL, without an intrauterine gestational sac raises concern for ectopic pregnancy.

Immediate evaluation is required for hypotension, tachycardia, syncope, peritoneal signs, severe anemia, or suspected ectopic pregnancy. Initial studies include CBC, type and screen, quantitative β-hCG, and pelvic ultrasound.

Amenorrhea: differential diagnosis and core investigations

The amenorrhea workup is organized around the hypothalamic-pituitary-ovarian-uterine axis. Normal menstruation requires pulsatile hypothalamic GnRH, pituitary FSH/LH secretion, ovarian estrogen/progesterone production, and an intact endometrium with a patent outflow tract.

Finding	Likely mechanism	Examples
High FSH, low estradiol	Primary ovarian failure due to loss of negative feedback	Turner syndrome, premature ovarian insufficiency, chemotherapy
Low/normal FSH and low estradiol	Hypothalamic or pituitary hypogonadism	Functional hypothalamic amenorrhea, pituitary mass, Sheehan syndrome
Normal estrogen with hyperandrogenism	Chronic anovulation	PCOS, nonclassic congenital adrenal hyperplasia
Normal hormones with cyclic pain	Outflow obstruction	Imperforate hymen, transverse vaginal septum, cervical stenosis

Recommended initial tests after excluding pregnancy are TSH, prolactin, FSH, and often estradiol. Elevated TSH can increase TRH, which stimulates prolactin release and suppresses GnRH. Prolactin levels are typically <20–25 ng/mL in nonpregnant women; levels >100 ng/mL strongly suggest prolactinoma, while >200 ng/mL is classically associated with macroprolactinoma. Persistent hyperprolactinemia warrants pituitary MRI, especially with headache or visual field defects.

FSH is interpreted with ovarian reserve: values repeatedly >25–40 IU/L with low estradiol support premature ovarian insufficiency in patients younger than 40. In primary amenorrhea with absent secondary sexual characteristics, obtain karyotype if gonadal dysgenesis is suspected. If secondary sexual characteristics are present but the uterus is absent, consider Müllerian agenesis or androgen insensitivity syndrome; serum testosterone and karyotype distinguish 46,XX Müllerian agenesis from 46,XY androgen insensitivity.

Dysmenorrhea: distinguishing primary from secondary causes

Primary dysmenorrhea is caused by excess endometrial prostaglandin F_2α, which increases uterine contractions and ischemic pain. Pain typically begins shortly before or at onset of menses and lasts 24–72 hours, without abnormal pelvic examination findings. Routine imaging is unnecessary when history is classic.

Secondary dysmenorrhea suggests pelvic pathology. Red flags include onset after age 25, progressively worsening pain, dyspareunia, infertility, noncyclic pain, abnormal bleeding, or pelvic mass. Evaluation includes pelvic examination, pregnancy test, NAAT testing for Chlamydia trachomatis and Neisseria gonorrhoeae when cervicitis/PID risk is present, and transvaginal ultrasound. Endometriosis is suggested by dysmenorrhea with dyspareunia and infertility; ultrasound may identify endometriomas but superficial implants require laparoscopy for definitive diagnosis.

Abnormal uterine bleeding: classification and investigations

The FIGO PALM-COEIN system classifies AUB in nonpregnant reproductive-age patients. PALM causes are structural: polyp, adenomyosis, leiomyoma, malignancy/hyperplasia. COEIN causes are nonstructural: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, and not otherwise classified.

Test	Indication	Interpretation
CBC and ferritin	Heavy or prolonged bleeding	Assesses anemia and iron deficiency; microcytosis suggests chronic blood loss
TSH, prolactin	Irregular cycles/anovulation	Thyroid disease or hyperprolactinemia disrupts GnRH pulsatility
PT, aPTT, von Willebrand testing	Heavy bleeding since menarche, easy bruising, epistaxis	von Willebrand disease is the most common inherited bleeding disorder
Transvaginal ultrasound	Suspected structural disease	Detects fibroids, polyps, adenomyosis, ovarian masses, endometrial thickening
Endometrial biopsy	Age ≥45 years, or younger with obesity, chronic anovulation, PCOS, unopposed estrogen, failed therapy, or persistent AUB	Evaluates hyperplasia and carcinoma

Postmenopausal bleeding is endometrial cancer until proven otherwise. On transvaginal ultrasound, an endometrial thickness of ≤4 mm has a negative predictive value exceeding 99% for endometrial carcinoma; thickness >4 mm or persistent bleeding requires endometrial sampling. In reproductive-age patients, endometrial thickness varies across the cycle and is less reliable as an isolated threshold.

Management, pharmacology and procedures

Initial principles: rule out pregnancy, instability, and structural disease

For any patient with amenorrhea, dysmenorrhea, or abnormal uterine bleeding (AUB), the first diagnostic and management step is a urine or serum β-hCG. Pregnancy-related bleeding, ectopic pregnancy, and pregnancy loss must be excluded before hormonal or procedural therapy. In AUB, assess hemodynamic status: tachycardia, orthostasis, syncope, pallor, or hemoglobin substantially below normal adult female range (~12–16 g/dL) suggests clinically significant blood loss. Acute unstable bleeding requires two large-bore IVs, crystalloid resuscitation, type and crossmatch, packed RBC transfusion when clinically indicated, and gynecologic consultation.

Acute abnormal uterine bleeding

AUB is classified by the PALM-COEIN system: structural causes (Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia) and nonstructural causes (Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified). Acute therapy aims to stabilize endometrium, promote vasoconstriction, and correct anemia.

Therapy	Typical dose	Mechanism and high-yield cautions
IV conjugated estrogen	25 mg IV every 4–6 h for up to 24 h, then transition to progestin or combined OCP	Rapidly promotes endometrial proliferation and hemostasis. Avoid in active/history of VTE, stroke, estrogen-dependent cancer, severe liver disease, or migraine with aura.
High-dose combined OCP	Monophasic pill containing 30–35 μg ethinyl estradiol, 1 tablet 3 times daily for 7 days, then daily	Estrogen stabilizes endometrium; progestin organizes and suppresses proliferation. Nausea is common; use antiemetic if needed.
High-dose oral progestin	Medroxyprogesterone acetate 20 mg PO 3 times daily for 7 days, then 10–20 mg daily	Best when estrogen is contraindicated. Converts proliferative endometrium to secretory/atrophic endometrium.
Tranexamic acid	1.3 g PO 3 times daily for up to 5 days during menses	Antifibrinolytic; inhibits plasminogen activation, reducing menstrual blood loss by ~30–50%. Avoid with active thromboembolism.
NSAIDs	Ibuprofen 600–800 mg every 6–8 h or naproxen 500 mg once, then 250–500 mg twice daily	Inhibit COX → decrease endometrial prostaglandins; reduce bleeding ~20–50% and treat dysmenorrhea. Avoid in renal disease, peptic ulcer disease, platelet dysfunction.

Endometrial sampling is recommended for AUB in patients ≥45 years, or younger patients with persistent bleeding, obesity, chronic anovulation/PCOS, Lynch syndrome, failed medical therapy, or other risk factors for unopposed estrogen. This tests for endometrial hyperplasia or carcinoma.

Long-term AUB control

Long-term management depends on etiology, desire for fertility, and contraindications to hormones. The 52-mg levonorgestrel intrauterine device releases approximately 20 μg/day initially and is among the most effective medical options for heavy menstrual bleeding; it causes endometrial glandular atrophy and stromal decidualization. Combined hormonal contraceptives suppress ovulation and regulate withdrawal bleeding. Cyclic progestins, such as medroxyprogesterone acetate 10 mg daily for 10–14 days each month, oppose estrogen in anovulatory cycles.

Correct iron deficiency with oral iron, commonly ferrous sulfate 325 mg containing ~65 mg elemental iron, once daily or every other day to improve absorption and reduce gastrointestinal adverse effects. Continue for about 3 months after hemoglobin normalization to replenish iron stores.

Amenorrhea management by mechanism

• Functional hypothalamic amenorrhea: due to decreased pulsatile GnRH from low energy availability, excessive exercise, stress, or eating disorder. Treatment is nutritional rehabilitation, weight restoration, reduced exercise intensity, and bone protection with calcium/vitamin D; combined OCPs may create withdrawal bleeding but do not correct the underlying hypothalamic suppression.
• PCOS: chronic anovulation causes unopposed estrogen and endometrial hyperplasia risk. Weight loss of even 5–10% can improve ovulation. Combined OCPs reduce LH-driven ovarian androgen production and increase hepatic sex hormone-binding globulin. Cyclic progestins protect the endometrium if contraception is not desired. Metformin improves insulin resistance but is not first-line solely for cycle control.
• Hyperprolactinemia: prolactin suppresses GnRH. Dopamine agonists restore ovulation by activating D2 receptors: cabergoline 0.25 mg twice weekly initially or bromocriptine 1.25–2.5 mg daily. Cabergoline has a long half-life of ~65 hours and is generally better tolerated.
• Primary ovarian insufficiency: low estrogen with high FSH before age 40. Provide physiologic estrogen plus progestin if uterus is present to prevent endometrial hyperplasia and maintain bone health until the average age of menopause (~51 years), unless contraindicated.
• Outflow tract obstruction or intrauterine adhesions: imperforate hymen or transverse vaginal septum requires surgical correction; Asherman syndrome is treated with hysteroscopic adhesiolysis.

Dysmenorrhea management

Primary dysmenorrhea results from excess endometrial prostaglandin F_2α, causing uterine hypercontractility and ischemic pain. First-line therapy is NSAIDs started 1–2 days before menses or at pain onset and continued for 48–72 hours. Hormonal contraception is also first-line, especially when contraception is desired; it suppresses ovulation, thins endometrium, and lowers prostaglandin production. Continuous combined OCP regimens reduce withdrawal bleeding frequency.

Secondary dysmenorrhea suggests endometriosis, adenomyosis, fibroids, pelvic inflammatory disease, or congenital obstruction. Endometriosis-associated pain may improve with continuous combined OCPs, progestins, depot medroxyprogesterone acetate 150 mg IM every 3 months, levonorgestrel IUD, or GnRH agonists such as leuprolide, which initially flare then downregulate pituitary GnRH receptors, decreasing LH/FSH and ovarian estrogen. Hypoestrogenic adverse effects include hot flashes and bone loss; “add-back” therapy reduces these effects.

Procedures, complications, and follow-up

Procedures are used when bleeding is severe, structural, refractory, or malignancy is suspected. Options include hysteroscopy with polypectomy, myomectomy for fertility-preserving fibroid treatment, uterine artery embolization for fibroids when fertility is not a priority, endometrial ablation only after malignancy is excluded and when future pregnancy is not desired, and hysterectomy as definitive therapy. Acute uncontrolled hemorrhage may require uterine tamponade, dilation and curettage, or operative management.

Follow-up focuses on symptom control, medication adverse effects, hemoglobin/ferritin recovery, and recurrence. Persistent amenorrhea, intermenstrual bleeding, postcoital bleeding, postmenopausal bleeding, or failure of empiric therapy warrants re-evaluation for pregnancy, endocrine disease, coagulopathy, structural lesions, and endometrial pathology.

Exam controversies and advanced synthesis

Guideline frameworks that unify exam questions

The most important synthesis point is that amenorrhea, dysmenorrhea, and abnormal uterine bleeding (AUB) are symptoms, not diagnoses. USMLE-style questions often test whether the first discriminating step is correctly chosen. In reproductive-age patients, pregnancy must be excluded first with urine or serum β-hCG, even when the history suggests “unlikely” pregnancy.

Presentation	High-yield initial framework	Classic pitfall
Primary amenorrhea	No menses by age 15 with normal secondary sexual development, or by age 13 without secondary sexual development	Failing to distinguish absent uterus from present uterus
Secondary amenorrhea	No menses for ≥3 months if previously regular, or ≥6 months if previously irregular	Forgetting pregnancy, hyperprolactinemia, thyroid disease, and hypothalamic suppression
AUB	FIGO PALM-COEIN classification	Calling all heavy bleeding “dysfunctional uterine bleeding”; that term is now outdated
Dysmenorrhea	Primary = prostaglandin-mediated pain without pelvic pathology; secondary = structural/inflammatory disease	Missing endometriosis when pain begins before menses, persists after menses, or is associated with dyspareunia/infertility

PALM-COEIN and biopsy thresholds

FIGO classifies AUB into structural causes—Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia—and nonstructural causes—Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified. This is more than terminology: it predicts mechanism. For example, anovulation causes prolonged unopposed estrogen stimulation, leading to proliferative, fragile endometrium and irregular heavy bleeding; von Willebrand disease causes impaired platelet adhesion and heavy bleeding from menarche.

Endometrial sampling is generally recommended for AUB in patients ≥45 years, and in younger patients with risk factors such as obesity, chronic anovulation/PCOS, Lynch syndrome, failed medical therapy, or persistent bleeding. This threshold is a frequent exam distinction: a 19-year-old with irregular anovulatory cycles is not managed the same way as a 52-year-old with new postmenopausal bleeding. Postmenopausal bleeding requires evaluation; a transvaginal ultrasound endometrial stripe of ≤4 mm has a very high negative predictive value for endometrial carcinoma, but persistent bleeding still warrants tissue diagnosis.

Pharmacologic mechanisms and clinically useful doses

Therapy	Typical use	Mechanism	High-yield dose/number
NSAIDs, e.g., ibuprofen, naproxen, mefenamic acid	Primary dysmenorrhea; ovulatory heavy bleeding	Inhibit COX → decreased prostaglandin F2α and E2 → decreased uterine contractions and ischemic pain	Ibuprofen 600–800 mg every 6–8 h; start 1–2 days before menses if predictable
Combined oral contraceptives	Dysmenorrhea, anovulatory AUB, endometriosis-associated pain	Suppress ovulation; stabilize endometrium; reduce menstrual volume	Ethinyl estradiol commonly 20–35 μg with progestin
Levonorgestrel intrauterine system	Heavy menstrual bleeding, endometrial protection	Local progestin → endometrial decidualization/atrophy	52-mg device releases approximately 20 μg/day initially
Tranexamic acid	Heavy menstrual bleeding, especially when hormonal therapy undesired	Lysine analog; inhibits plasminogen activation → antifibrinolytic	1.3 g orally three times daily for up to 5 days during menses
High-dose estrogen	Acute severe uterine bleeding in selected hemodynamically stable patients	Rapidly promotes endometrial regrowth and hemostasis	Conjugated estrogen 25 mg IV every 4–6 h for short course; avoid in high thrombotic risk

Controversies and “viva-level” distinctions

PCOS diagnostic criteria vary. NIH criteria emphasize hyperandrogenism plus oligo/anovulation, whereas Rotterdam criteria require any 2 of 3: oligo/anovulation, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology. For Step 1, remember the mechanism: increased GnRH pulse frequency favors LH over FSH, theca cells produce androgens, and peripheral aromatization in adipose tissue contributes to unopposed estrogen exposure and endometrial hyperplasia risk.

Endometriosis may be treated empirically, but laparoscopy is definitive. Ectopic endometrial glands and stroma respond cyclically to estrogen, causing bleeding, inflammation, fibrosis, and adhesions. Classic findings include dysmenorrhea, chronic pelvic pain, dyspareunia, dyschezia, infertility, “chocolate cyst” ovarian endometrioma, and powder-burn lesions. Exam questions may contrast this with adenomyosis: endometrial tissue within the myometrium causing a diffusely enlarged, boggy uterus and heavy painful menses, classically in multiparous patients.

The progesterone withdrawal test is conceptually useful but not the modern first step in all cases. Bleeding after progestin indicates estrogenized endometrium and patent outflow tract, suggesting chronic anovulation. No bleeding suggests low estrogen, endometrial damage such as Asherman syndrome, or outflow obstruction. Current algorithms usually begin with β-hCG, TSH, prolactin, and then FSH/estradiol guided by history.

Numerical endocrine interpretation

• High FSH with low estradiol suggests primary ovarian insufficiency or gonadal dysgenesis; menopause typically has FSH >25–40 IU/L depending on assay.
• Low or normal FSH/LH with low estradiol suggests hypothalamic or pituitary dysfunction, including exercise, weight loss, stress, chronic disease, or pituitary lesions.
• Hyperprolactinemia suppresses GnRH. Prolactin levels >200 ng/mL strongly suggest prolactinoma, although pregnancy, hypothyroidism, dopamine antagonists, and stalk effect can elevate levels.
• TSH elevation can increase TRH, which stimulates prolactin release, producing amenorrhea/galactorrhea.

Common exam traps

• Müllerian agenesis vs androgen insensitivity: both may have absent uterus. Müllerian agenesis has normal 46,XX ovaries and normal pubic hair; complete androgen insensitivity is 46,XY with testes, breast development from aromatized testosterone, and sparse pubic/axillary hair.
• Imperforate hymen: primary amenorrhea with cyclic pelvic pain and a bulging bluish hymen due to hematocolpos.
• Asherman syndrome: secondary amenorrhea after uterine curettage or infection due to intrauterine adhesions and damaged basalis layer.
• Coagulopathy clue: heavy bleeding since menarche, easy bruising, epistaxis, or family history suggests von Willebrand disease.