Step 2 CK · Obstetrics & Gynecology

Menstrual Disorders & Abnormal Bleeding

Name: Menstrual Disorders & Abnormal Bleeding
Creator: Veli Bakalov, MD

From the amenorrhea algorithm to PALM-COEIN and the pelvic pain syndromes

Obstetrics & Gynecology·Gynecology·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Primary amenorrhea is no menses by 15 with secondary sex characteristics (or by 13 without); secondary is ≥3 months absent after regular cycles; always rule out pregnancy first.
Absent uterus with primary amenorrhea: MRKH is 46,XX with female-range testosterone and pubic hair; androgen insensitivity is 46,XY with testes, male-range testosterone, and scant hair.
Secondary amenorrhea workup: β-hCG, then TSH and prolactin, then progestin challenge, then FSH (high = ovarian failure, low = hypothalamic).
No withdrawal bleed even after estrogen plus progestin means an outflow problem such as Asherman syndrome; hysteroscopy diagnoses and treats it.
PALM-COEIN organizes AUB; biopsy the endometrium at ≥45 or when younger with obesity, PCOS, chronic anovulation, unopposed estrogen, or tamoxifen.
Heavy menses since menarche with mucosal bleeding suggests von Willebrand disease, the most common inherited bleeding disorder.
Primary dysmenorrhea is prostaglandin-mediated and treated first with NSAIDs; endometriosis (dysmenorrhea, dyspareunia, dyschezia, infertility) is confirmed by laparoscopy.
Adenomyosis is a diffusely enlarged, boggy, tender uterus with menorrhagia in a parous woman in her 40s; hysterectomy is definitive.
POI (FSH >25 IU/L with 4 or more months of oligo/amenorrhea, low estrogen, before 40) needs estrogen replacement until menopausal age; PCOS (2 of 3 Rotterdam criteria) needs OCPs or cyclic progestin to protect the endometrium.

Amenorrhea: definitions and primary causes

Definitions. Primary amenorrhea is no menses by age 15 with normal secondary sex characteristics, or by 13 without them. Secondary amenorrhea is absence of menses for ≥3 months in a woman with previously regular cycles (or 6 months if cycles were irregular). The workups differ, but pregnancy is always ruled out first.

Classic causes of primary amenorrhea

Condition	Karyotype	Uterus	Breasts	Key findings
Turner syndrome	45,X	Present	Absent	Streak gonads, high FSH, short stature
Müllerian agenesis (MRKH)	46,XX	Absent (with upper vagina)	Normal	Normal ovaries, female-range testosterone, normal pubic hair; check for renal anomalies
Androgen insensitivity	46,XY	Absent	Normal (aromatized testosterone)	Female externals, blind vaginal pouch, testes, male-range testosterone, scant pubic hair
Imperforate hymen	46,XX	Present	Normal	Cyclic pelvic pain, hematocolpos, bulging bluish membrane

MRKH and androgen insensitivity both lack a uterus; testosterone level and karyotype separate them.

Androgen insensitivity carries a risk of malignancy in the undescended testes, so gonadectomy is performed, typically after puberty is complete. Hypogonadotropic causes of primary amenorrhea include constitutional delay and Kallmann syndrome (with anosmia).

Secondary amenorrhea, POI, and PCOS

β-hCGpregnancy is the most common cause—test before anything else
TSH and prolactinthyroid disease; hyperprolactinemia from a prolactinoma or dopamine-blocking drugs
Progestin challengewithdrawal bleed = estrogen present and outflow patent, so the problem is anovulation (e.g., PCOS)
No bleed → estrogen plus progestinstill no bleed = outflow problem (Asherman syndrome)
FSHhigh = ovarian failure; low or normal = hypothalamic-pituitary cause

Asherman syndrome. Intrauterine adhesions after a D&C or infection block the endometrium from responding, so even estrogen plus progestin produces no withdrawal bleed. Hysteroscopy is both diagnostic and therapeutic (adhesiolysis).

Ovarian and hypothalamic causes of secondary amenorrhea

Feature	Hypothalamic amenorrhea	Primary ovarian insufficiency	PCOS
FSH	Low or normal	High	Normal (LH often elevated)
Estrogen	Low	Low	Normal, unopposed
Progestin challenge	No bleed	No bleed	Withdrawal bleed
Setting	Stress, weight loss, excessive exercise, eating disorders	Before 40: Turner mosaicism, fragile X premutation, autoimmune oophoritis, chemo/radiation	Oligomenorrhea, hirsutism, acne, obesity, insulin resistance
Main risk	Bone loss	Bone loss, cardiovascular disease	Endometrial hyperplasia, diabetes

Primary ovarian insufficiency (POI) is loss of ovarian function before age 40—amenorrhea with high FSH and low estrogen (2024 guideline: oligomenorrhea or amenorrhea for 4 months or more plus a single FSH above 25 IU/L), often with hot flashes and vaginal dryness. Evaluate with a karyotype and FMR1 premutation testing, and screen for other autoimmune endocrine disease. Because it is hypoestrogenic, give estrogen replacement until the typical age of menopause to protect bone and cardiovascular health; pregnancy usually requires donor oocytes.

Polycystic ovary syndrome requires 2 of 3 Rotterdam criteria—oligo- or anovulation, hyperandrogenism (clinical or biochemical), and polycystic ovaries—after excluding thyroid disease, hyperprolactinemia, and nonclassic congenital adrenal hyperplasia. It is a leading cause of oligomenorrhea and anovulatory bleeding, with endometrial hyperplasia risk from unopposed estrogen. Combined OCPs or cyclic progestin restore withdrawal bleeding and protect the endometrium; weight loss and metformin address insulin resistance, spironolactone treats hirsutism, and letrozole induces ovulation.

Abnormal uterine bleeding

PALM-COEIN organizes any abnormal uterine bleeding (AUB) workup:

PALM (structural): Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia.
COEIN (nonstructural): Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified.

Workup. Evaluate AUB with β-hCG, CBC, TSH, and transvaginal ultrasound. Perform an endometrial biopsy to exclude hyperplasia or cancer if the patient is ≥45, or younger with risk factors: obesity, PCOS, chronic anovulation, unopposed estrogen, tamoxifen, or failed medical therapy.

Anovulatory bleeding (AUB-O) is common at the reproductive extremes—adolescence and perimenopause. Without ovulation there is no corpus luteum and no progesterone, so unopposed estrogen causes endometrial overgrowth and irregular, heavy shedding. Manage with combined OCPs or progestins. Acute heavy bleeding responds to high-dose estrogen or OCPs or tranexamic acid (D&C if unstable), and a levonorgestrel IUD is excellent maintenance.

Heavy menstrual bleeding since menarche—especially with easy bruising, epistaxis, or bleeding after dental work—suggests von Willebrand disease, the most common inherited bleeding disorder. Check a von Willebrand panel and CBC; treatment options include desmopressin, hormonal therapy, and tranexamic acid.

Dysmenorrhea, endometriosis, and adenomyosis

Primary dysmenorrhea has no pelvic pathology: prostaglandin-mediated cramping that starts with menses in young women and typically improves with age and after childbirth. NSAIDs are first-line (they inhibit prostaglandin synthesis), with combined OCPs as an add-on. Secondary dysmenorrhea implies an underlying lesion—endometriosis, adenomyosis, or fibroids—and often begins later in life.

Endometriosis vs adenomyosis

Feature	Endometriosis	Adenomyosis
Lesion	Endometrial tissue outside the uterus (ovaries, cul-de-sac, uterosacral ligaments)	Endometrial glands within the myometrium
Typical patient	Reproductive-age woman, often with infertility	Parous woman in her 40s
Symptoms	Dysmenorrhea, dyspareunia, dyschezia, infertility	Menorrhagia and dysmenorrhea
Exam	Fixed, retroverted uterus; cul-de-sac nodularity; endometriomas ("chocolate cysts")	Diffusely enlarged, boggy, tender uterus
Diagnosis	Laparoscopy with biopsy (gold standard)	MRI supports; histology after hysterectomy
Treatment	NSAIDs, OCPs, progestins, GnRH agonists (leuprolide); excision of implants	Hormonal therapy (e.g., levonorgestrel IUD); hysterectomy is definitive

A normal pelvic ultrasound does not rule out endometriosis—only laparoscopy visualizes implants. Fibroids, by contrast, make the uterus firm, irregular, and nontender.