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Summary Table

Category	Details
Risk Factors	African American descent, early menarche, nulliparity, obesity, age 30-50, family history, late menopause
Etiology	Benign monoclonal smooth muscle tumor of the myometrium; estrogen- and progesterone-dependent
Patient Presentation	Heavy menstrual bleeding (menorrhagia), pelvic pressure/fullness, bulk symptoms (urinary frequency, constipation)
Classic Physical Exam	Enlarged, irregularly shaped ("bulky") uterus on bimanual exam; firm, nontender, mobile
Key Diagnostic Results	Pelvic ultrasound showing well-circumscribed, hypoechoic myometrial masses; CBC often reveals iron deficiency anemia
Management	Medical: GnRH agonists, hormonal contraceptives. Surgical: myomectomy (fertility-sparing) or hysterectomy (definitive)
Keywords	"Bulky uterus," "whorled pattern," "irregular uterine contour," "heavy periods with clots," "pressure symptoms"

1. Pathophysiology

Uterine fibroids are benign monoclonal neoplasms arising from the smooth muscle cells of the myometrium. Each fibroid originates from a single progenitor cell that undergoes somatic mutation, leading to clonal expansion. Their growth is critically dependent on estrogen and progesterone, which is why fibroids enlarge during reproductive years, may grow rapidly during pregnancy (when hormone levels surge), and typically regress after menopause when hormonal stimulation declines.

At the molecular level, estrogen promotes fibroid growth by upregulating growth factors such as transforming growth factor-beta (TGF-B) and epidermal growth factor (EGF). Progesterone contributes by increasing cellular proliferation and inhibiting apoptosis within the tumor. This hormonal dependency is the fundamental principle behind medical therapy: if you remove the hormonal stimulus, the fibroid shrinks.

The clinical manifestations are directly tied to the location, size, and number of fibroids. Submucosal fibroids distort the endometrial cavity, increasing the endometrial surface area and disrupting normal hemostatic mechanisms during menstruation, which leads to heavy menstrual bleeding. This is why submucosal fibroids are the most symptomatic type even when small. Intramural fibroids sit within the myometrial wall and cause uterine enlargement, contributing to dysmenorrhea and pressure symptoms. Subserosal fibroids project outward from the uterine surface and compress adjacent structures: anterior fibroids press on the bladder (causing urinary frequency and urgency), while posterior fibroids compress the rectum (causing constipation or tenesmus).

A pedunculated subserosal fibroid can undergo torsion, presenting as acute pelvic pain, which mimics ovarian torsion or appendicitis on exam vignettes. Fibroids that outgrow their blood supply undergo various forms of degeneration. The most tested form is red (carneous) degeneration, which classically occurs during pregnancy and presents with acute localized pain, low-grade fever, and uterine tenderness. On histology, fibroids display a characteristic whorled pattern of smooth muscle bundles with well-circumscribed borders, distinguishing them from leiomyosarcoma.

2. Classification and Clinical Manifestation

By Location

Classification	FIGO Subtype	Clinical Manifestation
Submucosal	Type 0: Pedunculated intracavitary	Menorrhagia, intermenstrual bleeding, infertility, recurrent pregnancy loss
	Type 1: <50% intramural	Same as above, less severe
	Type 2: >=50% intramural	Menorrhagia, mild pressure symptoms
Intramural	Type 3: Contacts endometrium	Menorrhagia, dysmenorrhea, bulk symptoms
Intramural	Type 4: Entirely within myometrium	Uterine enlargement, pressure symptoms, dysmenorrhea
Subserosal	Type 5: >=50% intramural	Pelvic pressure, bladder/bowel compression
	Type 6: <50% intramural	Pressure symptoms, palpable abdominal mass if large
	Type 7: Pedunculated subserosal	Risk of torsion (acute abdomen), compression of adjacent organs
Cervical / Parasitic	Type 8: Other (cervical, broad ligament, parasitic)	Dyspareunia, obstructed labor, ureteral obstruction

By Degeneration

Degeneration Type	Context	Presentation
Hyaline degeneration	Most common type overall	Usually asymptomatic
Red (carneous) degeneration	Pregnancy (2nd trimester)	Acute pain, fever, localized tenderness, leukocytosis
Cystic degeneration	Advanced hyaline degeneration	Pelvic pressure
Calcific degeneration	Postmenopausal	Incidental "popcorn" calcifications on imaging
Sarcomatous degeneration	Rare (<1%), postmenopausal	Rapid uterine growth, postmenopausal bleeding

3. Diagnostic Workup

Test	Role	Key Findings
Pelvic ultrasound (transvaginal)	Best initial test	Well-circumscribed, hypoechoic, solid myometrial masses; may show calcifications
Saline infusion sonohysterography (SIS)	Best test for submucosal fibroids	Delineates intracavitary extension and endometrial distortion
MRI pelvis	Most accurate test (gold standard for mapping)	Precise location, size, number; distinguishes fibroid from adenomyosis; T2-weighted shows low-signal whorled masses
Hysteroscopy	Diagnostic and therapeutic for submucosal fibroids	Direct visualization and possible resection
CBC	Screening for anemia	Microcytic hypochromic anemia (iron deficiency from chronic blood loss)
Endometrial biopsy	Rule out endometrial pathology	Required in women >35 with abnormal uterine bleeding or in younger women with risk factors for endometrial cancer

Pelvic ultrasound (transvaginal preferred) is the first-line imaging for any woman presenting with abnormal uterine bleeding and an enlarged or irregular uterus on exam. Fibroids appear as well-defined, solid, hypoechoic masses within the myometrium. Ultrasound can identify size, number, and general location but is less reliable for distinguishing submucosal from intramural fibroids when the distinction matters clinically.

When submucosal location is suspected (i.e., the patient has disproportionately heavy bleeding relative to fibroid size), saline infusion sonohysterography is the next step. The instillation of saline into the uterine cavity allows the intracavitary component to be clearly delineated, which directly impacts surgical planning.

MRI is reserved for cases where ultrasound is inconclusive, when surgical planning demands precise anatomic mapping (e.g., before myomectomy in a patient with multiple fibroids), or when leiomyosarcoma must be excluded. On T2-weighted MRI, fibroids classically appear as well-circumscribed masses with low signal intensity (dark), reflecting their dense fibrous composition. This contrasts with leiomyosarcoma, which shows heterogeneous signal, irregular borders, and areas of necrosis.

A critical exam principle: any woman over 35 with abnormal uterine bleeding must have an endometrial biopsy to rule out endometrial hyperplasia or carcinoma before attributing the bleeding solely to fibroids. Do not skip this step in a vignette that mentions age over 35 or risk factors for endometrial cancer (obesity, anovulation, tamoxifen use).

4. Management and Treatment

Clinical Scenario	Treatment	Details
Asymptomatic fibroids	Observation	Serial ultrasound monitoring every 6-12 months
Mild symptoms / temporizing	Combined oral contraceptives or levonorgestrel IUD (Mirena)	Controls bleeding; does not shrink fibroids
Preoperative shrinkage	GnRH agonist (leuprolide 3.75 mg IM monthly)	Creates hypoestrogenic state; shrinks fibroids 30-50% over 3-6 months; limited to 6 months due to bone loss
Moderate bleeding, desires fertility	Myomectomy (hysteroscopic for submucosal, laparoscopic/open for others)	Fertility-sparing; 15-30% recurrence rate
Moderate symptoms, completed childbearing	Uterine artery embolization (UAE)	Minimally invasive; contraindicated if future pregnancy desired
Definitive treatment	Hysterectomy (total abdominal, laparoscopic, or vaginal)	Only cure with 0% recurrence; offered when childbearing is complete and symptoms are refractory
Acute heavy bleeding	IV conjugated estrogen 25 mg every 4-6 hours, then transition to OCP	Stabilizes endometrium acutely
Red degeneration in pregnancy	Supportive care: NSAIDs (avoid in 3rd trimester), IV fluids, rest	Self-limited; surgery is not indicated

Asymptomatic fibroids found incidentally require no treatment. The exam commonly tests this: a patient with an incidental finding of a small fibroid on ultrasound and no symptoms does not need intervention. The answer is observation with periodic imaging.

For symptomatic management, the approach depends on whether the patient desires future fertility. Hormonal therapy with combined oral contraceptives or a levonorgestrel-releasing IUD effectively reduces menstrual blood loss but does not decrease fibroid size. The levonorgestrel IUD is a strong first-line option for women with heavy bleeding who want nonsurgical management, but it may not be suitable if the fibroid distorts the uterine cavity (risk of expulsion).

GnRH agonists (leuprolide) are used as a bridge to surgery, not as standalone long-term therapy. They suppress gonadotropin secretion, creating a pseudomenopausal state that shrinks fibroids by 30-50% within 3-6 months. However, once discontinued, fibroids rapidly regrow. Long-term use beyond 6 months is limited by side effects: bone density loss, vasomotor symptoms, and vaginal atrophy. Add-back therapy with low-dose estrogen/progesterone can mitigate these effects. A newer oral GnRH antagonist, elagolix, achieves similar results with more convenient dosing.

Myomectomy is the surgical treatment of choice for women who want to preserve fertility. Approach depends on location: hysteroscopic myomectomy for submucosal fibroids (FIGO type 0-2), laparoscopic or open abdominal myomectomy for intramural/subserosal fibroids. The key limitation is a 15-30% recurrence rate, and patients must be counseled that repeat surgery may be necessary.

Uterine artery embolization (UAE) involves catheter-based injection of embolic particles into the uterine arteries, causing ischemic necrosis of the fibroids. It is effective for symptom relief but is contraindicated in women desiring pregnancy due to concerns about ovarian reserve and uterine integrity. A common exam trap is offering UAE to a patient who wants future children.

Hysterectomy is the only definitive cure. It eliminates recurrence entirely and is appropriate for women who have completed childbearing and have failed or declined other treatments. The route (vaginal, laparoscopic, or abdominal) depends on uterine size and surgical accessibility.

For red degeneration during pregnancy, management is conservative: analgesics (NSAIDs in the 2nd trimester, acetaminophen in the 3rd), hydration, and rest. Surgical intervention is avoided because it risks preterm labor and hemorrhage.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Adenomyosis	Enlarged uterus, heavy menstrual bleeding, dysmenorrhea	Uterus is diffusely enlarged and boggy/tender (not irregular); pain worsens progressively with menses; MRI shows junctional zone thickening >12 mm
Endometrial polyp	Abnormal uterine bleeding, intracavitary mass	Polyps are typically smaller, pedunculated, and echogenic on ultrasound; bleeding is often intermenstrual rather than heavy menses
Leiomyosarcoma	Pelvic mass arising from myometrium	Rapid growth especially postmenopausal; heterogeneous appearance on MRI with necrosis; elevated LDH; cannot reliably distinguish from fibroid preoperatively
Endometrial carcinoma	Abnormal uterine bleeding in older women	Postmenopausal bleeding, endometrial thickening >4 mm; diagnosed by endometrial biopsy, not ultrasound alone
Ovarian fibroma	Solid pelvic mass	Separate from the uterus on imaging; may present with Meigs syndrome (ascites + pleural effusion)
Pregnancy	Enlarged uterus, amenorrhea	Always obtain beta-hCG before attributing uterine enlargement to fibroids in a reproductive-age woman

6. Traps and High-Yield Pearls

The most common trap with uterine fibroids is confusing them with adenomyosis. Both cause an enlarged uterus and heavy menstrual bleeding, but the physical exam findings are different: fibroids produce an irregularly enlarged, nontender, firm uterus with a contour that feels "lumpy," while adenomyosis presents with a diffusely enlarged, globular, and tender uterus. If the vignette describes progressive dysmenorrhea with a uniformly boggy uterus, think adenomyosis. If it describes a woman with bulk symptoms and an irregular uterine contour, think fibroids.

Another frequently tested mistake is choosing the wrong surgical approach based on fertility goals. If the patient wants future pregnancies, the answer is myomectomy, not hysterectomy and not UAE. The exam will bury the fertility desire in one sentence mid-vignette to test whether you caught it. Always scan for the phrase "desires future fertility" or "has not completed childbearing" before selecting a management option.

A third trap involves the postmenopausal patient with a rapidly enlarging uterine mass. Fibroids should shrink after menopause due to estrogen withdrawal. If a fibroid is growing in a postmenopausal woman, the concern shifts to leiomyosarcoma, and the next step is surgical excision with pathologic evaluation, not observation.

Finally, never forget to check a pregnancy test in any reproductive-age woman with an enlarged uterus. The vignette may describe what sounds like a straightforward fibroid, but if the stem mentions missed periods or amenorrhea, beta-hCG must be obtained first. This tests whether you follow the fundamental principle of ruling out pregnancy before pursuing any gynecologic workup.

The core competency being tested with fibroids is the ability to match symptoms to fibroid location, select the correct imaging modality for the clinical question, and tailor treatment to the patient's reproductive goals. Test-writers expect you to reason through location-based pathophysiology, not simply memorize a treatment algorithm.

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