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You are here: Home / Podcasts / 163 Pelvic Pain Playbook – Endometriosis, Fibroids, Cysts & Torsion

163 Pelvic Pain Playbook – Endometriosis, Fibroids, Cysts & Torsion

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Endometriosis

  • Presence of endometrial glands and stroma outside the uterine cavity, most commonly on the ovaries, fallopian tubes, pelvic peritoneum, and uterosacral ligaments
  • The tissue behaves like endometrium: bleeds with every cycle, causing inflammation, adhesions, and scarring

Risk Factors

  • Nulliparity, early menarche, short cycles → increased lifetime exposure to retrograde menstruation
  • Family history → first-degree relatives have 7-10x higher risk
  • Retrograde menstruation is the dominant theory (Sampson’s theory)
  • Mullerian anomalies with outflow obstruction → accelerated disease

Clinical Presentation

  • Classic triad: dysmenorrhea (cyclic pelvic pain that starts before menses and worsens through the cycle), dyspareunia (deep, not superficial), and infertility
  • Pain is cyclic and progressive, gets worse over time, not better. If the student’s first instinct is “primary dysmenorrhea,” ask: is this getting worse, not better?
  • Dyspareunia in endometriosis is deep because of uterosacral ligament and posterior cul-de-sac involvement. Superficial dyspareunia points elsewhere.
  • Dyschezia (painful defecation during menses) when posterior lesions involve the rectovaginal septum
  • Ovarian endometriomas (“chocolate cysts”) can rupture and cause acute pelvic pain

Diagnostics

  • Pelvic ultrasound is first-line imaging. Identifies endometriomas (thick-walled, homogeneous hypoechoic ovarian cysts with ground-glass echogenicity) but does not diagnose peritoneal implants
  • Definitive diagnosis: laparoscopy with direct visualization and biopsy. No lab test or imaging confirms the diagnosis
  • On exam: fixed, retroverted uterus, uterosacral nodularity, adnexal tenderness
  • CA-125 may be elevated but is nonspecific, not a diagnostic test

Treatment

  • NSAIDs first for pain management
  • Hormonal suppression is the cornerstone: combined OCPs (continuous dosing), progestins, or GnRH agonists (leuprolide) for moderate-to-severe disease. GnRH agonists create a pseudomenopause state, highly effective for pain but used with add-back estrogen to prevent bone loss
  • Surgical (laparoscopic excision or ablation): definitive for diagnosis and treatment. First-line for infertility associated with endometriosis
  • Hysterectomy with bilateral salpingo-oophorectomy for women who have completed childbearing and failed other therapies
  • Pregnancy does not cure endometriosis, symptoms often return post-partum

Exam Keys

  • Cyclic pelvic pain + deep dyspareunia + infertility = endometriosis until proven otherwise
  • Definitive diagnosis requires laparoscopy, not imaging
  • Chocolate cyst = endometrioma on ultrasound
  • GnRH agonists suppress estrogen → pain relief, but use with add-back therapy to protect bone
  • Primary dysmenorrhea improves with age and after pregnancy. Endometriosis gets worse

Leiomyoma (Uterine Fibroids)

  • Benign smooth muscle tumors of the myometrium, most common benign gynecologic tumor and most common indication for hysterectomy in the US
  • Location determines symptoms: submucosal fibroids bleed, intramural fibroids cause bulk, subserosal fibroids cause pressure

Risk Factors

  • African American women have 2-3x higher incidence and more severe disease
  • Increased estrogen exposure: nulliparity, early menarche, obesity, exogenous estrogen
  • Family history
  • Fibroids grow under estrogen stimulation → enlarge during pregnancy, shrink after menopause

Clinical Presentation

  • Submucosal (into the uterine cavity): heavy menstrual bleeding (most common), prolonged periods, iron deficiency anemia. This is the type boards test for bleeding
  • Intramural (within the myometrium): pelvic pressure, dysmenorrhea, enlarged irregular uterus on exam
  • Subserosal (external surface): urinary frequency or urgency from bladder compression, constipation, pelvic fullness
  • Pedunculated fibroids can torse, causing acute pelvic pain. Think torsion when a known fibroid patient presents with sudden pain
  • Up to 50% are asymptomatic, found incidentally

Diagnostics

  • Pelvic ultrasound is first-line: well-circumscribed, hypoechoic masses within or adjacent to the uterus
  • MRI for surgical planning or when US findings are equivocal
  • CBC to assess for iron deficiency anemia if heavy bleeding
  • Hysteroscopy for submucosal fibroids when ablation or resection is planned

Treatment

  • Asymptomatic: observation. Fibroids shrink after menopause
  • Medical (to control bleeding):
    • Tranexamic acid (antifibrinolytic) or NSAIDs for acute heavy periods
    • Combined OCPs or progestins to regulate cycles
    • GnRH agonists (leuprolide): shrink fibroids preoperatively, short-term use only (bone loss)
    • Ulipristal acetate (progesterone receptor modulator): limited US availability
  • Surgical:
    • Myomectomy: preserves the uterus, preferred for women desiring fertility
    • Hysterectomy: definitive cure, only option that eliminates recurrence
    • Uterine artery embolization (UAE): minimally invasive, cuts off blood supply to shrink fibroids. Contraindicated if future pregnancy desired
    • Endometrial ablation for submucosal bleeding, effective for bleeding but does not treat the fibroid itself

Exam Keys

  • Heavy periods + irregular enlarged uterus + anemia = leiomyoma until proven otherwise
  • Location drives symptoms: submucosal → bleeding, subserosal → pressure
  • GnRH agonists shrink fibroids but are short-term only (bone loss)
  • Myomectomy preserves fertility. Hysterectomy is definitive
  • Fibroids grow with estrogen and shrink after menopause

Ovarian Cysts

  • Fluid-filled sacs on or within the ovary, most commonly functional cysts from normal follicular development
  • The key clinical question: functional vs. pathologic, and in postmenopausal women, benign vs. malignant

Types

  • Functional cysts (follicular and corpus luteum): reproductive age women, irregular ovulation
  • Endometrioma: endometriosis history
  • Dermoid cyst (mature teratoma): most common in women ages 20-40, contains ectoderm-derived tissues (hair, teeth, sebaceous material)
  • Cystadenoma: serous (thin-walled, watery) or mucinous (multilocular, large). Risk for malignant transformation, especially mucinous
  • Postmenopausal ovarian cysts have higher malignancy risk, require closer evaluation regardless of size

Clinical Presentation

  • Most ovarian cysts are asymptomatic, found incidentally on pelvic ultrasound
  • Symptomatic: dull, unilateral pelvic ache, bloating, pelvic heaviness, dyspareunia
  • Ruptured cyst: sudden onset sharp unilateral pelvic pain, often mid-cycle (follicular) or shortly after ovulation (corpus luteum). Usually self-limited. Hemorrhagic rupture can cause hemodynamic instability
  • Dermoid cysts: can torse because of the weight of their contents → acute pelvic pain. Ovarian mass with calcifications or fat density in a young woman is dermoid until proven otherwise

Diagnostics

  • Pelvic ultrasound is first-line. Characterize: size, unilocular vs. multilocular, solid components, septations, Doppler flow
  • Simple, thin-walled, unilocular cyst <10 cm in a reproductive-age woman: likely functional, observe
  • Complex features (thick walls, solid components, septations, internal flow): further workup, MRI or surgical evaluation
  • Dermoid: heterogeneous echogenicity on US, calcifications or hyperechoic components (fat)
  • Endometrioma: thick-walled, homogeneous hypoechoic (“ground-glass”) appearance
  • CA-125: elevated in epithelial ovarian cancer but also endometriosis, PID, and fibroids. Nonspecific in premenopausal women, more useful in postmenopausal women with complex cysts
  • Postmenopausal simple cyst <1 cm: usually benign, observe. Any complex features in a postmenopausal woman → surgical evaluation

Treatment

  • Functional cysts: observe for 2-3 menstrual cycles, most resolve spontaneously. OCPs prevent new functional cysts but do not shrink existing ones
  • Ruptured cyst (no hemodynamic compromise): analgesics, observation
  • Hemorrhagic rupture with hemodynamic instability: surgical intervention
  • Dermoid, cystadenoma, persistent or complex cysts: surgical excision (ovarian cystectomy if fertility preservation desired)
  • Postmenopausal complex cysts: surgical evaluation regardless of size

Exam Keys

  • Most ovarian cysts in reproductive-age women are functional and resolve in 2-3 cycles
  • Mid-cycle sudden unilateral pain = ruptured follicular cyst, usually self-limited
  • Dermoid = young woman, heterogeneous mass, calcifications, risk for torsion
  • Complex cyst features (solid components, septations, thick walls) → further workup, especially postmenopausal
  • CA-125 is only clinically useful in postmenopausal women with complex adnexal masses

Ovarian Torsion

  • Twisting of the ovary (with or without the fallopian tube) on its ligamentous supports, compromising venous outflow first, then arterial supply, leading to ischemia and necrosis
  • Surgical emergency. The window to preserve the ovary is narrow

Risk Factors

  • Ovarian cyst or mass (especially dermoid cysts) in reproductive-age women, the most common predisposing factor
  • Ovarian hyperstimulation syndrome (OHSS) from fertility treatments → enlarged ovaries, high torsion risk
  • Pregnancy (enlarged ovaries, lax ligaments)
  • Large adnexal masses are more likely to torse because they displace the ovary from its normal position
  • Right side more common than left because the sigmoid colon limits left-side mobility

Clinical Presentation

  • Sudden onset severe unilateral pelvic pain, most commonly right side
  • Nausea and vomiting are almost universal, boards will include this
  • Low-grade fever is a late sign indicating infarction and necrosis, early torsion is afebrile
  • Pain may be intermittent if torsion is partial or the ovary twists and untwists spontaneously
  • Adnexal tenderness and palpable adnexal mass on bimanual exam

Diagnostics

  • Pelvic ultrasound with Doppler is first-line
  • Reduced or absent Doppler flow suggests torsion, but normal Doppler flow does not rule it out. The ovary can have partial torsion with preserved flow early on
  • US may show enlarged, edematous ovary, free pelvic fluid, or the underlying cyst/mass that caused torsion
  • Diagnosis is ultimately surgical. If clinical suspicion is high, do not let a normal Doppler delay the OR

Treatment

  • Surgical detorsion via laparoscopy, performed urgently. Time to OR matters
  • Even a black, necrotic-appearing ovary can recover after detorsion. Cystectomy or oophorectomy decided intraoperatively based on viability
  • Do not empirically remove the ovary unless clearly non-viable
  • Postoperative oophoropexy (suturing the ovary to prevent recurrence) may be performed, especially with prior torsion

Exam Keys

  • Sudden pelvic pain + nausea/vomiting + known ovarian cyst = torsion until proven otherwise
  • Normal Doppler does not rule out torsion. High suspicion = go to the OR
  • Right side more common than left
  • Early = afebrile. Fever = late sign of necrosis
  • Treatment is surgical detorsion. Even a dark ovary may be salvageable

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