PA29.6-8 | Cervicitis, Endometriosis & Adenomyosis — Summary & Reflection

REFLECT

Pause and reflect before moving to the summary.

Connect the thread across all three conditions:

All three disorders you have studied today represent variations on the theme of endometrial tissue behaving outside its normal boundaries. In cervicitis, the offence is external — pathogens or trauma breaching the cervical epithelium. In endometriosis, endometrial tissue escapes the uterine cavity entirely and establishes ectopic colonies driven by estrogen. In adenomyosis, endometrium tunnels inward, colonizing the very muscle wall that should contain it.

Ask yourself:
1. Can a woman have all three conditions simultaneously? (Yes — and this combination is clinically relevant in the infertility workup.)
2. Why does endometriosis cause pre-menstrual pain while adenomyosis causes menstrual pain? (Think about which layer of endometrium is involved and its hormonal responsiveness.)
3. A gynaecologist performing a laparoscopy for infertility finds powder-burn lesions in the pouch of Douglas but the ovaries look normal. The histopathology comes back as 'fibrosis with hemosiderin deposits — no glands identified.' Is this endometriosis? (Yes — burnt-out endometriosis.)
4. Would treating adenomyosis with a GnRH agonist (which suppresses estrogen) be expected to relieve symptoms? Why?

If you can answer all four questions confidently, you have mastered the core concepts in this module.

KEY TAKEAWAYS

Module Summary — Cervicitis, Endometriosis & Adenomyosis

Cervicitis (PA29.6):
• Acute: neutrophilic; causes — N. gonorrhoeae, HSV-2, Trichomonas; mucopurulent discharge.
• Chronic: lymphoplasmacytic; causes — Chlamydia, normal flora, trauma, IUD; Nabothian cysts.
• Follicular cervicitis = lymphoid follicles in stroma → pathognomonic for Chlamydia trachomatis.
• Transformation zone is the key site — biologically vulnerable to HPV, cervicitis, and CIN.

Endometriosis (PA29.7):
• Endometrial glands + stroma outside the uterine cavity.
• Estrogen-dependent; theories: retrograde (Sampson, most accepted), metaplastic (Meyer), vascular/lymphatic (Halban).
• Sites: ovaries (chocolate cyst), pouch of Douglas, uterosacral ligaments, rarely distant.
• Powder-burn lesions (peritoneum); chocolate/endometrioma cyst (ovary).
• Microscopy: glands + stroma + hemosiderin-laden macrophages (2 of 3 needed).
• Clinical triad: dysmenorrhea (secondary, pre-menstrual) + dyspareunia + infertility.
• Complications: adhesions, ectopic pregnancy, rare malignant transformation (endometrioid/clear cell carcinoma).

Adenomyosis (PA29.8):
• Endometrial glands + stroma within the myometrium (>2.5 mm below junction).
• Mechanism: direct downgrowth of basalis (NOT implantation/metaplasia).
• Affects perimenopausal multiparous women; estrogen-responsive.
• Macro: diffusely enlarged, boggy, globular uterus; trabeculated cut surface; NO capsule.
• Micro: basalis-type glands in myometrium, reactive smooth muscle hypertrophy.
• Symptoms: menorrhagia + secondary dysmenorrhea (onset with flow, not pre-menstrual).
• Differs from endometriosis: internal, older age group, no adnexal disease, less infertility.
• Differs from leiomyoma: no capsule, boggy (not firm), hemorrhagic foci (not whorled).