Endometritis, endometrial hyperplasia, endometriosis

1. Endometritis

Definition

• Inflammation of the endometrium (inner uterine lining).
• Can damage fallopian tubes → infertility + ectopic pregnancy risk.

Pathogenesis

• Associated with retained products of conception (post-miscarriage / delivery).
• Foreign bodies (IUDs).
• Retained tissue / foreign body → nest for ascending infection (from vaginal/intestinal tract).
• Removal → resolution.

Classification

A) Acute endometritis

• Neutrophils within endometrial glands.
• Frequent organisms: N. gonorrhoeae, C. trachomatis.

B) Chronic endometritis

• Plasma cells + lymphocytes within endometrial stroma.
• Plasma cells are the defining feature.

Clinical features

• Fever + abdominal/pelvic pain + menstrual abnormalities + infertility + ectopic pregnancy.

2. Endometrial Hyperplasia

Definition

• Excessive endometrial proliferation due to prolonged estrogen excess (with relative progesterone deficiency).
• Progression: normal → disordered proliferation → hyperplasia → (atypia) → carcinoma.

Causes (estrogen excess)

• Failure of ovulation — perimenopause / anovulatory cycles.
• Prolonged unopposed estrogen therapy (without progestin).
• Estrogen-producing ovarian lesions: polycystic ovary syndrome, granulosa cell tumor.
• Obesity — adipose tissue converts steroid precursors → estrogen (aromatase).
• Other: tamoxifen, early menarche, late menopause, nulliparity.

Histological Distinction (key for risk)

Type	Progression risk	Management
Hyperplasia without atypia	1–3 %	Progestin therapy; surveillance
Hyperplasia with atypia (EIN)	20–50 %	Hysterectomy (or high-dose progestin in young patients)

• EIN = endometrioid intraepithelial neoplasia (precursor to endometrioid adenocarcinoma).

3. Endometriosis

Definition

• Endometrial glands + stroma located OUTSIDE the endometrium.
• Often multifocal: ovaries, fallopian tubes, uterine ligaments, peritoneal cavity, lymph nodes, distant organs.
• Adenomyosis = endometrium within uterine myometrium (related entity).

Epidemiology

• 10 % of women in reproductive age.
• 50 % of infertile women.

Pathogenesis — 4 Theories

1. Regurgitation (Sampson) theory — menstrual backflow through fallopian tubes → implantation in pelvis.
2. Metastatic theory — endometrial tissue spreads via blood vessels + lymphatics.
3. Metaplastic theory — endometrial differentiation from coelomic epithelium.
4. Stem cell theory — circulating stem cells differentiate into endometrial tissue.

Morphology

• Foci contain functioning endometrium that undergoes cyclic bleeding with hormones.
• Grossly: red-brown nodules (“powder burns”).
• Ovarian involvement: large blood-filled cysts → chocolate cysts (endometrioma) as blood ages.
• Triad of microscopic findings = endometrial glands + endometrial stroma + hemosiderin.

Clinical features

• Dysmenorrhea (painful menses) + pelvic pain (always present).
• Dyspareunia (painful intercourse) — uterus/bladder serosa involvement.
• Dyschezia (pain on defecation) — rectal wall involvement.
• Dysuria — bladder serosa involvement.
• Infertility — oviduct + ovary scarring.
• Risk of malignancy: ovarian endometrioid + clear cell adenocarcinoma can arise in long-standing endometriosis.

4. Three D’s of Endometriosis

• Dysmenorrhea
• Dyspareunia
• Dyschezia (± Dysuria, infertility)

💡 High-yield: Endometritis: acute (neutrophils + N. gonorrhoeae/Chlamydia, often post-partum/IUD), chronic (plasma cells = diagnostic) → infertility + ectopic. Endometrial hyperplasia = unopposed estrogen (PCOS, granulosa cell tumor, obesity, anovulation, tamoxifen); with atypia (EIN) = 20–50 % → endometrioid adenocarcinoma; without atypia = 1–3 %. Endometriosis = endometrial tissue outside uterus; 10 % of women, 50 % of infertile; chocolate cysts in ovary; classic Sx = dysmenorrhea + dyspareunia + dyschezia + infertility; 4 pathogenesis theories (regurgitation = Sampson #1).