Cycle Disorders and Dysfunctional Bleeding
Normally, the menstrual cycle is regulated by hormones: the proliferative phase is stimulated by estrogens, and the secretory phase by progesterone. Disruption of this sequence leads to dysfunctional uterine bleeding (DUB).
Most often, the culprit is ovarian pathology, and less frequently, disorders of the central nervous system, pituitary gland, or adrenal glands. Bleeding occurs against the background of:
- Anovulatory cycles (when the follicle fails to ovulate and the corpus luteum does not form).
- Insufficiency or persistence of the corpus luteum.
- Endometrial atrophy.
In clinical practice, such disruptions manifest as cycle abnormalities (dysmenorrhea), excessive bleeding during menstruation (menorrhagia), or irregular spotting outside the cycle (metrorrhagia). A serious and predictable outcome of these disorders is often infertility.
Endometrial Hyperplasia and Carcinoma
With hyperestrogenism, the endometrium proliferates excessively. The prognostic value of hyperplasia depends on its histological type, which determines the treatment strategy:
- Simple hyperplasia: irregular distribution of glands, cystic dilations, and stromal infiltration. Usually regresses spontaneously or after curettage.
- Complex (adenomatous) hyperplasia: glands become more tortuous with minimal intervening stroma. The risk of developing cancer is about 3%.
- Simple atypical: branching glands with hyperchromatic nuclei (8% risk).
- Complex atypical: bizarre-shaped glands closely fused together ("back-to-back" pattern). Cells lose polarity, and pathological mitoses are visible. Cancer risk is 30%.
Endometrial carcinoma is one of the most common female malignancies (mean age of onset is 55 years). It develops either against the background of hyperplasia (classical pathway) or rapidly without preceding endometrial thickening (about 1/3 of cases). In 85% of cases, the tumor is an adenocarcinoma. It metastasizes first via lymphatic pathways, and subsequently via hematogenous and implantation routes. Risk factors include obesity, diabetes, nulliparity, and estrogen replacement therapy.
Polyps and Uterine Leiomyoma
A dyshormonal background also promotes the formation of benign tumors and growths:
- Endometrial polyp: forms from the basal layer through monoclonal proliferation of mesenchyme. Macroscopically, these are smooth nodules ranging from microscopic to giant sizes (can occupy the entire uterine cavity). The main microscopic diagnostic criterion is the presence of thick-walled, tortuous blood vessels with wide lumens in the base (stalk) of the polyp.
- Uterine leiomyoma (fibroid): a benign tumor arising exclusively from smooth muscle tissue. It occurs in 15–30% of women over 35 years of age and almost always regresses postmenopause. The clinical presentation depends on the location of the nodules: patients complain of pain, menorrhagia, metrorrhagia, as well as constipation and urinary symptoms due to compression of the bowel and bladder by the large tumor.
Extrapelvic Endometriosis
In this condition, functional endometrial tissue is found outside the uterine cavity.
In 70% of cases, the ovaries are affected, where specific endometriotic cysts form. These cavities accumulate hemorrhagic fluid, earning them the name "chocolate cysts". The second most common site is the peritoneum (uterosacral ligaments, pouch of Douglas).
Endometriotic foci respond acutely to hormonal fluctuations, undergoing the same cyclical changes as eutopic endometrium. Periodic hemorrhages into the tissues cause severe aseptic inflammation. The ultimate result of this inflammation is pronounced scar-formation and adhesions that distort pelvic anatomy.