Fig. 19.14 ). Adherence of the inflamed tube to the ovary and adjacent ligamentous tissues may produce a tuboovarian abscess. This may in turn result in adhesions between the ovary and the tubes when the inflammation subsides. Even more serious are adhesions of the tubal plicae, which are associated with increased risk of tubal ectopic pregnancy (discussed later).
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Fig.19.14Pelvicinflammatorydisease,bilateralandasymmetric.Thetubeandovarytotheleftoftheuterusaretotallyobscuredbyahemorrhagicinflammatorymass.Thetubeisadherenttotheadjacentovaryontheotherside.
Follicle and luteal cysts in the ovaries are so commonplace that they may be considered variants of normal physiology. These innocuous lesions originate from unruptured graafian follicles or from follicles that rupture and then immediately seal. Such cysts often are multiple and develop subjacent to the serosa of the ovary. They typically are small (1–1.5 cm in diameter) and are filled with clear serous fluid. Occasionally, they become sufficiently large (4–5 cm) to produce palpable masses and pelvic pain. When small, they are lined by granulosa lining cells or luteal cells, but as fluid accumulates, pressure may cause atrophy of these cells. Sometimes these cysts rupture, producing intraperitoneal bleeding and peritoneal symptoms (acute abdomen).
Polycystic ovarian syndrome (formerly called Stein-Leventhal syndrome) is a complex endocrine disorder characterized by hyperandrogenism, menstrual abnormalities, polycystic ovaries, chronic anovulation, and decreased fertility. It usually comes to attention after menarche in teenage girls or young adults who present with oligomenorrhea, hirsutism, infertility, and sometimes with obesity.
The ovaries are usually twice the normal size, gray-white with a smooth outer cortex, and studded with subcortical cysts 0.5 to 1.5 cm in diameter. Histologic examination shows a thickened, fibrotic ovarian capsule overlying innumerable cystic follicles lined by granulosa cells with a hyperplastic luteinized theca interna. There is a conspicuous absence of corpora lutea in the ovary.
Damage to or obstruction of the tubal lumina may produce permanent sterility.
Once thought to be uncommon, primary adenocarcinomas of the fallopian tube may be the site of origin for many of the high-grade serous carcinomas long thought to arise in the ovary. Studies have identified the presence of serous tubal intraepithelial carcinoma (STIC) in the fimbriated ends of fallopian tubes. Like the precursor of uterine serous carcinoma, STICs have mutations in TP53 in more than 90% of cases. These lesions are found frequently in fallopian tubes removed prophylactically from women who carry mutations in BRCA1 and BRCA2 and less commonly in instances where tubes are removed from women without known genetic risk factors. This has led to the idea that sporadic “ovarian” serous carcinomas (discussed later) also originate in the fallopian tube. Because the fimbriated end of the fallopian tube is intimately associated with the ovary and has access to the peritoneal cavity, fallopian tube carcinomas frequently involve the ovary, omentum, and peritoneal cavity at presentation.