Non-neoplastic disorders of

endometrium

Dr Mohammad Manzoor Mashwani

Acute endometritis

Chronic endometritis

Causes: PID Postpartum Post-abortion (retained tissue) Foreign body (IUD) Tuberculosis (miliary or TB salpingitis)

Morphology

Clinical features

ADENOMYOSIS /Endometriosis interna• Adenomyosis refers to the growth of the basal layer of the

endometrium down into the myometrium.• Nests of endometrial stroma, glands, or both, are found deep in the myometrium interposed between

the muscle bundles. The aberrant presence of endometrial tissue induces reactive hypertrophy of the myometrium, resulting in an enlarged, globular uterus, often with a thickened uterine wall.

● Causes menorrhagia, pelvic pain during menstruation; rarely causes rupture during pregnancy● Occurs in 15% of uteri ● May be involved by hyperplasia or carcinoma

Morphology MacroscopicGrossly, the uterus may be

slightly or markedly enlarged. On cut section, there is diffuse thickness of the uterine wall with presence of coarsely trabecular, ill- defined areas of haemorrhages.

Microscopic• Benign endometrial islands

composed of glands as well as stroma deep within the muscular layer.

• The minimum distance between the endometrial islands within the myometrium and the basal endometrium should be one low-power microscopic field (2-3 mm) for making the diagnosis.

• Associated muscle hypertrophy is generally present.

ENDOMETRIOSISEndometriosis externa

• Endometriosis refers to the presence of endometrial glands and stroma in abnormal locations outside the uterus.

● Women 20-30 years old, up to 10% of all women affected● Consists of functional layers of endometrium that go through menstrual changes

The chief locations where the abnormal endometrial development may occur are as follows (in descending order of frequency):

3 theories about the histogenesis of endometriosis

1. Transplantation or regurgitation theory is based on the assumption that ectopic endometrial tissue is transplanted from the uterus to an abnormal location by way of fallopian tubes due to regurgitation of menstrual blood (Retrograde menstruation).

2. Metaplastic theory suggests that ectopic endometrium develops in situ from local tissues by metaplasia of the coelomic epithelium.

3. Vascular or lymphatic dissemination explains the development of endometrial tissue at extrapelvic sites by these routes (to lungs & nodes).

Clinical features

MorphologyTypically, the foci of endometriosis appear as blue or

brownish-black underneath the surface of the sites mentioned. Often, these foci are surrounded by fibrous tissue resulting in adherence to adjacent structures.

The ovary is the most common site of endometriosis and shows numerous cysts varying in diameter from 0.1 to 2.5 cm. Ovarian involvement is often bilateral. Larger cysts, 3-5 cm in diameter, filled with old dark brown blood form ‘chocolate cysts’ of the ovary.

Histology

Foci of endometrial glands and stroma, Old or new haemorrhages, Haemosiderin-laden macrophages and

surrounding zone of inflammation and Fibrosis

Abnormal Uterine BleedingMenorrhagia: profuse or prolonged bleeding at the time of the

period.Metrorrhagia: irregular bleeding between the periods.Postmenopausal bleeding. Common causes: endometrial polyps, leiomyomas, endometrial hyperplasia,

endometrial carcinoma, and endometritis.The probable cause of uterine bleeding in any given casedepends somewhat on the age of the patient.

Dysfunctional Uterine Bleeding

Abnormal bleeding from the uterus in the absence of an organic uterine lesion is called dysfunctional uterine bleeding. OR

Dysfunctional uterine bleeding (DUB) may be defined as excessive bleeding occurring during or between menstrual periods without a causative uterine lesion such as tumour, polyp, infection, hyperplasia, trauma, blood dyscrasia or pregnancy.

The various causes of abnormal uterine bleeding, both dysfunctional and that which is secondary to an organic lesion, can be segregated into four groups:

I.Failure of ovulation. Anovulatory cycles are very common at both ends of reproductive life, due to

(1) hypothalamicpituitary axis, adrenal, or thyroid dysfunction; (2) functional ovarian lesions producing excess estrogen; (3) malnutrition, obesity, or debilitating disease; and (4)

severe physical or emotional stress. Regardless of the cause, ovulatory failure results in an excess of estrogen relative to progesterone. Thus, the endometrium goes

through a proliferative phase that is not followed by the normal secretory phase. The endometrial glands may develop mild cystic changes or appear disorderly, while the

endometrial stroma, which requires progesterone for growth, may be scarce. This combination of abnormalities makes the endometrium prone to breakdown and abnormal bleeding.

Anovulatory or “disordered” endometrium containing dilated glands.

II. Inadequate luteal phase. The corpus luteum may fail to mature normally or may regress prematurely leading to a relative lack of progesterone. The endometrium under these circumstances fails to show the expected secretory changes.

III.Contraceptive-induced bleeding. Older oral contraceptives containing synthetic estrogens and progestin induced a variety of endometrial responses, including a lush, decidua-like stroma and inactive, nonsecretory glands. The pills in current use no longer cause these abnormalities.

IV. Endomyometrial disorders, including chronic endometritis, endometrial polyps, and submucosal leiomyomas.

Thank You