Endometrial dating ppt

Such superficial strips of papillary endometrium, which are generally atrophic, should be examined under high power to look for proliferative activity and nuclear atypia. Crushed endometrial glands and stroma may be extremely cellular and can cause concern. As with other tissues, crushed areas should not be viewed in isolation.

Tearing of the tissue is seen around the glands. Endometritis may result in symptoms of abnormal uterine bleeding and the pathologist should always exclude this.

Lymphocytes, including natural killer cells and lymphoid aggregates, are a normal component of the endometrium, and polymorphs are characteristic of the premenstrual and menstrual phases. The presence of plasma cells is widely regarded as the most useful criterion for a diagnosis of endometritis, although these are often admixed with other inflammatory cells, both acute and chronic, and may be a minor component of the inflammatory cell infiltrate. Other morphological features that alert the pathologist to a possible endometritis may also exist.

A degree of architectural complexity and cytological atypia may also be seen if the inflammatory cell infiltrate is marked, resulting in potential overdiagnosis of a hyperplasia or carcinoma. Problems in recognising plasma cells may occur, especially on histological sections that are less than optimal. Endometrial stromal cells may have a plasmacytoid appearance with eccentric nuclei, and the pathologist should be certain that classic plasma cells are present. It is emphasised that in the absence of the other morphological features of endometritis described earlier, an exhaustive search for plasma cells is not justified.

Occasional stromal plasma cells may be identified in an otherwise normal endometrium, and in these circumstances a diagnosis of endometritis should not be made. Plasma cells may be present in the stroma of endometrial polyps and also in association with an endometrial malignancy. Ancillary studies may aid in the diagnosis of endometritis, although they are not generally necessary.


My approach to the interpretation of endometrial biopsies and curettings

Antibodies against B and T lymphoid cells may also be of value. A recent study showed that in cases of endometritis, the number of T lymphocytes and natural killer cells did not differ from controls. This may be of value in diagnosing endometritis on small biopsy specimens in which the superficial endometrium is preferentially sampled. The endometrial glands are positive but the stroma is negative. Polyps are a common cause of abnormal bleeding in premenopausal and postmenopausal women.

The pathological diagnosis is generally straightforward if the gynaecologist is aware of the presence of a polyp, has conveyed this information to the pathologist and has removed the polyp intact. The gynaecologist may believe that a polyp is present, but histological examination shows a cyclical endometrium, often secretory in type, reflecting the fact that an abundant secretory endometrium may have a polypoid appearance. Often, the gynaecologist is not aware of the presence of a polyp.

When a biopsy is carried out for abnormal uterine bleeding, the pathologist should always consider the possibility of a polyp.

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On examination under low power, the initial clue to the presence of a polyp is often the admixture of fragments of a normal cyclical endometrium and fragments that are morphologically different. The glands within a polyp often show proliferative activity, even when the surrounding endometrium does not. The following points on endometrial polyps are worthy of mention:. It is useful to have a checklist of benign lesions other than those listed earlier, including granulomas, placental site nodules and the various forms of epithelial and stromal metaplasias.

These metaplasias will not be discussed in detail, as they have been reviewed recently. Assessing the underlying glandular architecture is problematic. This may result in consideration of a serous carcinoma or endometrial intraepithelial carcinoma. Hormones have varying effects on the endometrium and it is essential that the clinician supplies details to the pathologist regarding any hormone treatment. Such information is not always provided. Some hormone preparations, especially those that contain both oestrogen and progestogen most modern hormone replacement treatment regimens , characteristically result in a weak or poorly developed secretory endometrium, 27 , 28 whereas with other preparations the endometrium is atrophic.

This pseudodecidualisation is often most prominent just beneath the surface glands and is usually accompanied by an inflammatory cell infiltrate, largely comprising natural killer cells.

Pathology Outlines - Dating of endometrium

Similar appearances occur with the Mirena coil, an intrauterine device containing progestogen, which is widely used. Tamoxifen is widely used as adjuvant therapy in the management of breast cancer. The use of tamoxifen as a prophylactic agent in patients with a family history of breast cancer is now being investigated. The effects of tamoxifen on the endometrium has been the subject of several reviews.

Endometrial samples from women taking tamoxifen tend to be scanty, as tamoxifen may result in fibrosis of the endometrial stroma, making evaluation by biopsy difficult. The fibrosis can result in cystic dilatation of endometrial glands on an obstructive basis and this can be seen on hysteroscopy. The most common endometrial lesions seen in association with tamoxifen are benign polyps, which may be single or multiple. Indeed, as discussed previously, there is a peculiar tendency for serous carcinoma and EIC to arise within endometrial polyps, whether sporadic or associated with tamoxifen.

As women with breast cancer are more likely to develop endometrial carcinoma due to common risk factors, such as high socioeconomic status, low parity or hyperoestrogenic states, it is difficult to ascertain whether a true association exists between tamoxifen and the development of endometrial cancer. Most epidemiological studies, however, suggest that tamoxifen is associated with an increased risk of developing endometrial cancer, which is two to three times that in patients with breast cancer who are not taking tamoxifen.

As the effects of tamoxifen on the endometrium are believed to be due to oestrogenic activity, it is expected that most endometrial cancers should be endometrioid in type, as these neoplasms are hormone receptor positive. In my experience, various aspects related to endometrial hyperplasia commonly create problems for pathologists. In the following sections, I discuss some of these problematic areas.

Before diagnosing an endometrial hyperplasia, it is important to exclude the many benign mimics. The potential benign mimics of endometrial hyperplasia are listed in box 1. Most of these show an increase in the normal gland to stroma ratio, which is a defining feature of complex endometrial hyperplasia and is present in most cases of atypical hyperplasia complex atypical hyperplasia. One of the most common lesions to be misdiagnosed as a hyperplasia is an endometrial polyp, especially when this is removed piecemeal, and when the gynaecologist is not aware of the presence of a polyp and the suggestion of this is not conveyed to the pathologist.

The morphological features of endometrial polyps, as well as several of the other potential benign mimics of endometrial hyperplasia, have been discussed. A secretory endometrium and Arias—Stella effect endometrium often shows an increase in the gland to stroma ratio and may be misdiagnosed as an endometrial hyperplasia, especially when subnuclear vacuolation is not obvious.

In general, secretory activity is rare in endometrial hyperplasias, although this does occur, especially when hormone treatment has already been instigated. Cystic atrophy is distinguished from simple hyperplasia by the atrophic appearance of the glands, including the lack of proliferative activity.

Clinical history

In general, mitotic activity should be identified before diagnosing an endometrial hyperplasia. The term dysplasia should not be used with regard to the endometrium. The WHO classification was based on a seminal study of endometrial hyperplasia, 50 and divides hyperplasias into simple and complex forms depending on the glandular architecture. In simple hyperplasia, the normal gland to stroma ratio is largely maintained, although there may be a slight increase.

In complex hyperplasia, there is an increase in the gland to stroma ratio. Assessment of nuclear atypia is extremely subjective, resulting in marked interobserver variation, even among specialist gynaecological pathologists, in the classification of endometrial hyperplasia. In practice, atypia usually occurs in endometria with complex architecture and it is uncommon to diagnose simple atypical hyperplasia, although this rarely occurs.

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As a result, many pathologists use three categories of endometrial hyperplasia—simple, complex and atypical. The risk of developing an endometrioid adenocarcinoma after a diagnosis of atypical hyperplasia is difficult to ascertain, as, once atypical endometrial hyperplasia is diagnosed, it is treated either hormonally or more usually surgically. In a simple hyperplasia, the normal gland to stroma ratio is maintained or there is slight increase.

The endometrium shows proliferative activity, with cystically dilated glands of irregular sizes and shapes. No nuclear atypia is seen, the nuclei being oval and maintaining their orientation to the underlying basement membrane. A major problem is the distinction between simple endometrial hyperplasia and disordered proliferative endometrium, a term widely used, although the histological features are not well characterised.

The morphological features of these overlap and the distinction is poorly reproducible. In my practice, I require to see large numbers of dilated glands to diagnose simple hyperplasia, whereas if only occasional dilated glands are present, I diagnose this as disordered proliferative endometrium, especially if the patient is perimenopausal. Disordered proliferative endometrium is common in the perimenopausal years because of anovulatory cycles.

In any case, the management of simple endometrial hyperplasia and disordered proliferative endometrium is usually identical, in the form of progestogenic compounds. Furthermore, a continuum exists between disordered proliferative endometrium and simple hyperplasia. In complex hyperplasia, there is an increase in the gland to stroma ratio with glandular crowding.