Female Genital System and Breast

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Chapter 13 Female Genital System and Breast

Female Genital Tract – Anatomy and Physiology

The following diagrams summarise normal anatomy and physiology:

Diseases of the Endometrium

Endometritis is now unusual.

Acute infection is nearly always associated with childbirth and abortion – often related to retention of products of conception. Historically, criminal abortion in non-sterile conditions led to severe infection. Gonococcal infection does not commonly extend beyond the cervix but can lead to acute endometritis. Chlamydia may cause acute or chronic endometritis.

Chronic Endometritis

This can be seen in chronic pelvic inflammatory disease and in relation to retained products of conception.

Tuberculous Endometritis

This is now uncommon in UK. It is the result of infection spreading from the fallopian tubes. If the patient is still menstruating, the tubercles are shed each month: diagnostic biopsy should be done as late in the cycle as possible to allow new tubercles to develop. In some cases, menstruation ceases and caseation occurs.

Intrauterine Anti-Fertility Devices

A mild chronic inflammation may be associated with the use of these devices. There may be focal atrophy with mild plasma cell infiltration. Irregular bleeding may result.

Adenomyosis

Deep down growths of endometrium occur within the myometrium. There is an accompanying overgrowth of muscle and connective tissue. Two macroscopic forms occur:

Deposits are confined to inner part of myometrium. Foci of endometrium often brownish in colour

2. Localised

Resembling fibroid but with brownish foci

The endometrial deposits communicate with the uterine cavity, but despite this they often contain altered blood in the glands which become cystic. The diffuse type is commoner. Adenomyosis is not related to endometriosis.

Endometrial Hyperplasia

Endometrial hyperplasia occurs in 3 forms: Simple hyperplasia, complex hyperplasia and atypical hyperplasia. Of these, atypical hyperplasia is most important as it is associated with an increased risk of malignancy. Progressive molecular genetic alterations occur on the pathway to cancer.

Simple Hyperplasia

This tends to occur in the peri-menopausal period. It is due to excess oestrogen stimulation – particularly associated with anovulatory cycles, but rarely with oestrogen therapy or oestrogen-secreting tumours.

Clinically, there is irregular, frequent and heavy bleeding.

Complex Hyperplasia

In this form, hyperplasia is often focal and glands but not stroma are affected. Thus the glands appear crowded, but show no atypia. There is no increased risk of malignancy.

Atypical Hyperplasia

In this condition the hyperplasia is focal and cytological atypia with mitotic figures is common. Intervening endometrium may show simple hyperplasia. The importance of atypical hyperplasia is its relationship to the development of adenocarcinoma, i.e. it is considered to be pre-cancerous. Up to 40% have co-existing carcinoma in hysterectomy specimens.

Endometrial Polyp

This is a localised proliferation of endometrial glands which becomes pedunculated.

Sometimes polyps are associated with general endometrial hyperplasia. Progressive elongation of the pedicle may lead to venous congestion and bleeding.

Endometrial Carcinoma

This common gynaecological cancer particularly affects postmenopausal patients, who typically present with vaginal bleeding.

Carcinoma

This growth may form a localised plaque or polyp.

In some cases it appears as a diffuse change involving much of the endometrium. It grows initially within the endometrial layer, bulging into the uterine cavity.

Most growths are well-differentiated adenocarcinomas (endometrioid). These are graded from I – III

In some cases with a particularly poor prognosis malignant squamous epithelium is admixed with the adenocarcinoma – so-called adenosquamous carcinoma.

The endometrium possesses no lymphatics and invasion of the myometrium takes place slowly.

Local extension: this may take place in several directions.

Aetiology

Endometrial carcinoma is uncommon before the 5th decade. The most important factor is prolonged OESTROGENIC stimulation due to:

(a) endogenous overproduction, e.g. in cases of oestrogen-secreting ovarian tumours.

(b) exogenous oestrogen therapy.

(c) in obesity: increased conversion of androstenedione (from adrenals) to oestrone. atypical hyperplasia is an important precancerous stage.

Other endometrial malignancies:

Endometrial Stromal Sarcomas

These rare tumours may be of low grade or high grade.

Low grade tumours – infiltrate extensively through the lymphatics of the myometrium. The cells are cytologically bland and mitoses are few. About one fifth of patients eventually die from the disease.

High grade stromal sarcomas – are highly malignant spindle celled tumours, with poor prognosis. It may be difficult to separate these from uterine leiomyosarcomas.

Carcino-Sarcoma (Malignant Mixed Mullerian Tumours)

These uncommon tumours have features both of endometrial carcinoma and sarcoma. They often present as soft fleshy masses protruding through the cervix into the vagina.

Diseases of the Myometrium

Tumours of the myometrium are extremely common.

Leiomyoma (Fibroid)

This is a circumscribed growth derived from uterine muscle.

The cells are typical long spindle muscle cells, arranged in interlacing bundles

They vary in size from tiny (mm) growths to several cm in diameter and are frequently multiple.

Fibroids may be found in any part of the uterus.

Tumours beneath the endometrium tend to bulge into the cavity and may eventually develop to form a fibroid polyp.

Complications

Leiomyoma is one of the commonest tumours, occurring in 15–20% of women over the age of 35. Growth ceases at the menopause.

Leiomyosarcoma

This is a rare tumour which may arise from a preceding leiomyoma, but usually does not. Some tumours are highly malignant but in others with few mitotic figures it is difficult to predict the outcome – these are known as Smooth Muscle Tumours of Uncertain Malignant Potential (STUMP).

Diseases of the Cervix

The cervix constitutes the lower one third of the uterine body.

It is in two parts: endocervical and ectocervical with different lining epithelium.

The remainder of the cervical wall consists of circular smooth muscle lying in abundant fibroelastic tissue.

At the internal os, the structure gradually merges with that of the uterus proper, the branching glands giving place to the simple tubules of the endometrium, and the proportion of muscle increases greatly.

Cervicitis

Inflammation of the cervix may be acute or chronic. Acute cervicitis may be due to gonorrhoea or follow cervical laceration at childbirth.

Chronic cervicitis is commoner and may be due to candida, trichomonas (p.506) and chlamydia. The last is associated with reactive lymphoid follicles (follicular cervicitis).

Viral infections of the cervix include Herpes Simplex Virus (Type II) and human papilloma viruses (HPV). The latter can cause simple viral warts or be associated with cervical intraepithelial dysplasia and neoplasia (CIN) and invasive carcinoma (p.504).

Cervical Polyp

This is a local proliferation of endocervical mucosa which becomes pedunculated and may protrude through the cervix.

Cervical Intraepithelial Neoplasia (CIN)

The Transformation Zone

From puberty onwards and particularly in pregnancy the squamo-columnar junction presents on the vaginal surface of the external os. This is the area where squamous metaplasia occurs. It is important because cervical squamous carcinoma and its precursor cervical intraepithelial neoplasia (CIN) begin there. Within this metaplastic epithelium, dysplastic changes may develop. They are graded as CIN I, II and III. Later, in some cases, invasive squamous carcinoma develops.

Koilocytes (cells with a wrinkled pyknotic nucleus and perinuclear cytoplasmic clearing) are often seen in the suprabasal layers and indicate HPV infection.

Cytology and CIN

The cervical screening programme aims to detect CIN and thus prevent the development of invasive carcinoma. Cellular preparations from the squamo-columnar junction obtained by a cervical brush are stained by Papanicolaou’s method (liquid-based cytology). The cells can be examined for dysplasia – so-called dyskaryosis. Inflammatory changes, e.g. due to candida infection, may be seen.

The cytology is a screening test. Patients with abnormalities are referred for colposcopy where abnormal epithelium turns white on exposure to acetic acid (acetowhite). Punch biopsy to diagnose dysplasia is followed by laser ablation (laser loop excision of transformation zone). New techniques to identify proliferating and malignant cells are being rapidly developed.

Carcinoma of Cervix

Carcinoma

This is the most common malignant tumour of the female genital tract, even where there is a vigorous screening campaign for early diagnosis and eradication of dysplasia. The tumour is a squamous carcinoma in 90% of cases, and an adenocarcinoma in 10%. Most squamous carcinomas arise at the squamo-columnar junction: most adenocarcinomas arise within the endocervical canal.

The cervix becomes indurated with necrosis and ulceration

Later, a large fungating mass is produced

Microinvasive carcinoma is the earliest stage of invasive cancer – where spread is less than 5 mm in depth. This is associated with an excellent prognosis.

Spread

Until a very late stage, the disease is confined to the pelvic cavity. The patient commonly dies before distant metastases appear.

Local spread takes place in several directions:

1. Downward extension.

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