Endometriosis

 

Ectopic occurrence of endometrial tissue, frequently forming cysts containing altered blood.

 

Aetiology

 

Often unknown

 

Possibilities include

 

Implantation due to retrograde menstruation

 

Metaplasia of coelomic derivatives (pelvic peritoneum, some ovarian epithelium and Mullerian ducts are derived from the same embryological source)

 

Embolism of endometrial tissue in pelvic veins or lymphatics

 

 

Pathophysiology

 

The endometreum is the inside lining of the uterus

 

Endometrial deposits may be found in various parts of the body

 

Most common sites are the ovary and pelvis

 

Endometrial deposits can range from pin head size to larger cysts filled with altered blood - termed chocolate cysts

 

The ectopic endometrial tissue bleeds during menstruation due to systemic hormonal influences

 

Blood can cause a fibrous reaction resulting in stricture formation, e.g. in the bowel

 

 

Clinical features

 

Very variable and unrelated to the extent of the disease

 

Infertility

 

Menorrhagia

 

Deep seated dyspareunia

 

Pelvic pain before and during period

 

Congestive dysmenorrhoea, (secondary dysmenorrhoea caused by pelvic congestion secondary to increased blood supply secondary to pelvic disease)

 

Diagnosis is confirmed by laparoscopy

 

Management

 

Hormonal therapy - to induce pseudo pregnancy e.g. continuos progesterone therapy

 

Conservative surgery - e.g. removal or cortary of small ectopic areas of endometreum and removal of cysts

 

Radical surgery - in older women after reproduction

 

 

Complications

 

Rupture of a cyst can cause acute peritonism

 

Fixation of uterus

 

Other adhesions

 

Pain

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Pelvic inflammatory disease

 

 

Acute or chronic inflammation in the pelvic cavity, particularly, suppurative lesions of the upper female genital tract; e.g., salpingitis

 

A broad term to describe infection involving the tubes, ovaries and parametrium, (covering of the pelvic floor).

 

Aetiology

Ascending infection through the genital tract

Direct due to trauma delivery or abortion

Blood borne e.g. TB

Transperitoneal infection e.g. from appendicitis or diverticulitis

 

Pathophysiology

Inflammation caused by infection

May be acute or chronic

Other pelvic structures eg. Gut may be involved as a result of adhesions

 

Acute salpingitis

Fallopian tubes - congested, oedematous, infiltrated by neutrophils

Collection of pus in the tubes

 

Pus may leak into peritoneal cavity ------ acute pelvic peritonitis

 

Pelvic abscess may develop in the pouch of Douglas

 

Exudate collects in the tubes leading to adhesions

 

Clinical features

Acute lower abdominal pain and fever Pain usually bilateral

Possible vaginal discharge and deep dyspareunia Lower abdominal rebound tenderness

Diagnosis may be confirmed by laparoscopy

 

Complications

Adhesions in the tubes Rupture of masses causing generalised peritonitis

 

Management

High doses of antibiotics Analgesia Bed rest

 

Chronic PID

Low grade infection and effects of fibrous tissue causing adhesions

Acute exacerbations may occur

Persistent vaginal discharge

Deep dyspareunia Menorrhagia

Treat acute exacerbations conservatively Pelvic clearance may be performed

 

 

Benign tumours of the uterus

 

Polyps

 

Pathophysiology

Composed of fibrous tissue Often covered in functional endometrium

 

Clinical features

Irregular bleeding and menorrhagia Sometimes colicky pain

 

Management

Cervical dilation and uterine curettage

 

 

Fibroids

 

Pathophysiology

Uterine myomas Tumours derived from smooth muscle

Benign tumours Single or multiple

Small to very big

 

Aetiology

Unknown

 

Clinical features

May be asymptomatic Menorrhagia

Colicky pain Pressure symptoms

Complications of pregnancy

 

Management

Surgical excision to preserve function but hysterectomy is best

 

 

Malignant tumours of the uterus

 

Endometrial carcinoma

 

Factors

Obesity Nulliparous Late menopause

Diabetes mellitus Exogenous oestrogen

 

Pathology

Endometrial adenocarcinoma

 

 

Stages

 

 

 

 

Features

Post menopausal bleeding

Premenopausaly - irregular bleeding and menorrhagia

 

 

 

Prolapse of the uterus

 

Aetiology

Congenital in the young and nulliparous

Normally the uterus is held in by the pelvic floor muscles

Child birth - more common in parous women especially multiple or difficult deliveries

Oestrogen deficiency - postmenopausal atrophy - loss of muscle tone

Chronically raised intra-abdominal pressure - obesity, chronic cough, straining at stool, chronically stressed pelvic floor.

 

Pathophysiology

Prolapse means a downward eversion of a hollow organ - may involve the rectum, uterus or urethra

May be first second or third degree

 

Clinical features

Feeling of `something coming down`

Stress incontinence

Pain is variable

Sometimes backache

Complications involve the urinary system

 

Management

Prevent with good care of the pelvic floor muscles and perineum

Pelvic floor exercises

Avoid raised intra-abdominal pressure

Weight loss

Possible oestrogen HRT

Ring pessary, changed every 4 - 6 months

Oestrogen cream

Surgery

 

 

 

 

 

 

 

 

 

Cervical Cancer

 

Factors

Early age of first sex Multiple partners

A partner who has had multiple partners Human papilloma virus (HPV)

Herpes type 2 infection Smoking

Screening should start when sex does Oral contraception (100% increase after 10 years)

 

Features

Early disease is asymptomatic Post coital bleeding

Discharge Irregular bleeding

Pain with local invasion Involvement of bladder or rectum

 

Management

Depends on stage Local treatment

Cone resection and biopsy Hysterectomy

Radiotherapy

 

 

 

Ovarian Cancer

4th most common cause of cancer deaths in women

 

Aetiology

Unknown

May be related to ovulation - less in women who have taken oral contraception

 

Features

Usually presents late

Abdominal pain

Abdominal distension

Abnormal uterine haemorrhage

 

Pathology

Mostly epithelial

 

Management

Depends on stage

Abdominal hysterectomy with bilateral salpingo-oophorectomy

Cytotoxics

5-year survival is 25 - 30%

 

Benign ovarian neoplasia

 

May be solid, cystic or mixed

 

Commonly present as asymptomatic abdominal masses but may present

with pain or functional effects

 

 

 

Ovarian Cancer

 

Aetiology

The precise cause of ovarian cancer is unknown, but several risk and contributing factors have been identified.

 

Reproductive factors, women who have been pregnant have a 50% decreased risk for developing ovarian cancer compared to nulliparous women. Multiple pregnancies offer an increasingly protective effect. Oral contraceptive use decreases the risk of ovarian cancer. These factors support the theory that risk for ovarian cancer is related to ovulation and that conditions which suppress this ovulatory cycle play a protective role. Ovarian cancer may develop from an abnormal repair process of the surface of the ovary, which is ruptured and repaired during each ovulatory cycle. Therefore, the probability of ovarian cancer may be related to the number of ovulatory cycles.

 

Genetic factors, family history plays an important role in the risk of developing ovarian cancer. The lifetime risk for developing ovarian cancer is below 2% in the general population. This compares to a 4-5% risk when one first-degree family member is affected, rising to 7% when two relatives are affected. A history of breast cancer increases a woman's risk of developing ovarian cancer.

Hereditary ovarian cancer occurs in families in which multiple members have ovarian cancer. Fewer than 5% of all ovarian cancers have a hereditary predisposition. Breast/ovarian cancer syndrome is associated with early onset of breast or ovarian cancer. Inheritance follows an autosomal dominant transmission. It can be inherited from either parent. Most cases are related to the BRCA1 gene mutation. BRCA1 is a tumor suppressor gene that inhibits cell growth when functioning properly.

 

Pathophysiology

Accept any relevant discussion of the general pathophysiology of malignancy. Ovarian cancer describes a malignant neoplasm located in the ovaries. Disease may develop rapidly and might involve both ovaries. Metastasis occurs relatively early in the disease process. Early metastatic sites include the uterus, bladder and bowel. More than 90% of malignant tumors are epithelial tumors. Ovarian carcinoma can spread by local extension, lymphatic invasion, intraperitoneal implantation and haematogenous dissemination. Intraperitoneal dissemination is the most common and is a well recognized characteristic of ovarian cancer. Malignant cells can implant anywhere in the peritoneal cavity but are more likely to implant in sites of stasis along the pathways of peritoneal fluid circulation. The disease is staged into stages I, II, III, and IV. The disease is uncommon in patients younger than 40 years, after which incidence increases. Most cases are diagnosed in the seventh decade of life.

 

Clinical features

Unfortunately there are often no or few clinical features in the early development of the disease. The signs and symptoms of ovarian cancer are nonspecific. Most patients present with symptoms of several months duration. Symptoms include the following: abdominal/pelvic pain, vaginal bleeding, bloating, abdominal distension, irregular menses, change in bowel habit. Physical findings are uncommon in patients with early disease. Patients with more advanced disease might suffer from an ovarian or pelvic mass, ascites, pleural effusion.

 

Cervical cancer

 

Aetiology

Accept general principles of the aetiology of malignancy. The risk of developing cervical cancer increases with an early age of first sexual intercourse and history of sexually transmitted diseases. The more sexual partners a woman has, and the more partners any one of her sexual partners has had, the greater the risk. From this it can be seen young women should be advised to postpone beginning sexual activity and to choose a partner who has had few, if any previous partners himself. Unsafe sex is more risky than safe sex. The explanation for the sexually transmitted nature of cervical cancer is that 95% of cases are caused by human papillomavirus (HPV) infection.

HP virus is passed on during sex. HPV infection occurs in a high percentage of sexually active women. Most of these infections clear spontaneously within months to a few years, and only a small proportion progress to cancer. This means that other factors are involved in the process of carcinogenesis including the type and duration of viral infection, host conditions that compromise immunity, such as multiparity or poor nutritional status. Environmental factors probably include smoking, oral contraceptive use, vitamin deficiencies. There are many (77 so far identified) forms of HPV all based on DNA. The low-risk types consist of HPV 6b and 11, high-risk types, mostly HPV 16 and 18, are found in 50-80% of malignant cases. The virus effects the genetic machinery of the cell to resist apoptosis, causing uncensored cell growth after DNA damage. This ultimately results in progression to malignancy.

HIV infection also increases the likelihood of developing cervical cancer. There is also a positive association between duration of combined oral contraceptive use and incidence of cervical cancer; however it is not believed that this association is causal.

 

Pathophysiology

Accept general principles of cancer pathophysiology. Cervical cancer is a squamous cell carcinoma in most cases. Most commonly, malignant changes arise in the cervical os. The cervical os is the opening of the cervix into the vagina. In this area, there is a boundary between the stratified squamous cells of the vagina and the columnar cells of the cervix, known as the squamocolumnar junction. The columnar cells in the area of the squamocolumnar junction form a region called the transformation zone. It is the cells in this area which can change into malignant squamous cells. This process of cellular transformation is referred to as metaplasia. Uncommonly, cervical cancer may also arise from the glandular tissue associated with the columnar epithelium of the endocervix; this is an example of an adenocarcinoma.

 

The sequence of abnormal cell development goes through mild, moderate and severe dysplasia before finally becoming malignant. Dysplasia means a distinctive change in the type of cells found. Cytologists grade developing dysplasia in cervical cells using the CIN classification. CIN stands for cervical intra-epithelial neoplasia. CIN-1 is mild dysplasia, CIN-2 moderate and CIN-3 describes severe dysplasia and carcinoma in situ. After this the cancer will become locally invasive with metastases. The tumor grows by extending upward to the endometrial cavity, downward to the vagina, and laterally to the pelvic wall. It can invade the bladder and rectum directly. The common sites for distant metastasis include extrapelvic lymph nodes, liver, lung, and bone.

 

Clinical features

Cervical cancers usually affect women of middle age or older, but it may be diagnosed in any reproductive-aged woman. An abnormal cervical smear result. Clinically, the first symptom is abnormal vaginal bleeding, usually postcoital. Followed by bleeding in between periods. Post menopausal bleeding should always be investigated and explained as this may arise from a malignancy. Vaginal discomfort, malodorous discharge, and dysuria. Irregular shaped tumours increase the probability of infection becoming established. This leads to the development of a vaginal discharge, which is often very smelly. Chronic infection is a common problem in cervical cancer and may generate signs of chronic pelvic inflammation.

 

As the disease develops there will be pain during sex. Pain at other times usually indicates spread of the disease to the pelvic cavity. Local invasion often involves the bladder or rectum resulting in fistula formation. A fistula is an abnormal communication between two body cavities. This may result in urine or faeces coming out of the vagina. Direct spread backwards involves the sacral nerve plexus leading to severe sciatic pain. Systemic metastatic spread is via the lymphatics. Other symptoms may include constipation, haematuria, ureteral obstruction with or without hydroureter or hydronephrosis. The triad of leg edema, pain, and hydronephrosis suggests pelvic wall involvement.

 

In patients with early-stage cervical cancer, physical examination findings can be relatively normal. As the disease progresses, the cervix may become abnormal in appearance, with gross erosion, ulcer, or mass. These abnormalities can extend to the vagina. Rectal examination may reveal an external mass or frank blood from tumor erosion. Bimanual examination findings often reveal pelvic metastasis. Leg edema suggests lymphatic or vascular obstruction from tumor. If the disease involves the liver, some patients develop hepatomegaly. Pulmonary metastasis usually is difficult to detect upon physical examination unless pleural effusion or bronchial obstruction becomes apparent.

 

Fibroids

 

Aetiology

The cause of fibroid tumours of the uterus is unknown but fibroids may enlarge with oestrogen therapy (such as oral contraceptives) or with pregnancy. Growth seems to depend on regular oestrogen stimulation, showing up only rarely before the age of 20 and shrinking after menopause.

 

Pathophysiology

Uterine myomas, or leiomyoma. Benign neoplasms or tumours of smooth muscle cell origin that develop within or are attached to the uterine wall. 1 mm 30 cm in diameter. In the early stages when only muscle is involved the tumours are myomas, later as fibrous tissue forms between the muscles cells they becomes fibromyomas. As with other benign tumours the fibromyoma is surrounded by a capsule. Uterine fibroids are the most common form of pelvic tumour. Rare before the age of 20, present in the majority of women, if small ones are counted, during child bearing years. Most regress after the menopause. Oestrogen promotes growth.

 

Fibroids can be microscopic, but they can also grow to fill the uterine cavity. Growth normally continues up to the menopause. They may be single, but more commonly they will be multiple. They slowly enlarge and become more nodular, frequently intruding into the cavity of the uterus or growing out beyond the normal boundary of the uterus. Rarely, a fibroid will hang from a long stalk attached to the outside of the uterus. This is called a pedunculate fibroid. A fibroid may block a fallopian reducing fertility. Pressure may also occlude a ureter leading to hydronephrosis.

Existing fibroids will grow during pregnancy due to the increased blood flow and oestrogen levels.

Very rarely, malignant changes may occur; however, these usually take place in postmenopausal women. Very rarely a fibroid may become a sarcoma with rapid enlargement.

 

Clinical features

May be asymptomatic. Pelvic colicky pain, sensation of fullness or pressure in lower abdomen, abdominal fullness, increase in urinary frequency due to pressure on the bladder. Heavy menstrual bleeding (menorrhagia) due to ulceration of the thinned overlying endometrium, sometimes with the passage of blood clots, sudden, severe pain if a pedunculate fibroid twists causing the blood vessels feeding the tumour to kink. Pressure on the sigmoid colon may lead to alterations in bowel habit. A pelvic examination reveals an irregularly shaped, lumpy, or enlarged uterus. A transvaginal ultrasound or pelvic ultrasound is usually performed to confirm the findings. Prior to menopause, fibroids are likely to grow slowly. Women with known fibroids should have children early. Anaemia often develops as a result of the bleeding.