Ectopic occurrence of endometrial tissue, frequently forming cysts containing altered blood.
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
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
Very variable and unrelated to the extent of the disease
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
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
Rupture of a cyst can cause acute peritonism
Fixation of uterus
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).
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
Inflammation caused by infection
May be acute or chronic
Other pelvic structures eg. Gut may be involved as a result of adhesions
Fallopian tubes - congested, oedematous, infiltrated by neutrophils
Collection of pus in the tubes
Pus may leak into peritoneal cavity ------ acute pelvic peritonitis
abscess may develop in the pouch of
Exudate collects in the tubes leading to adhesions
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
Adhesions in the tubes Rupture of masses causing generalised peritonitis
High doses of antibiotics Analgesia Bed rest
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
Composed of fibrous tissue Often covered in functional endometrium
Irregular bleeding and menorrhagia Sometimes colicky pain
Cervical dilation and uterine curettage
Uterine myomas Tumours derived from smooth muscle
Benign tumours Single or multiple
Small to very big
May be asymptomatic Menorrhagia
Colicky pain Pressure symptoms
Complications of pregnancy
Surgical excision to preserve function but hysterectomy is best
Malignant tumours of the uterus
Obesity Nulliparous Late menopause
Diabetes mellitus Exogenous oestrogen
Post menopausal bleeding
Premenopausaly - irregular bleeding and menorrhagia
Prolapse of the uterus
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.
Prolapse means a downward eversion of a hollow organ - may involve the rectum, uterus or urethra
May be first second or third degree
Feeling of `something coming down`
Pain is variable
Complications involve the urinary system
Prevent with good care of the pelvic floor muscles and perineum
Pelvic floor exercises
Avoid raised intra-abdominal pressure
Possible oestrogen HRT
Ring pessary, changed every 4 - 6 months
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)
Early disease is asymptomatic Post coital bleeding
Discharge Irregular bleeding
Pain with local invasion Involvement of bladder or rectum
Depends on stage Local treatment
Cone resection and biopsy Hysterectomy
4th most common cause of cancer deaths in women
May be related to ovulation - less in women who have taken oral contraception
Usually presents late
Abnormal uterine haemorrhage
Depends on stage
Abdominal hysterectomy with bilateral salpingo-oophorectomy
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
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.
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.
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.
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.
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.
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.
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.
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.
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.