Oestrogen stimulates the repair of the endometrium. The surviving epithelial cells multiply and spread across the surface of the endometrium and form a new functional zone. As the endometrium thickens, endometrial glands develop and the arterioles coil and lengthen as they penetrate the stratum functionalis (Tortora and Grabowski).
Ovulation
By the time ovulation occurs, the functional zone is several millimetres thick and the endometrial glands are manufacturing mucus rich in glycogen.
In the ovaries the dominant follicle has matured into the graffian follicle. This matured follicle ruptures and releases a secondary oocyte in to the pelvic cavity at approximately day 14 of the cycle, this is ovulation.
Secretory Phase
This is the time post ovulation until the onset of the next menses from day 14 –28. The endometrial glands enlarge, steadily increasing their rates of secretion as the endometrium prepares for the arrival of a developing embryo. This activity is stimulated by progesterone and oestrogen produced by the corpus luteum. There is vascularisation of the superficial endometrium and it thickens to 12-18mm. Secretory activity peaks between days 21-28 of the menstrual cycle. If fertilisation does not occur, the level of progesterone declines due to degeneration of the corpus luteum. This causes menstruation and hence the start of a new menstrual cycle (Tortora and Grabowski).
Hydatidiform Mole
This is a disorder of pregnancy affecting approximately 1 in 1000 pregnancies in the world. It is a benign abnormal mass characterised by swollen, oedematous chorionic villi and trophoblastic hyperplasia. The uterus may or may not be ‘too large for dates’, see figure 1 in appendix 1. Macroscopically the placenta appears to be composed of multiple cystic, ‘grape-like’ structures (Underwood 1996), see figure 2 in appendix 1. It is common before the age of 20 and after 40. They usually present clinically with painless vaginal bleeding after 12-14 weeks after conception (Kumar, et al 1997). Govan, et al states that abortion is the usual outcome.
There are two types of mole:
- Partial mole – the vesicular degeneration of chorionic villi affects only part of the placenta. Malformed foetal parts and some normal placental villi are present, along with abnormal trophoblastic tissue. There is a low risk of subsequent development of malignancy (Stevens, et al 1995).
- Complete mole – this is a pregnancy lacking a foetus. No normal placenta is identified and the mole forms a bulky mass, which can fill the uterine cavity. No foetal parts or normal placental villi are present (Stevens, et al).
A small proportion of the moles show invasion of the myometrium by the molar components.
Endometrial Carcinoma
This is the most frequent invasive malignancy in the female genital tract. It occurs mainly in nulliparous women between 50-60 years of age. The incidence of carcinoma increases in obese, hypertensive or diabetic patients because they tend to have a higher level of blood oestrogen (Ross and Wilson). The first clinical indications are usually marked leukorrhoea and bleeding (Kumar et al). Macroscopically, small tumours appear as diffuse, solid areas or polypoid lesions in the endometrium, whereas larger tumours fill and distend the endometrial cavity with soft, white, friable tissue. Necrosis of the tumour is common and leads to a frequent presenting feature of post-menopausal bleeding (Stevens, et al).
The endometrium has no lymphatics, so lymph spread is delayed until there is extensive local spread that involves other pelvic structures i.e. bladder, ureters or rectum (see figure 3 in appendix 1). Invasion of the ureters leads to hydronephrosis and uraemia, which is commonly the cause of death (Ross and Wilson).
Fibroids (Leiomyoma)
These are common, multiple benign tumours of the myometrium. They are firm masses composed of smooth muscle encapsulated in compressed muscle fibres and they vary in size e.g. from 5 – 200mm. It can be found in any part of the uterus, see figure 4 in appendix 1 (Ross and Wilson 2001). It occurs in 15-20% of women over 35yrs and its growth ceases at menopause. A fibroid is generally white, hard and round with a whorled structure as can be seen in figure 5 in appendix 1 (Govan et al 1995), composed of complex interlacing bundles of smooth muscle fibres showing little or no mitotic activity (Underwood 1996).
Large tumours may undergo degenerative changes if they outgrow their blood supply. This leads to necrosis, fibrosis and calcification. They develop during the reproductive period and may be hormone dependant, enlarging during pregnancy and when oral contraceptives are used. They tend to regress in menopause. Larger fibroids can cause discomfort as they can compress structures in the pelvic cavity, and affect the frequency of micturition, they can also cause irregular bleeding, dysmenorrhoea and reduced fertility. Malignant change is rare (Ross and Wilson).
Endometriosis
Ross and Wilson state that endometriosis is the growth of endometrial tissue outside the uterus, most commonly in the ovaries, uterine tubes and other pelvic structures, see figure 6 in appendix 1. The ectopic endometrium still responds to cyclical hormonal stimulation, which causes menstrual type bleeding into the lower abdomen and the ovaries. The whole organ may be converted to a cystic mass contained brown, semi-liquid material (chocolate cyst). Recurrent haemorrhages cause the formation of fibrous adhesions and accumulation of haemosiderin pigment. When the peritoneum is involved, adhesions may cause bowel obstruction (Stevens et al 1995). The condition usually presents with cyclical pelvic pain, dysmenorrhoea, pelvic inflammation and infertility.
References
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Govan, MacFarlane, Callander (1995) ‘Pathology Illustrated’ Churchill Livingstone
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Kumar, Cotran, Robbins (1997) ‘Basic Pathology’ 6th edition, WB Saunders and Company
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Martini F., Bartholomew E. (2000) ‘Essentials of Anatomy and Physiology’ 2nd edition, Prentice Hall
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Ross, Wilson (2001) ‘Anatomy and Physiology in health and illness’, 9th edition, Churchill Livingstone
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Stevens A., Lowe J. (1995) ‘Pathology’, Mosby
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Tortora G., Grabowski S. (2003) ‘Principles of Anatomy and Physiology’, 10th edition. Wiley International
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Underwood E C J. (1996) ‘General and Systematic Pathology’ 2nd edition, Churchill Livingstone
