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On the conference of the Department

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on the conference of the Department

of Obstetrics and Gynecology with the Course

of Infant and Adolescent Gynecology

“____” _____________200 p.

protocol No

T.a.The Head of the department, Professor


Methodological instruction

on the themes singled out for independent study

Inflammatory diseases of female genitals in girls and women of reproductive age”


For 5 year students

of medical faculty

2 academic hours

Developed by assistant, PhD

Oksana Bakun

Chernivtsi, 2008

I. Scientific and methodical grounds of the theme

Inflammatory diseases of female genitals often take the first place among genital pathology, and often the cause of working ability loss, infertility, multiple complications.

II. Aim:

A student must know:

  1. Etiology and pathogenesis of acute and chronic female genitals diseases.

  2. Clinic symptoms of inflammatory gynecologic diseases.

  3. Peculiarities in the course of inflammatory gynecologic diseases in different age.

  4. Diagnostics methods of inflammatory gynecologic diseases.

  5. Differential diagnostics of inflammatory gynecologic diseases.

  6. Treatment methods of inflammatory gynecologic diseases.

A student should be able:

1. To carry out an objective gynecologic examination of a patient.

  1. To make up a plan of a patient’s examination.

  2. To evaluate the results of patient’s examination and to make a diagnosis.

  3. To write out a prescription of medicine.

III. Recommendations to the student


The vulva, vagina and ectocervix under normal conditions are the habitat of various types of infective agents, but they are only a threat if normal defence mechanisms are altered.

Defence mechanisms 1. Vaginal acidity.

Glycogen is produced by vaginal epithelium influenced by oestrogens and is converted to lactic acid by Doderlein's bacillus (a type of B. acidophilus). This maintains the vaginal pH between 3 and 4 which inhibits most other organisms.

2. Thick layer of vaginal squamous epithelium.

This is a considerable physical barrier to infection. Continual desquamation of the superficial keratohyalin layer and glycogen production, both dependent upon ovarian oestrogen action, combat bacteria. In children and post-menopausal patients the epithelium lacks oestrogen stimulation and is thin and easily traumatised or infected.

3. Closure of the introitus.

In children and virgin adults the vaginal canal is only a potential space kept closed by the surrounding muscles and provides another physical barrier. This, however, alters and becomes of little importance following sexual activity and pregnancy.

4. Glandular secretions from the cervix and Bartholin's glands maintain an outward fluid current helping to clear the canal of debris. In addition, cervical secretion contains immunoglobulins, especially IgA, and there are varying numbers of polymorphs, lymphocytes and macrophages.


Vulval inflammation is not uncommon but is usually an extension of infection from the vagina. A mild reaction may arise due to physical and anatomical conditions in the area, such as (a) moistness and (b) proximity of urethra and anus.

The area is not only naturally moist but also warm, particularly in obese patients. The folds of fat harbour moisture, and chafing occurs between them. The proliferation of bacteria is encouraged. Urinary incontinence and unsuspected glycosuria may add to this. It is important to test the urine for sugar in all patients.

Incidental factors may intensify any reaction resulting from these conditions e.g. the wearing of nylon underwear which is heat-retaining and non-absorptive. Associated with this may be chemical factors increasing the reaction such as washing underclothes with detergents, using toilet powders, perfumes and deodorants. The clinical result is irritation and itching leading to scratching. Continual itch-scratch-itch leads to maceration of the skin and may invite infection. Careful attention to personal hygiene is essential. Obese patients should be encouraged to lose weight and all of the incidental factors mentioned above should be avoided.

It must be remembered that itching may be a sign of a more serious disease such as impending liver failure or Hodgkin's disease.

Search for lice or scabies should be made where circumstances suggest the possibility.

One of the complications of vulvar inflammation is obstruction of the duct of Bartholin's gland. Cystic dilatation and abscess formation are apt to follow. The condition occurs during a woman's sexual life. Any organism, staphylococcal, coliform or gonococcal may be found.

The gland lies partly behind the bulb of the vestibule and is covered by skin and bulbospongiosus muscle. The duct is 2 cm long Orifice and opens into the vaginal orifice lateral to the hymen.


Marsupialisation (Gk. marsipos, a bag) The cyst or abscess is widely opened within the labium minus and drained and its walls sutured to the skin leaving a large orifice which it is hoped will form a new duct orifice and allow conservation of the gland. A ribbon-gauze pack is inserted for 48 hours by some operators.

LEUCORRHOEA. This means an excessive amount of normal discharge — a very subjective assessment. The patient will complain of constantly having to change her clothes but there will be no irritation and appearance will be normal. The smell will be the normal vulval odour (from the action of commensal bacteria on the secretions of the apocrine sex glands), microscopy will reveal normal appearances and culture will grow only lactobacilli.

The patient should be reassured and given an explanation of normal physiology. No local treatment is necessary.

Almost 20% of all patients attending gynaecological clinics complain of vaginal discharge, indicating some form of infection. The infective agents form three groups:

1. In 90% of cases the inflammation is usually relatively mild and is due to one of three

  • Candida albicans

  • Gardnerella vaginalis

  • Trichomonas vaginalis.

The remaining 10% are more serious. They may cause painful sores, tumour-like lesions, spread into the pelvis or cause generalised infection.


This is yeast and exists in two forms — slender branching hyphae or as a small globular spore which multiplies by budding. Source of infection

This organism may exist as a normal commensal in the rectum and small numbers may be found in the vagina, the acid medium suiting their survival without symptoms arising. The patient's fingernails may harbour the yeast. Sexual transmission is also possible. Symptomatic infection is most likely to arise when there are predisposing conditions e.g.

Pregnancy. The vagina provides a tropical micro-climate and the high concentration of sex steroids in the blood maintains an increased glycogen formation in the vaginal epithelium and may alter the local pH.

Immunosuppressive therapy. This includes cytotoxic drugs and corticosteroids. There is also thought to be a natural degree of immunosuppression during pregnancy.

Glycosuria. This may be due to undiscovered diabetes, but again a mild degree of glycosuria may exist in a normal pregnancy due to lowering of the renal threshold for sugar.

Antibiotic Therapy. Systemic antibiotics destroy the normal bacteria thus reducing the competition for nutrients leaving the field clear for C. albicans.

Chronic anaemia. Normal iron stores are needed to maintain an adequate immune reaction. This also entails adequate folic acid intake. The angular stomatitis of chronic anaemia is due to Candida infection.

Rarely, deficient cell mediated immunity is a predisposing condition.
Clinical features

The patient is usually between 20 and 40, when oestrogen support of the epithelial glycogen content is at its highest. The complaint is of irritant discharge and dyspareunia.


  • reveals an inflamed and tender vagina and vulva with white plaques

  • resembling curdled milk adhering to the vaginal wall and vulva.

  • Removal of the plaque reveals a red inflamed area. Pre-pubertal or post-menopausal infection is uncommon, but if it does occur after the menopause the symptoms tend to be severe.


A single 500 mg clotrimazole pessary, with external application of 1% clotrimazole cream offers convenient therapy. There is now doubt about the need to treat sexual partners, formerly advised. In persistent or recurrent infection, confirmation of the diagnosis by culture and determination of sensitivity to treatment are important. Oral fluconazole 150 mg or itraconazole 200 mg as a single dose, or monthly for 6 months may be effective. Nystatin 500,000 i.u. orally 4 x daily and Nystatin pessaries 2 x day for 3 or 4 months may be added. Boilable or disposable underwear should be worn.


For a long time a large number of cases of vaginitis were labelled non-specific because of disagreement regarding the infective agent. These cases were characterised by a non-irritating, foul smelling discharge. Ultimately, careful bacteriological studies have established the fact that although the discharge contains a mixture of bacteria, the one constant feature in 90% of cases is the presence of a tiny gram-negative cocco-bacillus which is a facultative anaerobe — Gardnerella vaginalis.

^ Clinical features

The patient complains of a foul-smelling discharge, and examination confirms both the discharge and the odour. In appearance the discharge is thin, greyish and sometimes shows bubbles. A vaginal smear reveals the presence of 'clue' cells. Gram staining is usually negative but can be variable.

Pus cells tend to be few in number. Doderlein's bacilli are also scanty but frequently many other bacteria are present. The pH of the fluid is raised. Although the main complaint is of malodorous discharge some patients will have pruritus, frequency, dysuria and dyspareunia.

Treatment. Oral Metronidazole 200 mg t.i.d. for 7 days or a single dose of 2 g appears to be effective. Clindamycin vaginal cream may also be employed. Male partners should also be treated.


Trichomonas vaginalis is a protozoan organism, which infests the vagina in the female and the urethra, prepuce and prostate in the male. It is a common cause of irritant vaginal discharge. T.Vaginalis is a single-cell organism about 20u x 10u, with four flagellae and an undulating membrane which gives it a characteristic jerky movement. It is transmitted mainly during sexual intercourse but can be acquired from infected articles such as a contaminated speculum.

Perhaps 18% of the female population. T.vaginalis is commonly found in patients with gonorrhoea, and has an association with cervical dysplasia. No cause-and-effect relationship has been proved.

Diagnosis is by observation of the motile organisms in a fresh smear diluted with saline and by laboratory culture.

Clinical features. In the acute phase the patient complains of severe vaginal tenderness and pain, and an irritant discharge. The vagina is seen to be inflamed, sometimes with a patchy strawberry vaginitis, and there is a copious offensive, frothy discharge. Frequently there is a burning sensation, pruritus, dysuria and dyspareunia. In the latent or dormant phases there are no symptoms although the presence of the organism can be demonstrated, often in a cervical smear.

Treatment. Always systemic and, if possible, including the patient's sexual partner. Metronidazole (Flagyl) 200 mg thrice daily for a week, or 2 g orally once, avoiding concurrent alcohol ingestion. Nimorazole (Naxogin) 2 gm as a single dose taken with food. Short courses are useful with patients whose cooperation is uncertain, but are more likely to cause nausea and gastritis.

The post-treatment vaginal smear should be normal, but T. vaginalis can linger in the urethra, Skene's and Bartholin's glands, and reinfection of the vagina may call for further treatment.

The nitroimidazoles are complex drugs and at least one of them, metronidazole, is active against anaerobic organisms and has also been used in alcoholism, Crohn's disease and rheumatoid arthritis. It is also effective as a potentiator of radiotherapy applied to hypoxic cancer cells, and a case of peripheral neuropathy has been reported after prolonged dosage. Care is necessary if the drug is being given to a pregnant woman, although no harmful effects on the fetus have been demonstrated.


Passing from host to host during coitus T. vaginalis attaches itself to the vaginal epithelium and multiplies rapidly, taking glycogen away from Doderlein's bacilli which disappear. The vaginal pH rises to about 5.5, allowing the increase of bacterial pathogens which aggravate the infection and resulting discharge.


This sometimes arises at times when ovarian activity ceases with the onset of the menopause, after surgical removal of the ovaries or following ablation by radiotherapy or chemotherapy.

Clinical features

Symptoms may be mild, consisting of irritation with discharge. In other patients the changes may be severe. Pain can be the main feature and the discharge purulent. Examination of the vaginal mucosa reveals a rash of petechial haemorrhages and there may be ulceration. Smears show rounded epithelial cells, with no glycogen, many polymorphs and bacteria. In neglected cases intra-vaginal adhesions may develop. Oestriol vaginal cream or pessaries and very low dose oestradiol preparations such as 0.025 mg vaginal tablet (Vagifem) or silastic ring pessary (Estring) give local benefits without significant systemic oestrogen effects.

^ VULVO-VAGINITIS in CHILDREN. This is a rare condition and only arises in certain circumstances viz.

In (a) the changes will be those of physical damage to the tissues. Infection will depend to some extent on whether the person guilty of the offence is a carrier of a specific agent. In this case infection may arise from bowel commensals. The diagnosis may be made by applying Sellotape (Scotch tape) to the vulva then pressing the tape onto a microscope slide for microscopic examination. Many of the examples of vulvo-vaginitis may arise from the irritation caused by threadworms. Scratching will lead to maceration of the skin which in turn will encourage bacterial contamination.

Vaginitis due to foreign bodies is sometimes seen in adults. Tampons, contraceptive devices and supportive pessaries used for prolapse may be left, forgotten, in situ. These give rise to an offensive purulent discharge. Bacteriological investigation will give an indication of the type of infection and the appropriate treatment following removal of the offending body.

A secondary vaginitis may arise due to contamination of the vagina through fistulous openings (vesico-vaginal or recto-vaginal) following injury, surgical operations or tumour growth. Repeated attacks of infection may occur. Treatment is obviously repair of the fistula where this is possible.

In all cases of vaginal discharge the possibility of malignant disease in the tract must be considered.


GENITAL HERPES. Herpes Simplex virus (HSV) types 1 and 2 may affect the lower genital tract or the mouth. It is highly infectious — 80% of women in contact with male carriers become infected. The initial attack may be severe. There may be, in 50% of victims, less severe recurring attacks every 3 or 4 weeks and they represent a potential for wide dissemination to others in the immediate environment. The incubation period is short — 3 to 7 days.

^ Clinical findings

The disease affects the vulvo-vaginal and perianal regions but may be transmitted to the mouth. The patient complains of burning, itching and hyperaesthesia of the area and the skin shows evidence of acute inflammation — oedema and erythema. There is usually a vaginal discharge. If the periurethral area is involved there may be dysuria and retention of urine.

The specific lesions start as small indurated tender papules which become vesicles and quickly break down to form shallow ulcers, 5 mm or more in diameter, with a yellowish grey slough in the base. These can be seen on the vulva and labia but in some cases they are confined to the vagina and cervix and there may be no external evidence of the disease. In these circumstances the ulcers may be large and could be mistaken for carcinoma of the cervix. The inguinal nodes are enlarged. The infection is accompanied by general symptoms of malaise, headache and even encephalitis. Sacral ganglion involvement causes neuralgia. There is no intense dyspareunia.

The acute phase lasts for 4-5 days. The lesions heal over 8-10 days and then a latent period ensues during which the virus remains in the sacral ganglia. Further attacks may follow. The disease may occur during pregnancy, and infection of the baby may prove fatal.


Clinical suspicion is confirmed by tissue culture isolation of virus or detection of virus antigen by immuno-fluorescence or ELISA techniques. Some degree of immunity may be conferred during recurrent attacks and a search for antibodies will help to differentiate primary from second attacks.


Ice packs, local analgesia (2% lignocaine), non-steroidal analgesic creams, saline bathing and systemic analgesics help relieve acute local symptoms. Acyclovir 3% ointment, applied repeatedly, is effective only if commenced at the onset of signs and symptoms. Oral Acyclovir, 200 mg 4 hourly for 5 days, may be commenced within 6 days of onset of a first episode. Antibiotics or povidone iodine control secondary infection. Acyclovir is less effective in recurrent episodes.

Acyclovir 800 mg daily, orally, has been used long-term when frequent recurrence is a problem. Famcyclovir and valciclovir have similar effect with less frequent administration.


Commonly called genital warts, these are caused by human papilloma viruses (HPV) which are transmitted sexually, with more that 50% of contacts developing lesions. Numbers 6 and 11 are particularly associated with condylomata. Infectivity is greatest just after appearance of a wart. Incubation varies from a few weeks to 9 months or more.

^ Clinical findings

A single warty growth quickly spreads to form multiple growths showing a tendency to fuse. They are pinkish with dry surfaces unless macerated and are of softer consistency than the ordinary skin wart. The growths become luxuriant in moist areas and especially during pregnancy. They affect the labia, perianal area, perineum, the lower part of the vagina and may even spread on to the thighs. Secondary infection may give rise to purulent discharge.

^ Differential Diagnosis

Syphilitic condylomata. These are more widespread and not confined to the genital area. They are also flatter and more rounded. Treponemes can be found in the tissue fluid. Serological tests will of course confirm the diagnosis.

Benign papilloma. This is commonly single and similar to ordinary skin warts.

^ Verrucous carcinoma. This is a locally malignant lesion but vulval carcinoma is rare in pre-menopausal patients. Biopsy will differentiate the two conditions.

Sometimes condylomata affect the cervix and can resemble carcinoma.


Podophyllin 20% in alcohol is often used, painted on the lesions. It may be ineffective and systemic absorption has proved fatal. It must not be used in pregnancy. Podophyllotoxin, the active ingredient, is available as liquid and cream for self-treatment of both sexes.

Cryocautery, electrocautery and laser ablation are employed. Lesions may recur.

^ MOLLUSCUM CONTAGIOSUM. This is a highly infective pox virus, one of the largest known and can be seen under the microscope. It is commonly transmitted by sexual contact but towels and clothing can carry the infection. Whitish papules with dark umbilicated centres are produced. They are firm in consistency. Mostly they affect the genital region but can spread to other parts of the body. Spread is rapid. The disease is common in infants. Sometimes there is a cheesy discharge from the warts.


This is a simple matter of killing the virus by local treatment to prevent spread of infection. Phenol can be applied to the centre of a nodule. Diathermy and cryosurgery are used in a similar fashion.

^ BACTERIAL INFECTIONS. CHLAMYDIA TRACHOMATIS. This is a widespread gynaecological infection.

Clinical features

The initial symptoms in women are often mild. Discharge may be present, varying from watery to frankly purulent according to the severity of the reaction to the disease. In severe cases there is obvious cervicitis which looks like an infected erosion. Sometimes there is a punctate haemorrhagic inflammation with micro-abscesses. Occasionally there are few changes in the vagina and the first evidence of infection is the appearance of a salpingitis. It is an important cause of chronic pelvic inflammation. A gelatinous exudate is formed in the pouch of Douglas which proceeds to multiple adhesions and tubal occlusion. It is an important cause of infertility. Ophthalmia neonatorum is very common as there is over 50% chance of transmission during delivery.

Reiter's syndrome with urethritis, arthritis and conjunctivitis is more common in the infected male. There may be spread to cause perihepatitis with so-called violin string adhesions to the parietal peritoneum. This is accompanied by acute pain in the upper right quadrant. The condition may be mistaken for cholecystitis or pancreatitis. It has been suggested that chlamydia may be involved as an aetiological agent in carcinoma of the cervix.


Endocervical cells, urethral cells or endosalpinx cells (salpingitis detected at laparotomy) must be obtained using a special cotton tipped swab and transferred immediately in special transport medium to an appropriate laboratory.

Nucleic acid amplification techniques are now commonly used to diagnose chlamydia from a vulval swab or a first-void urine sample, with 30% greater sensitivity than viral culture.

Treatment: Tetracycline 500 mg at 6 hourly intervals for 2 weeks. If the patient is pregnant erythromycin is preferable since there is a danger of hepatic damage with tetracycline therapy.

^ LYMPHOGRANULOMA VENEREUM (LGV). Previously thought to be viral, LGV is now attributed to a strain of chlamydia. Rare in the UK, it is mainly seen in the Far East, Africa and South America in seaports.

Clinical findings

The primary lesion is a small painless ulcer with raised irregular borders which may involve the labia, clitoris or urethra. It appears 1 to 3 weeks after infection. Several weeks later the inguinal and iliac lymph nodes enlarge, become soft and fluctuant and this is followed by rupture creating discharging sinuses. The lesions eventually heal with the creation of large fibrous scars. In the process the urethra may be virtually destroyed and the rectum stenosed. Recto-vaginal fistulae may form and extensive surgical treatment may be required. The pelvic organs may be involved in the same way giving rise to intestinal obstruction and various fistulous communications.

Treatment: Tetracyclines or erythromycin are effective.

^ GRANULOMA INGUINALE. Another tropical ulcerative condition, caused by the intra-cellular Gram-negative Donovania granulomatis, this begins as a painless genital, inguinal or peri-anal nodule, which ulcerates. Local lymphatic glands enlarge, but do not ulcerate. In pregnancy, abortion often occurs or there is high fetal morbidity. Secondary infection is common.

Treatment: The condition responds to tetracycline given for 2 or 3 weeks. Both of these diseases may be followed by squamous carcinoma.

CHANCROID. This lesion is due to infection by Haemophilus Ducreyii. After a short incubation period a red macule appears which quickly changes to a pustule and then an ulcer. The ulcers are numerous and vary in size from millimetres to several centimetres. They are well defined with projecting margins but shallow with a greenish slough in the base. These ulcers are soft and painful. This, together with the short incubation period helps to differentiate them from syphilitic lesions. The labia major, clitoris and perianal regions are affected. Two weeks later the local lymph nodes tend to enlarge and suppurate. There is usually secondary infection and the discharge is foul-smelling. Microscopically the lesions consist of granulation tissue infiltrated by lymphocytes and plasma cells. The bacillus can be demonstrated in scrapings from the ulcer stained by Giemsa.


Co-trimoxazole 960 mg twice a day by mouth is usually effective. Tetracycline may also be used. If the lymph nodes suppurate they should be aspirated through adjacent healthy skin, but do not incise.

GONORRHOEA. Gonorrhoea in the female carries a high risk of salpingitis and sterility, but early diagnosis is difficult to achieve. Symptoms are often mild or absent, and since the incubation period is about 2 weeks (longer than in the male) very few women consider the possibility of such an infection.

Clinical features. The classical history is of urethritis, vaginal discharge, menstrual upset of sudden onset, but any infection in the genital area however it presents, may be gonococcal. After the acute phase vaginal discharge will persist, followed in approximately 15% of cases by signs of pelvic inflammatory disease (PID).


The labia are held apart, and the urethra, Skene's ducts and Bartholin's ducts examined for signs of infection. These ducts should be 'milked' for specimens of pus, if any, and swabs are taken from the cervix which is the main reservoir of infection.

Diagnosis is a laboratory procedure.


In the UK, 1.2 mega units of procaine penicillin with 2 g of probenecid, or Amoxycillin 3 g orally plus probenecid lg orally are usually effective. In patient allergy or organism resistance, the latter very common outside of the UK, large oral doses of cephaloridine, tetracycline or doxycyline may be effective.

SYPHILIS. Syphilis is an uncommon disease in gynaecological practice, but any genital sore should come under suspicion. It is less uncommon in association with HIV.


The chancre (a corruption of 'cancer') has an incubation period of about a month and its appearance is often accompanied by pyrexia and malaise. The most common site is the vulva and then the cervix, but infection can occur anywhere. The chancre is the point at which the treponema enters the body.

The typical chancre is about 1cm in diameter and begins as a reddish papule which becomes ulcerated. It is painless and highly infective. The inguinal glands are markedly enlarged.

Diagnosis requires the identification of T. pallidum in the exudate of the chancre or in material aspirated from an enlarged gland. Treponemata are not easily recognisable in stained preparations and the dark-ground illumination of fresh specimens is used. Light is reflected off the edges of the organisms, making them easy to perceive and they are recognised by their shape and movement. ^ DIAGNOSIS OF SYPHILIS

Positive identification of T. pallidum is difficult for various reasons including the failure, so far, to grow the organism in vitro. The usual method of diagnosis is by serological tests which become positive 4-6 weeks after infection.

Treponemal Immobilisation Test (TPI).

This is a specific for syphilis but is expensive. Live T. pallida are used (from a rabbit chancre) and are seen to be immobilised if combined with syphilitic serum.

Fluorescent Treponemal Antibody Tests are becoming very widely used for verification of the 'positive WR'.

Enzyme immunoassay tests which detect anti-treponemal IgM and IgG antibodies are claimed to be both sensitive and specific. They are amenable to automation. Signs and symptoms of the spread of T. pallidum throughout the whole body appear usually about 2 months after the primary stage, and the disease may present in this phase to the gynaecologist.

There is likely to be a mild pyrexia and malaise, but the dominating signs are a generalised lymphadenopathy and mucocutaneous lesions. 'Snail track' ulcers appear on mucosal surfaces, and the skin develops a very wide variety of macular and papular rashes. In warm moist areas such as the breast flexures and the vulva, the papules become hypertrophic and flattened and present as 'condylomata lata' which are highly infective.

Diagnosis is by the demonstration of T. pallidum in the lesions and by serological tests.

Treatment of early contagious syphilis T. pallidum is sensitive to many antibiotics, but reactions are common and care is required in treatment. Most patients receiving effective treatment for early syphilis with any antibiotic will display some degree of the Jarisch-Herxheimer reaction — rigors, sweating, headache, for about 24 hours. It can be modified by giving prednisolone 5 mg 6-hourly.


This is an uncommon syndrome which can arise in women using tampons. It is caused by staphylococci which may be carried by the woman herself in various sites such as the vagina, cervix, perineum or nasopharynx. It is extremely dangerous and may prove fatal. The infection becomes established in the vagina, usually aided by the presence of a tampon.

^ Clinical signs

There is a rapid onset of fever often with vomiting, diarrhoea, muscular aches and skin erythema. The blood pressure drops to very low levels and the patient becomes confused and stuporose. Swabs should be taken from the various sites where the organism may be carried and tests of function should be made so far as possible in relation to the kidney, liver, muscle, central nervous system and blood platelets.

Treatment. Crystalloid solutions and plasma should be given rapidly to reverse the hypotension. Methicillin or oxacillin 1-2 g every 4 hours can be administered to subdue the infection. Check for a retained tampon.


This is the result of:

1. Spread from the lower tract of infections such as chlamydia, gonococcus or trichomonas and it begins in the cervix. It may not spread farther but it remains a potential threat, or 2. Diseases blood-borne from other parts of the body, or 3. A few cases may be related to obstetrical trauma or abortion.


An overgrowth of columnar epithelium replacing the squamous epithelium round the cervical os. It has a raw appearance and a velvety feel. It is an ectopy of columnar epithelium and in modern terminology is so described. This is physiological and no treatment is required.


An infection of the cervical epithelium and stroma, usually following ectopy.


There may be no symptoms with any of these conditions which are observed at examination, but usually there is a complaint of discharge, and they are potential causes of post-coital bleeding. Cervicitis has never been proved to have a special liability to malignant change.

CRYOSURGERY This has been developed as an alternative to cautery and diathermy and is useful as an outpatient procedure.

The cryoprobe temperature is reduced to about -50°C over 2 minutes by the endothermic action of nitrous oxide, taking in its latent heat as it is decompressed after being forced at high pressure hrough a narrow orifice.

Treatment takes about 2 minutes and is almost painless. Extreme cold causes adherence between tissues and metal and 30 seconds must be allowed for thawing before the probe is removed. The patient will have a watery discharge for 2 weeks, and coitus should be avoided for a fortnight.


More extensive lesions must be treated by surgical excision or by diathermy. In diathermy the infected tissue is destroyed by the great heat generated where the diathermy probe or point touches the cervix and sends high frequency current through the body to the indifferent electrode strapped to the leg.

The burnt tissue sloughs off over 2 weeks and the raw area is gradually re-epithelialised. This method requires general anaesthesia, and the discharge is more offensive than that following cryosurgery.


Laser therapy may be employed at a colposcopy clinic.



Acute inflammation may develop in response to infection following childbirth or abortion, or the insertion of a contraceptive device or as part of a gonorrhoeal infection. Actinomyces infection may be associated with neglected intra-uterine contraceptive devices and may be detected on a Papanicolaou smear.

Chronic Endometritis is a rare condition because of the frequency with which the endometrium is shed. The diagnosis is histological and there are no specific signs or symptoms, but the microscopic appearances are of infiltration mainly by plasma cells and lymphocytes.

Post-menopausal endometrium has little resistance to infection, and endometritis may arise from cervicitis or from tumour. If the cervix is stenosed by infection or tumour, the uterus becomes distended with pus and the condition is known as pyometra. Cervical dilatation will release the pus but curettage must be done to exclude malignancy and in such a situation it is very easy to perforate the uterus.

Metritis. Acute inflammation of the myometrium is a serious condition resulting from infection introduced during childbirth or abortion.

Treatment. If there is no organic cause, the menstrual irregularity may respond to sex steroid hormones. In the woman over 40 who wishes no more family, there is much to be said for simple hysterectomy. There may be a role here for progestogen releasing IUDs as these reduce the duration and amount of menstrual loss as well as giving excellent contraception.

^ GENITAL TUBERCULOSIS. Tuberculosis is a rare disease in gynaecology. It attacks the fallopian tubes and the endometrium, and lesions elsewhere in the genital tract are uncommon. It is possible that infection may be acquired from a sexual partner. The emergence of drug resistant strains of M.tuberculosis and the occurrence of tuberculosis in HIV-affected women and in developing countries may lead to a resurgence of genital tuberculosis.

^ Clinical Features

The patient is usually a young primary infertility or complaining of irregular menstruation, or perhaps abdominal pain.


Histological evidence from curettings. This is the commonest method and it is assumed that the tubes are also infected.

Laboratory culture (formerly guinea-pig inoculation).

Biopsy from any suspicious ulcerated area in the vagina or vulva.

By laparoscopic inspection and biopsy.

The tubes may appear normal (endosalpingitis) but usually display the distortion and swelling of chronic infection, and small pinhead tubercles appear on the serosa.

Once evidence of genital infection is obtained, the respiratory and urinary tracts must also be investigated.

The endometrium also shows tuberculous follicles, best developed in the premenstrual phase. There may be debris in endometrial glands.


  • Surgery

  • Chemotherapy


AIDS is now the most serious of all gynaecological infections. It was first recognised as a new entity in 1981. It has reached pandemic proportions affecting almost all countries and regions. In some parts of the world such as the sub-Sahara region of Africa and in some sections of the public in western countries, e.g. drug addicts in the USA, there are epidemics. The incidence is low in Arab countries. It is due to the human immune deficiency virus (HIV) or, in scientific terms, retrovirus oncornavirus.


There are several modes of infection and risk factors.

A. Sexual

Relationships with prostitutes. Multiplicity of sexual partners increases the risks. The same dangers exist with promiscuity. Male homosexual activities. Again there are likely to be multiple partners. Sexual contact with individuals of the same or opposite sex in southern parts of Africa.

Abrasions around the genital or anal regions increase the risk of infection.

B. Non-sexual


This depends upon the activities of lymphocytes, of which there are two basic types, B and T. lymphocytes. These are so called because they were first discovered in the bursa of Fabricius in the bowel of chickens.

When the body is invaded by a foreign antigen, such as in an infection, B lymphocytes are transformed and become plasma cells capable of secreting specific antibodies into the tissues and blood causing destruction of the antigen. This reaction is very rapid, almost immediate, and results in humoral immunity.

These B cells form 25% of the blood lymphocytes.

T lymphocytes are named thus because they are processed in the Thymus. They form 70% of blood lymphocytes.

T cells are also stimulated by foreign antigens and undergo transformation into several specific types whose function is to control and aid the B cells. There are 3 main types:

1. T cells which control the

production of B cell antibodies.

2. T cells which control the over-all production of lymphocytes.

These changes in T cells follow the B cell phase and are therefore delayed. They produce cell mediated immunity. The various activities of the T cells make certain, in normal circumstances, that the immune reaction is tailored to the needs of the body at any particular phase of infection.

3. Killer cells. These kill other cells by direct contact if the latter have been infected.

^ HIV INFECTION AND THE IMMUNE SYSTEM. The Human Immunodeficiency Virus (HIV) and the B lymphocytes.

The reaction is very slow and up to 6 months may elapse before antibodies appear in the blood. Usually, however, their appearance coincides with the eruption of symptoms. They seem to have little or no influence on the course of the disease and in the later stages they may disappear from the blood.

^ HIV and the T cells.

Although B cells react and produce antibodies, initially it is the effect of HIV on the T cells which ultimately destroys the whole immune apparatus. The virus attacks T cells, especially those of the helper variety commonly called T4 lymphocytes which stimulate production of antibodies and increase the number of lymphocytes.

Curiously one of the antigens of these lymphocytes, the differentiation antigen CD4, has an affinity for the virus and acts as a receptor. On the other hand, although brain tissue and muscle may be infected by the virus, there is no CD4 antigen to act as a receptor in these regions. Ultimately there is a progressive lymphopenia affecting both B and T cells.

T cells also influence polymorphs and macrophages in much the same way as lymphocytes. Normally, in infection they increase chemotaxis and phagocytosis. With HIV infection these activities will diminish and this explains the ease with which secondary infections by organisms of very low pathogenicity can establish themselves, spread rapidly and cause septicaemia.


The progress of the disease can be roughly divided into 4 phases, but these phases are ill-defined, variable in time of onset and duration.

Phase 1

Following infection there may be no symptoms but in a considerable proportion of infected individuals an acute illness resembling infectious mononucleosis appears with fever, night sweats, enlarged lymph nodes, diarrhoea and a blood lymphocytosis. Antibody formation occurs. In other individuals this feverish episode is delayed for varying periods.

Phase 2

A symptomless period usually ensues which may last for 7 years or more. Despite the lack of symptoms the virus goes on replicating within the body. During this period there is frequently enlargement of lymph nodes in various parts of the body. As a result the name 'Persistent generalised lymphadenopathy' is often applied to indicate a particular phase.

Phase 3

This is the turning point in the disease when the virus has replicated and is beginning to reduce the ability of the patient to mount an effective immune response to ordinary infections. Symptoms of the type observed in the initial phase may reappear. Further development means a change from mere infection by HIV to full-blown AIDS syndrome. Fifty per cent of infected individuals progress to phase 4 within 10 years. The phrase 'AIDS related complex' is used to indicate a particular stage in the disease but this phrase is not particularly useful because of the erratic behaviour of the infection.

Phase 4

The final phase is characterised by repeated attacks of intercurrent infection due to progressive immuno-deficiency. The core antigen increases. T4 helper lymphocytes progressively diminish. The viral DNA is integrated into the genome of infected cells producing more HIV.

Treatment. Specialised knowledge and experience are essential. Earlier forms of treatment were aimed at preventing and treating secondary infection in the final phases of the disease. They were directed especially at pneumonia due to Pneumocystis carinii which is common in these patients and, if untreated, causes death within 1 year.

Drugs have been used in a prophylactic manner to prevent secondary infection occurring. There are several preparations but some, such as nebulised pentamidine, while being effective against Pneumocystis, are too specific and have no influence on other common infections such as toxoplasmosis. Oral drugs e.g. co-trimoxazole, sulpha-methoxazole-pyrimethamine, dapsone and dapsone-pyrimethamine, have a more general action.

Four methods of treating or preventing the viral infection itself are in various stages of development:

1. Anti-viral drugs

These show some promise but whether they can produce a cure or merely modify the course of the disease is not yet clear. Zidovudine, lamivudine, indinavir, didanosine, nevirapine and didoxyinosine are such. The last has a disadvantage in that diabetes mellitus and Raynaud's syndrome have occurred during therapy. Combination therapies are more effective than single agents.

2. Genetherapy

An altered virus, a so-called mirror image of the AIDS virus has been constructed. The apparent idea is that the individual will be 'infected' with the artificial virus which will then occupy the viral receptors on T lymphocytes thus preventing entry of the AIDS virus and protecting the immune system.

3. Vaccination

It is obviously impossible to use whole AIDS antigen for vaccination for fear of actually infecting the individual. Sub-units of the antigen have been used and there are indications of some success but, unfortunately, while treatment may protect against systemic infection there is no protection against the mucosal invasion during sexual activity. There is also evidence that the antigenic sub-units can vary and so also does the degree of immunity.

4. A new drug treatment with benzodiazepine derivatives is being tried.

These drugs are known to interfere with reverse transcriptase reaction and would therefore stop the replication process.

^ IV. Control questions and tasks

1. Classification of inflammatory gynecologic diseases.

  1. What diseases are considered inflammatory processes of lower parts of female genitals?

  2. What is bartholinitis? Describe its clinic, diagnostics and treatment.

  3. What is vulvovaginitis? Describe its clinic, diagnostics and treatment.

  4. What is colpitis? What is its etiology? Diagnostic methods.

  5. Diagnostic and treatment methods of true and pseudoerosion of cervix uteri.

  6. Clinic, diagnostics and treatment principles of acute endometritis.

  7. Clinic and diagnostics of acute parametritis, peculiarities of its treatment.

  8. Clinic and diagnostics of acute adnexitis, peculiarities of its treatment

  9. Clinic and diagnostics of acute pelvioperitonitis, peculiarities of its treatment.

  10. Main principles of treatment of acute inflammatory diseases of upper parts of female genitalia.

  11. Antibiotic therapy - indications, principles of choice.

  12. Contemporary concept of gonococcus ultrastructure.

  13. Extragenital forms of gonorrhea, its clinic.

  14. Treatment methods of gonorrhea in women.

  15. Clinic of trichomoniasis.

  16. Urogenital infections, caused by chlamidia, mycoplasma, ureaplasma, special features of diagnostics and treatment.

  17. Candidiasis. Clinic, diagnostics, treatment.

  18. To name methods of provocations; used to reveal infection in occult sources.

V. List of recommended literature

1. Danforth’s Obstetric and gynaecology.-Seventh edition.-1994.-P.933-959

2. Gynecology. - Stephan Khmil, Zina Kuchma, Lesya Romanchuk. -


3. Infectious diseases of the female genital tract.-Richard L.Sweet, Donald S. Gibbs.-1985.-P.53-103

4. Gynaecology illustrated. David McKay Hart, Jane Norman.-Fifth Edition.-2000.-P.136-167

Approved on Session of Department of Obstetrics and Gynecology with course of Infant and Adolescent Gynecology_________________ protocol No___

T.a.The Head of Department:_______________ O.A.Andriiets’


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On the conference of the Department iconApplication form ХV international scientific conference «Ideas of Academician Vernadskyi and Problems of Regional Sustainable Development»
«Kremenchuk Plavni». The conference fee does not cover meals and accommodation. For foreign participants the conference fee may be...
On the conference of the Department iconApplication form ХІV international scientific conference «Ideas of Academician Vernadskyi, Problems of Research and Evaluation of Regional Sustainable Development»
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On the conference of the Department iconM. Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A. V., Ph. D. Rickets

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