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On the conference of the Department




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Approved

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

O.A.Andriiets’___________


Methodological instruction

on the practical class

Non-specific inflammatory diseases in gynecology”


Subject-gynecology

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.

  1. Clinic symptoms of inflammatory gynecologic diseases.

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

  3. Diagnostics methods of inflammatory gynecologic diseases.

  4. Differential diagnostics of inflammatory gynecologic diseases.

  5. 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

Pelvic infections are the most common conditions that gynecologists treat. There has been a dramatic increase in the recognition of pelvic infections because of new microbiologic and serologic techniques, because of educational efforts to increase physician awareness, and because of a rapid increase in the prevalence of sexually transmitted infections.

The impact of pelvic infections on the physical condition of women ranges from minor annoyance to serious illness and, in some instances, even death. The cost of treating pelvic infections is enormous if direct medical costs and indirect costs, including time lost from work, are calculated. For example, it has been estimated that by the year 2000, one of every four women who reached the reproductive age in the 1970s will have had an episode of pelvic inflammatory disease (PID). Of women with PID, 25% will have been hospitalized, 25% will have had major surgery, and 20% will be sterile.

All genital sites are susceptible to infectious organisms, while upper genital tract sites (endometrium, fallopian tubes, ovaries) are subject to ascending infection from lower genital tract sites. Certain agents preferentially infect certain sites and give rise to characteristic symptoms; other agents cause little symptomatology until major pathologic changes occur or until congenital neonatal infection or male partner infection occurs. The gynecologist should have special knowledge of the infections caused by Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum, genital mycoplasmas, Mycobacterium tuberculosis, and anaerobic bacteria, which may act alone or together to produce pelvic infections ranging from mild vaginitis to severe salpingitis.

^ VULVA Herpes

Today herpes simplex virus (HSV) infection is the most common cause of vulvar ulcers and viral genital infections. HSV genital infection usually occurs three to seven days after exposure. Symptomatic primary (first) genital infections typically consist of multiple vesicles that rapidly coalesce to produce ulcerations of the vulva, which may be exceedingly painful. The vagina and cervix may also be involved, producing a gray necrotic cervix and profuse leukorrhea. External dysuria is common, and bilateral inguinal lymphadenopathy is usual. Vulvar lesions may last for three or more weeks but healing is complete. Constitutional symptoms of fever, malaise, headache (aseptic meningitis), and urinary retention (myelitis) may persist for a week. It is also now apparent that the majority of primary infections result in minimal or no noticeable symptoms or signs.

After primary infection, latent HSV infection usually localizes in the sacral ganglion and perhaps in the dermis. The virus is probably not commonly transmitted during the latency period, when there are no symptoms and no physical evidence of infection despite well-documented sporatic random viral shedding. However, most patients develop a secondary (recurrent) infection from the latent virus weeks to months after the primary infection. Secondary lesions are usually less painful, more localized, and last for a shorter time (three to seven days) than those of primary infection. Systemic manifestations are unusual during secondary HSV.

From 75% to 85% of genital infections are caused by HSV type 2; the remainder of genital infections are caused by type 1 Herpesvirus hominis, which is the primary cause of oral infections. The two types of herpes infections are clinically indistinguishable. Vesicles and ulcers of HSV infection contain many virus particles that are highly infectious, and viral shedding occurs until the lesions re-epithelialize. Therefore, genital contact with a person who has either genital or oral lesions leads to a high infection rate. Transmission usually occurs from contact with ulcerative lesions, but transmission can occasionally occur from patients without lesions.

The diagnosis of herpes can be made clinically if typical, painful, multiple vulvar ulcers are present. Laboratory confirmation of atypical lesions and lesions that appear during pregnancy is best attained by virus isolation, which usually can be achieved within 48 hours. Pap smears or other cytologically examined material can identify intracellular inclusions and multinucleated cells, but unfortunately the cytologic methods, including fluorescein tagging and immunoperoxidase staining, are only 50% sensitive compared with culture in identifying HSV in-fections. Accordingly, a negative cytologic smear does not exclude HSV infection. Complement fixing and neutralizing antibodies appear within one week of the onset of infection; failure of an experienced laboratory to identify antibodies within three weeks is evidence against HSV infection. High antibody levels do not protect against recurrent HSV infection, although antibody passively transferred to the fetus appears to offer protection against neonatal infection.

The rising incidence of herpes infection and potential serious fetal effects have caused HSV to assume increasing importance in pregnancy.

HSV infection has been associated with cervical cancer. Women with cervical cancer have a higher prevalence of antibody and usually a higher antibody titer than do controls without cancer. However, the relation between herpes and cancer is not sufficient to establish that HSV causes human cancer. Nevertheless, women with HSV infection should receive frequent Pap smears and colposcopic examinations.

Local therapy of genital herpes is limited to the relief of pain. Most local treatment modalities either do not penetrate into virus-containing cells or are administered after epithelial damage has occurred. Many local antiviral compounds have been used, but rigorous double-blind and well-controlled studies have shown that most of them are ineffective. They neither shorten the duration of symptoms nor prevent recurrent infection. Corticosteroids and antibacterial and antifungal ointments are not only without benefit, but tend to prevent drying and, as a result, may delay healing. Local symptomatic therapy is often helpful (ten-minute sitz bath three or four times daily, followed by drying with a bulb light or a hair dryer). Oral acyclovir antiviral therapy (200 mg five times daily for seven to ten days) shortens the ulcerative phase and, when used continually two to five times daily for six to twelve months, reduces the frequency of recurrences. However, the expense and incomplete effectiveness of this drug limits its routine use.

^ Human Papillomavirus

Human papillomavirus (HPV) is a DNA virus of the family Papovaviradae that is distinct from the papovaviruses that cause the common wart. This virus thrives in the moist genital area and is usually sexually transmitted. The average incubation period is three months. Genital warts most commonly manifest gross lesions on the labia and posterior fourchette . They originally appear as individual lesions, although if neglected, large confluent growths up to several centimeters in diameter can occur. Vaginal and cervical warts are even more common than labial warts. Most cervical and vaginal warts are so-called flat lesions that are visible only by colposcopy. More than 40 HPV serotypes have been identified. Although visible genital warts are usually caused by types 6 and 11, the flat wart variant caused by types 16, 18, and 31 is usually visible only by colposcopy. When flat or atypical-appearing warts are found on the cervix, they may need to be biopsied to exclude cervical neoplasia; if so, treatment should be delayed until the nature of the lesion is determined. HPV types 16,18, and 31 have a high degree of association with cervical dysplasia and cancer when the HPV DNA is integrated into the cancer cell. Women with flat warts should have frequent Pap smears.

Vulvar warts must be differentiated from the less verrucous, flatter growths of syphilitic condyloma latum and carcinoma in situ of the vulva; punch biopsies may be required in order to exclude these lesions. Small to medium-sized verrucous lesions can usually be treated with cryotherapy (liquid nitrogen or carbon dioxide) or with 25% po-dophyllin in tincture of benzoin, which the patient must wash off after four hours. Small amounts (0.25 ml) should be used to avoid severe burns; the drug is contraindicated during pregnancy. Large amounts have produced coma in the adult and even caused fetal death in pregnant women. Atypical lesions should be biopsied before therapy is initiated because podophyllin causes bizarre histologic changes that persist for months. Cryotherapy, trichloroacetic acid, or laser ablation can be used on vaginal warts or during pregnancy. Recurrence rates of 50% probably relate to the failure of these methods to kill the virus in adjacent untreated areas. 5-Fluorouracil can be used intravaginally, but frequent burns and recurrences limit its routine use.

Vestibulitis

Patients with vestibulitis characteristically have pain with vaginal penetration (intercourse or tampon insertion), and in extreme cases they have difficulty sitting or wearing tight clothing. This condition is frequently treated as vaginitis because acidic vaginal discharge increases local irritation. Patients typically have an erythematous or even ulcerated area most commonly at four o'clock and seven o'clock just outside the hymenal ring. There is no clear evidence that microorganisms cause the inflammation. Treatment is frequently not effective, but regimens include topical corticosteroids (without an alcohol base), local corticosteroid injection, and skinning vulvectomy.

Furunculosis

Hair follicles or areas of hidradenitis in the vulva may become infected by staphylococci or other bacteria, giving rise to pustules. This condition must be distinguished from herpetic and syphilitic lesions. The diagnosis can be made by culture or by the finding of gram-positive cocci in Gram stains of pus. If only a few small lesions are present, treatment with hot, wet compresses or hexachlorophene scrubbing can be used. If a larger area is involved, administration of antistaphylococcal antibiotics is required until infection subsides, which often takes weeks.

Bartholinitis

Two stages of Bartholin gland infection occur. The first is an acute infection of the duct and gland usually caused by either N. gonorrhoeae or C. trachomatis. If the infection goes unchecked, duct obstruction results, leading to the second stage—abscess formation. Anaerobic bacteria can be isolated from the majority of abscesses. Rarely, synergistic vulvar gangrene has resulted from bartholinitis.

Cultures and a Gram stain of material expressed from the duct may identify gonococci. Cervical gonococcal and chlamydial cultures should be obtained, and if the patient has gonorrhea, a loading dose of penicillin followed by tetracycline should be administered for seven to ten days, as discussed later in this chapter. Patients in the second stage usually require abscess marsupialization or incision with placement of a catheter for three to six weeks. Simple incision and drainage usually lead to recurrent abscess or cysts. Recurrent infection from vaginal flora and mucus cyst formation are common sequelae of bartholinitis.

Chancroid

The soft chancre of chancroid is a painful ulcer with a ragged, undermined edge and a raised border. In contrast, the syphilitic chancre is painless and indurated. "Kissing ulcers" on apposing surfaces of the vulva occur. Tender, unilateral adenopathy is common, and suppuration occurs in about 50% of women with lymphadenopathy.

The incubation period of this uncommon, sexually transmitted disease is two to five days. The infection is caused by Haemophilus ducreyi, gram-negative bacteria that form a school-of-fish pattern when seen in the Gram stain preparation. The organism is fastidious, and it is best identified by culture of aspirated lymph nodes or the chancre onto specific selective media.

The differential diagnosis includes syphilis, which can be excluded by darkfield examination on at least three separate days. Chancroid may also resemble genital herpes and lymphogranuloma venereum. Treatment with erythromycin for seven days or one intramuscular injection of ceftriaxone, 250 mg, is preferred. Trimethoprim/sulfamethoxazole and amoxicillin/clavulanic acid are alternative regimens.

^ Granuloma Inguinale

Granuloma inguinale is rare in temperate climates. The organism is usually considered to be sexually transmitted, although gastrointestinal transmission can occur. The initial papular lesion typically ulcerates and develops into a soft, red, painless granuloma that can be covered by a thin gray membrane. The granuloma may spread over the course of many months to involve the anus and rectum. Lymph nodes are moderately enlarged and painless, but they do not suppurate. The infection is chronic, and longstanding disease may cause not only genital scarring and depigmentation, but also lymphatic fibrosis with consequent genital edema. Malignancy has been reported in granulomatous areas, but this is unusual.

The infection is caused by a gram-negative bacillus, Calymmatobacterium granulomatis, which is difficult to culture because it is an intracellular parasite. The identification is usually made from scraped or biopsied material obtained from the periphery of the lesion. Bipolar-staining bacteria are best identified within mononuclear cells (Donovan bodies) by Wright or Giemsa staining. A two- to three-week course of ampicillin, tetracycline, or erythriamycinis-the therapy of choice.

^ Lymphogranuloma Venereum

The incubation period for lymphogranuloma venereum (LGV) is two to five days. Thereafter, a transient, primary, painless genital or anorectal ulcer develops. Multiple large, confluent inguinal nodes develop two to three weeks later and eventually suppurate. Acute infection may cause generalized systemic symptoms. If untreated, the infection enters a tertiary phase that can lead to extensive lymphatic obstruction. This development, together with continued infection, causes fistulas and ulceration of the anal, urethral, or genital area Women with LGV are particularly susceptible to rectal stricture. Edema and elephantiasis of the external genitalia and lower extremities are serious sequelae.

The infection is caused by the sexually transmitted organism C trachomatis, an intracellular bacterium. Usually only L1-3 chlamydia immunotypes, which produce accelerated in vitro tissue destruction, cause LGV The diagnosis can be made by culturing chlamydia from genital lesions or lymph nodes. The most specific and sensitive serologic test is the microimmunofluorescent antibody test, in which the specific L immunotypes are identified. Complement fixation (CF) tests are positive in 95% of patients with LGV, but the CF test lacks specificity, it is often falsely positive in patients who do not have LGV, owing to previous exposure to other chlamydial infections.

The disease responds to two-week regimens of tetracycline, erythromycin, and sulfonamide drugs. Large lymph nodes should be aspirated to avoid chronic drainage. Surgical excision of scarred areas may be necessary

^ ACUTE URETHRAL SYNDROME

Acute cystitis is present in approximately 50% of women with symptoms of dysuria and urinary frequency Cystitis is defined by pyuria, and midstream urine cultures that contain more than 105 organisms per milliliter of cohform or staphylococcal organisms. Until recently the cause of symptoms in the remaining women was unknown. About one-half of the remaining women have less than 105 coliforms or Staphylococcus saprophyticus per milliliter isolated from urine obtained by suprapubic aspirates or urethral catheterization. Virtually all of these women have pyuria, defined as eight or more leukocytes per high-power field of urine. Pyuria among another 25% of women with recent onset of internal dysuria, urinary frequency, and negative urine cultures is termed acute urethral syndrome. C. trachomatis usually causes the "sterile" pyuria in patients with this syndrome. The remaining 25% of patients with these symptoms have no pyuria, bacteriuria, or chlamydia. Some women with external dysuria (labial pain with urination) have candidal or herpetic vulvitis. Although many women who have recently acquired gonorrhea develop transient dysuria, gonorrhea is only occasionally isolated from a general group of women with dysuria. Treatment of acute urethritis consists of therapy for the infectious agent, whether it is coliform, S. saprophyticus, or C. trachomatis.

A more chronic form of urethritis, which consists of periurethral gland inflammatory reaction that has responded to some degree to urethral dilatation, can be identified by cystoscopy. However, this entity has not been well studied bacteriologically, and it is unknown how many of these patients have a chlamydial or a low-bacterial-count coliform urethritis.

^ 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.

^ V. List of recommended literature

1. Danforth’s Obstetric and gynaecology.-Seventh edition.-1994.-P.933-938

2. Gynecology.-Stephan Khmil, Zina Kuchma, Lesya Romanchuk.-2003.-P.153-170

3. Gynecology. A clinical atlas.-1990.-P. 53-103

4. Gynaecology illustrated. David McKay Hart, Jane Norman.-Fifth Edition.-2000.-P.135-167


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’

Approved

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

O.A.Andriiets’___________


Methodological instruction

on the practical class

Specific inflammatory diseases in gynecology”


Subject-gynecology

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.

  1. Clinic symptoms of inflammatory gynecologic diseases.

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

  3. Diagnostics methods of inflammatory gynecologic diseases.

  4. Differential diagnostics of inflammatory gynecologic diseases.

  5. Treatment methods of inflammatory gynecologic diseases.
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