Download INFLAMMATORY DISEASES OF FEMALE GENITALS

Objectives: to learn how to diagnose and prescribe special therapy for mian women
with inflammatory diseases of the female genitals.
Professional motivation: The rate of inflammatory diseases is over 60% of all
gynecologic diseases and about 30%patients of women’s hospitals have the
inflammatory processes of the genital organs. Especially the quantity of
inflammatory diseases has enlarged because of an increased sexual activity at young
age, permissive sexual attitude, prostitution. Those at the highest risk are young
unmarried women with many sex partners. Primarily inflammatory diseases affect
human fertility because of infections of the female upper genital tract and their
consequences. Women with persistent viral infection are at particular risk for cervical
dysplasia and intrauterine fetal death.
Basic level:
1.
Normal vaginal microflora.
2.
Vaginitis (colpitis).
3.
Acute endometritis.
STUDENTS’ INDEPENDET STUDY PROGRAM
1.
Objectives for Students’ Independent Studies
You should prepare for the practical class using the available textbooks and lectures.
Special attention should be paid to the following:
1.
Inflammatory diseases of the external female genitals
2.
Classification of diseases of the external female genitals
3.
Examination and urgency aid for a women with inflammatory processes
4.
Bacterial vaginosis
5.
Acute and chronic endometritis
6.
Salpingoophoritis
7.
Tuboovarian abscess
Key words and phrases: inflammatory diseases.
Summary
INFLAMMATORY DISEASES OF THE
FEMALE GENITALS
The rate of inflammatory diseases is over 60% of all gynecologic diseases and about 30%
patients of female hospitals have the inflammatory processes of genital organs. Especially the
quantity of the inflammatory diseases has enlarged because of the increased sexual activity at the
young age, permissive sexual attitude, prostitution. Those at the highest risk are young unmarried
women with multiple sex partners. Primarily inflammatory diseases affect human fertility because
of infections of the female upper genital tract and their sequel. Women with persistent virus
infection are at particular risk for cervical dysplasia and intrauterine fetal death.
Normal flora has a significant role in defense against infection by genital pathogens. The
female genital tract, especially the vaginal secretions, contain from 108 to 109 bacteria per gram of
fluid examined. Lactobacilli produce lactic acid from glucose keeping the vagina at an acidic pH
(3,8-4,2). Glycogen is metabolized by vaginal epithelial cells to glucose, which then serves as a
substrate for Lactobacillus.
Normal vaginal microflora contains: Lactobacillus (70-90%), Staphylococcus epidermalis
(30-60%>), diphteroids (30-60%>), Hemolytic Streptococci (10-20%), nonhaemolytic streptococci (530%>), Escherichia coli (20-25%), Bacte-roides (5-15%), Peptococcus (10-60%),
Peptostreptococcus (10-40%), Clostridium (5-15%).
Presence of pathogenic flora without inflammation isn't a sign of pathologic processes.
It is considered that normal vaginal flora is represented by Lactobacillus. But not only
Lactobacillus acidophilus provide the self-cleaning of the vagina. The normal vaginal ecosystem of
reproductive age women contains 7 kinds of Lactobacillus: L acidophilus (42,8%), L. Paracasei, L.
Fermentum, L. Plantarum (10-18,6%)), L.cateforme, L.corineformis, L. Brevis (2,5-5,7%), H202
producing Lactobacillus may play an important role in acting as a natural microbicide within the
vaginal ecosystem.
Variation in vaginal colonization by Lactobacillus and other organisms could relate to estrogen level
metabolism products of vaginal microflora, vaginal pH, and the type of Lactobacillus initially
colonizing the vagina. Many endogenic and exogenic factors may change the balance of the vaginal
ecosystem. Some vaginal microorganisms may cause the inflammation in certain conditions. Both
vaginal and cervical epithelial cells have the capacity to convert glycogen to glucose, which is
further metabolized to lactic acid. Vaginal acidity depends on adequate levels of estrogens as well as
the presence of lactic acid-producing bacteria such as Lactobacilli. Concentrations of lactobacilli are
probably important determinants of vaginal pH as well. The increased concentration of lactic acid
producing bacteria in the vaginal fluid may result in a lower pH which determines decreased
susceptibility to infection. Estrogens have a direct effect on the number of organisms and composition
of the bacterial flora. The mucosal surface provides protection from invading pathogens. Mucous may
act to eliminate a variety of pathogens or antigens. Mucous also serves for attachment of
immunoglobulin A, lysozyme, lactoferrin and other biologically active substances. Mucous in the
female genital tract is under hormonal control. Any abnormalities with low estrogen secretion and
decreasing of estrogen level with age may damage defense mechanisms of the female genital tract.
Using of contraceptives, shower can effect into vaginal ecosystem by changing vaginal pH, altering
the vaginal fluid by direct dilution.
Bartholinitis
Bartholinitis is an inflammation of Bartholin's gland (large gland of vaginal vestibule). It may be
caused by Staphylococcus, E.coli and N. gonorrhea. Any type of the pathogen initiates ductal
inflammation and obstruction that can lead to Bartholin's abscess. There can be serous, serous-purulent,
or purulent inflammation.
Obstruction of the opening of the main duct into the vestibule leads to abscess formation. Infection
of Bartholin's glands can lead to secondary infections, abscess or cyst formation (fig 85). When the
gland becomes full and painful, incision and drainage is appropriate. Patients with abscess usually
require abscess incision with insertion of the catheter in abscess cavity. Recurrent infection from
vaginal flora and mucous cyst formation are common sequelae of bartholinitis. If the infection of
gland is caused by N. gonorrhea specific antibacterial treatment is prescribed.
Vulvitis
Vulvitis is a vulvar inflammation. It may be primary and secondary. Primary vulvitis is caused by
local irritants (including feminine hygiene sprays, deodorants, tight-fitting synthetic undergarments
in women with obesity or diabetes mellitus. Secondary vulvitis are caused by accompanying
discharge from vagina.
Fig. 85. Abscess
of Bartholin's "j gland
Reduced estrogens levels in reproductive age women, and more frequent in girls and
menopause women may lead to vulvitis.
Clinic. Erythema, edema of vulva and skin ulcers are all indices of the infection.
Patient's complains are itching or burning. Excoriation caused by the patient's scratching of
the skin of vulva are often seen in vulvar irritation.
To relieve inflammation and itching the main suspected cause must be removed. The
therapy includes local application of boric acid solution or KMn04 solution. Candidasis is treated
with Gyno-paveril 150mg in suppositories — 3 days, or Orungal lOOmg twice a day during 6-7
days orally, and then one capsule per day every first day of menstrual cycle during 3-6 cycles.
Treatment with local antibiotics and steroids is successful.
Vaginitis (colpitis)
Vaginitis (colpitis) is an inflammation of vagina. It is the most frequent cause of visits to
gynecologists. It may be caused by Staphylococcus, Streptococcus, E.coli and other.
Excessive vaginal discharge is associated with an identifiable microbiologic cause in 80% to 90%of
cases. Hormonal or chemical causes account for most of the remaining cases. Vaginitis may be
acute, subacute and chronic. There are two forms of vulvitis: purulent and granulosa-diffusional.
The main symptom is the increased, gray-white or yellow discharge generally serous or
purulent with rancid odour. The patients complain of dysuria, vulvar itching, burning and
dyspareunia. Examination may reveal edema or erythema of vulva and vagina, petechia or patches
in the upper vagina or on the cervix. In case of chronic vaginitis all these signs are not so expressed.The
cultures from vagina, cervix,urethra, ductus of Bartholin's gland should be microscopically examined.
Treatment of nonspecific vaginitis is comlex:
• using of antiinflammatory medicines
• treatment of neuroendocrinologic and immunodificiency conditions
• treating of male sexual partner; patients should avoid sexual contacts while therapy
Local treatment includes using of syringing with antiseptic fluid (KMn04, furacilin,
chlorhexidin) no more than 3-4 days. In case of acute or chronic vaginitis laser therapy may be used.
Metronidazol (vaginal suppositories), chlorhinaldin, terginan, betadin, gyno-paveril may be
prescribed. For normalization of vaginal ecosystem solkotry-chovac, vagilak, Lactobacterin and
Bifidumbacterin are used.
Bacterial Vaginosis
10-25% of all gynecologic patients have this disease. Among sexually transmitted diseases,
bacterial vaginosis is diagnosed in 60-65%> of women. Bacterial vaginosis is a result of an
overgrowth of both anaerobic bacteria and the aerobic bacteria Gardnerella vaginalis. Anaerobes and
G. vaginalis are normal inhabitants of vagina, but these bacteria overgrowth dominant of the normal
Lactobacillus flora results in the appearance of a thin, fishy odor, gray vaginal discharge that
adheres to the vaginal walls.
A small amount of vaginal discharge may be normal (2ml) particularly at the midcycle.
Bacterial vaginosis causes an increased vaginal discharge (15-20ml), vulvar irritation, pruritus,
dysuria and foul odour.
The diagnosis of bacterial vaginosis is based on the presence of the following characteristics
of the discharge:
• pH is higher than 4,5
• a homogeneous thin appearance
• a fishy amine odour produced by anaerobes when 10% KOH is added
presence of clue cells (vaginal epithelial cells to which organisms are attached).
Cultures aren't helpful because anaerobes and Gardnerella vaginalis can be recovered from
normal flora of healthy women, but the concentration of both bacteria is higher in patients with
bacterial vaginosis (fig. 86). Factors that lead to overgrowth of G.vaginalis and anaerobes have
not been identified.
Treatment includes elimination of anaerobic agent of microflora, inducement of local and
general immunity and then the normal microflora should be renewed.
Oral using of metronidazol (Flagyl) 500mg twice a day for 7 days or by intravaginal
Metrogel 0,75% cream twice a day for 5 days, 2% Clindamycin cream (Cleocin) once daily for
7 days.
For normalization of vaginal microflora the local bifidumbacterin insertion or 2-3%)
solution of Lactic acid is used. The treatment of the male parthner with Metronidazol can be
advocated only when bacterial vaginosis recurs, but effectiveness is not proven.
Endocervicitis
Endocervicitis is the inflammation of mucosa layer of the endocervix. Bacteria cause
infection of the columnar epithelium. Chlamidia trachomatis, Mycoplasma, Trichomonada
vaginalis, N. Gonorrhoeae, viruses, Candida, E.coli, Staphylococci cause endocervicitis.
Cervix is constantly exposed to trauma during childbirth, abortion.The abundant mucus
secretion of the endocervical glands both with the bacterial ascend from the vagina creates a
situation that is advantaging to infection.
The inflammatory process is chiefly confined to the endocervical glands. The squamous epithelium
of the exocervix may be involved into the process called acute exocervicitis. The extent of
endocervical involvement as compared with exocervical one appears to have some relation to the
infecting agent.
Chronic cervicitis manifestation is cervical erosion. Erosion indicates the presence around the
cervical os a zone of infected tissue that has a granular appearance. It implies the loss of superficial
layers of the stratified squamous epithelium of the cervix and overgrowth of infected endocervical
tissues.
The inflammatory process stimulates a reparative attempt in the form of an upward growth of
squamous epithelium, causing some of the ducts of the endocervical glands to be obstructed.
Retention of mucus and other fluid within these glands results in the formation of Nabothian cycts.
These cysts are endocervical glands filled with infected secretion. Their ducts become secondarily
included into the inflammation and reparative processes.
The most important in the diagnosis of chronic cervitis is the exclusion of the malignant
process. Before the begining of treatment, examination with colposcope should be carried out. The
cervicitis may appear as a reddish granulation raised above the surrounding surface, giving the
impression of being papillary.
A Papanicolaou smear should be obtained and suspicious areas should undergo biopsy.
Treatment Acute cervicitis is treated with appropriate antibiotics (it depends on bacterial agent).
Local treatment of acute phase is a real danger of dissemination of infection. Laser therapy is used in
treatment of acute and chronic cervicitis.
Electocautherization is the traditional treatment of chronic cervicitis, especially with erosion,
cervical ulcers or ectropion. Nowadays cryosurgery or laser surgery has replaced
electrocautherization.
Acute endometritis
Acute endometritis is an inflammation of endometrium (mucus layer of uterine). It may occur in
such cases as: endometritis after uterine curettage or suction and puerperal endometritis. Endometritis
is caused by bacterias, viruses, mycoplasmas. The most frequent the associations of 3-4 anaerobic
bacteria and 1-2 aerobic are the main reason of endometritis.
Anaerobic bacteria compose apart of the normal cervicogenital flora. There are two known
mechanisms which cause anaerobic infection: antibiotic selection that preferentially inhibits aerobic
bacteria and tissual trauma that occurs after surgery which reduces the redox potencial. Anaerobes
produce odorous metabolic products.
Uterus has endometrium factors of local immunity. There are T-lymphocytes and other factors of
cellular imunity in endometrial stroma. Lymphocytes and :utrophiels normally appear in the
endometrium in the second half of menstrual 'cle; their presence does not necessarily constitute
endometritis. The appearing 'plasma cells represents immune response, usually to foreign bacterial
antigen. The organism should be cultured before applying of antimicrobal therapy, s anaerobes
compose a part of normal flora, deep tissual cultures not mtaminated by surface bacteria are
required. Forty eight or more hours are quired for anaerobe recovery, and treatment usually is based
on clinical signs, here are nonspecific and specific endometritis. Specific endometritis is caused у М.
Tuberculosis, N. Gonorrhea, Chlamidia trachomatis, Actinomyces.
Fig. 87. Spreading
of inflammatory process
(scheme)
a — metroendometritis
b — parametritis
с — salpingitis
Clinic. Fever is the characteristic feature in the diagnosis of endometritis, nd it may be
accompanied by uterine tenderness. If the infection has spread to he parametrium and adnexa,
tenderness may be present there as well. Temperature :levation is probably proportionate to the
extention of the infection and when :onfmed to the decidua, the cases are mild and there is
minimal fever. Chills nay accompany fever. Women usually complain of abdominal pain. There
is enderaess on one or both sides of the abdomen and parametrial tenderness is ilicited upon
bimanual examination. The uterus is lightly enlarged.
A leukocytosis and increased erythrocyte's sedimentation rate is revealed n patient' blood test. In
some cases acute endometritis may become a chronic me;
Treatment Various choices of initial antibiotic therapy are used. Most of them are successful.
Single-agent therapy has the benefit of easy administration; Cephalosporins such as Cefotetan and
Cefoxitin are commonly used. A combination of Ampicillin and Aminoglycoside is also popular.
The combination of Clindamycin with Gentamicin or Metronidasol with Unasyn (Ampicillin with
Sulbuctam) and Gentamicin is applied. It is desirable to provide additional antibiotic coverage if there
has been no responce within 48 to 72 hours. Intravenous antibiotic therapy is continued until the
patient is asymptomatic and afebrile period lasts for at least 24 hours.
Local uterine douching with antiseptic solution of chlorhexidin or furacilin has a good effect. In
some cases uterine curettage is performed after temperature normalization.
Chronic endometritis
Chronic endometritis is a sequale of untreated acute endometritis or nona-dequate treatment of
postabortion or purperal endometritis. The chronic endometritis sometimes is associated with the use
of intrauterine device (IUD). In some cases it may occur without acute stage.
Clinic. The chronic endometritis results from organisms that are normally in lower genital
tract (Protei, E. Coli, Staphylococcus, Mycoplasma). Bacteria that can be recovered are usually of
low pathogenicity, but more virulent intrauterine bacteria occasionally cause the serous purulent'
discharge, abnormal uterine bleeding and moderate uterine tenderness. Diagnosis is based on
anamnesis and clinical manifestation. It could not be diagnosed unless plasma cells are found in the
endometrium. Ultrasonography can identify gas vesicules in uterine cavity, hyperechogenic places
(local fibrosis, sclerosis) in basal layer of endometrium.
Treatment. A complex treatment is used. It includes a medicines for curing of accompaning
deseases, desensibilisative medicines and additional general health measures, vitamines.
Physiotherapy has an important role. It improves pelvic hemodynamics. Diathermy on lower
abdomen, electrophoresis with copper, zinc, ultrasound, inductothermy, laser radiation are used. If
during physiotherapy the process becomes strained antibiotic therapy is recomended. While
remission antibiotic using is not proved.
Physiotherapy promotes to activation of hormonal ovarian function. If effect is not enouph than a
hormonal therapy is used (taking into account the patient's age, term of deseases, degree of ovarian
hypofunction). Health resort treatment is effective (balneologic therapy, mudcure resort).
Salpingoophoritis
Salpingoophoritis is the inflammation of the uterine tubes and the ovaries. Salpingoophoritis is
the most frequent among all pelvic inflammatory deseases. Most cases of oophoritis are secondary to
salpingitis. The ovaries become infected by the purulent material that escapes from fallopian tube. If
the tubal fimbriae are adherent to the ovary, the tube and ovary together may form a large retortshaped tubo-ovarian abscess.
Most patients with salpingoophoritis have lower abdominal, adnexal tenderness (unilateral or
bilateral) purulent cervical exudate or purulent vaginal discharge (fig. 88).
Clinic. There are four stages of salpingoophoritis. The first — salpingitis without irritation
(inflammation), of the peritoneum, the second—with signs of peritonitis, the third with occlusion of
uterine tubes and tuboovarian abscess and the fourth is the rupture of tuboovarian abscess. During
bimanual examination adnexal inflammatory mass is revealed.
The diagnosis of salpingoophoritis is based on the history, physical examination and laboratory
tests. Besides that additional ultrasonography and laparoscopy can be used.
Laparoscopy provides the most accurate way to diagnose the inflammatory process and its stage. It
should be used in cases when the diagnosis is unclear, especially in patients with severe peritonitis,
to exclude a ruptured abscess and
Fig. 88. Acute salpingoophoritis
appendicitis. Besides diagnostic laparoscopy is used to provide treatment procedures.
Ultrasound can be used to distinguish the presence of an abscess from an inflammatory mass
within the adnexal mass. It may also be helpful in defining mass in the obuse patient or if the
bimanual examination is unsatisfactory because of the excessive tenderness.
Treatment. All patients with acute salpingoophoritis should be hospitalized. Adequate therapy
of salpingitis includes the assessment of severity, antibiotic treatment, additional general health
measures.
Before the culture test performing the antibiotic therapy is provide with broad spectrum
antibiotics. The most effective is the combination of Clindamicin with Chloramphenicol, Gentamicin
andLincomicin, Doxycyclin, Clacid, Cefobid, Cyfran, Claforan, Dalacin С and Unasyn.
When anaerobic agents are suspected metronidazol should be used, in severe cases intravenously.
After temperature normalization and cessation of peritonitis signs antibacterial therapy is continued
for 5 days. Detoxycation is indicated and is provided by using of 5% glucose solution, polyglucin,
reopolyglucin, solutions of proteins, correction of pH balance by using of 4% solution of Sodium
bicarbo-nates. Among physical methods of treatment cold on the lower part of the abdomen is used.
Appropriate antibacterial treatment is combined with laparoscopy active drainage.
The tuboovarial abscess is drained of pus by puncture and rinsed with bacteriostatic solution and
local application of antibiotics. In subacute stage aloe, ultraviolet radiation, authohaemotherapy is
used. They prevent the chronic processes.
Chronic salpingoophoritis. In most cases chronic salpingoophoritis is the sequale of non
treated acute process. Chronic stage of the process is characterized by tubal occlusion with periovarial
adhesions, tubal dysfunction (fig. 89).
Clinic. The main complains of the patient are: mild tenderness in lower part of abdomen that
becomes severe during menstruation. Pelvic nerves have more painful sensitivity (pelvic plexitis,
ganglionevritis due to chronic inflammation). In some cases menstrual dysfunctions such as
oligomenorrhea, polymenorrhagia, algodismenorrhagia occur. Changing in uterine tubes and
hypofunction of ovaries lead to infertility or miscarriage. Secretory dysfunction like vaginal discharge
or cervical exudate may be observed as a clinical finding of colpitis or endocervitis. Some patients
complain of low libido, painful coitus, dysfunction of urinary bladder, liver tenderness.
Menstrual dysfunction (menorrhagia or metrorrhagia) is the most frequent symptom of chronic
salpingoophoritis as a sequel of disorders of neurohomoral regulation of menstrual function.
Metrorrhagia often occurs after cessation of menstruation and then the differential diagnosis should be
made in case of ectopic pregnancy.
Fig. 89. Chronic salpingoophoritis
Diagnosis. Correct history taking (reveal of inflammation after abortion, delivery or
dilatation and curettage) makes it possible to suspect the chronic inflammatory process. Primary
chronic salpingoophoritis is found in more than 60% of cases. Some information gives physical
examination and laboratory tests. Bimanual examination gives nonspecific information.
Enlargement, consistency and degree of adnexa mobility should be examined. Sometimes
because of peritubal and periovarian adhesions the sizes and mobility of adnexa are changed.
Additionally, ultrasound and laparoscopy, hysteroscopy should be held. Tomography or
endoscopy may be used. Laparoscopy is the most informative diagnostic method to
differentiate salpingoophoritis, external endometriosis, uterine myoma with inflammatory
changes, cysts. Disorders of adjacent organs (bladder, intestine) while serous inflammation is
present without structural changes. But women with disorders of urinary tract, gastro-intestinal
tract must be additionally examined (urography, irrigoscopy).
Treatment of chronic salpingoophoritis is provided with minding of pathogenesis and clinic.
Antibiotics are indicated in acute period, when there are signs of inflammation.
Nonsteroidal antiinflammatory drugs (Voltaren, Butadion) are prescribed. To stimulate immune
system immunomodulators are used: (Decaris, T-activin). FIBS, aloe, autohaemotherapy are also
used. Analgesia both by medicines and by reflextherapy is of great importance. Physiotherapy is
conducted in hospital while in case of acute process and remission it can be used in ambulatory
conditions. Ultrasound has analgetic and fibrinolityc influence and is prescribed in sinusoid and
modulate of high frequency. Laserotherapy is also used. To escape chronic salpingoophoritis the acute
salpingoophoritis must be treated in proper way and the quantity of abortion should be reduced.
Parametritis
Parametritis is an inflammation of parametrium. Inflammation of the whole pelvic cellular is
called pelviocellullitis. According to international statistics these diseases are classified as acute
parametritis or pelvic phlegmona.
Infection agents may be staphyloccocus, streptoccocus, E.coli, etc. It can be caused by one
microbic agent or microbe association. It occurs after pathologic delivery, abortion, operation on
genitals. The main way of infection spreading is lymphogenic. Morphologically parametritis is
characterized by all signs of inflammation: dilation of blood and lymphatic vessels, peripheral
edema, exudation. There are 3 stages in course of parametritis (infiltration, exudation, firming).
Exudation may be serous, and very rarely it is purulent. Sometimes it undergo resorbtion and
dissolves, sometimes a fibrose connective tissue grows and leads to uterine dislocation to the side of
previous inflammatory process.
Clinic. Moderate tenderness in lower parts of abdomen, in back, high body temperature (3839°C), tachicardia are found. Signs of peritoneal irritation and diminished or absent bowel sounds,
especially associated with ileus, indicate more serious infection, including the possibility of abscess
formation. Fever is a characteristic feature in the diagnosis of metritis and it is accompanied by uterine
tenderness. Bimanually before or behind on left or right side of the uterus infiltration may be
palpated. It is firm and immovable. Infiltration is classified into anterior, posterior and lateral.
Treatment begins from using antibiotic of broad coverage against a variety of common
microorganisms and is usually prescribed without cultures.
Various choices of initial antibiotic therapy are used. Most of them are successful.
Cephalosporins such as Cefotetan and Cefoxitin are commonly used. A combination of Ampicillin
and Aminoglucoside and also the combination of Clindamycin with Gentamicin are used.
A bottle with ice on the lower part of abdomen is used in case of infiltrative stage of disease. Bio
stimulators should be prescribed. Management of a persistent pelvic abscess includes drainage by
colpotomy, or laparotomy. Intraabdominal rupture of pelvic abscess is a surgical emergency. Sepsis
may occur in association with pelvic infection, with or without frank abscess formation.
Phisiotheraputic precedures are used for rehabilitation.
Tuboovarian abscess
Tuboovarian abscess (TOA) may occur as a complication of salpingoopho-ritis. It begins from
acute purulent salpingitis when all layers of uterine tubes are involved into the process. The tubes
characteristically become swollen and redde is the muscularis and serosa are inflamed. If exudate
drips from the fimbriated mds of the tubes a pelvic peritonitis is produced then it can give rise to
peritoneal idhesions. The swollen and congested fimbriaes may adhere to one another and
produce tubal occlusion. The fimbriae may occlude tubes producing permanent ubal infertility.
The swollen and congested fimbriae may adhere to ovary, trapping he exudate in the tube and
giving rise to pyosalpinx or if the ovary becomes nfected, a tuboovarian abscess (fig. 90). The
mucosal folds may adhere to one mother forming gland-like spaces that are filled with exudate.
If the infection subsides after agglutination of the fimbria and closure of the peripheral end of he
tube, secretion accumulates and distends the tube, forming pyosalpinx. Each •ecidive of chronic
salpingoophoritis has more clinical manifestation and is treated vith difficulty. TOA is associated
with IUD, microbe association, chronic salpingoophoritis.
Intoxication in case of TOA leads to liver disorders. Decreasing of albumin-globulin index is
observed while the level of general proteins is normal for a ong time. The degree of these
disorders depends on the time of duration of the process.
Clinic. Clinic of TOA depends on the volume of purulent damage of adnexa, duration of the process,
disorders of adjacent organs. There are some syndromes vhich are divided into local syndrome (pain,
purulent discharge, peritoneal symptoms and palpation of tuboovarian mass).
uterine body
tuboovarian abscesses
Fig. 90. Bilateral purulent tuboovarian cyst (TOA)
Inflammatory-intoxicative syndrome includes fever, tachycardia, nausea, vomiting.
Luecocytosis, decreasing of albumin-globulin index, C-reactive protein are observed in blood. Immune
syndrome (decreasing of lymphocytes and mono-cytis in blood) is found.
Syndrome of adjacent organs disorders (dysuria, urinary frequency, menstrual disorders) is also
possible.
Severe lower abdominal pain occurs, pelvic peritonitis may be present. Pain can irradiate to back,
pelvic bottom, in the chest. In such cases the examinations should be performed to exclude
pneumonia, pancreatitis, cholecystitis. Musclar defance which prevents abdominal palpation in the
lower quadrants, adnexa are tender to various degrees and cervix movement may cause pain in case of
bimanual examination. The adnexa often are either adherent to the posterior aspect of the uterine or
prolapsed in cul-de-sac, which may pull the uterine into a retroverted position. TOA is characterized
by pain and tenderness, fever or chills, temperature rises up 39°C, blood pressure decreases.
Abdomen takes part in breathing, and it is painful in lower parts. In blood analysis elevated white
blood count (9-10x107 1) erythrocytes' sedimentation rate more than 30mm/hour, positive Creactive protein, decreasing of albumin-globulin index till 0,8 are observed.
Sometimes there can be urinary syndrome with proteinuria, leucocyturia. There may be
disorders of filtrative kidney' function, even unuria. Changing of albumin-globulin index and
hypofybrinogenemia characterizes the liver dysfunction.
Diagnosis is based on clinic, bimanual examination, laboratory analyses and additional
methods of investigation (ultrasound, laparoscopy).
Treatment Tuboovarian abscess is treated by antibiotics, desensibilisative and nonsteroidal
antiinflammatory medicines, detoxication and immunostim-mulation. Best of all one should
combine taking of penicillin with tetracyclins. When anaerobic infection is suspected metronidazole
is used. Daily punctions of tuboovarian abscesses are indicated to remove purulent containts.
Indications to surgical removal of tuboovarian abscess are:
• abscence of efficiency of complex treatment with usage of punctions during 2-3 days
• suspicion on tuboovarian abscess perforation; volume of surgical intervention depends on process'
spreading, woman's age and extragenital pathology
Peritonitis
Pelvioperitonitis is an inflammation of pelvic peritoneum.The polymicrobial infection such as
Escherichia coli and other aerobic, enteric, gramnegative rods, group of p-hemolytic
staphylococci, anaerobic, streptococci, Bacteroides species, aphylococci, mycoplasms cause the
process. Pelvioperitonitis occurs secon-ary. Primary process is in uterine tubes, ovaries, uterus
and parametrium. In lost cases purulent damage of uterine adnexa lasts with pelvioperitonitis.
lfection can be spread by limphogenic or blood vessels, and from uterine tubes l case of
salpingitis, especially gonococcial infection.
Clinic characterizes the acute inflammation. High temperature, severe lower bdominal pain,
fever or chills, tachycardia are common. There can be nausea nd sometimes vomiting.
Muscular defence and rebound tenderness are the ymptoms of peritoneal irritation. Anterior
abdomen wall takes part in breathing ct.Tender adnexa are present at bimanual examination.
Cervical motion causes ain. Posterior fornix is painfull.
Laboratory tests reveal increasing of white blood cell count and erythrocyte edimentation
rate. C-reactive protein levels may appear. Generall blood test hould be done 4-5 times per day
to diagnose transformation of pelvioperitonitis о peritonitis.
Treatment All the patients should be hospitalized. Ideally, the antibiotic hould be selected
according to the organism present in the fallopian tube or items, but in most cases empiric
therapy must be used. Treatment includes intravenous doxycycline and either cefoxitin or cefotetan
or intravenous clindamycin ind gentamicin for at least 4 days followed by oral clindamicin or
tetracyclin for [0-14 days. Hospitalized patients who have peritonitis but do not have adnexal
ibscess usually respond rapidly to the regimens. In the presence of an adnexal ibscess, even if
the systemic manifestations are mild, antibiotics which eliminate 3.fragilis should be selected
because most pelvic abscesses contain this organism. Clindamycin, Metronidazol, Cefoxitin, or
Impinem should be used to treat pelvic ibscess. If there is an intrauterine device it should be
removed as soon as therapy s started. Surgery is indicated in the case of ruptured pyosalpinx or
ovarian ibscess. Colpotomy drainage usually is preferable when unruptured midline cul-de-sac
abscess is present. Laparotomy is required for such problems as unresolved abscess or adnexal mass
that does not subside, surgery should be limited to the most conservative procedures that will be
effective. Unilateral abscess respond to unilateral salpingoophorectomy.
Septic shock
Septic shock is associated with infection caused gram-negative aerobic coliform organisms those
are producing endotoxins. In gynecological practice it may occur in case of septic abortion, localized
or spreading peritonitis, thrombophlebitis. Septic shock is a special organism reaction that is
expressed in development of severe systemic disorders. It may be caused by using of broad spectrum
antibiotic in high doses, that results in releasing of great amount of endotoxin.
Endotoxin, a complex cell wall-associated lipopolysaccharide, is released into the circulation at the
time of bacterial death, resulting in multiple hemodynamic effects. The subsequent activation of
lymphocytic T-cells and mass cells results in histamine and kinin activation as well as the activation of
kallikrenin and decrease in kallikreinogen and kallikrein inhibitor. These changes result in the release
of bradykinin, a potent arterial dilator. Early septic shock is a classic example of distributive shock,
related to a systemic maldistribution of relatively normal or even increased cardiac output. Clinical
findings include hypotension, fever and chills. Initial hemodynamic findings include decreased systemic
vascular resistance and high normal or elevated cardiac output. The continued maldistribution of cardiac
output leads to local tissue hypoxia and to the development of lactic acidosis and organ dysfunction.
This decrease in systemic vascular resistance is caused by the release of vasoactive substances, as
well as by vascular endothelial cell injury, which promotes capillary plugging secondary to
complement induced leukocyte aggregation. These factors lead to increased arteriovenous shunting.
If the process continues a second hemodynamic phase of septic shock is developed. The
primary importance in this late phase is the development and progression of myocardial
dysfunction leading to ventricular failure. Studies assessing stroke work index and ventricular
ejection fraction have demonstrated depressed intrinsic ventricular function even in the early stage
of septic shock. Pulmonary hypertension, another important hemodynamic alteration is often
associated with septic shock, may have additional profound hemodynamic consequences. As the
sequalae of renal kidneys filtration disorders — the shock kidney is formed and acute renal
insufficiency is developed. Signs of liver disorders are hyperbilirubinemia, lipid metabolism
abnormalities.
Patients who recover from the initial hemodynamic instability of septic shock may suffer
prolonged morbidity secondary to endotoxin-mediated pulmonary capillary injury and
noncardiogenic pulmonary edema. Such lung failure is a major cause of death in patients whose
hypotension was prolonged and may experience acute tubular necrosis. Endotoxin mediated
endothelial cell injury and associated thromboplastine-like activity as well as prolonged shock from
any other cause may also lead to activation of the coagulation cascade and a clinical picture of
disseminated intravascular clotting syndrome (DIC).
Clinic and diagnosis. The clinical manifestation develops just after surgical operation on infected
organs. The body temperature rises till 39-40°C and is high during 1-3 days. Then the temperature
decreases, chills is a characteristic feature of the septic shock.
Among clinical findings there are hypotension without bleeding or nonade-quete to it,
tachycardia, 120-140 per minute. Decreasing of blood circulative volume leads to rising of shock
index till 1,5 (normally 0,5). Skin is pale and wet because of perspiration, later akrocyanosis can
appear. Breath disorders, like tachypnoe till 30-60 per minute, is the sign of shock lungs. Skin
may be colored in yellow, there may be blood vomiting.
The most dangerous complication of septic shock is kidney insufficiency. Clinical
manifestation at the beginning is oligouria — less than 30 ml per hour. Later anuria is
developed. All these changes in organism appear in very short time in 6-8 or sometimes 10-12
hours.
Diagnosis is based on the following signs:
• septic organ
• low blood pressure, nonadequate to blood loss
• nervoues system disorders
• pain of different parts of body
• decreasing of diuresis
• rash on the skin
The blood temperature should be taken every 3 hours, blood pressure is measured every 30
minutes, urine quantity must be measured. Bacterial culture from infected organ, blood analysis,
coagulogram and biochemical tests are performed.
Treatment of septic shock. The treatment of septic shock involves optimising preload relative
intravascular volume with crystalloid infusion as well as treating of the underlying infection. Although
some authorities advocate the use of colloid solutions for volume replacement, there is noconvincing
evidence that using of such solutions decreases the incidence of pulmonary edema or adult
respiratory distress syndrome. In most cases the infection is polymicrobial and broad spectrum
coverage for gram-negative and gram-positive aerobic and anaerobic organisms is most appropriate.
If an abscess is involved, promt surgical drainage after initial resuscitation is mandatory. Patients in
septic shock should be treated with dopamine hydrochloride. This agent in doses of less than
5mg/kg/minute improves renal blood flow by means of dopaminergic mesenteric vasodilatation; in
doses of 5 to 30 mg/kg/minute, a positive inotropic effect is also seen. The hemodynamic
manipulation of patients whose hypotension fails to respond rapidly to volume infusion may be assisted
by pulmonary artery catheterization, allowing the clinician to achieve optimal preload before the
institution of inotropic or vasoconstrictive therapy. High-dose corticosteroids are advocated (60-120
mg of prednizolone or 8-16 mg of dexamethazone). To renew Ph balance lactosol or bicarbonate
natrii are indicated.
SPECIFIC INFLAMMATORY DISEASES
(Sexually transmitted diseases)
To specific inflammatory diseases of the female reproductive organs belong tuberculosis and
sexually transmitted diseases. According to the WHO's classification, there are 21 such diseases.
Their frequency has been risen for the last years.
SEXUALLY TRANSMITTED DISEASES
(the WHO's classification)
Classic venereal diseases
Nosology
1. Syphilis
2. Gonorrhea
3. Chancroid
4. Lymphogranuloma venereum
5. Donovanosis, or granuloma inguinale
Microorganism
Treponema pallidum
Neisseria gonorrhoeae
Hemophilus ducrei
Chlamydia trachomatis
Callimmantobacteriumgranulomatis
3,4,5 are mostly in tropic countries
Other sexually transmitted infections
Nosology
Microorganism
A — that affect mostly genital tract
1. Syphilis
Treponema pallidum
1. Urogenital chlamydiasis
Chlamydia trachomatis
2. Urogenital trichomoniasis
Trichomonas vaginalis
3. Urogenital mycoplasmosis
Mykoplasma hominis
4. Candidosis vulvovaginitis
Candida albicans
5. Genital herpes
Herpes simplex virus
6. Genital warts
Papillomavirus hominis
7. Molluscum contagiosum
Molluscoviras hominis
8. Bacterial vaginosis
Gardnerella vaginalis та mini збудники
9. Urogenital shigellosis of homosexualists
Shigella species
10. Pediculosis pubis
Phthyrus pubis
11. Scabies
Sarcoptes scabiei
В — With mostly affection of other organs
1. Infection, caused by HIV
Human immunodeficiency virus
2. Hepatitis В
3. Cytomegalovirus infection
4. Amebiasis
5. Lambliosis
Hepatitis В virus
Cytomegalovirus hominis
Entamoeba hystolytica
Giardia lamblia
Gonorrhea
Gonorrhea is a contagious disease caused by Neisseria gonorrhoeae. Among the specific
inflammatory diseases of the female genital tract gonorrhea takes the second place and is in 525% of cases of all STDs.
Etiology and pathogenesis. Gonorrhea is caused by Neisseria gonorrhea (fig. 92). The
causative agent was found in 1879 by A. Neisser. Gram-negative N. gonorrhea is not stable in the
outer surrounding and dies quickly at the influence of antiseptic solutions, boiling, drying, but it is
rather stabile in human organism. In uncomfortable conditions they transform into L-forms,
which can transform into the usual form in the favourable conditions. In case of chronic
gonorrhea, N. gonorrhoeae are situated mostly in leukocytes and out of the cells, in case of the
acutening of the process they are found in the leukocytes.
Fig. 92. An agent of gonorrhea — gonococus
N. gonorrhea affects mostly those parts of urogenital tract, that are covered with cylindric
epithelium: mucosa of urethra, cervical canal, Bartholin's glands ducts, mucosa of uterine cavity,
uterine tubes, ovarian epithelium, peritoneum. During the pregnancy, childhood and menopausal
period there can be gonorrheal vaginitis.
The source of infection is a person with gonorrhea.
Ways of infecting:
• the disease is sexually transmitted
• homosexual contacts, orogenital contacts
• very rarely through sponges, towels, underwear
• during labour from mother (infected eyes, vagina in girls)
Incubational period lasts for 3-7 days, sometimes for 2-3 weeks.
According to the stage of spreading the process the gonorrhea of lowei part of genital organs
(gonorrheal urethritis, endocervicitis, Bartholinitis, vulvovaginitis) and gonorrhea of upper parts —
gonorrhea ascendens (endometritis, salpingitis, pelvioperitonitis) is classified.
According to duration there are such forms of gonorrhea:
• fresh gonorrheal infection with acute, subacute, torpid passing, which lasts less than two
months
• chronic gonorrheal infection, lasting more than two months
• latent gonorrheal infection
In women the clinic of gonorrhea depends on the localization of the process, virulency of
causative agent, age of woman, organism's reactivity, stage of the disease (chronic, acute).
Fresh gonorrhea in acute forms has expressed clinical manifestations. Subacute form is
characterized by subfebrile condition, sometimes by expressed clinical symptoms, which appeared
two weeks before. Torpid gonorrhea in acute form has mild clinical manifestations or is
asymptomatic, but N. gonorrhoeae are found in the patient. Latent form is diagnosed when there is
no bacteriologic and bacterioscopic confirment, no symptoms, but person is a source of infection.
Chronic gonorrhea lasts for more than 2 months, or without establishing of the beginning.
Gonococcal urethritis. Clinical manifestation appears within 3-5 days after infection and is
characterized by dysuria. Variable degrees of edema and erythema of the urethral meatus, purulent or
mucopurulent discharge are present.
Gonococcal Bartholinitis. It may occur when N. gonorrhea with vaginal discharge infects the
Bartholin's gland. It is manifested by edema, erythema around the duct's os. When the occlusion
occurs, pseudoabscess or Bartholin's abscess which are accompanied by purulent process
symptoms can develop.
Gonococcal endocervicitis. Inflammatory process develops in mucosal layer of the cervical
canal. Examination reveals edema and erythema of vagina and part of the cervix. There is a red
crown around the cervical os and a mucopurulent cervical discharge.
Gonococcal proctitis occurs very rarely. Rectum is involved into the process in the result of
contamination with the infected genital discharge. Clinic includes tenesmus and rectal pain.
Gonococcal endometritis is the first stage of the ascendant gonorrhea with infection of basal
and functional layer of endometrium. It is manifested by lower abdominal pain, high body
temperature, sometimes nausea, vomiting. Pain often has spasmatic character. Discharge is sanguinepurulent or mucopurulent. Uterus is painful at palpation. Chronic endometritis is characterized by
menstrual disorders.
Gonococcal salpingitis is the infection of the fallopian tubes, mostly bilateral. In acute stage the
pain in lower part of abdomen is common. It becomes stronger, motion, nausea, vomiting.
Menstrual disorders can occur.
Smears must be taken on the 2-4th day of the menstrual cycle and after provocation in 24, 48,
72 hours, that allows to reveal N. gonorrhea.
Treatment is provided in special clinic. Sometimes the patient is treated by the venerologist in
ambulatory.
To reveal another sexually transmitted diseases clinical and laboratory examination must be
performed. While prescribing medicines the clinical form, complications and severity of the
process should be taken into consideration.
The main medicines in gonorrhea treatment are antibiotics. Gonococcal infection very often is
accompanied with trichomoniasis, chlamidiasis, candidiasis, mycoplasmosis.
Antibiotics that have influence on the following agents such as: Ciprofloxacin, Doxycyclin,
Trobicyn, Sumamed, Cephtriaxon, Afloxacin in combination with Metronidazol, Tiberal, Naxogyn
should be prescribed. The dose of antibiotics is taken according to the methodical instructions of the
Ukraine МНР and annotation of medicines.
Gonovaccine is used after ineffective antibiotic treatment and relapse in the latent fresh torpid
and chronic form of the disease (200-300 mln. of microbe bodies, in 2-3 days intramuscularly).
During pregnancy immunotherapy and antibiotics with negative influence on a fetus are not used.
For toilet of external genital organs 0,002% solution of Chlorhexidine, Re-cutan, Baliz-2 are
prescribed. Local treatment of chronic gonorrhea is conducted after disappearing of the signs of
acute inflammation. In chronic and subacute stages physiotherapeutic methods are used: laser
radiation, paraffinotherapy, mud-cure, diathermy, inductothermy, U.H.F-therapy.
The control of the results of treatment: disappearing of subjective signs and microbe agents
in all the infected organs and discharge. On the 7-10th day after medical therapy the bacterioscopic
and bacteriologic methods are used to confirm the results of treatment. If there is no N. gonorrhea in
the material, then the combined provocation is conducted: injection of Gonovaccine (500 mln. of
microbe bodies), instillation of 1% Lugol's solution in urethra, 0,5% solution of Argentum Nitrate
into cervical canal. Discharge from this organ should be examined during 3 days. Smears are taken
during menstruation and then after provocation in 24, 48, 72 hours. Such examinations are
provided during 2-3 menstrual cycles. Women which have contacts or work with children are not
allowed to work.
Prophylaxis. Using of condom is the most effective prevention method. If the sexual intercourse has
happened without it, then the external genital organs should be washed with water and soap, and after
urination syringing with 0,05% Chlorhexidin solution should be performed.
Urogenital trichomoniasis
Urogenital trichomoniasis is caused by Trichomonas vaginalis and is a result f their invasion into
the lower part of genital tract and urethra.
Ethiology. Trichomonas vaginalis is a flagellate protozoan (fig. 93, 94) and t is transmitted by
sexual intercourse. It is not stable in outer environment, dies n few seconds under the influence of
antiseptic solutions, in water it dies during 5-45 minutes, and also when they wash hands with soap, it is
sensitive to drying, n human organism Trichomonas vaginalis can exist in 3 forms: common one
pear-shape form), amebiform with the expressed phagocytosis action (it can ihagocytise
mycoplasmas, N. gonorrhea and other bacteria that caused the recur-ence of mycoplasmas or
gonorrhea. This is the most spread disease among all he sexually transmitted ones. Its frequency
rate reaches 50-70% of sexually ictive women. According to the WHO statistics, 10% of world
population suffer rom trichomoniasis. Non-sexual transmission is very seldom: when they use
;ponges, underwear, towels.
Incubation period lasts for 5-15 days, the main places of trichomonas >arasitizing are mucose
membranes of vagina, cervical canal, uterus cavity, uterine ubes, Bartholin gland's duct, urethra,
urinary bladder.
Inflammatory process develops in the infected mucous membrane: edema, lyperemia, exudation,
desquamation affects epithelial cells.
Clinical manifestations. Vaginitis, urethritis, endocervicitis, proctitis are he most common
manifestations, ascendant infection meets rarely.
Fig. 93. An agent of trichomoniasis — vaginal trichomonas
bodies. Practically they don't cause the infection. Microscopy allows to identify both kinds of
bodies. Chlamidia has a complicated antigenic structure. It is very sensitive to disinfectant
substances. At 35-37°C during 24-26 hours outcellular Chlamidia become nonvirulent, at
temperature 95-1000C they die during 5-10 minutes. In cotton material they can survive up to 2
days at temperature 19-20°C.
The source of infection is the ill person.
Ways of transmission:
• sexual
• intrapartum (passing through the infected birth canal)
• nonsexual way (polluted hands, instruments, underwear, toilet, etc.)
Besides infection of urogenital organs, Chlamidia trachomatis can cause pharyngitis,
conjunctivitis, perihepatitis, otitis, pneumonia, other diseases (Rei-ter's syndrome).
Clinical manifestations. Incubational period lasts from 5 to 30 days. The main primary form
of chlamidial infection is endocervicitis with mild symptoms or without any. In acute stage purulent or
mucopurulent discharge from the cervix, edema and erythema of the vaginal part of the cervix are
observed. In chronic stage there is the mucopurulent discharge and pseudoerosion of the cervix.
Chlamidial urethritis can be asymptomatic or it manifests itself by dysuria. There are no
specific symptoms for clinical diagnostics of chlamidiasis.
Salpingitis, caused by Chlamidia trachomatis, is characterized by the same symptoms like the
process caused by other bacteria.
The sequale of chlamidial salpingitis is infertility.
Diagnosis is based on the history (both partners are ill, there is the infertility). Residual
diagnosis is established after revealing chlamidias in the scrap from the cervix and vagina. The
most exact are immuno-enzyme and immuno-fluorescent methods.
Treatment. It is necessary to cure the woman and her sexual partner. The woman should avoid
sexual intercourses, alcohol, psychical and physical overload.
Medicines from the tetracyclin group are prescribed (Doxycyclin, Rondo-micyn,
Morphocyclin), Sumamed, Tarivid, Macrolids (Clacid, Erythromycin).
To prevent candidosis Diflucanum in dose 150 mg is used, Nistatin or Levorin (2.000.000 IU per day
during treatment) are prescribed. Fromilid (Clarythro-mycin), an acid-resistant antibiotic from
macrolid group is recommended. An important property of this drug is its possibility to cell
penetration, that's why Fromilid is 8 times more active, than Erythromycin. It doesn't suppress
immune system, activates phagocyto-macrophagal system and some enzymes, that take part in
destroying of pathogenic bacterias. The dose of fromilid is 500 mg twice a day during 7-14 days in
case of fresh incomplicated chlamidiosis. In chronic forms the treatment course must be elongated
till 3-4 weeks.
At urogenital chlamidial infection medicines from ftorchinolon group, Ciprofloxacin (Ciprinol)
are used. Ciprinol is prescribed in the dose of 0,5g orally or 0,2g intravenously each 12 hours during
10-14 days. During treatment the ultraviolet irradiation including sun radiation are contraindicated.
Treatment of chlamidiasis demands from the doctor and patient accurate fulfilling of all the
indications (dose and duration of the therapy), especially at chronic, long-lasting forms of disease. At
the same time accompanying urogenital diseases should be treated. To reduce side effects of antibiotics
hepatoprotectors, antioxydants, polivitamins are used.
Urogenital mycoplasmosis
Ethiology. Microbal agents are Mycoplasma hominis, Mycoplasma genita-loum, Ureaplasma
urealiticum.
In the etiology of the inflammatory diseases of female genital organs the associaton of
mycoplasmosis with trichomoniasis, N. gonorrhea, Chlamidia trachomatis, anaerobes is of great
importance.
Mycoplasmas are transmitted sexually and they are highly spread among the population.
Clinic. Mycoplasmas infection can occur in acute and chronic form, and has no symptoms,
which are specific for this agent. It is often found in healthy women. Mycoplasmosis is characterized
by torpid course, sometimes the latent forms of the reproductive system inflammation are observed.
The agents may be activated under the influence of menstruation, oral contraceptives, pregnancy,
delivery. Ureaplasma is identified in the patients with vaginitis, cervicitis, urethritis, in association
with other bacteria the symptoms are typically and described in the part "Nonspecific inflammatory
diseases of the female genital organs".
Diagnosis. To reveal ureaplasmas the bacteriological method is used. Material is taken from the
purulent discharge of Bartholin's glands, from uterine tubes at salpingitis, tuboovatian tumors at
pelvic inflammatory disease. Test on the urease is done (colour index). It is based on the property of
ureaplasms to product urease, that changes the pH and the colour of indicator. Serological diagnosis
is also used. Immunogram in diagnosis of mycoplasmosis and other infection (Chlamidia, gonorrhea,
trochomoniases, herpes simplex virus) is indicated.
Treatment. Using of antimicrobal medicines from macrolid group (Erythromycin, Sumamed,
Roxitromycin), Tetracyclin group (Tetracyclin, Doxycyclin), Fluorochinolones (Ciprofloxacin) is
etiotropic treatment. They are prescribed for not less than 10-14 days with the following laboratory
control. Another course of treatment is immunity stimulation (Immunoglobulin, Levamizol, Tactivin, Ginseng Tincture).
Prophylaxis. Examination of the risk group (prostitutes, women with infertility, inflammatory
processes of genital organs), and keeping to the same measures for preventing sexually transmitted
diseases are used.
Candidiasis vulvovaginitis (Monilia vaginitis)
Candidiasis is a polyorganic disease, caused by yeast fungi (Candida albicans, C. glabrata, С
tropicalis) (fig. 95). It can be transmitted sexually. The most frequent localization is in vagina, vulva,
but there can be candidiasis endocervi-citis, endometritis, salpingitis.
Predisposing factors:
• endogenous long lasting diseases, such as diabetes mellitus, avitaminosis
• exogenous factors, that predispose fungal colonization and decrease the general reactivity of the
organism (long treatment with antibiotics) and local immunity in vaginal mucosa high virulency
of Candidas.
Fig. 95. An agent of candidiasis — Candida albicans
There are such kinds ofcandididas vulvovaginitis:
• primary
• antibiotics-induced (as a result of antibiotic treatment)
• as a sequale of changes in different systems of the organism (diabetes, pregnancy, using of
estrogens)
On the suppressed immunity of the organism fungi, that were previously saprophites,
become pathogenic. They adher to vaginal epithelial cells, causing superficial inflammation and
desquamation of vaginal cells. Genital candidiasis mostly doesn't cause a deep damage of
mucosa and spreading of the process, but if the agent has high virulence, it can penetrate into
intra- and subepithelium parts. In some cases there can be dissemination of candidiasis.
Clinical manifestations: Candidiasis vulvovaginitis is characterized by vulvar itching,
pruritus, cottage-cheese-like discharge.
Examination reveals edema and erythema of genital mucos with whitish adherent
discharge, that include pseudomicelium of fungi, exfoliated epithelial cells and leukocytes.
Diagnosis. Diagnosis is based on the clinical manifestations, vaginal examination,
colposcopy, bacterioscopic and bacteriological methods.
Treatment. Acute form is treated by Orungal 200 mg twice a day during 3 days; at chronic
form they use 100 mg twice a day during 6-7 days, then during 3-6 menstrual cycles 1 capsule on
the first day of menstrual cycle is taken. High effectiveness is observed while using Diflucan in
dose 150 mg per 1 reception, and Gyno-pevaril — one suppository (150 mg) during 3 days. In
case of relapse one suppository (50 mg) twice a day for 7 days and application of Gyno-pevaril
creme on glans penis during 10 days is recommended. The next step of treatment is normalization
of vaginal ecosystem.
Prophylaxis: rational antibiotic treatment with keeping to optional doses and duration of
the therapy course, in-time using of antimycotic medicines with the preventive aim. Avoiding of
premarriage and extramarital relationships, condom using for preventing fungal colonization of
the female genital tract.
Syphilis
Syphilis is an infective disease, that is transmitted sexually.
Etiology. The pathogene is Treponema pallidum. In microscopic examination it has spiral shape and is
movable. Optional temperature for reproduction of Treponema is 37°C. It is very sensitive to
different external conditions. It dies during boiling, drying, under the influence of different chemical
agents and 90% ethanol. While working with the infected persons hands are cleaned with ethanol. It
prevents from infection at contact with syphilitic rash having Treponema pallidum on its surface.
At 40°C (temperature for keeping blood for transfusion in refrigerator) Treponema pallidum dies in
24 hours.
The source of infection is the infected person.
Ways of transmission:
• sexual perversion (oro-genital, homosexual contacts)
• transplacental — congenital syphilis, when a child is infected by transplacental transmission
• professional — while examining the ill person with wet surfaced rash
• transfusion (very rarely) — as a sequale of blood transfusion from the ill person
Clinical manifestations. 3-4 weeks pass from the moment of agent penetration into organism
and till the first manifestations of the disease. This is the so-caled incubational period. The microbe
is already in human organism, but there are no complications and signs of the disease.
After finishing of incubational period the first signs appear only in the area of agent
inoculation. This is the so-called primary lesion (ulcerated shancre) (fig. 96). It appears as a painless
indurated papula on skin or mucos with erosion or necrosis of the surface. Is a hard-based, well-
Fig. 96. Ulcerated shancre of labia major
circumscribed lesion. There is no inflammation around it and it has smooth surface with serous
discharge. Its
size is from several mm to few cm, and it can be coated with whitish discharge like old fat. On
mucos of genital organs or anus it is like fissure. Sometimes shancre can gangrenize. Indurative
edema belongs to the atypical forms of shancres. Labia major enlarges in size, they are firm and
painless. Chancre on pubis, thighs and cervix can occur rarely.
If the shancre is situated on the genital organs, then after nearly 7 days the inguinal
lymphatic nodes enlarge on one side (scleradenitis, bubo), rarely on both sides. They are firm,
movable, painless. They are not connected with skin and have no suppuration. This is the
primary syphilis, that lasts for 6-8 weeks from the appearing of the shancre (the first 3-4 weeks
is primary seronegative period, when Wassermann reaction is negative, and next 3-4 weeks,
when Wassermann test is positive). Diagnosis in this period is based on the history taking
(sexual contact, incubation period, examination of sexual partner, revealing of Treponema pallidum
on shancre surface, positive serological reactions (Wasser-mann's, immunofluorescence).
Without identification of the agent or positive serological reactions diagnosis of syphilis is not
proved.
After 6-8 weeks of shancre development, the body temperature may rise, there is the night
headache, bone pain can appear. This is the so-called/?ro<iroma/ period. During this time the
agents are reproducted intensively, they appear in blood (treponems sepsis) and there is
disseminated rash on skin and mucosal layer. There appear the signs of secondary syphilis.
Firstly roseolas (little red macula 0,5-1 cm in size) appear on body skin. They disappear for a
while after the finger pressure, don't protuberate over the skin level. After some period papulas,
very rarely pustulas or hair shedding appear. In this time on skin and mucos of the female
genitals papula (erosion nodes) can appear. They are firm, without inflammation, up to 1 cm in
diameter, with moist surface, rich in microbal agents (Treponema pallidum), that make them very
infectious. There are no subjective feelings. As a result of irritation these nodes enlarge,
indurate and transform into the so-called condyloma lata, 0,5-1 cm and more in diameter,
indurated, prominating above skin level, without signs of acute inflammation, painless, with
smooth or tuberous, sometimes with moist surface.
There are plenty of agents on the surface of condyloma lata and they are very contagious.
They should differ it from viral pointed condylomas (soft, on the pedicle, with lobular, like
cauli-flower structure).
Diagnosis is confirmed by presenting erosional papulas and condyloma lata, positive
serological reactions (Wassermann's reaction, reaction of immobilization of Treponems).
Treatment of syphilis is provided by penicillin antibiotics (bicillin, retarpen, extencillin) in
venerologic dispensary, according to the instructions of the Ukrainian Ministry of Health Care.
Prophylactic measures: avoiding of extramarital relationships, using of condom. If coitus was
without condom or it has been torn, then the external genital organs should be washed with soap
and warm water, and during the first 2 hours the cleaning of genitals should be performed.
AIDS
Agent of AIDS is retrovirus, which affect immune system of organism.There are two types of
Human immunodeficiency virus, that caused acguired immunodeficiency syndrome (AIDS): HIV1 and HIV-2.
HIV-1 is spread in all the countries of the world. HIV (human immunodeficiency virus) is very
sensitive to heating, while at boiling it dies immediately, as well as after applying of 70% Ethanol,
0,2% solution of Natrii hypochlorate and other desinfective solution. But this virus survives in its
dried form during 4-6 days in 22°C temperature, in lower temperature even more. The source of
infection is the ill person or viral carrier. People with AIDS are infective all over the life.The quantity
of people with HIV in many times prevalents the quantity of ill person with AIDS. Infected person
becomes contagious in a very short time — 1 -2 weeks after infection.
The ways of infection:
• sexual, which insures natural viral transport from one person to another, as well as sequel of
homosexual contacts
• parenteral way of infection occurs when they break the sanitary rules making injections, especially
intravenous, when injections are made with one syringe, with changing only the needle
• professional way of infection of medical personnel occurs when blood of the person with
AIDS contacts with lesioned skin (microtrauma, fissure etc) or mucosal layer during
manipulations (injections and others)
• transfusional way occurs very rarely, when the infected blood is transfused to the healthy
person
• transplacental — from the infected mother to the child
So, HIV infection can be transmitted from people to people in direct contact: "blood to blood" or
"blood to sperm". Transmission of virus through saline during kissing is less possible. The virus isn't
transmitted by insect stings.
Clinical manifestations of AIDS: Incubation period can last from 1 month to 10 months or even
to years. Clinical manifestations may vary, they can be divided into some periods. In 30-50% of
the inspected persons in 2-4 weeks an acute period can be observed: fever, tonsillitis, enlarging of
neck lymphatic nodes, liver, spleen. This lasts for 7-10 days, and then the disease becomes latent.
The only sign of illness at this time may be the enlarged peripheral lymphatic nodes. They are
movable, not connected with tissues, some of them are painful at palpation. Such enlarging of
the nodes can indicate to the AIDS, if it lasts for more than 1,5-2 months. Later the so-called
AIDS-associated or premorbid complex of symptoms is developed. It can last from 1 to 6
months during some years. In this time many different symptoms and diseases which are not
specific for AIDS (up to 200) are developed. That is the long-term fever, generalized enlarging
of peripheral lymphatic nodes, periodical diarrhea, weight loosing (more than 10%), oral cavity
candidiasis, leukoplakia of tongue, folliculitis, different skin lesions.
This period lasts wave-likely while health becomes better till the clinic remission, when
person considers himself absolutely healthy.
The last period is AIDS. In such persons different infectious diseases occur (up to 170) on the
base of immunodeficiency, caused by HIV-infection. Nervous system is damaged (in 30-90% of
patients), poor orientation, bad memory and demention are develops. Pneumocystic pneumonia
(lung inflammation) occurs up to 60% with severe, sometimes with fulminant passing. In 60% of
cases severe and long-termed diarrhea is observed. Kaposhi's sarcoma very often progresses and
becomes the reason of death at young age In significant part of patients having AIDS, malignant
processes like lymphoma and others are developed as a result of virus influence on immune
mechanism of human being. Skin and mucosa are damaged with Candida fungi (candidiasis, Herpes
simplex and Circular herpes virus with severe, relapsing duration, they don't undergo to usual
methods of treatment.
Diagnosis. In AIDS the following diagnosis are mentioned:
• epidemiological history (homosexualism, drug abuse, prostitution, intravenous injections etc.)
• a long-term enlargening of peripheral lymphatic nodes, loosing of body weight, long-term
fever and diarrhea
• revealing of antibodies to HIV in blood by immunofluorescent analysis and others. 5 ml of
venous blood is taken, and it is kept in refrigerator at the tempreature of+2 — +4°C. Serum is
taken out after appearing of the blood the clot and sent to the laboratory not later than in 1-3
days Treatment. There are no medicines for treating AIDS. But remedies, that
inhibit development of the disease are used. Nowadays there is an effective preparation for
treatment of HIV infection and AIDS — Krixivan (protease inhibitor). Triple therapy of Krixivan
base (Krixivan+AZT+ZTS) has high effectiveness, decreases quantity of viruses in blood to
lower level. Immunostimu-lators, immunomodulators, symptomatic therapy depending on the
pathology is used.
Prophylaxis:
• sanitary and educational work among inhabits
• avoiding of pre- and extramatrial relationships
• using of condoms (decrease the transmission in 200-500 times)
• prophylaxis of drug abuse, parenteral (subcutaneous or intravenous) injectons of medicines proper
sterilization of medical instruments, using syringes and needles of single use
• using special defence agents by medical workers contacting with patients' blood and other
biological substances (special closes, double gloves, goggles, masks)
• control of donor blood
VIRAL DISEASES
The quantity of viral diseases of genital organs has been significantly inc-increasing for the last
time, especially among young people.
Viral infections can occur in latent form, with less symptoms and with expressed clinical
manifestation. That's why it is very difficult to diagnose them. These diseases have especially
negative influence on the pregnancy. There is a risk of viral transmission to fetus.
They can cause fetus diseases or defects of development, leading to fetus death or
miscarriage." Every pregnant woman with miscarried fetus must be examined on these infections
presence, because in the majority of such women Cytomegalovirus, Gripp virus, Hepatitis A and В
virus, Papillomavirus are revealed. Besides the influence on fetus, according to the recent
investigations, viral infection causes malignant growth in the female genital organs.
Herpesvirus infection
Herpesvirus diseases of genital organs are caused by Herpes simplex virus, mostly of the second
type (HSV-2). Source of the infection are infected persons and carriers. It may be revealed in young
sexually active women. It can be transmitted during orogenital contact. The virus is located mostly in
mucos membranes of urogenital tract in men and cervical canal in women, also in the nervous
ganglions of lumbar and sacral parts of sympathetic nervous system. Genital herpes is transmitted
sexually. During pregnancy it may cause miscarriage and malformations.
Genital herpes is considered to be all-life persistant infection, that's why it has a relapsing
passing.
Clinical manifestations. According to the clinical signs, the disease duration is divided into
typical, non-typical, and asymptomatic one (viral carrier).
Typical passing of the disease is characterized by genital and extragenital signs. Extragenital
signs: rising tempreature, mialgias, headache, nausea, viral rash on face, bad sleep. Genital signs
are present on the lower parts of genital system — vulva, vagina, cervix, near urethra os perineum.
Single or plural vesicles up to 2-3 mm in size, with erythema and edema, which exist for 2-3 days
appear in mucous membranes. After vesicle rupture erosion with incorrect form, covered with
yellow discharge appears. The erosion re-epitheliazes without scars in 2-4 weeks.
Patients complain of pain, irritation, itching in area with viral lesions.
Clinical manifestations are in three forms:
• I — acute primary
• II — chronic recurrent
• III — atypic
Depending on the localization, genital herpes is divided into three stages:
• the first one — herpes lesions of external genital organs
• the second — herpes lesions of the vagina, cervix, urethra
• the third — herpes lesions of the uterus, adnexa, bladder
Diagnosis is based on history taking, complaints, objective examination, revealing of
HSV-2 or its antibodies in the patient's serum.
The most informative method of identification is isolation of the virus from discharge of the
cervix, vagina, uterine cavity, urethra. For express-diagnosis a method of fluoriscine antibodies
and immunoperoxydase method are used. There is electro-microscopic method of HSV-2
identification and the method of viruses inoculation on tissue culture with the following studying
of their properties.
Treatment is difficult because of the relapses of the disease and possibility of reinfection.
Antiviral medicines belong to three main groups (according to the action mechanism):
• replication inhibitors of viral nucleic acid
• interferon and compounds, that have interferon-inductive action
• compounds with other antiviral action
Difficulties of treatment are caused by virus peculiarities (they are obligate intracellular
parasites).
As a result of investigation of virus nature on molecular level, new medicines were created.
They have the influence on viral growth and development of the virus. They are Zovirax
(Acyclovir, Valacyclovir), Alpizarin, Foscarnet, Valtrex, Herpevir. Acyclovir is used in dose of
600-1200 mg per day, orally or intravenously.
Local therapy by 3% Megasin ointment, 3% Bonaphton or 3% Alpizarin is also used.
For treatment of the recurrent herpes antiviral medicines, herpal vaccines, antirecidive
immunotherapy are used.
Condylomas acuminata
Ethiology. Condylomas acuminata are caused by Human Papillomavirus of 16 and 18 types.
They are transmitted sexually (fig. 98). Resistant to disinfective agents viruses may be killed by high
temperature during sterilization. Incubational period of condyloma acuminata lasts from 1 to 9 months.
The disease often occurs in sexually active persons. Papillomavirus causes genital cancer. These
patients have in 1-2 thousands times more chances to acquire a malignant process, than healthy
people. Condylomas acuminata can transform into cancer in 6-26% of cases.
Clinical manifestations: On the onset of disease single pink, sometimes grey warts, with
thin pedicle, rarely with wide base appears on skin surface of labia majora, perineal area and
mucosal layer of urethra, anus, vagina, cervix. Condylomas acuminatum can grow significantly
and fuse (fig. 99). They looks like cauliflower, with lobular structure, and have long-term
duration. Some patients with long-term duration of the process can have big condylomas, like
tumor. They can be complicated by abnormal vaginal discharge, due to the secondary vaginal
infection. Condylomas may cause some difficulties at walking, intercourse. During pregnancy
and delivery they can cause bleeding. In 15-17% of patients regression may occur, especially
during pregnancy.
Clinical diagnosis. Lobular surface, soft consistency, thin pedicle should be taken into
consideration.
Differential diagnosis for genital warts includes condylomata latum, which have wide base,
brown or red colour, and no lobular structure. Also other manifestations of syphilis are present
there.
Treatment If genital warts are large, laser vaporization is performed. It is more effective,
than criodestruction or surgical diathermy. For treatment of small condylomas 30% solution of
Podophyllin, Condilin or Resorcin are used. Modern effective remedy is Solcoderm.
Molluscum contagiosum
Ethiology. Molluscum contagiosum is caused by virus, that is transmitted by contact with
the ill persons or during using their things. In adults the main way of transmission is sexual
contact. Children are infected more often. Incubation period lasts from 2 till 9 months.
Clinical manifestations. On skin the small firm dome-shaped papules 5-7 mm in diameter,
occasionally enlarging to 1-3 cm conglomerates is appeared. The flesh-colored papules have
specific central umbilication (fig. 100). Lesions are located on the external genital organs,
perineum, pubis, hips, face.
Molluscum contagiosum can persist for a long time.
Clinical diagnosis. After direct pressure by forceps white caseous material can be got.
Treatment. The lesions are pressed by forceps and cleaned by Iodine solution or Betadine,
garlic juice or cryotherapy.
Cytomegalovirus infection
Infectional agent is Human cytomegalovirus. The percentage of the infected women according to
the world literature is very high. In Western Europe it is from 50 to 85%. Among pregnant women
with usual miscarriage 70% are infected.
Fig. 100. Molluscum contagiosum (histological picture)
After invasion cytomegalovirus persists in organism for a long time, spreading by saline and
sexual contacts.
Clinical manifestations. The main signs of the infection are extragenital symptoms: CNSlesions, thrombocytopenia, liver disorders, pneumonia. Infecting of the fetus during pregnancy leads to
intrauterine development defects (microcep-falus, deafness), diseases of the newborn (cerebral
paralysis, miasthenia). It is manifested by cervicitis, cervical erosions, vaginitis, vulvitis and other
inflammatory diseases, that have subclinical passing.
Diagnosis: Blood and urine tests for virus presence are performed. Cytoscope analysis of
saline and urine sediments are based on the properties of Cytomegalovirus to penetrate into the cells
and to make big intranuclear inclusions. Infected cell becomes bigger, it is the so-called
cytomegalovirus cell, "an owl's eye".
Serological methods: indication of antibodies components to HCMV (1:8 and more is
considered to be positive).
Non-direct immunofluoriescence method and DNA-diagnostics (chain polymerize reaction) are
used.
Treatment. The main purpose is the correction of the immune system disorders. Preparations for
immunity stimulation (Levamizol, T-activin, Immunoglobulin, Ginseng tincture) are used.
Application of ointment and injection of leukocyte interferon, immunoglobulin with high titred
cytomegalovirus antibodies ("Citotect") into cervix are used. Wide spectrum of antiviral preparations
(Valtrex, Acyclovir, Ribavirin, Gancyclovir, Bonaphton) are less effective.
Prophylaxis. Avoiding of pre- and extramarital sexual contacts, using of condom, keeping the
rules of personal hygiene.
Tuberculosis of genital organs
Genital tuberculosis is the secondary disease. Very often clinical focus is in lungs. The disease is
caused by Mycobacteria tuberculosis, which is transmitted hematogenically from lungs or intestine
to genital organs. Mostly women from 20 to 40 years of age become ill.
Tuberculosis infection is found in 5-8% of patients with inflammatory diseases of genital
organs, and in 1-3% of patients with salpongoophoritis.
Mycobacteria tuberculosis contaminate into genital organs mostly in childhood, but clinical
manifestations appear in the pubertyperiod, with the beginning of sexual life and after
supercooling.
Tuberculosis damages uterine tubes (85-90%), rarely uterus and ovaries (fig. 101, 102), and more
rarely — the cervix, vagina, external genital organs.
According to Aburela E. and Petersuc B. (1975) classification, there are four main forms of
specific process in the female genital organs:
• tuberculosis of genital organs with microdamages mostly with productive character, and latent
duration
tuberculosis of genital organs with macrodamages mostly with exudative-proliferative or
caseous character, and lasts like salpingoophoritis and endometritis, accompanying with ascites or
adhesive peritonitis
• associative tuberculosis of genital organs and tuberculosis of other organs (lungs, kidneys) or
tuberculosis of genital organs, combined with the other gynecological diseases (endometriosis,
sclerocystic ovaries, uterine myoma)
• clinically curable genital tuberculosis with posttuberculosis changes (petrification, adhesions,
degeneration)
Fig. 102. Tuberculisis of uterus, fallopian tubes, ovaries, parametrial tissue
Pathomorphological examination reveals inflammatory changes. Morphological specificity of
them is in presence of tuberculous granuloma in productive phase of inflammation a focus of
caseous decomposition with exudative phase of the process. If antituberculosis medecines are used
in exudative inflammation phase, the exudate resolves with complete or almost complete renewing of
tissue structure. Destruction of the tissue is substituted by the connective tissue in productive phase
of the process. Separation of the focus from intact tissue take place in case of caseous damage
resolvation of perifocal infiltration and fibrose transformation of the destruction zone with the
capsule. In such focus Mycobacterium tuberculosis can stay for a long time and in some cases it causes
relapsing.
Clinical manifestation. At "small" forms of tuberculosis pain syndrome is absent. Dominant
sign may be menstrual dysfunction (hypomenorrhea or algo-dysmenorrhea). Pain appears in case of
large damage. Almost all the patients with genital tuberculosis suffer from reproductive disorders, i.e.
primary or secondary infertility, ectopic pregnancy.
If the changes in endometrium are significant, amenorrhea (uterine form) can develop.
General changes in the patient's organism are accompanied by the signs of tuberculosis
intoxication: disorders of general state, weakness, sweating, sub-febrile temperature.
Diagnosis. Diagnosis is based on the history data (contact with tuberculosis patients,
previous tuberculosis of bones, lungs, bronchitis, pneumonia, long-lasting subfebrile condition),
objective examination (tuberculosis changes in organs or their sequel), bacteriological
examination, additional methods of examination, including histological. For confirming the
diagnosis of tuberculosis special tests are used (Mantu, Koch's). The Mantu test identifies only
the specific sensitization of the patient and has less diagnostic value. For diagnosis the Koch's test
is important. General, local and focal reactions appear after subcutaneous injection of 20 IU of
tuberculin in patients with tuberculosis. General one is manifested by high temperature,
headache, weakness. Focal reaction manifests itself in 48-72 hours by enlarging of adnexal
infiltration, they become more painful.
The Koch's test can be confirmed by changes in hemogram (high quantity of leukocytes at
the expence of the low amount of monocytes, eosinophiles and lymphocytes), proteinogram
(low amount of albumin and high amount of glo-bulines), immunogram. C-reactive protein and
high level of sialic acid appear in blood.
Bacteriological method is very important, it is in revealing of Mycobacterium tuberculosis in
uterine and adnexal tissue. Material for inoculation is discharge from uterus and vagina,
punctate from ovarian tumor or tissues taken during laparoscopy.
Laparoscopy is a valuable method, it allows to perform visual examination of abdominal
cavity and to take tissual samples for bacteriological and histological analysis.
roentgenological examination of genital organs and thoracic cavity are necessary,
especially in patients with first manifestations of the process in the uterus or adnexa (fig. 103).
Hysterosalpingography allows to estimate uterine cavity state, uterine tubes, their permeability
and other changes, caused by tuberculosis.
Histological examination of endometrium after uterine cavity curettage is important, too.
Ultrasonic echography for estimation of morphological changes in uterus and its adnexa is
also used.
Treatment of genital tuberculosis is complex and includes rational regimen, dietotherapy,
vitamins, symptomatic therapy and climatic health-resort cure.
The main is the antibiotic therapy. Antituberculosis agents, being in nse now, are: Rifampicin,
PAS A, Ethambutol, preparations of Izonicotine acid. For preventing mycobacterium persistation,
combination of remedies (Izoniazide + Rifampicin) are used. If the process is revealed for the first
time, or it has acute or subacute passing, three preparations are prescribed: antibiotic, one preparation
Fig. 103. Calcificates in tuberculosis
of Izonicotine acid (Izoniazide, Saluzid) and PASA. The last one has not only bacteriostatic action,
but also prevents from development of microorganisms resistention to antibiotics and preparations
of izonicotine acid, that's why they can be used for a long time. Treatment lasts for 1,5-2 years,
during the first 3-6 months the combination of 3 medicines is used, and later on for 6-8 months 2
agents are taken. After that supportive therapy is performed till 2 years.
Intramuscular and oral usage of medicines are combined with injection of some dose of
medicine in focus of lesion. Lidase with antibiotics and hydrocortisone are used for this purpose by
means of colpocentesis to the damaged organ. These medicines may be used during hydrotubations. 1
% solution of chimo-tripsin is used through posterior fornix and by electrophoresis. In some cases
surgical treatment is used. In spring and autumn antirecidive therapy is performed.
Rehabilitation of such patients is provided in specialized health resorts (Odessa, Alupka). For
resolvation of residual affects after tuberculosis physiotherapy and pelotherapy are used.
Assignments for Self – assessment.
II. Multiple Choise.
Choose the correct answer / statement
1.
The most freguent type of inflammatory diseases is:
A.
Iron-deficiency amenia;
B.
Folate-deficiency amenia;
C.
Pain;
2.
Which of the following is Not characteristic of inflammatory diseases?
A.
Decreased factor VII;
B.
Pain;
C.
Family history of the diseases;
D.
Prolonged bleeding time.
3.
Infants bom to mother with inflammatory diseases are at higher risk for:
A.
Neonatal patology;
B.
Neonatal hypoglycemia;
C.
Hypoglycemia;
D.
Polycythemia.
III.Answers to the Self- Assessment.1.C, 2.A, 3.A.
Students must know:
1.
Normal vaginal microflora.
2.
Vaginitis (colpitis).
3.
Acute endometritis.
Students should be able to make:
1.
Plan of management of the patients with inflammatory diseases;
2.
Plan the theatment of the patients with inflammatory diseases;
3.
Plan the delivery of the patients with inflammatory diseases;
4.
Plan the postpartum care of the patients with inflammatory diseases;
References:
1. Obstetrics – edited by Professor I.B. Ventskivska, Kyiv “Medicine”, 2008.
2. Gynecology and Obstetrics. - Norman F. Gant, F. Gary Cunningham. -1993. -- P. 406-412.
3. Obstetrics and gynecology. - Pamela S.Miles, William F.Rayburn, J.Christopher
Carey. - Springer-Verlag New York, 1994. - P. 62-64.