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Vaginal Discharge Dr.A Danesh

Vaginal Discharge Dr.A Danesh .

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Vaginal Discharge Dr.A Danesh

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  1. Vaginal DischargeDr.A Danesh

  2. Differential Diagnosis of the Abnormal Vaginal DischargeNormal (physiologic) vaginal secretionsVaginal infections Trichomoniasis Vulvovaginal candidiasis Bacterial vaginosisDesquamative inflammatory vaginitisCervicitis Infections NoninfectiousEstrogen deficiency

  3. TrichomoniasisEtiologyandPathogenesisProtozoan Trichomonas vaginalis Exogenous sexually transmitted infection Transmission almost always occurs through sexual contact.After an incubation period of a few days, patients develop a purulent discharge associated with varying degrees of vulvarirritation,dysuria, and dyspareunia. An abnormal odor is often present, usually signifying concomitant BV.

  4. Treatment Metronidazole and tinidazole A single 2g oral dose of metronidazole is the treatment of choice.500 mg can be given twice daily for 7 daystreatment all recent sexual partners

  5. If this treatment fails treatment of all current sexual partners should be assured Initial retreatment should be with oral metronidazole, 500 mg twice daily for 7 days. If this regiment is not successfuloral metronidazole in a single doseof 2 g can be prescried for 3 to 5 days.If the latter metronidazole regimen fails, the patient can be assumed to have clinically significant metronidazole resistance

  6. Alternative regimensHigh doses of metronidazole are usually oral (2.5 g daily)vaginal (0.5 g daily) metronidazole up to 3 weeks (Antiemetics) Intravenous regimensnext choice is usually tinidazolenonoxynol-9Furazolidone Zinc sulfate douches given in combination with oral metronidazole discontinuation of estrogen replacement treatment in a postmenopausal woman was associated with resolution of vaginal trichomoniasis

  7. Trichomoniasis in pregnancypremature rupture of the menbraneslow birth weight (theoretical mutagenicity oncogenicity)Pregnant women who have symptomatic trichomoniasis should be treated with 2g of metronidazole.

  8. Vulvovaginal CandidiasisEtiologyandpathogenesisCandida albicans 80% to 90% candida tropicalis 1% to 5% higher rate of recurrence Candida glabrata less intense itching and dyspareunia Non-alibecans infections are assoiated with recurrent disease with HIV infection

  9. Risk factorsantimicrobial treatment Antimicrobial treatmenthigh estrogen levels.Users of oral contraceptives Poorly controlled diabetes mellitus tight, insulating clothing impairment of phagocytic cells or of cell mediated immunity (transplantation, chemotherapy) HIV infection especially if they have low CD4 T-cell counts.Onset of sexual activity

  10. The severity of symptoms in vulvovaginal candidiasis is not directly related to the number of yeast cells present .An immunologic reaction has been suggested as the mechanism for symptomatic

  11. Classification of patients with vulvovaginalcandidiasisuncomplicated infection Sporadic No underlying disease caused by candida albicans patient is not pregnant Mild to moderate severityComplicated infectionUnderlying illnessHuman immunodefiencyvirus disease Diabetes mellitus Recurrent infection (four or more episodes per year) Caused by non-albicans species of candida Severe infection

  12. Treatment Uncomplicated vulvovaginal candidiasis short courses of vaginal nystatin, miconazole, clotrimazole, butoconazole, terconazole, and tioconazole , 1,3,7, or 14 days Oral antifungals fluconazole in a single 150 mg dose effetive as Ketoconazole and itraconazole, are effective but have not been approved by the FDA for the treatment of uncomplicated vulvovaginal candidiasis

  13. PregnantwomenShould be treated with topical agents for at least 7 days. Oral azole antifungal agents should not be used during pregnancy.

  14. Comlicatedtreatment should begin with a vaginal culturetreatment for 7 to 14 days or longer is usually required chronic suppressive treatment with an oral antifungal agent may e useful in preventing recurrences once the current infection has use of 100 mg of ketoconazole daily or flucomazole 100 to 200 mg of per week for at least 6 months

  15. not respond to the available topical and oral agents, intravaginal boric acid. powder (600mg)is placed into size 0 gelatin capsules and administered vaginally for 14 days. Treatment of sexual partnersUnpasteurzed yogurt product that contains live lactobacilli is prophylactic agent for recurrent vulvovaginal candidiasis

  16. Diagnosis B VGray and homogenousdischargeFishy vaginal odorDuring menstruationAfter intercourseMinimal itching or irritationVulvovaginal irritation is not prominent symptom-hence, “vaginosis’’ rather than “vaginitis”.

  17. Women who have BVIncreased risk for the development of infection with herpes simplexvirus type 2N. gonorrhoeae C.trachomatisBV is more prevalent and more persistent among HIV infected women. (Low CD4 T-cell)

  18. TreatmentOral metronidazole. 500 mg twice a day for 7 days.Oral clindamycin A single2g dose of metronidazole, is less effective.Vaginal preparations containing0.75% metronidazole gel or 2% clindamycin cream,ovules containing 100 mg of clindamycin lyophilized hydrogen peroxide-producing Lactobacillus acidophilus organisms.Intravaginal boricacid,600 mg at bedtime.Once the symptoms have been controlled, the dosing interval can be increased. Some patients remain symptom free using boric acid capsules once or twice a week.

  19. Postoperative infections occur more often in women undergoing gynecologic surgery.Vaginal cuff infections.Treatment of BV before induced abortion reduces the risk of subsequent pelvic inflammatory disease.

  20. BV during pregnancyPremature membrane rupture. Preterm birthpostpartum endometritis.Oral metronidazole or oral clindamycin. Topical agents do not appear to be as effective as oral agents. clindamycin cream has been associated with adverse events such as prematurity and neonatal infections.Treatment of sexual partners is not recommended.

  21. DESQUAMATIVE INFLAMMATORY VAGINITISEtiology and pathogenesisUnknown, cause it mimics estrogen deficiency vaginitis and trichomoniasis but usually occurs in women of reproductive age who have normal hormonal function and no evidence of any sexually transmitted conditions

  22. Occurs in perimenopausal women or After pregnancy role for changes in the level of estrogen background to have the A26 and B35 histocompatibility antigensgram positive cocci and group sreptococci can be recovered from some patients especially those who are perimenopausal local manifestation of a systemic illness such as systemic lupus erythematosusmay also have erosivelichen planus involving oral or genital mucous membranes always part of the lichen planus complex

  23. Diagnosis Purulent vaginal discharge varying degrees of vulvar irritation dysuria and dyspareunia there is of ten a history of multiple unsuccessful treatments with a variety of topical and oral antimicrobial agentsConfused with trichomoniasis

  24. TreatmentTopical corticosteroids and topical boric acid2% clindamycin vaginal creams 5 g of the cream (containing 100 mg of clindamycin) vagina at bedtime for 14 days.A few patients require a second 14 day course of treatment to induce a remission

  25. Relapses occur months to years later retreatment with topical clindamycinvery frequent relapses require continual biweekly intravaginal clindamycin or corticosteroids to remain in remission perimenopausal patients who are estrogen deficient may require estrogen replacement as well as topical clindamycin to sustain a remission

  26. CervicitisAcuteChronicInfectious cervicitis is endocervicitis.N.gonorrhoeae, C.trachomatis, Noninfectious cervicitis is usually ectocervicitis .Primary herpes simplex ectocervicitis.

  27. Examinationvulva and of the vaginal mucosa are usually normal infections endocervicitis the purulent secretions can be seen to flow from the endocervical canal noninfectious ectecervicitis the purulent secretions can be seen to emanate from the ectropionnoninfectious endocervicitis the abnormal secretions are solely endocervical presumably reflecting the noninfectious endocervicitis

  28. Treatmentif the volume of secretions arising from an ectropion is bothersome destruction of the ectopic endocervical mucosa of the ectropion with cryotherapy allows the ectocervix to become reepithelialized with squamous epithelium

  29. ESTROGEN DEFICIENCY VAGINITISEtiology and Pathogenesispostmenopausal Younger women who have become estrogen deficient because of disease or because of treatment with pharmaceuticals that interfere with the production or the activity of estrogen breast – feedingThinning of the mucosa may result in vulvar discomfort and introital dyspareunia. The thin vaginal mucosa may become infected, presumably enteric organisms and others that are able to colonize the vagina in the absence of lactobacilli. Frequent urinary tract infections may occur . Estrogen deficiency vaginitis overlaps with DIV.

  30. DiagnosisThe vestibular and vaginal mucosae are pale, often with patches of erythema . Vainal secretions, if present,may be purulent. Vaginal PH is elevated . No odor when the secretions are mixed with 10% KOH. Microscopic examination of the parabasalvaginal cells without leukocytes.

  31. TreatmentEstrogen replacement or cessation of antiestrogenic drugs or breast-feeding Topical antibacterial agents containing sulfonamides or clindamycin may improve symptomatic vaginitis, lubricating agents may relieve vaginal dryness and dyspareunia .Without estrogen replacement, symptoms may recur after cessation of treatment

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