Week 8: Vaginal Discharge And Sexually Transmitted Diseases

WEEK 8 PBL: VAGINAL DISCHARGE AND SEXUALLY TRANSMITTED DISEASES DIFFERENCE BETWEEN NORMAL AND ABNORMAL VAGINAL DISCHARGE Normal discharge Characteristics of normal vaginal discharge vary by the hormonal status of the patient. In reproductive-aged females, normal vaginal discharge consists of 1 to 4 mL of fluid (per 24 hours), which is white or transparent, thick or thin, and mostly odourless. The pH is typically 4.0 to 4.5 as measured with pH paper. This physiologic discharge is formed by mucoid endocervical secretions in combination with sloughing epithelial cells, normal vaginal flora, and vaginal transudate. Although normal discharge may be yellowish, slightly malodorous, and accompanied by mild irritative symptoms, it is not accompanied by pruritus, pain, burning or significant irritation, erythema, local erosions, or cervical or vaginal friability. The absence of these signs and symptoms helps to distinguish normal vaginal discharge from discharge related to a pathological process, such as vaginitis or cervicitis. Vaginal discharge consistency and character is also dependent on the role of estrogen. 1. 2. Estrogenized: In the presence of estrogen the nonkeratinized stratified squamous epithelium of the vagina is rich in glycogen. Glycogen from sloughed cells is the substrate for lactobacilli, which convert glucose into lactic acid, thereby creating an acidic vaginal environment (typically pH 4.0 to 4.5 as measured with pH paper. Absence of estrogen: common hypo estrogenic states are premenarche and post menopause. The lack of estrogen, and glycogen substrate, results in sparse presence of lactobacilli and an elevated vaginal pH (typically >4.5). Premenarche: Prior to estrogenization, physiologic vaginal discharge ranges from absent or scant. If present, fluid can be clear, white, or mucoid. The vaginal pH is alkaline. Postmenopausal: Leads to a reduction in quantity of the vaginal discharge and an increase in vaginal pH (typically > 4.5). Vaginal discharge may become more noticeable at times such as at midmenstrual cycle close to the time of ovulation or during pregnancy or use of OCP. Diet, sexual activity, medication and stress can also affect the volume and character of normal vaginal discharge. Abnormal discharge Disruption of the normal ecosystem can lead to conditions favourable for development of vaginitis with vaginal discharge. Some of these potentially disruptive factors include sexually transmitted diseases, antibiotics, foreign body, estrogen level, use of hygienic products, pregnancy, sexual activity, and contraceptive choice. 1. 2. Infectious: the most common causes of abnormal vaginal discharge are vulvovaginal candidiasis, bacterial vaginosis and trichomoniasis. Cervicitis, typically from sexually transmitted infections (STIs), such as gonorrhoea, chlamydia, and mycoplasma, can also present as nonspecific vaginal symptoms. Non-infectious: can be further grouped into Mechanical: foreign bodies like retained tampons or condoms. Chemical: vaginal washes and douches Systemic disorders like rheumatoid arthritis and systemic lupus. Clinical features: Individuals with abnormal vaginal discharge typically present with one or more of the following nonspecific symptoms; change in the volume, color or odor of vaginal discharge, pruritus, burning, irritation, erythema, dyspareunia and spotting. EVALUATION OF A PATIENT PRESENTING WITH VAGINAL DISCHARGE (History taking, physical exam, investigations and management) The main steps in the initial evaluation of individuals with symptoms of vaginitis are; History taking The initial history questions gather details of the patient's symptoms. Each symptom is further evaluated separately as more than one condition may be present. However, none of the findings from the history allows a definitive diagnosis since there is considerable overlap in symptoms among the different etiologies of vaginitis. 1. 2. 3. 4. 5. 6. Discharge: If discharge is present, what is the quantity, color, consistency, and odor? Classic descriptions of the vaginal discharge associated with the three most common vaginal infections are as follows: Bacterial vaginosis: The discharge of BV is typically malodorous, thin, gray (never yellow), and is a prominent complaint. Vaginal candidiasis: typically presents with scant discharge that is thick, white, odorless and often curd – like. Trichomoniasis: purulent, malodorous discharge, which may be accompanied by burning, pruritus, dysuria, frequency, and/or dyspareunia. Burning, irritation or other discomfort: Candida vulvovaginitis often presents with marked inflammatory symptoms (pruritus and soreness). In contrast, BV is associated with only minimal inflammation and minimal irritative symptoms. Burning and irritation can also be a symptom of non-infectious disorders such as vulvodynia. Pruritus: suggestive of a diffuse process such as infection, allergy, or dermatosis. Persistent or chronic focal pruritus is suggestive of a localized process such as neoplasia or malignancy. Vaginal bleeding: is not consistent with infectious vaginitis, with the exception of postcoital spotting, which may indicate cervicitis. If vaginal bleeding is present, the patient should be evaluated for cervicitis, erosive causes of vaginitis (eg, erosive lichen planus), and/or a uterine source. Timing of symptoms: Symptoms of candida vulvovaginitis often occur in the premenstrual period, while symptoms of trichomoniasis and BV often occur during or immediately after the menstrual period. Symptoms that develop soon after sexual intercourse are suggestive of STIs. Symptoms that develop after gynaecologic surgery such as hysterectomy can suggest a vaginal fistula. Estrogen status: Low estrogen levels can cause genitourinary syndrome of menopause (ie, vulvovaginal atrophy) that presents with symptoms of vaginitis, vaginal dryness, and dyspareunia. Menopausal individuals receiving systemic hormone therapy may not have adequate estrogen levels for vaginal health and thus remain prone to atrophic vaginitis unless additional low-dose vaginal estrogen is utilized. Physical Physical examination includes evaluation of the vulva, clitoris, vestibule, vagina, cervix, and pelvis. Sites of discomfort are identified and mapped. The clinician assesses the degree of vulvovaginal inflammation, characteristics of the vaginal discharge, and presence of lesions or foreign bodies. Other significant findings include cervical inflammation and pelvic or cervical motion tenderness. - - Vulva: normal findings are consistent with BV or leukorrhea Erythema, edema or fissures suggest candidiasis, trichomoniasis or dermatitis. Atrophic changes are caused by hypoestrogenemia and suggest the possibility of atrophic vaginitis. Changes in vulvovaginal architecture (eg, scarring) may be caused by a chronic inflammatory process, such as erosive lichen planus, as well as lichen sclerosus or mucous membrane pemphigoid rather than vaginitis. Pain with application of pressure from a cotton swab ("Q-tip test") on the labia or at the vaginal introitus may indicate an inflammatory process (candidiasis, dermatosis) or provoked vulvodynia (ie, vulvar pain of unclear etiology). Speculum: Speculum examination is performed to evaluate the vagina, any vaginal discharge, and the cervix. - Vagina: A foreign body (eg, retained tampon or condom) is easily detected and is often associated with vaginal discharge, intermittent bleeding or spotting, and/or an unpleasant odor due to - - inflammation and secondary infection. Removal of the foreign body is generally adequate treatment. Antibiotics are rarely indicated. Granulation tissue or surgical site infection can cause vaginal discharge or bleeding after hysterectomy or childbirth. The presence of multifocal rounded macular erythematous lesions (like a spotted rash or bruise), purulent discharge, and tenderness suggests erosive vulvovaginitis, which can be caused by trichomoniasis or one of several noninfectious inflammatory etiologies Necrotic or inflammatory changes associated with malignancy in the lower or upper genital tract can result in vaginal discharge; spotting is more common in this setting than in infectious vaginitis. Vaginal warts are skin-colored or pink and range from smooth flattened papules to a verrucous, papilliform appearance. When extensive, they can be associated with vaginal discharge, pruritus, bleeding, burning, tenderness, and pain. Bimanual exam: performed to assess for tenderness and/or abnormal anatomy. - Patients with vaginitis who also have pelvic or cervical motion tenderness are further evaluated for pelvic inflammatory disease (PID). Adnexal masses could represent a cyst or malignancy. While bimanual examination can also identify pelvic muscle spasm and tenderness reflecting pelvic muscle dysfunction, these entities are not usually associated with abnormal vaginal discharge. DIFFERENTIAL DIAGNOSIS OF A PATIENT PRESENTING WITH VAGINAL DISCHARGE AND RASH Vulvovaginitis DISCUSS PATHOPHYSIOLOGY OF SEXUALLY TRANSMITTED DISEASES (Etiology, risk factors, signs, investigations, prevention and management) Chlamydia Predominantly affects the genitourinary tract although it can cause pneumonia and neonatal conjunctivitis in infants born vaginally to infected mothers. It is causes by chlamydia trachomatis serotypes D – K and may be transmitted through genital to genital contact or oropharyngeal to genital contact. Clinical features The majority of infected individuals are asymptomatic. - Patients of any gender may present with urethritis (can cause dysuria; or polyuria) or proctitis Patients with female genitalia may additionally present with salpingitis, cervicitis, or symptoms of pelvic inflammatory disease.  (Muco)purulent vaginal discharge  Abnormal uterine bleeding  Postcoital bleeding -  Dyspareunia Symptoms of reactive arthritis may also be present. Diagnostics 1. 2. Preferred test: Nucleic Acid Amplification Test (NAAT) Detects Chlamydia trachomatis RNA or DNA, e.g., by PCR Specimen collection  Individuals with female genitalia: vaginal swab (preferred), cervical swab, or first-void urine  Individuals with male genitalia: first-void urine (preferred) or urethral swab  Suspected exposure from rectal intercourse: rectal swab Other diagnostic tests: not routinely recommended; a culture may be preferred over NAAT in select circumstances Management 1. 2. 3. 4. 5. Start antibiotic therapy (even if asymptomatic): doxycycline 100 mg PO BID for 7 d or azithromycin 1 g PO in a single dose. Doxycycline is contraindicated in the 2nd and 3rd trimesters of pregnancy. Pregnant patients should be treated with azithromycin. Evaluate and treat sexual partners (offer expedited partner therapy where available). All partners in the last 60 days OR, if no partners in the past 60 days, the most recent partner Test for common sexually transmitted coinfections All patients: HIV testing, gonorrhoea testing, syphilis testing Men who have sex with men (MSM) diagnosed with chlamydia on a rectal sample: Consider testing for LGV Offer patients counselling on safe sex practices including HIV PrEP where appropriate. Advise patients to abstain from sexual intercourse until all the following criteria are met: Completion of a 7-day regimen or for 7 days after a single-dose regimen Symptom resolution All sexual partners have completed treatment Antibiotic therapy When possible, provide the complete regimen and administer the first dose at the time of visit. Recommended regimens are; 1. 2. Non – pregnant individuals; First line: doxycycline Alternative: azithromycin or levofloxacin Pregnant Preferred: azithromycin Alternative: amoxicillin Patients with gonorrhea coinfection should be treated with oral doxycycline plus a single dose of intramuscular ceftriaxone. Follow up 1. 2. Pregnant patients: Perform a test of cure at 4 weeks Repeat after 3 months Individuals with ongoing risk factors for STIs should also be screened for chlamydia in the third trimester. Non – pregnant patients: - - Consider retesting at 4 weeks if any of the following are present.  Persistent symptoms  Concern for reinfection  Concern for poor adherence to treatment regimen Otherwise retest at 3 months Complications - PID Infertility Ectopic pregnancy Chronic pelvic pain Fitz – Hugh – Curtis syndrome Gonorrhea Gonorrhea is a sexually transmitted disease caused by the bacterium Neisseria gonorrhoeae that leads to genitourinary tract infections such as urethritis, cervicitis, pelvic inflammatory disease (PID) and epididymitis. The disease primarily affects individuals between 15–24 years of age and has an incubation period of 2–7 days. Etiology - Neisseria gonorrhea: gram negative, intracellular, aerobic, diplococci. Transmission: sexual and perinatal Risk factors: - Risky sexual behaviour like lack of barrier protection and multiple partners Asplenia, complement deficiencies. MSM Low socioeconomic groups Clinical features 1. 2. 3. 4. 5. 6. Urethritis: purulent urethral discharge that is yellow – green, possibly blood tinged Dysuria Increased urinary frequency Cervicitis: purulent yellow malodorous cervical discharge, cervical pain and bleeding on manipulation PID: fever, abdominal pain, dyspareunia, abnormal intermenstrual bleeding, Fitz – Hugh – Curtis syndrome Bartholinitis: pain, edema and discharge of the labia. Extra genital manifestations: 1. 2. 3. Pharyngitis (sore throat, pharyngeal exudate, cervical lymphadenitis) Proctitis Purulent discharge, possible anorectal bleeding and pain Rectal mucosa inflammation Rectal abscess (less common) Gonococcal conjunctivitis: may affect adults or neonates Disseminated gonococcal infection: Two distinct clinical presentations are possible Diagnostics 1. 2. 3. 4. 5. Specimens for testing include; First catch urine Swab specimens: urine, urethra, endocervix, pharynx For DGI: collect blood and synovial fluid (gained via arthrocentesis) Test of choice: NAAT Alternatives Gonococcal gram stain Gonococcal culture: useful in determining antibiotic resistance but has lower sensitivity than NAAT. Additionally, for arthritis: synovial fluid analysis which may be clear (non-purulent) or cloudy (purulent) with leukocyte count especially with segmented neutrophils. Screening for gonorrhea: Annual NAAT screening for sexually active women < 24 y/o, women > 24 years with risk factors. Evaluate for other STI’s. Treatment 1. 2. 3. 4. Uncomplicated gonorrhea First line: single dose ceftriaxone IM. In case chlamydia hasn’t been ruled out, add doxycycline PO twice a day for 7 days, or during pregnancy, add single dose azithromycin. Complicated gonorrhea: single dose ceftriaxone IM plus doxycycline PO for 10 -14 days. DGI: ceftriaxone IV every 24 hours for 7 days plus chlamydia prophylaxis. Then drain purulent joints. In all patients, evaluate and treat the sexual partners from the past 60 days. Treat the patient’s sexual partners with a single dose ceftriaxone IM Provide expedited partner therapy if the timely evaluation of sexual partners is not feasible. Complications: - Hymenal and tubal synechia, tubal motility disorders > infertility. Gonococcal conjunctivitis particularly in neonates DGI DISCUSS INFERTILITY (Define, classify, causes from both genders, investigations, diagnosis and management) Infertility is generally defined as the inability to achieve pregnancy despite regular unprotected sex after atleast one year in women under 35 years of age and after 6 months in women 35 years of age and over. - Primary infertility: infertility in persons who have never achieved pregnancy Secondary infertility: infertility in persons who have previously achieved atleast one pregnancy Recurrent pregnancy loss is the inability of a woman to carry to live birth even if conception is possible, due to myomas, antiphospholipid syndrome, etc Female infertility 1. 2. 3. System conditions: thyroid disorders, diabetes, hypertension, obesity, Cushing syndrome and chronic diseases. Ovary related causes: menstrual cycle abnormalities like functional hypothalamic amenorrhea, hyperprolactinemia, premature ovarian failure, pituitary adenoma, diminished ovarian reserve, PCOS and hypogonadotropic hypogonadism. Tubal / pelvic causes: PID, endometriosis, fallopian tube adhesions and / or obstruction. 4. 5. 6. Uterine causes: anatomical anomalies like septate and bicornuate uterus, uterine leiomyoma, endometrial polyps, asherman syndrome (mostly iatrogenic, scarring and fibrosis reduces the sensitivity of the endometrium to progesterone). Cervical causes: trauma, immune factors, DES exposure in utero and cervical anomalies Psychiatric causes: vaginismus, sexual arousal disorder Diagnostics 1. 2. 3. 4. Medical history of both partners especially gynaecological history Access ovulatory function Menstrual history Body temperature analysis to monitor menstrual cycle Hormone tests  Midluteal serum progesterone levels: progesterone should increase shortly after ovulation > failure to progesterone levels to rise indicates anovulation.  Ovulation prediction test to detect LH levels  Androgen levels: elevated levels induce negative feedback to the hypothalamus > inhibition GnRH secretion > decreased estrogen levels and suppression of ovulation  Ovarian reserve; early follicular FHS levels, early follicular estradiol levels and anti – Mullerian hormone levels  TSH levels  Prolactin levels Ovarian sonography: antral follicle count Endometrial biopsy: usually performed 1-3 days before menstruation to determine the thickness of the endometrium. A flat endometrium lining indicates a defect in the luteal phase of the menstrual cycle. Imaging: to assess the patency of fallopian tubes and uterus. Hysterosalpingography: an imaging technique involving the injection of contrast dye into the cervical canal and serial radiographs to evaluate the uterine cavity and morphology/patency of the fallopian tubes. Sonohydterosalpingography: an ultrasound technique in which fluid is inserted into the uterus via the cervix to examine the uterine lining. Examine cervix: physical examination, pap smear and testing for antisperm antibodies. Treatment 1. 2. 3. 4. Lifestyle modifications: cessation of alcohol, nicotine and recreational drug use as they contribute to subfertility. Treatment of underlying causes: levothyroxine for hypothyroidism, metformin for PCOS Ovulation induction Clomiphene citrate GnRH (pulsatile): stimulation of FSH and LH release > follicle maturation Gonadotropins (recombinant HCG, recombinant LH): stimulate final oocyte maturation > ovulation Tamoxifen; selective estrogen receptor modulator GnRH antagonists Assisted reproductive technology In vitro fertilization  The most common form of assisted reproduction technology  Involves hormonal follicular stimulation followed by a transvaginal follicular puncture for oocyte retrieval with ultrasound monitoring.  The recovered oocytes are mixed with processed spermatozoa and incubated  Two (in young women) to a maximum of five embryos (in > 40 years) are transferred into the uterus Intracytoplasmic sperm injection   - A form of in vitro fertilization A single spermatozoon is introduced into an oocyte under a microscope using an injection pipette, after which the same procedure is followed as described for in vitro fertilization. Intrauterine insemination: a procedure in which washed and concentrated sperm are introduced directly into the uterine cavity Complications Ovarian hyper stimulation syndrome: a potentially life threatening complication of ovulation induction with exogenous hcg. - Exogenous hCG is thought to be responsible for the massive luteinisation of the ovarian granulosa cells. Formation of multiple ovarian follicles and corpus luteum cysts with rapid ovarian enlargement. ↑ Release of vasoac ve mediators (e.g., VEGF) that induce an increase in capillary permeability and consequent third spacing into the abdominal cavity. Clinical features: the onset is between 3 days (early onset) and > 9 days (late onset) after hcg administration. - Abdominal pain and distention Nausea and vomiting Weight gain Ascites Oliguria or anuria Dyspnea Syncope Venous thrombosis Laboratory analysis indicates leucocytosis and elevated HCT. Check serum electrolyte concentrations, renal function tests and liver function tests. A transvaginal ultrasound may indicate ascites and ovarian enlargement. Management 1. 2. Mild to moderate cases are managed as outpatients. These are usually early onset cases. Limit physical activity Pain management with paracetamol Daily monitoring of body weight and urine output. Body weight should not increase by more than 1kg/day. Sufficient hydration of 1-2L/day Paracentesis to relieve symptoms of ascites. Severe cases (usually late onset) Hospitalization Multidisciplinary management approach: supportive care, monitoring and prevention of complications. Male infertility 1. 2. 3. 4. 5. 6. 7. Chronic conditions: liver cirrhosis and renal insufficiency Sperm disorders: reduced sperm count, impaired motility and reduced ejaculate volume. Testicular causes: scrotal injuries, testicular torsion, infections like mumps, scrotal hyperthermia, cryptorchidism Medication: anabolic steroids, spironolactone, corticosteroids, cimetidine Endocrine causes: thyroid disorders, hyperprolactinemia, pituitary and hypothalamic tumours Inherited causes: Klinefelter, Kallmann, Y chromosome microdeletion Sexual dysfunction: impaired libido, anejaculation Diagnostics 1. 2. 3. 4. 5. 6. Medical history of both partners Semen analysis Mixed antiglobulin reaction test for antisperm antibodies Antisperm antibodies form in disruption of the blood – testis barrier The antibodies can lead to immobilization and agglutination of sperm or have a spermatotoxic effect TSH levels Prolactin levels Karyotype test (Klinefelter syndrome) Treatment 1. 2. 3. 4. 5. Treatment of underlying cause Modification of lifestyle factors such as alcohol, nicotine and recreational drug use Medical therapy: clomiphene citrate, tamoxifen Assisted reproductive therapy Surgical treatment of testicular anomalies or defects DISCUSS PHYSIOLOGY OF CONTRACEPTIVE METHODS, FACTORS TO CONSIDER AND COMMON SIDE EFFECTS