Female Genitalia Path Flashcards
Herpes simplex clinical symptoms
Clinical symptoms will occur in ~1/3 of affected individuals
- lesions 3-7 days after intercourse
- painful red papules in vulva vesicles ulcers (contain virus particles)
- leukorrhea (white discharge) when cervix or vagina is involved
- systemic symptoms: fever, malaise, tender inguinal lymph nodes
Herpes simplex lesions & transmission
lesions heal spontaneously in 1-3 weeks, but infection remains latent in the regional nerve ganglia
-2/3 women suffer recurrence
transmission is possible whether active or latent phase
-greatest danger is to the neonate during birth
*may result in fatal systemic infection
-risk greatest during primary, active infections
Mycotic and yeast (Candida)
manifests as small white patches, leukorrhea, pruritus
10% of women are carriers
diabetes mellitus, oral contraceptives, and pregnancy promote development of infection
diagnosis: wet mount or culture
Trichomonas vaginalis
causes purulent discharge and discomfort "strawberry cervix" seen in 15% of women at STD clinics frothy discharge due to Trichomonas infection “strawberry cervix”
Bacterial vaginosis
most common vaginal infection in women of childbearing age
imbalance of bacterial flora, favoring harmful types
risk factors: multiple partners, douching, pregnancy, smoking
Bacterial vaginosis symptoms
signs/symptoms: fish-like odor; gray discharge; burning/itching; frequently asymptomatic
especially important to treat during pregnancy: associated with PROM/premature birth
may ascend and cause pelvic inflammatory disease
Bacterial vaginosis Amsel’s criteria
diagnosis by Amsel’s criteria (3 of the following):
microscopic “clue cells“
fishy odor on adding 10% KOH to secretions
vaginal pH > 4.5
thin homogenous discharge
Pelvic Inflammatory Disease (PID)
pelvic pain, adnexal tenderness, fever, vaginal discharge
infection by: gonococci, chlamydiae, enteric bacteria
Postpartum and postabortion infections: staphylococci, streptococci, coliform bacteria, Clostridium perfringes
Gonococcal PID
inflammatory changes in affected glands (e.g., Bartholin gland) 2-7 days post inoculation
-acute suppurative reaction; inflammation mainly in the superficial mucosa, submucosa
-cervix involvement
common
organisms may disappear over time; proteolysis of inflammatory cells results in accumulation of serous fluid
treatment: easily controlled with antibiotics in early stages; more difficult if abscesses have formed
Gonococcal PID involves & spares
usually spares endometrium and involves tubes
- acute suppurative salpingitis
- tubal serosa hyperemic; layered with fibrin
- tubal fimbriae leak exudate, the fimbriae seal to the ovary causing salpingo-oophoritis; tubo-ovarian abscess may develop
Postpartum and Postabortion PID
less exudation in tube lumens or mucosa, but greater deep involvement
- infection spreads throughout the wall to involve the serosa, and spreads up the uterus via lymphatics or blood supply
- bacteremia is a frequent complication
treatment: much more difficult to control with antibiotics than gonococcal PID; surgical removal of organs may be necessary
Vulvar Non-Neoplastic Epithelial Disorders (VNED)
spectrum of inflammatory lesions of the vulva
characterized by white, scaly, plaquelike mucosal thickenings that produce vulvar discomfort and pruritus
-biopsy is indicated to distinguish from other diseases
Lichen sclerosus (chronic atrophic vulvitis)
leads to atrophy of labia, subepithelial fibrosis, narrowing of the introitus
most common after menopause
Lichen sclerosus histological features
atrophy of the epidermis (disappearance of rete pegs)
degeneration of basal cells of the epidermis
dermal fibrosis
bandlike lymphocytic infiltrate
unclear pathogenesis; believed to be autoimmune
Lichen simplex chronicus
non-specific condition that results from rubbing or scratching the skin to relieve pruritus
characterized by acanthosis and hyperkeratosis of vulvar squamous epithelium
-epithelium thickened; may show mitotic activity in basal and prickle layers
VNED-associated vulvar cancer
hyperplasia -> cellular atypia -> VIN (= carcinoma in situ) treat with steroids to prevent cancer development
Condyloma Acuminatum (Venereal Wart)
benign papillomavirus-induced squamous lesion with verrucous appearance
-typically caused by HPV types 6 and 11
frequently multiple and coalesce
involve perineal, vulvar, and perianal regions, vagina, sometimes cervix
Condyloma Acuminatum (Venereal Wart) histological
acanthosis, parakeratosis, hyperkeratosis, koilocytosis
-frequently regress spontaneously and not considered to be precancerous lesions (just STD marker)
Carcinoma and Vulvar Intraepithelial Neoplasia (VIN)
1/8th as frequent as cervical cancer
-3% of all genital cancers
most frequent in women 65-75 yoa
-15% in women VIN
Carcinoma and Vulvar Intraepithelial Neoplasia (VIN) most frequent symptom & sign
Most frequent symptom = long history of pruritus
-Less common = vulvar bleeding discharge, dysuria, pain
Most common sign = vulvar lump or mass
-May be fleshy, ulcerated, leukoplakic, or warty
-Most unifocal and on the labia majora
-Expert opinion recommends annual visual inspection of the external genitalia, even if the patient is no longer receiving annual Papanicolaou smears
Vulvar Carcinoma
No diagnostic features – diagnosis based on biopsy alone
Lymphohematogenous dissemination
-Inguinal and femoral nodes metastasis common; rarely pelvic nodes
-Lungs, liver, other internal organs
A rare variant of squamous cell carcinoma is the verrucous carcinoma, which presents as a fungating tumor that resembles condyloma acuminatum (isn’t associated with HPV, however) biopsy any condyloma that doesn’t respond to therapy
Extramammary Paget Disease
Rare lesion of the vulva (sometimes perianal region) similar to Paget disease of the breast
-Manifests as pruritic, red, crusted lesion, usually on labia majora
*Sharply demarcated
*Sometimes with palpable submucosal thickening or tumor
~Prognosis is poor in uncommon cases associated with underlying carcinoma
Extramammary Paget Disease histology
Large tumor cells (Paget cells) distinguished by clear separation (“halo”) from surrounding epithelial cells
-Granular cytoplasm of Paget cells contains mucopolysaccharide that stains with periodic acid-Schiff (PAS)
Malignant Melanoma
Rare (5% of all vulvar cancers) -2% of all melanomas in women Peak incidence in 6th or 7th decade Tumors rapidly enter a vertical growth phase following inception -5-yr survival rate
Bartholin Cyst
obstruction of a Bartholin duct (usually due to preceding infection)
occur at all ages
symptoms: pain, local discomfort
cysts may become large (3-5 cm)
treatment: excision (recurrence likely) or marsupialization (opens the duct permanently)
Vaginal Intraepithelial Neoplasia and Squamous Cell Carcinoma
account for ~1% of malignant neoplasms of female genital tract
-(95% are squamous cell carcinomas)
most associated with HPV greatest risk factor is previous cervical or vulvar cancer
Vaginal Intraepithelial Neoplasia and Squamous Cell Carcinoma
most often affects upper posterior vagina along junction with ectocervix
- usually invades cervix and perivaginal structures by time of diagnosis
- metastasize to iliac and inguinal nodes
symptoms: - irregular spotting, leukorrhea
- may be clinically silent until urinary or rectal fistulas develop
Adenocarcinoma(Clear Cell Carcinoma)
increased frequency in young women whose mothers had been treated with diethylstilbestrol (DES) during pregnancy (for a threatened abortion)
usually in upper anterior wall of vagina (may also occur in cervix)
most commonly discovered between 15-20 yoa
tumors contain vacuolated, glycogen-containing cells (= “clear cell”)
Diethylstilbestrol (DES) during pregnancy
FDA issued advisory in 1971
used by 4 million females between 1938-1971
Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)
uncommon; most frequent in children
Cervicitis
some degree of cervical inflammation may be found in virtually all adult women, and is usually of little clinical significance
inflammations common and associated with mucopurulent to purulent vaginal discharge
-discharge contains white cells, atypical epithelial cells (due to inflammation), and possible microorganisms
*presence of microorganisms IS NOT diagnostic of infectious cervicitis
Endocervical Polyps
innocuous, inflammatory tumors
2-5% of adult women; more common in multiparous
produce irregular spotting or bleeding
cured by curettage or surgical excision; malignant transformation rare (
Cervix: Intraepithelial and Invasive Squamous Neoplasia
Invasive carcinomas of the cervix arise from precursor lesions referred to as CIN (cervical intraepithelial neoplasia)
= SIL (squamous intraepithelial lesion)
Represents a continuum of dysplasia with indistinct boundaries for classification
CIN terminology
Represents the precancerous changes that can be detected by cytologic exam
Spectrum of morphologic changes, ranging from:
CIN I = mild dysplasia; koilocytotic atypia, nuclear enlargement, and hyperchromasia
CIN II = moderate dysplasia; loss of polarity, increased mitotic figures, pleomorphism
CIN III = severe dysplasia (carcinoma in situ)
Important things to remember…
not all lesions start as condylomata or as CIN I; may enter at any point
CIN may regress spontaneously (especially CIN I in young women)
-Among LSIL lesions (= CIN I)
*50-80% regress in adult women
*90% regress in women 13-21
Not all CIN will progress to cancer, but we treat as if it will (especially CIN II/III)
-When it does progress, may take upwards of 20 years
The role of HPV in cervical oncogenesis
HPV is the most important agent in cervical oncogenesis
- “carcinogenic” types = 16 (primarily) and 18
- all other HPV types are “probably” or “possibly” carcinogenic (as defined by WHO) except for types 6 and 11
- A recent PCR test of a large international collection of cervical cancer specimens has shown that HPV DNA is present in 99.7% of cases!!!
risk factors of cervical cancer
cigarette smoking ↑ parity Oral contraceptives? Vit. A or C deficiency host factors
Invasive Carcinoma of the Cervix
Most (~75%) are squamous cell carcinomas
- Occur at any age, but peak incidence is 40-45 years
- Peak incidence of high-grade precancers (CIN II/III) is ~30 yoa
- > 50 yoa in countries with screening programs is rare, as well as
CIN and Cervical Cancer: Cytologic Screening
ACS screening recommendations include:
Screening should begin approximately 3 years after the onset of vaginal intercourse and no later than 21 yoa.
Women who are >70 yoa with an intact cervix and who have had 3 or more consecutive, normal results, with no abnormal cytology in the past 10 years, can elect to cease screening
Cervical screening should be performed annually. At age 30, women who have had 3 consecutive normal cytology results may be screened every 2-3 years (unless immunocompromised or were exposed to DES in utero)
Screening following total hysterectomy for benign gynecologic disease is not indicated, but should be continued in those with subtotal hysterectomy or history of CIN II/III.
WHO is evaluating HPV testing as an adjunct to Pap smear screening
CIN and Cervical Cancer: Histologic Diagnosis
Colposcopic exam
Many Pap smear abnormalities do not signify a precancerous or cancerous lesion
Abnormalities confirmed by punch biopsy
CIN I
CIN lesions characterized by white patches on the cervix after application of acetic acid
CIN and Cervical Cancer: Treatment
CIN I = Pap smear follow-up
CIN II/III = cryotherapy, laser, LEEP (loop electrosurgical excision procedures), cone biopsy
Invasive cancer = hysterectomy and lymph node dissection; radiation if advanced
-Small cell undifferentiated (oat cell) tumors have worst prognosis
CIN and Cervical Cancer: Prevention
Modify risk factors (e.g., cigarette smoking, sexual behavior)
Vaccination with papillomavirus-like particles (VLPs) for a variety of oncogenic types