1.

Infections of lower
Female Genital Tract
start
2. Herpes simplex
virus (HSV)
-typically HSV-2 but can also be HSV-1
-infections present with RED PAPULES 3-7 days after contact; these progress to VESICLES and painful,
coalescent ULCERS associated with fever, malaise, and tender lymphadenopathy
-although lesions spontaneously heal within 1-3 weeks, HSV establishes a latent infection in lumbrosacral
nerve ganglia and can be re-activated by stress, trauma, immunosuppression, or hormonal changes
*Diagnosis
-made on the basis of clinical findings and viral cultures
*ANTIVIRALS - can shorten the duration of symptomatic lesions, but they DO NOT eliminate latent infections
$$ MOST IMPORTANT consequence = transmission to neonate during birth
3. Molluscum
contagiosum
*a POXVIRUS infection of skin and mucous membranes
-type 1 - most common
-type 2 - most often sexually transmitted
*after a 6 week incubation period - characteristic dimpled, dome-shaped lesions erupt; these contain cells with
intracytoplasmic viral inclusions
4. Fungal infections -especially CANDIDIASIS
-common
*yeasts form part of the normal vaginal flora and can expand to cause symptomatic infections when the
characteristic host flora is disrupted (e.g. by diabetes, antibiotics, pregnancy, or immunosuppression)
5. Trichomonas
vaginalis
-flagellated protozoan transmitted by sexual contact
-can be asymptomatic or present with YELLOW FROTHY VAGINAL DISCHARGE, VULVOVAGINAL
DISCOMFORT, DYSURIA, or DYSPAREUNIA
6. Gardnerella
vaginalis
-gram-neg bacillus
*the major cause of bacterial VAGINITIS
-present with a THIN, GREEN-GRAY, FISHY SMELLING DISCHARGE
-such infections can precipitate premature labor
1006-1024
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7. PID *results from infections that arise in the vulva or vagina and ascend to involve the other genital tract structures (e.g.
cervix, uterus, fallopian tubes, and ovaries)
*Symptoms
-pelvic pain
-adnexal tenderness
-fever
-vaginal discharge
$$ GONOCCOCUS is the most important cause $$ followed by CHLAMYDIA and postabortal or postpartum
polymicrobial infections
*Ascending gonococcal infection tend to spread via the mucosal surfaces, eliciting an acute suppurative reaction
*Non-gonoccocal infections -are typically distributed through LYMPHATICS and VEINS
*Peritonitis and bacteremia (with systemic seeding) are COMPLICATIONS
-tubal scarring
-obstruction
-infertility
-increased risk of ectopic preg. **
-pelvic pain
-GI-pelvic adhesions ( fibrous bands that form between tissues and organs, often as a result of injury during surgery.
They may be thought of as internal scar tissue that connect tissues not normally connected.) that can cause intestinal
obstruction
8. Bartholin
Cyst
*common lesions resulting from occlusion of the draining ducts by inflammation
-typically lined by flattened epithelium and can be large (i.e. 3-5 cm) and painful
*TREATMENT - involves excision or permanent opening (marsupialization)
*Bartholin gland infections can also produce abscesses, requiring drainage
9. Lichen
Sclerosus
-lesions begin as papules or macules that eventually coalesce into smooth, white parchment-like areas
*Micro: there is epidermal thinning, superficial hyperkeratosis, and dermal fibrosis with a scant mononuclear
perivascular infiltrate
-the labia can become atrophic and stiffened, with constriction of the vaginal orifice
-an AUTOIMMUNE RESPONSE is implicated
10. Squamous
Cell
Hyperplasia
-aka LICHEN SIMPLEX CHRONICUS
-this is a non-specific response to recurrent rubbing or scratching to relieve pruritus
*characterized by WHITE PLAQUES that histologically reveal thickened epithelium, hyperkeratosis, and dermal
inflammation
-does not exhibit epithelial atypia and there is no increased predisposition to malignancy
11. Condyloma
Accuminatum
*Verrucuous (covered with warts or wart-like projections) lesions on the vulva, perineum, vagina, and (rarely) cervix
that are sexually transmitted by HPV types 6 or 11
*Histo: comprise sessile branching, epithelial proliferations of stratified squamous epthithelium
-mature superficial cells exhibit characteristic perinuclear cytoplasmic clearing with nuclear atypia (koilocytotic atypia)
-not considered pre cancerous
12. Vulvar Intraepithelial
Neoplasia and Vulvar
carcinoma
*Vulvar carcinoma is rare (mostly in women over 60)
-a third of cases are BASALOID or WARTY CARCINOMAS related to HPV infections
-2/3 are KERATINIZING SQUAMOUS CELL CARCINOMA unrelated to HPV
*Prognosis - depends on size, depth of invasion, and lymph node status (regional lymph node metastasis
portends a poor prognosis
-Uncommon variants (e.g. verrucous carcinoma and basal cell carcinoma) are locally aggressive but rarely
metastasize
*basaloid and warty carcinomas - arise from precancerous in situ lesions called CLASSIC VULVULAR
INTRAEPITHELIAL NEOPLASIA (VIN)
-most are positive for HPV16 and are often associated with vaginal and/or cervical HPV-related lesions
*Cancer risk increases with AGE and IMMUNOSUPPRESSION
13. Morphology *Classic VIN lesions
-discrete, hyperkeratotic, flesh-colored or pigmented, slightly raised plaques
-typically multicentric and demonstrate marked nuclear atypia with lack of cellular maturation
*Basaloid carcinoma
-can be exophytic or indurated, often with ulceration
-the tumors are characterized by nests and cords of small, tightly packed cells resembling immature basal
cells
*Warty Carcinoma
-exhibits exophytic architecture with prominent koilocytic (Koilocyte is a squamous epithelial cell that has
undergone a number of structural changes, which occur as a result of infection of the cell by human
papillomavirus) atypia
*Keratinizing squamous cell carcinomas
-arise in the setting of long-standing LICHEN SCLEROSUS or SQUAMOUS CELL HYPERPLASIA
-the immediately pre-malignant lesions are called DIFFERENTIATED VIN, distinguished by basal atypia
with apparently normal superficial epithelial maturation and differentiation
-risk of cancer development is a function of age, extent, and immune status
14. Morphology -these carcinomas typically dev. as nodules in a background of vulvar inflammation
-Histology reveals infiltrating nests and tongues of malignant squamous epithelium with prominent
keratin pearls
15. Papillary Hildradenoma -glandular neoplastic lesion
-benign tumor that arises from modified apocrine sweat glands
-presents as a sharply circumscribed nodule of tubular ducts lined by non-ciliated columnar cells atop a
layer of flattened myoepithelial cells
16. Extramammary Paget
Disease
-this malignant lesion appears as a red, crusted, sharply demarcated, map-like area
*Histo: large, anaplastic, mucin-containing tumor cells lying singly, or in small clusters within the
epidermis and its appendages
-most lesions are confined to the epidermis and invasion is rare, but even with wide excision, there is a
HIGH RECURRENCE RATE
17. Malignant Melanoma -Vulvar Melanomas = less than 5% of all vulvar malignancies and 2% of female melanomas
-peak incidence b/w 60-80 years
*Histo: comparable to melanomas at other sites, although 5 year survival is less than 32% due to delays in
detection and rapid progression to a vertical growth phase
18. Vaginal Dev. Anomalies *Septate Vagina (i.e. double) - accompanies a double uterus and arises from failure of complete fusion
of the MULLERIAN DUCTS
-Causes - genetic syndromes, in utero exposure to diethyl-stilbestrol (DES), or abnormalities of
epithelial-stromal signaling in fetal dev.
*Vaginal adenosis
-reflected by red, granular patches of remnant endocervical-type columnar epithelium that have not
been replaced by the normal squamous epithelium characteristic of adult vaginal mucosa
-It occurs at a low frequency in normal women, but is present in 35-90% of adult women exposed in
utero to DES; in that latter setting, vaginal adenosis can be a substrate for dev. of clear cell carcinoma
19. Vaginal intraepithelial
neoplasia and squamous cell
carcinoma
*PRIMARY vaginal carcinomas are rare
*virtually all are SQUAMOUS CELL CARCINOMAS associated with high risk HPV infection
-these arise from VAGINAL INTRAEPITHELIAL NEOPLASIA, which is analogous to malignant
precursor lesions in cervical carcinoma
$$ the UPPER POSTERIOR VAGINA is the most commonly affected site
20. Embryonal
Rhabdomyosarcoma
-an uncommon, highly malignant vaginal tumor in INFANTS and CHILDREN consisting of
embryonal rhabsomyoblasts
-the tumors are polyploid, bulky masses composed of grapelike clusters that can protrude from the
vagina
-tumor cells are small, with oval nuclei and small eccentric cytoplasmic protrusions
-tumors tend to invade locally and cause death by penetration into the peritoneal cavity, or by
obstructing the urinary tract
21. Cervix Inflammations *Acute Cervicitis
-lactobacilli are part of normal flora and produce lactic acid and hydrogen peroxide that keep the pH
below 4.5
-Higher pH caused by douching, bleeding, and sexual intercourse can reduce H2O2 levels, and
antibiotic therapy can decimate the bacteria --> overgrowth of pathogenic bacteria
*Chronic Cervicitis
-found at a low level in virtually all women; little clinical sig.
-however, infections with gonococci, chlamydiae, mycoplasmas, and HSV can produce sig. acute and
/or chronic cervicitis, and can --> upper genital tract disease and/or complications of pregnancy
22. Endocervical Polyps -benign exophytic growths present in 2-5% of women
-they can present with irregular vaginal "spotting"
-most arise in the endocervical canal and are soft mucoid lesions composed of a loose CT stroma
harboring dilated glands and inflammation, covered by endocervical epithelium
23. Cervical Premalignant and
Malignant Neoplasms
*Pathogenesis
-HPV 16 (60% of cases) and HPV 18 (10% of cases) are most important
-most HPV infections are asymptomatic and do not cause an tissue damage; 50% are cleared within 8
months and 90% by 2 years
**PERSISTENT INFECTION increases the risk of dev. malignancy
*HPV are DNA viruses that INFECT ONLY IMMATURE BASAL CELLS of the SQUAMOUS
EPITHELIUM (through a break in the epithelium) or metaplastic squamous cells at the cervical
squamocolumnar junction
*HSV by comparison, replicate in the maturing, normally non-proliferating squamous cells- must
reactivate the cellular mitotic cycle - does so primarily by interfering with function of the p53 and Rb
tumor suppressors
24. *Cervical Intraepithelial
Neoplasia
Precancerous cervical
epithelial histologic
changes are classified as
___ and ____
1) low-grade squamous intraepithelial lesions (LSIL)
-show only MILD DYSPLASIA, involving the more basal layers of the eputhelium
-while associated with productive HPV infection, there is not sig. alteration of the host cell cycle
-~60% of LSIL spontaneously regress within 2 years, while another 30% persist over that period
-only 10% progress to HSIL, and LSIL does not proceed directly to invasive carcinoma. It is therefore
not treated like a premalignant lesion
2) High-grade squamous intraepithelial lesions
-exhibit moderate to severe dysplasia and involve progressively more of the epithelial thickness
-this category also includes CARCINOMA IN SITU
-There is further HPV-driven deregulation of the cell cycle, with increased proliferation, decreased
epithelial maturation, and diminished viral replication
-~30% of HSIL will regress over 2 years, 60% will persist, and 10% will progress to carcinoma within a
2- to 10-year period
**More than 80% of LSIL and 100% of HSIL lesions are associated with high risk HPV; HPV 16 is the
most common type associated with both
25. Morphology *lesions classified according to distribution of cellular and nuclear atypia, including nuclear
enlargement, hyperchromasia, chromatin granularity, size variation, and koilocytosis
-in LSIL, the atypia is confined to the basal third of the epithelium
-in HSIL, the atypia extends to two thirds (or more) of the epithelial thickness
26. Cervical carcinoma *SQUAMOUS CELL CARCINOMA constitutes 80% of cervical cancers; ADENOCARCINOMA = 15%;
NEUROENDOCRINE and ADENOSQUAMOUS = 5%
-all are associated with HIGH RISK HPV
-PEAK INCIDENCE = 45 years
*Morphology
-Gross - lesions can be exophytic or infiltrative
-Micro - squamous lesions can be keratinizing or non-keratinizing; adenocarcinomas tend to be
glandular but relatively mucin depleted; adenosquamous lesions are composed of intermixed malignant
squamous and glandular elements; neuroendocrine tumors resemble small cell malignancy of the lung
*Clinical features
-early invasive cancer can be treated by cervical cone biopsy, but most are managed by hysterectomy and
lymph node dissection, with irradiation for advanced disease
-Prognosis and survival: 5 year for micro-invasive = 95%; 5 year for advance disease = 50%
-neuroendocrine have poor prognosis
27. Cervical cancer screening
and prevention
-false negative for pap smears is b/w 10-20% largely due to inadequate sampling
-Adjunct HPV DNA testing can be added to the routine cytology screening; positivity for high risk HPV
types mandates more frequent testing
-Abnormal pap smear is typically followed by a COLPOSCOPIC exam with selected biopsies
-LSIL lesions can be followed conservatively
-HSIL pathology is usually treated by cervical conization and life-long follow-up
-Prophylactic vaccines directed against HPV types 6 and 11 (condylomas), and 16 and 18 (cervical
cancer) can markedly reduce the incidence of HSIL but do not eliminate cancer risk from other HPV
types