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Flashcards in Female Genital Tract Deck (87)
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HSV Infection

  • red papules 3-7 days post contact.
  • progress to vesicles and painful, coalescent ulcers associated with fever, malaise, tender lymphadenopathy.
  • spontaneously heal within 1-3 wks but remains latent in lumbrosacral ganglia, reactivated during stress, trauma, immunosuppression, hormonal changes.
  • dx: clinical findings, viral cultures.
  • tx: antiviral agents to shorten.
  • can be transmitted to baby.


Molluscum Contagiosum

  • poxvirus infection of skin and mucous membranes.
  • type I = most common.
  • type II = most sexually transmitted.
  • 6wk intubation ⇒ dimpled, dome-shaped lesions.  contain cells with intracytoplasmic viral inclusions.


Fungal Infections

  • yeasts are part of vaginal flora.
  • expand when ecosystem disrupted = diabetes, antibiotics, pregnancy, immunosuppression.


Trichomonas Vaginalis

  • flagellated protozoan transmitted via sex.
  • asymptomatic or present with yellow, frothy vaginal discharge, vulvovaginal discomfort, dysuria, or dyspareunia.


Gardnerella Vaginalis

  • gram (-) bacillus, major cause of bacterial vaginitis.
  • presentation: thin, green-gray, fishy-smelling discharge.
  • can precipitate premature labor.


Pelvic Inflammatory Disease

  • from infections that arise in vulva or vagina and ascend to involve other genital tract structures.
  • causes: Gonococcus>Chlamydia>Staph, strep, coliforms, Clostridium perfringens.
  • gonococcal spread via mucosal surfaces, cause acute suppurative rxn
  • non-gonococcal distributed thru lymphatics and veins.
  • presentation: pelvic pain, adnexal tenderness, fever, vaginal discharge.
  • complications: peritonitis and bacteremia, tubal scarring and obstruction, infertility, ↑ risk of ectopic pregnancy, pelvic pain, GI pelvic adhesions cause intestinal obstruction.


Bartholin Cyst

  • from occlusion of draining ducts by inflammation.
  • lined by flattened epithelium, can be large (3-5cm) and painful.
  • can make abcesses needing drainage.
  • tx: excision, marsupialization (permanent opening).



  • opaque, white, plaque-like thickenings
  • accompanied by pruritus and scaling.


Lichen Sclerosus

  • papules or macules that coalesce into smooth, white parchment-like areas.
  • epidermal thinning, superficial hyperkeratosis, dermal fibrosis with scant mononuclear perivascular infiltrate.
  • labia can become atrophic, stiffened, with constricted vaginal orifice.
  • usually autoimmune.


Squamous Cell Hyperplasia

  • aka lichen simplex chronicus.
  • non-specific resopnse to recurrent rubbing or scratching to relieve pruritus.
  • white plaques, thickened epithelium, hyperkeratosis, dermal inflammation.
  • often present at margins of vulvar carcinoma.


Vulvar Fibroepithelial Polyps

  • skin tags


Squamous Papillomas (Vulva)

  • benign exophytic proliferations lined by non-keratinizing squamous epithelium.
  • single or numerous (vulvar papillomatosis).


Condyloma Acuminatum

  • verrucous lesions on vulva, perineum, vagina, and cervix (rare).
  • sexually transmitted via HPV types 6 and 11.
  • make sessile branching epithelial proliferations of stratified squamous epithelium.
  • koilocytotic atypia = perinuclear cytoplasmic clearing with nuclear atypia in mature superficial cells.


Vulvar Intraepithelial Neoplasia and Carcinoma

  • 3% female genital cancers.  women >60yrs.
  • 1/3 basaloid or warty carcinomas related to HPV infection.
  • 2/3 keratinizing squamous cell carcinoma unrelated to HPV.
  • verrucous carcinoma and basal cell carcinoma locally aggressive but rarely metastasize.


Keratinizing Squamous Cell Carcinoma

  • in setting of long-standing lichen sclerosus or squamous cell hyperplasia.  
  • pre-malignant lesion = differentiated VIN, has basal atypia with normal superficial epithelial maturation and differentiation. 
  • morphology: nodules with vulvar inflammation.
    • infiltrating nests and tongues of malignant squamous epithelium, prominent keratin pearls.


Basaloid and Warty Carcinomas

  • from precancerous in situ lesions = classic vulvular intraepithelial neoplasia (VIN), aka Bowen Disease.

    • positive for HPV type 16.

  • morphology: VIN = discrete hyperkeratotic, flesh-colored or pigmented slightly raise plaques.

    • multicentric with marked nuclear atypia, no maturation.

    • basaloid carcinoma = exophytic or indurated, ulceration.  nests and cords of small, tightly packed cells resembling immature basal cells.

    • warty carcinoma = exophytic with prominent koilocytic atypia.



Papillary Hidradenoma

  • benign, arises from modified apocrine sweat glands.
  • presentation: sharply circumscribed nodule of tubular ducts lined by non-ciliated columnar cells atop a layer of flattened myoepithelial cells.


Extramammary Paget Disease

  • malignant.  red, crusted, sharply demarcated, map-like area.
  • large, anaplastic, mucin-containing tumor cells in single layer or small clusters in epidermis and appendages.
  • confined to epidermis, invasion rare.
  • high recurrence rate.


Malignant Melanoma (Vulvar)

  • <5% vulvar malignancies, <2% female melanomas.
  • peak incidence btw ages 60-80.
  • 5 yr survival = <32% from delayed detection, rapid progression.


Septate Vagina

  • with a double uterus and is from failure of complete fusion of mullerian ducts.
  • causes: genetic syndromes, in utero exposure to diethyl-stilbestrol (DES), abnormalities of epithelial-stroma signaling in fetal development.


Vaginal Adenosis

  • red, granular patches of remnant endocervical-type columnar epithelium that weren't replaced by normal squamous epithelium of vaginal mucosa.
  • in 35-90% women exposed to in utero DES.
    • can be substrate for clear cell carcinoma.


Benign Vaginal Tumors

  • typically in reproductive-age women.
  • stromal polyps, leiomyomas, hemangiomas.


Vaginal Squamous Cell Carcinoma

  • primary vaginal carcinomas rare.
  • associated with high risk HPV infections.
  • arise from vaginal intraepithelial neoplasia (VIN).
    • analogous to VIN in cervical carcinoma.
  • most affects upper posterior vagina.


Embryonal Rhabdomyosarcoma

  • aka sarcoma botryoides.
  • highly malignant, uncommon. 
  • infants and kids, made of embryonal rhabdomyoblasts.
  • polypoid, bulky masses made of grapelike clusters, protrude from vagina.
  • tumor cells small, oval nuclei, small eccentric cytoplasmic protrusions.
  • invade locally, cause death by penetrating into peritoneum or obstructing urinary tract.


Acute Cervicitis

  • normal pH is below 4.5,  higher pH, from douching, bleeding, or sex, can lead to overgrowth by pathogens (acute cervicitis/vaginitis).
  • pH kept low by H2O2 and lactic acid.


Chronic Cervicitis

  • found at low level in all women.
  • infections with gonococci, chlamydiae, mycoplasms, HSV ⇒ significant acute/chronic cervicitis, lead to upper genital tract disease, complications with pregnancy.
  • can have abnormal cytologic smears from marked cervical inflammation causing reactive and reparative epithelial changes.


Endocervical Polyps

  • benign exophytic growths in 2-5% women.
  • presentation: irrgeular vaginal spotting.
  • come from endocervical canal, are soft mucoid lesions made of loose CT stroma with dilated glands and inflammation, covered by endocervical epithelium.


Cervical Carcinoma

  • pre-cancerous lesions well detected by Pap smear.
  • pathogenesis: risk factors = HPV types 16, 18, multiple partners, host immune response.
    • most HPV asymptomatic, 50% cleared in 8 months, 90% by 2 yrs.  persistent infection ↑ risk of malignancy.
    • HPV = DNA virus infecting immature basal cells of squamous epithelium or metaplastic squamous cells at cervical squamocolumnar junction.
    • have koilocytotic change in non-proliferating squamous cells where HPV replicates.
    • interferes with p53 and Rb via viral E6 and E7 proteins that cause:
      • ↑ cyclin E expression via E7 ⇒ ↓ RB
      • stop apoptosis via E6 ⇒ ↓ p53
      • centrosome duplication and instability via E6 and E7
      • ↑ telomerase expression via E6
    • all HPV ↑ proliferation and life span of infected cells.
    • 80% squamous cell, 15% adenocarcinoma, 5% adenosquamous or neuroendocrine.
    • peak incidence of invasive is 45 yrs.
  • morphology: exophytic or infiltrative.
    • squamous = keratinizing or not.
    • adenocarcinomas = glandular but mucin depleted.
    • adenosquamous = made of intermixed malignant squamous and glandular elements.
    • neuroendocrine = resemble small cell malignancy of lung.
  • presentation: early tx by cervical cone biopsy.  then hysterectomy and lymph node dissection, irradiation.
    • microinvasive = 95% 5 yr survival.
    • most advanced = <50% 5 yr survival.
      • neuroendocrine have poor prognosis.


Cervical Intraepithelial Neoplasia

  • precancerous epithelial changes, 2 types:
  • low grade squamous intraepithelial lesions (LSIL): 80% have high risk HPV (type 16).
    • mild dysplasia in basal layers of epithelium. no significant alteration of cell cycle. 
    • 60% regress within 2 yrs, 30% persist, 10% ⇒ HSIL.
    • not considered precancerous lesion.
  • high grade squamous intraepithelial lesions (HSIL): 100% associated with high risk HPV (type 16).
    • moderate to severe dysplasia, involves more of epithelium, includes carcinoma in situ.
    • HPV deregulates cell cycle (↑ proliferation, ↓ epithelial maturation, ↓ viral replication).
    • 30% regress over 2 yrs, 60% persist, 10% progress to carcinoma within 2-10 yrs.
  • morphology: LSIL = atypia only in basal third of epithelium.
    • HSIL = atypia extends to 2/3rds  or more of epithelial thickness.


Cervical Cancer Screening and Prevention

  • Pap test has false negative rate btw 10-20%.
  • can add HPV DNA testing.
  • abnormal pap followed up by colposcopic exam with biopsies.
  • LSIL lesions followed, HSIL treated with cervical cone and life-long follow up.
  • prophylactic vaccine against HPV types 6 and 11 (condylomas) and 16 and 18 (cervical cancer) reduce incidence of HSIL.