24 May 2009

Vulvar Lesions



Vulvar Lesions
Presentation by:Anna Mae Smith, MPAS, PA-C
Lock Haven University

Anatomy
* Mons pubis
* labia majora and minora
* clitoris
* vestibule
* urethral meatus
* It covers and protects the entrance to the vagina, vestibule, and urethra.

Vulvar Hygiene
* use mild, nondrying soap
* washing underwear with mild soap and rinsing well
* 100% cotton underwear
* avoid extra layers and tight slacks (unneeded medicines, tinted toilet tissue, all "feminine hygiene" products), excessive sweating without aeration, and public pools and hot tubs
* It is important to be keenly conscious of what "aggravates" the skin.
* A dermatologic cliche is to "dry wet lesions" (soaks and compresses) and "moisturize dry lesions" (creams and ointments).

Vulvar Cancer
* 4th most common site of gynecologic neoplasia
* Squamous neoplasia most common type of neplasia
* HPV (16,18) infections are most commonly associated with squamous cell changes of the vulva, vagina & cervix. However the vulva tends to be more resistant to oncogenesis

Histopathology of Vulvar Neoplasia
* Squamous
* Malignant melanoma
* Sarcoma
* Basal Cell
* Adenocarcinoma
* Paget’s Disease
* Undifferentiated


Classification of VIN
* VIN I - mild dysplasia with hyperplastic vulvar dystrophy with mild atypia
* VIN II - Moderate dysplasia, hyperplastic vulvar dystrophy with moderate atypia
* VIN III - Severe dysplasia, carcinoma in situ, Bowen’s Dz; hyperplastic vulvar dystrophy with severe stypia


Spread of vulvar Ca
* Local growth with extension to the perineum, anus, urethra, vagina & pelvic bone
* Lymphatics - inguinal & femoral nodes to the external iliac, common iliac, & para-aortic chains

Paget’s Disease
* presents with extreme pruritus and soreness, usually of long duration
* red or bright pink, desquamated, exzematoid areas among scattered, raised, white patches of hyperkeratosis
* borders are well demarcated and raised

Basal Cell Carcinoma
* very rare
* associated with a long history of pruritus
* occurs over the anterior two-thirds of the labia majora, with slightly elevated margins
* appears as condyloma
* does not respond to treatment for HPV

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VULVODYNIA



VULVODYNIA
Clinical Aspects and Research Initiative
Presentation by:Gloria A. Bachmann, M.D. and Nidhi Gupta, M.D.
Women’s Health Institute, UMDNJ-Robert Wood Johnson Medical School


Defining Vulvodynia
The International Society for Study of Vulvovaginal Diseases (ISSVD) defines vulvodynia as ‘chronic vulvar discomfort, characterized by the woman’s complaint of burning, stinging, irritation or rawness’

Types of Vulvar Pain
* PAIN from an IDENTIFIABLE ETIOLOGY
* VULVODYNIA

Pain from an Identifiable Etiology
* Infections such as chronic vulvovaginitis caused by Candida or other pathogens
* Dermatoses and Dermatitis that involve the vulva such as Lichen Sclerosus, Lichen Planus, irritants and allergic dermatitis
* Vaginismus

Vulvodynia: Vulvar Vestibulitis Subtype
* Friedrich’s criteria diagnostic:
* 1. Severe pain on vestibular touch or attempted vaginal entry.
* 2. Tenderness to pressure localized within the vulvar vestibule
* 3. Physical findings confined to vestibular erythema of various degrees
* Pain is provoked and localized
* Commonly seen in women aged 50 years or less

Dysesthetic Vulvodynia Subtype
* Pain is constant and may be felt beyond the confines of vulvar vestibule
* Usually pain is unprovoked
* Diagnosed mainly in women who are peri- or postmenopausal

Vulvodynia: Prevalence Statistics
* Harvard-based study (n=16,000) estimates a 16% life time prevalence*
* UMDNJ-based study estimates:

Vulvodynia: Demographics
* Older data suggest the highest prevalence in white women
* Accounts for 10 million doctor visits/year
* Upwards of 14 million women are affected in their lifetime
* Recent data suggest Hispanic women 80% more likely to have vulvar pain than other racial groups

Etiology: Vulvar Vestibulitis Subtype
* Prior vulvovaginal Candidiasis
* Hypersensitivity to chemicals
* Human Papilloma virus infection
* High levels of urinary oxalates
* Neurological dysfunction

Candida Etiology: Vulvar Vestibulitis Subtype
* In 1989 Ashman and Ott proposed cross reaction between Candida albicans antigens and self-antigen in vulvovaginal tissue
* Affected tissue has locally elevated concentrations of inflammatory cells and pro-inflammatory cytokines
* These suggest a hyper-immune response, possibly from persistent antigen from the Candida

Proposed Etiologies: Vulvar Vestibulitis Subtype
* Calcium oxalate crystals in urine may act as irritant to the vulva
* Reduced estrogen receptor expression causing alteration in vulvar sensation*
* CNS etiology, similar to other regional pain syndromes

Proposed Inflammatory Etiology: Vulvar Vestibulitis Subtype
* An inflammatory event releases cytokines that sensitize nociceptors in the nerve fibers of the vulva*
* Increased intraepithelial nerve endings in vestibulitis patients have been reported. Prolonged neuronal firing sensitizes neurons in dorsal horn of spinal cord, with subsequent abnormal interpretation as pain from touch**

Etiology: Dysesthetic Vulvodynia Subtype
* Etiology not definitively known
* Childhood trauma and OCP’s possible contributors
* Sympathetic pain loops caused by repeated irritation/trauma leads to continuous vulvar symptoms*

Vulvodynia: Assessment of the Patient

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Pathology and Neoplasia



Pathology and Neoplasia

1. Describe the pathogenesis and epidemiology of the common nonmalignant neoplasms that affect the external and internal genitalia.
2. Describe the role of oncogenes in the pathogenesis of premalignant lesions of the external and internal genitalia.


Lesions of the Vulva
* Dermatological conditions
* VIN
* Condyloma acuminatum

Condyloma
* Nevus
* Psoriasis
* Seborrheic Dermatosis
* Hidradenitis Suppurativa
* Lichen planus
* Lichen Sclerosis
* Lichen Simplex Chronicus
* Urethral Diverticulum or Caruncle
* Cysts
* Trauma
* Vaginal intraepithelial neoplasia (VAIN)

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