Vulval itch and Pathology Flashcards

1
Q

Differential diagnosis for Vulval itch

A
  • Lichen sclerosus
  • Dermatoses: Lichen simplex chronicus, Lichen planus
  • Vulval intraepithelial Neoplasia
  • Vulval carcinoma
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2
Q

Lichen Sclerosus History

A
  • Most common in postmenopausal women
  • severe non resolving itch
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3
Q

Lichen sclerosus Examination findings

A
  • Thin, wrinkly skin
  • Pearly white appearance
  • May be hyperkeratotic if concurrent squamous hyperplasia
  • Bilateral and symmetrical
  • Localised or figure 8 lesion
  • Does not extend into vagina or anus
  • Shrinkage of introitus with loss or fusion of labia minora
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4
Q

Lichen slerosus investigation

A

Biopsy: Epidermal atrophy
- hyalinisationof dermis
- underlying lymphocytic infiltrate

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5
Q

Lichen sclerosus treatment

A
  • Topical steroids and emollients
  • Start with potent or very potents for relief and then change to less potent or decrease frequency of use
  • 1% Hydrocort Mild
  • Potent: Betamethasone 0.1%
  • Very potent: Clobetasol propionate 0,05% or diflucorolone valerate 0,3%

No benefit to topical Oestrogen or testosterone identified
Nil Justification for surgery other than occasional separation of labial adhesions

NB: Longterm follow up every 6-12 months due to 2-5% risk of developing vulval carcinoma (Unsure re pathophys)

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6
Q

Lichen simplex chronicus Examination

A
  • dry scaly skin
  • non symmetrical
  • fissures due to scratching
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7
Q

Lichen Simplex Chronicus Treatment

A

Emollients and low potency steroids
Nigh sedation to avoid scratching

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8
Q

Lichen Planus examination

A
  • purple patches which become white
  • Wickhams striae which form a lacy white pattern
  • Also present on flexor aspects of wrists, gingival margins and oral mucosa
  • Can extend into vagina with adhesions and stenosis
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9
Q

Lichen planus diagnosis

A

Clinical diagnosis
Biopsy is non specific

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10
Q

Lichen planus treatment

A

Topical steroids
Systemic steroids and intravaginal steroids may be necessary

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11
Q

Psoriasis

A

Pink with irregular borders with satellite lesions
Rx with topical steroids

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12
Q

Vulval intraepithelial Neoplasia

A
  • Squamous premalignant lesion
  • Aietiology is oncogenic HPV
  • Risk factors; Smoking, immunosuppresion with HIV or medication, lichen sclerosus
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13
Q

VIN History

A
  • May occur in young women
  • Pruritis
  • Pain
  • Could be asymptomatic
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14
Q

VIN Examination

A
  • Variable appearance
  • white lesion if hyperkeratosis
  • Red lesion if thin skin
  • Brown due to increased Melanin
  • Raised papular and rough or macular with indistinct border
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15
Q

VIN investigation

A
  1. Histology: Lack of differentiation with disordered maturation
    - hyperchromatic
    - increased mitotic figures
    - increased nucleus to cytoplasm ratio
    occurs in original epithelium rather than metaplastic tissue as in the cervix. Nil TZ
    - Low risk of progression to invasive disease 6%
  2. Vulvoscopy : 5% acetic acid to reveal lesions and perform biopsy
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16
Q

VIN management

A
  1. Local excision: High recurrence rate. Reserved for florid lesions
  2. Topical Imiquimod widely used
  3. Laser ablation
  4. Long term follow up NB
    Be alert to signs of progression:
    - Ulceration
    - bleeding
    - swelling
    - soreness
    - Irritation
    Most progression will occur within 10 year of dx
17
Q

VIN classification

A
  • Vulval LSIL: Flat condyloma or HPV effect
  • Vulval HSIL
  • VIN: Differentiated type
18
Q

Vulval Carcinoma History

A
  • Predominantly older women with 80% > 65 years
  • rare
  • Pruritus of vulva
  • History of ulcer or mass
  • Bleeding
    Aetiology is that develops from range of skin abormalities
  • Lichen sclerosis: 66% of vulval CA occurs with history of Lichen Sclerosis although 2-5% LS develops into Vulval Ca
  • Vulval SIL- Secondary to oncogenic HPV
  • Pagets disease: Preinvasive lesion for adenoCa of vulva. 4-8% may be associatd with primary adenoCa elsewhere
  • Lichen planus: RARE
19
Q

Vulval Ca Examination

A
  • Ulcer
  • mass
  • labia Majora most common site, then minora, clitoris, posterior forchette, perineum and Bartholins gland
  • NB to chec Cervix for co-existing CIN or Cervix CA
20
Q

Vulval Ca examination

A
  • Biopsy of lesion to confirm diagnosis and depth of invasion
  • MRI: Check LN involvements
21
Q

Vulval Ca Management:

A
  • mainstay is surgery
    Depends on stage and LN involvement which is large determinant in survival rates

Nil Node involvement survival >90%
If nodes positiveL <60%

Should be managed By Gynae onc led MDT team
- stage 1a: WLE aim for margins >1cm
- Stage 1B- 4a: radical vulvectomy and bilateral groin node dissection via Separate incisions

Consider sentinel node mapping and if FZ negative then nil groin node dissection to reduce wound breakdown, lymphocyst formation and lymphoedema of lower limbs

  • Lateral lesions: Modified radical vulvectomy confined to affected side with ipsilateral GN dissection: If nodes clear: Leave other side GN. If positive: Dissect other side as well
  • Stage 3: Due to urethral or anal spread: Include incision of distal urethral or anus with Colostomy and GN dissection
  • Adj RadioRx if Nodes involved
  • May use Chemoradiation to avoid stomas: morbidity includes skin desquamation and pain
  • Stage 3 with unilateral nodes: Adj radiation to groin
  • Stage 4a: Local extension to pelvic cavity
  • Groin node dissection and radical exenterive surgery if nodes clear
  • 4a due to pelvic nodes or 4B;
  • poor prognosis
  • focus on disease control
  • may include surgery +/- radiation
  • Need to consider psychosecual morbidity