Disorders of the Vulva and Vagina Flashcards

1
Q

What are vulval symptoms?

A

 Pruritis
 Soreness
 Burning
 Superficial dyspareunia
 Can be due to infection, dermatological disease, malignant/premalignant disease and the vulval pain syndromes
 Skin disease affects the vulva, but rarely in isolation
 Systemic disease can predispose to vulval conditions e.g. DM & thrush

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2
Q

What causes pruritus valvulae?

A

 Infections

o Candidiasis + vaginal discharge, vulval warts (condylomata acuminata), pubic lice, scabies

Dermatological disease

o Any condition especially eczema, psoriasis, lichen simplex, lichen sclerosus, lichen planus and contact dermatitis

 Neoplasia
o Carcinoma

o Premalignant disease (vulval intraepithelial neoplasia, VIN)

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3
Q

How to we investigate pruritus valvulae?

A
  • FBC, ferritin (rule out IDA), TFTs, U&Es, LFTs, HbA1c and blood glucose
  • Vaginal swabs for candida and other infections
  • Refer for patch testing or skin biopsy
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4
Q

Define lichen simples/chronic vulval dermatitis

A

Localised plaque of eczematous inflammation created by repeated scratching/ rubbing of skin.

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5
Q

How does lichen simplex present?

A

Severe intractrable pruritis, especially at night
 Labia major is inflamed and thickened
 Shows hyper- and hypopigmentation
 Sx exacerbated by chemical or contact dermatitis
 Can be linked to stress or low iron stores

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6
Q

How do we manage lichen simplex?

A
  • Identify and avoid precipitating factors.
  • Consider prescribing a potent topical corticosteroid ointment (such as betamethasone), for 1–2 weeks to break the itch scratch cycle and bring the condition under control.
  • Consider prescribing a mildly anxiolytic antihistamine (for example hydroxyzine) for use at night.
  • Recommend an emollient as a soap substitute.
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7
Q

Define lichen planus.

A

Chronic inflammatory condition appearing as erosive glazed or glossy erythematous plaques; bluish purple, shiny, flat topped papules with small white dotes or lines (wickham’s striae). May be loss of vuva architecture and small increased risk of SCC.

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8
Q

What is the aetiology of lichen planus? Who does it affect?

A

May be AI but unknown

Affects all ages and is not linked to hormonal status.

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9
Q

How do we manage lichen planus?

A
  • Refer to secondary care to confirm the diagnosis.
  • Once the diagnosis is confirmed in secondary care, very potent corticosteroids are usually initiated by a specialist. Repeated, intermittent courses of topical steroids may be required for longer-term management.
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10
Q

Define lichen sclerosus.

A

Inflammatory condition affecting anogenital area most often (generally>50). Anywhere between the vagina and the anus can be affected however, vagina spared.

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11
Q

How does lichen sclerosus present?

A

 Autoimmune basis

o May coexist with vitiligo and thyroid disease

 40% develop autoimmune condition

 Typically postmenopausal, can affect young women

 Severe pruritis, worse at night
 Scratching → trauma and bleeding, skin splitting and sx of discomfort, pain and dyspareunia
 Pink white papules which coalesce to form parchment-like skin with fissures
 Inflammatory adhesions → fusion of labia and narrowing of intraoitus

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12
Q

What is the risk with lichen sclerosus?

A

Urinary and sexual problems as the skin tightens in those areas

Vulval carcinoma in 5% cases

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13
Q

How do you investigate lichen sclerosus?

A
  • It is a clinical diagnosis
  • Biopsy would be the gold standard
  • In cases where lesion is steroid resistant tissue biopsy should be done to rule out malignancy
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14
Q

How do we treat lichen sclerosus?

A
  • Refer to secondary care to confirm the diagnosis.
  • Once the diagnosis is confirmed in secondary care, very potent corticosteroids are usually initiated by a specialist. Repeated, intermittent courses of topical steroids may be required for longer-term management.
  • Tell the patient to use emollient soap instead
  • Moisturisers
  • High potency steroid ointments (clobetasol propionate)
  • Topical Calcineurin inhibitors such as Tacrolimus
  • Oral antihistamines
  • Treat co-existing infections e.g. thrush
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15
Q

How do we split vulvar dysaesthesias?

A

 Can be provoked or spontaneous vulvar dysaesthesia

 Subdivided into local (e.g. vestibular) or generalised

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16
Q

What is vulvar dysaesthesia associated with?

A

o Hx of genital tract infection

o Former use of OCP

o Psychosexual disorders

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17
Q

How do vulvar dysaesthesias present?

A

 Spontaneous vulvar dysaesthesia (essential vulvodynia)
o Burning pain
o More common in older patients

 Vulvar dysaesthesia of the vestibule  superficial dyspareunia or pain using tampons

o Younger women

o Exclude intraoital damage

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18
Q

How do we manage vulvular dysaesthesia?

A

amitriptyline or gabapentin sometimes used

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19
Q

What causes vulval infections?

A

 HSV, vulval warts, syphilis and donavanosis may affect the vulva

 Candidiasis

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20
Q

Who is at risk of getting a candidal infection?

A

o DM

o Obese
o Pregnancy
o Abx use
o Immunocomprimised
o Presents with irritation and

soreness of vulva and anus

21
Q

What is a Bartholin’s gland cyst/abscess?

A

 Two glands behind labia minora

 Secrete lubricating mucus for coitus

 Blockage of duct → cyst formation

o Infection with s. aureus or e. coli → abscess formation

22
Q

Who is at risk of a bartholin’s cyst?

A
  • Occurs in young women, with previous STIs
23
Q

How do bartholin’s cysts/abscesses present?

A
  • The worse symptoms are usually associated with an abscess
  • Unilateral vulvul swelling
  • often painless (cyst)
  • Dyspareunia
  • Difficulty walking
24
Q

How do we investigate Bartholin’s gland cyst/abscess?

A

Cyst fluid, cavity swab for microscopy, culture and sensitivity (MC&S)

25
Q

How do we manage Bartholin’s cysts?

A

Small Cyst:

  • Analgesia
  • Warm compress
  • Sitz bath

Symptomatic Cyst:

  • Marsupialisation* with Abx (trimethoprim)
  • OR catheter drainage with Word catheter + Abx (trimethoprim)
  • Surgical excision
  • Silver nitrate cauterisation

Large abscess:

  • Marsupialisation
  • Abx (trimethoprim)

*Marsupialisation: stitches on each side of a drainage incision to create a permanent opening less than 1/4-inch (about 6-millimeter) long. An inserted catheter may be placed to promote drainage for a few days after the procedure and help prevent recurrence)

26
Q

Define intraoital damage.

A

 Commonly after childbirth

 Overtightening, incorrect apposition at perineal repair or extensive scar tissue → superifical dyspareunia

27
Q

How do we manage intraoital damage?

A

 Sx resolve with time

 Too tight → vaginal dilators or surgery (Fenton’s repair)

28
Q

What do vaginal cysts look like? How should they be managed?

A

 Congenital cysts commonly arise in vagina

 Smooth white appearance

 Can be as large as a golf ball – often mistaken for prolapse

 Seldom cause sx

 Excise if dyspareunia

29
Q

Define vaginal adenosis.

A

 Columnar epithelium found in normally squamous epithelium of vagina

 Occurs in women whose mothers received DES (diethylstilboestrol) in pregnancy associated with genital tract abnormalities

30
Q

How should we manage vaginal adenosis?

A

 Can become malignant (clear cell carcinoma of vagina)

 DES exposure in utero → annual screening via colposcopy

 Can occur secondarily to trauma

31
Q

Define vulval intraepithelial neoplasia.

A

presence of atypical cells in vulval epithelium

32
Q

What are the types of VIN?

A

Depending on histological type:

  • Usual type VIN - associated with HPV 16, cigarette smoking and chronic immunosuppression
    • Warty or basaloid SCC
  • Differentiated -type VIN - rarer - associated with lichen sclerosis
    • linked to keratinising SCC of vulva
33
Q

What is the difference in

  • Aetiology
  • Type
  • Clinical appearance
  • Malignancy

between usual type and differentiate type VINs?

A
34
Q

How do VINs present? How do we manage them?

A

Pruritis or pain are common with VIN
 Emollients or steroids may help
 Gold standard – local surgical excision
 Confirm histology and exclude invasive disease
 15% of women have unrecognised invasive disease

35
Q

Describe the epidemiology of vulval carcinomas.

A
  • Over 1000 new vulval cancers are diagnosed each year in the UK.
  • A full time GP is likely to diagnose approximately one person with vulval cancer during their career.
  • Most common in those aged >60
36
Q

Describe the pathology of vulval cancer.

A

Pathology
 95% squamous cell carcinoma
 Rest = melanoma, BCC, adenocarcinoma and others e.g. sarcoma

37
Q

Describe the aetiology of vulval cancer.

A
  • Progression of certain vulval dermatoses
  • Progression of VaIN
  • 60% associated with HPV
  • Majority of SCC (melanoma and BCC are less common)
38
Q

How do vulval cancers present?

A

 History
o Pruritis, bleeding or discharge
o Mass
o Malignancy often presents late – unnoticed lesions or embarrassment
 Examination
o Ulcer or mass
o Most commonly on labia majora or clitoris

o Enlarged, immobile and hard inguinal LN

39
Q

How do vulval carcinomas spread?

A

Vulval carcinoma spreads locally and via LN
o Superficial inguinal → deep inguinal → femoral → external iliac
o Contralateral spread may occur

40
Q

What are the stages of vulval carcinoma?

A
41
Q

How do we investigate vulval carcinomas?

A
  • Tissue diagnosis 🡪 Full thickness biopsy
  • Cervical smear 🡪 Exclude CIN
  • Bloods
  • Imaging 🡪 MRI pelvis
  • Cystoscopy and sigmoidoscopy to define local spread
42
Q

How do we manage vulval carcinoms?

A
  • Surgery for early-stage disease: Wide radical local excision (10mm)
  • Ipsilateral or bilateral inguino-femoral lymph node dissection (stage 1b onwards)
  • Large/multifocal lesions:
    • Radical vulvectomy, ?ipsilateral or bilateral inguinofemoral lymph node dissection dependent on site and size of tumour.
  • Radiotherapy: External-beam radiation (advanced disease/” risk relapse in early disease).
    • • Adjuvant radiotherapy is indicated if the excision margins are close or in the presence of two or more groin node metastases •
    • Radical radiotherapy may be used instead of surgery if the patient is unfit for surgery
43
Q

Describe sentinel lymph node biopsy.

A
  • Untreated groin node metastases will be fatal
  • Affected nodes cannot be reliably identified with radiology
  • Current approach: full inguinofemoral lymphadenectomy (for all tumours with depth of invasion > 1 mm)

o NOTE: groin lymphadenectomy is a very morbid procedure with complications including wound healing problems, infection, VTE and chronic lymphoedema

o Groin nodes are involved in 15% of women with vulval cancer

o Full groin lymphadenectomy may be avoided by doing a sentinel lymph node biopsy (first node that the area drains to)

o A dye and radioactive nucleotide can be injected into the vulval tumour to identify the sentinel node

o If the sentinel node is positive for disease, then full groin lymphadenectomy is indicated

44
Q

What are the complications of surgical removal of lymph nodes?

A

o Wound breakdown
o Infection
o Leg lymphoedema
o Lymphocyst formation
o Sexual and body image problems

45
Q

What is the prognosis of vulval carcinomas?

A
  • No lymph node involvement = 5 year survival 80%
  • Lymph node involvement = 5 year survival <50%
46
Q

What causes secondary vaginal carcinoma?

A

 Common
 After local infiltration from cx, endometrium or vulva
 Or metastatic spread from cx, endometrium or GI tumour

47
Q

What causes primary vaginal carcinomas? How do they present? How do we treat them, whats the prognosis?

A

 2% genital tract Ca
 Affects older women

 Usually squamous
 Presentation
o Discharge
o Bleeding
o Mass or ulcer evident
 Tx
o Vaginal radiotherapy
o Radical surgery
 50% 5 year survival

48
Q

When are clear cell adenocarcinomas of the vagina present? Who is affected? How do treat them? What is the prognosis?

A

 Most common in late teenage years
 Rare complication of daughters of women who had taken DES to prevent miscarriage in late 1950searly
1970s
 Radical surgery + radiotherapy = good survival rates

49
Q

How do we stage vaginal cancers?

A