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Women's Health 1 > Disorders of Vulva & Vagina > Flashcards

Disorders of Vulva & Vagina Flashcards

1
Q

External vulvar anatomy

  • boundaries
  • structures included
A
  • Boundaries extend from mons pubis to anus to labial cural folds
  • Structures include: Labia majora, labia minora, paired Bartholin’s glands, Skene’s glands, urethra, anus, clitoris
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2
Q

Lymphatic drainage of vulva

A
  • Lymphatics of vulva drain from posterior to anterior traversing thru the mons pubis and into superficial and deep inguinal nodes
  • Tend to drain to ipsilateral side
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3
Q

What is the function of bartholin glands?

A

Secrete mucus for lubrication

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4
Q

What are the 3 tissue types and locations that make up bartholin glands?

A
  • Proximal = glandular epithelium
  • Distal = transitional epithelium
  • Opening = squamous epithelium
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5
Q

What causes a bartholin gland cyst?

A

Orifice of gland may become obstructed leading to mucus accumulation and cystic dilatation.

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6
Q

Characteristics of bartholin gland cyst

A
  • unilateral

- soft, painless mass

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7
Q

Which population should always have an excision of a bartholin gland cyst?

A

women over 40 to exclude carcinoma

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8
Q

How is a bartholin abscess different from a bartholin gland cyst?

A

-the cyst is now infected

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9
Q

Characteristics of bartholin gland abscess

A
  • very painful

- fluctuant, swollen, red, warm, mass

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10
Q

Tx of bartholin gland abscess

A

I&D with culture, consider drain placement (Word catheter)

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11
Q

What is a word catheter?

A
  • catheter that is placed into the area of the now empty abscess
  • it is inflated and left in place for 4-6 weeks
  • this promotes the formation of an epithelialized tract for drainage
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12
Q

Marsupialization of Bartholin Gland Abscess

A
  • Abscess cavity is incised 1-2 cm in length and drained
  • The edge of the cyst wall is grasped and everted open
  • The opening is then sutured open creating a new larger duct for drainage
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13
Q

List the non-neoplatic disorders (4)

A
  1. Lichen Sclerosis
  2. Lichen Simplex Chronicus/Squamous Cell Hyperplasia
  3. Lichen Planus
  4. Vulvar Psoriasis
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14
Q

What is the most common vulvar derm disorder?

A

Lichen sclerosis

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15
Q

Etiology of lichen sclerosis

A
  • Chronic, relapsing and remitting disorder (inflammatory)

- Peak Onset: Pre-pubertal and postmenopausal women

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16
Q

Appearance/sx of lichen sclerosis

A
  • *Figure 8/hourglass appearance**
  • Lesions appear as smooth, white plaques.
  • Surface is smoothed and resembles parchment or wrinkled cigarette paper.
  • Sx: intense pruritis, pain, dyspareunia
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17
Q

Etiology and anatomy of lichen sclerosis

A

Etiology is unknown:

  • Autoimmune
  • Genetic
  • Hormonal
  • labia minora, labia majora, clitoris, and perineum can all be involved
  • vagina is spared
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18
Q

Dx/Tx of lichen sclerosis

A

Diagnosis made by punch biopsy.
-Repeat biopsy if new lesions/symptoms as these patients are at increased risk for vulvar cancer.

Treatment:

  • Patient education
  • Topical corticosteroids
  • -Applied BID/daily until symptoms are controlled.
  • -Then 1-3 x weekly for maintenance.
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19
Q

List the drugs for tx of lichen sclerosis

A
  • Topical tacrolimus (Protopic 0.03 or 0.1%) or pimecrolimus (Elidel 1%) demonstrated effective but mainly use with taper.
  • Recalcitrant: oral hydroxychloroquine or cyclosporin
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20
Q

Etiology of Lichen Simplex Chronicus

A
  • AKA squamous cell hyperplasia – NOT a malignant precursor**
  • Secondary to chronic rubbing/scratching.
  • Associated with pruritis
  • Mostly in premenopausal women
  • Typically found on hair-bearing areas of labia majora
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21
Q

Describe clinical findings of lichen simplex chronicus

A
  • Characterized by benign epithelial thickening and hyperkeratosis from chronic irritation
  • Skin is thick with exaggerated skin markings
  • Usually bilateral and symmetric
  • *not a distinct entity but rather a description of morphologic alterations of vulva.
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22
Q

Dx/Tx of lichen simplex chronicus

A

Diagnosis is again made by biopsy.

Treatment:

  • Patient education
  • Identify and treat cause of itching (infection, contact dermatitis, etc.)
  • Topical corticosteroids
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23
Q

Etiology of Lichen Planus

A
  • Rare disorder believed to be autoimmune.
  • Affects skin and mucous membranes
  • Commonly affects the groin and the mouth**
  • Leads to intense pruritus, burning, dysuria, dyspareunia, and post coital bleeding
  • Mostly affects postmenopausal women
  • Almost 70% of patients have vaginal involvement
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24
Q

What is lichen planus characterized by??

A

Lesions characterized by bright erythematous erosions with white striae or white border (Wickham’s striae) visible along the margins

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25
Q

Complications of lichen planus

A
  • Recurrent exacerbations, slow healing and scarring are common
  • Scarring can cause significant anatomic disruption, stenosis of vaginal opening and urethral opening
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26
Q

Tx of lichen planus

A

Can be difficult to treat:

  1. Topical corticosteroids
  2. Oral corticosteroids
  3. Vaginal dilators
  4. Recalcitrant : hydroxychloroquine, thalidomide, apremilast (Otezla), cyclosporine, methotrexate, mycophenolate mofetil

There is no role for surgery

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27
Q

Etiology of vulvar psoriasis

A
  • Systemic skin disease characterized by silver-white scales.
  • Vulvar lesions sharply demarcated erythematous absent of the silver-white scale.
  • Moist and shiny
  • Can affect elbows, knees, back, scalp, and vulva.
  • It can be located just in one area, but it’s likely to be elsewhere on the body.
  • Associated with pruritis.
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28
Q

What is koebner phenomenon in regards to vulvar psoriasis?

A

Koebner phenomenon – skin lesions on lines of trauma

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29
Q

Dx/Tx of vulvar psoriasis

A

Diagnosis is made by vulvar biopsy.

Treatment includes:

  • Topical high potency steroids followed by maintenance therapy with lower potency steroids.
  • Tar creams
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30
Q

List the vulvar neoplasms (5)

A
  1. Extramammary Paget Disease
  2. Vulvar Intraepithelial Neoplasia (VIN)
  3. Vulvar carcinoma
  4. Bartholin gland carcinoma
  5. Vulvar melanoma
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31
Q

Etiology of Extramammary Paget Disease

A
  • Generally benign condition.
  • Pruritic, erythematous, with well-demarcated eczematoid appearance.
  • MC in postmenopausal, Caucasian women, 60s and 70s.
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32
Q

What nonvulvar locations will women have carcinoma in with extramammary paget disease?

A
  • Breast
  • Colon
  • Urethra
  • Bladder
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33
Q

Tx of extramammary paget disease

A

Treatment includes:

  • Patient education
  • Wide local excision
  • Chemotherapy – 5-FU, imiquimod
  • -These are typically used for widespread skin cancers: help to attract the bodies own immune system.
  • Microscopically positive margins are common.
  • Recurrence is common – 30-60%, 8-26% with MOHS.
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34
Q

What is vulvar intraepithelial neoplasia (VIN)?

A
  • Precancerous/dysplastic lesion.

- Spectrum of disease ranging from mild dysplasia to vulvar carcinoma in-situ

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35
Q

Describe the lesions in vulvar intraepithelial neoplasia (VIN)

A
  • Lesion appearance is highly variable but usually sharply demarcated.
  • May be white, hyperkeratotic plaques, hyperpigmented lesions or areas of erythema
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36
Q

Patient presentation with VIN

A

Patients may be asymptomatic or have pruritus, bleeding, or pain.

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37
Q

Etiology and risk factors of VIN

A
  • Incidence is increasing - particularly in younger women (related to HPV)
  • Bimodal distribution of patients:
  • -Younger, premenopausal women
  • -Postmenopausal women

Risk Factors:

  • HPV infection (90%)
  • Smoking
  • Immunodeficiency (HIV)
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38
Q

What is the importance of the “grades” of VIN?

A
  • The degree of dysplasia has to do with the depth into the epidermis/dermis.
  • Remember: carcinoma in-situ is full-thickness of the epidermis.
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39
Q

Describe mild dysplasia/VIN I

A
  • dysplasia confined to the lower third of epithelium.

- now thought to be benign reactive changes or HPV effect by low-risk HPV types

40
Q

Describe moderate dysplasia/VIN II

A

dysplasia confined to the lower two-thirds of epithelium

41
Q

Describe severe dysplasia/VIN III

A

dysplasia extending to the upper third of epithelium, but not involving full thickness

42
Q

Describe carcinoma in situ

A

full thickness involvement

43
Q

When can you classify invasive disease or cancer?

A

Invasive disease or cancer is NOT present until abnormal cells extend beyond the basement membrane and into the stroma below***

44
Q

Define usual type VIN (uVIN). What patient population is it seen in?

A

-most VIN 2 and 3.
-associated with oncogenic HPV infection.
HPV 16 is the most prevalent HPV type found in VIN and vulvar cancer***
-Tend to be multicentric.
-Younger women, multiple sex partners, STDs and smoking

45
Q

Define differentiated type VIN (dVIN). What patient population is it seen in?

A
  • Tend to be unifocal.
  • Older, non-smoking, post-menopausal (60-70s).
  • Oncogenic HPV uncommon.
  • More likely to progress to SCC vs uVIN***
46
Q

Define unclassified type VIN

A
  • pagetoid types

- Extramammary paget’s disease

47
Q

Dx/Tx of VIN

A

-Diagnosis is made by biopsy

Treatment options include:

  • Wide local excision – both for symptom relief as well as r/o invasion
  • Laser ablation
  • Topical imiquimod cream
  • Topical 5-fluorouracil cream
  • Patients should be counseled regarding smoking cessation.
  • Untreated lesions may persist, progress, or resolve.
  • Recurs frequently.
48
Q

Etiology of vulvular carcinoma

A

-Represents 5% of all gyn malignancies.
90% SCC
-< 20% are younger than 50 years: >50% in women older than 70

49
Q

Vulvular carcinoma in older women

A
  • Peak incidence in women ages 60–70 years

- Chronic inflammation - Lichen sclerosis OR genetic alterations

50
Q

Vulvular carcinoma in younger women

A
  • HPV-related- 50% cases.

* H/O smoking + H/O HPV genital warts have a 35–fold increased risk for developing vulvar cancer

51
Q

Vulvular carcinoma dx/tx

A
  • Diagnosis made by biopsy
  • Refer to Gyn for vulcoscopy- helps direct biopsy site selection (similar to colposcopy).
  • Biopsy via punch bx to allow evaluation for depth of invasion
52
Q

Tx of vulvar cancer

A

Surgical excision with 2 cm margin
-Modified radical vulvectomy

Sentinel lymph node biopsy
-For prognosis only

53
Q

Adjuvant therapy for vulvar cancer

A
  • Chemoradiation
  • Chemotherapy
  • Immune therapy
  • Targeted therapy
54
Q

Etiology of Bartholin Gland Carcinoma

A
  • 1% vulvar cancers
  • Painless vulvar mass.
  • Dyspareunia common first complaint
  • Size range from 1 – 7 cm.
  • Can get quite large before symptomatic.
  • Most appear in postmenopausal women  peak mid-60’s

REMEMBER: Bartholin gland enlargement in a woman older than 40 years and recurrent cysts or abscesses warrant a biopsy***

55
Q

What cancer types are most prominent in Bartholin Gland Carcinoma?

A
  • Squamous cell carcinoma (50%)
  • Adenocarcinoma (40%)
  • Adenoid cystic carcinoma
  • Transitional cell carcinoma
  • Adenosquamous carcinoma
56
Q

What is the criteria for diagnosis of Bartholin gland carcinoma?

A

1) arise at site of Bartholin gland
2) consistent histologically with primary Bartholin neoplasm
3) not be metastatic

57
Q

Explain the lymphatic spread of Bartholin gland carcinoma

A

Propensity for lymphatic spread into the inguinal and pelvic lymph nodes

58
Q

Tx of Bartholin gland carcinoma

A
  • Radical partial vulvectomy with inguinofemoral lymphadenectomy
  • Postoperative chemoradiation has been shown to reduce the likelihood of local recurrence
59
Q

Etiology of vulvar melanoma

A
  • 5-10% of all vulvar cancers, second most common vulvar cancer.
  • Postmenopausal**
  • MC arises in the region of the labia minora and clitoris
60
Q

Pigmented vs. nonpigmented vulvar melanoma

A
  • Nonpigmented melanoma may closely resemble squamous cell carcinoma
  • Pigmented vulvar neoplasia may be VIN, squamous cell carcinoma, Paget disease or melanoma
  • *sampling is mandatory
  • Staging and prognosis linked to depth of invasion.
61
Q

What kind of biopsy should you do for vulvar melanoma?

A

-Excisional biopsy
-Punch biopsy
**NOT shave biopsy
In shave biopsy, you use flat edge razor blade and get a little scoop of tissue - you’re not getting down through the whole dermis this way

62
Q

Tx of vulvar melanoma

A
  • Excision is the single best definitive therapy

- May consider adjuvant alpha interferon (IFN-α)

63
Q

List the vaginal neoplasms (2)

A
  1. Vaginal intraepithelial Neoplasia (VAIN)

2. Vaginal carcinoma

64
Q

Etiology of vaginal intraepithelial neoplasia (VAIN)

A
  • Pre-cancerous lesion/dysplasia.

- Less common than VIN or CIN.

65
Q

Risk factors for VAIN

A
  • HPV infection
  • Immunosuppression
  • Preceding or co-existing squamous cell carcinoma of the vulva, cervix, or anus.
  • At least ½ - 2/3 with VAIN have been treated for similar disease in either the cervix or the vulva
66
Q

Tx of VAIN

A

surgical excision or laser ablation

67
Q

Etiology of vaginal carcinoma

A
  • Rare, representing < 1% of malignancies of the female genital tract.
  • Vaginal cancer is more likely metastatic dz
  • *Mean age of diagnosis is 64 years
68
Q

Sx of vaginal carcinoma

A

painless vaginal bleeding, especially postcoital, vaginal discharge, or dysuria.

69
Q

Risk factors for vaginal carcinoma

A
  • HPV infection
  • Smoking
  • H/o previous vulvar or cervical cancer
70
Q

What tissue type is MC for vaginal carcinoma?

A

Majority of cases are squamous cell carcinoma.

71
Q

What is considered a primary tumor of vaginal carcinoma?

A
  1. Located in vagina
  2. No evidence of cervix or vulvar involvement

**Most tumors are in the upper 1/3 vagina and posterior wall.

72
Q

Tx of vaginal carcinoma

A
  • surgical excision in lower stage cancers if negative surgical margins can be obtained. + hysterectomy
  • Radiation therapy with chemotherapy
73
Q

Define cystocele

A

Prolapse of the anterior vaginal wall causing by bladder collapsing on weak vaginal muscle.

74
Q

Define rectocele

A

Rectum collapsing on weak vaginal muscle in the posterior wall.

75
Q

Define apical prolapse

A

AKA uterine prolapse

-uterus collapsing from the top of the vaginal wall

76
Q

What can cause pelvic organ prolapse?

A

Anterior and posterior vaginal relaxation, loss of pelvic floor muscle support, loss of connective attachments between the vaginal wall and the pelvic floor

77
Q

Etiology of pelvic organ prolapse

A
  • Large anterior vaginal prolapse (cystocele) is MC than posterior vaginal prolapse
  • Third MC indication for hysterectomy
  • Estimated that 30 to 65% of women presenting for routine gynecologic care have stage 2 prolapse
78
Q

Pelvic organ prolapse risk factors

A
  • Vaginal childbirth – especially if multiple
  • Increasing parity
  • Age
  • Obesity
  • Race - Black and Asian women show the lowest risk, whereas Hispanic and white women appear to have the highest risk
  • Hysterectomy
  • Repetitive increases in intraabdominal pressure (chronic constipation, COPD)
  • Connective tissue disorders
79
Q

Clinical Manifestations of pelvic organ prolapse

A
  • Bulge/pressure
  • “Something falling out”; “sitting on a ball”
  • Urinary incontinence, frequency
  • Back/pelvic pain
  • Effects on sexual function
80
Q

Pelvic organ prolapse management

A
  • tx indicated for symptomatic patients
  • conservative management:
  • -Pelvic floor muscle exercises/PT- Kegel exercises
  • -Pessary
  • Surgical management
81
Q

What are the 2 kinds of pessaries? How do they work?

A

**support and space-filling

Support pessaries rest in the posterior fornix behind the cervix and behind the pubic symphysis anteriorly.

Space filling crate suction between the pessary and vaginal walls, or by creating a larger diameter hiatus or both.

82
Q

What causes atrophic vaginitis?

A
  • Also called urogenital atrophy**

- Due to estrogen deficiency

83
Q

What population is atrophic vaginitis seen in?

A

40% postmenopausal women, but only 20-25% symptomatic seek medical attn.

84
Q

Explain how the vaginal epithelium responds to estrogen from birth to puberty

A

Vaginal epithelium responds to levels of circulating estrogen:

  1. Maternal estrogen – newborn epithelium rich in glycogen
  2. Puberty – thickens with copious amounts of glycogen
  3. Lactobacilli depend on glycogen
  4. Lactic acid produced by lactobacilli keep pH lower, essential for natural defense against vaginal and urinary infections
85
Q

Atrophic Vaginitis

-signs and symptoms

A
  • Long-term decrease in estrogen stimulation is generally required before symptoms
  • Decrease in vaginal lubrication is an early hallmark hormone insufficiency**
86
Q

Genital symptoms of atrophic vaginitis

A

Dryness, burning, dyspareunia, vaginal dryness, vulvar pruritus, feeling of pressure, itching and yellow malodorous discharge

87
Q

Urinary symptoms of atrophic vaginitis

A

Urethral discomfort, frequency, hematuria, urinary tract infection, dysuria and stress incontinence may be later symptoms

88
Q

What should be considered on your diff dx for atrophic vaginitis?

A
  • *Do not assume a diagnosis of atrophic vaginitis (or solely AV) in the postmenopausal patient who presents with urogenital complaint
  • Exogenous agents that may cause or further aggravate symptoms:
  • Perfumes, powders, soaps, deodorants, panty liners, spermicides and lubricants often contain irritant compounds.
  • In addition, tight-fitting clothing and long-term use of perineal pads or synthetic materials
  • Candidiasis, BV, Trichomoniasis
89
Q

Atrophic Vaginitis

-genital physical exam

A
  • Pale, smooth and shiny vaginal epithelium
  • Inflammation with patchy erythema, petechiae
  • Loss of elasticity or turgor of skin
  • Sparsity of pubic hair
  • Dryness of labia
  • Fusion of labia minora
  • Introital stenosis
  • Friable, unrugated epithelium
  • Pelvic organ prolapse/Rectocele
  • Vulvar dermatoses/lesions
90
Q

Atrophic vaginitis

-urethral physical exam

A
  • Urethral caruncle (benign fleshy outgrowth of posterior urethral meatus)
  • Eversion of urethral mucosa
  • Cystocele
  • Urethral polyps
  • Ecchymoses
  • Minor lacerations at peri-introital
91
Q

Diagnosis of atrophic vaginitis

A
  • Dx is usually clinical but serum hormone levels and Pap smear, can confirm
  • Elevated pH level (postmenopausal pH levels exceeding 5), pH strip in the vaginal vault
  • Vaginal US of the uterine lining demonstrates thin endometrium measuring between 4 and 5 mm - signifies loss of adequate estrogenic stimulation
92
Q

Tx of atrophic vaginitis

A
  • Estrogen replacement therapy helps to restore normal pH levels, thickens/revascularizes epithelium
  • -May alleviate existing symptoms or even prevent development of urogenital symptoms if initiated
  • Systemic administration
  • -Also helps with decrease in postmenopausal bone loss and alleviation of vasomotor dysfunction (hot flashes)
  • -Higher dosages may be necessary to alleviate atrophic sxs
  • -Up to 24 months of therapy may be necessary to totally eradicate dryness
93
Q

Transvaginal delivery tx for atrophic vaginitis

-advantages

A
  • creams, pessaries, hormone-releasing ring (Estring)

- Advantage may be decreased risk of endometrial carcinoma because a lower hormone amount is required**

94
Q

Transvaginal delivery tx for atrophic vaginitis

-disadvantages

A
  • patient dislike of vaginal manipulation
  • less prevention of postmenopausal bone loss and vasomotor dysfunction
  • decreased control of absorption with vaginal creams compared to oral and transdermal delivery
  • irregular treatment intervals that may cause patients to forget to administer
95
Q

What is the relationship between hormone concentration and transvaginal delivery for atrophic vaginitis?

A
  • Transvaginal rings offer convenience, constancy of hormonal concentration in the blood stream and a therapeutic value equivalent to creams without the need for frequent application
  • Atrophic vaginitis symptoms are relieved (dosage of 5 to 10 μg per 24 hours) without stimulation of endometrial proliferation, thereby eliminating need to add opposing progesterone
96
Q

Atrophic vaginitis tx

-moisturizers and lubricants

A
  • For those who choose no ERT or contraindicated BUT then should not use products with ginseng - may have estrogenic properties**
  • Length of effectiveness - generally less than 24 hours
97
Q

Sexual activity and atrophic vaginitis

A
  • Shown to encourage vaginal elasticity and pliability, and the lubricative response
  • Pts report fewer symptoms of atrophic vaginitis, less evidence of stenosis compared with sexually inactive women

Women's Health 1 (17 decks)

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