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X Women's Health > Vulvar and Ovarian Disease > Flashcards

Vulvar and Ovarian Disease Flashcards

1
Q

What is lichen sclerosus?

A

Autoantibodies attack extracellular matrix and basement membrane (immune dysfunction affecting all levels of the skin)–poorly understood so can be genetic or enviromental too

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2
Q

Environmental factors affecting pathophysiology of lichen sclerosus

A

Incontinence
Infection
Contact dermatitis
Trauma (Kobners phenomenon)

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3
Q

Presentation of lichen sclerosus

A

Mostly in postmenopausal women
Most common sxs is pruritus!!!
Pain (dysuria and dyspareunia)

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4
Q

What is seen on PE for lichen sclerosus?

A

Sharply, well-demarcated white plaques
Usually begins periclitorally with spread to perianal skin
(not usually seen as keratinized, hair-bearing labia majora or mucus membranes)

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5
Q

Pathognomonic for lichen sclerosus

A

Plaques demonstrate “cellophane paper” (also waxy and/or hyperkeratotic apperance)

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6
Q

Hallmark of lichen sclerosus

A

Fragility (purpura, erosions and fissues)

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7
Q

What can occur in untreated lichen sclerosus?

A

Squamous cell carcinoma (small amt)
Can also see pigmentary changes (benign but can see aytpical nevi and melanoma and take the pigmented lesions seriously)
Hypothyroidism

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8
Q

Risk factors of developing SCC from lichen sclerosus

A

Elderly

Hyperkeratotic lesions!!

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9
Q

How to confirm diagnosis of lichen sclerosus

A

Vulvar punch biopsy

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10
Q

Tx for lichen sclerosus

A

Topical ultrapotent steroid ointment!!! (first line is temovate .05% ointment applied twice daily until normal texture and can use 1-3x week for maintenance)
Lifelong!!!-thicker skin so can handle the steroid for a while

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11
Q

Side effects of temovate steroid for lichen sclerosus

A

Atrophy, dermatitis and rosacea

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12
Q

Other tx options for lichen sclerosus

A

Can use topical estrogen also but does not go away

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13
Q

What are Bartholin ducts?

A

Bilateral glands at 4 and 8 o clock positions in labia minora–ducts open into vestibule adjacent to vaginal introitus–secrete mucus like material to maintain moisture of vaginal mucosa

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14
Q

Pathophysiology of Bartholin cyst

A

Cysts form as result of ductal obstruction due to trauma or non specific inflammation
Abscess formation from infected cyst or primary gland infection (polymicrobial, STIs)

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15
Q

Presentation of Bartholin cyst

A

Acute, painful unilateral labial swelling
Dyspareunia
Pain with sitting or walking

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16
Q

What is seen on PE for Bartholin cyst?

A 
Tender, fluctuant labial mass
Surrounding erythema and edema
Cellulitis
Abscess formation
Fever
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17
Q

Tx for Bartholin cyst

A 
I&D with insertion of Word catheter
Culture purulent material
Empirical abx therapy (Keflex or Doxy)
Sitz baths for 2-3 days
No intercourse until cath is removed
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18
Q

Possible pathophysiology of vulvodynia

A 
Estrogen conc (onset around menopause, affects pain sensitivity and sensory discrimination)
Pelvic floor dysfunction
Psych (mood/anxiety disorders, poor allostasis)
Neuro sensitization (insult to vulvar mucosa causes chronic inflammation and sensation of touch becomes painful)
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19
Q

Presentation of vulvodynia

A

Vulvar discomfort described as burning sensation (stinging, irritated, sore, raw, stabbing)
Introital pain with intercourse
Generalized vs localized (sexual or nonsexual etc)

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20
Q

Important parts of PE for vulvodynia

A

Use Q tip to palapate vestibule, labia majora, perineum or interlabial folds
Pain is limited to vestibule
Single digit exam to feel for spasm or tenderness of pelvic floor musculature
Non-specific vestibular erythema

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21
Q

Tx for vulvodynia

A

No scented products, tight clothing, vigorous exercise or pads
Sitz baths BID followed by petroleum jelly
Couple counseling
Pelvic floor PT
Local nerve block

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22
Q

Pharm meds for vulvodynia

A

Topical vaginal estrogen .03% with T .1%
Nortriptyline 50 mg QHS (titrate up starting at 10)
Gabapentin 1200 mg TID (titrate up to it)

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23
Q

What is vulvar intraepithelial neoplasia?

A

Neoplastic cells confined to squamous epithelium

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24
Q

How to classify vulvar intraepithelial neoplasia

A

1, 2 or 3 (like CIN)

Now want to combine 2 and 3 b/c true precursors to vulvar cancer (Vinu and VINd based on morphologic manifestations)

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25
Q

Usual type of vulvar intraepithelial neoplasia

A

VINu

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26
Q

What is VINu associated with?

A

HPV 16 and 18 (seen in younger women so same risk factors as CIN)

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27
Q

Risk factors of CIN and VINu

A

Smoking
Immunosuppression
Multiple sex partners

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28
Q

How to diagnose VINu

A 
Vulvar colposcopy:
3-5% acetic acid and let sit for 3-5 min
Avoid using acetic acid in areas of inflammation and breaks in epithelium
See raised or flat lesions
Color is gray to white or red to black
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29
Q

Presentation of VINu

A

Most asymptomatic

Vulvar burning and pruritus in half

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30
Q

Association of VINu

A

High grade CIN (colposcopy is mandatory to rule out)

Biopsy all pigmented lesions!!

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31
Q

Tx for VINu

A

None provide a cure (reactivate latent)

All meds are off label

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32
Q

Off label meds for VINu

A

5FU cream (many s/es)
Interferon
Imiquimod 5% cream (apply 3 times weekly up to 20 wks so low compliance)
Must do vulvar assessments q 4wks during tx

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33
Q

Standard of care for VINu tx

A 
Surgery:
CO2 laser vaporization (destroy entire thickness of epithelium but don't do if invasion)
Local wide excision
Vulvectomy
Some high recurrence
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34
Q

What is VINd?

A

Differentiated type unrelated to HPV (not have same risk factors)
Seen in older women (>70)
Involves lower 1/3 of epithelium (so none abnormal cells in upper)

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35
Q

Pathogenesis of VINd?

A

Associated with squamous cell hyperplasia (lichen sclerosus, lichen simplex chronicus)
Unidentified carcinogenic agents combined with local environment of chronically irritated/inflamed skin lead to dysplastic cells

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36
Q

Tx for VINd

A

Prevent: tx of underlying

Tx is surgical excision tho

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37
Q

Follow up for VINu and VINd

A

Vaccination with Gardasil (VIN usual type)
Women with history of VIN considered at risk of recurrence
Must do post tx follow up of colposcopic vulvar inspection at 6 and 12 mos and then annually after

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38
Q

Incidence of vulvar cancer

A

Very uncommon tho
Etiology in 20-40 YO is HPV related (VINu)
60-70 YO is due to chronic irritation and poorly understood co-factors (VINd)–most have untreated lichen sclerosus, lichen simplex chronicus or squamous cell hyperplasia

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39
Q

Co-morbidities of vulvar cancer

A

Some have type 2 DM

Some are obese or hypertensive

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40
Q

Presentation of vulvar cancer

A

Asymptomatic (delays diagnosis so inspect vulva)
Pruritus is most common sx
Vulvar bleeding and pain

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41
Q

PE of vulvar cancer: squamous cell carcinoma

A

Varies in appearance from large, exophytic cauliflower like lesion to small ulcerative lesions with surrounding hyperkeratosis

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42
Q

PE of vulvar cancer: basal cell carcinoma

A

Raised lesion with ulcerated center and rolled borders

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43
Q

PE of vulvar cancer: malignant melanoma

A

Seen at labia minora and clitoris

Raised, darkly pigmented lesion

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44
Q

Tx for vulvar cancer

A

Staging based on fIGO
Primary: complete surgical removal of tumor with inguinal node dissection
Radiation therapy with lymph node spread!!

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45
Q

Background of vaginal intraepithelial neoplasia (VAIN)

A

-Precancerous disease of vagina (rare!!)
Seen mostly 35-55
HPV must be present to develop VAIN
Some have been previously treated for CIN or hysterectomy

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46
Q

Risk factors of vaginal intraepithelial neoplasia

A

Smoking, multiple sexual partners and early onset of sexual activity (same as CIN)
History of CIN III

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47
Q

Pathogenesis of vaginal intraepithelial neoplasia

A

HPV exposure but requires long time to develop
Frequency not as high as CIN since vaginal epithelium is different than cervical
Not very high progression to invasive cancer

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48
Q

Where are most lesions with vaginal intraepithelial neoplasia?

A

Upper 1/3 of vagina

49
Q

Classification of vaginal intraepithelial neoplasia (VAIN)

A

1: benign viral proliferation
2: intermediate risk
3: true precursor to vaginal cancer

50
Q

Labs for vaginal intraepithelial neoplasia

A

Detection is via pap smear (cytology)

Colposcopy

51
Q

Management for VAIN 1

A

Observation when younger

Cytology/HPV/colposcopy q 6 mos

52
Q

Management for VAIN 2/3

A

Surgical intervention or chemo

53
Q

Management for vaginal intraepithelial neoplasia in general

A

Vaginectomy (90% success)
Laser vaporization
Topical chemo/5FU (lower success but mostly used if other options not feasible)

54
Q

Most common cause of invasive vaginal cancer

A

Metastasis from endometrium, ovary or cervix (can only be called vaginal cancer when growth is from vagina says FIGO)

55
Q

Most common type of vaginal cancer

A

Squamous cell

56
Q

Presentation of vaginal cancer

A 
Asymptomatic
Leukorrhea
Vaginal odor
Post-coital bleeding
Abnormal pap smear (colposcopy with acetowhite changes, punctation or mosaicism)
57
Q

Tx for vaginal cancer

A

No standardized tx b/c rare

Combo vaginectomy and radiation (medium 5 yr survival rate)

58
Q

Pathophysiology of polycystic ovarian syndrome

A

Abnormal androgen and estrogen metabolism
Control of androgen production is unregulated (high T, androgens, DHEA)
Insulin resistance and hyperinsulinism
Decreased adiponectin
Increased androgens released from ovary are converted to estrogen

59
Q

Presentation of polycystic ovarian syndrome

A 
Most common is infertility
Oligomenorrhea/amenorrhea (anovulation)
Obseity
Acne and hirsutim
Male pattern baldness
Acanthosis nigricans
60
Q

NIH criteria to diagnose polycystic ovarian syndrome

A

NIH criteria:
Must have oligomenorrhea and hyperandrogenism
Must exclude hyperprolactinemis, CAH and Cushings

61
Q

Rotterdam criteria for polycystic ovarian syndrome

A

2 or 3 below must be present after exclusion of related disorders:
Oligomenorrhea
Clinical or biochemical signs of hyperandrogenism
Polycystic ovaries
(just expanded NIH)

62
Q

Ultrasound findings of polycystic ovarian syndrome

A

Presence of >12 follicles in each ovary measuring 2-9 mm in diameter (rotterdam)
String of pearls apperance!!
Ovarian vol >10 ml
No evidence of dominant follicle/corpeus luteum

63
Q

First lab for polycystic ovarian syndrome

A

Start by measuring total testosterone (normal is 40-60 ng/dl)
It is elevated if >60

64
Q

What labs must be seen with polycystic ovarian syndrome?

A 
Hyperandrogenism requires:
17-OH progesterone
DHEA-S
Cortisol
Prolactin (should be normal)
TSH (if increased can cause oligomenorrhea)
bHCG (rule out pregnancy)
65
Q

What elevated 17 OH progesterone could mean with polycystic ovarian syndrome?

A

Congenital adrenal hyperplasia

66
Q

What elevated DHEA-S could mean with polycystic ovarian syndrome?

A

Adrenal source for increased testosterone

67
Q

What elevated cortisol could mean with polycystic ovarian syndrome?

A

Cushings

68
Q

Most important component of polycystic ovarian syndrome tx

A

Weight loss!! (increased SHBG and decrease free testosterone to restore cycling)

69
Q

Other tx for polycystic ovarian syndrome

A

Metformin (only with hyperinsulinemia-500 BID)
COCs (low androgenic activity)—-only standard of care for these pts b/c truly helps them
Fertility consultation
Provera 10 mg QDx10 days (endometrial protection-so that they can have their normal period!)
Life long lifestyle

70
Q

Risks associated with polycystic ovarian syndrome

A 
Endometrial hyperplasia/carcinoma
Type 2 DM
HTN
HLD
CVD
Stroke
Infertility
Metabolic syndrome
Sleep apnea
71
Q

Ultrasound characteristics of benign adnexal mass

A

Thin walled
<3 cm premenopause of <1 cm post menopause (simple cyst)
Hyperechoic nodule with distal acoustic shadowing (teratoma)
Network of linear or curvilinear pattern (hemorrhagic cyst)
Homogenous echos (endometrioma)

72
Q

Ultrasound characteristics of malignant adnexal mass

A

Thick septations >2 mm
Solid component appears nodular or papillary
Blood flow to solid component

73
Q

Types of physiologic ovarian cysts

A 
Follicular cysts
Corpeus luteum cysts
Theca lutein cysts
Mature teratoma
Serous and mucinous cystadenomas
74
Q

Most common type of ovarian cyst

A

Follicular

75
Q

Characteristics of follicular ovarian cystq

A

2-8 cm
Non malignant
Results from failure or mature follicle to rupture (release ovum) or failure of non-dominant follicles to undergo atresia in presence of mature follicle

76
Q

Characteristics of corpus luteum ovarian cyst

A

3-11 cm
Less common
Following ovulation, blood accumulates in cavity of corpus luteum which stimulates resorption (if that doesnt occur and the luteum is greater than 3 cm it is a cyst)

77
Q

When do corpus luteum cysts usually resolve?

A

After 1-2 menstrual cycles

78
Q

Characteristics of theca lutein cysts

A

Seen with elevated chorionic gonadotropin levels (hydatidiform mole, choriocarcinoma, clomid therapy)
Usually bilaterally
Fluid is clear or straw colored
-Usually due to stimulation (fertility tx!!)

79
Q

When do theca lutein cysts resolve?

A

Spontaneously with tx of underlying disorder

80
Q

What are mature teratomas?

A

Half of benign neoplasms in reproductive age women

81
Q

Pathophysiology of mature teratoma

A

Parthenogenic theory: originate from primordial gem cells and teratomas found along migration pathway of germ cells from yolk sac to gonads)
Composed of well differentiated tissue derived from any of 3 derm layers (ectoderm, mesoderm, endoderm)

82
Q

Histology of mature teratoma

A

Cyst is lined with keratinized squamous epithelium with abundant sebaceous and apocrine glands
(can have hair and teeth!!!)

83
Q

Most common origin of mature teratoma

A

Ectodermal cell origin

84
Q

Presentation of mature teratoma

A

Asymptomatic (found on pelvic exam or incidental finding on other radiologic studies)
Pelvic pain (occurs secondary to torsion or rupture)
Frequency or urgency
Back pain

85
Q

What is seen on PE for mature teratoma?

A

Pelvic mass on bimanual exam

86
Q

Labs for mature teratoma

A

Transvaginal u/s (unilateral, complex xyst)

CEA, CA-125, AFP, bHCG (all should be normal b/c signs of ovarian cancer!)

87
Q

Tx for mature teratoma

A

Laparotomy vs laparoscopy
Ovarian cystectomy vs oophorectomy
Recurrence is low

88
Q

What is the background of ovarian cyst serous/mucinous cystadenoma?

A

30-50 YO

Represents 20-25% of benign neoplasm

89
Q

Histology of ovarian cyst serous/mucinous cystadenoma

A

Lined with columnar epithelium
Secrete think, gelatinous mucin (mucinous)
Thin walled, uni or multilocar and range in size from 5 to over 20 cm (mucinous greater than serous)

90
Q

Tx for ovarian cyst serous/mucinous cystadenoma

A

Surgical excision and ensure benign pathology

91
Q

2nd most common gynecologic cancer

A

Ovarian cancer

92
Q

Most common cause of gynecologic cancer death in US

A

Ovarian cancer

93
Q

Risk factors of ovarian cancer

A

Nulliparity!!, infertility tx, diets high in saturated animal fats, obese, talcum powder, personal Hx of breast cancer, family hx of breast, OVARIAN or colorectal cancer (higher with BRCA1 or lynch), Turners, early menarche!! or late menopause!!, estrogen replacement therapy, caucasian, endometriosis
***more women ovulates, more at risk she is

94
Q

Ways to reduce the risk of ovarian cancer

A 
Multiparity
Breast feeding
Long term oral contraceptive use (5 yrs drops it by 50%)
Bilateral tubal ligation
Low fat diet
Bilateral salpingectomy!!!!
95
Q

4 categories of ovarian cancer on histopathology

A

Epithelial (bilateral and older)
Germ cell (unilateral and younger)
Sex cord and stromal
Neoplasms metastatic to ovary

96
Q

Subtypes of epithelial ovarian cancer

A

High grade serous carcinoma
Endometriod carcinoma
Clear cell carcinoma
Mucinous carcinoma

97
Q

Subtypes of germ cell ovarian cancer

A 
Dysgerminoma
Endodermal sinus
Immature teratoma
Embryonal carcinoma
Choriocarcinoma
98
Q

Subtypes of sex cord and stromal ovarian cancer

A

Granulosa cell

Sertoli-stromal cell

99
Q

Examples of neoplastims metastatic to ovary

A

Tumors from stomach, colon or breast

100
Q

Theory of epithelial cancer based on location in ovary

A

Incessant ovulation therapy (repeated ovarian epithelital trauma by follicular rupture and subsequent epithelial repair and leads to malignant transformation)
Associated with endometriod, mucinous or clear cell cancer in ovary

101
Q

Theory of epithelial cancer based on location in fallopian tube

A

p53 tumor suppressor gene

Associated with high grade serous papillary cancer!!

102
Q

Types of ovarian cancer epithelial neoplasms

A 
High grade serous carcinoma MOSTLY (from fallopian tube- why salpingectomy decreases risk)
Endometriod carcinoma (from ovary)
Clear cell carcinoma (from ovary)
Mucinous carcinoma (from ovary)
103
Q

Background of germ cell ovarian cancer

A

20-30 YO mostly
Grow rapidly, favor lymphatic spread, contain mixture of tumor types and usually unilateral
They produce tumor markers
-*arises from internal party of ovary (epithelial is from outside)

104
Q

Types of germ cell ovarian cancer

A 
Dysgerminoma
Endodermal sinus tumor
Immature teratoma
Embryonal carcinoma
Choriocarcinoma
(mixed can be combo of 1-3)
105
Q

Characteristics of germ cell ovarian cancer: dysgerminoma

A

Most common!!
Unilateral mostly
Mostl < 30 YO

106
Q

Characteristics of germ cell ovarian cancer: endodermal sinus tumor

A

Bilateral
Displays most rapid growth of germ cell neoplasms
Produces alpha fetoprotein

107
Q

Characteristics of germ cell ovarian cancer: immature teratoma

A

2nd most common
Seen mostly <20 YO
Unilateral mostly
Produces alpha fetoprotein

108
Q

Characteristics of germ cell ovarian cancer: embryonal carcinoma

A

Uncommon
Rapid growth with extensive
Produces alpha fetoprotein and HCG

109
Q

Characteristics of germ cell ovarian cancer: choriocarcinoma

A

Seen with precocious puberty, uterine bleeding or amenorrhea
Very rare
Mostly 2nd decade of life

110
Q

Types of sex-cord stromal tumors associated with ovarian cancer

A

Granulosa cell

Sertoli-Stromal cell

111
Q

Characteristics of sex-cord stromal tumors associated with ovarian cancer: granulosa cell

A

Most common!
Causes hyperestrogenism (precocious puberty and post menopausal bleeding)
5th decade of life

112
Q

Characteristics of sex-cord stromal tumors associated with ovarian cancer: sertolid-stromal cell

A

Rare
Causes hyperandrogenism
3-4th decades

113
Q

Presentation of ovarian cancer

A

Acute: pleural effusion and bowel obstruction
Subacute sxs: adnexal mass, bloating/abd distention, early satiety, pelvic/abd pain, abnormal vaginal bleeding, altered BMs, dyspepsia

114
Q

What is seen on PE for ovarian cancer?

A

Ascites
Inguinal LAD
Pelvic mass

115
Q

Imaging for ovarian cancer

A

Transabd/vaginal u/s (BEST-verify mass)
Mammogram/colonoscopy rule out primary breast or colorectal cancer)
CT (reveal retroperitoneal involvment and metastais)
MRI (characteristics of neoplasms)
CXRs

116
Q

Labs for ovarian cancer

A

CA-125 elevated (suspected epitheltial ovarian cancer!!! >65 U/mL)
Elevated hCH, AFP, LDH or any variation of these 3 (suspected germ cell tumor!!!)
**order all four with an adnexal mass where suspicious for ovarian cancer

117
Q

Tx for epithelial ovarian cancer

A

Gyn ocology refer!!
Surgical staging (FIGO)
Chemo

118
Q

Tx for germ cell ovarian cancer

A

Consult gyn oncologist
Early diagnosis allows removal of involved adnexa with preservation of contralateral adnexa and uterus
Surgical staging (FIGO

X Women's Health (4 decks)

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