E2: Vulvar And Ovarian Disease Flashcards

1
Q

What is the clinical presentation of lichen sclerosis?

A
  • seen mostly in postmenopausal women
  • pruritis is the most common symptom
  • pain
  • usually begins periclitorally with spread to the perineal skin
  • Not usually seen at keratinized, hair bearing labia
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2
Q

On PE, you see sharply and well demarcated white plaques on the vulva. The plaques demonstrate “cellophane paper” appearance. What should you be suspicious of?

A

Lichen sclerosus

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3
Q

What is the hallmark of disease of lichen sclerosus?

A

Fragility: purpura, erosions, and fissures

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4
Q

What are patients with lichen sclerosus at increased risk for?

A

-Squamous cell carcinoma occurs in 5% of women with untreated lichen sclerosus (risk factors are elderly and hyperkeratoic lesions)

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5
Q

How is lichen sclerosus definitively diagnosed?

A

Vulvar punch biopsy

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6
Q

What is the treatment of lichen sclerosis?

A
  • Topical ultra potent steroid ointment, first line is Temovate 0.05% ointment applied twice daily until texture is normal, then 1-3x per week for maintenance
  • topical estrogen
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7
Q

What are the possible side effects of temovate?

A

Atrophy, dermatitis, rosacea

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8
Q

What is the pathophysiology of bartholin cysts?

A

-Cysts form as a result of ductal obstruction due to trauma or non-specific inflammation. Abscess formation results from an infected cyst or primary gland infection

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9
Q

What is the clinical presentation of a bartholin cyst?

A
  • Acute painful unilateral labial swelling
  • dyspareunia
  • pain with sitting or walking
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10
Q

What is the treatment of a bartholin cyst?

A
  • incision and drainage with insertion of word catheter
  • culture purulent material
  • possible and therapy with keflex or doxy
  • sitz baths for 2-3 days
  • no intercourse until catheter is removed
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11
Q

What is the clinical presentation of vulvodynia?

A
  • vulvar discomfort described as a burning sensation
  • introital pain with intercourse
  • On PE, pain is limited to the vestibule
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12
Q

What is the treatment of vulvodynia?

A
  • avoid scented products, tight clothing, vigorous exercise, and pads
  • Sitz baths BID followed by a thin film of petroleum jelly
  • topical vaginal estrogen 0.03% with testosterone 0.1%
  • Nortriptyline OR Gabapentin
  • Couples counseling
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13
Q

What is vulvar intraepithelial neoplasia (VIN)?

A
  • Neoplasticism cells confined to squamous epithelium

- Classified as VIN 1, 2, or 3

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14
Q

Which types of VIN are precursors to vulvar CA?

A

VIN 2 and 3

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15
Q

VINU is associated with HPV type ** and **.

A

16 and 18

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16
Q

How is VINU diagnosed?

A
  • Vulvar colposcopy with 3-5% acetic acid and allow to sit for 3-5 minutes. Reapply often.
  • Lesions are raised or flat and range in color from gray to whit or red to black
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17
Q

What is the presentation of VINU usual type?

A
  • Most are asymptomatic
  • vulvar burning and pruritis in 50% of cases
  • Associated with high grade CIN therefore colposcopy of the cervix is mandatory
  • Biopsy all pigmented lesions
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18
Q

What is the pharmacologic treatment of VINU?

A
  • None provide a guaranteed cure
  • All medical therapies are off-label use
  • 5FU cream
  • Interferon
  • Imiquimod 5% cream
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19
Q

What is the standard of care for VINU?

A
  • Surgical treate=meant with CO2 laser vaporization, which causes destruction of entire thickness of epithelium and do no perform if invasion is suspected
  • local wide excision
  • vulvectomy
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20
Q

What is VIND (differentiated)?

A
  • Unrelated to HPV and do no demonstrate same risk factors as VINU
  • Seen in older women
  • Involves the lower 1/3 of the epithelium
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21
Q

What is VIND commonly associated with?

A

Associated with squamous cell hyperplasia (lichen sclerosus, lichen simplex chronicus)

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22
Q

How can VIND be prevented?

A

Proper treatment of underlying condition

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23
Q

How is VIND treated?

A

Surgical excision

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24
Q

What is the recommended follow up for VINU and VIND?

A
  • Gardasil vaccination up to age 45 (especially VINU)
  • Should be considered at risk for recurrent throughout their lifetime
  • post treatment follow up includes colposcopic vulvar inspection at 6 and 12 months and then annually
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25
Q

What is he 4th most common malignancy of the female genital tract?

A

Vulvar cancer

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26
Q

What is the bimodal peaks of vulvar cancer?

A
  • Women 20-40 years is HPV related

- women 60-70 years is due to chronic irritation and poorly understood factors

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27
Q

What is the clinical presentation of vulvar cancer?

A
  • asymptomatic
  • pruritus is the most common symptom
  • vulvar bleeding and pain
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28
Q

What is the appearance of squamous cell carcinoma of the vulva?

A

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

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29
Q

What is the appearance of basal cell carcinoma of th vulva?

A

-Raised lesions with an ulcerated center and rolled border

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30
Q

What is the appearance of malignant melanoma of the vulva?

A

Seen at the labia minors and clitoris, raised and darkly pigmented lesion

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31
Q

What is the treatment of vulvar cancer?

A
  • Primary treatment is complete surgical removal of tumor with inguinal node dissection
  • Radiation therapy indicated with lymph node spread
  • Staging based on FIGO
32
Q

What has to be present for Vaginal intraepithelial neoplasia (VAIN)?

A

HPV infection

33
Q

What are the risk factors for VAIN?

A
  • Same as CIN (Smoking, multiple sex partners, and early onset of sexual activity)
  • History of CIN III
34
Q

What is the pathogenesis of VAIN?

A
  • HPV exposure
  • frequency of VAIN is not as high as CIN since vaginal epithelium is different than cervical
  • Most lesions are located in the upper 1/3 of the vagina
35
Q

What are the 3 classifications of VAIN?

A

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

36
Q

How is VAIN diagnosed?

A
  • Detection is via Pap smear

- Colposcopy

37
Q

What is the management of VAIN 1?

A
  • Observation is justified in younger women

- cytology/HPV/Colposcopy every 6 months

38
Q

What is the management of VAIN 2 and 3?

A

Surgical intervention vs chemotherapy

39
Q

What are the options for VAIN management?

A
  • Vaginectomy (90% success rate)
  • laser vaporization
  • total chemotherapy/ 5FU
40
Q

What is the most common cause of vaginal cancer?

A

Metastasis from endometrium, ovary, or cervix

41
Q

What is the most common type of vaginal cancer?

A

Squamous cell

42
Q

What is the clinical presentation of vaginal cancer?

A
  • Aymptomatic
  • Leukorrhea
  • vaginal odor
  • post-coital bleeding
  • Abnormal PAP
43
Q

What is the treatment of vaginal cancer?

A
  • Since occurrence is so rare there is no standardized treatment
  • combination of vaginectomy and radiation
  • 5 year survival rate is 61%
44
Q

What is the pathophysiology behind PCOS?

A
  • Abnormal androgen and estrogen metabolism
  • control of androgen production is unregulated
  • Insulin resistance and hyperinsulinemia
  • decreased adiponectin
  • Increased LH stimulates theca cells
  • FSH production is depressed
  • increased circulating insulin stimulates the ovary to produce more androgens
45
Q

What is the clinical presentation of PCOS?

A
  • Infertility
  • Oligomenorrhea/amenorrhea
  • Obesity
  • acne
  • hirsutism
  • male pattern baldness
46
Q

How is PCOS diagnosed?

A
  • NIH criteria
  • The following must be present: Oligomenorrhea and hyperandrogenism
  • The following causes must be excluded: hyperprolactinemia, CAH, Cushing syndrome
47
Q

What is the Rotterdam criteria for PCOS?

A

-Two of the three must be present after exclusion of related disorders: oligomenorrhea, clinical or biochemical signs of hyperandrogenism, and polycystic ovaries

48
Q

On pelvic US, you see a “string of pearls” on the ovaries. What should you suspect?

A
  • PCOS

- No evidence of dominant follicle/corpus luteum

49
Q

What is the treatment of PCOS?

A
  • weight loss
  • Metformin (only in patients with hyperinsulinemia and combin with Clomid for infertility)
  • COCs
  • Provera 10mgQD for endometrial protection
50
Q

If you see a thin walled adnexal mass that is <3cm in a premenopausal woman or <1cm in a postmenopausal woman, what should you suspect?

A

Simple adnexal cyst

51
Q

You see a hyperechoic nodule with distal acoustic shadowing of the adnexa. What should you suspect?

A

Teratoma

52
Q

What findings should you make you suspicious of a malignant adnexal mass?

A
  • Thick septations >2mm
  • Solid component appears nodular or papillary
  • blood flow to the solid component
53
Q

What US findings should make you thing of a hemorrhagic adnexal cyst?

A

Network of linear or curvilinear pattern

54
Q

What is the most common type of ovarian cyst?

A

Follicular

55
Q

What causes follicular ovarian cysts?

A
  • Failure of the mature follicle to rupture

- Failure of the non-dominant follicles to undergo atresia in the presence of the mature follicle

56
Q

What causes corpus luteum ovarian cysts?

A
  • Following ovulation, blood accumulates within the cavity of the corpus luteum which stimulates resorption. If resorption doesn’t occur and the corpus luteum is greater than 3cm it is considered a cyst
  • Usually resolves in 1-2 menstrual cycles
57
Q

What lab is often elevated with theca lutein cysts?

A

Elevated chorionic gonadotropin levels

58
Q

What is the pathophysiology of mature teratomas?

A
  • Benign neoplasms
  • originate from primordial germ cells, teratomas are found along the migration pathway of germ cells from yolk sac to gonads
  • Composed of well differentiated tissue derived from any of the 3 germ layers
59
Q

What is the most common origin of mature teratoma?

A

Ectoderm also germ (hair, teeth)

60
Q

What is the clinical presentation of mature teratomas?

A
  • Asymptomatic
  • Pelvic pain
  • Urinary frequency or urgency
  • Back pain
61
Q

What labs should be ordered for a mature teratoma?

A
  • Transvaginal US

- CEA, CA-125, AFP, and beta HCG (all tumor markers that should be within normal limits)

62
Q

What is the treatment of a mature teratoma?

A
  • Laparotomy vs laparoscopy

- Ovarian cystectomy vs oophorectomy

63
Q

What are serous/mucinous cystadenoma?

A
  • Benign neoplasms
  • lined with columnar epithelium, secretes a thick gelatinous mucin
  • May be uni or mulitlocular
64
Q

What is the treatment of serous/mucinous cystadenoma?

A

Surgical excision and ensure benign pathology

65
Q

What is the second most common gynecologic cancer?

A

Ovarian cancer

66
Q

What is the most common cause of GYN cancer death in the US?

A

Ovarian cancer

67
Q

What are the risk factors for ovarian cancer?

A
  • Nulliparity
  • early menarche
  • late menopause (increased menses= increased risk)
68
Q

What are the 4 types of ovarian cancer?

A
  • Epithelial
  • germ cell
  • Sex cord and stromal
  • neoplasms metastatic to the ovary
69
Q

What is the most common type of ovarian cancer?

A

Epithelial cancer

70
Q

What kind of ovarian cancer is associated with high grade serous papillary cancer?

A

Fallopian tube epithelial ovarian cancer

71
Q

What are the 4 types of ovarian cancer epithelial neoplasms?

A
  • high grade serous carcinoma (Fallopian tube, most common)
  • Endometrioid carcinoma (ovary)
  • Clear cell carcinoma (Ovary)
  • Mucinous carcinoma (Ovary)
72
Q

Does epithelial or germ cell ovarian cancer occur in younger women?

A

Germ cell, highest incidence at 20-30 years old

73
Q

What are the 5 types of germ cell ovarian cancer?

A
  • Dysgerminoma (Most common, unilateral)
  • Yolk sac tumor (unilateral)
  • Immature teratoma (unilateral)
  • Embryonal carcinoma (mixed germ cell tumors
  • Choriocarcinoma (mixed germ call tumors)
74
Q

What are the two types of sex-cord stromal tumors?

A
  • Granulosa cell (most common, causes hyperestrogenism and precocious puberty)
  • Sertoli stromal cell (rare, causes hyperandrogenism)
75
Q

If CA-125 is elevated, what should you be suspicious of?

A

Epithelial ovarian cancer

76
Q

If hCG, AFP, or LDH is elevated, what ovarian cancer should you be suspicious of?

A

Germ cell tumors because they produce high levels of these hormones