1 Vulvar and Ovarian Disease Flashcards

1
Q

Autoantibodies attack extracellular matrix and basement membrane —> immune dysfunction affecting all levels of the skin

A

Lichen Sclerosus

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2
Q

What are some environmental factors that can affect/exacerbate lichen sclerosus?

A

Incontinence
Infection
Contact dermatitis
Trauma (Kobner’s phenomenon)

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3
Q

What population is most likely to experience lichen sclerosus?

A

Postmenopausal women

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4
Q

Most common symptom for women with lichen sclerosus

A

Pruritis

Common for them to describe sleeping with ice packs to numb the vulva

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5
Q

Clinical presentation of lichen sclerosus

A

Typically postmenopausal women

Pruritis**
Dysuria
Dyspareunia

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6
Q

Physical exam findings for lichen sclerosus

A

Sharply, well-demarcated white plaques - “cellophane paper”, waxy, and/or hyperkeratotic in appearance

Fragility is hallmark - purpura, erosions, fissures

Usually begins periclitorally —> spread to perineal skin

Not usually seen in keratinized, hair-bearing labia majors or mucus membranes

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7
Q

“Cellophane paper” plaques

A

Lichen sclerosus

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8
Q

Sparing of keratinized, hair-bearing labia Majorca

A

Lichen sclerosus

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9
Q

_________ occurs in 5% of women with untreated lichen sclerosus

A

Squamous cell carcinoma

Risk factors = elderly, hyperkeratotic lesions

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10
Q

Patients with lichen sclerosus have a higher incidence of associated _______

A

Hypothyroidism

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11
Q

What lab do you need to diagnose lichen sclerosus?

A

Vulvar punch biopsy

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12
Q

Treatment for lichen sclerosus

A

Topical ultra potent steroid OINTMENT*** (b/c has to penetrate keratinized skin)

First line = Temovate 0.05% BID until texture is normal, then 1-3x/week for maintenance

Side fx = atrophy, dermatitis, rosacea (signs you’re using it too often)

Alternative = topical estrogen

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13
Q

What patient ed do you need to give for lichen sclerosus?

A

Does not go away - needs long term follow up

Encourage self exams and vulvar awareness

Side effects of topical steroid (atrophy, dermatitis, rosacea) indicate you’re using the steroid too much

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14
Q

Bilateral glands found at teh 4 and 8 o’clock positions within the labia minora

A

Bartholin glands

Open into teh vestibule adjacent to the vaginal Introitus —> secrete mucus-like material to maintain moisture of the vaginal mucosa

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15
Q

Bartholin cysts form as a result of _______ due to ________

A

Duct all obstruction

Trauma or non-specific inflammation

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16
Q

Bartholin abscess formation results from ….

A

An infected cyst or primary gland infection (polymicrobial, STI)

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17
Q

Clinical presentation of bartholin cysts

A

Abrupt onset of acute, painful unilateral labial swelling

Dyspareunia

Pain with sitting or walking

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18
Q

Physical exam findings for bartholin cyst/abscess

A

Tender, fluctuating labial mass

Surrounding erythema and edema

Cellulitis

Abscess formation

Fever

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19
Q

Treatment for bartholin cyst

A

Incision and drainage with insertion of Word catheter to prevent re-accumulation of pus)

Culture purulent material

+/- empirical abx (Keflex or Doxy)

Site baths 2-3 days after I&D

No intercourse until catheter removed

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20
Q

What causes vulvodynia?

A

We have no idea!

Maybe estrogen concentration (affecting pain sensitivity)?

Maybe pelvic flood dysfunction?

Maybe psychological factors?

Maybe neurologic sensitization (secondary to chronic inflammation)?

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21
Q

Clinical presentation of vulvodynia

A

Vulvar discomfort (“burning sensation”, stinging, irritated, sore, raw, stabbing)

Absent clinical findings and no underlying vulvar/vaginal pathology

Introital pain with intercourse

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22
Q

How to evaluate vulvodynia

A

Use a Q-tip to palpate vestibule, labia majora, perineum, interglacial folds

Pain is usually limited to vestibule

Single digit exam to feel for spasm or tenderness of the pelvic floor muscles

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23
Q

What is the of treatment for vulvodynia?

A

They’ll never get back to 100% but you want to get them back to functionality

Avoid scented products, tight clothing, vigorous exercise, pantyliners/pads

Sitz baths BID followed by thin film of petroleum jelly

Couples counseling

Pelvic floor therapy

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24
Q

Pharmacologic treatment for vulvodynia

A

Topical vaginal estrogen 0.03% w/ testosterone 0.1% (QD)

Nortriptyline 50 mg QHS (begin with 10mg and titrate up)

Gabapentin 1200 mg TID (begin with 100mg and titrate up)

Local nerve block (but it wears out)

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25
Q

Neoplasticism cells confined to squamous epithelium

A

Vulvar Intraepithelial Neoplasia (VIN)

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26
Q

What are the classifications of VIN

A

VIN 1, 2, or 3 (just like CIN)

But really, you could eliminated VIN 1 and combine 2/3 as the true precursors to vulvar cancer

VIN 2/3 are further differentiated into VIN-U and VIN-D

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27
Q

VIN 2/3 are subdivided into _____ and ______ based on _____.

A

VIN-U (usual type)

VIN-D (differentiated)

Based on morphologic manifestations, HPV content, and clinical characteristics

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28
Q

Which type of VIN:

Associated with HPV type 16 and 18

A

VIN-U

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29
Q

Which type of VIN:

Seen in younger women

A

VIN-U

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30
Q

Risk factors for VIN-U

A

Same as for CIN

Smoking (50-80%)
Immunosuppression
Multiple sex partners

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31
Q

How is VIN-U diagnosed?

A

Vulvar colposcopy

3-5% acetic acid applied, wait 3-5 min, maybe reapply

Avoid using acetic acid in areas of inflammation and breaks in epithelium

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32
Q

Colposcopy findings consistent with VIN-U

A

Lesions are raised or flat

Range in color from gray to white or red to black

Must biopsy all pigmented (or hypopigmented) lesions**

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33
Q

How do patients with VIN-U typically present?

A

Most are ASYMPTOMATIC

Vulvar burning and pruritis in 50%

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34
Q

Why are colposcopies mandatory for VIN-U?

A

Associated with high grade CIN

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35
Q

What is the cure for VIN-U?

A

THERE IS NONE!

Frequent failure to include all lesions when surgically treating

Re-activation of latent HPV common

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36
Q

What are the off-label use medical therapies for VIN-U?

A

5FU (Efudex) cream (lots of S/E’s so women don’t like)

Interferon (Intron-A)

Imiquimod (Aldara) 5% cream - low compliance b/c freq application

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37
Q

What treatment is the standard of care for VIN-U?

A

Surgical
• CO2 laser vaporization (destruction of entire thickness of epithelium)
• Local wide excision
• Vulvectomy

Post-treatment recurrence rate is 30-50%

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38
Q

Which type of VIN:

Unrelated to HPV

A

VIN-D

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39
Q

Which type of VIN:

Seen in older women (>70)

A

VIN-D

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40
Q

Which type of VIN:

Involves lower 1/3 of epithelium

A

VIN-D

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41
Q

Which type of VIN:

Associated with squamous cell hyperplasia (ie - untreated Lichen Sclerosus or Lichen Simplex Chronicus)

A

VIN-D

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42
Q

What is the treatment for VIN-D?

A

Surgical excision

NO CO2 laser - you want clear margins

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43
Q

What is the recommended follow up for VIN?

A

If VIN-U, vaccination with Gardasil

Women w/ a hx of VIN should be considered at risk for recurrence throughout lifetime

Post treatment f/u includes colposcopy at 6 and 12 months then annually thereafter

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44
Q

Is vulvar cancer common?

A

Hahaha, NOPE

Only accounts for 5% of gyn cancers - it’s extremely rare

But for some reason she then put it’s the fourth most common malignancy of the female genital tract 🙄

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45
Q

10% of women with vulvar cancer also have ______ and 30-50% are _______ or _______.

A

Type II DM

Obese or Hypertensive

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46
Q

What age is most affected by vulvar cancer?

A

Incidence has a bimodal peak

20-40 year olds = HPV related (VIN-U)

60-70 year olds = due to chronic irritation or squamous cell hyperplasia (VIN-D)

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47
Q

Vulvar cancer that develops from VIN-U typically affects ______ and is related to ______

A

20-40 yo

HPV

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48
Q

Vulvar cancer that develops from VIN-D typically affects ______ and is related to ______

A

60-70 yo

Untreated, long-lasting lichen sclerosus, lichen simplex chronicus, or squamous cell hyperplasia

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49
Q

Clinical presentation of vulvar cancer

A

ASYMPTOMATIC (—> delayed diagnosis)
• Always inspect the vulva!

Pruritis is most common Sx if they have any

Also, vulvar bleeding and pain

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50
Q

What are the three types of vulvar cancer?

A

Squamous cell carcinoma

Basal cell carcinoma

Malignant melanoma

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51
Q

You inspect a woman’s vulva during her well-woman exam and find lesions varying in appearance, from large, exophytic cauliflower-like lesions to small ulcerative lesions with surrounding hyperkeratosis.

What you think?

A

Squamous cell carcinoma

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52
Q

You inspect a woman’s vulva during her well-woman exam and find a raised lesion with an ulcerated center and rolled borders.

What you think?

A

Basal cell carcinoma

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53
Q

You inspect a woman’s vulva during her well-woman exam and find lesions on the labia minora and clitoris that are raised and darkly pigmented.

What you think?

A

Malignant melanoma

Good for you for finding it! Most dermatologists are idiots and don’t bother looking at the hoo-ha

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54
Q

What is the primary treatment for vulvar cancer?

A

Complete surgical removal of tumor with inguinal node dissection

Radiation therapy indicated with lymph node spread

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55
Q

What has to be present for a woman to develop VaIN?

A

HPV

51-62% have been previously treated for CIN

25% have undergone hysterectomy for CIN

75% have preceding or co-existing squamous cell carcinoma of the vulva or cervix

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56
Q

Mean age of incidence for VaIN?

A

35-55

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57
Q

Risk factors for VaIN?

A

Same as CIN!

Smoking
Multiple sex partners
Early onset of sexual history

History of CIN III

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58
Q

What is the pathogenesis of VaIN?

A

HPV EXPOSURE IS A MUST!

Development of VaIN following HPV exposure requires greater period of time

Frequency of VaIN not as high as CIN since vaginal epithelium is different from cervical

59
Q

Most VaIN lesions are located in the ______

A

Upper 1/3 of the vagina

60
Q

What are the different classifications of VaIN?

A

VaIN 1 = benign viral proliferation

VaIN 2 = intermediate risk

VaIN 3 = true precursor to vaginal cancer

61
Q

How do you diagnose VaIN?

A

Detection via Pap smear (cytology) —> colposcopy

62
Q

What are the differences in management between the different classifications of VaIN?

A

VaIN 1 = observation in younger women, with cytology/HPV/Colposcopy q6 months

VaIN 2/3 = surgical intervention vs chemo

63
Q

What is the treatment for VaIN?

A

Vaginectomy - 90% success rate but you lose your vagina

Laser Vaporization - 63-90% successful

Topical chemotherapy (5FU) - 50-85% successful
• Only used if other treatment options aren’t feasible (not FDA approved for this indication)
64
Q

Most common cause of invasive cancer in the vagina

A

Metastasis from endometrium, ovary, or cervix

FIGO states only when the primary site of growth is from the vagina can it be called vaginal cancer

65
Q

Age for vaginal cancer

A

> 50

Only <20% are diagnosed before 50

66
Q

Most common type of cancer in the vagina

A

Squamous cell (80-92%)

67
Q

Clinical presentation of vaginal cancer

A

ASYMPTOMATIC

Leukorrhea
Vaginal odor
Post-coital bleeding
Abnormal Pap smear

68
Q

Your patient’s Pap smear is abnormal. You do a colposcopy. What changes are indicative of vaginal cancer?

A

Acetowhite changes, punctation, or mosaicism

69
Q

Treatment for vaginal cancer

A

It’s super duper rare, so no STANDARD treatment

Combo vaginectomy and radiation

5 year survival rate is 61%

70
Q

Polycystic Ovarian Syndrome results from…

A

Abnormal androgen and estrogen metabolism —> unregulated androgen production —> high serum testosterone, androstenedione, and DHEA

71
Q

What is the relationship between PCOS and insulin?

A

PCOS —> insulin resistance and hyper insulin emit

Increased insulin alters gonadotropin (FSH/LH) effects on ovarian function

Increased insulin decreases synthesis of sex hormone binding globulin (SHBG) and insulin-like growth factor

72
Q

What happens to adiponectin in PCOS patients?

A

Decreased

Adiponectin regulates lipid metabolism and glucose levels, so decreased adiponectin further exacerbates PCOS symptoms

73
Q

What role do gonadotropins play in PCOS?

A

Increased LH stimulates theca cells to produce androgens

FSH is depressed (b/c negative feedback) —> decreased aromatase in the ovary —> decrecreased conversion of androgens to estrogens

74
Q

In PCOS, increased androgens released from the ovary are converted to estrogen by…

A

Adipose tissue

This causes negative feedback to anterior pituatary and further decrease in FSH production

75
Q

In PCOS, increased circulating insulin stimulates…

A

The ovary to produce more androgens —> elevated circulating free testosterone

76
Q

Most common symptom of PCOS

A

Infertility

77
Q

Clinical presentation of PCOS

A
Infertility
Oligomenorrhea/amenorrhea**** 
Obesity
Acne****
Hirsutism****
Male pattern baldness
Acanthosis nigricans
78
Q

What conditions must be ruled out when diagnosing PCOS?

A

Hyperprolactinemia
Congenital adrenal hyperplasia
Cushing’s syndrome

79
Q

What is the Rotterdam Criteria of 2003 for PCOS?

A

2/3 must be present after exclusion of related disorders:
• Oligomenorrhea
• Clinical or biochemical signs of hyperandrogrenism
• Polycystic ovaries

Did not replace NIH definition, just expanded it to include polycystic ovaries

80
Q

Ultrasound findings in PCOS

A

Presence of >12 follicles in each ovary 2-9mm

“String of pearls” appearance

Ovarian volume >10ml

No evidence of dominant follicle/corpus luteum

81
Q

What lab do you order first if suspecting PCOS?

A

Total testosterone

Normal = 40-60 ng/dL

Elevated if >60 ng/dL —> further lab eval

82
Q

So your patient who you suspect has PCOS had a total testosterone >60 ng/dL.

What you wanna order next?

A

17-OH progesterone

DHEA-S

Cortisol

Prolactin

TSH

ßHCG

83
Q

Why order this test when working up PCOS?

17-OH progesterone

A

R/o congenital adrenal hyperplasia

84
Q

Why order this test when working up PCOS?

DHEA-S

A

R/o adrenal source for increased testosterone

85
Q

Why order this test when working up PCOS?

Cortisol

A

R/O cushing’s

86
Q

Why order this test when working up PCOS?

Prolactin

A

R/o hyperprolactinemia

87
Q

Why order this test when working up PCOS?

TSH

A

Increased thyroid can cause oligo/amenorrhea

88
Q

Why order this test when working up PCOS?

bHCG

A

Because pregnancy is the most common cause of secondary amenorrhea

89
Q

Treatment for PCOS

A

WEIGHT LOSS!!!! Restores predictable cycling

Metformin ONLY for patients with hyperinsulinemia (500mg BID) - combine with Clomid for infertility

Combined oral contraceptives (pick one with low androgenic activity)

Fertility consult

Provers 10mg QD x 10d for endometrial protection

90
Q

PCOS puts patients at risk for …

A
Endometrial hyperplasia/carcinoma
T2DM
Hypertension
Hyperlipidemia
CVD
Stroke
Infertility
Metabolic syndrome
Sleep apnea
91
Q

What types of adnexal masses are benign?

A
Thin walled on U/S
Endometrioma
Hemorrhagic 
Teratoma
Simple cysts (<3cm in premenopausal, <1cm in postmenopausal)
92
Q

U/S shows Homogenous echos

A

Endometrioma (benign)

93
Q

U/S shows network of linear or curvilinear pattern

A

Hemorrhagic cyst

94
Q

U/S shows cyst <3 cm in a premenopausal woman

A

Simple cyst

<1cm in postmenopausal woman

95
Q

U/S shows hyperechoic nodule with distal acoustic shadowing

A

Teratoma

96
Q

U/S findings that suggest malignancy for adnexal masses

A

Thick septations (>2mm)
Solid component, appears nodular or papillary
(+) blood flow to solid component

97
Q

What are the different types of ovarian cysts

A
Follicular*** (most common)
Corpus luteum cyst
Theca lutein cyst
Mature teratoma
Serous/mutinous cystadenoma
98
Q

Follicular ovarian cysts range in diameter

A

2-8 cm

99
Q

Are follicular cysts bad?

A

Nope - common and non-malignant

Will regress after 1-2 menstrual cycles

100
Q

Follicular cysts result from …

A

Failure of the mature follicle to rupture (no ovum released)

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

101
Q

Corpus luteum cysts range in size

A

3-11 cm

102
Q

How do corpus luteum cysts form?

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 resolve after 1-2 menstrual cycles

103
Q

When do you patients develop theca lutein cysts?

A

With elevated chorionic gonadotropin levels (those going through infertility treatment

Usually seen bilaterally

104
Q

Fluid in theca lutein cysts is…

A

Clear, straw colored

105
Q

Where do mature teratomas originate from?

A

Parthenogenic theory:
• Originate from primordial germ cells
• Teratomas are found along the migration pathway of germ cells from yolk sac to gonads

106
Q

Which germ layer is the most common type of mature teratoma?

A

Ectodermal

That’s why you get hair, teeth, etc in them

107
Q

What does the histology look like for mature teratomas?

A

Cyst is lined with keratinized squamous epithelium with abundant sebaceous and apocrine glands

108
Q

How do mature teratomas present?

A

Asymptomatic - found via pelvic exam or incidental finding on other radiologic studies

Pelvic pain is usually secondary to torsion or rupture (rare)

Urinary frequency/urgency

Back pain

109
Q

What do you need to do to diagnose mature teratomas?

A

PE - pelvic mass on bimanual exam

Transvaginal U/S - shows unilateral, complex cyst

CEA, CA-125, AFP, and ßHCG all should be within normal limits

110
Q

Treatment for mature teratoma

A

Laparotomy vs laparoscopy (depends on size)

Ovarian cystectomy vs oophorectomy

Recurrence is ~10%

111
Q

Who usually gets serous/mutinous cystadenomas?

A

Women 30-50 yo

112
Q

Histology of serous/mutinous cystadenomas

A

Lined with columnar epithelium

Secrete thick, gelatinous mucin

Thin-walled, uni- or multilocular, and range in size from 5 to over 20 cm

113
Q

How do you treat serous/mutinous cystadenomas?

A

Surgical excision

Ensure benign pathology

114
Q

2nd most common gynecologic cancer

A

Ovarian cancer

2nd most common but most common cause of gynecologic death in the US

115
Q

Highest incidence of ovarian cancer is in women…

A

65-74 yo

116
Q

Risk factors for ovarian cancer

A
NULLIPARITY****
Infertility treatment
Obesity and diets high in sat fat
Talcum powder
Personal hx of BC
Family hx of breast, ovarian, or colorectal cancer
Turner’s Syndrome
Early menarche****
Late menopause****
Estrogen replacement therapy 
Caucasian race
Endometriosis
117
Q

Protective factors for ovarian cancer

A
Multiparity***
Breastfeeding
Long-term oral contraceptive use**** (at least 5 years of use reduces the relative risk of ovarian cancer by 50%)
Bilateral tubal ligation
Low fat diet
Bilateral salpingectomy
118
Q

What are the four categories of ovarian cancer?

A

Epithelial
Germ cell
Sex cord and stromal
Neoplasms metastatic to the ovary

119
Q

What are the subtypes of epithelial ovarian cancer?

A

High-grade serous carcinoma
Endometriod carcinoma
Clear cell carcinoma
Mucinous carcinoma

120
Q

What are the subtypes of germ cell ovarian cancer?

A
Dysgerminoma 
Endodermis sinus
Immature teratoma
Embryonal carcinoma
Choriocarcinoma
121
Q

What are the subtypes of sex cord and stromal ovarian cancer?

A

Granulosa cell

Sertoli-stromal cell

122
Q

Most common origin for metastatic ovarian cancer

A

Stomach
Colon
Breast

123
Q

Pathophysiology of epithelial ovarian cancer in the ovary

A

Incessant ovulation theory - repeated ovarian epithelial trauma by follicular rupture and subsequent remain —> malignant transformation

Associated with endometriod, mucinous, or clear cell cancer

124
Q

Pathophysiology of epithelial ovarian cancer in the Fallopian tube

A

p53 tumor suppressor gene

Associated with high grade serous papillary cancer

125
Q

Which type of epithelial ovarian cancer is most common?

A

High-grade serous carcinoma

Arises from the Fallopian tube

126
Q

Which epithelial neoplasms arise from the Fallopian tube?

A

High-grade serous carcinomas

127
Q

Which epithelial neoplasms arise from the ovary?

A

Endometriod carcinoma
Clear cell carcinoma
Mucinous carcinoma

128
Q

Highest incidence of germ cell ovarian cancer is in women…

A

20-30 years

129
Q

What are the characteristics of germ cell ovarian cancers?

A

Younger women

Tend to grow rapidly

Favor lymphatic spread

Contain mix of tumor types

Usually unilateral

Produce tumor markers (helpful in tx)

130
Q

Most common type of germ cell neoplasm

A

Dysgerminoma

Unilateral in 85-90%

90% in women <30

131
Q

Unilateral or bilateral:

Endodermis Sinus Tumor

A

Bilateral

132
Q

Which germ cell neoplasm type displays the most rapid growth?

A

Endodermal sinus tumor

133
Q

Which germ cell tumors are associated with alpha fetoprotein?

A

Endodermal sinus tumor

Immature teratoma

Embryonal carcinoma

134
Q

2nd most common type of germ cell neoplasm

A

Immature teratoma

Seen most commonly in patients <20

Usually unilateral

135
Q

Which germ cell neoplasm is associated with both AFP and HCG?

A

Embryonal carcinoma

Rapid growth with extensive spread

136
Q

Which type of germ cell neoplasm is seen with precocious puberty, uterine bleeding or amenorrhea?

A

Choriocarcinoma

Seen most commonly in the 2nd decade of life

137
Q

Most common type of sex-cord/stromal tumor

A

Granulosa cell (70%)

138
Q

(Sex-cord stromal tumors)

_______ cause hyperestrogenism

_______ cause hyper androgens

A

Granulosa cell

Sertoli-stromal cell

139
Q

Acute sx of ovarian cancer

A

Pleural effusion

Bowel obstruction

140
Q

Subacute sx of ovarian cancer

A
Adnexal mass
Bloating/abdominal distention
Early satiety
Pelvic/abdominal pain
Abnormal vaginal bleeding
Altered bowel habits
Dyspepsia
141
Q

PE findings for ovarian cancer

A

Ascites
Inguinal LAD
Pelvic mass

142
Q

What labs/imaging you wanna order if suspecting ovarian cancer?

A

Transabdominal/vaginal U/S
Mammogram/colonoscopy
CT
MRI
CXR
CA-125 (suspected epithelial ovarian cancer)
hCG, AFP, LDH (suspected germ cell tumor)

143
Q

Treatment for epithelial ovarian cancer

A

GYN onco consult

Surgical staging (FIGO)

Chemo

144
Q

Germ cell ovarian cancer treatment

A

GYN onco consult

Early dx allows removal of involved adnexa with preservation of contralateral adnexa and uterus

Surgical staging (FIGO)