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Womens Health > Exam 2 Vulvar and Ovarian dz > Flashcards

Exam 2 Vulvar and Ovarian dz Flashcards

1
Q

Etiology, description and potential risk of Lichen Sclerosis

A

Poorly understood

  • autoimmune
  • genetic
  • environmental

Benign chronic inflammatory process; fragility is hallmark

SCC occurs in 5% of untx

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2
Q

How do pt with Lichen Sclerosus Present

A

Primarily in postmenopausal
- Pruritus, dysuria, dyspareunia

Usually begins periclitoral and spread to perineal skin

Pigment changes are usu benign but may be a/w atypical nevi or melanoma

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3
Q

What PE findings would be indicative of Lichen Sclerosus

A
  • Demarcated white plaques
  • Cigarette/ CELLPHANE PAPER - waxy &/or hyperkeratotic appearance
  • Fragility - purpura, erosions, fissures
  • Not usually seen at keratinized, hair bearing labia major or mucus membranes (vestible, vagina, rectal mucosa)
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4
Q

Labs and dx for Lichen Sclerosus

A

Labs/dx: vulvar punch biopsy

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5
Q

Tx of Lichen Sclerosus

A
  1. Stop Itch/scratch cycle
  2. Topical superpotent steroid OINTMENT (Clobetasol) qhs for 6-12 wk then 1-3x/wk for LIFE (se: atrophy, dermatitis)
  3. Topical estrogen for atrophy
  4. *educate pt that Lichen sclerosis is CHRONIC and RECURRING if tx stopped
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6
Q

DX:

Think of Ps→ Postmeno, pruritis, dysPareunia, Poorly understood pathophys, Plaques, (cigarette) Paper, Purpura, Punch biopsy, Periclitoral to Perineal, Potent steroid, Potential Progression to CA, Pigment imPortant

Sclerosus to Squamous

A

Lichen Sclerosus!

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7
Q

Bartholin Gland: function and etiology of cysts?

A
  • Bartholin glands secrete mucus like material to maintain moisture of vaginal mucosa
  • Cysts form as a result of ductal obstruction due to trauma or inflammation
  • abscess formation if infected cyst or primary gland infection
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8
Q

How would pt with Bartholin Cyst present?

A

USU acute UNILATERAL

Painful labial swelling w/ dyspareunia & pain w/ walking or sitting

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9
Q

What PE exam findings are indicative of Bartholin Cyst

A
  • Tender, fluctuant labial mass with Erythema, edema,
  • Cellulitis
  • Possible abscess &
  • Fever

CATS fever (cellulitis, abscess, surrounding erythema/edema, tender labial mass)

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10
Q

Bartholin Cyst: tx

A
  • I&D w/ word catheter
  • Culture purulent material
  • +/- empirical abx (if cellulitis): Bactrim (TMP-SMX)
  • Sitz baths 2-3d after I&D
  • Avoid intercourse w/ catheter
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11
Q

Tips for remembering Bartholin Gland info…

A

Bartholin Bathes the vaginal mucosa*

Bartholin – Bactrim and Baths (sitz)

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12
Q

What is VIN and how is it categorized

A

Vulvar intraepithelial Neoplasia

Neoplasia confined to squamous epithelium

VIN1-3: 1 gone, 2/3 comb
VIN2/3 differentiate into VINu & VINd based on morph, HPV content, & clinical characteristics

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13
Q

Characteristics of VINu?

A
  • 90% assoc w HPV 16, 18
  • Commonly younger women
  • Risks same as CIN: smoking, immunosuppression, mult sex partners
  • Usu asymp
  • Vulvar burning, pruritus in 50%
  • a/w high grade CIN - must do colposcopy
  • Biopsy all pigmented lesions
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14
Q

Characteristics/ etiology/ location/ association of VINd?

A
  • Unrelated to HPV (does not have same risk factors as VINu)
  • Older women, lower 1/3 of epithelium (d is down)
  • a/w squamous cell hyperplasia (lichen sclerosus, Lichen Simplex Chronicus)
  • carcinogenic agents combined w/ local chronic irritation & inflammation of skin lead to dysplastic cells
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15
Q

What is ACOG/ASCCPs position statement regarding women with hx of VIN

A
  • Woment with hx of VIN should be considered at risk for recurrence throughout their lifetime
  • Post tx f/u includes colposcopic vulvar inspection at 6 and 12 mth then yearly Follow up:
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16
Q

Describe the process of Vulvar colposcopy

A
  • 3-5 % acetic acid:
  • Accentuates white lesions and abnormal vascular patterns
  • Biopsy multiple sites
  • Shows flat or raised lesions of gray to white or red to black

*Biopsy ALL pigmented lesions

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17
Q

How should you manage VINu?

A 
•	If concern for invasion → surgical tx recommended (wide local excision)
•	If CA not suspected →
o	CO2 laser vaporization
o	Med: Imiquimod (Aldara) 
•	Post tx recurrence rate 30-50%
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18
Q

How should you manage VINd?

A

Prevention: tx underlying condition (ie lichen sclerosus - clobetasol, topical estrogen)

Tx: SURGICAL EXCISION

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19
Q

Vulvar CA: incidence, frequency, risk?

A 
Uncommon, 5% gyn CA
Bimodal Peak
•	Younger: HPV & VINu related
•	Older: Chronic irritation and poorly understood cofactors (VINd)
Smoking increases risk
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20
Q

Hint for remembering VINu and HPV association

A

HPV is a USUAL std, the vinUsual is associated with HPV”

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21
Q

Vulvar CA: presentation/sx

A
  • Asymptomatic →delays Dx (INSPECT THE VULVA!!)
  • Pruritus most common sx
  • Vulvar bleeding
  • Vulvar pain
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22
Q

What are the potential types of Vulvar CA

A

Squamous, BCC, Malignant Melanoma

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23
Q

How do you distinguish the different types vulvar CA on PE

A

Squamous - varied appearance, exophytic, cauliflower like lesion to small ulcerative lesion with surrounding hyperkeratosis

Basal cell- raised lesion w/ ulcerated center rolled border

Melanoma - raised, dark lesion seen at labia minora and clitoris

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24
Q

How do you treat Vulvar CA

A

Staging - FIGO
Complete surgical removal of tumor w/ inguinal nodes
Radiation if lymph spread

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25
Q

Vulvar CA Prognosis

A

70% 5 yr survival

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26
Q

VaIN: what is it, incidence/associations, risk factors?

A
  • Rare
  • Mean age: 43-60 yo
  • > 90% aw HPV
  • 50-66% of pt w VaIN have/had cervical or vulvar neoplasia
  • Same risks as CIN & VINu: smoking, mult sex partners, immunosuppression

[CIN, VINu and VaIN same risk factors]

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27
Q

Pathogenesis of VaIN

A
  • HPV exposure
  • Dev. of VaIN after HPV exposure (requires time)
  • CIN more freq than VaIN bc vaginal epithelium is diff than cervical
  • Most lesions upper 1/3 of vagina (vinD is lower 1/3)

“the vain upper class (upper 1/3 vagina)”

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28
Q

How is VaIN classified/categorized?

A

VaIN 1: involves basal epithelial layers

VaIN 2: 2/3 vag epithelium

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29
Q

VaIN: presenation and labs/sutdies

A

Usually asymp, +/- postcoital spotting, vaginal dc; abnormal pap

Labs: Colposcopy for VaIN

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30
Q

Mgmt of VaIN?

A

VaIN 1: observation
VaIN 2/3: surgery is mainstay; meds: imiquimod (aldara) and 5-FU

Prognosis: 20-30% recurrence

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31
Q

Vaginal CA: Occurence, type, label

A
  • Invasive most commonly due to metastasis from ovary, cervix, or endometrium
  • Primarily W>55yo
  • Usu squamous cell (80-90%)

According to FIGO, can only label as vaginal CA if primary site is the vagina

32
Q

Vaginal CA: Presentation

A
  • Asymptomatic,
  • Painless Vaginal Bleeding
  • Vaginal dx
  • Pelvic Pain
33
Q

Tx of Vaginal CA

A

SO rare - no standardized
*vaginectomy, radiation, chemo

5 yr survival 42%

34
Q

Types of Ovarian cycsts

A

4 physiologic types:

  1. Follicular,
  2. Corpus luteum,
  3. Theca Lutein,
  4. Mature teratoma*
35
Q

Steps in folliculogenesis

A
  1. Egg, ovulation
  2. Corpus Lutein, degenerating corpus luteum
  3. Primary oocytes
  4. Dev of oocyte and follicle
  5. Continued dev of follicle
  6. Primary oocyte
  7. Secondary oocyte
  8. Mature follicle
36
Q

Of the Four type of Ovarian cysts, what is the most common cause of this cyst? Size, prognosis?

A 
folllicular cyst most common 
•	Results from failure of a mature follicle to rupture
•	Size: ~3-8 cm 
•	NON MALIGNANT
•	Most spontaneously regress w/in 6w
37
Q

Corpus Luteum Ovarian Cyst: size, cause, prognosis

A
  • 3-11 cm
  • Due to failure to resorb the blood after ovulation and the CL is >3 cm then considered a cyst
  • Usu resolves in 1-2 menstrual cycles
38
Q

THeca Lutein Cysts (Ovarian Cyst): association, characteristics, prognosis

A
  • Seen w ↑chorionic gonadotropin (hydatidiform mole, choriocarcinoma, clomid tx (infertility))
  • Usu bilateral
  • Clear, straw colored fluid
  • Cysts regress spontaneously with tx of underlying disorder (ie get rid of pregnancy or stop infertility tx)
39
Q

Snowstorm appearance on Ovarian UTZ…

A

hydatidiform mole

40
Q

Benign ovarian neoplasm - Mature Teratoma:

incidence, composition?

A
  • 40-50% benign neoplasms
  • Reproductive age women
  • Composed of well diff tissue derived from any of the 3 germ layers (ectoderm, mesoderm, endoderm)
41
Q

Mature Teratoma (Benign Ovarian Neoplasm): Presenting s/sx

A
  • Asymptomatic (found on pelvic exam or incidental finding on other radiologic studies)
  • Pelvic pain (secondary to torsion or rupture; rare)
  • Urinary frequency or urgency,
  • Back pain
42
Q

Mature Teratoma (Benign Ovarian Neoplasm): PE findings, Labs/studies

A

PE: Pelvic mass on bimanual

Labs/studies
• Transvaginal US (unilateral complex cyst)
• CEA, CA125, AFP, hCG (all should be wnl)

43
Q

Mature Teratoma (Benign Ovarian Neoplasm): tx

A

Laparotomy v Laparoscopy
Ovarian cystectomy v Oophorectomy
Recurrence ~10%

44
Q

Ovarian CA frequency, mortality and age range

A
  • 5th most common cause of CA related death in US females
  • High probability of mortality
  • Half of all ovarian CA found in women >63yo
45
Q

4 of the many Theories of Ovarian CA etiology include

A
  1. incessant ovulation,
  2. Gonadotropin stimulation
  3. excess androgenic stimulation
  4. inflammation
46
Q

Risk factors for Ovarian CA

A

BRCA, HNPCC (Lynch), BRCA, family hx, genetic , endometriosus, infertility, PCOS, smoking, OC, breast feeding >12mth, tubal ligation, previous preg

47
Q

Increased risk of Ovarian CA…

A

Delayed childbreaing, early menarch, late menopause
Low parity, Fam hx, estrogen replacement,, genetic
high fat diet, endometriosus

48
Q

Decreased risk of Ovarian CA

A

Breastfeeding for >18 mth
Early menopause
Multiparity, OC, Tubal Ligation, Hysterectomy
Late menarche, low fat diet

49
Q

SGO recommendations re Salpingectomy and ovarian CA prevention

A

after completion of childbearing, BRCA women or women at risk should undergo bilat salpingectomy for Ovarian CA prevention and oophrectomy

50
Q

Categories of Ovarian CA include..

think GEMSS

A

Germ cell
Epithelial
Mets to ovary
Sex/stromal

51
Q

Which of the types of ovarian histopathologies is most common? Origin and categorization/subtypes of this cancer?

A

**Epithelial neoplasms = 90% ovarian tumors
[CA-125 elev]

  1. Serous: Most common type (~80%), (Fallopian tubes)
  2. Endometrioid: a/w endometriosus, (Endometrium)
  3. Mucinous: Often >20cm, (Endocervix)
  4. Clear cell: a/w hyperCa and Hyperpyrexia (Mesonephros)
  5. Brenner (resembles kidney)
52
Q

What is the most common Epithelial Neoplasm in Ovarian CA? histology, location?

A

Serous is 75-80% of Ovarian CA Epithelial Neoplasms

  • Bilateral 50%
  • Fallopian histo
53
Q

Mucinous Ovarian CA epithelial Neoplasm

A

Less likely bilateral, often >20cm

*endocervix histo

54
Q

Endometroid Epithelial Neoplasms (ovarian CA): bilateral? association? histo?

A

Bilateral 40% cases
a/w endometriosus
histo similar to endometrium

55
Q

Clear Cell: Epithelial Neoplasm in ovarian CA

A

<1% of epithelial tumors
Rarely reach size of serous or mucinous
a/w hyperCa and Hyperpyrexia
**Mesonephros histo

56
Q

Brenner Cell: epithelial neoplasm in ovarian CA

A

looks more like renal cells ; <1% of epithelial tumors

57
Q

Germ cell Neoplasms (Ovarian CA) most common in

A

2nd to 3rd decade; younger population!
Produce tumor markers helpful in tx response
elev hCG, AFP, LDH

58
Q

What are the two types of Sex cord stromal tumors (Ovarian CA)

A
  1. Granulosa: most common 70%, hyperestrogenism

2. Sertoli-Stromal: rare, hyperandrogenism

59
Q

Clinical presentation of Ovarian CA (recent updates)

A

• Historically called “silent killer” bc considered asymp till advanced HOWEVER new research suggests the following sx to be correlated w early stage ovarian CA:
o Bloating
o Pelvic or abdominal pain
o Difficulty eating or feeling full fast
o Urinary urgency/frequency
• IF these sx are almost daily for more than few wks, women should see their doctor

60
Q

PE findings Ovarian CA

A

Pelvic mass, inguinal LAD, ascites

61
Q

Ovarian CA labs/imaging

A
  • Pelvic US
  • CA-125 elev: suspect epithelial ovarian CA (>65)
  • elev hCG, AFP, LDH: think germ cell CA
  • CT: reveals if retroperitoneal involvement, or Mets
  • MRI: reveals char of neoplasm
  • CXR
62
Q

Tx of Epithelial Ovarian CA

A
  • Consult GYN oncologist
  • Surgical stage: FIGO (remove tumor and mets, biopsy, peritoneal washings, biopsy pelvic and paraaortic lymph nodes, complete abdominal exploration, hysterectomy)
  • Chemo
63
Q

Tx germ Cell Ovarian CA

A

• Consult GYN oncologist
• Early dx allows removal of involved adnexa with preservation of contralateral adnexa and uterus
• Stage: FIGO
o Biopsy, Peritoneal washing, Lymph node bx (pelvic, paraarotic)
o Full abd exploration

64
Q

Recommendations: BRCA testing for non ash Jewish

A
    • send to genetic counselor 1st
      a) 2 first deg one 50;
      b) 3 or more 1st + 2nd deg;
      c) comb of breast & ovarian CA among 1st & 2nd deg
      d) first deg with bilateral breast CA,
      e) two or more 1st or second deg with ovarian,
      f) Hx breast ca in male
65
Q

Recommendations: BRCA testng for Ash Jewish

A

any 1st deg with breast or ovarian

or two 2nd degree on same side

66
Q

When is genetic risk assessment recommended for Lynch syndrome

A

Endometrial or ovarian CA with synchronous CRC dx before 50yo

67
Q

Background and features of PCOS

A

Pathophys not fully understood
Major Features: menstrual dysfunction and hyperandrogenism
Affects 5-10% women repro age

68
Q

Pathophysiology of PCOS

A

• Abnormal androgen and estrogen metab
• Control of androgen production is unregulated → high serum concentrations of testosterone, androstenedoine, DHEA-S
• Insulin resistance and hyperinsulinemia
o ^ insulin alters gonadotropin (FSH/LH) effects on ovarian function
o ^ insulin decreases synthesis of SHBG and IGF ( hyperandrogenism)
• Decreased Adiponectin: regulated lipid metab and glucose levels (CV & T2DM risk)

unregulated high levels of LH –> Theca cells –> androgen (no aromatase conversion in granulosa cells bc insufficient FSH) –> unopposed estrogen in body tissues

69
Q

PCOS presentation

A
  • Infertility, Oligomenorrhea/amenorrhea
  • Obesity, Sleep apnea
  • Acne, hirsutism (upper lip and chin), male patterned baldness, skin tags
  • Acanthosis nigricans, Metabolic syndrome
70
Q

What criteria is used to dx PCOS? what are the requirements?

A

ROTTERDAM criteria (2003)
2/3 of the following after exclusion of related d/o
1. An/Oligo-ovulation
2. Clinical or biochemical signs of hyperandrogenism
3. Polycystic ovaries

r/o hyperPRL, Congenital adrenal hyperplasia, androen insensitivity

71
Q

What US findings support dx of PCOS

A
  • > 12 follicles in each ovary measuring 2-9mm diameter
  • “String of pearls” appear
  • Ovarian volume >10mL
72
Q

Labs for dx PCOS

A

Fasting lipid profile to screen dyslipidemia
Fasting serum glu for insulin resistance
Free T (>200 sugg androgen secreting tumor)
LH: abn ^ suggest PCOS
LH:FSH (^ more than 2:1 suggest PCOS)
Liver enzymes: abn ^ AST and ALT to screen for NASH

*also order DHEAS to r/o adrenal hyperplasia

73
Q

ddx PCOS

A 
Cushing (24 h urine cortisol)
Androgen secreting tumor (free T)
Congenital hyperplasia (morning 12-hyroxyprog)
HyperPRL (serum PRL)
Thyroid dysfunction (serum TSH, FT)
74
Q

Tx of PCOS

A
  1. First line: WEIGHT LOSS AND DIET
2. COC 
•	Low androgenic activity
•	Desires preg or not an Est. candidate, Cyclic Provera
3. METFORMIN: 
•	For pt w hyperinsulinemia
•	Combine with CLOMID for infertility
4. Fertility consult
75
Q

Risks of PCOS

A

T2DM
Endometrial hyperplasia/CA
Metabolic syndrome (HTN, dyslipidemia),
NASH

Womens Health (3 decks)

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