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Women's Health > Exam pt 2 > Flashcards

Exam pt 2 Flashcards

1
Q

what is the 4th most common CA in women

A

uterine CA

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2
Q

what is a hallmark of ovarian CA

A

intra-peritoneal spreads

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3
Q

2nd most common gynecologic malignancy with the highest mortality

A

Ovarian CA

*incidence increases w/ age and risk of relapse of advanced stage is 70%

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4
Q

pathogenesis hypotheses for ovarian CA

A
  1. repeated ovulation/ trauma/ repair to ovarian epithelium allow genetic mutations and neoplasia
  2. excess gonadtotropin secretion –> increased estrogen –> epithelial proliferation and potential for malignant transformation
  3. starts as carcinoma insitu in fallopian tubes –> breaks free and invades ovaries
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5
Q

____% of primary ovarian tumors derive from epithelial cells

A

90% *mostly serous

3% germ cells and 7% sex cord-stroma

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6
Q

___% diagnosed with stage III/IV ovarian CA

A

75%

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7
Q

____% 5 year survival of advanced stage ovarian CA

A

20%

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8
Q

risk factors for ovarian CA

A
  1. women w/ ovaries
  2. long ovulation hx
  3. unexplained infertility
  4. nuliparity
  5. fhx of breast or ovarian CA / BRCA**
  6. diet
  7. estrogen replacement
  8. hx of endometriosis
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9
Q

factors that decrease your risk for ovarian CA

A
  1. increased parity*
  2. oral contraceptive use*
  3. tubal ligation
  4. hysterectomy

*decreased ovulation

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10
Q

symptoms of ovarian CA

A

bloating, fatigue, increased abdominal size, urinary urgency, constipation

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11
Q

how do u evaluate an adenxal mass?

A
  1. transvaginal sonography (TVS)
    - if normal rescan in 1 yr
    - if abnormal evaluate tumor morphology index score, CA-125 biomarker, and color doppler
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12
Q

prevalence of adenxal mass

A

2-7%

*7.8% of premenopausal women had adenxal masses 2.5cm or larger on random u/s (ovarian cysts)

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13
Q

factors to consider when evaluating adenxal masses by TVUS

A

tumor size
borders
density
*morphology index score above 5 is concerning

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14
Q

what is an elevated CA-125 in a premenopausal woman and a postmenopausal woman

A

premenopausal >200
postmenopausal >35

*biomarker for ovarian CA but not specific!

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15
Q

how to treat an ovarian cyst

A

laparoscopy

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16
Q

tumor markers

A

HE4: ovarian CA
CA-125: ovarian and others
CEA: mostly GI tract
CA 19-9: mucinous tumors, pancreatic tumors
( if HE4 normal and CA125 elevated in premenopausal likely endometrosis)

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17
Q

screening for ovarian CA

A

there is no screening tool!
*just educate on signs

Can measure 5 protein in blood:
Transthyretin
apolipoprotein A-1
B2 microglobulin
Transferrin
CA 125 II
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18
Q

surgical staging for ovarian CA. What should be done?

A
  1. hysterectomy
  2. both tubes and ovaries (BSO)
  3. pelvic washings
  4. pelivic lymph nodes
  5. periaortic lymph nodes
  6. peritoneal biopsies
  7. diaphram scraping
  8. omentectomy/biopsy
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19
Q

stages for ovarianCA

A

Stage 1- stays where it started
Stage 2- spread next to the origin
Stage 3-spread outside pelvis
Stage 4- distally spread

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20
Q

treatment of ovarian CA

A
  1. chemotherapy (IV or intraperitoneal)
  2. platiunum and taxane (6 cycles of 21 days)
  3. clinical trials
  4. surgery

**Platinum drugs are the most effective (carboplatin or cisplatin)- but some are resistant to it

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21
Q

surveillance of ovarian CA after no evidence of disease

A
  1. 5 yr prognosis
  2. visit every 3 months for 2 years, then may space out
  3. H and P
  4. CA125
  5. imaging?
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22
Q

what percent of ovarian CAs are genetic?

A

10%
of that:
BRCA1 ~70-75%
BRCA2~ 20%

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23
Q

what is a significant family hx of ovarian CA

A

-2 first degree relatives (Breast or ovarian CA OR 1

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24
Q

screening for ovarian CA if BRCA +

A
  1. monthly BSE starting at 18
  2. annual mammograms at 25
  3. annual breast MRI
  4. 2x yearly ovarin screening w/ us and CA125 at 35
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25
Q

how can u reduce ones risk of ovarian CA if they are BRCA +

A
  1. screening
  2. surgery
  3. chemoprevention

*BSO reduces ~95%
Mastectomy ~40-50%

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26
Q

most common gyn malignancy in developed countries

A

endometrial CA

95% of uterine CA are endometrial, 5% are sarcomas

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27
Q

median age of endometrial CA

A

61

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28
Q

major risk factor for type I and type II endometrial CA

A

type I- unopposed estrogne

type II- age

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29
Q 
80% of endometrial CA
race: caucasian > black
differentiation: well differentiated
histology: grade 1 or 2, endometrioid
Prognosis: favorable
A

type 1 endometrial CA

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30
Q 
10-20% of endometrial CA
race: caucasian = black
differentiation: poorly differentiated
histology: grade 3, serous, clear cell, mucinous, etc. 
Prognosis: poor
A

type 2 endometrial CA

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31
Q

risk factors of endometrial CA

A
  1. unopposed estrogen (type 1 only)
  2. obestity
  3. late menopause
  4. nulliparity
  5. diabetes
  6. hypertension
  7. tamoxifen
  8. endometrial hyperplasia
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32
Q

% risk of
simple endometrial hyperplasia w/o atypia
complex endometrial hyperplasia w/o atypia
simple endometrial hyperplasia with atypia
complex endometrial hyperplasia with atypia

A

1%
5%
10%
25%

*think coin size

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33
Q

factors that decrease risk of endometrial CA

A
  1. decrease estrogen or increased progesterone
  2. oral contraceptives
  3. pregnancy
  4. smoking
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34
Q

signs and symptoms of endometrial CA

A

abnormal bleeding

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35
Q

what do u do if someone presents w/ abnormal bleeding?

aka how do u dx endometrial CA

A

Biopsy!!!- endocervix and endometrium

-US:

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36
Q

___% of endometrioid ovarian CA have a synchronous endometrial CA

A

20%

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37
Q

what other CA has a 40-60% lifetime risk of endometrial CA

A

hereditary non-polyposis colorectal CA syndrome (Lynch syndrome)
**recommend prophylactic hysterectomy

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38
Q

spread patterns of endometrial CA

A
  1. direct extension- most common
  2. transtubal
  3. lymphatic
  4. hematogenous- mostly lungs
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39
Q

treatment of endometrial CA

A
  1. surgical staging
  2. postop radiation or chemo
  3. medical managment (progesterone, anti-estrogen?)** used as palliative care
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40
Q

prognostic variables of endometrial CA

A

young worse than old
2cm
hormone receptor status: + better than neg.

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41
Q

prognosis for stage IA endometrial CA

prognosis for stage IVB endometrial CA

A

88%

15%

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42
Q

most common gynocologic CA worldwide but not in US because of screening prevention

A

cervical CA

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43
Q

risk factors of cervical CA

A 
HPV infection
smoking
multiple partners
multiparity
HIV
STDs
OCP use
low socioeconomis status
poor diet (Vit. deficiency)
alcoholism
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44
Q

screening for cervical CA

A

PAP

*76% reduction in incidnece of invasive cervical CA

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45
Q

what HPV strains cause the most cervical CA

A

HPV 16 and 18 cause >70%

HPV 16 alone causes about 50%

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46
Q

symptoms of cervical CA

A

frequently asymptomatic

  • abnormal vaginal bleeding
  • postcoital bleeding
  • vaginal discharge: watery, mucoid, purulent, and/or malodorous
  • do not confuse with cervicitis
  • pelvic or lower back pain
  • bowel or urinary symptoms
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47
Q

treatments of cervical CA

A
  1. radical hysterectomy
    • radiation
  3. chemoradiation
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48
Q

lower urinary tract dysfunction ranges from ___-___% following radical hysterectomy

A

20-80%

*most common types of dysfunction:
voiding, storage, recurrent UTI, UI

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49
Q

signs and symptoms of vulvar CA

A

pruritus (severe itching)
burning
nonspecific irritation
appreciation of a mass

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50
Q

how do you dx vulvar CA

A

biopsy everything

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51
Q

most common vulvar CA subtypes

A

squamous 90%
melanoma 5%
Basal 2%

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52
Q

Staging of vulvar CA is based on what

A

midline lesion?
radical vulvectomy
inguinal lymphnodes (>1mm invasion)

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53
Q

Stages of vulvar CA

A

Stage 1: confined to vulva
Stage 2: extension to adjacent structures
Stage 3: positive inguinal femoral lymph nodes
Stage 4: upper 2/3 of urethra, upper vagina, distant

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54
Q

treatment of paget disease of the vulva

A

-wide local excision or vulvectomy 2cm margins is preferred
-radical vulvectomy
+/- lymph node dissection
+/- chemo/radiation
*60% experience local recurrence and may require 5cm margins

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55
Q

vulva is diffusely involved, with very thin, whitish epithelial areas, termed “onion skin” epithelium or “cigarette paper”

A

lichen sclerosus

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56
Q

an itch that rashes
itching contributes to epidermal thickening or hyperplasia and inflammatory cell infiltrate, which in turn leads to heightened sensitivity that triggers more mechanical irritation

A

Lichen Simplex Chronicus

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57
Q

rare inflammatory skin condition that can be generalized or isolated to the vulva and vagina
Sx:
whitish, lacy bands of keratosis near the reddish ulcerated-like lesions
chronic vulvar burning
pruritus
insertional dyspareunia
profuse vagina discharge

A

Lichen Planus

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58
Q

lesion: atrophic, thin, whitish epithelium w/ frequent perianal halo or keyhole distrubution

A

lichen sclerosis

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59
Q

lesion: pale red to yellowish pink plaques, often oily appearing, scaly crust

A

seborrheic

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60
Q

lesion: eczematous lesions w/ underlying erythema

A

dermatitis (allergic, irritant, or atopic)

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61
Q

lesion: annular pink plaques with silvery scalre that bleed if removed (auspitz sign)

A

psoriasis

62
Q

lesion: lichenified, hyperplastic plaques of red to reddish brown

A

lichen simplex chronicus

63
Q

lesion: white lacy network (wickham striae) w/ flat-topped lilac papules and plaques

A

lichen planus

64
Q

hallmark: other hair-bearing areas often affected-scalp and chest, also back and face

A

seborrheic

65
Q

hallmark: symmetric w/ extension into areas of irritant or allergen contact

A

dermatitis (allergic, irritant, or atopic)

66
Q

hallmark: elbows, knees, scalp also affected

A

psoriasis

67
Q

hallmark: erosive vaginitis w/ demarcated edges

A

lichen planus

68
Q

hallmark: symmetric w/ variable pigmentation

A

lichen simplex chronicus

69
Q

hallmark: cigarette paper, parchment-like skin, halo or loss of elasticity

A

lichen sclerosis

70
Q

fiery, red background mottled w/ whitish hyperkeratotic areas

A

pagets disease

** high risk of underlying internal carcinoma, particularly of the colon and breast

71
Q

most common presenting complaint of vulvar CA

A

pruritus
*may notice a red or white ulcerative or exophytic lesion arising most commonly on the posterior 2/3s of either labum majus

72
Q

what is the most common non-SCC of the vulva

A

melanoma

73
Q

another word for uterine leiomyomata

A

fibroids and myomas

74
Q

represent localized prliferation of smooth muscle cells surrounded by a pseudocapsule of compressed muscle fibers

A

uterine leiomyomata

75
Q

_____ are the most common indications for hysterectomy, accouting for approximately 30% of this operation

A

leiomyomata

76
Q

leiomyomata centered in the muscular wall of the uterus

A

intramural leiomyomata

77
Q

leiomyomata just beneath the uterine serosa

A

subserosal leiomyomata

78
Q

leiomyomata just beneath the endometrium

A

submucosal leiomyomata

79
Q

leiomyomata that remains connected to the uterus by a stalk

A

pedunculated leiomyoma

*subtype of subserosal

80
Q

uterine malignancy is imore typical in postmenopausal patients who present with

A

rapidly enlarging uterine massess, postmenopausal bleeding, unusual vaginal discharge, and pelvic pressure

81
Q

menstrual blood loss of >80 mL

A

menorrhagia

82
Q

on abdominopelvic examination, uterien leiomyomata usually present as a __

A

a large, midline, irregular-contoured mobile pelvic mass w/ a characteristic “hard feel” or solid quality
-the degree of enlargement is usually state in terms “weeks size” that are used to estimate equivalent gestational size

83
Q

treatment for uterine myomas

A

most do not require (surgical or medical) treatment

84
Q

___ is commonly sused before a planned hysterectomy to reduce blood loss as well as the difficulty of the procedure. It can also be used as a temporizing medical therapy until natrual menopause occurs

A

gonadoropin-releasing hormone agonist (GnRH analogs)

85
Q

a surgical treatment is warranted in patients who desire to retain childbearing potential or whose fertility is compromised by the myomas, creating significant intracavitary distortion

A

myomectomy

**otherwise a hysterectomy

86
Q

indications for a m yomectomy include

A

a rapidly enlarging pelvic mass
symptoms unrelieved w/ medical management
enlargement of an asymptomatic myoma to the point of causing hydronephrosis

87
Q

what is the def of infertility

A

1 yr attempting conception

88
Q

% of male infertility

A

35%

89
Q

% of tubal/pelvic infertility

A

35%

90
Q

pretesticular reasons for infertility

A
  1. hypogonadotropic hypogonadism (Kallman’s, tumor, trauma, empty sella, iatrogenic)
  2. coital disorder (ED)_
  3. Ejaculatory failure (psychosexual, post-genitourinary surgery, neural, drug-related)
91
Q

what hormone decreases fertility in males (decreases sperm count)

A

testosterone

*shuts down hormonal signally needed to make sperm

92
Q

testicular reasons for infertility

A
  1. genetic (Klinefelters-XXY, Y chromosome deletions, immotile cilia,)
  2. Congenital (cryptorchidism, infective- orchitis)
  3. Antispermatogenic (heat, chemo, drugs, irradiation,)- vascular, torsion, immunologic, idiopathic
93
Q

post-testicular reasons for infertility

A
  1. Epididymal (congenital, infective)
  2. Vasal (genetic: CF-abnormal development of vas deferens, acquired: vasectomy)
  3. Accessory gland infection
  4. immunologic
  5. idiopathic
94
Q

red lesion indicates

A

newer lesion

95
Q

a chocolate cyst

A

endometrioma

96
Q

_____% of infertile women will have endometriosis

A

25-50%

97
Q

best treatment for endometrioma

A

removal of cyst bc has less recurrence and side effects than drainage

98
Q

screening test for endometriosis

A

no screening test

-surgery is diagnostic and treatment

99
Q

treatment options for endometriosis

A
  1. conservative: remove the endometriosis
    70-100% relief of pelvic pain
    *generally recommend hormone suppression after to decrease recurrence risk
  2. Radical: remove the uterus and fallopian tube
    90% relief of pelvic pain
    ovarian conservation if ovaries uninvolved
100
Q

medical therapy of endometriosis

A
  1. NSAIDS
  2. Continuous OCs (pseudopregnancy)
  3. Progestogens (depo provera/norethindron, Mirena, implanon)
  4. Anti-progestins
  5. Aromatase inhibitors (off label)
  6. Danazol (androgen- suppresses FSH and LH)
  7. GnRH agonists
101
Q

How do GnRH agonists help tx endometriosis

A

GnRH causes ovaries to shut down by removing pulsatile release of GnRH–> no FSH and LH release from pituitary–> no ovulation

**causes pt to go into medical menopause and may have associated symptoms (use add-back therapy to treat symptoms)

102
Q

how should the flow of treatment go for endometriosis pain

A

try NSAIDs and birth control pill

  • still pain, treat w/ GnRH
  • still pain, treat w/ laparoscopy

*if you suspect someone has endometriosis and they are trying to get pregnant soon, do surgery sooner

103
Q

% of ovulatory disorders

A

15%

104
Q

2 causes of anovulation

A
  1. Estrogenized (PCOS)

2. Not estrogenized (hypothalamus or pituitary)

105
Q

what is the most common endocrine defect that causes infertility

A

PCOS

5-10% reproductive age women

106
Q

DDX of PCOS

A

CAH
hypercortisolism
PRL
thyroid

107
Q

clinical features of PCOS used to diagnose

A

need at least 2 out of 3

  1. oligo- or anovulation
  2. chemical or clincal signs of hyperandrogenism (elevated serum androgen concentration, or hirsutism, male pattern hair loss, acne)
  3. Polycystic-appearing ovaries

*diagnose by exclusion

108
Q

Pathophysiology: increased LH over FSH release from pituitary –> increased androgen production from theca cells in ovary

  • insulin–> acts synergistically w/ LH to enhance ovarian androgen production
  • insulin –> inhibits production of SBHG from liver (increased levels of free testosterone)
A

PCOS

109
Q

how to evalute PCOS

A
  1. Gonadotropins (FSH, LH) and E2
  2. TSH
  3. Prolactin
  4. Pelvic US
  5. Testosterone, DHEAS
  6. 17OHP
  7. Glucose screening
  8. lipid panel
110
Q

medical concerns related with PCOS

A
  1. prevention of endometrial hyperplasia
  2. prevention of DM2
  3. infertility
111
Q

normal hgbA1c and for DM2

A

nl: 6.4%

* not as sensitive but easier to perform

112
Q

treatment for DM2

A

metformin

statins

113
Q

insulin sensitizer:

  • disubstituted biguanide
  • modest glucose disposal improvement
  • primary: reduces hepatic glucose output
A

metformin

114
Q

insulin sensitizer:

  • thiazolidinedione
  • improves sensitivity at liver, skeletal muscle, adipose
  • modest: hepatic glucose output
  • primary:glucose disposal improvement
A

Rosiglitazone

115
Q

how to treat PCOS menstrual irregularity

A
  • combined oral contraceptives (also helps manage testosterone levels)
  • progestins

*estrogen causes endometrial lining to grow, which increases endometrial hyperplasia and increases risk of endometrial CA if not shedding

116
Q

how to treat PCOS infertility

A
  • lifestype modification (5% decrease in fat can help)
  • injectable gonadroptropins
  • ovarian drilling
  • aromatase inhibitors (ex. letrozole)
117
Q

best treatment of PCOS and infertility

A

best to use both or clomiphene alone

*Metformin does not help fertility but does help with endocrine issues

118
Q

how does aromatase inhibitor, Letrozole work

A

causes low estrogen level to increase FSH level which causes ovulation
*better live birth rate (better rate of ovulation)

119
Q

Causes of central anovulation

A
  1. defects within HP unit
    (hypothalamic lesions, GnRH deficiency, prolactin excess, pituitary defects-adenoma, empty sella, tumors)
  2. CNS-Hypothalamus
    (nutrition, exercise, anorexia nervosa, stress, female athlete triad
120
Q

how to evaluate and treat central anovulation

A

evaluate w/ MRI

Tx w/
lifestyle modification
gonadotropins
pulsatile GnRH

*clomide and letrozole won’t help because hypothalamus is the problem not the pituitary

121
Q

% of unexplained (+ age-related) infertility

A

10%

122
Q

how do you measure ovarian reserve

A

-Day 3 FSH/Estradiol. Anti-mullerian hormone

123
Q

unexplained inferility definition

A

failure to conceive after 12 months in the setting of:
regular menses
at least 1 patent fallopian tube (HSG)
normal sperm count

124
Q

treatment for unexplained infertility

A

superovulation/IUI

IVF

125
Q

Cost-effectiveness 2010 study showed what

A

FSH/IUI added no additional value

126
Q

studies show women with infertility have similar stress levels to those with:

A

CA
HIV
going through a divorce

127
Q 
which of the follwing is an epithelial cell tumor?
dermoid cyst
sertoli-leydig cell
lymphoma
muscinous cystadenoma
A

muscinous cystadenoma

128
Q 
which of hte followin gis a germ cell tumor
brenner cell
lymphoma
endometrioid
teratoma
A

teratoma

129
Q 
which of the follwing is an ex of a stromal cell neoplasm
serous cystadenoma
dysgerminoma
endometrioid
sertoli-leydig cell
A

sertoli-leydig cell

130
Q 
what tumor of the ovary should always be treated with hysterectomy, bilateral salpinogo-oophorectomy, and staging
theca lutein cyst
dysgerminoma
cystadenocarcinoma
brenner cell tumor
A

cystadenocarcinoma

131
Q 
a pt not using OCP, with regular periods, presents w/ acute pain late in luteal phase. this is most c/w
dermoid cyst
mucinous cystadenoma
serous cystadenoma
hemorrhagic corpus luteum
A

hemorrhagic corpus luteum

132
Q

coelomic epithelium gives rise to what ovarian neoplasm

A

serous cystadenoma

133
Q

gonadal stroma gives rise to what ovarian tumor

A

granulosa theca

134
Q

germ cells result in what ovarian neoplasm

A

teratoma

135
Q

what percent of serous cystadenomas are benign

A

70%

136
Q

most common type of benign epithelial cell neoplasm

A

serous

137
Q

when a child or adolescent presents w. an ovarian neoplasm, the most common type is

A

benign cystic teratoma

138
Q

Brenner cell tumors may be associated with

A

mucinous tumors

139
Q

which of the following neoplasms can contribute to precocious puberty in a female child

A

granulosa theca cell tumor

140
Q

in the reproductive age group, about what percent of nonfunctional ovarian neoplasms are benign

A

70%

141
Q 
which ovarian tumor has the highest malignant potential
dermoid
serous cystadenoma
mucinous cystadenoma
brenner tumore
A

serous cystadenoma

142
Q

malignant ovarian epithelial cell tumors spread primarily by

A

direct extension w/in peritoneal cavity

143
Q

women with BRCA1 gene have a cumulative lifetime risk of ___ for developing breast CA and ___ for developing ovarian CA

A

50-80%

15-45%

144
Q

what is the primary surgical approach involved in the treatment of ovarian carcinoma

A

cytoreductive surgery or “tumor debulking”

145
Q 
which of the follwiong is a tumor that is metastatic to the ovary from other sites
fibrosarcoma
krukenberg tumor
immature teratome
malignant mesodermal sarcoma
A

krukenberg tumor

146
Q

what is a pathognomic sign of tubal carcinoma

A

profuse serosanguineous vaginal discharge

147
Q 
which of the following is the most common virilizing ovarian tumor
gynandroblastoma
arrhenoblastoma
adrenal rest tumor
leydig cell tumor
A

arrhenoblastoma

148
Q

the presence of signet-ring cell type in ovarian tumors ism ost characteristic of

A

krukenberg tumors

149
Q

breast CA metastatic to the ovary is found in what proportion of cases

A

25%

150
Q

what percent of epithelial ovarian carcinomas occur in familial or hereditary patterns

A

5%

151
Q

meigs syndrome couples ascites and right pleural effusion with ___

A

ovarian fibroma

Women's Health (3 decks)

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