Cervical and Uterine Abnormalities Flashcards

1
Q

What is a Nabothian cyst?

A

Cystic structure that forms when columnar epithelium is covered by squamous epithelium

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2
Q

Presentation of Nabothian cyst

A

Appear as translucent or yellow, millimeters to 3 cm

Benign and asymptomatic seen during speculum exam

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3
Q

Tx for Nabothian cyst

A

Excision is not required

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4
Q

Presentation of cervical polyps

A

Usually <3 cm
Benign
May cause post-coital bleeding or abnormal uterine bleeding

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5
Q

Tx for cervical polyps

A

Polypectomy for symptomatic pts

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6
Q

What is in the exocervix?

A

Stratified squamous epithelium

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7
Q

What is in the transformation zone?

A

Squamo-columnar junction
Metaplastic squamous epithelium
*most important part
Most sample it b/c this is where HPV goes

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8
Q

What is in the endocervical canal?

A

Single layer mucin-producing columnar cells

must get this to get adequate sampling

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9
Q

Which HPV is related to which cervical cancers?

A

16- squamous cell carcinoma

18-adenocarcinoma

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10
Q

What do pts with adenocarcinoma have concurrently?

A

HSIL cytology

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11
Q

High and low risk HPV

A

High: 16 and 18
Low: 6 and 11

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12
Q

Risk factors for HPV infection

A

Multiple sex partners
Early onset of sexual activity, history of STDs, smoking (carcinogens in cervical mucus), immunosuppression, long term oral contraceptive use, multiparity (maintenance of transformation zone)

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13
Q

HPV vaccines

A

Gardasil 9 (6, 11, 16, 18, 31, 33, 45, 52, 58)
Cervarix (16 and 18)
-if get vaccination then get ongoing Paps based on age guidelines
-potential to prevent 45% of HPV associated cancers
*** look at slide for what it decreases!!

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14
Q

Types of pap smears

A

ThinPrep and SurePath

Very specific

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15
Q

Type of HPV DNA testing

A

Cervista and Hybrid capture high risk HPV test

Very sensitive and specific

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16
Q

2 components of pap smear

A

Cytology (cellular makeup of cervix)
HPV testing (in conjunction with pap smear to assess for HPV DNA)
*only screening for cervical cancer

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17
Q

Best screening test for cervical cancer

A

Pap smear/ HPV DNA testing (Cobas does just HPV but best to do both)

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18
Q

When is screening for cervical cancer initiated?

A

Start at 21 despite age of sexual debut!

  • only .1% occur before 20–screening before 21 doesn’t reduce rate of cervical cancer
  • doesn’t apply to high risk (immunocompromised)
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19
Q

Most cases of HPV infection

A

Cleared within 1-2 yrs without producing neoplastic change

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20
Q

What should all adolescent encounters contain?

A
Contraceptive counseling
STI screens (no speculum when asymptomatic)
Gardasil education and administration
Safe sex practices
No pap unless high risk
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21
Q

Screening for HPV in women 21-29

A

Cytology performed alone q 3 years

DO NOT perform HPV DNA testing

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22
Q

Screening for HPV in women 30-64

A

Cytology (+) HPV DNA testing q 5 yrs OR
Cytology alone q 3 years OR
HPV alone q 5 years

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23
Q

Who is at high risk for developing cervical cancer and need yearly screening?

A
HIV positive women
Immunocompromised
Personal history of cervical cancer
History of CIN II/III
Exposure to diethylstilbestrol (DES) in utero
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24
Q

What is diethylstilbestrol?

A

Given to pregnant women to reduce risk of pregnancy complications and losses
Causes vaginal/cervical malignancies, breast cancer, malformations of reproductive tract and infertility

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25
Q

Cervical cancer screening for HIV positive women

A

q 6 mos the year of diagnosis then q year and begin screening at age of diagnosis

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26
Q

When to stop screening for cervical cancer

A

Stop at age of 65 if in past 10 years:

  • Pt has evidence of 3 prior consecutive negative results with cytology alone
  • 2 consecutive negative Co-testing results
  • Most recent test has to have occurred within 5 yrs
  • Cannot have history of CIN 2+ within last 20 yrs
  • not when high risk, do not resume screening even if woman reports a new sexual partner
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27
Q

When to stop screening for cervical cancer in women with hysterectomy?

A

Stops at time of surgery
Hysterectomy performed for benign disease
No history of CIN 2+ within 20 yrs

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28
Q

What must be done during speculum exam when note abnormal cervical lesion?

A

Biopsy not pap smear (b/c biopsy is diagnostic)

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29
Q

How to further define an abnormal pap smear

A

ASCUS
LSIL
HSIL

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30
Q

What is ASC-US?

A

Atypical cells of undetermined significance

  • Causes of ASCUS cytology in absence of HPV are chlamydia, herpes simplex, vulvovaginal atrophy
  • If no HPV, then treated as normal pap
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31
Q

What is LSIL?

A

Low grade

  • Lesions usually consistent with CIN I
  • Cellular features include enlarged, hyperchromatic nuclei, abundant cytoplasm
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32
Q

What is HSIL?

A

High grade (assume HPV DNA is present)

  • Lesions usually consistent with CIN II-III, AIS
  • Cellular features include enlarged, hyperchromatic nuceli, little/no cytoplasm
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33
Q

No endocervical cells or unsatisfactory pap smear report

A

Negative cytology, no endocervical cells (so didn’t get transformation zone)
Unsatisfactory cytology due to insufficient squamous component (HPV test may be falsely negative due to insufficient sampling)

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34
Q

Association with persistently positive HPV DNA test (x2)

A

CIN II/III will be present in 36 mos in some ppl

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35
Q

Cervical intraepithelial neoplasia I (based on colposcopy biopsy)

A

Lesions typically regress in 12 mos (involves lower third of epithelial lining)

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36
Q

Cervical intraepithelial neoplasia II

A

43% of lesions regress and 35% persist and 22% progress (involves lower 2/3 of epithelial lining)

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37
Q

Cervical intraepithelial neoplasia III

A

32% of lesions regress, 56% persist and 14% progress

more than 2/3 of epithelial lining

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38
Q

How to classify colposcopy results

A

Satisfactory: complete visualization of transformation zone
Unsatisfactory: incomplete visualization of transformation zone, have to do endocervical curettage (ECC)
May need magnified view of cervix with 5% acetic acid-vinegar turns them white
Acetowhite epithelium

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39
Q

What is the loop electrosurgical excision procedure?

A

High electrical current density results in rapid heating of nearby tissue and steam envelop surrounding wire is created to vaporize adjacent tissue (sent to pathology)
*goal is to take off transformation zone
Replaced laser surgery for tx of CIN

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40
Q

When is loop electrosurgical excision procedure C/I?

A

If invasion is suspected, have glandular abnormality on pap or pregnant

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41
Q

Education for loop electrosurgical excision procedure

A

No heavy lifting for 4 wks to avoid bleeding
May have malodorous vaginal discharge for 2-3 wks
Avoid intercourse for 4 wks
Avoid douches, creams and tampons for 4 wks
First menses after is heavier due to partial removal or endocervical canal

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42
Q

Complications of loop electrosurgical excision procedure

A

Bleeding, infection, cervical obliteration/incompetence/ stenosis, pre-term delivery (after PPROM)

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43
Q

3rd most common GYN cancer in US

A

Cervical cancer

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44
Q

Characteristics of cervical squamous cell cancer

A

Mostly HPV 16 and 18
Prevalence is falling
Microinvasion (<3 mm)
Invasive (>3 mm or visible lesion)

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45
Q

Characteristics of cervical adenocarcinoma

A

HPV 16 and 18 associated with more cases then squamous
Prevalence is rising
Typers (endocervical, endometrioid, clear cell, adenoid cystic)

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46
Q

Cytology of cervical cancer

A

Columnar cells with elongated nuclei
Nuclear enlargement
Hyperchromatic nuclei
Mitosis and apoptotic bodies

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47
Q

Presentation of cervical cancer

A

Frequently asymptomatic but most common sxs if abnormal vaginal bleeding!!
Postcoital bleeding
Pelvic pain, unilateral with radiation into hip or thigh (advanced)
Vaginal discharge (watery, mucoid, purulent, malodorous)

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48
Q

How to stage cervical cancer

A

***(only one that is clinically staged-rest are when go in for surgery)
Clinical exam of bladder, uterus and rectum
(CXR or CT for thoracic involvement)

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49
Q

Where do uterine fibroids come from?

A

Smooth muscle cells within uterine wall (made of collagen, smooth muscle and elastin surrounded by pseudocapsule)
-More common in AA women

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50
Q

Pathophys of uterine fibroids

A

Estrogen is implicated in growth (myomas have higher conc of estrogen that in surrounding myometrium)
Progesterone may increase mitotic activity and suppress apoptosis

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51
Q

How to classify uterine fibroids

A

By anatomic locations within myometrium:
Submucosal: just beneath endometrium (0, I, II)
Subserosal: just at serosal surface of uterus
Intramural: lie within uterine wall

52
Q

Presentation of uterine fibroids

A
About 1/2 have sxs (often due to location and size)
Abnormal uterine bleeding
Pain
Pelvic pressure
Infertility
Spontaneous abortion
53
Q

Abnormal uterine bleeding of uterine fibroids

A

Submucosal fibroids increase SA of endometrium leading to menorrhagia

54
Q

Pain with uterine fibroids

A

Due to degeneration, myometrial contractions, dyspareunia

55
Q

Pelvic pressure with uterine fibroids

A

Mass effect, compression of surrounding organs

56
Q

Infertility with uterine fibroids

A

Submucosal fibroids (impingement of intrauterine cavity)

57
Q

What might be seen on bimanual for uterine fibroids?

A

Enlargement
Irregular shape
Masses

58
Q

Imaging used for uterine fibroids

A
Transvaginal u/s
Saline-infused sonohystogram
Hysteroscopy
MRI
H and H
59
Q

What is saline-infused sonohystogram?

A

Under US guidance a ped catheter is advanced within intrauterine cavity and H2O is instilled to define size and location of fibroid

60
Q

Hysteroscopy

A

Utilize camera advanced into intrauterine cavity to define size and location

61
Q

How to think about tx for uterine fibroids

A

Sxs drive the tx (no standard of care)

62
Q

Medical options for uterine fibroids

A

GnRH analogs
Steroids
Tranexamic acid

63
Q

Surgical options for uterine fibroids

A
Hysteroscopic resection
Endometrial ablation
Laproscopic myomectomy
Abd myomectomy
Laproscopic radiofrequency ablation
64
Q

Other tx options for uterine fibroids

A

Uterine artery embolization

Magnetic resonance guided focused ultrasonography

65
Q

Depot Lupron for uterine fibroids

A

GnRH agonist that will decrease fibroid sixe
Improves anemia prior to surgery
Decrease blood loss during surgery

66
Q

How to use Depot Lupron

A

May be primary role in tx near menopause

Not for over 6 mos use

67
Q

When to use steroidal therapies for uterine fibroids

A

Pts with prolonged heavy menses with NO submucosal fibroids

68
Q

Types of steroidal therapies for uterine fibroids

A

OCPs

Mirena, Ortho Evra, NuvaRing

69
Q

When is Lysteda (tranexamic acid) used in uterine fibroids?

A

Pts with prolonged, heavy menses with no submucosal fibroids

-oral antifibrinolytic for menorrhagia

70
Q

When to use Lysteda

A

During menstrual cycle (two 650 mg tablets TID)

71
Q

Myomectomy for uterine fibroids

A

Preserves fertility and uterus!!

Delay pregnancy for 3-6 mos b/c c-section secondary to uterine rupture

72
Q

When to do myomectomy

A

Intramural, subserosal and pedunculated fibroids

Pressure sxs

73
Q

Laparoscopic myomectomy for uterine fibroids

A

With robotic assistance

Depends on number and size of fibroids so may need to convert to laparotomy

74
Q

Complications of laparoscopic myomectomy

A

Hemorrhage, re-operation, adhesions, vascular and visceral injuries

75
Q

Hysteroscopy for uterine fibroids

A

Preserves fertility/uterus
Only on submucosal fibroids
Non-ionic solution used as distention media
Heated loop to resect fibroid

76
Q

Risks of hysteroscopy

A

Fluid overload and hyponatremia

77
Q

Education for hysteroscopic resection

A

Outpatient-anesthesia by paracervical block or general
Return to normal daily activities in 1-2 days
Can have sex 1 mo post-op

78
Q

Endometrial ablation for uterine fibroids

A

Minimally invasive and preserves uterus
Tx of menorrhagis
No major distortions of uterine cavity
Cavity should be <9 cm to prevent reoccurrence of menses

79
Q

Very important to tell pt with endometrial ablation

A

No future childbearing so must continue contraceptives! (they cannot have kids!!!-placenta apreva)

80
Q

Pros of endometrial ablation

A
Outpatient or in office
General lor paracervical block
Medium is small amount of CO2 so no fluid overload
2 min procedure and can go home in 2 hrs
Any time during menstrual cycle
81
Q

Cons of endometrial ablation

A

B/c not distort cavity, polyps and submucosal fibroids must first be removed
Doesn’t address fibroid symptomatology in general
May have amenorrhea
Poor childbearing and reproductive outcomes b/c destory endometiral lining

82
Q

Uterine artery embolization for uterine fibroids

A

Preserves uterus NOT fertility
Arteriogram IDs blood supply to fibroid
Puth cath in uterine artery and embolizing agent infused until blood flow stops

83
Q

Who is a candidate for uterine artery embolization?

A

Pt doens’t desire future childbearing
C/I: numerous and large fibroids
A lot will get the pre-op MRI and then decide to do something else

84
Q

Side effects and complications of uterine artery embolization

A

Postembolization syndrome (overnight admit to manage pain)
Non-purulent vaginal discharge
Endometritis and uterine infection
Recurrence
Embolization agent in non-target tissues and cause premature ovarian failure
Uterine necrosis, sepsis, bacteremia and death

85
Q

What is adenomyosis?

A

Growth of endometrial glands and stroma into uterine myometrium

86
Q

Why does adenomyosis occur?

A

Think ovarian hormones implicated
Invagination of endometrium (myometrium weakens with degeneration)
Parity

87
Q

Presentation of adenomyosis

A

Menorrhagia
Dysmenorrhea
Pelvic pain
History of previous uterine surgery (C-section, myomectomy)

88
Q

What is seen on bimanual exam for adenomyosis

A

Diffuse uterine enlargements (globular) but size does not exceed >12 wk gestation

89
Q

How to diagnose adenomyosis

A

Histologic examination AFTER hysterectomy

imaging can aid in it but suggestive and must look at uterus after take it out-u/s or MRI

90
Q

Medical options to treat adenomyosis

A

Improve dysmenorrhea and menorrhagia

OCPs, Mirena, NuvaRing

91
Q

Surgical options for adenomyosis

A
Hysterectomy (definitive)
Uterine artery embolization (not much recurrence of sxs)
Endometrial ablation (high failure rate and increased pain after)
92
Q

What is endometriosis?

A

Presence of endometrial glands and stroma outside endometrial cavity and uterine musculature
Increased risk of ovarian cancer

93
Q

Where do you usually see glands in endometriosis?

A

Pelvis (ovaries, posterior cul-de-sac or uterine surface) but can be other places

94
Q

Most common diagnosis for hospitalization of women 15-44 YP

A

Endometriosis

95
Q

Pathophys of endometriosis

A

Retrograde menstruation (endometrial tissue goes into fallopian tubes and peritoneum)
Deficient cellular immunity (Increase risk of AI disorders)
Hereditary

96
Q

Presenation of endometriosis

A
Premenstrual pelvic pain!!
Infertility
Dysmenorrhea
Dyspareunia
Elevated CA-125
97
Q

Premenstrual pain in endometriosis

A

Lesion growth is stimulated by estrogen and progesterone
Lesions grow and are secretory but expansion is inhibited by surrounding fibrosis (pressure and inflammation leads to pain)
Pain subsides after menses-b/c hormones have subsided do they’re not affecting it!!!!

98
Q

PE for endometriosis

A

Tenderness at posterior cul-de-sac
Fixed or retroverted uterus (secondary to adhesions)
Endometrioma cause adnexal masses or tenderness

99
Q

How to diagnose endometriosis

A

Laparoscopy (only way to diagnose):
Erythematous, petechial lesions on peritoneal surface
Surrounding peritoneum thickened and scarred
Ovaries can have lesions or endometriomas (chocolate cysts)
Adhesions

100
Q

Most common site of endometriosis

A

Ovaries

101
Q

Tx for mild endometriosis

A

Expectant management

NSAIDs

102
Q

Tx of moderate to severe endometriosis

A

*want to interrupt stimulation of endometrial tissue
OCPS, progestins (mirena is best for this!!!), Depot Lupron, laparscopy with excision or hysterectomy with bilateral salpingo-oophorectomy

103
Q

OCPS for endometriosis

A

Causes atrophy of endometrial tissue
Decrease risk of ovarian cancer
(continuous with no placebo week)

104
Q

Depot Lupron for endometriosis

A

Suppression of estrogen and progesterone by down-regulation of pituitary gland
12 mo therapy: norethindrone acetate to prevent bone loss

105
Q

Risk factors of endometrial hyperplasia and cancer

A

OBESITY!!!
Early menarche <12, late menopause >52, infertility or nulliparous, tamoxifen, unopposed estrogen therapy, DM, PCOS, history of breast or ovarian cancer, radiation for pelvic cancer, HNPCC (lynch syndrome)

106
Q

Classification of endometrial hyperplasia

A

Simple hyperplasia without atypia
Complex hyperplasia without atypia
Simple atypical hyperplasia
Complex atypical hyperplasia

107
Q

Pathophys of endometrial hyperplasia

A

Estrogen stimulates proliferation of endometrium
Progesterone has antiproliferative effects to endometrial lining sheds
Unopposed estrogen leads to it (adipose tissue releases estrogen)

108
Q

Presentation of endometrial hyperplasia

A
Asymptomatic
Post-menopausal bleeding
Menorrhagia
Intermenstrual bleeding
Prolonged menses (>7 days)
Decreased menstrual interval (<21 days)
Oligo or amenorrhea
109
Q

What to do when suspect endometrial hyperplasia

A

Pelvic exam and pelvic u/s (endometrial thickness-< 4 mm malignancy is unlikely)
Endometrial biopsy!!!
D&C hysteroscopy

110
Q

D&C hysteroscopy for endometrial hyperplasia

A

Performed if lining too think to rely on EMB results or insufficient sample
Cervical stenosis
Persistent irregular or PMB despite - EMB

111
Q

Tx for endometrial hyperplasia without atypia

A

Mirena IUD
Provera 10 mg QD 3-6 mos
Reassess with EMB to ensure resolution

112
Q

Tx for endometrial hyperplasia with atypia

A

Increased risk of endometrial cancer
TOC: hysterectomy (half have underlying endometrial cancer)
High dose progesterone therapy (megace 40-80 mg BID, mirena IUD, reassess q 3 mos until resolved)

113
Q

Most common gynecologic cancer

A

Endometrial cancer (seen at 50-69)

114
Q

Pathophys of endometrial cancer

A

Estrogen!

Progression from endometrial hyperplasia

115
Q

Type 1 endometrial cancer

A

Arise due to unopposed endogenous or exogenous estrogen

Favorable prognosis b/c well-differentiated tumors

116
Q

Type 2 endometrial cancer

A

Arise independently of estrogen and seen with endometrial atrophy
Poorly differentiated with poor prognosis

117
Q

Most common type of endometrial cancer

A

Adenocarcinoma!!! (type 1)-80%

118
Q

Adenocarcinoma with squamous differentiation

A

Type 1 endometrial cancer (20%)

119
Q

Serous carcinoma

A

Type 2 endometrial cancer
Not associated with hyperestrogenic state!!
Seen when relapse from stage 1-poor prognosis
Looks histologically like serous carcinoma of ovary so tx is same

120
Q

Clear cell carcinoma

A

Type 2 endometrial cancer
Not associated with hyperestrogenic state!
High grade, aggressive with deep invasion

121
Q

Presentation of endometrial cancer

A

Abnormal vaginal bleeding (menorrhagis, intermenstrual spotting, post-menopausal bleeding!!)
Abd cramping, back pain, weight loss, dyspareunia

122
Q

What to do with women with Lynch syndrome (HNPCC)?

A

Screening for endometrial cancer- Colaris testing

123
Q

Labs for endometrial cancer

A
CBC
Endometiral biopsy
D&amp;C (dilatation and curettage)
Transvag u/s!!!1
Paps (not really part of the work-up tho, indicator for cancer if seen on pap)
CA-125 (seen elevated in stage 1)
MRI/CT
124
Q

Tx for endometrial cancer

A

Hysterectomy with bilateral salpingoophorectomy
Radiation
Chemo (infrequent, usually just advanced)

125
Q

When to use radiation for endometrial cancer

A

Pts with contraindications to surgery

Advanced pelvic disease prior to TAH (total abd hysterectomy)