Gynecologic oncology-Erin wright Flashcards

1
Q

What is the most common CA in both men and women?

A

lung cancer

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2
Q

What is the MC cancer in women?

A

breast CA

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3
Q

How does CA occur?

A
  • increased division of abnormal cells, or
  • decreased apoptosis = this is how cancer occurs
  • and loss of normal growth control, with multiple** mutations
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4
Q

Describe somatic mutations

-list ex’s

A

=sporadic mutations (Cancer)

-typically from exposure
Smoking
Environmental carcinogens
Viruses
Hormones
Alcohol
High fat diet
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5
Q

Describe germline mutations

A

=hereditary (cancer)

mutations you are born with

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6
Q

_________ is the key to dx and tx of CA

A
  • *pathology
  • Once you know cell type, you evaluate location and extent of cancer to determine staging
  • You can then decide treatment or management options
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7
Q

CA cells spread in the body in a series of steps:

A
  1. growing into, or invading nearby normal tissue
  2. moving through the walls of nearby lymph nodes
  3. Traveling through lymphatic system and blood to other body parts
  4. Stopping in small blood vessels at a distant location, invading the blood vessel walls, and moving into surrounding tissue
  5. Growing in tissues until a tiny tumor forms
  6. Causing new blood vessels o grow, which creates a blood supply that allows the tumor to cont. to grow
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8
Q

Bladder CA mets to–>

A

bone
liver
lung

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9
Q

Breast CA mets to–>

A

bone
brain
liver lung

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10
Q

TNM staging=

A

T – Extent of the primary tumor
N- absence or presence of regional lymph node involvement
M- absence or presence of distant metastases

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11
Q

Primary tumor (T):

  • TX=
  • T0=
  • T1..
A

TX: Main tumor cannot be measured.

T0: Main tumor cannot be found.

T1, T2, T3, T4: Refers to the size and/or extent of the main tumor. Thehigher the number after the T, the larger the tumor or the more it has growninto nearby tissues. T’s may be further divided to provide more detail, suchas T3a and T3b.

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12
Q

Regional lymph nodes (N):

-NX=

A

NX: Cancer in nearby lymph nodes cannot be measured.
N0: There is no cancer in nearby lymph nodes.
N1, N2, N3: Refers to the number and location of lymph nodes that containcancer. The higher the number after the N, the more lymph nodes thatcontain cancer.

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13
Q

Distant Metastasis (M)

A

MX: Metastasis cannot be measured.
M0: Cancer has not spread to other parts of the body.
M1: Cancer has spread to other parts of the body.

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14
Q

Tumor grade:

  • GX=
  • G1=
A

GX: Grade cannot be assessed (undetermined grade)
G1: Well differentiated (low grade)
G2: Moderately differentiated (intermediate grade)
G3: Poorly differentiated (high grade)
G4: Undifferentiated (high grade)

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15
Q

Goals of Treatment:

  • Prophylaxis:
  • Cure ?
A

Prophylaxis:
-Preventative surgery. The goal of prophylactic surgery is to remove additionaltissue or organs from the body which, although it currently shows no signs ofcancer, carries a high risk of developing cancer in the future

Cure:

  • -Aggressive treatment to obtain best outcome for cure (early stage)
  • Cancer type is responsive to treatment
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16
Q

Goals of Tx:

  • control?
  • Palliative?
A
  • Management of cancer to diminish tumor burden or spread
  • Maintain quality of life
  • Increase length of life

Palliative: Control cancer causing symptoms, improve QOL

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17
Q

Mainstays of CA tx: (list the 4 realms)

A
  • Surgical: **Curative intent, palliative intervention
  • Radiation: Localized theray for solid tumors or mets, total body for SCT
  • Chemotherapy: neo-adjunct, adjuvant, palliative
  • Biotherapy: immunotherapy, targeted therapy, gene therapy
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18
Q

Endometrial Cancer – Epidemiology / Risk:

  • How common?
  • ___% lifetime risk of developing endometrial CA
  • Risk increases with _______
A
  • MC gynecologic malignancy in developed countries
  • 3%
  • advancing age
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19
Q

Endometrial CA:

  • age over ___ indicates increased risk
  • _____ syndrome increases risk
  • _______ therapy increases risk
A
  • > 45 yo

- lynch syndrome, unopposed estrogen therapy increases risk

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20
Q

T/F: use of tamoxifen increases risk for endometrial CA

A

true

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21
Q

Endometrial Cancer – Clinical Presentation:
-cardinal sx?
-

A
  • **abnormal uterine bleeding
  • -70-90% of Pts w/ endometrial CA present w this Sx
  • *6-19% of women with postmenopausal vaginal bleeding have endometrial cancer
  • Any postmenopausal bleeding should prompt evaluation for endometrial cancer
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22
Q

Endometrial Cancer:

-PE findings=

A

Typically enlarged uterus or palpable mass is not present

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23
Q

Endometrial Cancer – Diagnostic Evaluation:

  • labs?
  • US?
  • Gold standard test?
A
  • Hgb/Hct– eval for anemia
  • Hcg– r/o pregnancy
  • tumor markers–CA125

-**pelvic US–> ***shows Endometrial thickening or stripe >4mm indicates need for biopsy

-*****Endometrial sampling – GOLD STANDARD
Office biopsy vs hysteroscopy vs dilation and curettage

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24
Q

endometrial CA- prognosis

A
  • if you catch this early, GOOD survival rate

- most women get caught early cuz they are symptomatic

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25
Q

Endometrial Cancer – Screening

-is routine screening of asymptomatic women advised?

A

NO, dont screen asymptomatic women.

  • High percentage of symptomatic women with disease
  • Majority diagnosed with disease confined to the uterus
  • 90% five year survival rate
  • No screening test that is sensitive and specific
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26
Q

Lynch syndrome holds lifetime risk of developing endometrial cancer at ____%

A

12-54%

–Risk-reducing hysterectomy

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27
Q

Cervical CA:

  • how common?
  • _____ is detected in 99.7% of cervical CA’s
A
  • 3rd MC gynecologic malignancy & cause of death in US
  • 2nd MC female malignancy and cause of death from CA in countries w/out access to screening

-**HPV

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28
Q

Cervical Cancer – Risk Factors

A

Early onset sexual activity
Multiple sexual partners
High risk sexual partner
Known HPV positive or multiple sexual partners
History of sexually transmitted infections
History of vulvar or vaginal squamous intraepithelial neoplasia or cancer
Immunosuppression

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29
Q

65 yo woman with vaginal bleeding

–work them up for?

A

**ENDOMETRIAL CA

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30
Q

Cervical CA: HPV is detected in 99.7% of cervical cancers

–Vaccinations have ______ incidence

A
  • decreased cervical cancer incidence by 75% over the last 50 years
  • It has been estimated that 75-80% of sexually active adults will acquire genital tract HPV by the age of 50
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31
Q

Disease burden of genital HPV infection

(list ex’s)

A

Vulvar cancer, vaginal cancer, penile cancer, anal cancer, anogenital warts

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32
Q
  • 40 genital mucosal HPV types
  • ___ are oncogenic
  • HPV ___ and ____ are found in over 70% of all cervical CA’s
A
  • 15

- HPV 16 and 18 (KNOW)

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33
Q

_______ helps prevent infection by HPV 16, 18, 6, and 11 as well as 31, 33, 45, 52, and 58

A

**Gardisil 9. (KNOW)

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34
Q

Cervical CA- pathophys:
-Squamous Cell carcinoma ___%
(what types of HPV?

A

Sqauamous cell carcinoma (69%)

-HPV 16 (59%), 18 (13%), 58(5%), 33 (5%, 45 (4%)

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35
Q

Cervical CA- pathophys:

  • adenocarcinoma ___%
  • HPV types?
A

Adenocarcinoma (25%)

-HPV 16 (36%), 18 (37%), 45 (5%), 31 (2%), 33 (2%)

36
Q

Cervical CA- pathophys:

-HPV infection must _____ to progress to cancer

A

persist

  • Initial infection > high grade cervical intraepithelial neoplasia > invasive cancer
  • Average of 15 years
37
Q

________ infection as a cofactor in cervical cancer pathogenesis has been reported

A

Herpes simplex virus-2

38
Q

Cervical Cancer – Clinical Presentation:

  • early on?
  • MC sx?
  • Advanced disease?
A

-early–frequently asymptomatic
-MC: Irregular or heavy vaginal bleeding,
Postcoital bleeding, May have vaginal discharge mistaken for vaginitis or cervicitis

-advanced: Pelvic or lower back pain
Bowel or urinary symptom

39
Q

Cervical Cancer – Physical Exam:

-which exam must be performed?

A
  • *Pelvic exam in any women with suggestive Sx
  • Visualization of cervix may appear normal or cervical lesion may be visible
  • **Anything raised or friable should be biopsied
40
Q

Cervical Cancer – Diagnostic Testing:
-cervical cytology=
-Cervical Bx=
-

A
  • **pap smear
  • cervical bx taken from area which looks most suspicious
  • Colposcopy– used if there is no visual lesion but high suspicion of abnormal cytology, Helps visualize the squamocolumnar junction and transformation zone, Application of acetic acid to aid visualization
41
Q

what causes cervical CA?

A

**HPV

42
Q

Cervical CA:

-Imaging?

A
  • not routinely part of initial diagnosis of cervical cancer

- CT scans for staging

43
Q

Cervical Cancer - Screening:

-ages?

A

Age < 21: No screening recommended

Age 21 – 30: Recommend screening with papanicolaou every 3 years
–May consider reflex to HPV testing, but HPV testing is not recommended per ACOG guidelines

Age 30-65: Recommend screening with Pap test and HPV test every 5 years or Pap test every 3 years

Age > 65: May consider discontinuing screening if you have no history of abnormal cells or you have had 3 negative Pap tests in a row or two negative co-tests in a row within 10 years and most recent testing within 5 years

44
Q

Cervical Cancer – Abnormal Screening:

-Atypical Squamous cells (ASC)–>

A

-Differ from normal cells but do not meet premalignant disease
ASC – US (unknown significance)
ASC – H (HSIL cannot be excluded)

45
Q

Cervical Cancer – Abnormal Screening:

-cytologic findings?

A

Squamous intraepithelial neoplasia (SIL) - premalignant condition of the cervix

46
Q

Cervical Cancer – Abnormal Screening:

-Histologic findings?

A

Cervical intraepithelial neoplasia (CIN) - premalignant condition of the cervix

Note: CIN and HSIL are testing the same thing

47
Q

Cervical CA:

CIN 1=

A

=Low-grade lesion

Mildly atypical cellular changes in the lower third of the epithelium

HPV cytopathic effect (koilocytotic atypia) is often present

LSIL

48
Q

Cervical CA:

CIN 2=

A

High-grade lesion

Moderately atypical cellular changes confined to the basal two-thirds of the epithelium with preservation of epithelial maturation

-**If HPV-16 negative, it’s considered LSIL; otherwise HSIL

49
Q

Cervical CA:

CIN 3=

A

**High-grade lesion

  • Severely atypical cellular changes encompassing greater than two-thirds of the epithelial thickness and includes full-thickness lesions
  • HSIL
50
Q

Breast CA:

-how common?

A

-2nd MC cancer worldwide, leading cause of death in women, 2nd MC CA death in the US

51
Q

Breast CA: risk factors?

  • personal hx of _____
  • family hx?
A

-ovarian, peritoneal, or breast cancer

  • ovarian, peritoneal, or breast cancer
  • Genetic predisposition: BRCA genetic mutation

-Chest wall radiation between the ages of 10 and 30

52
Q

Breast Cancer – Clinical Presentation:

-in developed countries, most women present with _____

A

abnormal mammogram

  • -15% present with mass not detected on mammogram
  • -30% present with mass in interval between mammograms
  • Hard, immobile, single dominant mass
53
Q

Breast CA:

-describe a locally advanced dz

A

Axillary adenopathy
Erythema, thickening, dimpling of the skin (peau d’orange)
Suggests inflammatory breast cancer

54
Q

Breast CA:

-describe metastatic disease– MC sites of mets?

A

bone, liver, lungs

55
Q

Breast Cancer – Diagnostic Imaging:

  • Mammogram findings:?
  • breast US ?
A
  • Soft tissue mass or density, **Spiculated, high-density mass
  • US: Hypoechogenicity, internal calcifications, shadowing, spiculated/indistinct/angular margins
56
Q

Breast CA: imaging

-breast MRI results?

A

*Irregular or spiculated mass margins, heterogeneous internal enhancement, and enhancing internal septa

57
Q

Breast Cancer – Additional Diagnostic Testing

-labs?

A
  • Elevated alkaline phosphatase or bone pain >bone scan
  • Elevated liver enzymes > CT abdomen/pelvis
  • Pulmonary Sx: –> get CT chest
  • Stage III or higher > whole body PET/CT
58
Q

Breast Cancer – Pathology

-list ex’s

A
  • Infiltrating ductal carcinoma
  • Infiltrating lobular carcinoma
  • Mixed ductal/lobular carcinoma
  • Other: metaplastic, mucinous, tubular, medullary, and papillary carcinomas (less than 5%)
59
Q

How common is Infiltrating ductal carcinoma?

A

MC type of invasive breast CA **

60
Q

How common is Infiltrating lobular carcinoma?

A

-8% of invasive breast CAs

61
Q

Mixed ductal/lobular carcinoma:

-how common?

A

=a Mixed invasive carcinoma, 7% of invasive breast cancers.

62
Q

Breast Cancer - Pathology:
-Receptor testing:
list ex’s

A
  • ER positive/negative (estrogen receptor)
  • PR positive/negative (progesterone receptor)
  • HER-2 positive/negative (human epidermal growth factor 2)–> Approximately 20% positive
63
Q

Breast Cancer - Pathology:
-Receptor testing:
triple negative breast CA (test negative for all 3 receptors) approx. ____% of Pts
-prognosis?

A
  • 13%

- poor prognosis

64
Q

Ductal carcinoma in situ (DCIS)=

A

a heterogeneous group of *****PREcancerous lesions confined to the breast ducts and lobules and is potentially a precursor lesion to invasive breast cancer

-characterized by the size of the lesion, nuclear grade, presence and extent of comedo necrosis, and architectural pattern

65
Q

Breast Cancer - Screening:

  • age <40 ?
  • age 40-49 ?
  • age 50-74?
  • age 75+
A
  • No recommended screening for average risk individuals
  • Recommend screening mammography every two years, Consider patient input
  • Recommend screening mammography every two years
  • Recommend screening mammography every two years if life expectance is >10 years
66
Q

Breast Cancer – Screening

-high risk Pts need ?

A
  • *MRI
  • *Breast ultrasound

-Self breast exams–> Monthly
Controversial as to efficacy

67
Q

Ovarian CA:

  • how common?
  • avrg age of dx?
A
  • 2nd MC gynecologic CA in US, MC cause of gyno CA death in US
  • 63 yo
68
Q

Ovarian Cancer – Risk Factors (list)

A

Age
BRCA mutation
-Risk of ovarian cancer reaches 2-3% in women with aBRCA1gene mutation at age 35 andwithBRCA2mutation at age 50

-Hereditary cancer syndromes–>The typical age at diagnosis of ovarian cancer in women with Lynch syndrome is 43 to 50years old

Infertility

Nulliparity

Less risky risk factors:
Endometriosis, PCOS, Postmenopausal hormone therapy, Obesity, Smoking, Asbestos

69
Q

Ovarian Cancer – Protective Factors (list)

A

Multiparity
Breastfeeding
Oral contraceptives

Salpingo-oophorectomy: Include removal of fallopian tubes to prevent peritoneal carcinoma
Tubal ligation
Hysterectomy

70
Q

Ovarian Cancer - Pathophysiology:

- ______ carcinoma (95%)

A
  • Epithelial carcinoma (95%)
  • -Serous carcinoma – most common histologic subtype

-Germ cell tumors or sex cord stromal tumors (5%)

71
Q

Ovarian Cancer – Clinical Presentation:

-acute ?

A

Typically advanced disease requiring urgent care and evaluation
Pleural effusion
Bowel obstruction
Venous thromboembolism

72
Q

Ovarian Cancer – Clinical Presentation:

Subacute presentation?

A

-Adenxal mass
-Pelvic/abdominal Sx:
Bloating, urinary urgency or frequency, early satiety, pelvic/abdominal pain

73
Q

Ovarian Cancer – Clinical Presentation:

-majority of ovarian CA’s are diagnosed at _____

A
-advanced stage 
Confined to primary site (15%)
Spread to regional lymph nodes (17%)
Distant metastases (61%)
Unstaged (7%)
74
Q

Ovarian Cancer – Diagnostic Testing

A
  • Full surgical removal as opposed to bx is preferable
  • CT abdomen/pelvis and/or Pelvic Ultrasound
  • CA-125
75
Q

Ovarian Cancer - Prognosis:

-5 year survival?

A
  • Stage 1 disease >90%
  • Regional disease 75-80%
  • Distant metastatic disease <25%
  • Overall five-year survival in women with ovarian cancer is less than 45%

–Largely due to the spread of cancer beyond the ovary at the time of clinical detection in 75% of patients

76
Q

Risks of screening w/ ovarian CA

A

Although ovarian cancer is an important cause of cancer death, it’s incidence and prevalence is fairly low

  • False positive screening tests could lead to surgical intervention with complications
  • Currently no recommendations for screening
  • Risk stratification for individual: Preventive measures
77
Q

Vulvar Cancer:

-how common?

A

-4th MC gyno malignancy

78
Q

Vulvar Cancer – Risk Factors

A
Vulvar or cervical intraepithelial neoplasia (VIN)
Prior history of cervical cancer
Cigarette smoking
Vulvar lichen sclerosus
Immunodeficiency syndromes
Northern European ancestry
HPV infection
79
Q

Vulvar Cancer:
HPV was detected in ____% of vulvar intraepithelial neoplasia
-and ____% of invasive vulvar CA cases

A
  • 87%

- 29%

80
Q
Vulvar CA:
HPV subtypes (list 3**)
A
HPV 16 (73%)
HPV 33 (7%)
HPV 18 (5%)
81
Q

Vulvar Cancer – Clinical Presentation:

-abnormal finding on the _____ _____ is MC

A
  • labia majora
  • Labia minora, perineum, clitoris and mons are less common
  • Unifocal vulvar plaque, ulcer or mass
  • Can be fleshy, nodular, or warty
82
Q

Vulvar Cancer – Clinical Presentation:

-which Sx is MC?

A
  • **vulvar pruritus
  • -vulvar bleeding or pain
  • Dysuria, dyschezia, rectal bleeding, an enlarged lymph node in the groin, or lower-extremity edema
83
Q

Vulvar Cancer – Diagnostic Eval ?

A

-biopsy

84
Q

Vulvar Cancer - Pathology:

– ______% are squamous cell carcinoma

A
  • 75%
  • Keratinizing, differentiated, or simplex type is MC
  • Older individuals
  • Not associated with HPV infection
  • Associated with vulvar dystrophies (lichen sclerosis)
85
Q

Vulvar Cancer:

  • Classic, warty, ______ type is MC in younger women
  • associated with HPV ____, ____, and ____
A
  • Bowenoid type

- HPV 16, 18, and 33

86
Q

Vulvar Cancer – Pathology(cont)

A
  • Verrocouscarcinoma: Variant of squamous cell carcinoma
  • Basal cell carcinoma: Non-metastasizing

Melanoma: 2nd MC

-Sarcoma: Poor pronosis

  • Paget disease of the vulva
  • -Intraepithial carcinoma

-Bartholin gland carcinoma–> most often adenocarcinomas or squamous cell carcinomas, but transitional cell carcinomas, adenosquamous, and adenoid cystic carcinomas may also develop

87
Q

Marjoity of vulvar cancers are diagnosed at an _____ stage

A

early

  • Confined to primary site (59%)
  • Regional disease (30%)
  • Distant metastatic disease (6%)
  • Five-year survival after dx is 72%
  • Median age at death= 78 years