Gynonco Flashcards

1
Q

1st line chemo for advanced ovarian cancer

A

6 cycles of Taxol+ carboplatin

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2
Q

Ovarian cystectomy revealed borderline serous ovarian tumor

A

Limited staging, USO

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3
Q

Granulosa cell tumor immunohistochemical marker:

A

immunostaining for inhibin antibody, eosinophilic call-Exner bodies

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4
Q

Beta-unit similarity btw — and B-hcg : the same amino acids consequences

A

LH

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5
Q

Cannonball appearance in the lungs:

A

Mets

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6
Q

Phantom Bhcg :

A

Due to heterophilic Ab

To dx: do urine pregnancy test

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7
Q

Do not give NSAIDS and carboxyl compound containing products.” Like penicillin” along with chemotherapy that toxic to nephro

A

Warn

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8
Q

Medical management of fibroids:

A

selective progesterone receptor modulators

like ulipristal acetate (UPA)

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9
Q

Pedunculated UFs localized in the submucosa, extending inside the uterine cavity, are classified as type

A

0

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10
Q

submucosal UFs that have ±50% of intramural location considered types …,…

A

1 and 2

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11
Q

Uterine Fibroids are completely located intramural with contact to the endometrium considered type:

A

Type 3

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12
Q

UFs are intramural lying entirely in the myometrium considered type

A

type 4

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13
Q

subserosal UFs with ±50% of intramural location considered types

A

Types 5–6

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14
Q

UTERINE FIBROIDS THAT attached to the serosa by a stalk (pedunculated) CONSIDERED TYPE…

A

7

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15
Q

all other UFs not related to the myometrium such as cervical or parasitic lesions considered type

A

8

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16
Q

Increased LDH in

A

Dysgerminoma

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17
Q

Increased A-FP in which ovarian Tumor type

A

Endodermal sinus Tumor

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18
Q

Dysgerminoma mode of transmission

A

Lymphatic

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19
Q

Dysgerminoma percentage of being bilateral

A

15 %

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20
Q

Indications of cone bx:

A
  • Discrepancy btw pap and Colpo
  • Diagnostic conization is indicated in the following situations:
    Finding epithelial cell abnormalities, in particular high-grade squamous intraepithelial lesions (HSIL) or low-grade squamous intraepithelial lesions (LSIL) in the absence of gross or colposcopic lesions of the cervix
    Unsatisfactory colposcopy, defined as the examiner’s inability to view the entire transformation zone, including the squamocolumnar junction, in women with epithelial cell abnormalities
    Uncertainty regarding the presence or absence of microinvasion or invasion following the diagnosis of CIN by directed biopsy
    Finding CIN or microinvasive cancer during endocervical curettage
    Cytologic or histologic evidence of premalignant or malignant glandular epithelium
    Cytologic diagnosis inconsistent with histologic diagnosis based on directed biopsy findings
  • Therapeutic conization
    -Therapeutic conization is currently the preferred modality to treat CIN grades 2 and 3. All described approaches (ie, cold-knife, laser, LEEP) are equally effective, as found by Mitchell and colleagues.
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21
Q

Simple hysterectomy only for which stage of Cervical ca

A

Stage 1A1

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22
Q

serum glycoprotein CA-125 concentration (normal range 0–35 kU/L) is elevated in 80% of women with ovarian cancer. However, the levels can be within the normal range in 50% of women with stage I disease. What malignancies can be high with?

A

epithelial ovarian, colon, or breast cancer.

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23
Q

-

A

USS and measurement of serum levels of CA-125 should be performed every 4 months. If there is no change in the size of the cyst or the cyst has resolved after 1 year of follow-up, then the patient can be discharged from follow-up.

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24
Q

In postmenopausal Women at intermediate risk of malignancy (RMI <200) with Simple, unilateral, unilocular ovarian cysts, management ?

A

can be suitable for laparoscopic surgery. Laparoscopic management of ovarian cysts in post-menopausal women should involve oophorectomy (usually bilateral), rather than cystectomy.

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25
Q

In postmenopausal Women at high risk of malignancy (usually RMI >200 or clinical suspicion) presenting with adnexal mass, mangament ?

A

need to be managed by a gynae- cological oncologist in a cancer centre. The aim of surgery in these cases is to confirm the diagnosis, to assess the extent of the disease, and to attempt optimal debulking. The laparotomy should be performed through a midline incision and include: collection of peritoneal fluid for cytology, bilateral salpingo-oophorectomy and hysterectomy, omentectomy, appendicectomy, biopsies from any suspicious peritoneal surfaces, and para-aortic lymph node sampling.

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26
Q

Endometrial hyperplasia percentage to convert to endometrial cancer based on WHO classification

A

Simple without atypia 1%, with 8-10%
Complex without atypia 3%, with atypia 29-30%

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27
Q

Atypical polyploid adenomyosis associated with

A

Uterine adenocarcinoma

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28
Q

Occasionally, the plateauing or increasing hCG levels are a result of a false-positive laboratory test result caused by heterophilic antibodies cross-reacting with the hCG test. Such false-positive test results, also known as “___________,”

A

phantom hCG

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29
Q

Mode of metastasis of ovarian cancer:

A

Cell exfoliation

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30
Q

Sex cord–stromal tumors accounts for approximately -% of ovarian neoplasms

A

Sex cord–stromal tumors accounts for approximately 6% ( 3 to 5% -William-) of ovarian neoplasms

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31
Q

characteristic microscopic pattern of Granulosa cell tumors

A

Call-Exner bodies, eosinophilic bodies surrounded by granulosa cells.

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32
Q

granulosa cell tumor clinical presentation:

A

Approximately 5% occur before puberty and they can be one cause of precocious puberty.
increased levels of blood estrogens, uterine bleeding, and occasionally endometrial carcinoma. It is estimated that approximately 5% of the granulosa cell tumors in adults are associated with endometrial carcinoma. In menstruating women, the functional granulosa cell tumor can produce abnormal menstrual patterns, menorrhagia, and even amenorrhea.

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33
Q

Krukenberg tumor most characteristic pathological feature

A

characterized by mucin-laden, signet-ring cells within ovarian stroma.

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34
Q

A 45-year-old woman with history of vulval itching and soreness for past two years attends the gynaecology clinic. She is a smoker. She gives a history of using high potency steroid ointment previously with no symptom relief. A biopsy in the clinic reports vulval intraepithelial neoplasia (VIN) 3. You counsel her for excision of the lesion. What percentage of VIN ultimately have unrecognised invasion detected on excision?
A. 5%
B. 10%
C. 15%
D. 20%
E. 25%

A

D. 20%

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35
Q

Approximately … percent of inherited ovarian cancers result from germline mutations in the BRCA I, BRCA.2, or other homologous recombination deficiency genes.

A

Approximately 75 percent of inherited ovarian cancers result from germline mutations in the BRCA I, BRCA.2, or other homologous recombination deficiency genes.

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36
Q

The BRCA I gene is located on chromosome 17 q21. Patients with a proven mutation have a dramatically elevated risk of developing ovarian cancer (-%). BRCA2 is located on chromosome 13q12 and in general is less likely to lead to ovarian cancer (-%). The estimated lifetime risk of breast cancer with a BRCA I is ….. % and BRCA 2 mutation is —- %

A

The BRCA I gene is located on chromosome 17 q21. Patients with a proven mutation have a dramatically elevated risk of developing ovarian cancer (39 to 46%). BRCA2 is located on chromosome 13q12 and in general is less likely to lead to ovarian cancer (10 to 27%). The estimated lifetime risk of breast cancer with a BRCA I (65%) and BRCA 2 mutation is 70% (Kuchenbaecker,2017) وفي رواية ( btw 45 to 85 % )

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37
Q

In low-risk patients who are not BRCA. carriers, risk-reducing salpingectomy also is now considered in those undergoing hysterectomy or permanent sterilization. Ovarian cancer risk is reduced up to –%

A

In low-risk patients who are not BRCA. carriers, risk-reducing salpingectomy also is now considered in those undergoing hys-terectomy or permanent sterilization. Ovarian cancer risk is reduced up to 65%

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38
Q

In BRCA carriers, BSO procedure is approximately –% effective in preventing epithelial ovarian cancer (Kauff, 2002; Rebbeck, 2002). Prophylactic BSO also reduces the risk of developing breast cancer by -% (Rebbeck, 2002). Predictably, the protective effect is strongest among premenopausal women (Kramer, 2005). In women with HNPCC, the ovarian cancer risk reduction approaches -%

A

In BRCA carriers, the procedure is approximately 90-percent effective in preventing epithelial ovarian cancer (Kauff, 2002; Rebbeck, 2002). Prophylactic BSO also reduces the risk of developing breast cancer by 50 % (Rebbeck, 2002). Predictably, the protective effect is strongest among premenopausal women (Kramer, 2005). In women with HNPCC, the ovarian cancer risk reduction approaches 100 %

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39
Q

Endometrial cancer incidence is

A

3% in general population or 1/42.

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40
Q
  • Ovarian cancer incidence is
A

1/72 or 1.5% in general population.

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41
Q

Pseudo-pseudo Meigs’ syndrome (PPMS) or Tjalma syndrome

A

rare manifestation of patients with systemic lupus erythematosus (SLE), defined by the presence of ascites, pleural effusions and an elevated CA-125 level.

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42
Q

psammoma bodies can be seen in which type of gyne tumors

A
  • serous cystadenocarcinoma of the ovary
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43
Q

Management Abnormal Pap Smear
IF Cytology negative, HPV+

A
  • occur in less than 10 percent of screened patients . • Cotesting is repeated in 12m. ( risk of high-grade lesion is low, and most HPV infections will resolve during this time)
    • Colposcopy is recommended for persistently positive HPV DNA test results.
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44
Q

IN ASCUS — WHAT IS THE risk OF CIN 2/3

A

5-10%, cancer 1-2/1000.

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45
Q

Management of ASCUS If repeated pap abnormal
or if ASCUS, HPV positive :

A

colpo
• Reflex HPV testing >25 y/o (acceptable 21-24, recommended if HIV+)

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46
Q

Management of ASCUS , HPV negative:

A

cotest 3 years or cytology alone after one year if <25.

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47
Q

Management of ASCUS Without HPV testing

A

— repeat cytology 1y (preferred age 21-24)

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48
Q

in LSIL- what is the risk of CIN2/3

A

15-30%

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49
Q

management of LSIL, w.out HPV tesing or HPV positive:

A

COLPO
Reflex testing is not indicated in reproductive age women as 75-85% will be positive. Can consider reflex testing in postmenopausal women without HPV test.

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50
Q

management of LSIL, HPV negative:

A

repeat cotest 1y preferred, colpo acceptable
Age 21-24 w/LSIL : cytology follow up preferred.
HIV: colpo (ACOG)

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51
Q

Management of Abnormal Pap Smear
if ASC-H:

A

Colpo — if inadequate, diagnostic excisional procedure indicated.

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52
Q

if ASC-H: the risk of HSIL

A

25%

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53
Q

Management of Abnormal Pap Smear
in HSIL:

A

• Colpo- immediate LEEP also an option “see- and- LEEP approach.”
• Colpo may miss high grade lesion and the most HSIL cytologies eventually result in excision for diagnosis or tx.
• Inadequate colpo for excision.

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54
Q

if pap smear showed HSIL: what is the risk of CIN2/3 and invasive SCC?

A

70% CIN2/3, 1-2% invasive SCC

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55
Q

Management of Abnormal Pap Smear

if AGC, AGC favor neoplasia, AIS

A

• Colpo, endocervical sampling • Endometrial sampling in patients 35 years and older or in younger women with RF.
• Atypical endometrial cells: initial endometrial and endocervical sampling acceptable with colpo if negative.
• Diagnostic excision is indicated following AGC favor neoplasia and AIS pap results if initial colpo evaluation does not result in a cancer diagnosis

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56
Q

pap smear showed Unsatisfactory Pap tests, next step?

A

repeated in 2 to 4 months.
• If atrophy or a specific infection is present, treatment before repeat cytology may be helpful.
• If the result is unsatisfactory again, colposcopy is recommended as this persistent result confers increased CIN risk

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57
Q

Colposcopy is recommended for pts with:

A
  • ASC-H cytology, regardless of HPV
  • HPV18+ NILM ( Negative for intraepithelial lesion or malignancy ) and HPV16+ NILM
  • After 2 consecutive unsat screening tests
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58
Q

Incidence of Cervical Cancer in all races + (Asian?)

A

7.3 (Asian 6.4)

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59
Q
A

2.3

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60
Q

It is the second most common cancer in women worldwide, and the third most common cause of female cancer mortality in developing countries

A

Cervical cancer
(4th world wide among all malignancies in women per WHO 2019)

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61
Q

Types of cervical cancer include

A

squamous cell carcinoma (most common), invasive adenocarcinoma, small cell neuroendocrine carcinoma, and other rare histologic types.

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62
Q

Evaluation of cervical cancer

A
  • Early stage disease is usually asymptomatic and detected by screening with cervical smear.
  • Symptoms, if present, are usually vaginal bleeding or blood-stained vaginal discharge.
  • Diagnosis is usually made using colposcopically directed cervical biopsy.
  • Imaging should be done for clinical staging and risk assessment (Strong recommendation).
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63
Q

Management For early invasive cervical cancer (small tumors ≤ 4 cm confined to cervix) initial treatment is

A

surgery or radiation (Strong recommendation).

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64
Q

Approximately … percent of all breast cancers are due to mutations in the BRCA2 gene

A

Approximately two percent of all breast cancers are due to mutations in the BRCA2 gene

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65
Q

HPV 16 commonly associated with which type of cancer

A

Squamous cell carcinoma

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66
Q

HPV 18 commonly associated with which type of cancer

A

Adenocarcinoma and Neuroendocrine tumors

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67
Q

HPV 6 and 11 can cause

A

Benign genital warts

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68
Q

If Atypical glandular cell found in Pap smear the risk of CIN 2&3

A

10%

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69
Q

In Pt with low risk HPV (presented with genital warts) because the risk of getting high risk HPV the follow-up plan ?

A

Yearly Pap test screening for 2-3 years if negative then for it will be back every 3 years
(?American association)

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70
Q

vulval adenocarcinoma prevalence

A

rare histological diagnosis found in less than 10% of vulval cancers.

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71
Q

the most common vulvar malignancy

A

1st Squamous cell carcinoma (accounts for 4%-5% of all gynecologic malignancies)
And account approximately 90 percent of vulvar carcinoma
2nd most common is Malignant melanoma

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72
Q

Vulvar squamous cell carcinoma (VSCC) is often categorized by

A

the presence or absence of human papillomavirus (HPV) in the tumor.

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73
Q

Diseases associated with HPV-negative VSCC ( vulvar squamous cell carcinoma)

A

Dermatological diseases involving chronic inflammation (such as lichen sclerosis and lichen simplex chronicus)

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74
Q

risk factor for HPV-associated VSCC.

A

Smoking

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75
Q

Vulvar cancer prevalence

A

1.1% of all female cancers and 3.6% of all gynecological cancers

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76
Q

Schiller duval bodies

A

Endodermal sinus tumor

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77
Q

When do you Stop cervical cancer screening?

A

after age 65 years if there is consecutive normal testing for prior 10 years, or after hysterectomy for benign condition with removal of the cervix (Strong recommendation).

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78
Q

What are the Three major categories of malignant ovarian tumors.

A

1) Epithelial ovarian cancers account for 90 to 95 percent of malignant ovarian tumors
2) Germ cell 2-3%
3) sex cord-stromal ovarian tumors account for 6%

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79
Q

the most common subtype of all germ cell tumors accounts for 95 percent of

A

The mature cystic teratoma, also called dermoid cyst

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80
Q

Malignant germ cell tumors

A

dysgerminoma, yolk sac tumor, endodermal sinus tumor, polyembryoma, embryonal ,immature teratoma, choriocarcinoma,mixed.

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81
Q

Three clinical features distinguish malignant germ cell tumors from epithelial ovarian cancers. Which are ..?

A

First. individuals typically are younger, usually in their teens or early 20s. Most have stage I disease at diagnosis. Last, prognosis is excellent-even for those with advanced disease–due to exquisite tumor chemosensitivity. Fertility-sparing surgery is the primary treatment for women seeking future pregnancy, although most will require postoperative chemotherapy.

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82
Q

2nd line of endometrioid tumors and positive estrogen receptor status

A

Systemic hormonal: Tamoxifen or a combination of tamoxifen and progestin (used for patients who wish to preserve fertility and for patients with advanced or recurrent disease in a palliative setting)
(Letrozole can be given as well

Systematic Review (Weelden,2019)

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83
Q

Modified WHO Classification of Ovarian Germ Cell Tumors

A

Dysgerminoma
Yolk sac tumor (former endodermal sinus tumor)
Embryonal carcinoma
Nongestational choriocarcinoma
Mature teratoma Solid Cystic (dermoid cyst)
Immature teratoma
Mixed germ cell tumor

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84
Q

Monodermal teratoma and highly specialized types arising from a mature cystic teratoma which includes

A

Thyroid turners (struma ovarii: benign or malignant)
Carcinoids
Neuroectodermal tumors
Carcinomas (squamous cell or adeno-)
Sebaceous tumors

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85
Q

the most common ovarian malignancy detected during pregnancy.

A

Dysgerminoma

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85
Q

the most common ovarian malignancy detected during pregnancy.

A

Dysgerminoma
(This is believed to be an age-related coincidence, however, and not due to gestation)

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86
Q

Five percent of ******* are discovered in phenotypic females with karyotypically abnormal gonads, specifically, with a normal or abnormal Y chromosome (Morimura, 1998). Commonly, this group includes those with Turner syndrome mosaicism (45,X/46,XY) and with Swyer syndrome (46,XY, pure gonadal dysgenesis)

A

dysgerminomas
(The dysgenetic gonads of these individuals often contain gonadoblastomas, which are benign germ cell neoplasms. These tumors may regress or alternatively may undergo malignant transformation, most commonly to dysgerminoma. Because approximately 40 percent of gonadoblastomas in these individuals undergo malignant transformation, both ovaries are removed)

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87
Q

the only germ cell malignancy with a significant rate of bilateral ovarian involvement-15 to 20 percent.

A

Dysgerminomas

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88
Q

characterized microscopically by a relatively monot~ nous proliferation of large, rounded, polyhedral dear eel Is that are rich in cytoplasmic glycogen. These contain uniform central rounded or squar~ged nuclei with one or a few prominent nucleoli.

A

Dysgerminoma

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89
Q

Dysgerminoma tumor cells closely resemble the primordial germ cell of the embryo and are histologically identical to **** of the testis.

A

seminoma

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90
Q

The standard treatment of dysgerminoma

A

usually involves fertility-sparing surgery with unilateral salpingo-oophorcctomy (USO). In some extenuating circumstances, ovarian cystectomy may be considered (Vicus, 2010). Surgical staging is generally extrapolated from epithelial ovarian cancer, but lymphadenectomy is particularly important (Chap. 35). Of the malignant germ cell tumors, dysgerminoma has the highest rate of nodal metastases, approximately 25 to 30 percent (Kumar, 2008). Although staging deviations do not adversely affect survival, comprehensive staging allows a safe observation strategy for stage IA tumors (Billmire, 2004; Palenzuela, 2008). Preservation of the contralateral ovary leads to “recurrent” dysgerminoma in 5 to 10 percent of retained gonads during the next 2 years.

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91
Q

Dysgerminomas have the best prognosis of all malignant ovarian germ cell tumor variants. Two thirds are stage I at diagnosis, and the 5-year disease-specific survival rate approximates

A

99 %
Even those with advanced disease have high survival rates following chemotherapy. For example, those with stage II-IV disease have a greater than 98-percent survival rate with platinum-based agents (Chan, 2008). a result carboplatin may be preferable to cisplatin in these patients due to equivalent outcomes with reduced long-term toxicity (Shah, 2018; Skalleberg, 2017).

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92
Q

Yolk sac tumors (previously called endodermal sinus rumors) account for ** percent of all malignant ovarian germ cell tumors

A

10 to 20

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93
Q

the most common gynecologic malignancy

A

endometrial cancer

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94
Q

Risk factors of endometrial cancer

A

obesity and advancing age.
excess-estrogen environment (type I endometrial cancer)
Polycystic ovarian syndrome Long-term, high-dose unopposed menopausal estrogens Early age of menarche Late age of natural menopause Infertility Nulliparity Menstrual irregularities North America or northern Europe residence Higher education or income level White race Older age Tamoxifen, hereditry (lynch syndrome), high cumulative doses DM, CHTN, or gallbladder disease Lower risk with Long-term COC use Cigarette smoking

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95
Q

The cornerstone of treatment of endometrial cancer

A

hysterectomy with bilateral salpingo-oophorectomy (BSO) and surgical staging that includes lymph node assessment for most women. Of affected women, 67 percent will have stage I disease that is potentially curable by surgery alone, although high-risk stage I patients often receive adjuvant therapy (Siegd, 2019).

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96
Q

the sixth leading cause of cancer deaths among women

A

Endometrial cancer

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97
Q

Endometrial adenocarcinomas are categorized as

A

type I or type II based on histology.
Type I, that is, endometrioid type, makes up 80 to 90 percent of all cases (Felix, 2010).
The other 10 to 20 percent are type II cancers, namely, the non-endometrioid histologic types that include serous and clear cell adenocarcinomas and carcinosarcoma.

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98
Q

The lifetime risk of developing endometrial cancer

A

3-percent (1:32)

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99
Q

If EC invades the Bowel stroma not mucosa what stage

A

IIIB

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100
Q

the most common extracolonic manifestation of Lynch syndrome (hereditary nonpolyposis colorectal cancer [HNPCC])

A

Endometrial cancer
Of all endometrial cancer cases, 2.3 percent are attributable to Lynch syndrome, and these cases develop more than 10 years earlier than sporadic endometrial cancer (Resnick, 2009).

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101
Q

Lynch syndrome (hereditary nonpolyposis colorectal cancer [HNPCC]) mode of Inheritance

A

This autosomal-dominant syndrome results primarily from mutations in the mismatch repair genes MLH1, MSH2, MSH6, and PMS2
Gene mutation prevents repair of base mismatches, which are commonly produced during DNA replication. Inactivity of this DNA repair system leads to mutations that can promote carcinogenesis. Mutation carriers have a risk of developing endometrial cancer that ranges from 40 to 60 percent. Among affected women, endometrial cancer often develops at a young age, and the risk for this cancer actually exceeds that for colorectal cancer

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102
Q

Tamoxifen causes a – to – fold higher risk of developing endometrial cancer by its modest “unopposed” estrogenic effect on the endometrium

A

Tamoxifen causes a two-to three fold higher risk of developing endometrial cancer by its modest “unopposed” estrogenic effect on the endometrium.
(cancer rates rise linearly with the duration and cumulative dose of tamoxifen therapy)
Accordingly, women taking tamoxifen are counseled regarding this endometrial risk and should report vaginal spotting, bleeding, or discharge. That said, unless a tamoxifen-treated patient has such symptoms, routine endometrial surveillance does not improve early detection rates (American College of Obstetricians and Gynecologists, 2019c}.

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103
Q

combination oral contraceptive (COC) use for at least 1 year confers as much as a — to – percent reduced endometrial cancer risk. Risk reduction extends for 10 to 20 years.

A

combination oral contraceptive (COC) use for at least 1 year confers as much as a 30-to 50-percent reduced endometrial cancer risk. Risk reduction extends for 10 to 20 years.

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104
Q

Endometrial hyperplasia is defined as

A

endometrial thickening with proliferation of irregularly sized and shaped glands and an increased gland-to-stroma ratio.
(In the absence of such thickening, lesions are best designated as disorderly proliferative mdometrium or focal glandular crowding)

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105
Q

The classification system of endometrial hyperplasia used by the World Health Organization {WHO) and International Society of Gynecological Pathologists designates two different types with varying malignant potential

A

1) Hyperplasia without atypia is characterized by exaggerated endometrial gland proliferation and an increased gland-to-stroma ratio compared with normal proliferative endometrium, but without significant cytologic atypia.
2) Atypical endometrial hyperplasias are clearly associated with the subsequent development of adenocarcinoma
Although endometrial hyperplasias are formally classified in these two different groups, they tend to be morphologically heterogeneous, Endometrial intraepithelial neoplasia (EIN) is a term introduced to more accurately distinguish the two very different clinical categories of hyperplasia.

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106
Q

Endometrial intraepithelial neoplasia (EIN) is a term introduced to more accurately distinguish the two very different clinical categories of hyperplasia. These are:

A

(1) nonnal polyclonal endometrium diffusely responding to an abnormal hormonal environment and
(2) intrinsically proliferative monoclonal lesions that arise focally and confer an devated risk of adenocarcinoma
The ElN classification system is a more accurate and reproducible way to predict progression to cancer and is recognized by the American College of Obstetricians and Gynecologisu and Society of Gynecologic Oncology (2017a). However, it is not been universally implemented

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107
Q

Pipelle office endometrial biopsy (EMB) indications:

A

The American College of Obstetricians and Gynecologists (2016) recommends such a sample for women older than 45 years with AUB. EMB is also considered for those younger than 45 with chronic excess estrogen exposure (exogenous or endogenous), failed medical management, and persistent AUB.
All patients older than 35 years with AGC cervical cytology should undergo endometrial biopsy. Endometrial biopsy also is recommended for women of any age with AGC cytology and risk factors for endometrial cancer (eg, abnormal
bleeding, obesity, anovulation) or cytologic diagnosis of AGC, favor endometrial origin.

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108
Q

Cut-off point for endometrial thickness that mandate endometrial sample in symptomatic postmenopausal women

A

For these women, endometrial stripe thickness measurements less or equal to 4 mm and associated with bleeding that is a.attributed to endomcttial atrophy (Amerian College of Obstmicians and Gynecologim, 2018b). Postmcnopausal women with a thicker endometrium warrant biopsy. Sonography may also identify abnormal echostructural changes in the endometrium. Cystic endometrial changes suggest polyps, homogeneously thickened endometrium may indicate hyperplasia, and a heterogeneous structural pattern is suspicious for malignancy. However, these sonographic findings show great overlap and cannot be used alone.

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109
Q

Cut-off point for endometrial thickness that mandate endometrial sample in asymptomatic postmenopausal women

A

Endometrial thickness >4 mm may be identified in postmenopausal women undergoing sonographic evaluation for reasons unrelated to postmenopausal bleeding. The positive predictive value of an •abnormal” endometrial thickness in asymptomatic women would be expected to be low, because the disease prevalence in asymptomatic patients is low. It is therefore reasonable to use a higher threshold value for these patients. The Society of Obstetrics and Gynecology of Canada suggests 11 mm as the threshold in asymptomatic women (Wolfman, 2010).

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110
Q

yolk sac tumor pathognomic histopathology feature

A

Schiller-Duval body (This structure consists of a central caplllary surrounded by tumor cells, present within a cystic space that may be lined by flat to cuboidal tumor cells)

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111
Q

Features of yolk sac tumor age of population:

A

One third of individuals are premenarchal at the time of initial presentation. Involvement of both gonads is rare, and the other ovaty is usually involved with metastatic disease only when other metastases are found in the peritoneal cavity.

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112
Q

In immature teratoma, survival is predicted most accurately by stage and by histologic grade of the tumor. How to counsel the patient ?

A

almost three quarters of immature teratomas are stage I at diagnosis and have a 5~year survival rate of 98 percent (Chan, 2008). Those with stage IA grade 1 immature teratomas have an excellent prognosis and do not require adjuvant chemotherapy (Bona,1994; Marina, 1999). Patients with stage II-IV disease have a 5-year survival rate ranging from 73 to 88 percent (Chan, 2008).

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113
Q

the standard care of management for immature teratoma and other malignant germ cell tumors in reproductive-aged women

A

Unilateral salpingo-oophorectomy

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114
Q

The most frequent site of dissemination of immature teratoma is

A

the peritoneum and much less commonly the retroperitoneal lymph nodes.

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115
Q

The most common Malignant Transformation variant of Mature Cystic Teratomas

A

Squamous cell carcinoma is most common and is found in approximately 1 percent of mature cystic teratomas typically develop in postmenopausal women

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116
Q

Steps of surgical staging of ovarian cancer:

A
  • vertical abdominal incision is still traditionally recommended if an advanced ovarian malignancy is suspected.
  • If present, ascites is evacuated and sent for cytologic evaluation. Otherwise, washings of the pelvis and paracolic gutters are collected for analysis prior to manipulation of the intraperitoneal contents.
  • The entire peritoneal cavity is systematically inspected. The ovaries are assessed for size, tumor involvement, capsular rupture, external excrescences, and adherence to surrounding structures.
  • Fertility-sparing USO is performed in all reproductive-aged women diagnosed with malignant ovarian germ cell tumors, as this conservative approach in general does not adversely affect survival
    who has completed childbearing and would derive little benefit from retaining an ovary, hysterectomy with bilateral salpingo-oophorectomy (BSO) is appropriate
  • lymphadenectomy is most important for dysge.rminomas, whereas staging peritoneal and omental biopsies are particularly valuable for yolk sac tumors and immature teratomas
  • Cytoreductive surgery is recommended for advanced-stage nondysgenninomatous malignant ovaiian germ cell tumors if it can be accomplished with minimal residual disease (Ovarian dysgerminomas are so chemosensitive they do not generally require aggressive attempts at debulking)
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117
Q

Chemotherapy standard regimen for malignant germ cell ovarian tumors

A

The standard regimen is a 5-day course of bleomycin, etoposide, and cisplatin (BEP) given every 3 weeks (Gershenson, 1990; Williams, 1987). Modified 3-day BEP combinations also are safe and effective (Chen, 2014; Dimopoulos, 2004). Carboplatin and etoposide, given in three cycles, has shown promise as an alternative for selected patients (Williams, 2004). For women with incompletely resected disease, at least four courses ofBEP are usually recommended (Morgan, 2016).

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118
Q

the preferred treatment for recurrent ovarian germ cell tumors in women initially managed with surgery alone.

A

At least four courses of BEP chemotherapy, Patients who achieved a sustained clinical remission of greater than 6 months after completing BEP or another platinum-based chemotherapy regimen may be treated again with BEP. Because their tumors are generally more responsive, these “platinum-sensitive” patients have a much better prognosis.
However, women who do not achieve remission with BEP chemotherapy or relapse within a few months (fewer than 6) are considered “platinum-resistant,” and treatment options are limited. Chemorefractory cases with dysgerminoma or immature teratoma appear to have a better outcome than other subtypes, and surgical salvage aimed at achieving no residual disease may benefit some patients (Li, 2007). Other palliative options for this group include vincristine, dactinomycin, and cyclophosphamide (VAC) or paclitaxel (Morgan, 2016).

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119
Q

Mature cystic teratomas (dermoid cysts) make up —- of tumors resected during pregnancy

A

Mature cystic teratomas (dermoid cysts) make up one third of tumors resected during pregnancy

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120
Q

Management of germ cells tumor in pregnancy

A

Surgical staging as non pregnant
for patients with nondysgerminomatous tumors (mainly yolk sac tumors and immature teratomas) and those with incompletely resected disease, chemotherapy during pregnancy is strongly considered.

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121
Q

Age of population of sex cord stromal ovarian tumors

A

ovarian SCST s typically affect women of all ages. This range contains a unique bimodal distribution that reflects inherent tumor heterogeneity. For example, juvenile granulosa cell tumors, Sertoli-Leydig cell tumors, and sclerosing stromal tumors are found predominantly in prepubertal girls and women within the first three decades of life (Schneider, 2005). Adult granulosa cell tumors commonly develop in older women, at an average age in the mid-50s (van Meurs, 2013).

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122
Q

Genetic etiology behind SCST (sex cord stromal ovarian tumors)

A

The etiology of SCSTs is largely unknown. However, a single, recurrent FOXL2 gene mutation is present in vinually all adult-type granulosa cell tumors (Schrader, 2009; Shah, 2009). Also, women with a germline DICER1 mutation are predisposed to developing SCSTs (Heravi-Moussavi, 2012)

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123
Q

ovarian SCSTs develop in association with several defined hereditary disorders at a frequency that exceeds mere chance. These include

A

Ollier disease, which is characterized by multiple benign but disfiguring cartilaginous neoplasms, and Peutz-Jeghers syndrome, characterized by intestinal hamartomatous polyps (Stevens, 2005).

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124
Q

serum testosterone levels> ISO ng/dL or dehydroepiandrosterone sulfate (DHEAS) levels >8000 µg/L strongly suggest the possibility of

A

an androgen-secreting tumor

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125
Q

Modified WHO Classification of Ovarian Sex Cord-Stromal Tumors

A

*Pure stromal tumors: Fibroma/fibrosarcoma Thecoma Sclerosing stromal tumor Leydig cell tumor Steroid cell tumor
*Pure sex cord tumors: Granulosa cell tumor Adult type Juvenile type Sertoli cell tumor Sex cord tumor with annular tubules
*Mixed sex cord-stromal tumors: Sertoli-Leydig cell tumors Sex cord-stromal turners, NOS

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126
Q

Embryonic origin of granulosa and Sertoli cells

A

develop from the sex cords and thus from the the coelomic epithelium ( misoderm)

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127
Q

thoca cells, Lcydig cells, and 6broblasts are derived from .

A

the mesechyme

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128
Q

Seventy percent of ovar· ian SCSTs are

A

granulosa cell tumors

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129
Q

the most definitive treatment of endometrial hyperplasia

A

Hysterectomy

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130
Q

Management of Premenopausal women with nonatypical endometrial hyperplasia

A

a 3-to 6-month course of low-dose progestin therapy. Cyclic medroxyprogesterone acetate (MPA) (Provera) given orally for 12 to 14 days each month at a dose of 10 to 20 mg daily is commonly used. Continuous daily dosing with MPA 10 mg is suitable and may be more effective than cyclic administration in reversing hyperplastic changes. Another frequently used option is COC pills for those without contraindications. The levonorgestrel-releasing IUD also is effective (Gallos, 2010; 0rbo, 2014; Scarselli, 2011).

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131
Q

Managment of Postmenopausal women with nonatypical endometrial hyperplasia

A

low-dose oral cyclic MPA or a continuous 10-mg daily regimen, Importantly, in older women, providers should be confident that the sample obtained is adequate to exclude cytologic atypia. D & C may be indicated at times, especially if the tissue from Pipelle sampling is scant or if recurrent bleeding is noted. Affected postmenopausal patients who have a contraindication to progestin therapy or who cannot tolerate the therapy can be expectantly managed. Complex hyperplasia without atypia is usually treated chronically with progestins. Office endometrial biopsy is recommended every 3 to 6 months until lesion resolution is achieved.

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132
Q

In cases of endometrial hyperplasia without atypia, the risk of progression to endometrial cancer is

A

only 1 to 3 percent. The overall clinical and pathologic regression rates to progestin therapy range from 70 to 80 percent for nonatypical endometrial hyperplasia (Rattanachaiyanont, 2005; Reed, 2009).

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133
Q

Patients on progestins with persistent endometrial hyperplasia without atypia on repeated biopsy may be switched to

A

higher-dose regimen such as MPA 40 to 100 mg orally daily. Also, megestrol acetate (Megace), 160 mg daily or 80 mg twice daily, is suitable. It can be increased even up to 160 mg twice daily if no regression is initially achieved. Again, a clinician must confirm that hormonal ablation has occurred by resampling the endometrium after a suitable therapeutic interval, usually 3 to 6 months. Hysterectomy may also be considered for lesions that are refractory to medical management.

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134
Q

TLH Vs. LAVH

A

LAVH is preferred in patients with a mass involving the lower segment or a relatively large uterus. (A uterus >12 weeks gestation in size was the only factor considered for LAVH)

135
Q

the risk of progression to cancer over time with Atypical endometrial hyperplasia

A

approximates 29 percent.

136
Q

the preferred treatment for women with atypical endometrial hyperplasia

A

Hysterectomy

137
Q

Management Premenopausal women with Atypical endometrial hyperplasia who strongly wish to preserve fertil~ ity can be treated with progestins

A

High-dose progestin therapy, megestrol acetate 80 mg orally twice daily, is an option for motivated patients who will be compliant with surveillance (Randall, 1997). The IUD that releases 20 µg of intrauterine levonorgestrel daily (Mirena, Llletta) also is suitable (0rbo, 2014).

138
Q

How to check for Resolution of atypical endometrial hyperplasia in pt using hormonal ablation

A

must be confirmed by serial endometrial biopsies every 3 months until response is documented.

139
Q

ENDOMETRIAL CANCER TYPES

A
  • type I endometrioid adenocarcinomas constitute most cases. They are estrogen-dependent, low grade, and derived from atypical endometrial hyperplasia.
  • type II cancers are serous, carcinosarcoma, or clear cell histology; have no precursor lesion; and portend a more aggressive clinical course.
140
Q

routine screening of hyperplasia or endometrial cancer is not advocated. Instead, at the onset of menopause, women are counseled on the risks and symptoms of endometrial cancer and strongly encouraged to report unexpected bleeding or spotting to their provider. One screening exception is the woman with Lynch syndrome. Which is

A

For these individuals, EMB is recommended every 1 to 2 years beginning at age 30 to 35 years (American College of Obstetricians and Gynecologists, 2019a; Smith, 2019).

141
Q

Lynch Syndrome Genetic Screening Recommendations

A

Patients with endometrial or colorectal cancer and tumor evidence of:
Microsatellite instability or DNA mismatch repair protein loss
First-degree relative with endometrial or colorectal cancer who was diagnosed: Before age 60 years or Is at risk for Lynch syndrome based on personal and medical history First-or second-degree relative with a known DNA mismatch repair gene mutation

142
Q

Lynch syndrome screening is performed by

A

histochemistry staining of the tumor to search for the four most important Lynch syndrome proteins expressed by the mismatch repair (MMR) genes MLHl, MSH2, MSH6, and PMS2.For patients who have negative screening results but who are still suspected of having Lynch syndrome based on family history, further testing for microsatellite instability may be performed. The combination of intact protein expression and lack of microsatellite instability predicts a very low risk of Lynch syndrome.

143
Q

women with Lynch syndrome have such a high lifetime risk of developing endometrial cancer account to – to – %

A

(40 to 60 percent)

144
Q

Because women with Lynch syndrome have such a high lifetime risk of developing endometrial cancer (40 to 60 percent), what prophylactic step can be taken ?

A

prophylactic hysterectomy is recommended once affected women reach the early to mid 40s and have completed childbearing.
BSO also is performed due to the 9-to 12-percent lifetime risk of ovarian cancer. Prior to hysterectomy, colon cancer screening with colonoscopy should be up to date (American College of Obstetrician and Gynecologists, 2019a).

145
Q

Seventy percent of ovarian SCSTs are

A

granulosa cell tumors (the adult form, which comprises 95 percent of cases, and the juvenile type, accounting for 5 percent)

146
Q

In this tumor Cells are typically crowded and contain scant pale cytoplasm. Their elongated nuclei may have a longtudinal fold or groove that gives them a coffee bean appearance. Call-Exner bodies are ldentified by their rosette appearance.

A

Granulosa cell tumor

147
Q

Related to this oestrogen excess, coexisting pathology such as endometrial hyperplasia or adenocarcinoma has been found in – to – percent of patient with adult granulosa cell tumor

A

Related to this esttogen excess, coexisting pathology such as endometrial hyperplasia or adenocarcinoma has been found in 25 to 30 percent of patienu with adult granulosa cell tumor

148
Q

Adult granulosa cell tumors features are

A

low-grade malignancies that typically demonstrate indolent growth. Ninety-five percent arc unilateral, and 70 to 90 percent are stage I at diagnosis The 5-year survival for patients with stage I disease is 90 to 95 percent (Colombo, 2007; Zhang, 2007). However, 15 to 25 percent of stage I tumors will eventually relapse. The median time to recurrence is 5 to 6 years but may be several decades (Abu-Rustum, 2006; East, 2005)

149
Q

Poor prognostic factors of granulosa cell tumors are

A

advanced stage, large tumor size, and residual disease (Seagle, 2017). Patients with stage II-IV tumors have a 5-year survival we of 50 to 80 percent (Seagle, 2017). Cellular atypia and mitotic count may help in determining the prognosis but are difficult to reproducibly quantify (Miller, 2001).

150
Q

the fifth leading cause of cancer-related death

A

ovarian cancer

151
Q

Numerous reproductive, environmental, and genetic risk factors have been associated with ovarian cancer (Armstrong, 2019). The most important is

A

a family history of breast or ovarian cancer, and up to 25 percent of patients have an inherited genetic predisposition (American College of Obstetricians and Gynecologists, 2017a).

152
Q

patients without children have — the risk of developing ovarian cancer

A

patients without children have double the risk of developing ovarian cancer

153
Q

long-term combination oral contraceptive (COC) use reduces the risk of ovarian cancer by up to –%

A

50% . The duration of protection persists for more than 30 years after the last use (Collaborative Group on Epidemiological Studies of Ovarian Cancer, 2008). In contrast, hormone replacement therapy after menopause carries an elevated associated risk (Lee, 2016).

154
Q

By how many fold is A family history of ovarian cancer in a first-degree relative, that is, a mother, daughter, or sister, increased a woman’s lifetime risk.

A

triple

155
Q

Women Who Should Undergo Genetic Testing

A

Epithelial ovarian cancer at any age
Breast cancer diagnosed at age 45 or younger
Breast cancer with two distinct and sequential primaries, first one diagnosed at age 50 or younger
Breast cancer that is triple-negative and diagnosed at age 60 or younger
Breast cancer at any age, with at least one close relative diagnosed at age 50 or younger
Breast cancer diagnosed at any age, with two or more close relatives with breast cancer; one close relative with epithelial ovarian cancer; or two close relatives with pancreatic cancer or aggressive prostate cancer
Breast cancer, with a close male relative with breast cancer at any age
Breast cancer and Ashkenazi Jewish ancestry Individuals from a family with a known deleterious mutation

156
Q

In Cowden syndrome which gene is mutated ? and what cancers that increase risk to ? What prophylactic measures can be offered ?

A

Mutated gene is PTEN , increase risk of breast, uterus , thyroid, renal, colorectal cancers
To Discuss hysterectomy after childbearing

157
Q

Age of prophylactic BSO

A

prophylactic BSO should be offered to BRCAl carriers at age 35 to 40 years. For BRCA.2 carriers, BSO is recommended between 40 and 45, and at age 45 to 50 years for other HR deficiency (BRIP 1, RAD 51 CJ carriers (American College of obstetricians and Gynecologists, 2017a).

158
Q

prophylactic BSO is approximately —percent effective in preventing epithelial ovarian cancer

A

90%

159
Q

Prophylactic BSO also reduces the risk of developing breast cancer by – percent (Rebbeck, 2002).

A

Prophylactic BSO also reduces the risk of developing breast cancer by 50 percent (Rebbeck, 2002).

160
Q

prophylactic BSO In women with HNPCC, the ovarian cancer risk reduction approaches – percent

A

100%

161
Q

Histologically, LMP tumors are distinguished from benign cysts by having at least two of the following features:

A

nuclear atypia, epithelial stratification, microscopic papillary projections, cellular pleomorphism, or mitotic activity

162
Q

Unlike invasive carcinomas, Low Malignant Potential tumors lack

A

stromal invasion. However, up to 10 percent of LMP turners will exhibit areas of microinvasion, defined as foci measuring <3 mm in diameter and forming <5 percent of the tumor

163
Q

The prognosis is excellent for patients with ovarian LMP tumors. Five-year survival rates range from %

A

96 to 99 percent for stages I-III, whereas it reaches 77 percent for stage IV disease (Trimble, 2002). Overall, more than 80 percent have stage I disease. Fertility-sparing surgery is associated with up to a 15-pcrcent risk of rdapsc, usually in the contralatcral ovary, but remains highly curable by rcoperation and resection. (Park, 2009; Rao, 2005).

164
Q

What are the endometriosis–associated rumors ?

A

Endometrioid
Clear cell
Seromucinous

165
Q

The serum CA125 level is integral to epithelial ovarian cancer management. In 90 percent of women presenting with malignant nonmucinous tumors. CA125 Ievels are elevated.

A

to bear in mind during adnexal mass evaluation. Half of stage I ovarian cancers will have a normal CA125 measurement (false negative). Also. an elevated value (false positive) may be associated with various common benign indications such as pelvic inflammatory disease, endometriosis, leiomyoma, pregnancy. and even menstruation. Thus. in postmenopausal women with a pelvic mass. a CA125 measurement may better predict a higher likdihood of malignancy

166
Q

World Health Organization Histological Classification of Ovarian Carcinoma

A

Serous adenocarcinoma
Mucinous adenocarcinoma
Endometrioid adenocarcinoma
Clear cell adenocarcinoma
Malignant Brenner tumor
Mixed epithelial and mesenchymal:( Adenocarcinoma Carcinosarcoma )
Squamous cell carcinoma
Mixed carcinoma
Undifferentiated carcinoma
Small cell carcinoma

167
Q

During frozen section analysis, ———– are essentially pathognomonic of an ovarian-type serous carcinoma.

A

During frozen section analysis, psammoma bodies are essentially pathognomonic of an ovarian-type serous carcinoma.

168
Q

Mucinous adenocarcinomas compose – to – percent of true epithelial ovarian cancers.

A

Mucinous adenocarcinomas compose 5 to 10 percent of true epithelial ovarian cancers.

169
Q

Clear Cell Adenocarcinoma Comprising – to – percent of epithelial ovarian cancers

A

Clear Cell Adenocarcinoma Comprising 5 to 10 percent of epithelial ovarian cancers

170
Q

———- adenocarcinomas are most frequently associated with pelvic endometriosis.

A

clear cell adenocarcinomas are most frequently associated with pelvic end.ometriosis.

171
Q

Microscopically, both clear and “hobnail” cells are characteristic to

A

Clear cell carcinoma

172
Q

Transitional cell carcinoma accounts for fewer than – percent of ovarian cancers.

A

Transitional cell carcinoma accounts for fewer than 5 percent of ovarian cancers.

173
Q

Transitional cell carcinoma prognosis

A

Microscopically, these tumors resemble a primary bladder carcinoma, often with squamous differentiation, but have an immunoreactive pattem consistent with. an ovarian origin (Lee, 2003). Thus, transitional cell carcinoma is considered a high-grade form of serous carcinoma but carries a better prognosis (Guseh, 2014). The rare malignant Brmnn tumor characteristically lw transitional cell carcinoma coupled with foci of benign or borderline Brenner features. 1b.e&e twnors classically have a dense, abundant fibrous stroma with. embedded nests of transitional epith.dium. They carry a better prognosis than pwe transitional cell carcinomas.

174
Q

Small cell carcinoma prognosis

A

rare, extremely malignant,Recent data suggest these highly lethal tumors arise via a specific muta· tion in the SMARCA4 gene Odinic, 2014).In general, patients with small cell carcinoma die within 2 years from rapid disease progression.

175
Q

Small cell carcinoma types

A
  • hyperkalcemic type, which typically develops in young women. Nearly all tumors arc unilateral, and two thirds are associated with elevated serum caJ. cium levels that resolve postoperatively (Young, 1994).
  • The pulmonary type resembles oat cell carcinoma of the lung and develops in older women. Half of these women have bilateral ovarian disease (Eichhorn, 1992).
176
Q

Small cell carcinoma types

A
  • hyperkalcemic type, which typically develops in young women. Nearly all tumors arc unilateral, and two thirds are associated with elevated serum caJ. cium levels that resolve postoperatively (Young, 1994).
  • The pulmonary type resembles oat cell carcinoma of the lung and develops in older women. Half of these women have bilateral ovarian disease (Eichhorn, 1992).
177
Q

Up to – percent of”typical” epithelial ovarian cancers are actually primary peritoneal carcinomas that develop de novo from the lining of the pelvis and abdomen.

A

Up to 15 percent of”typical” epithelial ovarian cancers are actually primary peritoneal carcinomas that develop de novo from the lining of the pelvis and abdomen.

178
Q

Criteria for Diagnosing Primary Peritoneal Carcinoma When Ovaries Are Present

A
  • Both ovaries must be normal in size or enlarged by a benign process
  • The involvement in the extraovarian sites must be greater than the involvement on the surface of either ovary - The ovarian tumor involvement must be either nonexistent, confined to the ovarian surface epithelium without stromal invasion, or involving the cortical stroma with tumor size less than 5 x 5 mm.
    لكن ولله الحمد
    In general, the stag· ing, treauncnt, and prognosis of primary peritoneal carcinoma are the same as for epithelial ovarian cancc:r (Mok, 2003). The differential diagnosis mainly includes malignant mesothelioma. :)
179
Q

metastatic mucinous/signet ring cell adenocarcinoma

A

Krukenburge tumor Malignant rumors that metastasize to the ovary are almost invariably bilateral that typically originates from primary tumors of the intestinal tract, characteristically the stomach. Ovarian metastases often represent a late disseminated stage of the disease in which other hematogenous metastases also are found (Prat, 2003).

180
Q

Management of Early-Stage epithelial Ovarian Cancer

A
  • Surgical Staging
  • Fertility-Sparing Management if disease appears confined to one ovary. Although many patients will be “up-staged” as a result of the operative findings, those with surgical stage I disease have an excellent long-term survival following unilateral adnexectomy (Armstrong, 2019).
  • Postsurgical Management In women with stage lA or IB, grade 1 or 2 epithelial ovarian carcinoma, observation without further treatment following surgery is appropriate (Armstrong, 2019).
181
Q

Post surgical management of epithelial ovarian cancer

A

Postsurgical Management In women with stage lA or IB, grade 1 or 2 epithelial ovarian carcinoma, observation without further treatment following surgery is appropriate (Armstrong, 2019). However, one third of patients who appear to have disease confined to the ovary will be up-staged by surgical staging and require postoperative chemotherapy. Women with stage lA or IB, grade 3 epithelial ovarian cancer and all stage IC and II tumors are treated with platinum-based chemotherapy (Armstrong, 2019). In a Phase III Gynecologic Oncology Group (GOG) trial (protocol #157), women with earlystage disease were randomly assigned to either three or six cycles of carboplatin (Paraplatin) and paclitaxel (T axol). Overall, three cycles resulted in a relapse rate comparable to that fur six cycles but caused less toxicity (Bell, 2006). However, in a subanalysis of patients in this study who had serous tumors, treatment with six cycles decreased the relapse risk (Chan, 2010a). Despite chemotherapy, more than 20 percent of women with early-stage disease develop recurrences within 5 years.

182
Q

Surveillance after complete treatment of early stage ovarian cancer

A

After treatment completion, women with early-stage ovarian cancer may be followed every 2 to 4 months for the first 2 years, twice yearly fur an additional 3 years, and then annually. At each visit, complete physical and pelvic examinations are performed. In addition, a serum CA125 level may be indicated if it was initially elevated (Armstrong, 2019). However, one multi-institutional trial evaluated the utility of CA125 levels for ovarian cancer monitoring after primary therapy completion. Women with relapsed ovarian cancer did not live longer by starting chemotherapy earlier based on a rising CA125 level compared with delaying treatment until symptoms developed. The group monitored with CA125 tests received 5 more months of chemotherapy overall, whereas women who were diagnosed and treated later for clinically evident recurrence had higher quality-of-life measures (Rustin, 2010). Whether suspected by examination, CA125 level elevation, or new symptoms, recurrent disease must be confirmed with the aid of imaging. Of modalities, CT is initially most helpful to identify intraperitoneal disease.

183
Q

Candidates of neoadjuvant chemotherapy

A

unresectable disease. Other patients may be too medically compromised, may not have received initial care by a gynecologic oncologist, or may have large-volume “suboptimal” residual disease despite attempted debulking. In such circumstances, three to four courses of chemotherapy are used to shrink disease before attempting an “interval” cytoreductive surgery.

184
Q

Adjuvant chemotherapy used for epithelial ovarian ca

A

the most widely used intravenous (IV) regimen in the United States is six courses of carboplatin and paclitaxel. If additional cycles are required to achieve clinical remission, this suggests relative tumor chemoresistance and usually leads to an earlier relapse. In Europe, single-agent carboplatin often is used. This preference is based on two large Phase III trials of the International Collaborative Ovarian Neoplasm (ICON) Group

185
Q

maintenance chemotherapy in Management of Patients in Remission stage of advanced ovarian cancer

A
  • monthly paclitaxel was disappointing and caused significant neuropathy(Markman, 2003, 2009). In a later Phase III trial of 1157 patients, neither lower-dose paclitaxd nor CT-2103 (paclitaxd poliglumex) reduced the death rate compared with no maintenance therapy.
    -Bevacizumab, an antiangiogenic agent, also has been studied as maintenance therapy in several Phase III trials. In GOG protocol #218 and the Gynecologic InterGroup Trial (ICON7) studies noted earlier (p. 749), bevacizumab was combined with paclitaxel and carboplatin and then continued alone for a year of maintenance therapy. This regimen demonstrated only a 2-to 4-month prolongation of progression-free survival and no overall survival benefit (Tewari, 2019)
  • Pazopanib, an oral multikinase inhibitor of the vascular endothelial growth factor (VEGF} receptor, also shows some promise as maintenance therapy. In a Phase III trial, patients receiving pazopanib had a 5.6-month improvement in progression-free survival compared with placebo. Still, it was associated with significant toxicity and lack of overall survival benefit (duBois, 2014).
186
Q

The overall 5-year survival rate of all stages of epithelial ovarian cancer approximates — percent, uterine __ percent , cervical cancer (__ percent).

A

The overall 5-year survival rate of all stages of epithelial ovarian cancer approximates 45 percent, far lower than uterine (84 percent} or cervical cancer (73 percent).

187
Q

Most Important Favorable Prognostic Factors for Ovarian Cancer

A

No ascites
Younger age
Early-stage disease
Well-differentiated tumor
Otherwise good health status
Histologic type other than mucinous or clear cell
Small disease Volume prior to surgical debulking
Small residual tumor following primary cytoreductive surgery

188
Q

Management of Recurrent Ovarian Cancer

A

Tamoxifen may be administered when only “biochemical” evidence - means elevation in CA-125 only- indicates disease progression. It has some activity in ueating recurrent disease, and its toxicity is minimal (Hurteau, 2010).

189
Q

usually the first sign of ovarian cancer relapse

A

Gradual elevation of the CA125 level

190
Q

Management of Those who relapse within 6 months of completing chemotherapy have “platinum-resistant” ovarian cancer

A

should be encouraged whenever possible, response rates typically range from 5 to 15 percent using nonplatinum FDA-approved conventional cytotoxic drugs such as paclitaxel, pegylated liposomal doxorubicin (Doxil), docetaxel (Taxotere), topotecan (Hycamtin), or gemcitabine (Gemzar). Recendy, bevacizumab in combination with weekly paclitaxel, doxorubicin, or topotecan was shown to provide a 27-percent response rate. This was more than double the rate with single-agent chemotherapy alone in patients with platinum-resistant disease (Pujade-Lauraine, 2014).

191
Q

the best candidates for secondary cytoreductive surgery have:

A

(1) platinum-sensitive disease,
(2) a prior long disease-free interval,
(3) a solitary-site recurrence, and
(4) no ascites (Chi, 2006; Armstrong, 2019).

192
Q

Patients with a germline BRCAI or BRCA2 gene mutation who develop resistance to platinum may benefit from

A

targeted therapy with olaparib, niraparib (Zejula), or rucaparib (Rubraca). All three PARP inhibitors are now FDA-approved for this indication

193
Q

Worldwide, cervical cancer is common, and it ranks —- among all malignancies for women

A

Fourth (World Health Organization, 2019).

194
Q

Causes of cervical cancer

A
  • HPV: 99.7 percent of cervical cancers are associated with an oncogenic HPV subtype (W alboomers, 1999).
  • herpes simplex virus 2, may play a concurrent causative role.
195
Q

– percent of invasive cervical cancer cases were attributable to HPV serotype 16.
Serotype 18 was associated with – percent of invasive disease cases ( Guan, 2012).

A

63 percent of invasive cervical cancer cases were attributable to HPV serotype 16. Serotype 18 was associated with 16 percent of invasive disease cases ( Guan, 2012).

196
Q

HPV 16 is more commonly associated with —— carcinoma of the cervix, whereas HPV 18 is a risk factor for —– carcinoma (Bulk, 2006).

A

HPV 16 is more commonly associated with squamous cdl carcinoma of the cervix, whereas HPV 18 is a risk factor for cervical adenocarcinoma (Bulk, 2006).

197
Q

Among HPV-infected women, current and former smokers have a —to —fold greater incidence of highgrade squamous intraepithdiallesion (HSIL) or invasive cancer.

A

Among HPV-infected women, current and former smokers have a two-to threefold greater incidence of highgrade squamous intraepithdiallesion (HSIL) or invasive cancer.

198
Q

women with seven prior full-term pregnancies have an approximately —fold risk of having HPV and cervical cancer, and those with one or two have a –fold risk compared with nulliparas (Munoz, 2002)

A

women with seven prior full-term pregnancies have an approximately fourfold risk, and those with one or two have a twofold risk compared with nulliparas (Munoz, 2002)

199
Q

COCP and cervical cancer

A

Long-term combination oral contraceptive (COC) use is another factor. In women who are positive for cervical HPV DNA and who use COCs, cervical carcinoma rates rise by up to fourfold compared with women who are HPV -positive and never users (Moreno, 2002). Additionally, current COC users and women who are within 9 years of use have a significandy higher risk of developing both squamous cell and adenocarcinoma of the cervix (International Collaboration of Epidemiological Studies of Cervical Cancer, 2006). Encouragingly, the relative risk to COC users appears to decline after cessation. Data from 24 epidemiologic studies showed that by 10 or more years following COC cessation, cervical cancer risk returns to that of never users (International Collaboration of Epidemiological Studies of Cervical Cancer, 2007).

200
Q

cervical lymphatic drainage

A

From the parametrial and paracervical nodes, lymph subsequently flows into the obturator lymph nodes and into the internal, external, common iliac lymph nodes, and ultimately the paraaortic lymph nodes. Accordingly, pelvic and paraaortic lymph nodes are also traditionally removed concurrently with radical hysterectomy. In contrast, lymphatic channels from the posterior cervix course through the rectal pillars and the uterosacral ligaments to the rectal lymph nodes. These nodes also are encountered and are removed during the extended resection of the uterosacral ligaments that is characteristic of radical hysterectomy.

201
Q

Management of woman presents with uncontrolled hemorrhage from cervical tumor bed (spontaneously or after punch biopsy)

A

bleeding can often be controlled with a combination of Monsel paste (ferric subsulfate) and vaginal packing. Topical acetone can also be used to obtain hemostasis, especially in cases refractory to Monsel paste (Patsner, 1993). Burning from acetone makes it a less desirable choice than Monsel paste. With vaginal packing, the patient ideally remains at bed rest, and a Foley catheter is concurrently inserted to drain the bladder. The pack may interfere with normal voiding, and the catheter also allows for accurate monitoring of urine output during volume resuscitation. If bleeding continues, emergent radiation can be delivered. Alternatively, internal iliac artery embolization or ligation can be performed in cases of refractory hemorrhage. However, caution is used for these latter two options, as tumor oxygenation is impaired if the blood supply is occluded. Radiation therapy is a primary component of advanced-stage cancer, radiation’s effects are diminished in low-oxygen environments. This can translate into worsening diseasespecific survival rates (Kapp, 2005). In those with significant bleeding, hemodynamic support of the patient

202
Q

cervical cancer may mirror the appearance of ( ddx of cervical ca)

A

cervical leiomyoma, cervical polyp, vaginitis, cervical eversion, cervicitis, threatened abortion, placenta previa, cervical pregnancy, condyloma acuminata, herpetic ulcer, chancre, or a prolapsing uterine leiomyoma, polyp, or sarcoma.

203
Q

Pap testing has a sensitivity for detecting high-grade lesions on any given single test about – to – %

A

53-to 80-percent
( thus, the preventive power of Pap testing lies in regular serial screening ) >_*
يعني أذا ما ضبطت هالمرة يمكن تضبط الجاية

204
Q

What is the sensitivity of pap smear in women who have stage I cervical cancer of single cytologic smears obtained are read as positive for cancer?

A

only 30 to 50 percent
Hence, Pap testing alone for evaluation of a suspicious lesion is discouraged. Instead, these lesions arc directly biopsied with TUchler biopsy forceps or a Kevorkian

205
Q

What is the FDG-PET ?

A

a radiolabeled analogue of glucose, fluorodeoxyglucose (FDG), is injected intravenously and is taken up by metabolically active cells such as rumor cells in PET scan.
Important note: PET is insensitive for lymphatic metastasis <5 mm. Moreover, its role in early-stage smaller, resectable rumors is limited (Sironi, 2006; Wright, 2005)

206
Q

Cervical Cancer Survival Rates According to Stage Stage 5-Year Survival

A

lA 100%
IB 88%
IIA 68%
lIB 44%
Ill 18-39%
IVA 18-34%

207
Q

EARLY-STAGE PRIMARY DISEASE TREATMENT of Stage lA ( microinvasive cervical cancer )< invasion depth to <5 mm

A

Stage IA1 These microinvasive tumors invade <3 mm and are associated with low risk of spread into the parametrial or uterosacral nodes, these lesions may be effectively treated with cervical conization alone.
However, a total extrafascial hysterectomy (type I hysterectomy) is preferred for women who have completed childbearing.

208
Q

Squamous cervical cancers with stromal invasion < 1 mm have a – percent risk of nodal metastasis, and those with 1 to 3 mm of stromal invasion carry a –percent risk.

A

1% , 1.5 %

209
Q

In stage IAI microinvasive cancers, the presence of LVSI increases the risk of lymph node metastasis and cancer recurrence to approximately – percent. Suggested treatment ?

A

In stage IAI microinvasive cancers, the presence of LVSI increases the risk of lymph node metastasis and cancer recurrence to approximately 5 percent. these cases are managed with modified radical hysterectomy (type II hysterectomy) and pelvic lymphadenectomy. Radical trachelectomy with pelvic lymph node dissection can be considered in those patients desiring fertility preservation (Olawaiye, 2009).

210
Q

General Treatment for Primary Invasive Cervical Carcinoma for stage IA2 (These microinvasive cervical lesions have stromal invasion that measures 2=3 mm to <5 mm. These cancers have a 7-percent risk of lymph node metastasis and carry a >4-percent risk of disease recurrence)

A

Radical hysterectomy+ PLND (consider SNLB) or Radical trachelectomy+ PLND (consider SNLB) for selected patients desiring fertility

211
Q

patient may be considered for pelvic exenteration if the triad of (1)(2)(3) is absent

A

(1) lower extremity edema,
(2) back pain,
(3) hydronephrosis
If present, these suggest disease extension to the pelvic sidewalls, which would contraindicate surgery.
In addition, regional and distant metastasis should be excluded by both physical c:xamination and radiologic imaging, which typically is a PET /CT scan.

212
Q

What is the most common type of Borderline tumor

A

Serous 50%
Mucinous 30%

213
Q

Factors associated with para-aortic lymph node dissemination include

A

advanced stage, high histological grade, deep myometrial invasion, cervical involvement, lymphovascular space involvement, and the presence of pelvic lymph node metastases.

214
Q

Mode of delivery of pregnant lady with micro invasive squamous cell cervical carcinoma found during conization that measures <3 mm and contains no LVSI (stage IAl)

A

may deliver vaginally and be reevaluated 6 weeks postpartum. Moreover, for those with stage IA or IB disease, studies find no greater maternal risk if treatment is intentionally ddayed to optimize fetal maturity regardless of the trimester in which the cancer was diagnosed. Given the outcomes, a planned treatment dday is generally acceptable for women who are 20 or more weeks’ gestational age at diagnosis with stage I disease and who desire to continue their pregnancy.

215
Q

Risks factors of vulvar cancer

A

Women who are infected with human papi/Jomatlirus (HPV) have a greater risk of vulvar cancer. Specifically, 50 to 75 percent of invasive vulvar cancers are associated with highrisk HPV serotypes (Gargano, 2012). Strong correlations also can be seen between high-risk HPV infection and preinvasive TABLE 31-1. Vulvar Cancer Histologic Subtypes Vulvar c:ardnomas Squamous cell carcinoma Adenocarcinoma Carcinoma of Bartholin gland Adenocarcinoma Squamous carcinoma Transitional cell Vulva Paget disease Merkel cell tumors Verrucous carcinoma Basal cell carcinoma Vulvar malignant melanoma Vulvar sarcoma Leiomyosarcoma Malignant fibrous histiocytoma Epithelial sarcoma Malignant rhabdoid tumor Metastatic cancers to vulva Yolk sac tumors lesions of the vulva (Gargano, 2012). HPV becomes a stronger contributor when combined with other cofactor& such as smoking or herpes simplex virus (HSV) infection (Madele.ine, 1997). Women who have smoked and have a history ofHPV genital warts have a 35-rold greater risk fOr developing vulvar cancer compared with women without these predispositions (Brinton, 1990; Kirschner, 1995).

216
Q

VIN is categorized as

A

1) Usual type VIN is associated with highrisk HPV infection and develops usually in young women.
2) the differentiated type VIN occurs in postmenopausal women with chronic skin conditions such as lichen sclerosis (Reyes, 20 14). Of these two, differentiated type VIN has a significantly stronger association with squamous cell carcinoma compared with usual type VIN (Eva, 2009).

217
Q

The nonavalent vaccine (Gardasil 9) is effective against which HPV sero-types

A

high-risk HPV scrotypes 16 and 18 (Huh, 2017).

218
Q

Overall survival rates of women with squamous cell carcinoma of the vulva are relarivdy good and approximate

A

65 percent (Razzagh.i, 2018).

219
Q

SEER (2018) data from 2008 to 2014 show that anticipated a 5-year survival rate for :
- local disease (stage I and II)
- higher stages are poorer, can be expected for regional (stage III and IV A) disease
- for stage IVB.

A
  • rate 86 percent for local disease (stage I and II)
  • rate of 54 percent for stage III and IV A
  • rate of 16 percent for stage IVB.
220
Q

Apart from FIGO stage. other important prognostic factors of vulvar cancers(any any cancer) include

A

lymph node metastasis, lesion size, depth of invasion, resected-margin status, and lymphatic vascular space involvement.

221
Q

Depth of tumor invasion is another prognostic element of vulvar cancer This depth is measured from

A

from the epidermis basement membrane to the deepest point of invasion into the dermis and subcutaneous layer (Kurman, 2014). Tumors with a depth of invasion < 1 mm carry little or no risk of inguinal lymph node metastasis. However, depth of invasion positively correlates with increased nodal metastasis.

222
Q

the single most important vulvar cancer predictor

A

Lymph node metastasis, since inguinal node mewtasis reduces long-term sutvival rates by 50 percent (Farlas.-Eisner, 1994

223
Q

In vulvar cancer Surgical margins that are tumor-free lower local tumor recurrence rates. Thus, at a minimum

A

a 2-cm tumor-free margin is desired. More specifically, two large retrospective series demonstrated that a tumor-free surgical margin > or = 8 mm at final pathologic analysis yielded a high rate of local controL In contrast, if tumor was found within this 8-mm margin, the recurrence rate was 23 to 48 percent (Chan, 2007; Heaps, 1990)

224
Q

lnguinofemoral Lymphadenectomy is recommended for all vulvar squamous carcinomas that ( who are the candidates?)

A

invade deeper than 1 mm on initial biopsy or that have a tumor diameter > 2 cm regardless of invasion depth (stages IB- IV A). To maximize metastatic disease detection and staging accuracy, surgical evaluation of the inguinal nodes is recommended.

225
Q

One trial by the GOG reported the sensitivity of selective lymph node biopsy (SLNB) exceeded – percent, and the false negative predictive value was – percent for tumors measuring < 4 cm in diameter (Frurnovitz, 2005).

A

exceeded 90 percent, and the false negative predictive value was 2 percent for tumors measuring < 4 cm in diameter (Frurnovitz, 2005).

226
Q

In stage IV poorly resectable,. locally advanced vulvar cancers can be effectively treated with

A

neoadjuvant chemoradiation to minimize the surgical resection required. Two GOG studies GOG have demonstrated the feasibility of this approach using cisplatin regimens (Moore,. 1998, 2012).

227
Q

SURVEILLANCE After completing primary treatment of vulvar cancer

A

all patients receive thorough physical examination that includes inguinal lymph node palpation and pelvic examination every 3 months for the first 2 to 3 years. Surveillance examinations are then scheduled every 6 months to complete a total of 5 years. Thereafter, disease-free women may be seen annually (Salani, 20 17). Biopsies are performed if concerning areas are noted. Radiologic imaging and targeted biopsies to diagnose possible tumor recurrence are completed as indicated.

228
Q

VERRUCOUS CARCINOMA rare variant of vulvar squamous cell carcinoma treatment

A

Surgery is preferred, and most tumors are excised by wide local excision that ensures a 1-cm surrounding margin. Inadequate margins risk local recurrence. Verrucous carcinomas are resistant to radiotherapy and if exposed may undergo anaplastic transformation to become more aggressive and invasive. Enlarged groin lymph nodes are evaluated preoperatively by FNA because they usually are inflammatory.

229
Q

Ddx of vulvar melanoma

A

Benign conditions like lentigo simplex, vulvar melanosis, acanthosis nigricans, seborrheic keratosis, and nevi.
And malignant lesions like pigmented vulvar neoplasia may be VIN, squamous cell carcinoma, or Paget disease.

230
Q

Treatment of melanoma

A

Vulvar melanoma has limited response to both chemotherapy and radiotherapy. Thus, excision is the single best definitive therapy (Conservative surgery, such as wide local acis.ion or a radical partial wlvectomy).

231
Q

for treatment of metastatic or unresectable melanoma

A
  • Vemurafenib (Zelboraf), a BRAF inhibitor, was approved by the Food and Drug Administration (FDA} for that exhibits the BRAF mutation (Robert, 2011).
  • Imatinib (Gleevec) may be used for tumors with the c-KIT mutation.
232
Q

Primary malignant tumors arising from the Bartholin gland can be

A

adenocarcinomas, squamous cell carcinomas, or transitional cell carcinomas.

233
Q

growth fraction

A

The speed with which tumors grow and double in size is largely regulated by the number of cells that are actively dividing

234
Q

Adjuvant chemotherapy

A

is given to destroy remaining microscopic cells that may be present after the primary tumor is removed by surgery.

235
Q

Neoadjuvant chemotherapy

A

refers to drug treatment directed at an advanced cancer to decrease preoperatively the extent or morbidity of a subsequent surgical resection.

236
Q

Consolidation (or maintenance) chemotherapy

A

is given after cancer has disappeared following the initial therapy and ainu to prolong the duration of clinical remission or to prevent ultimate relapse.

237
Q

salvage (or palliative) chemotherapy

A

Therapy applied to recurrent disease or to a tumor that is refractory to initial treatment.

238
Q

Gemcitabine MOA, uses and side effects

A

antimetabolite is FDA approved to be used with other agents for treannent of recurrent ovarian cancer but is also commonly used for uterine sarcoma, Myelosuppression, especially neutropenia. is the main dose-limiting side effect. Gastrointestinal (GI) toxicity, such as nausea. vomiting. diarrhea, or mucositis, also is common.
Approximately 20 percent of patients will develop a flulike syndrome, including fever, malaise, headache, and chills. Pulmonary toxicity is infrequent. but reported.

239
Q

Ifosfamide uses, side effects

A

Recurrent ovarian CA, cervical CA, CNS and uterine sarcoma(not FDA approved)

BMD, cystitis, N&V ,alopecia, and renal toxicity, its metabolic activation occurs more slowly and leads to a greater production of chloracetaldehyde, a possible neurotoxin. neurotoxicity, manifested as lethargy, confusion, seizure, ataxia, hallucinations, and occasionally coma, is more likely.

240
Q

Cyclophosphamide uses, MOA, side effects

A

Cyclophosphamide is the “C” of EMACO in GTN, used as salvage therapy for recurrent epithelial ovarian cancer.
It’s alkylating agents is characterized by positively charged alkyl groups that bind to negatively charged DNA to form adducts. Binding leads to DNA breaks or cross-links and a halt to DNA synthesis. In general, these drugs are cell cycle-nonspecific agents.
Myelosuppression, mainly neutropenia, is the usual doselimiting side effect. One of its metabolites, acrolein, can alkylate and inflame the bladder mucosa. As a result, hemorrhagic Cystitis is a classic complication that may follow from 24 hours to several weeks after administration. To prevent this effect, adequate hydration is imperative to aid acrolein excretion. In addition, Gl toxicity, such as nausea, vomiting, or anorexia, is common. Alopecia. secondary malignancy rates are increased, particularly acute myelogenous leukemia and bladder cancer. ovarian function damage. Preventatively, adjuvant gonadotropin-releasing hormone (GnRH) agonists may lower rates of chemotherapy-induced ovarian failure (controversial) ovarian tissue cryopreservation make it likely that the removal of oocytes prior to treatment will become the preferred approach when feasible

241
Q

Dactinomycin uses, MOA, excretion,side effects

A

antitumor antibiotic FDA approved to treat GTN as a single agent or as part of combination chemotherapy, Dactinomycin (Cosmegen), also known as actinomycin D, is the “A” of the EMA-CO chemotherapy combination.
Dactinomycin becomes anchored into purine-pyrimidine DNA base pairs, resulting in DNA synthesis inhibition. It also produces toxic oxygen free radicals that cause DNA breaks.
excreted mainly through the biliary system.
Myelosuppression is the main dose-limiting side effect and may be severe.GI toxicity, including nausea, vomiting, mucositis, and diarrhea, Alopecia, potent vesicant.

242
Q

Bleomycin uses, MOA, side effects

A

antitumor antibiotic FDA approved for malignant pleural effusion treatment or for palliative therapy of recurrent squamous cervical or vulvar cancer. An off-label use includes bleomycin as the “B” in BEP (bleomycin, Etoposide, cisplatin) regimens, which are used as adjuvant treatment of malignant ovarian germ cell or sex cord-stromal tumors.used in GlN salvage treatment.
Bleomycin (Blenoxane), when complexed with iron, creates activated oxygen free radicals, which cause DNA strand breaks and cell death. It is maximally effective during the G2 phase. Pulmonary toxicity is the main dose-limiting side effect, not myelosuppressive. However, skin reactions are common and include hyperpigmentation or erythema.

243
Q

the main dose-limiting side effect of bleomycin is Pulmonary toxicity, by how much percentage ? And how to monitor/dx it ?

A

developing in 10 percent of patients and causing death in 1 percent. Accordingly, for women prescribed bleomycin, chest radiographs and pulmonary function tests (PFTs) are performed at baseline and obtained regularly before every one or two treatment cycles. The most important PFT measurement is the diffusing capacity of the lung for carbon monoxide (DLCO). The DLCO measures the ability to transfer oxygen from the lungs to the blood stream. If the DLCO declines by 15 to 30 percent, it indicates development of restrictive lung disease. Fibrosis often presents clinically as pneumonitis with cough, dyspnea, dry inspiratory crackles, and infiltrates on chest radiograph.

244
Q

Doxorubicin uses, MOA, metabolism and excretion, side effects

A

antitumor antibiotic is FDA approved to treat epithelial ovarian cancer, but doxorubicin (Adriarnycin) is more frequently used for uterine sarcoma.
This agent intercalates into DNA to inhibit DNA synthesis, inhibits topoisomerase II, and forms cytotoxic oxygen free radicals. The drug is metabolized extensively in the liver and eliminated through biliary excretion.
Myelosuppression, particularly neutropenia, is the main dose-limiting side effect. However, cardiatoxicity is a classic complication. irreversible dilated cardiomyopathy associated with congestive heart failure. Gastrointestinal toxicities are generally mild, but alopecia is universal.

245
Q

cardiatoxicity is a classic complication of treatment with doxorubicin, how to monitor?

A

Patients are monitored with a multiple-gated acquisition (MUGA) radionuclide scan at baseline and periodically during therapy. The risk of cardiotoxicity is higher in women older than 70 and those with cumulative doses exceeding 550 mg/m2.

246
Q

Doxorubicin Liposome uses , MOA, side effects

A

antitumor antibiotic is FDA approved and commonly used for the salvage treatment of recurrent epithelial ovarian cancer. The liposomal encapsulation of doxorubicin (Doxil) dramatically alters the pharmacokinetic and toxicity profiles of the drug. Researchers developed liposomal doxorubicin to reduce cardiotoxicity and to selectively target tumor tissues. contrast to doxorubicin, administration of the encapsulated liposome is associated with minimal nausea, vomiting, alopecia, Infusion-related reactions develop in less than 10 percent of patients and are most common during the first treatment course. However, an increased rate of stomatitis and palmar-plantar erythrodysesthesia (PPE) is noted.

247
Q

palmar-plantar erythrodysesthesia (PPE) is characterized by

A

Patients may initially complain of tingling sensations on their soles and palms that generally progress to swelling and tenderness to touch. Erythematous plaques typically develop that can become extremely painful and often lead to desquamation and skin cracking. Symptoms result from the prolonged blood levels of cytotoxic agent and may last several weeks.

248
Q

Vinca Alkaloids (Vincristine, vinblastine, and vinorelbine) uses, MOA, side effects

A

are cell cycle-specific in the M phase. These compounds inhibit normal microtubular polymerization by binding to the tubulin subunit at a site distinct from the taxane-binding site. vincristine is the “O” of EMA-CO combination chemotherapy for GTN treatment.
the most common dose-limiting toxicity and may include peripheral neuropathy, autonomic nervous system dysfunction, cranial nerve palsies, ataxia, or seizures. Moreover, concurrent administration with other neurotoxic agents such as cisplatin and paclitaxel may increase severity. GI toxicity also is common, including constipation, abdominal pain, and paralytic ileus. However, myelosuppression is typically mild.

249
Q

Topotecan MOA, uses, side effects

A

This TOPO I inhibitor binds to and stabilizes a transient TOPO I-DNA complex. This results in double-strand breakage and lethal DNA damage.
FDA approved as salvage therapy of recurrent epithelial ovarian cancer and recurrent cervical cance.
Myelosuppression, most commonly neutropenia, is the main dose-limiting side effect. GI toxicity also is frequent and includes nausea, vomiting, diarrhea, and abdominal pain. Systemic symptoms such as headache, fever, malaise, arthralgias, and myalgias are typical. Alopecia.

250
Q

Etoposide MOA, uses, side effects

A

cell cycle-specific agent has maximal activity in the late S and G2 phase. Etoposide “poisons” the TOPO II enzyme by stabilizing an otherwise transient form of the TOPO II-DNA complex. As a result, DNA cannot unwind, and double-strand DNA breaks form.
This agent is not FDA approved for gynecologic cancers. However, it is most often used IV as part of combination chemotherapy. Etoposide (VP-16) represents the “E” of the EMA-CO regimen, which is used for GTN. In BEP regimen, used for ovarian germ cell or sex cord-stromal tumors.
Up to 95 percent of etoposide is protein-bound, mainly to albumin. Thus, decreased albumin levels result in a higher fraction of free drug and potentially a higher incidence of toxicity. Myelosuppression, most commonly neutropenia, is the main dose-limiting side effect. GI symptoms of nausea, vomiting, and anorexia are usually minor, except with oral administration. Most patients will develop alopecia, later secondary malignancy is a small (approximately 1 in 1000) but significant risk. Acute myelogenous leukemia is the most common secondary cancer.

251
Q

Carboplatin MOA, uses, side effects

A

cell cycle-nonspecific drugs, produces DNA adducts that inhibit DNA synthesis. This agent is one of the most widely used, particularly in adjuvant or salvage treatment of epithelial ovarian cancer, and is FDA approved for this indication. It is also frequendy used off-label for endometrial cancer.
Myelosuppression, most commonly thrombocytopenia, is the main dose-limiting side effect. GI toxicity and peripheral neuropathy are notably less severe than with cisplatin. Hypersensitivity reactions will eventually develop in up to 25 percent of women receiving more than six cycles.

252
Q

Cisplatin MOA, uses, side effects

A

this agent produces DNA adduces that inhibit DNA synthesis. Cisplatin is one of the oldest and most widely used agents and is FDA approved for ovarian, cervical, and germ cell cancer. It may be given concomitandy with radiation as a radiosensitizing agent for primary treatment of cervical cancer or given as a single agent or in combination for recurrent cervical cancer. Alternatively, cisplatin is part of combination chemotherapy as the “P” of BEP, given for ovarian germ cell or sex cord-stromal tumors. Cisplatin has several significant toxicities. Of these, nephrotoxicity is the main dose-limiting side effect. Accordingly, patients must be aggressively hydrated before, during, and after drug administration. Mannitol (1 0 g) or furosemide (20 to 40 mg) may be necessary to maintain a urine output of at least 100 to 150 mL/hour. With cisplatin, electrolyte abnormalities, such as hypomagnesemia and hypokalemia, are common. In addition, severe, prolonged nausea and vomiting can be dramatic without adequate premedication. metallic taste and loss of appetite following treatment. Neurotoxicity, usually in the form of peripheral neuropathy, can also be dose limiting and irreversible. Ototoxicity typically manifests as high-frequency hearing loss and tinnitus. Similar to carboplatin, hypersensitivity reactions may develop with prolonged use. Overall, cisplatin is significandy more toxic than carboplatin, except for its reduced hematologic toxicity.

253
Q

megestrol acetate (Megace) MOA, uses, side effects

A

Synthetic derivative of progesterone and has activity on tumors through its antiestrogenic effects.
is most often used to treat endometrial intraepithelial neoplasia (EIN), nonoperable endometrial cancer, and recurrent endometrial cancer, especially in those patients with grade 1 disease.
Megestrol acetate has minimal toxicity, but patients often gain wdght from a combination of 8uid retention and increased appetite. Thromboembolic events are rare. Patients with diabetes mellitus arc carefully monitored because of the possibility of exacerbating hyperglycemia due to its concurrent glucocorticoid activity.

254
Q

bevacizumab (Avastin) uses, MOA, side effects

A

FDA approved for persistent, recurrent, or metastatic cervical cancer. For advanced epithelial ovarian cancer, bevacizumab is coupled with chemotherapy after initial surgery and then wed as single-agent maintenance. Last, it is suitable for relapsed platinum-resistant epithelial ovarian.
GI perforation may occur in up to 10 percent of patients (Cannistra, 2007). This complication is more likely in women with preexisting inflammatory bowel disease or in those with bowel resection at their primary surgery for advanced ovarian cancer (Burger, 2014). Elevated blood pressure is common and may lead to hypertensive crisis. Other possible toxicities include incomplete wound healing. weakness, pain, nosebleed. and proteinuria.

255
Q

Poly(ADP) Ribose Polymerase Inhibitors (PARP inhibitors) uses, MOA, side effects

A

Homologous recombination (HR) is an important pathway that repairs double-strand breaks, and PARP repairs single strand breaks. In the functioning cell, if HR does not repair the break. PARP will. If PARP repair is prevented, cancer cell DNA cannot be repaired and cells die. In contrast, normal cells are unaffected.
PARP inhibitors are now FDA approved for maintenance treatment of recurrent epithelial ovarian cancer following a complete or partial response to platinum-based chemotherapy. All three prolong survival, regardless of HR deficiency gene status, yet allow suitable quality of life during therapy. Olaparib is used for BRCAl and BRCA2 mutation carriers with relapsed ovarian cancer that has demonstrated resistance to platinum drugs. The most frequent toxicity is anemia. but other side dfects are fatigue, nausea or abdominal pain Niraparib has Most signficant side effects are hematologic and can be managed with dose adjustments. Rucaparib is used for patients with a BRCA mutation (germline or somatic) and with recurrent epithelial ovarian cancer treated by two or more courses of therapy.

256
Q

pembrolizumab uses, MOA, side effects

A

passive immunotherapy agents a therapeutic humanized antibody that targets and blocks the programmed cell death 1 (PD-1) receptor of T cell lymphocytes. approved for any unresectable or metastatic solid tumor with MSI-H or MMR deficiencies and for advanced cervical cancer in PD-Ll-positive patients. the response rate approximates 15 percent. Side effects are few and include rash and fever.

257
Q

Management of emetogenic cytotoxic medications

A

Mild nausea and vomiting can often be managed effectively by prochlorperazine (Compazine} with or without dexamethasone.

258
Q

Peripheral neuropathy can be seen with which chemotherapies

A

cisplatin, paclitaxel, and the vinca alkaloids. Cisplatin-induced neurotoxicity usually resolves slowly, due to axonal demyelination and loss. To counter this toxicity, amifostine (Ethyol) may be administered, but substitution of carboplatin will avoid much of the toxicity. Gabapentin (Neurontin) is the usual treatment for neuropathic pain

259
Q

Electromagnetic Radiation Energy Deposition Three mechanisms are involved in energy transfer:

A

(1) photoelectric effect,
(2) Compton effect,
(3) pair production
The photoelectric effect is dominant if the incident energy is low (less than 100 kV). The Compton effect dominates in mid-to high energy ranges (1 MY to 20 MV) and is the most important in clinical radiation therapy. Last, pair production occurs when a photon beam with very high energy (beyond 20 MV) strikes the electromagnetic field of the nucleus.

260
Q

Radiosensitivity of Some Selected Cancers Sensitivity

A

Highly sensitive: Lymphoma, dysgerminoma, small cell cancer, embryonal cancer
Moderately sensitive: Squamous carcinoma, adenocarcinoma
Poorly sensitive: Osteosarcoma, glioma, melanoma

261
Q

Taxanes, such as paclitaxd and docetaxd MOA, uses, side effects

A

causing microtubule dysfunction and blocking cells at the G2/M junction
enhance the effects of radiation with platinum agent

262
Q

Postoperative radiation is employed in the treatment of many gynecologic malignancies. Such as

A

For cervical cancer, postoperative radiation is recommended in those with lymphovascular invasion, deep stromal invasion, or large tumor size
Postoperative chemoradiation is offered if positive parametria, positive margins, or positive lymph nodes are found.
For uterine cancer, postoperative radiation is frequendy used for patients with stage IB or greater disease. intermediate-risk endometrial adenocarcinoma (includes older age, lymphovascular invasion, deep myometrial invasion, or intermediate-or high-grade disease )for adjuvant pelvic radiation.

263
Q

the most consistent sequela of radiation therapy is

A

Atrophy, It affects all lining epithelia-including skin and the epithelia of the gastrointestinal, respiratory, and genitourinary tracts and of the endocrine glands. Additionally, necrosis and ulceration may develop. Within the submucosa and deep soft tissues, fibrosis frequendy follows radiation therapy, leading to tissue contracture and stenosis

264
Q

Side effects of radiotherapy

A

Tissue atrophy
acute vaginal mucositis, formation of vaginal synechiae or tdangiectasia, and most commonly, vaginal stricture. Less frequently, rectovaginal or vesicovaginal fistulas may devdop after radiation therapy, especially with advanced-stage cancers.
acute cystitis symptoms within 2 to 3 weeks of beginning treatment.
acute malabsorption syndrome ensues to cause nausea, diarrhea, vomiting, and cramping. Adequate fluid intake and a low-lactose, low-fat, and low-fiber diet is recommended. acute radiation nephropathy typically appear 6 to 12 months after radiation exposure. Affected patients develop hypertension, edema, anemia, microscopic hematuria, proteinuria, and decreased creatinine clearance. Radiation-induced insufficiency fractures. Radiation therapy can significantly deplete bone marrow hematopoietic stem cells that include erythrocyte, leukocyte, and platelet precursors. if platelet levels measure <35,000 X 109/L and leukocyte counts are <1.0 X 109/L, then radiation may be held until these values rise. For anemia, transfusion is recommended To spare bone marrow injury, IMRT may be beneficial
- proctitis
- POI (less with ovarian transposition)

265
Q

Clear cell ovarian carcinoma assoociated with paraneoplastic

A
  • paraneoplastic hypercalcemia
  • VTE
266
Q

The risk of developing endometrial cancer in known patient with MMR gene mutetion (lynch syndrome)

A

40-60 %

267
Q

abnormal cells solely confined to the lower third of the squamous epithelium of the cervix referred as ….. , if extend into the middle third it’s ……, if into the upper third …… and full-thickness involvement,……

A

mild dysplasia or CIN 1
moderate dysplasia or CIN 2,
severe dysplasia or CIN 3;
carcinoma in situ (CIS)

268
Q

HPV 16 is the most oncogenic and accounts for the largest percentage of CIN 3 lesions (– percent) and cervical cancers (– percent). It is also the dominant type linked to other HPV-rdated anogenital and oropharyngeal cancers (Schiffman, 2010; Smith, 2007).

A

HPV 16 is the most oncogenic and accounts for the largest percentage of CIN 3 lesions (45 percent) and cervical cancers (55 percent). It is also the dominant type linked to other HPV-rdated anogenital and oropharyngeal cancers (Schiffman, 2010; Smith, 2007).

269
Q

HPV causes nearly all cervical cancers and approximately – percent of anal cancers, – percent of vaginal, and – percent of vulvar cancers.

A

HPV causes nearly all cervical cancers and approximately 90 percent of anal cancers, 70 percent of vaginal, and 40 percent of vulvar cancers.

270
Q

HPV 18 type is found in – percent of cervical squamous cell carcinomas, and in an even higher proportion of cervical adenocarcinomas and adenosquamous carcinomas (approximately – percent) (Bruni, 2010; Smith, 2007).

A

HPV 18 type is found in 13 percent of cervical squamous cell carcinomas, and in an even higher proportion of cervical adenocarcinomas and adenosquamous carcinomas (approximately 40 percent) (Bruni, 2010; Smith, 2007).

271
Q

HPV type – is the third most common type found in cervical cancers (de Sanjose, 2019)

A

HPV type 45 is the third most common type found in cervical cancers (de Sanjose, 2019)

272
Q

The risk of progression of biopsied but untreated CIN 3 to invasive cancer approximates – percent over – years (McCredie, 2008).

A

The risk of progression of biopsied but untreated CIN 3 to invasive cancer approximates 30 percent over 30 years (McCredie, 2008).

273
Q

In BRCA carriers epithelial ovarian cancer prevention percentage of prophylactic steps
Of interventions like OCP use, hysterectomy, BSO.

A

Prolonged use of OCP RR for 50% (prolog: 80%), hysterectomy 30%, BSO 90%

274
Q

Most common non epithelial vaginal cancer:

A

Rhabdomyosarcoma

275
Q

Mode of inheritance of BRCA1 &2 genes

A

Autosomal dominant

276
Q

A74yearoldpatientisseeninclinic.Shehasbeenfoundtohaveanovarianepithelialcancerwithmalignantcellsonpleuraleffsuionaspirate.SheisdiagnosedwithstageIVovariancancer.Whatisthe5yearsurvivalforstage4ovariancancers?

A

17%

277
Q

lifetime risk of breast/ ovarian cancer is?
In normal population vs. BRCA genes mutations

A

In the general population 12% of women will develop breast cancer during their lifetime. The lifetime risk of developing breast cancer with BRCA 1 is 55-65% and BRCA 2 is 45%
In the general population 1.3% of women will develop ovarian cancer during their lifetime. The lifetime risk of developing ovarian cancer with BRCA 1 is 40% and BRCA 2 is 15%

278
Q

Glandular neoplasia is often associated with cervical intraepithelial neoplasia (in –% of cases) and an underlying malignancy (adenocarcinoma) in –% of the cases.

A

Glandular neoplasia is often associated with cervical intraepithelial neoplasia (in 50% of cases) and an underlying malignancy (adenocarcinoma) in 40% of the cases.
Therefore, one smear test reported as glandular neoplasia needs urgent referral to colposcopy and the woman needs to be seen in the clinic within 2 weeks of referral (target referral).

279
Q

woman with a normal smear 3 years ago has her current smear reported as mild dyskaryosis, next step ?

A

According to recent NHS cancer screening guidelines, women with borderline and mild dyskaryosis are triaged to have high-risk HPV test. If the high-risk HPV virus is positive then they are referred for colposcopy. If the colposcopy is normal, they then go on to have routine recall in 3 or 5 years’ time depending on the screening age of patient. If the high-risk HPV test is negative then they go on to have routine recall in 3 years’ or 5 years’ time depending on the screening age of the patient.

280
Q

FIGO staging of uterine sarcoma ( leiomyosarcoma, endometrial uterine sarcoma and adenosarcoma)

A
281
Q

FIGO surgical staging of endometrial cancer

A
282
Q

Summary of syndromes with malignant manifestations associated with ovarian or breast ca

A
283
Q

Cowden syndrome : mode of inheritance, disease features , cause, associated neoplasm?

A
284
Q

Li-fraumeni syndrome, mode of inheritance , gene mutation, associated neoplasm?

A
285
Q

Lynch syndrome, associated neoplasm and percentages

A
286
Q

Lynch syndrome-associated endometrial cancer accounts for up to –% of all endometrial cancer

A

Lynch syndrome-associated endometrial cancer accounts for up to 6% of all endometrial cancer

287
Q

The modified Amsterdam criteria have only –% sensitivity to identify individuals with an HNPCC mutation.

A

The modified Amsterdam criteria have only 40% sensitivity to identify individuals with an HNPCC mutation.

288
Q

Criteria for Lynch Syndrome Screening

A

Modified Amsterdam Criteria:
• In very small families, two cases of colorectal cancer in first-degree relatives spanning at least two generations
• In families with two first-degree relatives with colorectal cancer, a third relative with an unusual early-onset cancer or endometrial cancer
Revised Bethesda Criteria:
• Colorectal cancer diagnosed in an individual younger than 50 years
• Presence of synchronous or metachronous colorectal cancer or other Lynch-associated tumors, regardless of age
• Colorectal cancer with microsatellite instability diagnosed in patients younger than 60 years
• Colorectal cancer diagnosed in one or more first-degree relatives with a Lynch-associated tumor, with at least one being diagnosed before age 50 years
• Colorectal cancer diagnosed in a patient with two or more first- or second-degree relatives with a Lynch-related tumor, regardless of age

289
Q

The spectrum of BRCA mutation-associated gynecologic cancer includes

A

ovarian cancer of predominantly serous and endometrioid histologies, tumors of the fallopian tube, and primary peritoneal cancer.

290
Q

Criteria for Genetic Risk Assessment
Patients with greater than an approximate 20–25% chance of having an inherited predisposition to breast cancer and ovarian cancer and for whom genetic risk assessment is recommended:

A

• Women with a personal history of breast cancer and ovarian cancer*
• Women with ovarian cancer* and a close relative† with ovarian cancer, premenopausal breast cancer, or both
• Women with ovarian cancer* who are of Ashkenazi Jewish ancestry
• Women with breast cancer at 50 years or younger and a close relative† with ovarian cancer* or male breast cancer at any age
• Women of Ashkenazi Jewish ancestry in whom breast cancer was diagnosed at age 40 years or younger
• Women with a close relative† with a known BRCA1 or BRCA2 mutation

291
Q

Criteria for Genetic Risk Assessment:
Patients with greater than an approximate 5–10% chance of having an inherited predisposition to breast cancer and ovarian cancer and for whom genetic risk assessment may be helpful:

A

• Women with breast cancer at age 40 years or younger
• Women with ovarian cancer, primary peritoneal cancer, or fallopian tube cancer of high grade, serous histology at any age
• Women with bilateral breast cancer (particularly if the first case of breast cancer was diagnosed at age 50 years or younger)
• Women with breast cancer at age 50 years or younger and a close relative† with breast cancer at age 50 years or younger
• Women of Ashkenazi Jewish ancestry with breast cancer at age 50 years or younger
• Women with breast cancer at any age and two or more close relatives† with breast cancer at any age (particularly if at least one case of breast cancer was diagnosed at age 50 years or younger)
• Unaffected women with a close relative† that meets one of the previous criteria

292
Q

Tumor markers

A
293
Q

Anti-Yo progressive cerebellar degeneration

A

most commonly is associated with ovarian or breast carcinoma. Frequently, the neurologic disorder predates discovery of the tumor. The Yo antigen is one of three cerebellar degeneration-related antigens identified by expression cloning and causes direct toxicity to Purkinje cells, which may not be restored. Progressive cerebellar degeneration renders patients unable to walk, and dysarthria is frequently severe. Once the disorder reaches this stage, treatment with immunosuppression or effective treatment of the underlying malignancy rarely produces significant improvement.

294
Q

What is the molecular pathway associated with serous borderline tumors?

A

BRAF/KRAS

295
Q

Molecular pathway in epithelial ovarian tumours

A

Serous (KRAS , BRAF)
Endometrioid (PTEN)
Mucinous (KRAS)

296
Q

In BRCA carriers Risk reduction with OCP use for 5 years ranges btw —-—-%

A

Risk reduction with OCP use for 5 years ranges btw 33-38%

297
Q

– to – percent of epithelial ovarian cancers have histologic and biologic features that are intermediate between clearly benign cysts and frankly invasive carcinomas.

A

Ten to 15 percent of epithelial ovarian cancers have histologic and biologic features that are intermediate between clearly benign cysts and frankly invasive carcinomas.

298
Q

Age of population of borderline tumors

A

patients are in their mid-40s, which is 15 years younger than women with invasive ovarian carcinoma.

299
Q

lymphadenectomy has been reported to be no longer deemed necessary for the subset of Endometrial cancer patients with low-risk features
low-risk features have been defined as;

A

“endometrioid type EC, FIGO grade 1 or 2 histology, myometrial invasion (MMI) ≤50%, and primary tumor diameter (PTD) ≤2 cm.

all other patients have been defined as high-risk and introduced as candidates for systematic lymphadenectomy up to the renal veins

300
Q

For risk-reducing salpingo-oophorectomy in patients with hereditary breast and ovarian cancer syndromes, chance of finding occult malignancy at surgery or during final pathologic analysis approximates – percent (Finch, 2006; Manchanda, 2011). Thus, preoperative serum CA125 level and pelvic sonography should evaluate for malignancy.

A

For risk-reducing salpingo-oophorectomy in patients with hereditary breast and ovarian cancer syndromes, chance of finding occult malignancy at surgery or during final pathologic analysis approximates 5 percent (Finch, 2006; Manchanda, 2011). Thus, preoperative serum CA125 level and pelvic sonography should evaluate for malignancy.

301
Q

Pelvic ultrasonography of the ovaries can be useful for evaluating the presence of an ovarian androgenproducing neoplasm in patients with markedly elevated testosterone concentrations, rapidly progressive hirsutism, or signs of virilization.

A

Many of the ovarian androgen-producing neoplasms can be small and may not be clearly identified on ultrasonography. Sometimes the only way to identify an ovarian neoplasm is by noting asymmetry of the ovaries on ultrasonography or growth over time.

302
Q

Patients with a history of a BRCA1 mutation, a BRCA2 mutation, or Lynch syndrome are at increased risk of ovarian cancer by which percentages

A

(69%, 41–45%, and 5–10%, respectively, for ovarian cancer by age 70 years).

303
Q

Proximal fallopian tube occlusion has been classified into three types:

A

nodular (eg, salpingitis isthmic nodosa, endometriosis), non-nodular (eg, true fibrotic occlusion), and “pseudo” occlusion (eg, debris, polyps, hypoplastic tubes).

304
Q

The most common HPV associated with VIN and squamous cell cancer is

A

16

305
Q

Hormonal Treatment for Endometrial Intraepithelial Neoplasia*

A
306
Q

Types of cervical cancer

A

squamous cell carcinoma (most common), invasive adenocarcinoma, small cell neuroendocrine carcinoma, and other rare histologic types.

307
Q

Sedlis criteria for external pelvic radiation after radical hysterectomy in node-negative, margin-negative, parametria-negative cases

A
  • lymphovascular space invasion (LSVI) plus deep one-third stromal invasion plus primary tumor of any size
  • LVSI plus middle one-third stromal invasion plus primary tumor size ≥ 2 cm
  • LSVI plus superficial one-third stromal involvement plus primary tumor size ≥ 5 cm
  • no LSVI plus middle or deep one-third stromal invasion plus primary tumor size ≥ 4 cm
308
Q

Squamous cell carcinomas represent –% of all cervical cancer, and adenocarcinomas account for –% of cervical cancers. The other cell types are rare.

A

Squamous cell carcinomas represent 70% of all cervical cancer, and adenocarcinomas account for 25% of cervical cancers. The other cell types are rare.

309
Q

Pap testing has only a —to —percent sensitivity for detecting high-grade lesions on any given single test

A

Pap testing has only a 53-to 80-percent sensitivity for detecting high-grade lesions on any given single test.
Moreover, in women who have stage I cervical cancer, only 30 to 50 percent of single cytologic smears obtained are read as positive for cancer

310
Q

relative contraindications to radiation include

A

These contraindications include diabetes, pelvic inflammatory disease, hypertension, collagen disease, inflammatory bowel disease, or adnexal masses.

311
Q

Clinically, a patient may be considered for pelvic exenteration if the triad of — , —, — are absent.

A

Clinically, a patient may be considered for pelvic exenteration if the triad of lower extremity edema, back pain, and hydronephrosis are absent.

312
Q

Natural History of Cervical lntraepithelial Neoplasia (CIN) Lesions

A

The risk of progression of biopsied but untreated CIN 3 to invasive cancer approximates 30 percent over 30 years (McCredie, 2008).

313
Q

Cytology-negative and HPV-positive test results will occur in <10 percent of screened patients

A

co-testing is repeated 12 months later. Colposcopy is recommended for recurrent, positive HPV results or an abnormal repeat cytology.
An alternative strategy is now available for the manage- ment of normal cytologic findings but a positive HPV result. A reflex test specifically for HPVs 16 and 18, (genotyping) can be performed in many settings. If HPV 16 or 18 is found, immediate colposcopy is recommended (American College of Obstetricians and Gynecologists, 2018a; Saslow, 2012).

314
Q

Endocervical sampling is cur- rently recommended during colposcopy for the following situ- ations (American College of Obstetricians and Gynecologists, 2018b; Massad, 2013):

A

• The SCJ is not fully visualized.
• The SCJ is fully visualized, but no lesion is identified.
• Initial evaluation of ASC-H, HSIL, AGC, or AIS cytology
test results.

315
Q

IF Histologic LSIL (HPV changes or CIN 1) WAS found
WHAT IS THE PROPER MANGAMENT ?

A

exhibits high rates of spontaneous regression. The LSIL diagnosis is poorly reproducible by cytology or histology and is thus unreliable. Pt should not be told they have HPV infection based upon LSIL cytology or biopsy alone. For these reasons, HPV change found by biopsy is not treated, and CIN 1 is no longer treated immediately. When diagnosed after a “lesser” cytologic abnormality such ASC-US, LSIL, or an NILM, HPV-positive screening, it can be observed indefinitely. Treatment is accept- able only ifCIN 1 persists for more than 2 years. This is regard- less of colposcopic examination adequacy or presence of CIN 1 in an endocervical sampling. Treatment of CIN 1 in younger women or chose concerned about the possible effects of treat- ment on future pregnancy is discouraged. Current guidelines for surveillance without treatment and criteria that return a woman to routine screening should be followed and may involve periodic cytology or co-testing.
Ifdeemed appropriate, persistent CIN 1 can be treated by ablation. Criteria require that the SCJ and all lesions are fully seen during colposcopy and that the endocervical sampling lacks HSIL (CIN 2/3) or ungraded CIN. If these criteria are not met and treatment is indicated, excision is recommended and ablation is unacceptable.
CIN 1 diagnosed after an ASC-H or HSIL Pap test result carries a higher risk of undiagnosed high-grade CIN. Depending on patient age and colposcopic findings, either a diagnostic excision or surveillance with colposcopy, cytology, HPV testing, or a combination of these at prescribed intervals will be recommended by current guidelines. Persistent, unex- plained HSIL or AGC cytology generally warrants an excision procedure, if only CIN 1 is found with colposcopic biopsy.
(CIN severity, colposcopic findings, age, and reproductive plans play key roles in cervical disease man- agement. Guidelines are complex and applied on an individual- ized basis. They cannot address all patient scenarios and cannot prevent all cases o f cervical cancer.)

316
Q

Management of HSIL:CIN2 and CIN3 ?

A

Treatment modalities include either ablation or excision of the entire TZ.
An unequivocal histologic diagnosis of CIN 3 is always treated and not observed in nonpregnant patients regardless of age or reproductive history. With a CIN 3 biopsy, if HSIL or ungraded CIN is found in the endocervical sampling or if col- poscopy did not fully visualize the SCJ and the upper limits ofall lesions, a diagnostic excision is indicated to exclude occult inva- sive cervical cancer. Recurrent or persist HSIL after treatment is managed with repeat excision, not ablation. Hysterectomy as primary therapy is unacceptable. Hysterectomy may be indi- cated if repeat excision is needed but not anatomically feasible or if high-grade CIN recurs or persists and invasive cancer has been thoroughly excluded. For young women, particularly of low parity, with CIN 2 or HSIL (CIN 2/3, not otherwise specified) surveillance or treat- ment is acceptable, ifthe SCJ and all lesions are fully seen during colposcopy. In this context, “young women” refers to individu- als for whom the possible risk to future pregnancies from treat- ment outweighs the risk of progression to malignancy, although both are difficult to quantify. No upper age limit is specified for surveillance. Surveillance o f specified CIN 2 is preferred in younger women, because this histologic diagnosis is less reli- able and spontaneous regression of lesions over time is com- mon. Even in younger women or those concerned with future reproduction, treatment is indicated ifcolposcopy does not fully visualize the SCJ and lesions present, biopsy shows CIN 3, or if CIN 2 or CIN 2/3 is persistent. Current guidelines for surveil- lance testing, intervals for reassessment, and acceptable upper time limits for persistence should be consulted.

317
Q

Ifan excision margin or endocervical curettage performed immediately after an excision is positive for HSIL (CIN 2 or CIN 3), next step ?

A

repeat excision may be indicated.
Repeat excision is indicated for special circumstances such as AIS or microinva- sive carcinoma at the excision margins.

318
Q

Vulvar cancer treatment (based on staging)

A

1) Wide local excision (AKA simple partial vulvectomy) can be appropriate for preinvasive disease and microinvasive tumors (stage IA) of the vulva and some rare histologic types with a 1-cm surgical margin is obtained around the lesion. Deep surgical margins corresponds to Colles fascia measuring 1 cm.
2) radicalpartial vulvectomy, tumor-containing portions of the vulva are completely removed, wherever they are located. Skin margins are ideally 2 cm, and excision extends deep to the perineal membrane.
3) Radical partial vulvectomy is typically reserved for lesions that are not too large or extensive, with an otherwise normal vulva.
Radical total vulvectomy is a complete dissection ofvulvar tissue to the level ofthe perinea! membrane and the periosteum of the pubic rami or symphysis.

319
Q

Microinvasive Tumors (Stage IA) vulvar ca management

A

these patients can undergo wide local excision with a 1-cm margin. Lymphadenectomy is not indicated because associated lymph node metastasis is rare.

320
Q

For women with local tumor recurrence, the 5-year survival rate is — percent. This compares with a rate >— percent in women with no recurrence (Woelber, 2016).

A

For women with local tumor recurrence, the 5-year survival rate is 67 percent. This compares with a rate >80 percent in women with no recurrence (Woelber, 2016).

321
Q

Vaginal intraepithelial neoplasia (ValN) is a precursor to invasive vaginal cancer, and up to — percent of patients with VaIN will progress to invasive cancer (Ratnavelu, 2013; Zeligs, 2013).

A

Vaginal intraepithelial neoplasia (ValN) is a precursor to invasive vaginal cancer, and up to 3 percent of patients with VaIN will progress to invasive cancer (Ratnavelu, 2013; Zeligs, 2013).

322
Q

Of primary vaginal adenocarcinoma types(Histologic types include clear cell, endometrioid, mucinous, and serous carcinomas), the ———- is most closely associated with DES exposure.

A

Of primary vaginal adenocarcinomas types, the clear cell type is most closely associated with DES exposure,

323
Q

the most common malignancy of the vagina in infants and children,

A

embryonal rhabdomyosarcomas

324
Q

Endometrial adenocarcinomas are categorized as rype I or rype II based on histology. Type I, that is, —- rype, makes up 80 to 90 percent ofall cases. The other 10 to 20 percent are rype II cancers, namely, the ——— hiscologic rypes that include

A

Endometrial adenocarcinomas are categorized as rype I or rype II based on histology. Type I, that is, endometrioid rype, makes up 80 to 90 percent ofall cases. The other 10 to 20 percent are rype II cancers, namely, the non-endometrioid hiscologic rypes that include serous and clear cell adeno- carcinomas and carcinosarcoma.

325
Q

Postmenopausal bleeding is particularly worrisome and carries a – to –percent likelihood of diagnosing endometrial carcinoma (Clarke, 2018; van Hanegem, 2017). Abnormal vaginal discharge may be another symptom in older women.

A

Postmenopausal bleeding is particularly worrisome and carries a 5- to 10-percent likelihood of diagnosing endometrial carcinoma (Clarke, 2018; van Hanegem, 2017). Abnormal vaginal discharge may be another symptom in older women.

326
Q

postmenopausal women with endometrial cells are occasionally recorded on a routine Pap test report what is her risks of endometrial cancer ? percentages

A

postmenopausal women with such findings have a 3- to 5-percent risk ofendometrial cancer (Simsir, 2005) In those using H RT, the prevalence of benign endometrial cells on smears is greater, and the risk of endometrial malignancy is low (1 to 2 percent)

327
Q

Only three classes of cytotoxic drugs with definite activity for endometrial cancer have been identified,Which are

A

and paclitaxel (Taxol), doxorubicin {adriamycin), and cisplatin (TAP) chemotherapy is one of the adjuvant treatment options for advanced endomtrial cancer following surgery. In one GOG trial of273 women (protocol #177) A less toxic alternative to TAP chemotherapy is paclitaxel plus carboplatin. Routinely used for ovarian cancer, this regimen is effective in advanced-stage endometrial cancer (Hoskins, 200 I; Sovak, 2006, 2007). One GOG trial (protocol #209) compared TAP and the regimen of carboplatin plus paclitaxel. Results demonstrated that carboplatin plus paclitaxel was not inferior to TAP in terms of progression-free and overall survival rates.

328
Q

In one study, — percent of invasive cervical cancer cases were attributable to HPV serotype 16. Serotype 18 was associated with — percent ofinvasive disease cases (Guan, 2012).

A

In one study, 63 percent of invasive cervical cancer cases were attributable to HPV serotype 16. Serotype 18 was associated with 16 percent ofinvasive disease cases (Guan, 2012).

329
Q

are the most common germ cell tumors and account for 20% to 25% of all ovarian neoplasms

A

Benign cystic teratomas (dermoids) are usually unilateral, but 10% are bilateral.

330
Q

The most common cause of death in ovarian cancer is

A

Malignant bowel obstruction

331
Q

Women with hereditary breast and ovarian cancer syndrome have a —% to —% lifetime risk of breast cancer and a —% to —% (BRCA1) or a —% to —% (BRCA2) risk of ovarian cancer.

A

Women with hereditary breast and ovarian cancer syndrome have a 65% to 74% lifetime risk of breast cancer and a 39% to 46% (BRCA1) or a 12% to 20% (BRCA2) risk of ovarian cancer.

332
Q

Women with an RMI of <25 have low risk of developing ovarian cancer (<-%).
Women with an RMI of 25–250 have moderate risk of developing
ovarian cancer (—%).
Women with an RMI of >250 have high risk of developing ovarian
cancer (—%).

A

Women with an RMI of <25 have low risk of developing ovarian cancer
(<3%).
Women with an RMI of 25–250 have moderate risk of developing
ovarian cancer (20%).
Women with an RMI of >250 have high risk of developing ovarian
cancer (75%).

333
Q

with lichen planus, the risk of progression to vulvar cancer is approximately

A

3–6%.

334
Q

Approximately x-x% of patients who have lichen sclerosus will have coexisting squamous cell carcinoma, so diagnosis should be confirmed by biopsy.

A

Approximately 2–5% of patients who have lichen sclerosus will have coexisting squamous cell carcinoma, so diagnosis should be confirmed by biopsy.

335
Q

Treatment of ovarian cancer:
• Primary treatment can be surgical, via primary debulking surgery (PDS) or with NACT.
• Surgery usually consists of an exploratory laparotomy, abdominal cytology, hysterectomy, BSO, omentectomy, and cytoreduction.

A

with evidence of up to stage IIIB cancer should be surgically staged to include peritoneal biopsies and a pelvic and PA-LND. Three-fourths of advanced-stage cancers will have positive retroperitoneal LN. LN drainage tends to follow the ovarian vessels. Dissection around the high precaval and PA regions is important.