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30 Cards in this Set

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Describe Each Tanner Stage
Tanner I  no glandular tissue; areola follows the skin contours of the chest (prepubertal) [typically age 10 and younger]

Tanner II  breast bud forms, with small area of surrounding glandular tissue; areola begins to widen [10-11.5]

Tanner III  breast begins to become more elevated, and extends beyond the borders of the areola, which continues to widen but remains in contour with surrounding breast [11.5-13]

Tanner IV  increased breast size and elevation; areola and papilla form a secondary mound projecting from the contour of the surrounding breast [13-15]

Tanner V  breast reaches final adult size; areola returns to contour of the surrounding breast, with a projecting central papilla. [15+]
Describe each tanner stage for pubic hair.
Pubic hair (both male and female)

Tanner I  no pubic hair at all (prepubertal Dominic state) [typically age 10 and younger]

Tanner II  small amount of long, downy hair with slight pigmentation at the base of the penis and scrotum (males) or on the labia majora (females) [10–11.5]

Tanner III  hair becomes more coarse and curly, and begins to extend laterally [11.5–13]

Tanner IV  adult-like hair quality, extending across pubis but sparing medial thighs [13–15]

Tanner V  hair extends to medial surface of the thighs [15+]
List the highlights of the cycle
Follicular phase
Egg matures

Ovulation
Egg released

Luteal phase
Corpus luteum
Endometrium
Prep for blastocyst

No Pregnancy
Menses
Polycystic ovaries are?
>8 follicles per ovary less than 10mm in diameter
On microscopy, also seen is “hyperthecosis” – I.e. enlarged thecal cells, assoc w/ elev insulin levels –Therefore, ovary itself is enlarged.
Special note on secondary hirsuitism:
Karyotype for patients with premature ovarian failure <30yo

If hirsutism is present, consider PCOS, congenital adrenal hyperplasia, Cushing’s, or ovarian tumors: check free testosterone
Special note on secondary hirsuitism:
Karyotype for patients with premature ovarian failure <30yo

If hirsutism is present, consider PCOS, congenital adrenal hyperplasia, Cushing’s, or ovarian tumors: check free testosterone
With secondary amenorrhea, the purpose for inducing menses at least every 3 months is?
to prevent endometrial hyperplasia and cancer
Key Point

Select information about the safety and appropriate use of GARDASIL® [Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine] is presented in this slide.

Background
GARDASIL is a vaccine indicated in girls and women 9 to 26 years of age for the prevention of cervical cancer, precancerous or dysplastic lesions, and genital warts caused by HPV Types 6, 11, 16, and 18.

Select Safety Information
GARDASIL is contraindicated in individuals who are hypersensitive to the active substances or to any of the excipients of the vaccine.

Vaccination with GARDASIL does not substitute for routine cervical cancer screening, and women who receive GARDASIL should continue to undergo screening per standard of care.
Key Point

Select information about the safety and appropriate use of GARDASIL® [Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine] is presented in this slide.

Background
GARDASIL is a vaccine indicated in girls and women 9 to 26 years of age for the prevention of cervical cancer, precancerous or dysplastic lesions, and genital warts caused by HPV Types 6, 11, 16, and 18.

Select Safety Information
GARDASIL is contraindicated in individuals who are hypersensitive to the active substances or to any of the excipients of the vaccine.

Vaccination with GARDASIL does not substitute for routine cervical cancer screening, and women who receive GARDASIL should continue to undergo screening per standard of care.
Key Point

Select information about the safety and appropriate use of GARDASIL® [Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine] is presented in this slide.

Background
Select Safety Information (cont)
Vaccination with GARDASIL may not result in protection in all vaccine recipients.

GARDASIL is not intended to be used for treatment of active genital warts; cervical cancer; CIN, VIN, or VaIN.

GARDASIL has not been shown to protect against diseases due to non-vaccine HPV types.

The vaccine-related adverse experiences that were observed among recipients of GARDASIL at a frequency of at least 1.0% and greater than placebo were pain, swelling, erythema, fever, nausea, pruritus, and dizziness.
Key Point

Select information about the safety and appropriate use of GARDASIL® [Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine] is presented in this slide.

Background
Select Safety Information (cont)
Vaccination with GARDASIL may not result in protection in all vaccine recipients.

GARDASIL is not intended to be used for treatment of active genital warts; cervical cancer; CIN, VIN, or VaIN.

GARDASIL has not been shown to protect against diseases due to non-vaccine HPV types.

The vaccine-related adverse experiences that were observed among recipients of GARDASIL at a frequency of at least 1.0% and greater than placebo were pain, swelling, erythema, fever, nausea, pruritus, and dizziness.
Key Point

In studies of sexually active women, most had not been exposed to all HPV types contained in GARDASIL. Although GARDASIL does not protect against disease caused by previously acquired HPV types, GARDASIL will help protect against disease caused by vaccine types to which the patient is naïve. ACIP, ACOG, and other professional societies recommend vaccination of females 13 to 26 years of age, regardless of previous HPV infection or abnormal Pap test results.

Background
The decision to vaccinate sexually active females is supported by several key factors. First, there is clinical evidence of the efficacy of GARDASIL in these types of patients.1 Although GARDASIL will not protect from disease caused by HPV types that these patients had already contracted, GARDASIL will still help protect against the types patients have not encountered. Data suggest that most sexually active women in the vaccination age group had not been exposed to all 4 vaccine HPV types.

Second, professional organizations, including ACIP, ACOG, AAFP, and SAM recommend catch-up vaccination for females 13 to 26 years of age who were not previously vaccinated or who have not completed the full vaccine series. Furthermore, these organizations recommend vaccination, regardless of previous HPV infection or abnormal Pap test results, and continuation of Pap testing after vaccination.2–4

GARDASIL is a prophylactic vaccine and therefore will not treat current lesions.
Key Point

In studies of sexually active women, most had not been exposed to all HPV types contained in GARDASIL. Although GARDASIL does not protect against disease caused by previously acquired HPV types, GARDASIL will help protect against disease caused by vaccine types to which the patient is naïve. ACIP, ACOG, and other professional societies recommend vaccination of females 13 to 26 years of age, regardless of previous HPV infection or abnormal Pap test results.

Background
The decision to vaccinate sexually active females is supported by several key factors. First, there is clinical evidence of the efficacy of GARDASIL in these types of patients.1 Although GARDASIL will not protect from disease caused by HPV types that these patients had already contracted, GARDASIL will still help protect against the types patients have not encountered. Data suggest that most sexually active women in the vaccination age group had not been exposed to all 4 vaccine HPV types.

Second, professional organizations, including ACIP, ACOG, AAFP, and SAM recommend catch-up vaccination for females 13 to 26 years of age who were not previously vaccinated or who have not completed the full vaccine series. Furthermore, these organizations recommend vaccination, regardless of previous HPV infection or abnormal Pap test results, and continuation of Pap testing after vaccination.2–4

GARDASIL is a prophylactic vaccine and therefore will not treat current lesions.
Key Point

ACIP recommendations for the quadrivalent HPV vaccine indicate routine vaccination for females 11 to 12 years of age with catch-up vaccination in females 13 to 26 years of age.

Background
Recommendations for use of quadrivalent HPV vaccine1:
Routine vaccination with 3 doses of quadrivalent HPV vaccine is recommended for females 11 to 12 years of age. The vaccination series can be started in females as young as 9 years of age.
Catch-up vaccination is recommended for females 13 to 26 years of age who have not been vaccinated previously or who have not completed the full vaccine series. Ideally, vaccine should be administered before potential exposure to HPV through sexual contact. However, females who might have been exposed to HPV should be vaccinated.
Quadrivalent HPV vaccine can be administered at the same visit that other age- appropriate vaccines are provided, such as Tdap and quadrivalent meningococcal conjugate (MCV4).
– NOTE: Although ACIP states that the quadrivalent HPV vaccine can be administered with these other vaccines, per the prescribing information, co-administration of GARDASIL® [Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine] with these vaccines has not been studied.
Key Point

ACIP recommendations for the quadrivalent HPV vaccine indicate routine vaccination for females 11 to 12 years of age with catch-up vaccination in females 13 to 26 years of age.

Background
Recommendations for use of quadrivalent HPV vaccine1:
Routine vaccination with 3 doses of quadrivalent HPV vaccine is recommended for females 11 to 12 years of age. The vaccination series can be started in females as young as 9 years of age.
Catch-up vaccination is recommended for females 13 to 26 years of age who have not been vaccinated previously or who have not completed the full vaccine series. Ideally, vaccine should be administered before potential exposure to HPV through sexual contact. However, females who might have been exposed to HPV should be vaccinated.
Quadrivalent HPV vaccine can be administered at the same visit that other age- appropriate vaccines are provided, such as Tdap and quadrivalent meningococcal conjugate (MCV4).
– NOTE: Although ACIP states that the quadrivalent HPV vaccine can be administered with these other vaccines, per the prescribing information, co-administration of GARDASIL® [Quadrivalent Human Papillomavirus (Types 6, 11, 16, 18) Recombinant Vaccine] with these vaccines has not been studied.
Key Point

The quadrivalent HPV vaccine is not recommended for use in pregnancy.

Background
The quadrivalent HPV vaccine is not recommended for use in pregnancy.1
Any exposure to vaccine during pregnancy should be reported to the vaccine pregnancy registry (1-800-986-8999).1
Precautions1:
– Quadrivalent HPV vaccine can be administered to females with minor acute illnesses (eg, diarrhea or mild upper respiratory tract infections, with or without fever). Vaccination of people with moderate or severe acute illnesses should be deferred until after the patient improves.
– Syncope can occur after vaccination, most commonly in adolescents and young adults.
Key Point

The quadrivalent HPV vaccine is not recommended for use in pregnancy.

Background
The quadrivalent HPV vaccine is not recommended for use in pregnancy.1
Any exposure to vaccine during pregnancy should be reported to the vaccine pregnancy registry (1-800-986-8999).1
Precautions1:
– Quadrivalent HPV vaccine can be administered to females with minor acute illnesses (eg, diarrhea or mild upper respiratory tract infections, with or without fever). Vaccination of people with moderate or severe acute illnesses should be deferred until after the patient improves.
– Syncope can occur after vaccination, most commonly in adolescents and young adults.
Key Point

American College of Obstetricians and Gynecologists (ACOG) guidelines are in line with ACIP recommendations. ACOG also recognizes that well-visits of adolescents and young women 16 to 26 years of age are a strategic time to discuss HPV and the potential benefit of the HPV vaccine, and to offer vaccination to those who have not already received it.

Background 
ACOG guidelines are in line with ACIP recommendations. The ACOG Committee on Adolescent Health Care and the ACOG Working Group on Immunization recommend the vaccination of females 9 to 26 years of age against HPV.1

Although pediatricians primarily care for younger-aged patients, any visit by females 9 to 26 years of age is critical to the widespread use of the vaccine. Adolescents and young women 16 to 26 years of age who are in the vaccination age groups, including women of college age, may visit their OB/GYN for primary care. These visits provide a strategic time to discuss HPV and the potential benefit of the HPV vaccine and to offer vaccination to those who have not already received it.1

Well-visits by adolescents and young women 16 to 26 years of age (for primary care, contraceptive or other gynecologic needs, or pregnancy-related services) also provide strategic opportunities for OB/GYNs to discuss HPV and other sexually transmitted infections (STIs), review the potential benefit of the HPV vaccine, and administer the HPV vaccination.1
Key Point

American College of Obstetricians and Gynecologists (ACOG) guidelines are in line with ACIP recommendations. ACOG also recognizes that well-visits of adolescents and young women 16 to 26 years of age are a strategic time to discuss HPV and the potential benefit of the HPV vaccine, and to offer vaccination to those who have not already received it.

Background 
ACOG guidelines are in line with ACIP recommendations. The ACOG Committee on Adolescent Health Care and the ACOG Working Group on Immunization recommend the vaccination of females 9 to 26 years of age against HPV.1

Although pediatricians primarily care for younger-aged patients, any visit by females 9 to 26 years of age is critical to the widespread use of the vaccine. Adolescents and young women 16 to 26 years of age who are in the vaccination age groups, including women of college age, may visit their OB/GYN for primary care. These visits provide a strategic time to discuss HPV and the potential benefit of the HPV vaccine and to offer vaccination to those who have not already received it.1

Well-visits by adolescents and young women 16 to 26 years of age (for primary care, contraceptive or other gynecologic needs, or pregnancy-related services) also provide strategic opportunities for OB/GYNs to discuss HPV and other sexually transmitted infections (STIs), review the potential benefit of the HPV vaccine, and administer the HPV vaccination.1
Key Point

ACOG also recognizes that the HPV vaccine can benefit sexually active women.

Background 
The quadrivalent HPV vaccine has been classified by the Food and Drug Administration (FDA) as pregnancy category B. Although its use in pregnancy is not recommended, no teratogenic effects have been reported in animal studies. In clinical studies, the proportion of pregnancies with an adverse outcome was comparable in women who received the quadrivalent HPV vaccine and in women who received a placebo. The manufacturer’s pregnancy registry should be contacted if pregnancy is detected during the vaccination schedule. Completion of the series should be delayed until pregnancy is completed.1

Sexually active women can receive the quadrivalent HPV vaccine. Women with previous abnormal cervical cytology or genital warts also can receive the quadrivalent HPV vaccine. These patients should be counseled that the vaccine may be less effective in women who have been exposed to HPV before vaccination than in women who were HPV naïve at the time of vaccination. Women with previous HPV infection will benefit from protection against disease caused by the HPV vaccine genotypes with which they have not been infected. The need for annual cervical cytology screening should be emphasized.1
Key Point

ACOG also recognizes that the HPV vaccine can benefit sexually active women.

Background 
The quadrivalent HPV vaccine has been classified by the Food and Drug Administration (FDA) as pregnancy category B. Although its use in pregnancy is not recommended, no teratogenic effects have been reported in animal studies. In clinical studies, the proportion of pregnancies with an adverse outcome was comparable in women who received the quadrivalent HPV vaccine and in women who received a placebo. The manufacturer’s pregnancy registry should be contacted if pregnancy is detected during the vaccination schedule. Completion of the series should be delayed until pregnancy is completed.1

Sexually active women can receive the quadrivalent HPV vaccine. Women with previous abnormal cervical cytology or genital warts also can receive the quadrivalent HPV vaccine. These patients should be counseled that the vaccine may be less effective in women who have been exposed to HPV before vaccination than in women who were HPV naïve at the time of vaccination. Women with previous HPV infection will benefit from protection against disease caused by the HPV vaccine genotypes with which they have not been infected. The need for annual cervical cytology screening should be emphasized.1
Approximately 10% of women with ovarian cancer are carriers of a breast/ovarian cancer susceptibility gene. The proportion of cases of ovarian cancer due to such a gene decreases with age and is estimated to be 14% for women diagnosed in the fourth decade, dropping to 7% for women diagnosed in the sixth decade. Gene carriers have a greater than fifteen-fold risk of ovarian cancer compared to noncarriers. The lifetime risk for ovarian cancer in the general population is 1.3%, while estimates for gene carriers range from 10% to 60%. BRCA1 and BRCA2 together have been estimated to account for 85% of breast-ovarian cancer families. Both BRCA1 and BRCA2 are transmitted in an autosomal dominant fashion. Certain ethnic groups, such as Ashkenazi Jews, have high rates of specific mutations of these genes. The large number of mutations described makes genetic testing and patient counseling complex, and illustrates the need for genetic counseling by a qualified health care provider.
BRCA1. BRCA1 is a gene associated with increased risk for breast and ovarian cancer. The lifetime risk of breast cancer is estimated to be 55-85%, while the lifetime risk of ovarian cancer is 20-40%, with some studies suggesting as high at 60%. The proportion of ovarian cancers in the general population attributable to this gene is estimated to be 5.9% for women in the third decade or younger, and steadily declines with increasing age, dropping to 1.8% in the seventh decade [Ford 95]. Features suggestive of a BRCA1 mutation include a family history of:
Two or more cases of ovarian cancer
Breast and ovarian cancer in the same woman
One or more cases of pre-menopausal breast cancer with or without a case of ovarian cancer diagnosed at any age
Two or more cases of post-menopausal breast cancer and one or more cases of ovarian cancer diagnosed at any age
Male breast cancer
BRCA2.The BRCA2 tumor suppressor gene is also associated with high rates of breast and ovarian cancer. The lifetime risk of breast cancer has been reported to be similar to that of BRCA1 (55-85%), while the lifetime risk of ovarian cancer is estimated to be 10-20%. BRCA2 is also associated with a 5-6% risk of male breast cancer, as well as increased risk of pancreatic cancer and melanoma. BRCA2 features are similar to those outlined for BRCA1, but also include a family history of pancreas cancer in addition to breast and/or ovarian cancer
Approximately 10% of women with ovarian cancer are carriers of a breast/ovarian cancer susceptibility gene. The proportion of cases of ovarian cancer due to such a gene decreases with age and is estimated to be 14% for women diagnosed in the fourth decade, dropping to 7% for women diagnosed in the sixth decade. Gene carriers have a greater than fifteen-fold risk of ovarian cancer compared to noncarriers. The lifetime risk for ovarian cancer in the general population is 1.3%, while estimates for gene carriers range from 10% to 60%. BRCA1 and BRCA2 together have been estimated to account for 85% of breast-ovarian cancer families. Both BRCA1 and BRCA2 are transmitted in an autosomal dominant fashion. Certain ethnic groups, such as Ashkenazi Jews, have high rates of specific mutations of these genes. The large number of mutations described makes genetic testing and patient counseling complex, and illustrates the need for genetic counseling by a qualified health care provider.
BRCA1. BRCA1 is a gene associated with increased risk for breast and ovarian cancer. The lifetime risk of breast cancer is estimated to be 55-85%, while the lifetime risk of ovarian cancer is 20-40%, with some studies suggesting as high at 60%. The proportion of ovarian cancers in the general population attributable to this gene is estimated to be 5.9% for women in the third decade or younger, and steadily declines with increasing age, dropping to 1.8% in the seventh decade [Ford 95]. Features suggestive of a BRCA1 mutation include a family history of:
Two or more cases of ovarian cancer
Breast and ovarian cancer in the same woman
One or more cases of pre-menopausal breast cancer with or without a case of ovarian cancer diagnosed at any age
Two or more cases of post-menopausal breast cancer and one or more cases of ovarian cancer diagnosed at any age
Male breast cancer
BRCA2.The BRCA2 tumor suppressor gene is also associated with high rates of breast and ovarian cancer. The lifetime risk of breast cancer has been reported to be similar to that of BRCA1 (55-85%), while the lifetime risk of ovarian cancer is estimated to be 10-20%. BRCA2 is also associated with a 5-6% risk of male breast cancer, as well as increased risk of pancreatic cancer and melanoma. BRCA2 features are similar to those outlined for BRCA1, but also include a family history of pancreas cancer in addition to breast and/or ovarian cancer
OVARIAN GERM CELL TUMORS
Germ cell tumors account for approximately 5 percent of all ovarian malignancies. They almost always occur in women of reproductive age and are most frequently found in women in their teens or twenties. Many types of germ cell tumors are extremely aggressive, fast-growing malignancies. In the past they were often fatal within two years even though frequently confined to one ovary at the time of diagnosis. With surgery and modern multi-agent chemotherapy, the cure rate is excellent.
Types
There are six main cell types: dysgerminoma, endodermal sinus tumor, embryonal carcinoma, choriocarcinoma, immature teratoma and mixed germ cell tumors.
There are also rare cell types such as struma ovarii, carcinoid and malignant transformation of a benign dermoid.
How It Spreads
Ovarian germ cell tumors can spread directly to the adjacent pelvic organs and through the lymph system to the pelvic, aortic, chest (mediastinal), groin and neck lymph nodes. They may also spread to the surfaces of the abdominal cavity and to distant organs such as the liver, lungs and brain.
OVARIAN GERM CELL TUMORS
Germ cell tumors account for approximately 5 percent of all ovarian malignancies. They almost always occur in women of reproductive age and are most frequently found in women in their teens or twenties. Many types of germ cell tumors are extremely aggressive, fast-growing malignancies. In the past they were often fatal within two years even though frequently confined to one ovary at the time of diagnosis. With surgery and modern multi-agent chemotherapy, the cure rate is excellent.
Types
There are six main cell types: dysgerminoma, endodermal sinus tumor, embryonal carcinoma, choriocarcinoma, immature teratoma and mixed germ cell tumors.
There are also rare cell types such as struma ovarii, carcinoid and malignant transformation of a benign dermoid.
How It Spreads
Ovarian germ cell tumors can spread directly to the adjacent pelvic organs and through the lymph system to the pelvic, aortic, chest (mediastinal), groin and neck lymph nodes. They may also spread to the surfaces of the abdominal cavity and to distant organs such as the liver, lungs and brain.
Malignant transformation of the ovarian surface epithelium (OSE) accounts for most ovarian carcinoma. Detection of preneoplastic changes in the OSE leading to overt malignancy is important in prevention and management of ovarian cancer. We identified OSE proteins with altered expression derived from women with a family history (FH) of ovarian and/or breast cancer and mutations in the BRCA1 tumor suppressor gene.
Proteome Changes in Ovarian Epithelial Cells Derived from Women with BRCA1 Mutations and Family Histories of Cancer *
Malignant transformation of the ovarian surface epithelium (OSE) accounts for most ovarian carcinoma. Detection of preneoplastic changes in the OSE leading to overt malignancy is important in prevention and management of ovarian cancer. We identified OSE proteins with altered expression derived from women with a family history (FH) of ovarian and/or breast cancer and mutations in the BRCA1 tumor suppressor gene.
Proteome Changes in Ovarian Epithelial Cells Derived from Women with BRCA1 Mutations and Family Histories of Cancer *
Ovarian Cancer Screening

CA-125 is a marker that is elevated in approximately 80% of women with ovarian cancer with sensitivities of 50% in women with stage I disease and 90% in patients with advanced disease,22 However, it can be elevated in many other conditions, including gynecologic etiologies such as endometriosis, uterine fibroids, and pregnancy, and nongynecologic conditions such as gastroenteritis, pancreatitis, cirrhosis, and congestive heart failure.16, 17, 18 As such, the specificity of CA-125 is limited and is not recommended for routine screening purposes in the general population.15
Urine or serum beta human chorionic gonadotropin (ß-hCG) should be obtained in women of reproductive age to rule out pregnancy and pregnancy-related etiologies of adnexal masses.
Other serum markers such as AFP and LDH can be helpful when a germ cell tumor is suspected
CA-125 is a marker that is elevated in approximately 80% of women with ovarian cancer with sensitivities of 50% in women with stage I disease and 90% in patients with advanced disease,22 However, it can be elevated in many other conditions, including gynecologic etiologies such as endometriosis, uterine fibroids, and pregnancy, and nongynecologic conditions such as gastroenteritis, pancreatitis, cirrhosis, and congestive heart failure.16, 17, 18 As such, the specificity of CA-125 is limited and is not recommended for routine screening purposes in the general population.15
Urine or serum beta human chorionic gonadotropin (ß-hCG) should be obtained in women of reproductive age to rule out pregnancy and pregnancy-related etiologies of adnexal masses.
Other serum markers such as AFP and LDH can be helpful when a germ cell tumor is suspected
Imaging StudiesOvarian Carcinoma
The most commonly performed test to evaluate an adnexal mass is transabdominal or transvaginal ultrasonography.5, 6, 7, 23
This test helps demonstrate the presence of the mass and its location (eg, ovarian, uterine, bowel). It also provides the mass size, consistency, and internal architecture. Scoring systems, such as that suggested by DePriest and associates, can then be used to determine the likelihood of a malignant component.24
Hysterosonography (ultrasonography with the presence of fluid in the uterine cavity) may be used to help distinguish between uterine masses and those arising from other pelvic structures.
Color Doppler ultrasonographies can be used to evaluate the resistive index of the mass vessels, which, when low, has been indicative of a malignancy.
Pelvic radiographs are generally not helpful in the evaluation of adnexal masses. A dermoid cyst generally contains areas of calcification that may be picked up on a plain radiograph.
CT scans are most useful for assessing the remainder of the abdomen and pelvis when metastatic disease is suspected. Incidental adnexal masses are sometimes found when CT is performed for evaluation of other conditions. As with ultrasonography, CT scan can help identify the size, location, and relationship to other organs. CT scan is less effective than ultrasonography for determining the internal architecture of these masses.
MRI scans can help characterize adnexal mass characteristics in select cases when ultrasonographic findings are limited.4
Imaging Studies
The most commonly performed test to evaluate an adnexal mass is transabdominal or transvaginal ultrasonography.5, 6, 7, 23
This test helps demonstrate the presence of the mass and its location (eg, ovarian, uterine, bowel). It also provides the mass size, consistency, and internal architecture. Scoring systems, such as that suggested by DePriest and associates, can then be used to determine the likelihood of a malignant component.24
Hysterosonography (ultrasonography with the presence of fluid in the uterine cavity) may be used to help distinguish between uterine masses and those arising from other pelvic structures.
Color Doppler ultrasonographies can be used to evaluate the resistive index of the mass vessels, which, when low, has been indicative of a malignancy.
Pelvic radiographs are generally not helpful in the evaluation of adnexal masses. A dermoid cyst generally contains areas of calcification that may be picked up on a plain radiograph.
CT scans are most useful for assessing the remainder of the abdomen and pelvis when metastatic disease is suspected. Incidental adnexal masses are sometimes found when CT is performed for evaluation of other conditions. As with ultrasonography, CT scan can help identify the size, location, and relationship to other organs. CT scan is less effective than ultrasonography for determining the internal architecture of these masses.
MRI scans can help characterize adnexal mass characteristics in select cases when ultrasonographic findings are limited.4
If a carcinoma has become very advanced and sent seedlings to a number of different sites in a number of different organs or tissues then it can be said to have become 'carcinomatosis'. So if, for example, a primary carcinoma of the breast had just spread to affect one or more of the nearby lymph glands under the arm, this certainly would not be 'carcinomatosis'. But if a breast cancer had become much more advanced and spread to involve lots of areas in, say, the bones, the liver and the lungs, then this could be called 'carcinomatosis'.
Although, strictly speaking, the word carcinomatosis should only be used for epithelial cancers, or carcinomas, it is sometimes used to describe other types of cancer that have spread widely throughout the body.
If a carcinoma has become very advanced and sent seedlings to a number of different sites in a number of different organs or tissues then it can be said to have become 'carcinomatosis'. So if, for example, a primary carcinoma of the breast had just spread to affect one or more of the nearby lymph glands under the arm, this certainly would not be 'carcinomatosis'. But if a breast cancer had become much more advanced and spread to involve lots of areas in, say, the bones, the liver and the lungs, then this could be called 'carcinomatosis'.
Although, strictly speaking, the word carcinomatosis should only be used for epithelial cancers, or carcinomas, it is sometimes used to describe other types of cancer that have spread widely throughout the body.
Surgical Care for Ovarian Cancer:
If the tumor is well differentiated or moderately well differentiated, total abdominal hysterectomy and bilateral salpingo-oophorectomy with omentectomy is adequate for patients with stage IA and stage IB disease. The undersurface of the diaphragm should be visualized and biopsied; pelvic and abdominal peritoneal biopsies and pelvic and para-aortic lymph node biopsies are required and peritoneal washings should be obtained routinely.[1] In selected patients who desire childbearing and have grade I tumors, unilateral salpingo-oophorectomy may be associated with a low risk of recurrence.[2]
Prognosis in ovarian cancer is influenced by several factors, but multivariate analyses suggest that the most important favorable factors include:[17-21]
Younger age.
Good performance status.
Cell type other than mucinous and clear cell.
Lower stage.
Well-differentiated tumor.
Smaller disease volume prior to any surgical debulking.
Absence of ascites.
Smaller residual tumor following primary cytoreductive surgery.

For patients with stage I disease, the most important prognostic factor is grade, followed by dense adherence and large-volume ascites.[22] DNA flow cytometric analysis of stage I and stage IIA patients may identify a group of high-risk patients.[23] Patients with clear cell histology appear to have a worse prognosis.[24] Patients with a significant component of transitional cell carcinoma appear to have a better prognosis.[25]
If the tumor is well differentiated or moderately well differentiated, total abdominal hysterectomy and bilateral salpingo-oophorectomy with omentectomy is adequate for patients with stage IA and stage IB disease. The undersurface of the diaphragm should be visualized and biopsied; pelvic and abdominal peritoneal biopsies and pelvic and para-aortic lymph node biopsies are required and peritoneal washings should be obtained routinely.[1] In selected patients who desire childbearing and have grade I tumors, unilateral salpingo-oophorectomy may be associated with a low risk of recurrence.[2]
Prognosis in ovarian cancer is influenced by several factors, but multivariate analyses suggest that the most important favorable factors include:[17-21]
Younger age.
Good performance status.
Cell type other than mucinous and clear cell.
Lower stage.
Well-differentiated tumor.
Smaller disease volume prior to any surgical debulking.
Absence of ascites.
Smaller residual tumor following primary cytoreductive surgery.

For patients with stage I disease, the most important prognostic factor is grade, followed by dense adherence and large-volume ascites.[22] DNA flow cytometric analysis of stage I and stage IIA patients may identify a group of high-risk patients.[23] Patients with clear cell histology appear to have a worse prognosis.[24] Patients with a significant component of transitional cell carcinoma appear to have a better prognosis.[25]
Chemotherapy for Ovarian Cancer:

Treatment options:
If the tumor is grade III, densely adherent, or stage IC, the chance of relapse and death from ovarian cancer is as much as 30%.[3-6] Clinical trials evaluating the following treatment approaches have been performed:
Intraperitoneal P-32 or radiation therapy.[1,7,8]
Systemic chemotherapy based on platinums alone or in combination with alkylating agents.[1,7,9-11]
Systemic chemotherapy based on platinums with paclitaxel.

Drug Category: Chemotherapy agents
Cisplatin, carboplatin, and paclitaxel are chemotherapy agents approved for the initial treatment of ovarian cancer. Results from randomized studies have shown that platinum-containing regimens are superior to those that do not contain platinum. In addition, the combination of platinum and paclitaxel is superior to a regimen that does not include paclitaxel.
Treatment options:
If the tumor is grade III, densely adherent, or stage IC, the chance of relapse and death from ovarian cancer is as much as 30%.[3-6] Clinical trials evaluating the following treatment approaches have been performed:
Intraperitoneal P-32 or radiation therapy.[1,7,8]
Systemic chemotherapy based on platinums alone or in combination with alkylating agents.[1,7,9-11]
Systemic chemotherapy based on platinums with paclitaxel.

Drug Category: Chemotherapy agents
Cisplatin, carboplatin, and paclitaxel are chemotherapy agents approved for the initial treatment of ovarian cancer. Results from randomized studies have shown that platinum-containing regimens are superior to those that do not contain platinum. In addition, the combination of platinum and paclitaxel is superior to a regimen that does not include paclitaxel.