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Case Study: Abby DuthlerLemmen-Holton Cancer Pavilion02.25.2016RIT 495.01Presenting Signs and Symptoms This patient is a 64-year-old Caucasian female. She has a history of irregular periods and infertility. She has never had radiation therapy before. She has a history of hypertension. She has asthma, diabetes, hypothyroidism, history of gallstones, history of irritable colon. She underwent menarche at 13-years-old, and she underwent menopause at 50-years-old. She has used hormone replacement therapy for 10 years. She has never used alcohol or smoked. She is obese, though she has lost weight due to a change in diet within the last year. She has a sister that had thyroid cancer, a maternal aunt that had colon cancer, and a paternal aunt that had some sort of cancer, possibly colon cancer. She has not had her period in years, and she started having vaginal bleeding for about 4 months with worsening pelvic pain. Epidemiology About 52,000 women develop gynecologic cancer in the US every year. The leading gynecologic cancer in developing countries is endometrial cancer. In 2008, 288,800 women were diagnosed with uterine cancer worldwide. There are more than 600,000 survivors with about 8,600 deaths. In developed countries, uterine cancer was the most common gynecologic malignancy. The most common age range of developing endometrial cancer is 50-69 years old. Caucasian women are more likely to develop endometrial cancer while African American women are more likely to die from endometrial cancer (Chen & Berek, 2015).EtiologyThere are many factors that increase a woman’s chance of developing a endometrial cancer. These include hormone imbalance, hormone therapy, birth control pills, higher number of menstrual cycles, pregnancy, obesity, Tamoxifen, polycystic ovarian syndrome, age, diet and exercise, diabetes, family history, breast or ovarian cancer, prior pelvic radiation therapy, and endometrial hyperplasia. A woman’s hormone balance is a key component to whether or not she will develop endometrial cancer. This has to do with two main female hormones: estrogen and progesterone. When the balance tips towards more estrogen, a woman is at higher risk of developing uterine cancer. This is the reason why estrogen therapy for menopause, some birth control pills, no pregnancies, obesity, more total menstrual cycles in a lifetime, Tamoxifen for breast cancer, Polycystic ovarian syndrome, ovarian tumors that create estrogen, and breast cancer are risk factors for endometrial cancers. The risk of endometrial cancer increases with age. A high-fat diet can be a risk factor for uterine cancer. Endometrial cancer is about 4 times more common in women with diabetes. Uterine cancer is genetic and runs in families. These genes also tend to cause colon cancer. Radiation increases chances of cancer. Endometrial hyperplasia is an increased growth of the endometrium and has a chance of becoming a cancer if it is categorized as atypical (American Cancer Society, 2014). Compare Patient to Typical This patient is a pretty typical patient that would develop endometrial cancer. She is 64-years-old, so within the 50-69 age range. She has been taking hormone therapy drugs for 10 years, most likely due to obesity and menopause. She has had a poor diet for most of her life, thus making her obese, and diabetic. She also has a family history of cancer, specifically colon cancer. The genes that cause colon cancer are linked to the genes that cause endometrial cancer. Her irregular periods throughout her lifetime were probably due to hormone imbalances. This is another cause of endometrial cancer. Patient Work-up InformationDateProcedureResults11/10/2015Presented with unusual vaginal bleeding and underwent endometrial biopsyThe pathology showed grade 1 endometrial adenocarcinoma with mucinous features12/09/2015Robotic total abdominal hysterectomy and salpingo-oopherectomyMeasured 3x2cm. No myometrial invasion. Cervix was not involved. No angiolymphatic invasion. Pelvic lymph nodes were all negative for metastatic disease. Staged as 1A. 12/29/2015ConsultationDiscussed post-op radiation therapyAnatomy Endometrial cancer is found in the uterus. The uterus is in the pelvis of a woman, and it is where babies grow before being born. The uterine wall is made up of three layers. In order from deep to superficial, they are endometrium, myometrium, and perimetrium. The endometrium is the layer that is shed every month during a woman’s period. The myometrium is the layer that is muscle used for contractions. The perimetrium is the outer thin layer that holds it all (see figure 1). On either side of the uterus are an ovary and a fallopian tube (see figure 1). The ovaries store the eggs, and the fallopian tubes are a pathway for the eggs into the uterus. The bottom of the uterus into the vagina is called the cervix (see figure 1). This is what helps hold the baby in until it is ready to be born. In front of the uterus is the bladder that holds urine (see figure 2). Behind the uterus are the rectum and some bowel that contains waste from the body (see figure 2). The bones of the pelvis area are the pelvic bone, the head of the femur, sacrum and coccyx, and the lumbar vertebrae. The pelvic bone is the main bone that contains the organs of the pelvis. The femoral head is the part of the femur that fits into the pelvic bone at the acetabulum and creates the hip joint. The sacrum and coccyx create the posterior border of the pelvis. The lumbar vertebrae are superior of the sacrum (see figure 3). The blood vessels of the pelvis are the descending aorta, inferior vena cava, left and right ovarian veins and arteries, left and right common iliac arteries and veins, left and right internal and external iliac veins and arteries. The descending aorta brings blood from the heart to the lower body while the inferior vena cava brings blood from the lower body to the heart. The left and right ovarian arteries bring blood from the aorta to the reproductive organs while the right and left ovarian veins bring blood from the reproductive organs to the inferior vena cava. The left and right common iliac blood vessels bring blood to and from the hips. The left and right internal iliac blood vessels bring blood to and from the pelvis. The left and right external iliac blood vessels bring blood to and from the legs (see figure 4) (O'Loughlin, 2012). Lymphatic DrainageThe lymphatic drainage of the pelvis follows the blood vessels of the pelvis. There are the paraaortic lymph nodes, the left and right common iliac lymph nodes, and the left and right external and internal iliac lymph nodes. The paraaortics follow the aorta, the common iliac nodes follow the common iliacs, and the external and internal iliac nodes follow the external and internal iliacs (see figure 5) (O'Loughlin, 2012).Anatomy GraphicsFigure 1 2 3 4 5 Pathological examination is key to the diagnosis of endometrial cancer. About 80% of all endometrial carcinomas are of the endometrioid type. Endometrioid refers to the endometrial-type glands of varying differentiation that can easily be recognized with a microscope. Squamous differentiation is common in endometrioid carcinoma. An endometrioid carcinoma with a malignant squamous component is referred to as adenocarcinoma. Most endometrioid carcinomas arise from endometrial hyperplasia. Serous and clear-cell carcinomas are two kinds of endometrial cancers that are not endometrioid. Both are considered high grade simply by definition. Serous carcinoma is the most aggressive type of endometrial cancer. Serous cancer is diagnosed by the presence of papillae covered by highly pleomorphic tumor cells. Clear-cell carcinoma is another nonendometrioid endometrial cancer. This is categorized by the epithelium of the endometrial surface and underlying glands replace by pleomorphic tumor cells (Amant, Moerman, Neven, & Timmerman, 2005). The endometrium undergoes modification in specialized cells in response to fluctuations of estrogen and progesterone during the menstrual cycle. Long-lasting estrogen exposure leads to endometrial hyperplasia, which increases the chances of developing atypical hyperplasia and endometrial cancer (Amant et. al., 2005).StagingUterine cancers use a staging system called TNM. The “T” stands for tumor size and can range from small (T1) to large (T4). The “N” stands for lymph nodes involved and can range from none (N0) to many (N2). The “M” stands for if it has metastasized and can range from it has not metastasized (M0) to it has metastasized (M1). For uterine cancers, each category is specific. The T categories are Tis through T4. Tis is for a carcinoma that is preinvasive. T1 is for a tumor that is confined to the corpus uteri to a tumor that invades the myometrium. T2 is for a tumor that invades stromal connective tissue of the cervix without extending beyond the uterus. T3 is for a tumor that involves serosa and/or adnexa or a tumor that has vaginal or parametrial involvement. T4 is for a tumor that has invaded the bladder or bowel mucosa. The N categories range from N0 to N3. N0 is for a tumor that has not spread to the nearby lymph nodes. N1 is for tumors that have spread to regional pelvic lymph nodes. N2 is for a tumor that has spread to paraaorticc lymph nodes. The M categories range from M0 to M1. M0 is for a tumor that has not spread to distant organs. M1 is for a tumor that has spread to distant organs (Greene & American Joint Committee on Cancer, 2002). The stages range from 0 to IV. The relation of stage and the TNM system can be seen in the following chart (Greene & American Joint Committee on Cancer, 2002):Stage 0TisN0M0Stage IT1N0M0Stage IIT2N0M0Stage IIIT3T1-T3T1-T3N0N1N2M0M0M0Stage IVT4T anyN anyN anyM0M1Another staging system that is used for endometrial cancer is called the International Federation of Gynecology and Obstetrics Staging (FIGO). The following table shows the FIGO system:StageDescriptionITumor confined to uterine corpusIANo or less than half myometrial invasionIBInvasion to or in more than half of the myometriumIITumor invades the cervical stroma but doesn’t extend beyond the uterusIIILocal or regional spread of the tumorIIIATumor invades the serosa and/or adnexaeIIIBVaginal or parametrial involvementIIICMetastases to the pelvic and/or paraaortic lymph nodesIIIC1Positive pelvic nodesIIIC2Positive paraaortic lymph nodes with or without positive pelvic nodesIVTumor invades bladder or bowel mucosa or distant metastasesIVATumor invasion of bladder and/or bowel mucosaIVBDistant metastasis, including intraabdominal metastases and/or inguinal lymph nodes(Sorosky, 2012).GradingEndometrial carcinoma uses a four-grade system. This system ranges from GX to G4. GX is for tumors that the grade cannot be assessed. G1 is for tumors that are well differentiated. Well differentiated means that the cancer cells look more like normal tissue. G2 is tumors that are moderately differentiated. G3 is for tumors that are poorly differentiated. G4 is for tumors that are undifferentiated. Undifferentiated means that the cancer cells look nothing like normal tissue. Undifferentiated tumors tend to grow more rapidly than well differentiated tumors (Greene & American Joint Committee on Cancer, 2002). Patient’s Pathology, Stage, and GradeThis patient’s tumor is FIGO stage 1A (T1N0M0), grade 1 endometrial adenocarcinoma of the uterus. FIGO stage 1A means that her tumor invaded less than half of the myometrium. T1 meaning that her tumor has not spread beyond the corpus uteri. N0 meaning that no lymph nodes were involved. M0 meaning that her cancer had not spread. Grade 1 means that her cancer is well differentiated, or that is has cells that look similar to normal cells and are mostly predictable. Adenocarcinoma refers to tumors that have a malignant squamous component. Treatment Plan and PrescriptionThis patient has the following prescription:LocationTreatment VolumeTotal Dose (cGy)ModalityFxPxDose/fx (cGy)Isodose (%)UterusPTV3000Brachytherapy51/4days600100Treatment Information and Set-up The patient was placed on the treatment table supine, with her head towards the machine. A pillow was placed under her head. Her hands held on to a ring on her chest. Her legs were straight with her feet banded. Reference tattoos were placed on the patient’s lateral sides and one on her anterior side to line up to the laser system in the simulation room. Photographs of her marks were taken and placed in her chart. Treatment Type and DeliveryTypeSizeBlocksBBsLocationIntracavitary (Vaginal Cylinder)3.0 cm24Above symphysisComplications and Side EffectsThe patient did not experience any side effects aside from a bit of fatigue. Rest was recommended for the patient in order to help with the fatigue. Adjuvant TherapiesFor uterine cancers, a few adjuvant therapies may be used. These include surgery, chemotherapy, and hormone therapy. Surgery can be used to biopsy and/or remove part or the entire organ. The main kind of surgery for uterine cancer is a hysterectomy, which is the removal of the uterus and cervix. This is typically done with a bilateral salpingo-oophorectomy, which is the removal of the ovaries and fallopian tubes. Lymph node dissection of the pelvic and para-aortic lymph nodes is also done to determine the stage of disease. Possible side effects from surgery may include infertility and possibly lymphedema. Lymphedema is a build up of fluid in the legs typically caused by lymph node dissection followed by radiation (American Cancer Society, 2015). Chemotherapy is the chemical treatment of a disease. This can either be through IVs or prescribed pills. Some side effects of chemotherapy could include loss of appetite, fatigue, hair loss, increased chance of getting sick, nausea and vomiting. Loss of appetite may be treated by setting routine meal times, drinking more water, and eating high calorie foods. Fatigue may be treated by eating enough, letting others help, and getting enough rest. Hair loss cannot be treated, but a wig or scarf can help cover it up. Increased chance of sickness can be treated by washing hands well, staying away from germs, and trying not to get cuts. Nausea and vomiting can be treated with anti-nausea medicine (Chemotherapy Side Effects Sheet, 2012). Hormone therapy is also used in treating endometrial cancers. The main hormone treatment used for endometrial cancer uses progesterone-like drugs called progestins. Other less common treatments use tamoxifen, gonadotropin-releasing hormone agonists, and aromatase inhibitors. All of these drugs are used to target hormones within the body to treat cancer (American Cancer Society, 2015). Patient’s Adjuvant TherapiesThis patient had surgery along with her radiation therapy. The surgery that she underwent was a robotic abdominal hysterectomy with a bilateral salpingo-oophorectomy. This means that she had her uterus, cervix, ovaries, and fallopian tubes removed. Critical Structures and TolerancesOrganTD 5/5 (cGy)InjuryBladder6000ContractureCartilage & Bone6000Necrosis, FractureArteries and veins>8000sclerosisLymph Nodes5000Atrophy, sclerosisMuscle6000FibrosisOvary200-300SterilizationSkin5500Acute and Chronic DermatitisRectum6000Ulcer, StrictureUterus7500StrictureIntestine4500Ulcer, perforation, hemorrhageSpinal Cord4500Infarction, NecrosisVagina9000Ulcer, fistulationKidney1500Acute and chronic nephrosclerosis(Washington & Leaver, 2010)Routes of Spread Endometrial cancer spreads locally, then through direct extension, then to lymphatics, then to distant sites. To spread locally, the tumor must spread to the endometrium and other layers of the uterus. To spread by direct extension, the tumor must spread to other organs nearby such as ovaries, fallopian tubes, cervix, and vagina. To spread by lymphatics, the tumor must spread to the lymph nodes of the pelvis and paraaortics. Finally, to spread to distant sites, the tumor must spread to distant organs, most likely to the lungs, liver, bones, and brain (Sorosky, 2012).Prognosis and Survival The most important prognosis factors are the FIGO stage, differentiation grade, and histological type. Most of these are independent of each other. The FIGO stage reflects the 5-year survival, which can vary but is about 85% for stage 1, 75% for stage 2, 45% for stage 3, and 25% for stage 4. The differentiation grade is considered when looking at a stage I disease and ranges from over 95% for a low-grade (1 or 2) to 42% for a high-grade (3 or 4) disease. Non-endometrioid endometrial cancers such as serous and clear-cell carcinomas make up about 10% of all endometrial cancers but account for about 50% of recurrences and deaths from endometrial cancer. Therefore, these cancers would have a low prognosis (Amant et. al.,2005).Patient Prognosis and Survival This patient’s prognosis is most likely high. This is due to her FIGO stage 1 with a 5-year survival rate of 85%, her low grade with a 95% 5-year survival, and her common histologic cancer type. Her 5-year survival is most likely 92%..SourcesAmant, F., Moerman, P., Neven, P., Timmerman, D., & al, e. (2005). Endometrial cancer.?The Lancet,?366(9484), 491-505. Retrieved from Cancer Society. (2014, February 20). In?American Cancer Society. Retrieved January 23, 2015, from Side Effects Sheets. (2012, December 10). Retrieved January 29, 2015, from , L., & Berek, J. (2015, January 26). Endometrial Carcinoma: Epidemiology and Risk Factors.?UpTDate. Retrieved from , F. L., & American Joint Committee on Cancer. (2002).?AJCC cancer staging manual. New York: Springer.O'Loughlin, M. (2012).?Human Anatomy?(International ed., Vol. Third, pp. 118-139, 440-512). New York City: McGraw-Hill.Sorosky, J. (2012, August). Endometrial Cancer.?Obstetrics & Gynecology,?120(2), 383-397. Retrieved from , CM & Leaver, D. (2010). Principles and practices of radiation therapy. (3rd ed.). St. Louis, MO: Mosby Publishers. ................
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