Discussion w11-12 652

Q-1

Testicular cancer

Pathology – Testicular cancer is a heterogeneous disease that occurs during or after puberty (Pyle & Nathanson, 2016). Most testicular cancers are germ cell tumors from the sperm and can be classified into two subtypes: seminomas, which are the most common, and nonseminomas, the more aggressive type.

Etiology - The cause of testicular cancer is unknown, but incidences are higher by genetics, typically, among close male relatives. It is the most common malignancy affecting males between the ages of 15-35.

Risk factors – Non-modifiable risk factors include gender, ages 15-35, family history, and genetic disorders including Klinefelter syndrome and Down syndrome (Pyle & Nathanson, 2016). Cancers can be caused by changes in chromosomes that turn off tumor suppressor genes which slow down cell division or turn on oncogenes which help cells grow and divide. Most testicular cancer cells have extra copies of a part of chromosome 12 which may be a contributing factor (Pyle & Nathanson, 2016). Men with a history of cryptorchidism and prior orchiopexy are also at increased risk. Some studies show a mild association between risk of testicular cancer and high intake of saturated fat, dietary cholesterol, and dairy products. Additionally, regular use of marijuana may increase the risk about twofold.

Signs/symptoms – Testicular tumors typically present as a nodule or swelling of one testicle that is typically painless. Male patients will report a dull ache or a heavy sensation in the lower abdomen, perianal area, or scrotum (Bjelaković et al., 2020). If it is metastatic, symptoms may vary depending on the site including neck mass, cough, or dyspnea related to pulmonary metastasis, anorexia, nausea, vomiting, and/or bone pain. Additionally, gynecomastia may occur due to a systemic endocrine manifestation of testicular germ cell tumors (Bjelaković et al., 2020). A testicular examination is essential as abnormalities of firm, hard, or fixed areas within the tunica albuginea should be considered suspicious. Testicular tumors are ovoid and may spread to the epididymis or spermatic cord.

Diagnostics – A physical examination is essential, in which both testicles should be examined and compared for size, tenderness, symmetry, and presence of nodules. A scrotal ultrasound is the gold standard for diagnosis, which is a rapid and reliable technique for suspected testicular tumor, as well as, to exclude hydrocele or epididymitis (Bjelaković et al., 2020). Radiographic testing and serum tumor markers, such as beta-human chorionic gonadotropin and alpha-fetoprotein, are helpful to determine the histologic type and extent of the disease. A CT is recommended if the metastatic disease involves the chest/peritoneum.

Treatment – Regardless of staging, radical orchiectomy is done initially. If cancer has spread, treatments including radiation or chemo should be considered.

 

References 

Bjelaković, M. D., Vlajković, S., Bjelaković, G., & Antić, M. (2020). Testicular cancer stem cell hypothesis - diagnostic and therapeutic implications. Vojnosanitetski Pregled: Military Medical & Pharmaceutical Journal of Serbia, 77(11), 1210–1215. https://doi.org/10.2298/VSP170821197D

Pyle, L. C., & Nathanson, K. L. (2016). Genetic changes associated with testicular cancer susceptibility. Seminars in Oncology, 43(5), 575–581. https://doi.org/10.1053/j.seminoncol.2016.08.004

Q-2

Acute Myeloid Leukemia (AML)

Acute myeloid leukemia the most common form of cancer in adults. As mentioned by (Tamamyan et al., 2017), the average age at diagnosis is 70. The disease is seen as more common in males than females, and prevalence is higher in withes than blacks. Treatment of the disease has progressed significantly. This was confirmed by (Tamamyan et al., 2017) wherein they mentioned that back in 1964, long-term survival was less than 5% and currently is nearing 30–40%.

Etiology: According to (Domino, 2020) the exact cause remains unknown, but there are many risk factors in developing the disease.

Modifiable and Nonmodifiable risk factors: There are many predisposing risk factors. Some may be adjustable such as environmental and lifestyle factors. Unfortunately, some are nonmodifiable such as genetic and blood disorders. As mentioned by (Tamamyan et al., 2017), the risk factors are genetic factors: Down's syndrome and Klinefelter syndrome. Environmental factors and lifestyle: smoking alcohol use, tobacco use, and pesticide exposure. Drugs: Alkylating agents, chloramphenicol, and chloroquine. Antecedent blood disorders: myelodysplastic syndrome, aplastic anemia, and polycythemia vera. As stated by (Tamamyan et al., 2017), there is a noteworthy connection between tobacco smoking and AML.

Pathology: AML is a diversified and complex disease. (Tamamyan et al., 2017) explain the characteristics as a proliferation of immature, abnormal blast cells and impaired production of normal blood cells that are out of control. (Domino, 2020) add that these cells are unable to advance into more mature elements. This, in turn, progresses to bone marrow failure.

Pertinent signs and symptoms: The signs and symptomatology are not specific to the disease, but further workup will pinpoint towards the diagnosis. According to (Tamamyan et al., 2017), clinical manifestation is mainly related to pancytopenia and blast proliferation. A list of common signs and symptoms would include generalized weakness, fatigue, fever, easy bruising, bleeding, organomegaly (hepatomegaly and splenomegaly), and lymphadenopathy, dizziness, blurred vision, headache, and infections with difficulty clearing the same.

Diagnostics: The diagnosis process per (Tamamyan et al., 2017) is primarily dependent on bone marrow aspiration with the identification of 20% or more myeloid blasts in the bone marrow and/or peripheral blood. Initial testing, according to (Domino, 2020) would include a CBC that would identify abnormal RBCs, neutrophils, and platelets, ESR, LDH, and uric acid, which may be elevated. COAG’s profile may be normal, but in DIC will be prolonged. Imaging of the abdomen, such as ultrasound or CT scan, may elicit organomegaly. Confirmation of the disease is performed through bone marrow aspiration and biopsy. In agreement with (Domino, 2020) confirmations studies will show hypercellular bone marrow with effaced architecture and a blast count of 20% or more.

Treatment regimens to include both pharmacological and non-pharmacological: An oncologist will guide appropriate management of the disease. (Domino, 2020) asserts that the basis of the treatment is chemotherapy. (Ferri, 2021) summarizes the treatment by mentioning that immediate therapy will be offered to those presenting with Acute Promyelocytic Leukemia (APML) to correct metabolic, infectious, or hyperleukocytosis emergencies. Those without APML will begin with induction therapy to gain remission, defined as a blast count of <5% in the bone marrow, absolute neutrophil count of >1000/mcl, platelet count >100,000/mcl, and transfusion freedom. Consolidation therapies consist of intensive chemotherapy or stem cell transplantation with the intent to prevent relapses. Non-pharmacological management would include bone marrow transplantation. This is intended for high-risk patients, and as previously mentioned, stem cell transplantation to prevent relapses.

Nutritional approaches: As acknowledged by (Stauder et al., 2020), when patients with oncologic disease have co-existing malnutrition, the prognosis is poor, as it negatively affects their quality of life. The treatment plan may require modification which often leads to poor treatment outcomes and increased adverse events. With this said, (Domino, 2020) advises that each patient must maintain a balanced diet with adequate calorie and vitamin intake. If needs be, the patient may be started on total parenteral nutrition for aggressive support.

References

Domino, F. J. (2020). The 5-minute clinical consult (R. A. Baldor, J. Golding, & M. B. Stephens, Eds.; 28th ed.). Wolters Kluwer.

Ferri, F. F. (2021). Ferri's clinical advisor 2021: 5 books in 1 (1st ed.). Elsevier.

Stauder, R., Augschoell, J., Hamaker, M. E., & Koinig, K. A. (2020). Malnutrition in older patients with hematological malignancies at initial diagnosis – association with impairments in health status, systemic inflammation and adverse outcome. HemaSphere, 4(1), e332. Retrieved May 12, 2021, from  https://doi.org/10.1097/hs9.0000000000000332

Tamamyan, G., Kadia, T., Ravandi, F., Borthakur, G., Cortes, J., Jabbour, E., Daver, N., Ohanian, M., Kantarjian, H., & Konopleva, M. (2017). Frontline treatment of acute myeloid leukemia in adults. Critical Reviews in Oncology/Hematology, 110, 20–34. Retrieved May 12, 2021, from  https://doi.org/10.1016/j.critrevonc.2016.12.004

Q-3

Ovarian cancer (OC) is one of the most common gynecologic cancers that rank 7th among women and has a worse prognosis and highest mortality rate caused by being asymptomatic and secret growth of the tumor, delayed onset of symptoms, and lack of proper screening that results in its diagnosis in advanced stages. Most tumors appear to originate from other gynecological tissues and involve the ovary secondarily and low- and high-grade tumors arising from fallopian tube epithelium and other endometrioid tumors are genetically mutated and aggressive and differ histopathological and molecular subtype (Reid, Permuth, & Sellers, 2017). The majority of OC has an epithelial origin which is more invasive, and others have a non-epithelial origin which is less invasive, and epithelial OC may be mucinous and non-mucinous, non-mucinous are serous, endometrioid and clear cell and unspecified types (Momenimovahed, Tiznobaik, Taheri, & Salehiniya, 2019).

The non-modifiable risk factors are increasing age, locality such as European and Asian countries such as China, India, Singapore, Kazakhstan, and Brunei and in USA & Africa. Other non-modifying risk factors were pelvic inflammatory diseases, chlamydia trachomatis infection of GU tract, endometriosis, and tube ligation led to the upward trend of OC, family history of OC, BRCA mutations, Lynch syndrome (Momenimovahed, Tiznobaik, Taheri, & Salehiniya, 2019). The modifying risk factors were urban life, decreased pregnancy, duration of lactation, oral contraceptive pills, hormone replacement therapy, infertility treatments have a beneficial effect on ovarian cancer, consumption of high cholesterol diet with fewer vegetables, obesity and less physical activity, alcohol caffeine and cigarettes, reduced lactation and low income and low literacy all contributed to risk of OC.

According to Freij et al, (2018), the three highest known symptoms of OC recognized were extreme fatigue, back pain, and persistent pain in the pelvic area. Other general symptoms can be fever, loss of appetite, weight loss, nausea and vomiting, anemia, neutropenia, constipation, urinary frequency, and abdominal distension. Diagnosis of OC is by signs and symptoms and through detection of tumor markers such as CA125 and HE4, PRSS8, FOLR1, KLK6/7, GSTT1, and mi RNAs, and through trans vaginal ultrasonography, CT of abdomen pelvis and MRI, and tissue biopsy with histopathologic studies (Giampaolino et al, 2019). In my history taking going through risk factors, family history and symptoms and clinical examination will guide for my diagnostic tests in the patient. Once there the diagnosis made, a referral to a hematologist, oncologist surgery, and another rehabilitation team will be needed.

Frontline chemotherapy for endometrial OC is a combination of intravenous paclitaxel and carboplatin administered every 3 weeks has remained the standard of care and other alternative therapy intraperitoneal administration of chemotherapy and use of other antiangiogenic agent’s bevacizumab (Marth, Reimer, & Zeimet, 2017), immunotherapy, hormone therapy. Other non-pharmacological treatments are surgical removal of the tumor in combination with radiation and/or with chemotherapy along with nutritional therapy and another form of therapy like holistic healing. Correcting nutritional deficiency is an important part of the therapy to replenish electrolytes, protein, and vitamins and through enteral feeding tubes or TPN. Malnutrition leads to low-performance status, impaired quality of life, unplanned hospital admissions and reduced survival and hence oncologist and clinical nutritionist needs to plan the nutrition therapy and interventions for the success of the cancer therapy (Cotogni et al, 2019)

Reference.

Momenimovahed, Z., Tiznobaik, A., Taheri, S., & Salehiniya, H. (2019). Ovarian cancer in the world: epidemiology and risk factors. International journal of women's health, 11, 287. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6500433/

Reid, B. M., Permuth, J. B., & Sellers, T. A. (2017). Epidemiology of ovarian cancer: A review. Cancer biology & medicine, 14(1), 9. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5365187/

Giampaolino, P., Della Corte, L., Foreste, V., Vitale, S. G., Chiofalo, B., Cianci, S., ... & Bifulco, G. (2019). Unraveling a difficult diagnosis: the tricks for early recognition of ovarian cancer. Minerva medica, 110(4), 279-291. Retrieved from https://europepmc.org/article/med/31081307

Marth, C., Reimer, D., & Zeimet, A. G. (2017). Front-line therapy of advanced epithelial ovarian cancer: standard treatment. Annals of oncology, 28, viii36-viii39. Retrieved from https://www.sciencedirect.com/science/article/pii/S0923753420346615

Freij, M., Al Qadire, M., Khadra, M., ALBashtawy, M., Tuqan, W., Al Faqih, M., ... & Abd El-Razek, A. (2018). Awareness and knowledge of ovarian cancer symptoms and risk factors: A survey of Jordanian women. Clinical nursing research, 27(7), 826-840. Retrieved from https://journals.sagepub.com/doi/abs/10.1177/1054773817704749

Cotogni, P., Pedrazzoli, P., De Waele, E., Aprile, G., Farina, G., Stragliotto, S., ... & Caccialanza, R. (2019). Nutritional therapy in cancer patients receiving chemoradiotherapy: Should we need stronger recommendations to act for improving outcomes?. Journal of Cancer, 10(18), 4318. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691712/