Podcast Presentation about 2 Diabetes and Cancer Patients
Question 1: your patient/client has malignant tumour that metastasised. Your patient has a friend, named Alex who has been diagnosed with abnormal growth also, but Alex doctor tells them their tumour is benign and localised. Explain the underline terms, and explain what this means for your patient and for their friend, Alex.
As we know that if the tumour tis benign it won’t be able to enter nearby tissue or other parts of body, and it can be removed by surgery and the tumour is less worrisome unless it is pressing other nerves or tissue (Samah, Fauzi & Mansor, 2017), in Alex case surgery can be supportive in removing the tumours before it became malignant. On other hand, Neil (my patient) has malignant tumour that means it made of cancer cells and it can enter nearby tissue, metastasised means that cancer can spread to other part of the body, this type of cells can grow rapidly, they have abnormal chromosome and DNA characterised by dark large nuclei, and can spread by blood stream carry risk of recurring after the removal. Malignant tumour can secrete substances that cause weight loss and fatigue (Reshi, Amin, Jeelani & Rasheed, 2019), therefore aggressive treatment like surgery, immunotherapy, chemotherapy, etc. require urgently.
Question 2: choose two factors that could be contributing to development and/or accelerate the growth of cancer in your patient/client (one genetic mutation and one hormonal factor). Explain how these factors contribute to cancer development in your person/client. (i.e., the pathophysiology). Hint. You may find it useful to refer to the regulation of the cell cycle and control of cell division/growth.
Inherited mutations of the BRCA 1 and BRCA2 genes are related to an increased prostate cancer risk in men (Pestell, 2019). Not many cases of prostate cancer are not linked to inherited/mutated gene, the cancer related with somatic mutation take place only in certain cells in the prostate. On other hand, hormonal factor such as obesity and substance abuse might be the reason contributing to development/accelerate growth of cancer. Hormone changes due to obesity changes the local profile of immune cells, for instance, macrophages and myeloid-derived suppressor cells in prostate cancer, and tumour related B cells, and neutrophils, B cells may stimulate prostate cancer due to obesity (Lin et al., 2017).
Question 3: some of clinical manifestations of cancer include:
- Increased risk of infection
Choose one clinical manifestation from group A and one clinical manifestation from group Band relate them to the underlying pathophysiology for your patient/client.
Clinical manifestation from group A
Cachexia: cachexia is a metabolic syndrome that cause overall weight, muscle and fat loss, inflammation, insulin resistance and poor appetite. The cachexia is very prevalent in patient about 60% in prostate cancer. Earlier, cachexia was defined as a unintentional weight loss or body mass index of <20>
Clinical manifestation from group B
Anaemia: patient with advanced prostate cancer may suffer from Anaemia that is caused by several factors such as nutritional decline, androgen deprivation, treatment related toxity, inflammation, and bone marrow infiltration (Wu et al., 2020). Symptoms caused by Anaemia are fatigue, dyspnoea, etc. Castration is a known cause of anaemia, as testosterone is essential for the development of erythropoietin creation in the kidney and also for the centre action of erythropoiesis but after castration, red blood cell mass decreases 10%, red blood cell diameter decreases 40%, and osmotic fragility increases (Wu et al., 2020).
Question 4: the following treatments are used in the management of neoplastic growths:
Active surveillance (watch and wait)
Describe one non-pharmacological and one pharmacological approach from the table above, and explain why they are beneficial in management of neoplastic growths. You should also discuss whether they are appropriate treatments for your person/client given they have metastasised and malignant tumour.
Radiation therapy: this treatment involve use of high energy x rays and other types of radiation to keep the cancer cells from growing (Shipley et al., 2017), in Neil case as the tumour malignant and carry risk of spreading in other part of organ this approach will be beneficial in managing the condition. There are different type of radiation therapy. External radiation therapy use machine to send radiation toward the cancer from outside the body. Hypofractionated radiation therapy is a treatment in which dose of radiation is larger than usual dose given in the day (Litwin & Tan, 2017). Radiopharmaceutical therapy uses a radioactive substance to treat cancer if it is spread in bone. This is appropriate treatment for the patient as patient (Neil) has increased risk of spreading the cancer in other part of the body.
Hormone therapy: this therapy used in removing hormones or blocking the action to hinder/stop the cancer cells from growing (Mckenna, 2017), this is appropriate treatment considering the Neil condition of malignant tumour that is metastasised. As hormones are made by glands and circulated in the blood stream, in prostate cancer blocking the hormones might be supportive in treating the patient condition. Hormone therapy for prostate cancer comprise abiraterone acetate to stop prostate cancer cells from making androgens, Antiandrogens to block action of androgens, drugs to prevent adrenal glands from making androgens, and Orchiectomy that involves surgery of removing both testicles (James et al., 2017).
Anker, M. S., Holcomb, R., Muscaritoli, M., von Haehling, S., Haverkamp, W., Jatoi, A., & Anker, S. D. (2019). Orphan disease status of cancer cachexia in the USA and in the European Union: a systematic review. Journal of cachexia, sarcopenia and muscle, 10(1), 22-34.
James, N. D., de Bono, J. S., Spears, M. R., Clarke, N. W., Mason, M. D., Dearnaley, D. P., ... & Matheson, D. (2017). Abiraterone for prostate cancer not previously treated with hormone therapy. New England Journal of Medicine, 377(4), 338-351.
Lin, D., Ettinger, S. L., Qu, S., Xue, H., Nabavi, N., Choi, S. Y. C., & Fleshner, N. (2017). Metabolic heterogeneity signature of primary treatment-naive prostate cancer. Oncotarget, 8(16), 25928.
Litwin, M. S., & Tan, H. J. (2017). The diagnosis and treatment of prostate cancer: a review. Jama, 317(24), 2532-2542.
Mckenna, D. (2017). Improving Hormone Therapy for Prostate Cancer. Oncology News, 12(2), 47-49.
Pestell, R. (2019, September). Extending genetic portraits of human prostate cancer. In 7th International Pacific Rim (PacRim) Breast and Prostate Cancer Meeting (Vol. 1). BioScientifica.
Reshi, R., Amin, J., Jeelani, T., & Rasheed, R. (2019). Benign and Malignant Tumors of Parotid Gland: A Retrospective Two Year Study. Journal of Current Medical Research and Opinion, 2(06), 180-183.
Samah, A. A., Fauzi, M. F. A., & Mansor, S. (2017, September). Classification of benign and malignant tumors in histopathology images. In 2017 IEEE International Conference on Signal and Image Processing Applications (ICSIPA) (pp. 102-106). IEEE.
Shipley, W. U., Seiferheld, W., Lukka, H. R., Major, P. P., Heney, N. M., Grignon, D. J., ... & Pisansky, T. M. (2017). Radiation with or without antiandrogen therapy in recurrent prostate cancer. New England Journal of Medicine, 376(5), 417-428.
Wu, F. J., Li, I. H., Chien, W. C., Shih, J. H., Lin, Y. C., Chuang, C. M., ... & Kao, L. T. (2020). Androgen deprivation therapy and the risk of iron-deficiency anaemia among patients with prostate cancer: a population-based cohort study. BMJ open, 10(3), e034202.