MSN570 Week 2 Case Studies
A 47-year-old female presents with Stage IV breast cancer.
Today, the PET scan reveals brain metastasis.
1. Define proliferation and differentiation and relate these
changes to cancer.
2. Describe invasion, angiogenesis and metastasis.
3. There are three underlying causes of growth and maturity
abnormalities: telomerase, pRB changes and 53 changes.
Ace my homework – Write my paper – Online assignment help tutors – Discuss these in relation to the patient.
4. Ace my homework – Write my paper – Online assignment help tutors – Discuss tumor suppressor genes, oncogenes and DNA
repair genes.
A 30-year-old presents with a history of IV drug use, HIV +, and is
today diagnosed with pneumonia.
1. Does the patient have an acute or chronic state of
inflammation? Explain the rationale.
2. What is the significance of cellular replication in a patient
with HIV?
3. What is viral load and what is the relationship with CD4 T
cells?
4. How did the pneumonia occur?
A 25-year-old male presents with chronic sinusitis and allergic
rhinitis.
1. Define innate vs. acquired immunity.
2. Define active vs. passive immunity.
3. Ace my homework – Write my paper – Online assignment help tutors – Discuss the genetic predisposition of allergens.
4. Describe the antigen-antibody response.
5. What is the pathology of sinusitis?
A 40-year-old has an endometrial biopsy report: benign
endometrial hyperplasia.
1. Explain the diagnosis.
2. Which cells are implicated in this diagnosis? Compare and
contrast atrophy vs. hyperplasia.
3. How does dysplasia differ from hyperplasia?
4. Does hyperplasia lead to neoplasia? Defend your answer. Ace my homework – Write my paper – Online assignment help tutors – Discussion Prompt
Part 1: Choose a condition from the following case studies: (Week 2 Case Study Details). You may work in small groups of up to 3 students if desired.
Part 2: Select two different students/topics and discuss the condition encompassing clinical experiences and critique the post.
_______________________________
Case Study 1: A 47-year-old female presents with Stage IV breast cancer. Today, the PET scan reveals brain metastasis.
Proliferation and differentiation play crucial roles in the development and progression of cancer. Proliferation refers to the uncontrolled and excessive growth of cells, leading to the formation of a tumor. Differentiation, on the other hand, refers to the process by which cells mature and acquire specific functions. In cancer, these processes become disrupted. Cancer cells lose their ability to differentiate into specialized cell types and continue to proliferate uncontrollably, resulting in the formation of malignant tumors.
Invasion, angiogenesis, and metastasis are key processes involved in the spread of cancer. Invasion refers to the ability of cancer cells to invade surrounding tissues by breaking through the normal tissue barriers. Angiogenesis is the formation of new blood vessels to supply nutrients and oxygen to the growing tumor. Metastasis occurs when cancer cells break away from the primary tumor, travel through the bloodstream or lymphatic system, and establish secondary tumors in distant organs or tissues.
The patient’s condition may be influenced by the underlying causes of growth and maturity abnormalities. Telomerase is an enzyme that maintains the length of telomeres, which are protective caps at the ends of chromosomes. Changes in telomerase activity can contribute to uncontrolled cell proliferation seen in cancer. Alterations in the pRB (retinoblastoma) gene can disrupt cell cycle regulation and lead to abnormal cell growth. Changes in the p53 gene, a tumor suppressor gene, can impair DNA repair mechanisms and promote the survival and proliferation of damaged cells, increasing the risk of cancer development.
Tumor suppressor genes are involved in regulating cell growth and preventing the formation of tumors. Mutations or inactivation of these genes can result in the loss of their tumor-suppressing function, allowing uncontrolled cell growth and increased cancer risk. Oncogenes, on the other hand, are genes that have the potential to cause cancer. Activating mutations or overexpression of oncogenes can drive cell proliferation and contribute to the development of cancer. DNA repair genes are responsible for maintaining the integrity of the genome by fixing DNA damage. Mutations in these genes can impair DNA repair mechanisms, leading to an accumulation of genetic abnormalities and an increased risk of cancer.
Part 2: I will discuss the condition of the 40-year-old with benign endometrial hyperplasia and the 30-year-old with pneumonia.
Regarding the 40-year-old with benign endometrial hyperplasia:
The diagnosis of benign endometrial hyperplasia indicates an abnormal increase in the number of cells in the endometrium (the inner lining of the uterus). It is considered benign because the cells are still relatively normal in appearance and have not acquired the ability to invade nearby tissues or metastasize.
The cells implicated in this diagnosis are the endometrial cells. Atrophy refers to the shrinkage or decrease in size of cells or tissues, while hyperplasia refers to an increase in the number of cells. In atrophy, there is a loss of cells, whereas in hyperplasia, there is an overgrowth of cells.
Dysplasia is a term used to describe the abnormal growth and development of cells that may progress to cancer if not treated. It is characterized by cellular changes that are more severe than hyperplasia but not as severe as cancer.
Hyperplasia itself does not necessarily lead to neoplasia (the formation of a new, abnormal growth). However, if the underlying causes of hyperplasia, such as hormonal imbalances or genetic mutations, persist or worsen, it can increase the risk of neoplastic changes and the development of cancer. Regular monitoring and appropriate management are important to prevent progression to malignancy.
As for the 30-year-old with pneumonia, I will leave that discussion open for another student to contribute.
