Portage Learning Pathophysiology NURS 231/BIOD 331 Module 2 Exam All Versions Latest, Exams of Pathophysiology

Download Portage Learning Pathophysiology NURS 231/BIOD 331 Module 2 Exam All Versions Latest and more Exams Pathophysiology in PDF only on Docsity! All Versions Of Exam 2 Categorized By Question Types 2024-2025 NURS 231/BIOD 231 Pathophysiology Portage Learning. Question Type Breakdown ➢ True and false: ➢ Matching, multiple choice and short answer: ➢ Clinical questions: Only questions are provided for clinical questions as examinees are strongly encouraged to answer them in their own words. All the Best! True And False: Cell differentiation is the process of increasing cell numbers by mitotic cell division. False Cell proliferation is the process of increasing cell numbers by mitotic cell division. True Blood tests for tumor markers can make a diagnosis of cancer. Why or why not? False, only tissue can diagnose. Tumor markers are helpful to assess response to therapy or reoccurrence. Matching Multiple Choice And Short Answer: What are two important properties that stem cells possess? potency and self-renewal Which of the following are risk factors for developing cancer? Select all that apply. Hbv, Alcohol, High intake of smoked meats What are molecular and cellular mechanisms in genes that increase susceptibility to cancer? Select all that apply. Lack of cellular senescence, Angiogenesis, Mutations in growth factor signaling pathways Malignant tumors have which of the following characteristics? Select all that apply. Variable rate of growth, Spreads by metastasis Which of the following are most likely to have arisen from an adult stem cell? epithelial (they are constantly being replaced) What is the most important procedure in diagnosing the correct cancer and histology? tissue biopsy All of the following viral agents are correctly paired with the associated lesion except: know the following pairings: HPV & genital warts, cervical cancer EBV & lymphoma, nasopharyngeal cancer Hep B: hepatocellular carcinoma HHV-8 & Kaposi sarcoma Clinical questions: Only questions are provided for clinical questions as examinees are strongly encouraged to answer them in their own words. Explain the TNM system: T is the size and local spread of the primary tumor. N is the involvement of the regional lymph nodes. M is the extent of the metastatic involvement. 1. List two signs or symptoms a patient may present with that might indicate a cancer diagnosis: S+S: Bleeding; sore that doesn't heal; fluid in the pleural, pericardial, or peritoneal spaces; chest pain, shortness of breath, cough, abdominal discomfort or swelling. Other possible answers can include a mass or lump, pain (need to be specific), fatigue, fevers, weight loss 2. What are two systemic manifestations of cancer exhibited by cancer patients? Systemic: Weight loss, wasting of body fat and muscle tissue, weakness, anorexia, and anemia, fatigue, sleep disturbances 1. What are the three possible goals of cancer treatment? Curative, control, palliative 2. How does radiation kill cancer cells? Genetic instability is a hallmark of many cancers, as the accumulation of genetic errors can lead to uncontrolled cell growth, evasion of apoptosis (programmed cell death), and other malignant traits. Does Genetic Instability Increase or Decrease with Cancer? Increase: Genetic instability increases with cancer. As cancer progresses, cells acquire more mutations that promote uncontrolled growth, metastasis, and resistance to treatments. The instability in the genome provides the raw material for the evolution of cancerous traits, making it a central factor in tumor development and heterogeneity. 3. Growth Factor Independence, Definition of Cell-Density-Dependent Inhibition: Cell-density-dependent inhibition (also known as contact inhibition) is a regulatory mechanism that prevents cells from dividing once they reach a certain population density. In normal tissues, when cells become too crowded, signals are triggered that stop cell division. This mechanism helps maintain tissue organization and prevents excessive growth. In healthy cells, this inhibition plays a critical role in limiting growth and maintaining the architecture of tissues by stopping cells from proliferating when they come into contact with neighboring cells. Does Cell-Density-Dependent Inhibition Increase or Decrease with Cancer? Decrease: In cancer, cell-density-dependent inhibition decreases or is lost entirely. Cancer cells often do not respond to the usual growth-inhibitory signals caused by crowding, allowing them to continue dividing even when packed closely together. This uncontrolled growth contributes to the formation of tumors and the disruption of normal tissue structure. Loss of this regulatory mechanism is a key feature of cancerous transformation. 4. Cell-Density-Dependent Inhibition, Cell-Density-Dependent Inhibition (also called contact inhibition) is a phenomenon where normal cells stop proliferating (growing or dividing) when they become crowded and come into contact with each other. This process is a regulatory mechanism that ensures that cells do not overgrow and that tissue remains properly structured. It is part of the body's normal control of cell division. Relationship with Cancer: In cancer, cell-density-dependent inhibition decreases or is lost. Cancer cells do not respond to the usual signals to stop dividing when they come into contact with other cells, which allows them to continue growing uncontrollably. This contributes to tumor formation, as the cells no longer obey the normal regulatory mechanisms that limit growth. Thus, cancer cells exhibit a loss of density-dependent inhibition, which leads to unchecked cell proliferation. 5. Cell Cohesion And Adhesion, Cell Cohesion and Adhesion refer to the ability of cells to stick together and to the extracellular matrix (ECM), playing a crucial role in maintaining the structural integrity and proper functioning of tissues. Cell Cohesion: The tendency of similar cells within a tissue to stick together. This helps maintain the structural organization and proper function of tissues. Cell Adhesion: The attachment of a cell to neighboring cells or the extracellular matrix via specialized molecules, such as cadherins, integrins, and other adhesion proteins. Relationship with Cancer: In cancer, cell cohesion and adhesion generally decrease. Cancer cells often lose their ability to stick to each other and to their surrounding tissue. This loss of adhesion allows cancer cells to become more mobile, leading to: Invasion: The ability of cancer cells to spread into surrounding tissues. Metastasis: The ability of cancer cells to detach from the primary tumor and spread to distant organs through the bloodstream or lymphatic system. The reduction in cell adhesion is a hallmark of epithelial-to-mesenchymal transition (EMT), a process critical for cancer metastasis. 6. Anchorage Dependence, Anchorage Dependence refers to the requirement of normal cells to attach to a solid surface (like the extracellular matrix) to grow, divide, and survive. This attachment triggers signals that allow the cell to proceed through the cell cycle and perform its functions. Relationship with Cancer: Decrease with Cancer: Cancer cells typically lose anchorage dependence, meaning they can grow and divide without needing to attach to a solid surface. This is one of the hallmarks of cancer, allowing cancer cells to proliferate uncontrollably and metastasize (spread to other parts of the body). This loss of anchorage dependence enables cancer cells to survive in the bloodstream or other non-adherent environments. 7. Cell-To-Cell Communication, Cell-to-Cell Communication refers to the processes by which cells send and receive signals to coordinate their activities. This can occur through direct contact (e.g., gap junctions), chemical signals (e.g., hormones, neurotransmitters), or other forms of signaling (e.g., autocrine, paracrine, or endocrine signaling). Proper communication is crucial for maintaining tissue homeostasis, growth regulation, and immune responses. Relationship with Cancer: Decrease with Cancer: In many cancers, cell-to-cell communication decreases or becomes dysfunctional. This impairment allows cancer cells to evade normal regulatory signals that control growth and apoptosis (programmed cell death). For example: Reduced gap junction communication: Cancer cells often lose direct communication channels with neighboring cells, enabling them to grow independently of normal tissue control. Altered signaling pathways: Cancer cells may alter signaling molecules, receptors, or downstream pathways, leading to unchecked growth or survival signals. This disruption of communication contributes to tumor progression, invasion, and the ability of cancer cells to avoid immune detection. 8. Life Span, Life Span (Cellular Life Span) refers to the number of divisions or the duration a normal cell can undergo before it stops dividing and enters senescence (a state of permanent growth arrest) or undergoes apoptosis (programmed cell death). Normal cells have a limited life span due to mechanisms like telomere shortening, which acts as a biological clock for cell division. Relationship with Cancer: Increase with Cancer: In cancer cells, the cellular life span often increases abnormally. Cancer cells gain the ability to bypass normal limits on cell division, allowing them to divide indefinitely. This is mainly due to: Telomerase activation: Cancer cells often reactivate or upregulate the enzyme telomerase, which extends telomeres (protective ends of chromosomes), allowing them to evade the normal limits on cell division. Avoidance of apoptosis: Cancer cells often avoid programmed cell death, allowing them to survive much longer than normal cells. This increase in cellular life span is one of the hallmarks of cancer and contributes to tumor growth and persistence. 9. Antigen Expression, Antigen Expression refers to the presence of specific proteins (antigens) on the surface of cells. These proteins can be part of normal cellular processes or can be associated with disease states, including cancer. In the context of cancer: Tumor Antigens: These are proteins that are expressed at higher levels on cancer cells compared to normal cells. Their expression often increases with cancer as they are produced or upregulated due to the malignancy. Tumor-Specific Antigens (TSAs): These are unique to cancer cells and not present on normal cells. Their expression is usually increased with cancer as they are specifically associated with tumor cells. Tumor-Associated Antigens (TAAs): These are proteins that are present in both cancerous and normal cells but are expressed at higher levels or in abnormal forms in cancer cells. Their expression generally increases in the context of cancer.