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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.
- 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
- 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
- What are the three possible goals of cancer treatment? Curative, control, palliative
- How does radiation kill cancer cells?
(3) Yearly low-dose chest CT. List 4 of the 7 risk factors linked to cancer as stated in the module. Heredity, Hormonal factors, Obesity, immunologic mechanisms, Environmental agents such as chemicals, radiation, and cancer-causing viruses. List three characteristics of cancer cells and briefly explain what it means: *know definitions of the following, and whether they increase or decrease with cancer: *
- Anaplasia, Anaplasia refers to the loss of cell differentiation and organization, which is a hallmark of cancerous (malignant) cells. In normal cells, there is a structured growth pattern and cells retain specialized functions. However, in anaplastic cells: They become undifferentiated. They lose the characteristics and functions of their original tissue. They often display abnormal shapes, sizes, and organization. Anaplasia is typically associated with aggressive cancers and signifies that the cells have lost control over their growth and division processes. Does Anaplasia Increase or Decrease with Cancer? Anaplasia increases with cancer, particularly with more aggressive and advanced malignancies. The higher the level of anaplasia, the more poorly differentiated the cells are, which generally correlates with a worse prognosis. Highly anaplastic tumors are often resistant to treatment and can grow and spread rapidly.
- Genetic Instability, Definition of Genetic Instability: Genetic instability refers to an increased tendency of an organism's genetic material (DNA) to acquire mutations. This instability can involve various types of genetic alterations, including: Point mutations: Changes in a single base pair in the DNA sequence. Chromosomal rearrangements: Structural changes in chromosomes such as deletions, duplications, inversions, or translocations. Aneuploidy: Abnormal numbers of chromosomes.
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.
- 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.
- 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.
- Cell Cohesion And Adhesion,
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.
- 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.
- 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.
In summary, antigen expression related to cancer usually increases as the tumor develops, due to the production of new antigens or the upregulation of existing ones.
- Enzyme/Hormone Production, Enzyme/Hormone Production refers to the synthesis and release of specific biological molecules that play roles in various physiological processes. In the context of cancer: Enzyme Production: Cancer-related Enzymes: Some cancers can lead to the increased production of certain enzymes that are either involved in tumor growth, metastasis, or are a result of the cancerous process. For example, matrix metalloproteinases (MMPs) can be upregulated in cancer to help tumors invade surrounding tissues. Generally, the production of such enzymes increases with cancer. Normal Enzymes: In contrast, the production of some normal enzymes might decrease if their expression is suppressed by the cancer or if the cancer disrupts normal cellular functions. Hormone Production: Cancer-related Hormones: Certain cancers, such as hormone-secreting tumors, can lead to increased production of specific hormones. For instance, some tumors of the adrenal gland can increase cortisol production, while certain breast cancers might increase estrogen levels. Normal Hormones: In some cases, the production of normal hormones can decrease if the cancer affects the organs that produce them. For example, cancers that affect the thyroid gland can lead to reduced production of thyroid hormones. Overall, whether enzyme or hormone production increases or decreases with cancer can depend on the specific type of cancer and the roles of the enzymes or hormones in question
- Cytoskeletal Changes Cytoskeletal Changes refer to alterations in the network of protein filaments and tubules that provide structural support to cells, including microfilaments, intermediate filaments, and microtubules. In the context of cancer: Microfilaments: These are composed mainly of actin. In cancer cells, changes in the organization and dynamics of microfilaments can lead to increased cell motility and invasiveness. For example, actin filaments may become more dynamic, which can enhance the cancer cell's ability to move and invade surrounding tissues. Typically, the reorganization and activity of microfilaments increase with cancer progression. Intermediate Filaments: These provide structural stability to cells. In cancer, intermediate filament proteins such as keratins and vimentin may be aberrantly expressed or redistributed. For instance, epithelial cancers often show altered keratin expression patterns, which can decrease cell-cell adhesion and contribute to cancer metastasis. Changes in the expression of intermediate filaments are often associated with cancer and can increase in terms of dysregulation.
