PROJECT

Overview of Project 2:
Patient Scenario Assignment
Addresses Learning Outcomes:
• Use knowledge of biological principles and the Scientific Method to ask and answer relevant questions about human health and disease
• Analyze information to distinguish between diseased and healthy structure and functioning.
• Analyze how internal and external factors cause disruption of healthy body function, leading to disease and disorders.
Patient: Mr. Smith is 60 years old. He was diagnosed with prostate cancer five years ago. Over the past few days, Mr. Smith has been feeling increasingly tired and has also been suffering from a headache that did not respond to over-the-counter medications. He scheduled an appointment with his physician.
His physician performed a physical examination and recommended a battery of laboratory tests and imaging procedures.
His blood pressure is 165/100 mmHg. MRI reveals metastasis of prostate cancer to osseous tissue. Abdominal CT shows obstruction of intestine due to nodular enlargement of adrenal glands.
The table below shows Reference values in the right-hand column. These values reflect the normal range of values for patients without disease or illness. The center column reflects the resulting values for medical test results obtained for Mr. Smith.
Take note whether Mr. Smith’s values are within normal limits.
Laboratory results from Mr. Smith’s second hospital admission and medical tests show following findings:
Mr. Smith Reference Values
K+ 2.6 mmol/L 3.8-4.9mmol/L
Hb 7.3 g/dl 13.8 to 18.2 g/dL
Hct 20.4% 45-52%
Platelet Count 20×109/L 150-400×109/L
HCO3 38 mmol/l 22-26 mmol/L
Urinary K+ 70 mmol/L/24 hr 25-120 mmol/L/24 hr
Blood Glucose 460 mg/dl 64.8-104.4 mg/dL
Serum Aldosterone 1 ng/dl <31 ng/dL
24 hour Urinary Aldosterone 8.4 mcg/24 hr 2.3-21.0 mcg/24 hr
Renin 2.1 ng/ml/hr 0.65-5.0 ng/ml/hr
ACTH (Adrenocorticotropic Hormone) 1082 pg/ml 9-46 pg/ml
Cortisol 155.5 microg/dL 0-25 microg/dL
CONCLUSION AND DIAGNOSIS
Laboratory findings, MRI and CT confirmed metastatic prostate adenocarcinoma, hypertension and refractory hypokalemia due to ectopic ACTH production. High levels of circulating cortisol caused continuous activation of mineralocorticoid receptors resulting in hypokalemia, metabolic alkalosis and hypertension.
After reading provided scenario, answer the following questions:
1. What are the components of physical examination? Describe each component. (See Module 1, Topic B, Part B.2)
2. Mr. Smith’s blood pressure was 160/100 mmHg.
a. How does a medical provider take or measure blood pressure?
b. What do the top (numerator) and bottom (denominator) numbers mean in the biological sense?
c. What is the significance the size of these two numbers?
d. Is Mr. Smith’s blood pressure within normal range? Explain how you concluded whether Mr. Smith’s blood pressure is/is not within normal range.
e. Discuss the possible health issues anticipated for a person with a blood pressure of 165/100 mm Hg.
3. Based on the data provided, what laboratory tests were performed and what samples were taken from the patient? Select one of the laboratory tests ordered for Mr. Smith and discuss why Mr. Smith’s physician might have ordered the test and the information she might have expected to obtain from that particular test.
4. Value analysis.
a. Compare Mr. Smith’s values with reference values and indicate whether Mr. Smith’s values are below, above, or within normal range (compare Mr. Smith’s values with the Reference values) for each laboratory tests in the table above from the second set of tests.
b. Select one of the values outside of normal range from the table above and discuss possible medical concerns related to the identified change in Mr. Smith’s values.
5. What imaging procedures did Mr. Smith undergo? Discuss the distinctions and similarities between the two different imaging approaches. What were the results of imaging procedures in Mr. Smith’s case?
Guidelines:
•?????????You should answer all five questions concisely and complete all parts of each question.
•?????????Clearly number each question answer 1-5.
•?????????Do not provide original question in your submitted document.
•?????????Submit your completed answers as a document (.doc, .docx, .rtf, or .txt only) into your assignment folder. Your grade will depend upon the content, clarity and originality of responses written in your own words. Good writing practices, including the use of correct grammar, sentence and paragraph structure, and punctuation, and presence of logical reasoning, will account for a portion of your grade.
•?????????Use in text citations as needed using APA format within your answer text.
•?????????Provide full citations in APA format at the end of the assignment.
Grading: Your grade for the Patient Scenario assignment will be based on the following components:
1. Answered all five questions and all sub-parts of each question—up to 18 points
2. Student provides original, detailed responses, written in student’s own words, showing presence of logical reasoning – up to 24 points
3. Student provides correct or logical answers to each question—up to 42 points
4. Student incorporates terms and concepts learned from assigned materials – up to 8 points
5. Student correctly cites resources in APA format – up to 4 points
6. Form – grammar, spelling, style – up to 4 points

HELPFUL HINTS.

How Do Cancerous Cells Differ from Healthy Cells?
Precancerous and cancerous cells differ in their shapes and sizes when compared to healthy cells of the same tissue. Moreover, the size and shape are inconsistent from one cancer cell to another. Well-differentiated cancerous cells will resemble the original tissue, whereas poorly differentiated cells will look quite different from the tissue of origin. Other distinguishing characteristics of cancerous cells are
• atypical shapes and sizes of nuclei
• multiple nuclei per cell
• hyperchromatic (chromatin consists of DNA and associated proteins that stain excessively) nuclei
• missing stroma (supportive framework of cells, tissues, and organs)
• increased irregular mitosis (process of cell division that results in the production of two genetically identical cells from one parent cell)
2. What Causes Cancer?
The answer to this question is not as simple as it may seem from the information available from mass media. Cancer is a multifactorial disease where not just one, but several factors contribute to the changes in the cell from normal to cancerous. The interplay of internal and external factors including viruses, the activation of cancer-promoting and the inhibition of cancer-suppressing genes, exposure to chemical substances and radiation, and inherited predispositions for some types of cancer all contribute to the changes in a cell leading to a cancer.
Both DNA and RNA viruses play a role in the etiology (study of causes, for example, causes of disorders) of cancer. Examples of DNA viruses associated with cancer are Human papillomavirus (HPV) and Epstein-Barr virus. HPV is associated with cervical cancer and Epstein-Barr virus with cancer of the nose and throat. Human immunodeficiency virus (HIV), an RNA virus, has been linked to Kaposi’s sarcoma.
Cigarette smoke is probably the most discussed carcinogen that is associated with an increased risk of lung cancer. However, other chemicals have also been linked to cancer. Exposure to asbestos is associated with lung cancer, excessive intake of alcohol is linked to esophageal cancer, and a low-fiber diet plays a role in the development of colon cancer. Overall, nearly half of the cancers are related to smoking and diet (Lipsky, n.d.). Excessive sun exposure is associated with accelerated aging of the skin and also with skin cancer.
3. What Is the Role of Oncogenes in Cancer Development?
Most cells in the body divide on a regular basis. Each division requires replication of the original DNA. Therefore, alteration in a single cell’s DNA may lead to an uncontrolled division and ultimately to a cancer. The cell’s division and growth are under genetic control. Proto-oncogenes are genes necessary for proper replication, transcription, and cell growth. A proto-oncogene (a normal gene that has the potential to turn into an oncogene) can turn into an oncogene (a gene that can make a normal cell become cancerous) by insertion of a retroviral promoter, translocation of a chromosome (part of a broken chromosome attaches to a different chromosome), point mutation (a single nucleotide base substitution), or gene amplification (production of multiple copies of a single gene). Other genes that play a role in carcinogenesis are tumor-suppressor genes. Gene alteration can cause tumor-suppressor gene inactivation (see Figure 1.6) (Schneider, 1993).
Figure 1.6
Function of Normal and Mutated Tumor-Suppressor Genes

Source: Gray-Mitsumune, M. (2002). Genetic basis of cancer. Retrieved 26 March, 2009, from Geocities Web site: http://www.geocities.com/madokagm/BIOL1551/lecture_notes_Nov_29.htm
Furthermore, DNA repair genes can also be damaged by mutations, inherited or acquired. These mutations may lead to an accumulation of ineffective products and may participate in the development of cancer (see Figure 1.7). In Figure 1.7, move your mouse over the green words to see more information.
Figure 1.7
Etiology and Pathogenesis of Cancer

Based on Lipsky, M. M. (n.d.). Carcinogenesis. Retrieved March 28, 2009, from University of Maryland Web site: http://aquaticpath.umd.edu/appliedtox/module7.html, section 6, p. 3 of pdf file
Malignant tumors are grouped together based on the tissue of origin. Two of the most prevalent malignancies are carcinomas and sarcomas (see Table 1.5).
Table 1.5
Common Malignancies with Tissues of Origin and Examples
Name of the Malignancy Tissue of Origin Example
Carcinoma (most common type of cancer) Epithelial tissue
Squamous
Adenomatous (glandular)
Transitional • Skin cancer
• Adenocarcinoma of the lung
• Bladder cancer
Sarcoma Connective tissue
Bone
Muscle
Fat
Blood • Bone cancer (osteosarcoma)
• Myosarcoma
• Liposarcoma
• Leukemia
4. Tumor Grading and Staging
Like schoolchildren, tumors are graded. However, unlike schoolchildren, who want to get the highest numbers of points, in the case of tumors lower numbers are better for treatment and prognosis. Tumors are graded based on biopsy results. In histopathological analysis (microscopic analysis of tissue searching for microscopic, disease-related changes in the tissue) of tissue samples from the tumor, the degree of cellular differentiation and the resemblance of the samples to the original tissue are evaluated under the microscope. Well-differentiated tumors have lower scores (1 and 2) and thus a better prognosis.
Tumors are also staged to determine how far the cancer has advanced, what treatment plan is appropriate, and what the prognosis is. Staging assesses the tumor’s location, the level of infiltration of surrounding tissue, the involvement of the lymph nodes, and the presence of metastases. A TNM system is used for tumor staging. T stands for the primary tumor. Tis indicates tumor in situ, or a cancer localized to its area of origin. T1 through T4 indicate the size of the primary tumor; the smaller the number, the smaller the tumor. N stands for a node, and N0 means no evidence of cancer presence in regional nodes. N1 through N3 indicate the presence of cancer in the regional node. N4 indicates cancer in the nearby regional nodes. M stands for distant metastasis of the tumor. If M0 is assigned to a tumor, it means that there is no sign of metastases. M1 indicates the presence of metastases.
5. How Is Cancer Treated?
Depending on the type and the stage of the tumor, the following therapeutic options are available:
• surgical procedures
• chemotherapeutic drugs
• radiation therapy
• hormonal therapy
• immunotherapy
• bone marrow transplant
6. Can We Prevent Cancer?
Yes and no. We can definitely take preventative steps to decrease our risk for developing a cancer, but we cannot eliminate all risk factors from varied causes of cancer. Moreover, cancer has a definite genetic component.
Prevention involves changes in biological and environmental factors and screening. Everyone can make lifestyle changes aimed at prevention. For example, you can quit smoking, eat more dietary fiber, and decrease your exposure to the sun. Commonly used cancer screening methods are the Pap test for cervical cancer, mammography for breast cancer, fecal occult blood test and colonoscopy for colorectal cancer, and the prostate-specific antigen (PSA) test for prostate cancer.
As we mentioned, cancer has a strong genetic component. Therefore, awareness of your family history can suggest whether you might be at increased risk for certain types of cancer such as breast, ovarian, and colon cancers. Knowledge of your family history allows you to keep a watchful eye for early symptoms of cancer.
Often it is the patient who makes the biggest difference between early and late detections of cancer. It literally pays to pay attention to nonspecific symptoms such as indigestion, long-lasting cough, skin lesions that are not healing, visible changes in warts or moles, the presence of a lump, and unusual bleeding or discharge (Martini, 2000).
Assessment 1.8: Human Tissue Types

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