You must prepare answers to these questions along with references. Anything taken from a paper in a journal, a text, etc. must include a citation. e.g. Jones and Jones (1972) reported that ......... or It has been shown that ........ (Smith and Smith 1980).
BIO 5333-51 ADVANCED PATHOPHYSIOLOGY Midterm Exam, Spring 2019 DIRECTIONS: 1. BEFORE YOU START: Begin by consulting the Exam Information Page (under “Offline Component Information”), paying special attention to the “How to’s,” “Meditations . . .” and the FAQ’s. You may find valuable suggestions and answers to many questions about writing essay exams. Please feel free to e-mail me any questions. 2. WHAT TO ANSWER: Please be prepared to write one essay on each of the four units below (A, B, C and D). Note that you have a choice of 2 questions within each unit. Please label your choices clearly (e.g., A1, B2, etc.). Total number of questions to be answered: 4 (25 points each). Be sure to label each page with a header or foot with your name and page number. 3. GENERAL APPROACH: Keep in mind that this is a PATHOPHYSIOLOGY course, and frame your answers in this context (i.e., try to avoid issues such as “patient considerations,” “nursing implications,” and “need for further nursing research. . .”). The course’s required textbook is a good starting point, but I expect you to go WAAAAAAY beyond it. . . Use the literature. There is new information on all of these topics. 4. FORMAT: Please keep each essay to NO MORE THAN ONE SINGLE-SPACED PAGE (maximum), not including the bibliography list. Consulted references list may appear at the end of each essay (preferably), or they could be placed as a total list at the end of the exam (in the latter case, please identify the answer to which the references apply). Please DO NOT USE fonts smaller than 11pts. 5. REFERENCES: In answer to the age-old question . . . you should use as many references as it takes to answer your questions; this is a matter of quality and appropriateness, not quantities. References must be recent, say, within the last 10 years. When you using electronic references, the Websites must be specific to the subject discussed. In other words, if your answer is on asthma, don’t cite the URL address of the National Lung Association; the article you consulted and whose URL you are providing has to be specific to asthma. This site you use must have a URL address where I can retrieve it and see where you got your information (http:// www., etc.). When you use Google (highly recommended), be sure to call for Google Scholar, to reach the best and reliable scholar publications. Stay away from generic information (Merck Manual), and sources aimed at patient education. Be careful in quoting from the WWW. There is a lot of junk out there . . . A. PULMONARY DISEASE CASE STUDY: A 45-year-old white female is rushed to the OR because of shock due to postoperative (cholecystectomy) bleeding; during intubation she vomits and aspirates that day’s breakfast. Physical examination: tachycardia, tachypnea, fever, hypotension; central cyanosis; warm, moist skin; intercostal retraction; inspiratory crepitant rales heard over both lung fields. ABGs: severe hypoxemia no improvement with 100% O2. Imaging: alveolar filling process suggestive of non-cardiogenic pulmonary edema. Pathology: hyaline membranes; pulmonary edema; widespread atelectasis; stiff lung. Micropathology: endothelial and alveolocapillary damage with edema, hyaline membrane formation, and inflammatory infiltrate; loss of surfactant. QA1. Based on the above information, and on additional material researched, suggest a possible diagnosis for this condition, and DISCUSS, at the cellular level, the pathogenesis of this common and often fatal disease that is usually triggered by an inflammatory reaction. QA2. COMPARE and CONTRAST the pathophysiology of the adult and infantile variants of this disease. Please EXPLAIN how a reduction in alveolar radius enhances the deleterious effect of surface tension in hyaline membrane disease of prematurity. (Hint: Laplace’s law . . .) B. CARDIOVASCULAR SYSTEM DISORDERS: HEART DISEASE CASE STUDY: A 63-year-old overweight male came to the EC clutching his chest. The patient is diaphoretic and pale. When questioned, the man stated that his chest pain is dull, radiating down his left arm, and started without physical activity. He has had some palpitation the past week. His father died at age 55 from a myocardial infarction. He works as a stock broker. He admits no physical activity due to his high stress job. He smokes at least one pack of cigarettes a day and was recently diagnoses with diabetes mellitus. Since he and his wife divorced 3 years ago, he has lived off take-out, because he is not a good cook. He denies any nausea. His heart rate is 103, BP 142/93, and he is having difficulty breathing. His LDL is 168 and his total cholesterol is 140. The patient has elevated CK, CK-MB and troponin. A 12 lead EKG reveals some abnormalities. The patient was taken to the cath lab, which reveal coronary artery blockage. (Source: M.C., MSN). QB1. Based on the above information, and on additional material researched, DISCUSS the pathophysiology of myocardial cell death, and EXPLORE the concept of apoptosis. QB2. Based on the above information, and on additional material researched, DISCUSS the pathophysiology of atherosclerosis, and EXPLORE the inflammatory mechanisms involved in plaque rupture and coronary obstruction. Please distinguish between stable and unstable (vulnerable) plaque. C. RENAL DISEASE CASE STUDY: The patient is a 36-year-old female pharmacist who presents to the clinic complaining of bilateral flank pain increasing in severity over the past 3 days, with periods of worse pain. She reports urine output of one episode a day and the urine has a pink tinge to it. She is having some intermittent nausea associated with the episodes of worse pain. She also reports being more tired with episodes of SOB for the past 5 days. Past medical history reveals that she was seen at this office and treated for a streptococcal pharyngitis one month ago. She finished a course of Amoxicillin 20 days ago. The patient lives with her husband of 12 years and their 8-year-old daughter. She reports being sexually active and monogamous; no tobacco use; drinks alcohol at the rate of 1 to 2 beers or glasses of wine per week; no history of illicit drug use. Family history indicates that both her parents are living. Her father (age 59) has a history of HTN, and her mother (age 58) has a history of HTN and rheumatoid arthritis (x 2 years). Laboratory and diagnostic findings: Urinalysis reveals (normal values in parenthesis): Appearance: clear (clear), pink (light yellow) urine. Specific gravity: 1.003 (1.005-1.030); pH: 4.5 (4.5-8.0). The following results are negative (i.e., within normal ranges): ketones, glucose, protein (4+), bilirubin, leukocyte esterase, and nitrite. BUN: 41 (8-20); creatinine: 1.4 (0.7-1.4); albumin: 2.1 (3.1-5.0). Renal ultrasound shows enlarged kidneys. CXR shows mild pulmonary edema in posterior lobes. Differential diagnoses: Glomerulonephritis; renal stones; nephritic syndrome; acute renal failure; chronic renal failure. (Source: M.E., MSN) QC1: Based on the above information, and on additional material researched, suggest a possible diagnosis for this condition, and JUSTIFY your opinion by explaining the pathophysiology of the chosen disease process. If the patient had systemic lupus erythematosus, EXPLAIN (in detail) how it can cause rapidly progressive glomerulonephritis. QC2: Imagine that this patient is 66 years old, and DISCUSS what physiological changes could have occurred to glomerular function, renal tubule function, and alterations in the Renal-Angiotensin-Aldosterone-System (RAAS) as a result of the aging process. D. THYROID DISEASE CASE STUDY: Ms G. is a 32‑year‑old social worker who was brought to the emergency room in a state of cardiovascular and neuromuscular hyperactivity, following a family crisis that resulted in an episode of acute stress. Clinical assessment revealed severe agitation, heat intolerance with excessive perspiration, tachycardia and palpitations. She had a fixed, wide eye gaze, with bilateral lid retraction, and ophthalmoplegia. She was diagnosed as experiencing a thyroid storm as a result of poorly controlled hyperthyroidism. Her ocular manifestations are consistent with Graves’ disease. Past History: Ms G.'s symptoms began 3 months ago and have increased in severity since that time. She has lost 26 pounds, despite increased appetite and adequate nutrition. During a previous visit to the endocrinology service, Ms G. reported finding herself in a constant state of restlessness and increased physical activity. Because of this, and as a result of the ensuing fatigue, she has been experiencing difficulty in falling asleep in the evenings, and in remaining sound asleep during the night. She complained of being very irritable all the time, with her heart racing and pounding during those episodes, and even during rest periods. Ms G. also complained of being constantly hot, even in cool rooms. She noticed that the collars on her clothing seem too tight and that her vision often seems blurred. Although she has always had a history of regular menses, she has not had a period in 2 months. Current Status: Ms G. is a thin, pale woman, who appeared anxious as she waited to be examined. Her eyes have a bulging, staring appearance, with decreased eye movement. A mass can be seen on the anterior aspect of her neck. Her skin is smooth, warm, and moist. She is sweating profusely, in spite of a room temperature set at 70 degrees Fahrenheit. At admission Ms G. weighed 102 lbs, a loss of 26 lbs from her normal weight. Her hair is very fine and soft. Her vital signs are as follows: oral temperature, 99 degrees F; heart rate, 120 at rest; respiratory rate, 20; BP, 110/50. Laboratory results: triiodothyronine (T3), 160 mg/dl; thyroxine (T4), 20 mg/dl; cholesterol, 50 mg/dl. Radioactive iodine uptake was increased (40% uptake in 6 hrs). After appropriate treatment, Ms G. was discharged to the endocrine service for management of her hyperthyroidism and follow-up. QD1: Based on the above information, and on additional material researched, DISCUSS (in detail) the pathophysiology of hyperthyroidism, EMPHASIZING the connection between immunity and Graves’ disease. QD2: DISCUSS (in detail) the concept