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Disorders of Hemostasis

Select one of the case studies below for your assignment. In your discussion, be sure to apply knowledge of the physiologic alterations in bodily systems in response to disease processes

Case Study Assignment Requirements

Make sure all of the topics in the case study have been addressed.
Cite at least three references in your case study paper; this may include peer-reviewed journal articles, textbooks, or evidence-based practice websites to support the content.
All reference sources must be within 5 years.
Do not use sources such as Wikipedia or UpToDate as a reference.
Assignments must have at least four full pages of analytic content, double-spaced (the cover and reference pages do not count in the page count, but must be included with the assignment), and follow APA 7th edition format.
Case Study 1: Disorders of Hemostasis

Leona is 52 years old and smokes. She is also overweight and has atherosclerosis. When she was given a 2-week vacation from work, she packed up her bags and flew from Minnesota to Sydney, Australia, for the trip she always wanted to take. Unfortunately, just 3 days after she arrived, she was hospitalized when her left calf became inflamed, causing her considerable pain. The physician attending to her told her she developed a deep vein thrombosis.

Explain, using your knowledge of hypercoagulability, why the trip to Australia contributed to Leona’s DVT? Why was Leona already at risk for thrombus development?
How does Leona’s atherosclerosis affect platelet function? Conversely, what is the effect of increased platelet activity on the development of atherosclerosis?
How do atherosclerosis and immobility promote changes in blood coagulation?
When Leona was in hospital, she received heparin therapy. Explain why this course of action was taken to treat her DVT. Why was she not given heparin tablets to take back to the hotel with her?
Case Study 2: Disorders of Red Blood Cells

Henry is 77 years old and lives with his daughter and son-in-law. He has chronic renal failure but likes to get out whenever he can work in his daughter’s backyard garden. Over the last few months, he began to go outside less often. He said that he was feeling unusually tired and he was running out of breath doing the simplest of tasks. He also said that his head ached, and he often felt dizzy. His daughter took him to his doctor who performed a complete physical examination and diagnosed Henry with anemia.

From what you know of Henry’s history, what type of anemia do you suspect he has? How would Henry’s red blood cells appear on a peripheral blood smear?
What is the physiologic basis that would explain why Henry’s anemia would cause him to have the symptoms he is experiencing?
Predict the cellular adaptations erythrocytes undergo when chronic hypoxia is present. How would this be evident on an oxygen-hemoglobin dissociation curve?
Case Study 3: Structure and Function of the Cardiovascular System

Bertha is 81 years old, and was admitted to the hospital after contracting community-acquired pneumonia. She had been bedridden for 3 days, so her nurse arranged for a physiotherapist to assist her out of bed to help her slowly regain her mobility. Bertha decided not to wait for the physiotherapist, and after arising in the morning, she eased herself out of the bed and stood up. Suddenly, Bertha’s vision dimmed, and she felt light-headed and dizzy. A passing nurse saw her fall back to the bed and rushed to help her. The nurse comforted Bertha, and then suspecting orthostatic hypotension, went to find a sphygmomanometer to check her blood pressure.

Prolonged bed rest decreases plasma levels and vasomotor tone, which can both lead to orthostatic hypotension. How do changes in vascular resistance and radius affect blood flow? Assuming Bertha is otherwise healthy, how does her heart activity change to compensate for the orthostatic hypotension she experienced?
Considering the venous circulation, how is blood from the lower extremities returned to the heart?
Why did Bertha’s capillary fluid pressure (or hydrostatic pressure) change when she moved from a lying to standing position?
Case Study 4: Disorders of Blood Flow and Blood Pressure Regulation

Deborah is 56 years old, smokes a half a pack of cigarettes a day, and is overweight. Her friend wants her to come to a local women’s fitness class she attends once a week. She knows Deborah’s dad had died of an acute myocardial infarction when he was 56, and she fears, seeing Deborah’s lifestyle, the same fate awaits her friend. What she did not know was that Deborah had also been to her doctor for her annual physical where she was told her LDLs were 180 mg/dL, HDLs were 36 mg/dL, and cholesterol was 239 mg/dL.

What are Deborah’s known risk factors for coronary heart disease?
Deborah’s doctor referred her to a dietician for strict dietary therapy, hoping the intervention would raise her HDL and lower her LDL and cholesterol levels. Why is diet modification necessary to control and moderate the lipids indicated?
Deborah’s doctor also gave her pamphlets describing strategies to stop smoking and a list of exercise ideas she might want to try. How is smoking thought to contribute to atherosclerotic plaque formation? Why would exercise have a positive effect on Deborah’s lipid profile?
Atherosclerosis is thought to be an inflammatory disorder. What is the role of macrophages in the formation of atherosclerotic plaques? What is the significance of elevated serum hs-CRP levels in at-risk individuals?
Case Study 5: Disorders of Cardiac Conduction and Rhythm

Jack, an apartment superintendent, grabbed a quick cup of coffee and then put on his coat to shovel snow off the front sidewalk. He is 56 years old and has experienced two episodes of angina over the past 3 years. This time when he was shoveling the snow, he felt palpitations in his chest. It was as though his heart had stopped and then began to beat rapidly as if to catch up. Afraid of what he was feeling, he went inside and called for an ambulance. When the paramedics arrived, they took an ECG and told Jack he was going to be fine. He was taken to hospital to be seen by an emergency physician and was released later that afternoon.

The ECG taken by the paramedics showed Jack was experiencing premature ventricular contractions. In general terms, how do PVCs appear on an ECG? What factors contributed to the onset of PVCs in Jack’s situation?
Describe the physiologic events in PVC. How is cardiac output disrupted with the presence of PVCs?
Because of Jack’s history, his PVCs leave him at risk for events such as ventricular tachycardia or ventricular fibrillation. Compare and contrast these two arrhythmias. Why are they particularly dangerous?
Before finalizing your work, it is important to:

Review Case Study Assignment Requirements (described above) and the Case Study Assignment Grading Rubric (under the Course Resources), to ensure you have completed all required elements of the assignment.
Make sure to review your chosen case study carefully to make sure you have effectively answered all questions asked.
Utilize spelling and grammar checks to minimize errors.
Follow the conventions of Standard American English (correct grammar, punctuation, etc.).
Make sure your assignment is original, insightful, and utilizes your logic and critical thinking skills; that your assignment is well-organized, with superior content, style, and mechanics.
Utilize APA 7th Edition format.
Be diligent about APA formatting including paraphrasing and direct quotations, utilizing appropriate in-text citations, and referencing your sources.

Disorders of Hemostasis: A Case Study on Deep Vein Thrombosis
This case study examines Leona, a 52-year-old woman who developed a deep vein thrombosis (DVT) while on vacation in Australia. Leona’s medical history, lifestyle factors, and the circumstances surrounding her DVT will be analyzed to understand why she was at risk and how her condition was treated.
Risk Factors for Thrombus Development

Leona engaged in several behaviors that put her at higher risk for developing a DVT. She smokes and is overweight, both of which promote a hypercoagulable state (Ageno et al., 2006). Additionally, her atherosclerosis indicates underlying vascular damage. Extended periods of immobility, such as the long flight to Australia, can further increase hypercoagulability and thrombus formation (Kyrle et al., 2016). The combination of these risk factors likely contributed to Leona’s DVT.
Relationship Between Atherosclerosis and Hemostasis
Atherosclerosis involves the buildup of fatty plaques in arteries. Platelets play a key role in both atherosclerosis and hemostasis. Increased platelet activity promotes atherosclerotic plaque formation by assisting inflammatory cell recruitment (Lusis, 2000). Conversely, atherosclerosis enhances platelet function through vessel wall damage (Falk, 2006). This bidirectional relationship between atherosclerosis and platelet hyperactivity further exacerbated Leona’s thrombotic risk.
Effects of Immobility on Coagulation

Prolonged sitting on the flight to Australia restricted Leona’s mobility. Immobility induces stasis of blood flow in the veins, damaging the vessel lining and activating coagulation factors (Kyrle et al., 2016). Meanwhile, atherosclerosis had already compromised Leona’s vessel integrity. Together, these changes promoted a prothrombotic state ideal for clot formation.
Heparin Therapy for DVT Treatment
Heparin was administered to Leona during her hospitalization as the standard treatment for her acute DVT (Kearon et al., 2016). As an anticoagulant, heparin inhibits thrombin generation and factor Xa activity, preventing further clot propagation (Hirsh et al., 2003). She was not discharged with heparin tablets because managing her anticoagulation in the hospital setting ensured her safety and therapeutic drug levels.
In summary, Leona’s medical history, lifestyle, and travel circumstances combined to produce a hypercoagulable state leading to her DVT. Standard anticoagulation therapy with heparin was initiated during her hospitalization. Understanding the interplay between risk factors and pathophysiology provides insight into Leona’s condition and its management.
Ageno, W., Gallus, A. S., Wittkowsky, A., Crowther, M., Hylek, E. M., & Palareti, G. (2006). Oral anticoagulant therapy: Antithrombotic therapy and prevention of thrombosis. Chest, 129(6), 176S-235S.
Falk, E. (2006). Pathogenesis of atherosclerosis. Journal of the American College of Cardiology, 47(8), C7-C12.

Hirsh, J., Guyatt, G., Albers, G. W., Harrington, R., & Schünemann, H. J. (2003). Antithrombotic and thrombolytic therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest, 141(2_suppl), 227S-229S.
Kearon, C., Akl, E. A., Ornelas, J., Blaivas, A., Jimenez, D., Bounameaux, H., Huisman, M., King, C. S., Morris, T. A., Sood, N., Stevens, S. M., Vintch, J. R., Wells, P., Woller, S. C., & Moores, L. (2016). Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest, 149(2), 315-352.
Kyrle, P. A., Eichinger, S., & Pabinger, I. (2016). Deep vein thrombosis. The Lancet, 388(10063), 1830-1841.
Lusis, A. J. (2000). Atherosclerosis. Nature, 407(6801), 233-241.

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