Assignment 2.1: BIO 526 Cellular Adaptation, Injury, and Death Case Study 

Assignment 2.1: BIO 526 Cellular Adaptation, Injury, and Death Case Study

Assignment 2.1: BIO 526 Cellular Adaptation, Injury, and Death Case Study

Maria Case Study
Maria is a sedentary, 68-year-old woman who is overweight. She complains that her hands and feet are always cold and she tires quickly when cleaning the house. Maria comes in for a visit. When she comes in for a visit, her blood pressure is one-eighty-four over ninety-eight. She has edema around her ankles and legs. You are concerned about an echocardiogram that indicates Maria has an enlarged heart.

Identify two reasons why Maria will have tissue ischemia. How might this lead to hypoxia?
What are the two early and reversible changes that occur to tissue cells when they are hypoxic?
What specific type of cellular adaptation has taken place in Maria’s enlarged heart? What made you come to this conclusion?

ORDER A CUSTOMIZED, PLAGIARISM-FREE PAPER HERE

Good News For Our New customers. We can write this assignment for you and pay after Delivery. Our Top -rated medical writers will comprehensively review instructions , synthesis external evidence sources(Scholarly) and customize a quality assignment for you. We will also attach a copy of plagiarism report alongside and AI report. Feel free to chat Us

Assignment Guidelines
You may also submit your completed work using the Maria Case Study (Word) document. Please make sure to include your name on your case study submission.

Turnitin
This assignment will be scanned using Turnitin software. Turnitin is an online service that highlights matching text in written work. It indexes Internet sources, databases of subscription services, and written work submitted through its website. Assignments sent through Turnitin are scanned against all of its sources and a report is generated that summarizes and highlights matching text and where it was found. It is up to instructors and students to interpret the report to determine if plagiarism occurred.

You may submit your assignment to Turnitin prior to its due date to assess your work against Turnitin’s database. You may use the Originality Report’s results to address any originality concerns in your work, and then resubmit your assignment for grading. You may resubmit until the assignment’s due date. Any work that has been submitted at the time the assignment is due will be considered your final submission, and this will be the submission used for grading.

Visit the Bradley University Turnitin student page for tips and resources, including a video tutorial on how to submit an assignment using Turnitin.

Submission
Submit your assignment and review full grading criteria on the Assignment 2.1: Cellular Adaptation, Injury, and Death Case Study page.

ORDER A CUSTOMIZED, PLAGIARISM-FREE PAPER HERE

Bi-Weekly Case Study RubricCriteriaRatingsPtsRelevance of Answer

view longer description

20 to >15 pts

Meets all Expectations

Answers are complete with adequate specificity and detail.

15 to >10 pts

Meets Most Expectations

Answers are complete, yet critical details are missing.

10 to >0 pts

Partially Meets Expectations

Answers are incomplete or not all answers are correct.

0 pts

Does Not Meet Expectations

Answer does not address case study questions.

/ 20 pts

Total Points: 0

ORDER A CUSTOMIZED, PLAGIARISM-FREE PAPER HERE

Maria Case Study
Maria is a 68-year-old lady who is overweight and leads a sedentary lifestyle. She presented with complaints of easy fatigability with simple tasks and persistent coldness of her feet and hands. Assessment reveals a high blood pressure of 184/98 mmHg. She also has bilateral lower limb edema at her ankles and legs. Findings from an echocardiogram show that she has an enlarged heart.
Reasons Why Maria Will Have Tissue Ischemia
Maria is at risk of tissue ischemia. Ischemia is characterized by the inadequate blood supply to tissues with resultant hypoperfusion (Cameron et al., 2018). The restricted blood supply to organs leads to tissue hypoxia with subsequent anaerobic respiration, and impaired elimination of metabolic wastes. The patient in this case study may have tissue hypoxia secondary to atherosclerosis and the existing edema.
The patient likely has atherosclerosis since she is overweight and sedentary. Atherosclerosis leads to the progressive build-up and progression of atherosclerotic plaques within vascular walls (Scheen et al., 2018). This leads to the narrowing of the vascular lumen and eventual occlusion due to plaque rupture and thrombosis (Scheen et al., 2018). The consequent reduction in blood flow results in hypoperfusion of distal tissues which may cause tissue ischemia. The most commonly encountered effects include myocardial infarction and ischemic stroke.
The lower limb edema may also predispose the patient to tissue ischemia. Edema may be a direct consequence of ischemia due to disrupted cellular membrane integrity and homeostasis or an exacerbating factor for tissue ischemia (Simon et al., 2018). Edema reduces tissue perfusion by increasing the diffusion distances for oxygen delivery (Simon et al., 2018). Additionally, edema causes direct compression and pressure on blood vessels thus further restricting blood flow to affected tissues (Simon et al., 2018). This process is cyclic and progressive and with no interventions, irreversible tissue damage and infarction may occur. Restricted blood supply with resultant inadequate delivery of oxygen to metabolically active cells attributable to both edema and atherosclerosis leads to hypoxia. This can further be worsened by a compromised cardiovascular system evidenced by an enlarged heart on echocardiogram which may result in reduced cardiac output.
Early and Reversible Changes in Hypoxic Tissue Cells
Oxygen is integral to various cellular functions and processes. Oxygen drives various biochemical reactions and the presence of hypoxia causes cellular stress with various reversible and irreversible changes (Lee et al., 2020). The two early reversible changes in hypoxic cells are a reduction in the production of adenosine triphosphate (ATP) and cellular membrane dysfunction (Lu et al., 2022). ATP provides energy that drives cellular function. Its optimal generation through metabolic processes of glycolysis and mitochondrial respiration via oxidative phosphorylation in the electron transport chain requires oxygen (Dunn et al., 2022). Hypoxia limits these processes and mitochondrial activity with a consequent resort to anaerobic respiration for energy production (Lu et al., 2022). The outcome of anaerobic respiration is significantly reduced ATP and lactic acidosis. Increased production of reactive oxygen species during hypoxia also inhibits mitochondrial activity further diminishing the production of ATP.
Hypoxia causes reversible disruptions in the integrity of the cellular membrane. Reduction in ATP levels attributed to hypoxia also leads to a subsequent reduction in phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-biphosphate which are integral in maintaining homeostasis of the cellular membrane (Lu et al., 2022). Additionally, inadequate ATP supply leads to the failure of ATP-dependent Na+/K+ transmembrane ion channels (Simon et al., 2022). These lead to the derangement of electrolyte ion gradient with the influx of sodium and calcium ions and efflux of potassium ions. The intracellular shift of sodium ions is accompanied by a concurrent shift of fluid with resultant cellular swelling and tissue edema. The edema worsens the preceding tissue hypoperfusion.
Type of Cellular Adaptation
Pathological cardiac hypertrophy is the cellular adaptation that has occurred with resultant cardiomegaly. Cardiac myocytes are terminally differentiated by birth and thus cannot increase in number through cell division (Nakamura et al., 2018). Cellular adaptation to physiological and pathological processes in cardiac myocytes thus occurs only through hypertrophy which is the increase in cellular size (Nakamura et al., 2018). Pathological cardiac hypertrophy occurs in response to ventricular wall stress, hemodynamic stress, and increased cardiac workload caused by disorders such as hypertension, ischemic heart disease, and cardiomyopathy (Daines et al., 2021). The patient’s cardiomegaly can be attributed to hypertension based on high blood pressure measures. She is also overweight and leads a sedentary lifestyle thus is predisposed to ischemic heart disease and myocardial infarction secondary to atherosclerotic processes.
Pathological cardiac hypertrophy can gradually progress to cardiac failure. This progression can be exacerbated by oxidative stresses, increased pro-inflammatory activity, calcium ion handling abnormalities, and cardiac myocyte apoptosis (Oldfield et al., 2020). Cardiac hypertrophy increases oxygen demand. Existing inadequate supply stemming from reduced cardiac output further worsens cardiac dysfunction. Early intervention is thus pivotal in preventing the progression of pathological cardiac hypertrophy and cardiomegaly to overt heart failure.
Conclusion
Tissue hypoxia causes oxidative stress to cells and cellular functions. Tissue hypoxia is attributed to the inadequate blood supply to tissues from various causes such as atherosclerosis and reduced cardiac output. Tissue edema also exacerbates tissue hypoperfusion by increasing diffusion distance and compressing adjacent blood vessels. Tissue hypoxia can result in reverse changes such as reduced ATP production, lactic acidosis, and cellular membrane dysfunction. Oxidative stress from tissue ischemia and hypoxia can lead to adaptive cellular responses such as pathological cardiac hypertrophy which eventually leads to heart failure.

References
Cameron, S. J., Mix, D. S., Ture, S. K., Schmidt, R. A., Mohan, A., Pariser, D., Stoner, M. C., Shah, P., Chen, L., Zhang, H., Field, D. J., Modjeski, K. L., Toth, S., & Morrell, C. N. (2018). Hypoxia and ischemia promote a maladaptive platelet phenotype. Arteriosclerosis, Thrombosis, and Vascular Biology, 38(7), 1594–1606. https://doi.org/10.1161/atvbaha.118.311186
Daines, B., Rao, S., Hosseini, O., Prieto, S., Abdelmalek, J., Elmassry, M., Sethi, P., Test, V., & Nugent, K. (2021). The clinical associations with cardiomegaly in patients undergoing evaluation for pulmonary hypertension. Journal of Community Hospital Internal Medicine Perspectives, 11(6), 787–792. https://doi.org/10.1080/20009666.2021.1982488
Dunn, J., & Grider, M. H. (2022). Physiology, Adenosine Triphosphate. In StatPearls. StatPearls Publishing.
Lee, P., Chandel, N. S., & Simon, M. C. (2020). Cellular adaptation to hypoxia through hypoxia-inducible factors and beyond. Nature reviews. Molecular cell biology, 21(5), 268–283. https://doi.org/10.1038/s41580-020-0227-y
Lu, J., Dong, W., Hammond, G. R., & Hong, Y. (2022). Hypoxia controls plasma membrane targeting of polarity proteins by dynamic turnover of PI4P and PI(4,5)P2. eLife, 11, e79582. https://doi.org/10.7554/eLife.79582
Nakamura, M., & Sadoshima, J. (2018). Mechanisms of physiological and pathological cardiac hypertrophy. Nature reviews. Cardiology, 15(7), 387–407. https://doi.org/10.1038/s41569-018-0007-y
Oldfield, C. J., Duhamel, T. A., & Dhalla, N. S. (2020). Mechanisms for the transition from physiological to pathological cardiac hypertrophy. Canadian journal of physiology and pharmacology, 98(2), 74–84. https://doi.org/10.1139/cjpp-2019-0566
Scheen A. J. (2018). De l’athérosclérose à l’athérothrombose: D’une pathologie chronique silencieuse à un accident aigu critique [From atherosclerosis to atherothrombosis : from a silent chronic pathology to an acute critical event]. Revue medicale de Liege, 73(5-6), 224–228.
Simon, F., Oberhuber, A., Floros, N., Busch, A., Wagenhäuser, M., Schelzig, H., & Duran, M. (2018). Acute limb ischemia—much more than just a lack of oxygen. International Journal of Molecular Sciences, 19(2), 374. https://doi.org/10.3390/ijms19020374