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Posted: January 7th, 2021

Advanced Pathophysiology

· Discussion: Alterations in Cellular Processes
· Photo Credit: Getty Images
· At its core, pathology is the study of disease. Diseases occur for many reasons. But some, such as cystic fibrosis and Parkinson’s Disease, occur because of alterations that prevent cells from functioning normally.
· Understanding of signals and symptoms of alterations in cellular processes is a critical step in diagnosis and treatment of many diseases. For the Advanced Practice Registered Nurse (APRN), this understanding can also help educate patients and guide them through their treatment plans.
· For this Discussion, you examine a case study and explain the disease that is suggested. You examine the symptoms reported and explain the cells that are involved and potential alterations and impacts.
A 27-year-old patient with a history of substance abuse is found unresponsive by emergency medical services (EMS) after being called by the patient’s roommate. The roommate states that he does not know how long the patient had been lying there. Patient received naloxone in the field and has become responsive. He complains of burning pain over his left hip and forearm. Evaluation in the ED revealed a large amount of necrotic tissue over the greater trochanter as well as the forearm. EKG demonstrated prolonged PR interval and peaked T waves. Serum potassium level 6.9 mEq/L.
Post an explanation of the disease highlighted in the scenario you were provided. Include the following in your explanation:
The role genetics plays in the disease.
· Why the patient is presenting with the specific symptoms described.
· The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
· The cells that are involved in this process.
· How another characteristic (e.g., gender, genetics) would change your response.
McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
· Chapter 1: Cellular Biology; Summary Review
· Chapter 2: Altered Cellular and Tissue Biology: Environmental Agents (pp. 46-61; begin again with Manifestations of Cellular Injury pp. 83-97); Summary Review
· Chapter 3: The Cellular Environment: Fluids and Electrolytes, Acids, and Bases
· Chapter 4: Genes and Genetic Diseases (stop at Elements of formal genetics); Summary Review
· Chapter 5: Genes, Environment-Lifestyle, and Common Diseases (stop at Genetics of common diseases); Summary Review
· Chapter 7: Innate Immunity: Inflammation and Wound Healing
· Chapter 8: Adaptive Immunity (stop at Generation of clonal diversity); Summary Review
· Chapter 9: Alterations in Immunity and Inflammation (stop at Deficiencies in immunity); Summary Review
· Chapter 10: Infection (pp. 289–303; stop at Infectious parasites and protozoans); (start at HIV); Summary Review
· Chapter 11: Stress and Disease (stop at Stress, illness & coping); Summary Review
· Chapter 12: Cancer Biology (stop at Resistance to destruction); Summary Review
· Chapter 13: Cancer Epidemiology (stop at Environmental-Lifestyle factors); Summary Review

Genetics plays a role, as certain genetic mutations can cause deficiencies in enzymes involved in muscle metabolism, making individuals more susceptible. In this case, the patient’s history of substance abuse, particularly if involving stimulants, could be a triggering factor by overworking the muscles.
The patient is presenting with burning pain in the hip and forearm, along with necrosis (death of cells/tissue) in these areas. This is because skeletal muscle breakdown releases myoglobin, potassium, urate, phosphate, and creatine kinase into the bloodstream. Myoglobin specifically can damage the kidneys if in high enough amounts. The elevated serum potassium and EKG changes seen here indicate hyperkalemia, a dangerous medical emergency caused by excessive potassium release from damaged muscle cells.
At the cellular level, excessive contraction and overexertion of skeletal muscle fibers leads to injury of the sarcoplasmic reticulum and T-tubules, disrupting calcium regulation. The increased intracellular calcium triggers proteolytic enzymes like calpain to degrade structural and contractile proteins within the muscle cell. This autodigestion process causes the muscle cell to essentially digest itself from within.
The cells primarily involved are skeletal muscle myocytes. As you noted, gender could impact risk factors – for example, males may be more prone to exertional rhabdomyolysis from activities like bodybuilding due to higher muscle mass. Genetic disorders affecting muscle metabolism would also alter the presentation.
I hope this explanation helped provide insight into the cellular mechanisms at play. Please let me know if you need any clarification or have additional questions.
Vanholder, R., Sever, M. S., Erek, E., & Lameire, N. (2000). Rhabdomyolysis. Journal of the American Society of Nephrology, 11(8), 1553–1561.
Wallimann, T., Wyss, M., Brdiczka, D., Nicolay, K., & Eppenberger, H. M. (1992). Intracellular compartmentation, structure and function of creatine kinase isoenzymes in tissues with high and fluctuating energy demands: the ‘phosphocreatine circuit’ for cellular energy homeostasis. Biochemical Journal, 281 ( Pt 1), 21–40.
Bosch, X., Poch, E., & Grau, J. M. (2009). Rhabdomyolysis and acute kidney injury. New England Journal of Medicine, 361(1), 62–72.
Ismail, O. Z., & Ismail, A. A. (2017). Rhabdomyolysis: Pathophysiology and Predisposition. Acta neurologica Belgica, 117(2), 321–328.

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