NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

NURS 6501 Advanced Pathophysiology Week 1 Discussion Alterations in Cellular Processes

This paper is a case study involving a 27-year-old patient with a history of substance abuse who is found unresponsive by emergency medical services. The patient becomes responsive after being administered naloxone. The essay examines the role of genetics, reasons for patient’s symptoms, physiological response, cells involved, and influence of other characteristics.

Genetics play a role in substance use disorders. For example, opioid use disorder has large risk of being inherited in families. Genes such as OPRM1 variates and A118G also predispose individuals to substance abuse disorder. Individuals of European descent with OPRD1 genes also have high predisposition to opioid use disorder. Additional genes include KCNG2, CNHIH3, KCNC1, RGMA, and APBB2 genes (Crist et al., 2019; Liu et al., 2019).

The patient presented with symptoms such as unresponsiveness due to central nervous system depression by the opiate overdose. The patient became response following the administration of naloxone since its an opiate antagonist that reverses the depressing effects of opiates. The patient reported pain in left hip and forearm because the effects of the opiates had ben reversed, hence, perception of pain. There is also tissue necrosis that may have developed due to poor tissue perfusion from depressed central nervous system, which affected circulation and respiratory system (Parthvi et al., 2019). The patient also developed respiratory acidosis, which increased serum potassium, hence, hyperkalemia and ECG changes.

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The cells involved in the patient’s symptoms include mast cells, neutrophils, and macrophages. These cells induce the induction and transition of the pain the patient experience. Adaptive immune cells such as B and T cells also initiate and resolve pain. Characteristics such as age would change my response in this case study (Machelska & Celik, 2020). For example, the elderly patients have low sensitivity to pain stimuli and potentially worse outcomes due to opiate overdose. These changes will affect the treatment interventions.

In summary, substance abuse has genetic predisposition. The patient developed the given symptoms because of the effects of opioid overdose and naloxone. Age would affect the clinical symptoms and management of opiate overdose.

References

Crist, R. C., Reiner, B. C., & Berrettini, W. H. (2019). A review of opioid addiction genetics. Current Opinion in Psychology, 27, 31–35. https://doi.org/10.1016/j.copsyc.2018.07.014

Liu, M., Jiang, Y., Wedow, R., Li, Y., Brazel, D. M., Chen, F., Datta, G., Davila-Velderrain, J., McGuire, D., Tian, C., Zhan, X., Choquet, H., Docherty, A. R., Faul, J. D., Foerster, J. R., Fritsche, L. G., Gabrielsen, M. E., Gordon, S. D., Haessler, J., … Vrieze, S. (2019). Association studies of up to 1.2 million individuals yield new insights into the genetic etiology of tobacco and alcohol use. Nature Genetics, 51(2), Article 2. https://doi.org/10.1038/s41588-018-0307-5

Machelska, H., & Celik, M. Ö. (2020). Opioid Receptors in Immune and Glial Cells—Implications for Pain Control. Frontiers in Immunology, 11. https://www.frontiersin.org/articles/10.3389/fimmu.2020.00300

Parthvi, R., Agrawal, A., Khanijo, S., Tsegaye, A., & Talwar, A. (2019). Acute Opiate Overdose: An Update on Management Strategies in Emergency Department and Critical Care Unit. American Journal of Therapeutics, 26(3), e380. https://doi.org/10.1097/MJT.0000000000000681

This paper is being written to explain the pathology of cystic fibrosis. I personally have a friend who

has this disease and have learned from her. The topics that will be covered are, how cystic fibrosis is created at a cellular level, genetics role in cystic fibrosis, the reasoning for the symptoms that the patient presented with, the description of the cells involved in cystic fibrosis, and how other characteristics would change the child’s response to cystic fibrosis. In short what I remember from nursing school is that cystic fibrosis is a genetic disorder which is an autosomal recessive gene that is carried by both the mother and the father. The abnormality occurs in chromosome 7 which is where creates an inability to transport small molecules across the cell’s membrane, which in turn, dehydrates the cells of the epithelium and this then creates dry secretion. This is a broad overview of what this disease is, but I will go into further detail below.

 The Role Genetics Plays in the Disease

Genetics play an important role in this disease, according to an article published in PubMed titled Cystic fibrosis genetics: from molecular understanding to clinical application states that due to a defective epithelial cell that is defective, this cell is inherited and is an autosomal recessive gene. The genetic information that is in the cell, which is the recipe for the cell to make proteins (Cutting, 2015).  According to Pathophysiology of disease: An introduction to clinical medicine, if a person receives a cystic fibrosis transmembrane conductance regulator gene (CFTCR), or a person can receive two copies of the CFTCR gene. This copy has a mutation of the cystic fibrosis gene, furthermore these two copies of the CFTR gene have stored a mutation which is the on chromosome seven. So, when the recipe is being presented to the cell to be made, the genetic information is then stored into the deoxyribonucleic acid which is known as DNA.  This is part of the twenty-three pairs of chromosomes, but on the seventh chromosome, the cystic fibrosis recipe is stored in that chromosome. In the DNA, where the CFTCR gene recipe lives, if there is one copy of the recipe than the gene will not show up in the person but will be a carrier but if there are two copies of the recipe being stored in the chromosome than the cystic fibrosis gene than the person will have cystic fibrosis (McCance at el., 2019).

 Why the Patient is Presenting with the Specific Symptoms Described

The baby’s symptoms included salty skin, a swollen stomach on occasion, and a failure to gain weight normally. According to an article published in the Journal of Cystic Fibrosis titled Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy, epithelia make up the major organ systems. The sweat glands, liver’s bile duct, and intestines in the gastrointestinal tract are all affected in this patient. The article goes on to explain that the patient suffers from malnutrition and does not grow normally as a result of the loss of pancreatic function. As a result, enzyme replacement is critical for this patient in order to prevent cell clogging caused by an inability to breakdown a key nutrient (Cutting, 2015).

The physiologic response to the stimulus presented in the scenario and why you think this response occurred

After reading different sources, I was able to breakdown the pathology behind this patient’s symptoms. This disease starts with the CFTR gene protein being mutated in the chromosome seven, which there are two copies of the recipe, this mutation causes the decrease of chloride acceptance and ion being transported, then this makes the absorption of water to increase which throws off ciliary from completing the job and there is mucus that is dry, this is what causes the skin to be salty of the baby. The stomach inflammation and swelling that is being experienced, is due to the CFTR gene protein not having the right recipe present to the epithelial cell, this is causing malfunction by changing the reabsorption of the sodium, chloride and potassium in the cell, the recipe tells the cell to keep the sodium, chloride and potassium outside of the cell, this causes a back-up of outside of the cell structure and blocks the cell from absorbing the nutrients especially, proteins, fats and vitamins that are fat soluble.

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The Cells that are Involved in this Process

The cells involved in this process begin with epithelial membranes found in the digestive tract, pancreas, airways, and reproductive area. According to an article in Apoptosis Journal, cystic fibrosis is caused by epithelial cell dysfunction, which leads to inflammation and an inability to create homeostasis due to the CFTR gene’s constant inflammation. Furthermore, the epithelial cells fail and undergo apoptosis as a result of the inflammation that occurs in the endoplasmic reticulum (Soleti at el., 2013).

How another characteristic (e.g., gender, genetics) would change your response

For cystic fibrosis, it is important to understand that this would not be a disease if the parents did not carry the gene. The

gene is the CFTR gene mutation, mentioned throughout this paper. According to a study done by Harvard Stem Cell Institute, where a lung cell was isolated to examine the function of the CFTR gene. It was shown in the study that if the ionocytes in the cell are not doing their job because it is expressing CFTR gene in increased levels, then the symptoms are created in the cell (Montoro at el., 2018). This occurs in the form of thick mucus and creates the response in the body that does not allow for the patient to regulate sodium, chloride, and potassium in a normal fashion.

Conclusion

During this journey of studying disease in depth and truly understanding how they work will help in the future of my career. I believe that if screening done at the hospitals before they leave would be beneficial. When parents are informed about the possibility of something occurring and what it means, parents will be empowered and get treatment before or if cystic fibrosis symptoms could show up. Also, encouraging parents to come to their baby checkups, will also allow for the medical staff to ask the right questions and treat the baby early, if they see symptoms. Cystic fibrosis is a challenge some patients may struggle with and it is our job as practitioners to catch things before extreme measures need to be taken.

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.

To prepare:

By Day 1 of this week, you will be assigned to a specific scenario for this Discussion. Please see the “Course Announcements” section of the classroom for your assignment from your Instructor.

By Day 3 of Week 1

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.

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Read a selection of your colleagues’ responses.

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By Day 6 of Week 1

Respond to at least two of your colleagues on 2 different days and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not

it is true that cells are the basic structural components of the body and are specialized to conduct different functions in the body. The central dogma also illustrates the pivotal role of genes in dictating the specialization of cells and subsequent events. Disease can alter the nature of cells thereby interfering with the normal cell functions. I find your case analysis quite intriguing, there are many patients who complain of sore throat that is related to allergic conditions and your analysis through genetic involvement is informative (Centers for Disease Control and Prevention,2021).

Group A streptococcus pharyngitis among children and adolescents is common and the identification of the genes associated with the common occurrence provides an avenue for solving the menace. Hypersensitivity relation to genetic composition also provides a better understanding of the recurrence of such cases (McCance & Huether, 2019). I also think that the bod defense system is triggered by recognition of the pathogen and the process of acting against the identified antigen leads to the symptoms, which include inflammation that would be felt as sore throat.

I agree hat the physiological processes upon identification of the antigen includes a variety of cells mediators that take part in the inflammatory pathway. These processes cause heat, swelling and redness. The patient characteristics that define different responses include age as age relates to immunity. Children are more susceptible to some diseases as compared to adults. Elderly people are also prone to some diseases that are not so common among young adults. Allergy to drugs also links to age as the allergy increases with age (Soderholm et al., 2018). I concur with you that severe allergic reaction would definitely be a concern

References

Soderholm, A. T., Barnett, T. C., Sweet, M. J., & Walker, M. J. (2018). Group A streptococcal

pharyngitis: Immune responses involved in bacterial clearance and GAS‐associated immunopathology. Journal of leukocyte biology, 103(2), 193-213.

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in

adults and children (8th ed.). Mosby/Elsevier.

Centers for Disease Control and Prevention. (2021, November 23). Pharyngitis (strep throat): Information for clinicians. Retrieved March 1, 2022, from https://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html

Kidney transplant is an effective treatment for patients suffering from end-stage renal disease. However, some patients develop adverse effects including kidney rejection. The management of kidney transplant rejection depends on the type and patient factors. Therefore, this paper examines why a patient with acute kidney transplant developed the described symptoms, genes associated with kidney transplant rejection and process of immunosuppression.

Why the Patient Presented the Symptoms Described

The patient presented symptoms that include gaining weight, decreased urinary output, fatigue, and running temperatures up to 101 F. The patient gained weight because of the increased body fluid volume level. The kidneys excrete excess fluids from the body. Impaired kidney function as seen in the case study affects the regulation of fluids in the body, hence, its accumulation and weight gain. The decline in renal function also impaired normal urine output. This led to reduced urine production, as seen in the case study. The rejection altered the normal renal function in the excretion process, leading to oliguria. The kidneys also eliminate toxins from the body. This includes excess ammonia in urine. Impaired kidney problems affect the elimination of these toxins, which lead to symptoms such as fatigue, poor concentration, acidosis, and anemia. Therefore, this explains the patient’s experience of fatigue. Patients with end-stage renal disease and those with kidney transplant rejection problems also experience immunosuppression (Rauen et al., 2020). This predisposes them to infections, hence, the fever that the patient has.

Genes Associated with the Development of the Disease

Genes have been linked with kidney transplant rejection. They include cytochrome p450 2EI (CYP2EI), CYP3A5, cytotoxic T-lymphocyte associated protein 4 (CTLA4), C-X-C motif chemokine ligand 8 (CXL8), epoxy hydrolase 2, coagulation factor II thrombin, and coagulation factor V genes. In addition, Forkhead box P3, Fc fragment of IgG receptor IIA, major histocompatibility complex class II, I, DO alpha, and interleukin 1 beta, 2, 2-receptor subunit beta genes also play a role in the development of the rejection in kidney transplant. Genes such as interleukin genes are inflammatory cytokines that inhibits inflammatory processes once a person received an allograft. On the other hand, this gene also downgrades the maturation of antigens and cells that develops host’s immunity following the transplant (Arnold et al., 2022; Spicer & Runkel, 2019; van Vugt et al., 2022). Other genes such as ATP-binding genes increase the body’s resistance towards drugs used in suppressing the immune system following the transplant.

Process of Immunosuppression

Immunosuppression refers to the state in which the ability of the body to fight infections is reduced. The immune system is lowered to a level that it cannot counteract any disease causing organisms from invading the body. The causes of immunosuppression include the use of medications that are used in conditions such as cancer. The other cause is conditions that depress the immune system such as cancer and HIV. Treatments for cancer such as radiotherapy and chemotherapy also cause immunosuppression. The effects of immunosuppression are varied. They include increasing the vulnerability of patients to infections. It also increases costs that patients incur due to frequent hospitalizations (Gupta et al., 2021). Prolonged infections also affect the patients’ quality of life. Patients may also die in cases where the immune system is severely compromised.

Conclusion

In conclusion, the patient presented the symptoms because of reduced renal functioning. Genes are involved in the development of kidney transplant rejection. The rejection may result in immunosuppression, which has negative effects on health.

References

Arnold, M.-L., Heinemann, F. M., Oesterreich, S., Wilde, B., Gäckler, A., Goldblatt, D., Spriewald, B. M., Horn, P. A., Witzke, O., & Lindemann, M. (2022). Correlation of Fc Receptor Polymorphisms with Pneumococcal Antibodies in Vaccinated Kidney Transplant Recipients. Vaccines, 10(5), Article 5. https://doi.org/10.3390/vaccines10050725

Gupta, R., Woo, K., & Yi, J. A. (2021). Epidemiology of end-stage kidney disease. Seminars in Vascular Surgery, 34(1), 71–78. https://doi.org/10.1053/j.semvascsurg.2021.02.010

Rauen, T., Wied, S., Fitzner, C., Eitner, F., Sommerer, C., Zeier, M., Otte, B., Panzer, U., Budde, K., Benck, U., Mertens, P. R., Kuhlmann, U., Witzke, O., Gross, O., Vielhauer, V., Mann, J. F. E., Hilgers, R.-D., Floege, J., Floege, J., … Hilgers, R.-D. (2020). After ten years of follow-up, no difference between supportive care plus immunosuppression and supportive care alone in IgA nephropathy. Kidney International, 98(4), 1044–1052. https://doi.org/10.1016/j.kint.2020.04.046

Spicer, P., & Runkel, L. (2019). Costimulatory pathway targets for autoimmune and inflammatory conditions: Clinical successes, failures, and hope for the future. Expert Opinion on Investigational Drugs, 28(2), 99–106. https://doi.org/10.1080/13543784.2019.1557146

van Vugt, L. K., Schagen, M. R., de Weerd, A., Reinders, M. E., de Winter, B. C., & Hesselink, D. A. (2022). Investigational drugs for the treatment of kidney transplant rejection. Expert Opinion on Investigational Drugs, 31(10), 1087–1100. https://doi.org/10.1080/13543784.2022.2130751

Naloxone is an FDA-approved medication intended to counteract the effects of opiate misuse and overdose. The medication is an opioid antagonist that competes with opiates for opioid receptors, resulting in a significant reduction in the effects of opioids (Dunne, 2018). With larger dosages, opioids are known to produce bradycardia and breathing suppression, which can lead to fainting. Moreover, naloxone is only effective against opioids. Consequently, the patient’s fast response after the medicine was provided shows that his immediate state was caused by opiate misuse or overdose.

However, Rhabdomyolysis is my diagnosis of the patient’s sickness after examining all of the presenting signs and symptoms. The illness is a fatal medical ailment that involves the deterioration of muscle tissue and the entry of such tissues into the blood circulatory system. The tissue causes broad harm to the body, most notably renal failure (Kruijt et al., 2021). The appearance of necrotic tissue on the patient’s hip and forearm, as well as discomfort in those areas, suggest substantial muscle tissue deterioration. This could be a result of cellular damage from a fall or injury, or abuse of injectable narcotics (Waldman et al., 2020). At the cellular level, a shortage of ATP or muscular damage causes an influx of intracellular sodium and calcium. Sodium causes swelling and rupture of the membranous structure by drawing water into the cell. Excess intercellular calcium promotes actin-myosin cross-linking, myofibrillar contraction, and ATP consumption. Reperfusion induces leukocyte migration into injured muscles, resulting in a rise in cytokines, prostaglandins, and free radicals (Stanley et al., 2022). This causes increased muscle fibre necrosis and the release of muscle breakdown byproducts such as potassium, creatine kinases, phosphate, uric acid, and myoglobin into the bloodstream.

Genetic factors play a role in the development of the condition. Hereditary diseases such as mitochondrial disorders, metabolic muscle disorders, muscular dystrophies, excitation-contraction coupling abnormalities, and intramuscular calcium release disorders make one more susceptible to Rhabdomyolysis (Scalco et al.,2015). Establishing a genetic relationship to rhabdomyolysis is challenging due to the various possible genetic conditions that can predispose one to the medical condition. However, it may be crucial clinically to prevent future crises.

This patient’s ECG revealed a prolonged PR interval and peaked T waves. Peaking T waves are early indicators of hyperkalemia  (Hunter & Bailey, 2019). The potassium level was 6.9 mEq/L, indicating mild hyperkalemia. Therefore, the patient is suffering from a secondary case of hyperkalemia due to the release of potassium from cellular breakdown into the bloodstream.

References

Dunne, R. B. (2018). Prescribing naloxone for opioid overdose intervention. Pain Management, 8(3), 197-208. https://doi.org/10.2217/pmt-2017-0065

Hunter, R. W., & Bailey, M. A. (2019). Hyperkalemia: pathophysiology, risk factors and consequences. Nephrology Dialysis Transplantation, 34(3), iii2-iii11. https://doi.org/10.1093/ndt/gfz206

Kruijt, N., van den Bersselaar, L. R., Kamsteeg, E. J., Verbeeck, W., Snoeck, M. M. J., Everaerd, D. S., … & Voermans, N. C. (2021). The etiology of rhabdomyolysis: an interaction between genetic susceptibility and external triggers. European Journal of Neurology, 28(2), 647-659. https://doi.org/10.1111/ene.14553Links to an external site.

Scalco, R. S., Gardiner, A. R., Pitceathly, R. D., Zanoteli, E., Becker, J., Holton, J. L., Houlden, H., Jungbluth, H., & Quinlivan, R. (2015). Rhabdomyolysis: a genetic perspective. Orphanet journal of rare diseases, 10(1), 51. https://doi.org/10.1186/s13023-015-0264-3

Stanley, M., Chippa, V., Aeddular, N., Quintanilla Rodriguez, B., & Adigun, R. (2022). Rhabdomyolysis – statpearls – NCBI bookshelf. National Library of Medicine. Retrieved March 4, 2023, from https://www.ncbi.nlm.nih.gov/books/NBK448168/

Waldman, W., Sein Anand, J., & Kabata, P. (2020). The characteristics and outcomes of toxin-induced massive rhabdomyolysis. International Journal of Occupational Medicine and Environmental Health, 33(5). https://doi.org/10.13075/ijomeh.1896.01532Links to an external site.

My scenario is: 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.

• The role genetics plays in the disease.
  • The patient could have had a genetic predisposition to substance abuse which contributed to his current situation of an overdose and associated rhabdomyolysis
• Why the patient is presenting with the specific symptoms described.
  • The patient is likely presenting with opiate overdose due to history of substance abuse and response to naloxone. Additionally the patient is likely suffering from infection of drug administration sites and AKI rhabdomyolysis from laying on the floor for an extended period of time.
• The physiologic response to the stimulus presented in the scenario and why you think this response occurred.
  • The unconscious state is directly related to the opiate overdose. The necrosis is directly related in response to physical trauma and infection from drug use as well as mechanical trauma from having fallen and remaining in a fixed position. The hyperkalemia is as a result of the AKI caused by rhabdomyolysis from the patient having been down for an extended period of time.
• The cells that are involved in this process.
  • Epithelial cells that are damaged as result of the trauma, cells within the kidney responsible for protein clearing as well as potassium excretion,
• How another characteristic (e.g., gender, genetics) would change your response.
  • A much older patient would have changed my rationales as they would be at a higher risk for accidental overdose and would be at an increased risk for falls and AKI with multiple comorbidities.

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