Case: End-Stage Kidney Disease

    Compose a 3- to 4-page case analysis (in addition to a title page, abstract, and reference list page) written in APA Style citing at least 3 references with one non-Internet reference. The following should be covered in the paper: • Title Page: Case Title, Full Name, Section, Date, Instructor, and Campus • Abstract: Summarize the case o One non-indented paragraph on a separate page. This will be page 2. • Introduction: The physiological importance of the liver, pancreas, and kidneys for the proper functioning of the human body • Body: Response to the prompts: Organize your analysis with headings that thoroughly answer the prompts (e.g., “Abnormal Glucose Levels” for question 1). o Explain each prompt in depth with physiological concepts and provide sufficient evidence from the literature for each prompt. o Include normal physiological ranges (if it applies). o Maintain the order of questions when answering. • Conclusion: Summarize the paper in a paragraph. Support your opinions with evidence from your readings and research. Review the rubric for complete grading criteria. ________________________________________ Case: End-Stage Kidney Disease Cynthia, a 53-year-old female presented to the emergency room due to feeling constantly tired, hungry, thirsty, and with frequent urination. Her past medical history is significant for cirrhosis and end-stage kidney disease. Physical examination had revealed yellowish discoloration to the skin, multiple bruises, bilateral edema, and weakness lasting more than three weeks. Laboratory tests were ordered (results provided below) after which she was prescribed metformin and informed to contact a doctor if she starts experiencing nausea, vomiting, fast breathing, and/or lethargy, as metformin has been known to cause metabolic acidosis. Complete Blood Count (CBC) Sodium 126 mEq/L Glucose 220 mmol/L Calcium 7.1 mg/dl Red blood cell count 3.9 cells/ul Iron 40 mcg/dL Albumin 2.5 g/dl Vitals Blood pressure 92/64 mmHg Hormone Panel Renin Low ADH Elevated Aldosterone Low Vitamins Vit D Low Vit K Low Vit E Low Vit A Low Urine and Stool Sample Stool color Gray Stool content Increase fat content Urine color Clear Complete Blood Count (CBC) Glucose Present Answer the following questions regarding Cynthia’s case: 1. What hormone is not functioning properly causing Cynthia’s glucose levels to be abnormal? Furthermore, explain in depth how this hormone regulates blood glucose levels. 2. What other hormone(s) are responsible for maintaining normal glucose levels? Explain in depth how they work. 3. Explain why Cynthia is presenting with excessive thirst (polydipsia), tiredness and hunger (polyphagia), and frequent urination (polyuria). 4. Explain why Cynthia is experiencing hypotension. How does the body and its various organ systems bring the blood pressure back towards homeostasis? 5. What do you expect Cynthia’s heart rate and end-diastolic volume (EDV) to be (elevated, normal, or low) and justify your expectation with cardiovascular formulas such as cardiac output (CO) and stroke volume (SV). 6. What is the importance of iron in the body and the consequence of it being 40 mcg/dL? 7. Explain in detail what gluconeogenesis is and where in the body it occurs? Knowing that gluconeogenesis helps maintain blood glucose level, what is the effect of metformin on the management of diabetes mellitus type 2? 8. Looking at Cynthia’s albumin levels, what effect does it have on her (a) blood osmolarity (b) glomerular filtration rate (GFR) and (c) urine volume? 9. Explain how glucose is normally reabsorbed by the kidneys? What is happening in Cynthia’s kidneys resulting in glucosuria and what effect does glucosuria have on her blood pressure? 10. If Cynthia ends up developing metabolic acidosis, what would the levels of her pH, CO2, and HCO3 be in the blood? Furthermore, how would the body compensate and address both renal and respiratory compensation (optional: show the compensation via a flow chart)?
Case Title: A Case Study of End-Stage Kidney Disease and its Impact on Hormonal Regulation and Metabolic Processes Full Name: [Your Full Name] Section: [Your Section] Date: [Date] Instructor: [Instructor's Name] Campus: [Campus Name] Abstract This case analysis explores the physiological consequences of end-stage kidney disease (ESKD) in a 53-year-old female patient, Cynthia. The case examines the impact of ESKD on hormonal regulation, metabolic processes, and overall health. Specifically, the analysis focuses on the abnormal glucose levels, polydipsia, polyphagia, polyuria, hypotension, anemia, and metabolic acidosis experienced by Cynthia. The case also discusses the role of the liver, pancreas, and kidneys in maintaining normal physiological functions. Introduction The liver, pancreas, and kidneys play crucial roles in the proper functioning of the human body. The liver is involved in various metabolic processes, including glucose metabolism, protein synthesis, and detoxification. The pancreas produces hormones such as insulin and glucagon, which regulate blood glucose levels. The kidneys are responsible for filtering waste products from the blood and maintaining fluid balance. Body
  1. Abnormal Glucose Levels
The hormone primarily responsible for regulating blood glucose levels is insulin. Insulin is produced by the beta cells of the pancreas. When blood glucose levels rise, insulin stimulates glucose uptake by cells in the liver, muscle, and adipose tissue. This leads to a decrease in blood glucose levels. In Cynthia's case, the elevated glucose levels suggest a deficiency or resistance to insulin. This could be due to the underlying ESKD, which can impair pancreatic function and reduce insulin sensitivity.
  1. Other Hormones Regulating Blood Glucose Levels
In addition to insulin, other hormones also play a role in regulating blood glucose levels. These include:
  • Glucagon: Produced by the alpha cells of the pancreas, glucagon increases blood glucose levels by stimulating the breakdown of glycogen in the liver.
  • Cortisol: A stress hormone produced by the adrenal glands, cortisol can increase blood glucose levels by stimulating gluconeogenesis.
  1. Polydipsia, Polyphagia, and Polyuria
Cynthia's symptoms of excessive thirst, hunger, and urination (polydipsia, polyphagia, and polyuria) are classic signs of hyperglycemia. The elevated blood glucose levels can lead to osmotic diuresis, where excess glucose in the blood draws water into the urine, resulting in increased urination and fluid loss. This can lead to dehydration and increased thirst.
  1. Hypotension
Cynthia's hypotension is likely due to a combination of factors related to her ESKD. The kidneys play a crucial role in regulating blood pressure by producing renin, an enzyme that activates the renin-angiotensin-aldosterone system (RAAS). In ESKD, the kidneys may be unable to produce enough renin, leading to decreased aldosterone levels and a reduction in blood volume. This can result in hypotension. The body has several mechanisms to compensate for hypotension, including:
  • Increased heart rate: The heart pumps faster to increase cardiac output and maintain blood pressure.
  • Vasoconstriction: Blood vessels constrict to increase blood pressure.
  • Fluid retention: The kidneys retain more fluid to increase blood volume.
  1. Heart Rate and End-Diastolic Volume
Given Cynthia's hypotension, I would expect her heart rate to be elevated to compensate for the decrease in blood pressure. The increased heart rate would lead to an increased cardiac output. However, the end-diastolic volume (EDV) might be low due to decreased blood volume and reduced venous return to the heart. Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate
  1. Importance of Iron
Iron is essential for the production of red blood cells, which carry oxygen to tissues throughout the body. A low iron level (40 mcg/dL) can lead to anemia, characterized by a decreased red blood cell count and reduced oxygen-carrying capacity. This can result in fatigue, weakness, and other symptoms.
  1. Gluconeogenesis
Gluconeogenesis is the process of converting non-carbohydrate sources, such as amino acids and lactate, into glucose. It occurs primarily in the liver and kidneys. Gluconeogenesis is important for maintaining blood glucose levels during fasting or when carbohydrate intake is limited. Metformin, a medication used to treat type 2 diabetes, works by inhibiting gluconeogenesis. By reducing the production of glucose by the liver, metformin can help lower blood glucose levels.
  1. Albumin and its Effects
Albumin is a protein produced by the liver that plays a crucial role in maintaining blood volume and oncotic pressure. A low albumin level, as seen in Cynthia's case, can have several effects:
  • (a) Blood osmolarity: Decreased albumin can lead to a decrease in blood osmolarity, which can affect fluid balance and electrolyte levels.
  • (b) Glomerular filtration rate (GFR): Albumin plays a role in maintaining the glomerular filtration barrier. A low albumin level can lead to increased proteinuria, which can damage the kidneys and reduce GFR.
  • (c) Urine volume: Decreased GFR can lead to decreased urine output and fluid retention.
  1. Glucose Reabsorption and Glucosuria
In the kidneys, glucose is normally reabsorbed from the glomerular filtrate in the proximal tubules. This reabsorption process is mediated by specific transport proteins. In Cynthia's case, the excessive glucose levels in the blood likely overwhelm the reabsorption capacity of the kidneys, leading to glucosuria. Glucosuria can contribute to dehydration and increased urination.
  1. Metabolic Acidosis
If Cynthia develops metabolic acidosis, her blood pH would be low, CO2 levels would be normal or low, and HCO3 levels would be low. The body would compensate for the acidosis through both renal and respiratory mechanisms.
  • Renal compensation: The kidneys would attempt to excrete more hydrogen ions and retain bicarbonate ions to increase blood pH.
  • Respiratory compensation: The lungs would increase the rate and depth of breathing to eliminate more carbon dioxide, which can help to raise blood pH.
Conclusion This case analysis highlights the complex interplay of hormonal regulation, metabolic processes, and kidney function in maintaining overall health. Cynthia's ESKD has led to a cascade of physiological abnormalities, including abnormal glucose levels, polydipsia, polyphagia, polyuria, hypotension, anemia, and metabolic acidosis. Effective management of ESKD requires a comprehensive approach that addresses these underlying issues and provides appropriate treatment.  

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