Case Study 6 Analysis: Will’s Case
Case Study 6 Analysis: Will’s Case
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Case Study 6
Acute Renal Injury and Chronic Kidney Disease
Will is a 68-year-old male with a history of hypertension. Eight months ago, he started regular dialysis therapy for ESRD. Before that, his physician was closely monitoring his condition because he had polyuria and nocturia. Soon it became difficult to manage his hypertension. He also lost his appetite, became weak, easily fatigued, and had edema around his ankles. Will debated with his physician about starting dialysis, but she insisted, before the signs and symptoms of uremia increased, the treatment was absolutely necessary.
1. What is the difference between azotemia and uremia?
2. Two years ago, Will’s physician told him to decrease his protein intake. In spite of what the physician ordered, Will could not stop having chicken, beef, pork, or eggs at least once a day. Why did his physician warn him about his diet?
3. Will’s feelings of weakness and fatigue are symptoms of anemia. Why is he anemic?
4. Knowing what you do about Will’s history, why is left ventricular dysfunction a concern for his physician?
Case Study 6 Analysis: Will’s Case
Question 1 Differences between Azotemia and Uremia
These two terms are associated with the disorders of the renal system. As such, both Azotemia and Uremia relate to the build-up of metabolic wastes in the blood. According to (Porth, 2011), Azotemia can be explained as the presence of nitrogenous waste products such as uric acid, urea nitrogen and creatinine in the blood which is asymptomatic in nature. As such, Azotemia is a leading indicator of acute renal failure. On the other hand, Uremia, as the word suggests, refers to the presence of urine in the blood. Contrast to Azotemia, Uremia develops with chronic kidney disease (CKD). Further research suggests that Uremia occurs with acute kidney failure (AKI). Furthermore, Uremia presents a chronic condition to a patient due to its symptoms of shallow breath, drastic energy loss, reduced exercise tolerance, massive weight loss, body swelling as a result of fluid retention, skin frost, and in due course organ failure that leads to death, if not treated (Thompson, et al., 2015). Porth (2011) suggests that Azotemia is a mild manifestation of Uremia. Arguably, the two conditions are different is such a way that Azotemia occurs as an acute condition and Uremia occurs as a chronic condition. To add on, there are three types of Azotemia; prerenal, intrarenal, and postrenal, and these types are differentiated with the elevation levels of urea nitrogen (BUN) and creatinine in the kidney. Postrenal Azotemia is associated with Uremia.
Question 2: Protein Intake and Renal Failure
As a patient with a history of hypertension, Will might have thought that there is need to eat more protein to lower the systolic blood pressure as suggested by Buendia, Bradlee, Singer, Moore (2014). Even though protein intake helps lower blood pressure, for the purposes of renal sufficiency, the kidney is not sufficiently able to secrete the waste products associated with metabolism of protein. Arguably, low intake of proteins can help decrease symptoms of Uremia as well as lowers the development of renal failure. Studies suggest that proteins modulate the renal functioning, particularly, high dietary intake of protein promotes renal failure since the inability of the renal system to secrete wastes of protein metabolism initiates the persistent and chronic increase in the glomerular pressure and hyperfiltration. Consequently, a decreased glomerular filtration rate (GFR) is a defining characteristic of renal failure. Furthermore, hypertension is a risk factor in the development of Chronic Renal Failure or CKD.As such, Will was on the verge of developing Uremia and/or Azotemia, and this is the main reason why the physician advised on a low dietary intake of proteins.
Question 3: Why Anemic?
In regards to the patient in question, it is evident that he presents a case of renal failure. The underlying symptoms of renal failure include; a decreased secretion of erythropoietin, low production of red blood cells (RBCs), and accumulation of the nitrogenous wastes. First, anemia relates to the clinical condition that presents a decreased number of healthy RBCs in the blood of an individual. Critically, erythropoietin hormones (ERO) are produced by a healthy kidney with the purposive aim of prompting the bone marrow to produce RBCs (Kutuby, Wang, Desai, & Lerma, 2015). As such, in cases of renal failure, the kidney will produce inadequate ERO that will result in a reduced production of RBCs, a symptom of anemia. Also, renal failure being characterized by the presence of excess nitrogenous waste in the blood indicates that the life span of RBCs will be shortened leading to a predisposition of anemic condition on the body of an individual (Lammert & Zeeb, 2014, p. 261). Lastly, Will presents an anorexic condition that limits him from iron intake which will predispose him to develop an iron-deficiency anemia.
Question 4: Left Ventricular Dysfunction
Will has a history of
hypertension which increases oxygen demand as well as the workload of the left
ventricle. The left ventricle is responsible for the pumping of oxygenated blood
to other parts of the body. Left ventricular hypertrophy, as s pathophysiologic
condition can be caused by inherent stimuli such as a form of cardiomyopathy or
an extrinsic stimulus such as volume and pressure overload. First, the doctor
was critical of the patient developing Left ventricle hypertrophy since it is
evident that renal failures are associative with patients with anemia and
hypertension. In regards to renal failure which leads to the production of
fewer RBCs, the blood will tend to be less oxygenated making the left ventricle
to increase its wall pressure for sufficient supply of oxygenated blood (Chang, Chen,
Huang, Su, & Chen, 2014). Additionally,
anemia is associated with ischemic events that contribute to left ventricular
hypertrophy. These conditions are all indicators that led the physician to have
a concern of the LV to have a dysfunction.
Buendia, J. R., Bradlee, M. L., Singer, M. R., & & Moore, L. L. (2014, September 6). Diets higher in protein predict lower high blood pressure risk in Framingham Offspring Study adults. American Journal of Hypertention, 28(3), 372-379.
Chang, J. M., Chen, S. C., Huang, J. C., Su, H. M., & Chen, H. C. (2014). Anemia and left ventricular hypertrophy with renal function decline and cardiovascular events in chronic kidney disease. The American journal of the medical sciences, 347(3),183-189.
Kutuby, F., Wang, S., Desai, C., & Lerma, E. V. (2015). Anemia of chronic kidney disease. Disease-a-Month, 61(10), 421-424.
Lammert, E., & Zeeb, M. (2014). Metabolism of Human Diseases: Organ Physiology and Pathophysiology. New York: Springer Science & Business Media.
Porth, C. (2011). Essentials of Pathophysiology: Concepts of Altered Health States (3rd ed.). Philadelphia, Pennisylvania, United States of America: Lippincott Williams & Wilkins.
Thompson, S., James, M., Wiebe, N.,Hemmelgarn, B., Manns, B., Klarenbach, S., & Tonelli, M. (2015). Cause of death in patients with reduced kidney function. Journal of the American Society of Nephrology, 26(10), 2504-2511.