Acute Renal Injury and Chronic Kidney Disease
The pathophysiologyof uraemia is associated with certain fluid or electrolyte thatcauses the hormone imbalance which causes renal problems. When theblood urea nitrogen (BUN) has increased in the blood it implies thatan individual will suffer from azotemia. The level of BUN should be8-20mg/dl and serum level should be 0.7-1.4 mg/dl. The symptom ofUraemia indicated that there was urine in the blood (Juncos, 2012).One of the important roles of the kidney is to ensure thatnitrogenous waste is eliminated in the body since they are formedwhen protein and amino acid processes take place. Urea and uric acidare formed when proteins are broken-down, and thus it has to befiltered in the kidney where it is excreted as urine. It is anindication that when Will had symptoms of uraemia there was apresence of some urea in the blood. When uraemia is experienced, itshows that one has an acute kidney failure, and thus the kidney doesnot function at all. It is an indication that the glomerularfiltration is below the recommendable rate of 60ml/min, and thiscauses a high concentration of urea in the blood. Symptoms like lossof appetite, weight and body swelling, nausea and vomiting arecommon. To treat uraemia it is important to perform kidney dialysiswhich removes the entire uric acid that is in the body as describedin Will case study.
From Will casestudy, it indicates that before uraemia was experienced there was anindication of azotemia that is as a result of increased nitrogen inthe blood. There is a difference between uraemia and azotemia sinceuraemia is experienced when plasma has increased urea. On the otherhand, azotemia is as a result of nitrogen in the blood. This is awarning sign that when one has azotemia he or she if not hospitalizedresults to uraemia. The proteins and amino acids after they arebroken-down they form nitrogenous waste products that are supposed tobe filtered out so that they will not get access to the blood. Thenormal range of BUN (Blood Urea Nitrogen) should be 8-20mg/dl, andthe serum should be 0.7-1.4 mg/dl. The glomerular filtration issupposed to be about 125ml/min. When BUN increases in the body and isallowed 20-30 percent and the glomerular filtration decreases to70ml/dl it indicates that one is suffering from azotemia.
From Will casestudy, the physician told him two years ago that he should decreasehis protein intake. In spite of what the physician ordered, Willcould not stop having chicken, beef, pork, or eggs at least once aday that are a source of protein. Having diagnosed of uraemia, it isan indication that food that has a lot of protein increases themetabolism of proteins and amino acids that are broken-down in thekidney resulting to urea and uric acid that is formed when thoseproteins are broken-down (Yunfu, 2012). Based on the fact that thekidney is not function well it will not be able to filter the proteinthat will result in urine going to the blood making his conditionworse. Additionally, when proteins are taken it implies that there isthe formation of nitrogen in the blood that should be maintainedbetween 8-20 mg/dl. When the blood urea nitrogen increases when thereis a high intake of proteins that is broken down to nitrogen azotemiais experienced later result to uraemia. The protein intake in thebody should be regulated based on the fact that it overworks thekidneys since it will have to filter all the protein.
Anemia is acondition that is experienced when the body does not have enoughblood or when red blood cells are not function well (Gardner andJackson, 2011). On the other hand, hemoglobin plays an important rolein making sure that there is adequate oxygen in the lungs that willlater be taken by the blood to the entire body. The symptoms ofanemia are characterized by feelings of weakness and fatigue and itis an indication that he is anemic. This is because the blood is notenough in the body since it has urea and nitrogen that is acidic tothe body resulting in the destruction of the red blood cell. When thered blood cells are destroyed by the urea and BUN in the body, itimplies that symptoms like feeling weak and tired will be the orderof the day. Based on Will, is suffering from ureamia it means thathis blood has urea, and thus there is a shortage of iron in the bodysince the blood is not enough or it is contaminated and thus therewould be no production of red blood cells.
The function of theleft ventricle is to receive oxygenated blood from the far end of theleft atrium through the mitral valve that is later pumped by the leftventricle to the aorta. The oxygenated blood is pumped into the aortavia an aortic valve that makes the blood circulate systemic in theheart. Conditions like ventricular hypertrophy may cause challengesor interfere with the left ventricle since it enlarges and hardenswhich results to uncontrolled hypertension or high blood pressure. Itis imperative that when the left ventricle valves to the aorta hardenit implies at there will be no blood that can pass to the other rightventricle and thus heart failure results. The left ventricularhypertrophy (LVH) is a risk factor to the cardiovascular (CV), and itresult in high mortality.
When a patient hasleft ventricular hypertrophy chances of suffering from stroke andheart failure and heart diseases can be experienced (Zhu, 2014). Thesudden cardiac death is a result of the failure of oxygenated bloodto penetrate in the valves of the left ventricle when it creates ashape like a curve and hardens making it impossible to supply theblood to the other ventricles. When the blood is trying to penetratein the valves of the left ventricle, it pushes with force causing aneffect like hypertension to be experienced. This implies that thepatient has to be under the medication since it causes discomfort tothe patient. The clinical data has to be followed accurately so thatthe physician will know how long the patient needs to be under themedication. When the heart failure occurs, it implies that there isno medication since sudden death occurs. It is important forindividuals to visit clinics so that blood pressure and how thevalves pass the blood can be noted since it will thwart suchoccurrence of sudden death.
Gardner, R., & Jackson, C. (2011). 4 The classical causes ofheart failure. Oxford Textbook of Heart Failure.
Juncos, L. (2012). Prerenal Azotemia. Clinical Decisions inNephrology, Hypertension and Kidney Transplantation, 175-182.
Yunfu, L. (2012). Changes of Peripheral Blood Cells in Patients withCirrhotic Portal Hypertension. Portal Hypertension – Causes andComplications.
Zhu, X. (2014). Double Outlet of Left Ventricle. Surgical Atlas ofCardiac Anatomy, 451-458.