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.
What is the difference between azotemia and uremia?
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?
Will's feelings of weakness and fatigue are symptoms of anemia. Why is he anemic?
Knowing what you do about Will's history, why is left ventricular dysfunction a concern for his physician?
Both azotemia and uremia describe the accumulation of metabolic wastes (normally excreted as urine) in the blood. Azotemia is the presence of nitrogenous wastes (urea, uric acid, and creatinine) in the blood and is often asymptomatic. Uremia results when all the products of urine accumulate in the blood and cause systemic manifestations. Uremia includes acid-base, electrolyte, and fluid imbalances. Without treatment, uremia results in multiorgan failure, coma, and death.
In renal sufficiency, the kidneys have difficulty in secreting the waste products of protein metabolism. A low-protein diet during this time can slow the progression of renal failure and decrease the symptoms of uremia.
In renal failure, erythropoietin secretion declines and red blood cell production falls below the needs of the body. The life span of RBCs is also shortened due accumulation of nitrogenous waste. Finally, if Will's anorexia was significant, a deficiency in dietary iron would also be a factor in the development of his anemic state.
Hypertension increases workload on the left ventricle and increases oxygen demand. Anemia contributes to left ventricular hypertrophy and ischemic events. Together, coupled with extracellular fluid overload, are all factors in Will's history that predispose him to left ventricular dysfunction or congestive heart failure.
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