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Clinical Examination of Mr Robinson Who Suffers from Gastrointestinal Bleeding

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Age, lifestyle habits, stress and diet are important risk factors determining the course of upper GI bleeding. Hematemesis is the vomiting of bright red blood or coffee-ground colored material resulting from previous bleeding, and it indicates an upper GI source proximal to the ligament of Treitz (Humes 2001). In the United States each year 100 patients per 10,000 are hospitalized for upper GI bleeding and about 20 patients per 100,000 are hospitalized for lower GI bleeding (Mushlin & Greene 2009). Blood specimen A of Mr Robinson exhibit the serum sodium value of 139 mmol/L, serum potassium of 4.5mmol/L, serum creatinine of 97mmol/L and Urea of 15mmol/L. Serum Sodium and Potassium: The normal serum sodium and potassium of Mr.

Robinson’ s blood analysis suggests that the kidney tubules have not undergone necrosis and the capability of active reabsorption and secretion of electrolytes is retained by the renal tubular cells. Any renal tubular necrosis would have resulted in deterioration of the serum electrolytes with an increase in serum potassium and decline of serum sodium. Renal tubular necrosis is presented with increased fractional sodium excretion, more than 1 percent, signifying the loss of tubular function to reabsorb sodium (Tierney et al.

2008). Prerenal azotemia is characterized by increased serum creatinine to serum urea ratio, due to increased absorption of urea, but near to normal serum sodium and potassium levels as the tubular function is preserved. Prerenal azotemia is caused mainly due to hypoperfusion of the kidney. The creatinine to blood urea nitrogen ratio exceeds 20:1 however, the fractional excretion of sodium is maintained at less than 1 percent (Tierney et al. 2008). Serum Urea and Creatinine: The urea is increased significantly in Mr Robinson as compared to serum creatinine which can be described as a result of prerenal azotemia and also as a consequence of absorption of nitrogenous products of blood in the small intestine (Mushlin & Greene 2009).

The increased protein load in the gut leads to increased production of urea, leading to elevated serum urea levels. Increased blood urea nitrogen can also be explained because of the dehydrated status of Mr. Robinson.  

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