Urinary Calculi

Urinary Calculi: Case Study
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1 Discuss possible factors that may have been responsible for the development of the stone and use this case to show how the patient’s diet and water intake can help analyze the composition of the calculi.
Urinary calculi formation is secondary to the increased saturation of the urine. Subsequently, it leads to the crystallization of particles, nucleation, progression in size, fixation, and further growth in size. Ultimately, it obstructs the renal, urinary system, or both, leading to the symptoms felt by the patient, such as flank pain, dysuria, and hematuria. There are different types of urinary calculi, and each has a distinct mechanism of formation. The differences are secondary to physiologic and pathological processes altered by a diseased state or the individual’s diet (Ratkalkar & Kleinman, 2011).
Calcium oxalate formation is increased with a high intake of nuts, legumes, spinach, rhubarb, and wheat bran, increasing the formation of oxalate. Its formation is also enhanced by increased sodium intake, which has high amounts in canned, packaged, and fast foods, high in preservatives. It is also enhanced by the intake of animal protein, particularly red meat. Similarly, calcium phosphate stones are formed with increased animal protein and sodium intake, while uric acid stone formation is directly proportional to animal protein intake. Lastly, cystine stone formation is primarily associated with the decreased water intake (NIDDK, 2017). In this case, the patient is a grocer sales clerk, and his occupation predisposes him to the risks of buying foods with high preservatives, which contribute to urinary calculi formation.
Promoters and inhibitors also influence stone formation. The promoters are the following: 1) High urate or uric acid. This stimulates the attachment of the calcium oxalate cells. It leads to nucleation and aggregation of crystal particles.; 2) Acidic urine pH induces calcium oxalate, uric acid, and the subsequent nucleation of calcium oxalate to calcium phosphate; 3) Increased intake of Vitamin D and Calcium plus the enhanced release of calcium from bones direct the saturation of the crystals; 4) Congenital diseases affecting the metabolism of oxalate results to its overproduction. Conversely, its inhibitors include the alkalinization of urine, increased citrate, pyrophosphate, magnesium, glycoproteins, and phytate (Gupta & Shamsher, 2018).
2 What would be the test results of his white blood cells, blood calcium levels, CT scan, and x-ray?
Obstruction in...