Urinary tract stone disease, depict

Urinary tract stone disease, depicted below, is likely caused by two basic phenomena.
The first phenomenon is supersaturationทำให้อิ่มตัว of the urine by stone-forming constituents, including calcium, oxalate, and uric acid. Crystals or foreign bodies can act as nidi, upon which ions from the supersaturated urine form microscopic crystalline structures. The resulting calculi give rise to symptoms when they become impacted within the ureter as they pass toward the urinary bladder.
The overwhelmingทำให้รู้สึกท่วมท้น majority of renal calculi contain calcium. Uric acid calculi and crystals of uric acid, with or without other contaminating ions, comprise the bulk of the remaining minority. Other, less frequent stone types include cystine, ammonium acid urate, xanthine, dihydroxyadenine, and various rare stones related to precipitation of medications in the urinary tract. Supersaturation of the urine is likely the underlying cause of uric and cystine stones, but calcium-based stones (especially calcium oxalate stones) may have a more complex etiology.
The second phenomenon, which is most likely responsible for calcium oxalate stones, is deposition of stone material on a renal papillary calcium phosphate nidus, typically a Randall plaque (which are always composed of calcium phosphate). Evan et al recently proposed this model based on evidence accumulating from several laboratories.[4]
Calcium phosphate precipitates in the basement membrane of the thin loops of Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal papilla. The subepithelial deposits, which have long been known as Randall plaques, eventually erode through the papillary urothelium. Stone matrix, calcium phosphate, and calcium oxalate gradually deposit on the substrate to create a urinary calculus.
Development of renal colic pain and renal damage
The colicky-type pain known as renal colic usually begins in the upper lateral midback over the costovertebral angle and occasionally subcostally. It radiates inferiorly and anteriorly toward the groin. The pain generated by renal colic is primarily caused by the dilation, stretching, and spasm caused by the acute ureteral obstruction. (When a severe but chronic obstruction develops, as in some types of cancer, it is usually painless.)
In the ureter, an increase in proximal peristalsis through activation of intrinsic ureteral pacemakers may contribute to the perception of pain. Muscle spasm, increased proximal peristalsis, local inflammation, irritation, and edema at the site of obstruction may contribute to the development of pain through chemoreceptor activation and stretching of submucosal free nerve endings.
The term "renal colic" is actually a misnomer, because this pain tends to remain constant, whereas intestinal or biliary colic is usually somewhat intermittent and often comes in waves. The pattern of the pain depends on the individual’s pain threshold and perception and on the speed and degree of the changes in hydrostatic pressure within the proximal ureter and renal pelvis. Ureteral peristalsis, stone migration, and tilting or twisting of the stone with subsequent intermittent obstructions may cause exacerbation or renewal of the renal colic pain.
The severity of the pain depends on the degree and site of the obstruction, not on the size of the stone. A patient can often point to the site of maximum tenderness, which is likely to be the site of the ureteral obstruction (see the image below).