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  Obstruction is one of the most important abnormalities of the urinary tract, since it eventually leads to decompensation of the muscular conduits and reservoirs, back pressure, and atrophy of renal parenchyma. It also invites infection and stone formation, which cause additional damage and can ultimately end in complete unilateral or bilateral destruction of the kidneys.


  Both the level and degree of obstruction are important to an understanding of the pathologic consequences. Any obstruction at or distal to the bladder neck may lead to back pressure affecting both kidneys. Obstruction at or proximal to the ureteral orifice leads to unilateral damage unless the lesion involves both ureters simultaneously. Complete obstruction leads to rapid decompensation of the system proximal to the site of obstruction ,with immediate muscular failure. For example, acute retention occurs if the obstruction is distal to the bladder, and anuria occurs if obstruction involves both ureters. Partial obstruction leads to gradual progressive muscular hypertrophy followed by gradual dilation. decompensation ,and hydronephrotic changs. Vesicoureteral reflux may develop in some cases.




  Acquired urinary tract obstruction may be due to inflammatory or traumatic urethral strictures, bladder outlet obstruction (benign prostatic hypertrophy or cancer of the prostate), vesical tumors, neuropathic bladder, extrinsic ureteral compression (tumor, retroperitoneal fibrosis, or enlarged lymph nodes), ureteral or pelvic stones, ureteral strictures, or ureteral or pelivic tumors.




  Regardless of its cause, acquired obstruction leads to similar changes in the urinary tract, which vary depending on the severity and duration of obstruction.


  a. Urethral Changes: Proximal to the obstruction, the urethra dilates and balloons. Aurethral diverticulum may develop, and dilatation and gaping of the prostatic and ejaculatory ducts may occur.


  b. Vesical Changes: Early, the detrusor and trigonal thickening and hypertrophy compensate for the outlet obstruction, allowing complete bladder emptying . This change leads to progressive development of bladder trabeculation, cellules, saccules, and then, diverticula. Subsequently, bladder decompensation occurs and is characterized by the above changes plus incomplete bladder emptying, resulting in residual urine. Trigonal hypertrophy leads to secondary urteral obstruction owing to increased resistance to flow through the intravesical ureter. With detrusor decompensation and residual urine accumulation, there is strectching of the hypertrophied trigone, which appreciable increases ureteral obstruction. This is the mechanism of back pressure on the kidney in the presence of vesical outlet obstruction (while the urterovesical junction maintains its competence)。 Catheter drainage of the bladder relieves trigonal stretch and improves drainage from the upper tract.


  A very late change with persistent obstruction (more frequently encountered with neuropathic dysfunction) is decompensation of the ureterovesical junction, leading to reflux. Reflux aggravates the back pressure effect on the upper tract by exposing it to abnormally high intravesical pressures——in addition to favoring the onset or persistence of urinary tract infection.


  c. Ureteral Changes: The first noted change is a gradually progressive increase in uretereal distention. This increases ureteral wall stretch, which in turn increase contractile power and produces ureteral hyperactivity and hypertrophy. Because the ureteral musculature runs in an irregular helical pattern, stretching of its muscular elements leads to lengthening as well as widening. This is the start of ureteral decompensation, where tortuosity and dilatation become apparent. These changes progress until the ureter becomes atonic, with infrequent and ineffective or completely absent peristalsis.


  d. Pelvicaliceal Changes: The renal pelvis and calices, being subjected to progressively increasing volumes of retained urine, progressively distend. The pelvis first shows evidence of hyperactivity and hypertrophy and then progressive dilatation and atony. The calices show the same changes to a variable degree, depending on whether the renal pelvis is intrarenal or extrarenal. In the latter, caliceal dilatation may be minimal in spite of marked pelvic dilatation. In the intrarenal pelvis, caliceal dilatation and renal parenchymal damage are maximal. The successive phases seen with obstruction are rounding of the fornices, followed by flattening of the papillae and finally clubbing of the minor calices.

  d.肾盂肾盏改变:肾盂肾盏由于承受的残余尿容量逐渐增加而扩张。肾盂早期表现是蠕动增强及肥厚,以后逐渐扩大及无张力。肾盂根据其是肾内肾盂抑或外肾盂,而呈不同程度的同样改变。如为后者,虽然肾盂已明显扩大,肾盏扩张可能不明显;而若为肾内肾盂,肾盏扩张和肾实质损害均严重。其梗阻连续相(Successive phase)所见为穹窿呈圆形,接着肾乳头呈扁平,最后肾小盏呈杵状。

  e. Renal Parenchymal Changes: With progressive pelvicaliceal distention, there is parenchymal compression against the renal capsule. This, plus the more important factor of compression of the arcuate vessels as a result of the expanding distended calices, results in a marked drop in renal blood flow. This leads to progressive parenchymal compression and ischemic atrophy. Lateral groups of nephrons are affected more than central ones, leading to patchy atrophy with variable degrees of severity. The glomeruli and proximal convoluted tubules suffer most from this ischemia. Associated with the increased intrapelvic pressure, there is progressive dilation of the collecting and distal tubules, with compression and atrophy of tubular cells.


  Clinical Findings


  a. Symptoms and Signs: The findings vary according to the site of obstruction:


  Infravesical obstruction——Infravesical obstruction leads to difficulty in initiation of voiding, a weak stream, and a diminished flow rate with terminal dribbling. Burning and frequency are common associated symptoms. A distended or thickened bladder wall may be palpable. Urethral induration of a stricture, benign prostatic hypertrophy, or cancer of the prostate may be noted on rectal examination. Meatal stenosis and impacted urethral stones are readily diagnosed by physical examination.


  Supravesical obstruction——Renal pain or renal colic and gastrointestinal symptoms are commonly associated. Supravesical obstruction may be completely asymptomatic when it develops gradually over a period of several weeks or months. An enlarged kidney may be palpable. Costovertebral angle tenderness may be present.


  b. Laboratory Findings: Evidence of urinary infection, hematuria, or crystalluria may be seen. Impaired kidney function is noted by elevated blood urea nitrogen and serum creatinine, with the ratio well above the normal 10:1 because of urea reabsorption.


  c. X-Ray Findings: Radiologic examination is usually diagnostic in cases of stasis, tumors, and strictures. Dilatation and anatomic changes occur above the level of obstruction, whereas distal to the obstruction, the configuration is usually normal. This helps in localizing the site of obstruction .Combined antegrade imaging by intravenous urograms and retrograde imaging by ureterograms or urethrograms, depending on the site of obstruction, is sometimes needed to demonstrate the extent of the obstructed segment. In supravesical obstruction, demonstration of stasis and delayed drainage is essential to establish and measure the severity of obstruction.


  d. Special Examinations:


  Antegrade urography via percutaneous needle or tube nephrostomy is of particular value when the obstructed kidney fails to excrete the radiopaque material on excretory urography. This procedure allows application of the Whitaker test, during which fluid is introduced into the renal pelvis at varying rates. The fluid transport can be measured and the degree of obstruction estimated by the use of a pressure monitor.

  顺行时尿路造影:当阻塞的肾脏在排泄性尿路中造影剂不能排泄时,使用经皮针或者说导管行肾造瘘特别有价值,这种操作可施行Whitaker试验, 在试验期间液体可以不同程度注入肾盂。可测量液体转移,以压力监测器来估计梗阻程度。

  Ultrasonography——This will reveal the degree of dilatation of the renal pelvis and calices and allows for diagnosis of hydronephrosis in the prenatal period.


  Isotope studies——A technetium Tc 99m DMSA scan portrays the degree of hydronephrosis, as well as renal function. Use of diruretics during the scan can provide information similar to that obtained with the Whitaker test.

  同位素检查:用锝99M DMSA扫描可了解肾盏积水程度及肾功能。在扫描时使用利尿剂可得到与Whitaker试验相似的效果。

  CT scan——This may be of value in revealing the degree and site of obstruction as well as the as the cause in many cases. The use of contrast agents will allow estimation of residual renal function.




  The most important complication of urinary tract obstruction is renal parenchymal atrophy as a result of back pressure. Obstruction also predisposes to infection and stone formation, and infection occurring with obstruction leads to rapid kidney destruction.




  The aim of therapy is relief of the obstruction(eg, catheterization for relief of acute urinary retention)。 Surgery is often necessary. Simple urethral stricture may be managed conservatively by dilation or urethrotomy. However, urethroplasty may be required. Benign prostatic hypertrophy and obstructing bladder tumors require surgical removal.


  Impacted stones must either be removed or bypassed by a catheter if it is thought that they may pass spontaneously. If they do not pass spontaneously, the stones must be removed surgically later.


  Ureteral or ureteropelvic junction obstruction requires surgical revision and plastic repair, either by ureterovesicoplasty, ureteroureteral anastomosis, bladder flaps to bridge a gap in the lower ureter, transureteroureteral anastomosis or ureteropyeloplasty. Penal stones may be removed instrumentally via percutaneous nephrostomy or by irrigation through a tube placed directly into the kidney.


  Preliminary drainage above the obstruction is sometimes needed to improve kidney function. Occasionally, permanent drainage and diversion by cutaneous ureterostomy, ileal or colonic loop diversion, or permanent nephrostomy is required. If damage is advanced, nephrectomy may be indieated.




  The prognosis depends on the cause, site, duration, and degree of kidney damage and renal decompensation. In general, relief of obstruction leads to improvement in kidney function except in seriously damaged kidneys, especially those destroyed by inflammatory scarring.


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