Renal stone

- flank pain, hematuria, pyelonephritis, previous stone passage.
- costovertebral tenderness
- red cells in urine
- stone visualized on urography, ultrasonography, or spiral CT scan.

If the stone acutely obstructs the ureteropelvic junction or a calix, moderate to severe Renal pain will be noted, often accompanied by nausea, vomiting, and ileus. Hematuria is common. Staghorn calculi which may form a cast of all calices and the pelvis. Symptoms of infection , if present, will be exacerbated.
Laboratory:
Leukocytosis is to be expected. Urinalysis may reveal red and white blood cells and bacteria. A pH of 7,6 or higher implies the presence of urea-splitting organisms. A pH below 5,5 is compatible with the formation of uric acid or cystine stones. If the pH is fixed between 6 and 7, Renal tubular acidosis should be considered as a cause of nephrocalcinosis. A 24 hours urine collection for calcium may reveal hypercalciuria, which occurs with hyperparathyroidism and idiopathic hypercalciuria.
Imaging:
90% of calculi are radiopaque: calcium, cystine.
Nonopaque stone will be seen as radiolucent defect in the opaque contrast media.
Stone analysis:
Stone chemical composition should be analyzed.
Treatment:
- a high fluid intake 3-4L/d
specific:
* calcium stone formers, stop vitamin D suplements.
* oral orthophosphates are effective in decreasing urine calcium and increasing inhibitor activity
* thiazide diuretics, decreasing the calcium/oxalate content in urine by 50%.
* antibiotics
* percutaneous nephrostomy and percutaneous nephrolithotomy
* pulverization by means of ultrasonic, electrohydraulic, or laser probes passed through the nephrostomy tract may also be useful.
* residual infection stones may be dissolved by percutaneous irrigation with hemiacidrin
* extracorporeal shock wave lithotripsy/ eswl
* open surgical removal of stones

Benign prostatic hyperplasia

*prostatism: nocturia, hesitancy, slow stream, terminal dribbling, frequency
*residual urine
*acute urinary retention
*uremia in advanced cases
BPH is probably related to hormonal factors. Hyperplasia of the prostate causes increased outflow resistance. A higher intravesical pressure is required to accomplish voiding, causing hypertrophy of the vesical and trigonal muscles.
Stagnation of urine can lead to infection.
The size of the prostate rectally is not of primary diagnostic importance. The american urological association (AUA) developed a seven-items that can assist the patient and physician in evaluating the patients lower urinary tract symptoms (LUTS).
Laboratory:
Urinalysis reveal evidence of infection.
Residual urine is commonly increased >50cc.
Time urinary flow rate will be decreased <10-15 cc/s.
Serum prostate-specific antigen may be slightly elevated <4 ng/mL if it is over >10 ng/mL , cancer should be suspected.
Imaging:
The enlarged gland may cause an identation in the inferior surface of the bladder, which may result in a " J hook" deformity of the distal ureter. Pelvic ultrasound can obviate bladder catheterization and can also accurately predict the amount of residual urine.
Cystoscopic:
It will reveal secondary vesical changes (trabeculation) and enlargement of the periurethral prostatic glands. It may identify other conditions: bladder stones and tumors.
Treatment:
Conservative: alfa adrenergic blocking agents to relax the prostatic capsule and internal sphincter . 5alfa reductase inhibitors or antiandrogens to decrease the volume of the prostate. Catheterization is mandatory for acute urinary retention. Catheter should be left indwelling for 3 days while detrusor tone returns.
Surgical: indications are impairment of or threat to renal function and bothersome symptoms. Prostatectomy: transurethral resection/incision of the prostate(<50g), retropubic, suprapubic, and perineal.
- transurethral vaporization
- transurethral microwave chemotherapy
-transurethral needle/ultrasound ablation
-laser Prostatectomy