2.  Urinary stones have afflicted humankind since antiquity, with the earliest recorded example being bladder and kidney stones detected in Egyptian mummies dated to 4800 BC.  The specialty of urologic surgery was recognized even by Hippocrates, who wrote, in his famous oath for the physician, "I will not cut, even for the stone, but leave such procedures to the practitioners of the craft" ( Clendening, 1942).Clendening

3.  The prevalence of urinary tract stone disease is estimated to be 2% to 3%, and the likelihood that a white man will develop stone disease by age 70 years is about 1 in 8.  The recurrence rate without treatment for calcium oxalate renal stones is about 10% at 1 year, 35% at 5 years, and 50% at 10 years ( Uribarri et al, 1989).Uribarri  In 1993, urolithiasis cost the American economy $1.7 billion, including indirect costs from loss of productivity.

4.  Until the 1980s, urinary stones were a major health problem, › with a significant proportion of patients requiring extensive surgical procedures and › a sizable minority losing a kidney.

5.  BASED ON: - › Locations.  Nephro,(kidney)- Lithiasis.  Calyco,(Calyces)-lithiasis.  Pyelo, (Pelvis)- lithiasis.  Ureter,(Ureter) – lithiasis.  Vesico [cysto], (urinary bladder) – stone.  Prostato, (prostatic) – lithiasis.  Urethro (Urethral) –lithiasis.  Etc. › Compositions.

6.  Oxalate stones  Phosphatic stones.  Uric acid & Urate stones.  Cystine stones.  Xanthine Stones.  Indigo stones derived from indicans.

7.  Popularly known as the mulberry stone.  Mainly calcium oxalate and others  Usually single  Surface covered with projections.  Usually hard and very radio-opaque.

8.  Usually calcium phosphate /Others,(Ammonium, Magnesium & or combined).  Smooth  Dirty white.  Enlarges very fast in an alkaline medium.  May take the shape of the structure in which it is found. e.g. staghorn calculus.  Radio-opaque.

9.  Intrinsic factors. › Sex and age. › Genetics.  Extrinsic factors. › Geographical. › Climatic and seasonal factors. › Water intake. › Diet. › Occupation. › Stress and kidney association.

10. Many theories.  Thermodynamic Solubility Product, Saturation, and Super saturation.  Nucleation, Crystal Growth, and Aggregation  Free Particle Nucleation and Fixed Nucleation or Crystal Retention.  Modifiers of Crystal Formation: Inhibitors, Complexors, and Promoters.  Role of Matrix

11.  Urinary stones do not occur unless crystals of the offending substance form in urine.  For crystals to occur, the urine should be supersaturated with the salt in consideration.  An increase in urinary excretion of the chemicals that constitute the crystals results in an increase in the potential for crystallization.  Urine does not need to be continuously supersaturated for crystals to form or grow:

12.  Intermittent super saturation, as is seen during periods of dehydration or after meals, is sufficient.  Because urine is a complex solution, several factors affect the availability of ions required for crystallization.  Thus, the crystallizing potential of calcium oxalate is related not so much to the total concentration of calcium or oxalate in urine but to the chemical activity of the ions in solution.

13.  Compounds such as › citrate and phosphate form complexes with calcium, › and elements such as magnesium and sodium form complexes with oxalate, › effectively reducing the free ionic concentrations of each.

14.  Urinary super saturation alone cannot explain the formation of urinary stones.  Urinary crystals can be seen in most urine specimens, particularly after storage, yet most individuals do not form stones.  Stone formers as a group excrete larger crystals and crystal aggregates than do healthy individuals.

15.  Normal subjects have inhibitors of Lithologenesis. › crystal formation, › Crystal growth, and › Crystal aggregation in their urine.

16.  Free crystals formed within the kidney do not have the ability to grow to a size large enough to occlude a collecting duct and form a stone in a free-flowing urinary system.  Crystal aggregation and retention within the urinary tracts are prerequisites for urinary crystals to be converted to urinary calculi.

17.  Crystal aggregation is enhanced in individuals who lack inhibitors of aggregation.  The urinary glycoprotein nephrocalcin and Tamm-Horsfall protein are potent inhibitors of crystal aggregation in simple solutions,  whereas citrate and magnesium are inhibitors of crystal growth.

18.  These include low-molecular-weight compounds, such as citrate and pyrophosphate, and larger molecules, such as › glycosaminoglycans, › nephrocalcin, and › Tamm-Horsfall protein.  Urine from patients with recurrent calcium oxalate stones tends to have higher calcium and oxalate saturations and lower inhibitors than does urine from patients without stones.  A mathematically derived saturation-inhibition index has been reported to differentiate between the groups with more than 90% accuracy.

19.  Anatomic abnormalities, such as Medullary sponge kidney or ureteropelvic junction obstruction, or increased "stickiness" of the tubular epithelium can predispose to increased crystal retention.  Urate and calcium oxalate crystals anchor to surfaces of cultured renal epithelial cells and may adhere in vivo to tubular cells or urothelium.

20.  Although it is not proven, bacterial infection may promote calcium oxalate stone formation by increasing urinary matrix, which, in turn, promotes crystal adherence.  Finally, altered transport of calcium and oxalate by renal epithelial cells may result in interstitial or intracellular crystallization. These crystals are retained in the kidney and can become the nidus for stone formation.

21.  Asymptomatic. › Accidental findings in the course of assessment of an individual for some other pathological conditions. › Sometimes even for ordinary medical exams.  Symptomatic.  Acute Stone Episode.  Chronic.  Acute on chronic.

22.  Symptoms due to the primary disease conditions.  Symptoms due complications.

23.  Pain.  Dysuria.  Haematuria.

24.  Constitutional Changes. › Fever. › Headache. › Loss of appetite.  Others. › Swellings › Symptoms of renal failure.

25.  Urinalysis.  Chemical analysis.  Radiographic Examination.  Plain Abdominal Films.  Intravenous Urogram.  Ultrasonography.  Endoscopy.  Retrograde Cysto - urethrography.  Computed Tomography.  Magnetic Resonance Imaging.  HASTE MR

26.  MR sequencing using half-Fourier acquisition single- shot turbo spin-echo (HASTE) imaging has been reported in the assessment of ureteral obstruction. In one report, HASTE MR urography correctly diagnosed obstruction in 41 kidneys (100%), and the technique had a high correlation with IVU in identifying level of obstruction as well.  The study also identified the presence of perirenal fluid in 87% of obstructed kidneys and identified the site on the first 13-second scan in 80% of the studies performed. The ability to identify perirenal fluid is believed to be of value in differentiating acute from chronic obstruction.

27.  WATCHFUL WAITING › Dietary control e.g. Avoid diet rich in cacium e. g.  MEDICAL › Copious fluid intake › Treat associated medical conditions. › Dietary control › Use of Drugs.  SURGICAL.

28. Pre – op treatment. Intra - op. Treatment Post – op treatment.

29.  Open › Minimally invasive  Basket extraction e.g. Dormia basket.  Litholopaxy and washout.  Per cutaneous approach e. g. use of balloon catheter, ultrasonic lithotriptor › Invasive.  LITHOTOMY  ECTOMY.  Closed. › ESWL