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Renal

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Answer
90% of stones are:   radiopaque (visible): Ca & struvite). Uric acid & cystine stones are radiolucent.  
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Calcium oxalate or Ca phosphate stones   75%; occasionally with chronic hypercalcemia (hyperparathyroidism)  
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Magnesium – ammonium – phosphate (struvite) stones: prevalence   10-15%  
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Uric Acid / cystine stones: prevalence (%)   Uric Acid 5-8% of all kidney stones. Cystine 1-3%  
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Stones: DDx   AAA; Appendicitis; Tuboovarian Abscess (TOA); Ectopic Pregnancy  
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Urolithiasis: dx imaging   noncontrast CT (high sensitivity); US (hydronephrosis; good for PG); KUB (less specific)  
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Urolithiasis admission criteria   Infection / Sepsis; Complete Obstruction; Deteriorating renal fn; Intractable N/V; Solitary kidney; Very large or proximal stones  
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Renal stones lodge at:   UPJ (kidney stones), ureterovesicular junction/UVJ (bladder stones), or ureter at level of iliac vessels  
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Urolithiasis RFs   Prior stones, FH, low Ca/fluid intake, high oxalate/pro/Na intake, gastric bypass (RYGB); gout, DM, obesity, chronic UTIs, chronic diarrhea  
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Struvite stones form in pts with:   recurrent UTI (urease forming bacteria: proteus / klebsiella). Staghorn: often struvite  
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Urolithiasis clinical features   colicky flank pain +/- hematuria +/- fever/chills, N/V  
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Symptoms of renal stone in upper ureter:   radiate to anterior abdomen  
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Symptoms of renal stone in lower ureter:   radiate to ipsilateral groin, testes/ labia  
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Symptoms of renal stone in UVJ:   urgency, frequency, pelvic pain  
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ADPKD comorbididities   Berry aneurysms of the circle of Willis; cerebellar hemangioblastomas; hepatic cyst; hypertension (<50% of pts); valvular heart dz; divertic; renal failure  
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Meds contributing to stone formation   Antacids, carbonic anhydrase inhibitors (raise urine pH). Loop diuretics (increase urine Ca concentrations), thiazides (uric acid stones). Large doses vitamin C (-> hyperoxaluria)  
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Dietary factors on stone formation   Animal protein metabolism -> metabolic acidosis -> more Ca filtered/hypercaliuria. Meat (purine) -> uric acid. Green leafy (oxalate) -> Ca oxalate stones  
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Secondary causes of stones   HyperPTH, hyperthyroid, Cushing, granulomatous (sarcoid/TB/dissem candida), immobility, vit D intox, bone dz  
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Kidney stone dx   Stone analysis to ID. Noncontrast CT is TOC. US can show obstruction & hydro. 24hr urine, Urine Ca:Cr ratio. Check PTH in chronic pt if Ca elevated.  
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Kidney stone mgmt   IV fluids, analgesia. Most <5mm stones pass spontaneously. 5-10mm may need removal. Diet to lower Ca/ oxalate  
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UA findings in stones   pH <5.0 = uric acid & cystine. pH > 7.2 = struvite  
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Stones removed by:   lithotripsy (ESWL) or ureteroscopy w/extraction. Stones >10mm may require admission for lithotripsy or percutaneous nephrolithotomy  
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Medullary sponge kidney characteristics   Benign. Hereditary AD: MCKD1 or MCKD2 mutation on chromosomes 1 & 16. Dx in 4th-5th decade.  
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ADPKD genetics   Chromosome 16 short arm defect (90%). Chromosome 4 (10-15%), slower w/longer life expectancy  
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Epithelium-lined cavities filled with fluid or semisolid that develop from renal tubular elements =   cysts (70% of all renal masses)  
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Dx study for medullary sponge kidney   Intravenous pyelogram (IVP) - will show striations in papillary portions (=contrast accumulation in dilated collecting ducts)  
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Large echogenic kidneys on US =   ADPKD  
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