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Obat Tx BG/SK
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Why is it important?
Prevalence 2% to 3% Likelihood that a white man will develop stone disease by age 70 1 in 8. Recurrence rate without treatment for calcium oxalate renal stones 10% at 1 year, 35% at 5 years, and 50% at 10 years
(Uribarri et al, 1989).
Epidemiology
Rare in Native Americans, blacks of African or American decent, and native born Isrealis Bladder stones more common in malnourished, kidney disease more common in affluent
Epidemiology
Genetic
Evidence not clear Does appear in certain genetic disorders
Familial renal tubular acidosis Cystenuria Hereditary xanthinuria dehydroxyadeninuria
Epidemiology
Age and sex
Peak occurrence in 20s to 40s Males > females Women are more likely to have infectious or hereditary cause
Ind.
termasuk daerah sabuk batu (stone belt) BSK (Subadi,1999) Retensi urin; 28,58 % karena BKM & Uretra (Barus, 1999)
Wiranto, 1999 meneliti BSK di RSUP Dr. Sarjito dari Jan 93-Des 97 menemukan 317kasus
Batu saluran kemih dapat diderita siapa saja dari bayi sampai usia lanjut. Gilsanz, dkk 1985 10 bayi prematur dg Nefrolithiasis. Penderita BSK di RSUP Dr.Sardjito termuda laki-laki usia 2,5 th. & tertua 86 th. Pasien 79,6 %; 20,4 % dan terbanyak ditemukan umur dekade kelima yaitu 30 % (Wiranto, 1999).
Patogenesis terjadinya BSK * Teori presipitasi kristalisasi * Teori pembentukan inti matrik * Teori ketiadaan inhibitor * Teori penghambatan sistem limfa Teori yg konsisten pd bbrp pmbntk batu: pengeluaran bhn/unsur pokok pmbtk batu & pH. ( Teori presipitasi kristalisasi)
Stones apparently form in an organized manner influenced by: -Composition of the environment -urinary solutes -urinary particles, i.e. bacteria, sloughed urothelium -uromucoids large arrays or protein formed in the urinary tract -glycoaminoglycans group of substances which coat the urinary tract
-Nature of the bed of origin -urothelium (transitional cell epithelium) -Field characteristics -magnetic -gravitational possibly influence of gravity on certain particles -Nature of Nidal forces it is assumed that every stone starts as a central core
Physical Chemistry
Supersaturation
Central event in stone formation Dependant on concentration, temperature, pH, other chemicals
Urine
Contains inhibitors which allow supersaturation metastable concentration
Stone formation once the process stone formation has begun, we are no longer dealing with a biological driven system, it is all a chemical process from that point on.
Symptoms/signs
Moderate to severe colicky flank pain, may radiate towards the testis, vulva or loin Radiation indicates that the stone has migrated toward lower third of ureter Some may even present with ureteral obstruction, unexplained persistent UTIs, or painless hematuria
Full workup
Pt. have h/o diarrhea, UTIs, or gout? FHx of stones? Urine pH, culture if UA shows signs of infection Serum calcium, phosphorous, parathyroid hormone, sodium, oxalate, citrate, uric acid, creatinine 24 hour urine collection for: calcium, sodium, oxalate, citrate, urate, creatinine Further imaging
Treatment
Percutaneous
ESWL the most frequent treatment modality for stones in the upper ureter and the kidneys Endourolology
Laser
ultrasound Extraction
Open lithotomy
Treatment
Normal calcium intake (lowers stone events by 50%) Low sodium diet High fluid intake (UO should be >2L/day) Hypercalcuria worsened by: high sodium diet, loop diuretics, high intake of animal protein For recurrent stones: thiazide diuretic and/or amiloride
What is amiloride?
Mild potassium-sparing diuretic Unique class, acts on distal convoluted tubule and collecting duct Action is independent of aldosterone Cannot use in patients with renal insufficiency Can cause hyperkalemia
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Hyperoxaluria
Results from fat malabsorption (IBD, chronic pancreatitis, jejunoileal bypass) excessive dietary consumption (leafy greens), or recessive metabolic syndrome Treatment: cholestyramine, low-fat, low oxalate diet, calcium supplements given with meals
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Hypocitrauria
Citric acid helps to prevent calcium stones by complexing wth free urinary calcium May be alone or found in combination with other disorders (RTA, chronic diarrheal illness Treatment: alkali, usually complexed with potassium instead of sodium Alkali increase urinary excretion of citrate
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Hyperuricosuria
Can cause calcium oxalate stones High urinary uric acid causes supersaturation of calcium oxalate Mainly from excessive dietary purine consumption Treatment: low dietary purine, allopurinol
Struvite stones
From urease-producing organisms, most often Proteus mirabilis Infection can occur from chronic obstruction, instrumentation, or chronic antibiotic therapy Treatment: antibiotics, removal of staghorn calculus, which is frequently infected
Cystine Stones
Genetic defect in amino acid transport in the GI brush border and renal tubules Suspect when stones are formed at a young age Stones are radioopaque Treatment: hydration (UO>3L/day), alkalinization, and D-penicillamine or alpha-mercaptoproprionyl glycine
other
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