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FARMAKOTERAPI OBAT
PADA PENYAKIT
BATU SALURAN KEMIH
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Tx BG/SK
OT
Tempuyung
Obat
Pembedahan
Metode lain:Litotripsi aa
+_
Di Ind. dikenalsbg obat u/ BSKHeyne, 1987
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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).
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(Laerum & Murtagh, 2001)
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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
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Epidemiology
Genetic
Evidence not clear
Does appear in certain genetic disorders
Familial renal tubular acidosis
Cystenuria
Hereditary xanthinuria dehydroxyadeninuria
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Epidemiology
Age and sex
Peak occurrence in 20s to 40s
Males > females
Women are more likely to have infectious or
hereditary cause
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Ind. termasuk daerah sabuk batu (stone
belt) BSK (Subadi,1999)
Retensi urin; 28,58 % karena BKM & Ure-tra (Barus, 1999)
Wiranto, 1999 meneliti BSK di RSUP Dr.Sarjito dari Jan 93-Des 97 menemukan317kasus
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Batu saluran kemih dapat diderita siapa sajadari 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).
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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 pmbtkbatu & pH. ( Teori presipitasi kristalisasi)
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Stones apparently form in an organized mannerinfluenced by:
-Composition of the environment-urinary solutes
-urinary particles, i.e. bacteria, sloughed
urothelium-uromucoidslarge arrays or protein formed in
the urinary tract
-glycoaminoglycansgroup of substances whichcoat the urinary tract
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-Nature of the bed of origin
-urothelium (transitional cell epithelium)
-Field characteristics
-magnetic
-gravitationalpossibly influence
of gravity on certain particles
-Nature of Nidal forcesit is assumedthat every stone starts as a central core
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Physical Chemistry
Supersaturation
Central event in stone formation
Dependant on concentration, temperature, pH,other chemicals
Urine
Contains inhibitors which allow supersaturation
metastable concentration
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Stone formationonce theprocess stone formation has
begun, we are no longer dealing
with a biological driven system,
it is all a chemical process from
that point on.
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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
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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
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Treatment
Percutaneous Ultrasound
Laser
Electrohydrolic
ESWL
the most frequent treatment modality forstones in the upper ureter and the kidneys
Endourolology
Laser
ultrasound
Extraction
Open lithotomy
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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/oramiloride
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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) excessivedietary consumption (leafy greens), or
recessive metabolic syndrome
Treatment: cholestyramine, low-fat, lowoxalate diet, calcium supplements given with
meals
go
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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 otherdisorders (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
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Uric acid stones
Urate stones are radiolucent
Hyperuricosuria AND low urinary pH (usually less
than 5.5) Assoc. conditions: myeloprolferative disorders (with
or without chemo), Lesch-Nyhan
Treatment: alkalinization of urine with bicarb or
citrate, hydration, allopurinol
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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
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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-mercaptoproprionylglycine
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Penanganan batu saluran kemih
Konservatif: Hidrasi, Diet.
Obat (Simptomatik: Analgesik, spasmolitik),
(kausatif).
Tindakan (Invasif, noninvasif)
Obat tradisional dari berbagai jenis tana-
man: daun (keji beling, gempur batu,
tempuyung, urat,wungu, kaki kuda); akar
(pohon enau, bt. Pepaya); rimpang(temulawak). Farmakologinya ???
other
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Tanaman Tempuyung (Sonchus arvensis L.
other
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Allopurinol - Zyloric
Cholestyramin - Questran
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other
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go
other
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Basitrasin
Vankomisin
AmfoterisinNistatinSulfonamid, Trimetoprim
Metronidazol, INH, Asam
Nalidiksat, vidarabin,
A l i
Linkomisin
Klindamisin
1
23
4
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