FARMAKOTERAPI OBAT

PADA PENYAKIT
BATU SALURAN KEMIH
 Obat
Metode lain:
_
aa +
 Tx BG/SK
Litotripsi
Pembedahan
OT Di Ind. dikenal
sbg obat u/ BSK
Tempuyung Heyne, 1987
 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).
Incidence/prevalence
 1-5% of the population
 Men have twice the risk of women
 Usual age of onset depends on
composition of stone
 Additional stones form in 35% of
patients at 2 years and 52% at 10
years

9/30/2004 2
(Laerum & Murtagh, 2001)
 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 20’s to 40’s
– 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 & Ure-
tra (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.
 Pharmacotherapeutic
• 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

go other
 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
 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
 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
 Allopurionol  Uric acid stone
• Allopurinol is approximately 90% absorbed
from the gastrointestinal tract. Peak plasma
levels generally occur at 1.5 hours and 4.5
hours for allopurinol and oxipurinol,
respectively, and after a single oral dose of
300 mg allopurinol, maximum plasma
levels of about 3 mcg/mL of allopurinol and
6.5 mcg/mL of oxipurinol are produced.
• Approximately 20% of the ingested
allopurinol is excreted in the feces. Because
of its rapid oxidation to oxipurinol and a
renal clearance rate approximately that of
the glomerular filtration rate, allopurinol
has a plasma half-life of about 1-2 hours.
Oxipurinol, however, has a longer plasma
half-life (approximately 15 hours), and
• therefore effective xanthine oxidase
inhibition is maintained over a 24-hour
period with single daily doses of
allopurinol. Whereas allopurinol is cleared
essentially by glomerular filtration,
oxipurinol is reabsorbed in the kidney
tubules in a manner similar to the
reabsorption of uric acid.
Thiazide
• Hydrochlorothiazide
Bioavailibility 75 % Vd
0,8 l/kg PB 64 %
Eliminasi: hampir
sempurna dieliminasi
renal tanpa diubah dg
sekresi yg bersaing dg
uric acid. terjadi
reabsorpsi Ca2+ pd dct
• Indikasi klinis: • Toksisitas
Hipertensi Alkalosis metabolik hipo
Gagal jantung kongestif kalemik hiperurikemia
Nefrolitiasis hiperkalsi- Gangguan toleransi
uria idiopatik karbohidrat
Diabetes insipidus Hiperlipidemi
Hiponatremi
Reaksi alergi
Toksisitas lain: kelema-
Kontraindikasi:
han, kelelahan, pares-
>Sirosis hati, ggl ginjal
tesi, impotensi
Gagal jantung kongestif other
Diuretika hemat kalium
• Spironolacton (Sp)
(antagonis aldosteron)
• Triamteren, Amilorid
menghambat kanal ion
Na+
• (Sp) Bioavailibility 70
% Vd 0,05 l/kg PB
>98 % t½ plasma 10
mnt metabolit aktif
(Cantrenoat t½ 17
jam)
• Indikasi klinis • Toksisitas
Kondisi mineralokorti- Hiperkalemia
koid berlebihan (sin- Asidosis metabolik
droma Conn) atau al- hiperkloremik
dosteronisme sekunder Ginekomasti
(CHF, CH, SN)
Gagal ginjal akut
Batu ginjal

Kontraindikasi:
go
Hiperkalemia, insufisiensi
ginjal kronis, penyakit hati other
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
Tanaman Tempuyung (Sonchus arvensis L.
other
 Penyakit Infeksi
 Farmakologi Antibiotik = sudah diberikan
pada blok 9