Bu Widy_ginjal (Patofisiologi & Penatalaksanaan Ggk)
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Transcript of Bu Widy_ginjal (Patofisiologi & Penatalaksanaan Ggk)
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PATOFISIOLOGI & PENATALAKSANAAN GAGAL GINJAL KRONIK
Dra. WIDYATI, MClin Pharm, Apt
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DEFINISI
Kidney damage for ≥ 3 months as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifest by either: pathological abnormalities; or markers of kidney damage, including abnormalities in the composition of the blood or urine; or abnormalities in imaging tests.
GFR < 60 mL/min/1.73m2 for ≥ 3 months, with or without kidney damage.
(NKF-KDOQI)
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CHRONIC KIDNEY DISEASE
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PATOFISIOLOGI
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CKD Manifest as a loss of renal reserve As CKD progress Pt may remain
asymptomatic As renal function worsen susceptible to
infection, poorly controlled hypertension
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ESRD
Clinical state irreversible loss of endogenous renal function RRT permanent
Azotemia Uremic syndrome: anemia, malnutrition;
impaired carbohydrate metabolism,fats,and proteins; defective utilization of energy and metabolic bone disease
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Symptoms & Signs Develop slowly and nonspecific Can be asymptomatic until stage 5 Manifestation: General: malaise, fatigue, weakness GI: anorexia, nausea, vomit, hiccup Neurologic: insomnia, irritable,twitch, paresthesia,
restless leg Libido , mens irregularity Cardiopulmonary: cardiomegaly, oedema, pericarditis Uremic encepahlopathy: asterixis, myoclonus, confusion-
coma
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PENYEBAB CKD
Non-Diabet: Hipertensi, Renal Artery Stenosis Policystic kidney disease Glomerular disease Tubulointerstitial disease Obstructive Nephropathies Diabetes Mellitus
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DIABETIK NEFROPATI Def: laju ekskresi albumin urin>300mg/24jam pd
Pt dg DM tanpa adanya penyakit ginjal lain (Selby,JAMA 1990)
Terjadi hampir 1/3 DM Tk albuminuria berhubungan dg tk gagal ginjal Faktor resiko perkembangan DN: Kontrol gula yg
buruk, HT, intake protein ,smoking, ,cholesterol Treatment: Insulin terapi, ACE inhibitor, restriksi
diet protein. Monitor: albuminuria, BP, komplikasi
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COMPLICATIONS
HYPERKALEMIA ACID-BASE DISORDER CARDIOVASCULAR HEMATOLOGIC NEUROLOGIC DISORDERS OF MINERAL METABOLISM ENDOCRINE DISORDERS GI DISORDER HYPERURICEMIA
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HYPERKALEMIA
K balance usually remain intact until GFR < 10ml/min
Endogenous causes: hemolysis, trauma, acidemic states, hyporeninemic hypoaldosteronism
Exogenous causes: diet, drugs that K secretion (spironolactone, ACE, NSAID)
Hyperkalemia arytmia, ECG change (QRS widen)
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ACID-BASE DISORDER Inability of kidney to excrete acid generated
from protein metabolism Primarily due to loss of renal mass Ammonia production & urine buffer
production pH is maintained at 7,33-7,37 & bicarb
15meq/L Excess of H+ buffered by CaCO3 & CaPO4
Renal osteodystrophy
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CARDIOVASCULAR
HYPERTENSION PERICARDITIS CONGESTIVE HEART FAILURE
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HYPERTENSION
Causes: Salt & water retention due to inability to
excrete, adjust to variation in intake water, Na as renal failure worsen
Hyperreninemic states Exogenous erythropoetin Failure to control HT lead to progression of
renal damage
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Pericarditis
Cause: retention of metabolic toxins Symptoms & signs: chest pain, fever,
pericardial effusion CO poor with distended Jugular Venous
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Congestive Heart Failure
HT
Myocardial work ↑
O2 demand ↑
Atherosclerosis ↑
PTH
CHF
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HEMATOLOGIC
ANEMIA COAGULOPATHY
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ANEMIA
Characteristic: normochromic, normocytic Cause: erythropoetin production, Fe deficiency Low grade hemolysis Blood loss from platelet dysfunction HD
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Coagulopathy
Platelet dysfunction Bleeding is prolong Platelet shows abnormal adhessiveness
and aggregation Sign: petechiae, purpura
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NEUROLOGIC
Uremic encephalopathy Occur at CKD stage 5 or ESRD Cause: hiperPTH; Ca >12-15mg/dL Symptoms: difficulty in concentrating,
lethargy,confusion, coma Physical: nystagmus, weakness, asterixis,
hypereflexia Neuropathy: can be peripherally (restless legs, distal
pain, lost of tendon reflexes) and others (impotence, autonomic dysfunction)
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DISORDERS OF MINERAL METABOLISM Renal Osteodystrophy: disorder of Ca, P and
bone. Form: osteomalacia, osteitis fibrosa cystica
GFR falls <25% impaired P excretion, renal conversion of vit D3, gut absorption of Ca
Hyperphosphatemia hypocalcemia PTH secretion bone turnover ↑
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OTHERS
GI DISORDERS include: nasea, vomiting, anoreksia, gastric/duodenal ulcer
HYPERURICEMIA; impaired excretion of uric acid as renal function worsen
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ENDOCRINE DISORDER
Renal insulin clearance insulin level↑ Glucose intolerance can occur when GFR<10-
20ml/min due to pheripheral insulin resistance. Testosterone libido, impotence Estrogen anovulatory Abnormalities in thyroxine, GH, aldosterone,
cortisol level
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PHARMACOTHERAPY
1. Treating Reversible Causes of Renal Dysfunction
2. Slowing the Progression of Renal Disease
3. Treating Complications
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Treating Reversible Causes Factors responsible for acute decrements in renal
function in CKD: volume depletion, CHF, nephrotoxic drugs, radiocontrast
Hypovolemia treatment: repletion, dose of diuretic,↑ Na intake
CKD + CHF treatment: Loop diuretic (maintaining fluid balance)
Use of Nephrotoxic drug: adjust dose, avoid Radiocontrast: use non-ionic contrast,hydration 12
hours before procedure
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Slowing the Progression of RD
Systemic HT Generates ↑intraglomerular pressures and accelerate
glomerular sclerosis and RD Antihypertensive protect both renal & cardiovascular
Antihypertensive in non-proteinuric CKD unable to slow the progression
Agents: ACE,ARB, diuretic, Diltiazem, Verapamil, β-blocker
Dietary Protein intake Protein restriction to 0,6g/kg/day in pt not on dialysis Glycemic control Strict glycemic control
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Treating Complication
HYPERKALEMIA Treatment: iv Ca gluconate, insulin +glucose, Nabic, ion exchange
resin, dialysis ACIDOSIS Treatment: Nabic 0,51mEq/kg/d target Nabic level>22mEq/L HEMATOLOGIC Anemia: erythropoetin started 50U/kg 1-2 x/week s.c.(iron stores
must be adequate), iron supplementaion if ferritin < 100g/ml with 1-3 x 325mg FeSO4
DISORDER OF MINERAL METABOLISM PTH↑, Ca Calcitriol, Ca CO3
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Treating Complication
HIPERURICEMIA Krn kegagalan ginjal mengekskresi as urat. Terapi: Allopurinol atau dialisis.
ABNORMALITAS GI (lihat ARF)
Karakterisitik: anoreksia, gastrik/duodenal ulcer
Penyebab: prod. amonia , siklus internal amonia-urea
Terapi: Antasid, H2-bloker, sukralfat
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PHARMACEUTICAL CARE
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TREATMENT OUTCOME
PREVENT PROGRESSION OF RENAL DISEASE
PREVENT & MANAGE COMPLICATIONS
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COMMON PROBLEM
PROBLEM MEDIK: Anemia, kelainan hematologi Hipertensi yang tidak terkontrol dg>3 AHT Uremia, acidosis Hiperuricemia, Hiperkalemia/Hipokalemia Gangguan GIT DRP: Over/low dose, cek apakah perlu penyesuaian Adrac Pemilihan obat yang kurang tepat
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IMPLIKASI FARMASI KLINIK
Estimasi fungsi ginjal: Cockroft-Gault, klirens kreatinin
Tinjau perlu-tidaknya penyesuaian dosis. Sesuaikan dosis khususnya pada Renally excreted drug/metabolit
Ketahui metabolisme, aktivitas, DOA, dan metode ekskresi.
Pilih obat dg nefrotoksisitas minimal Lakukan TDM Hindari penggunaan lama
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IMPLIKASI FARMASI KLINIK Monitor efektifitas, ADR, toksisitas lebih ketat Gangguan GI:awasi peresepan antasid Plasma protein binding:awas obat highly protein
bound (ikatan protein>90%) Na & air retensi: cek Na-content Awasi tekanan darah & efektivitas antihipertensi Farmakodinamik: awasi obat yg CNS sensitivity Dialisis: sesuaikan dosis obat terdialisis
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Estimate Renal Function
Goal: to assess the need of dossage adjustment COCKROFT-GAULT
CrCl = 1.23(pria)or 1.04 (wanita) x(140-umur)x BB Serum creatinine(mol/L)BB: gunakan IBW kecuali BB<IBWIBW : Pria 50+2.3/inch (TB>150 cm) Wanita: 45.5 + 2.3/inch (TB>150 cm) Pengukuran CrCl melalui urin tampung 24 jamCrCl= Uvol x [U Cr] [Cr*] x t* kadar pada midpoint pengumpulan urin
Populasi: Critically ill, trauma, post-op
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Estimate Renal Function
Modified Diet in Renal Disease (MDRD) GFR (mL/min/1.73 m 2) = 186 x [Cr] –
1.154 x (Age) – 0.203 x (0.742 if female) x (1.210 if African – American)
SCr: serum creatinine in mg/dL; age in years
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MONITORING BIOKIMIA: Cr, BUN, elektrolit (Na, K, Ca, PO4),
keseimbangan asam-basa, albumin, BSL, Asam urat.
Hematologi: Hb, platelet, hematokrit, white cell count,
profil koagulasi Karakteristik Pasien: BP, BB, temp.,KU, kulit. Terapi Obat: TDM, dosis, efek, adverse drug
reaction, nefrotoksisitas
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CASE1
Ny MS, 60 th, BB 55kg RP:DM, ESRD (routine on Dialysis) RO: Dexacap 3x25mg, Diltiazem 3x30mg,
Glurenorm1-0-0.Neurovit E 1x1tab,Allopurinol2x1tab
PC: Hyperglikemia, sesak napas, batuk kering,febris, hypertension ( 200/120mmHg)
Lab: Leukocyt 18000, Na 128 meq/dl,K 5,6 meq/dL, BSL 200mg/dl, Urat5,6mg/dl Cr PHD 7,5 mg/dl, BUN 89 mg/dl
Dx: CRF + febris,encephalopathy
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Case 2 Ny H, 24th, BB 45kg TB 150cm PC: lemah, muntah, sesak napas RP: Hipertensi RO: Blopress 8mg Lab: Cr 14,7mg/dL, BUN 124 mg/dL, SGOT
(N), SGPT (N), Na 115meq/L, K 2,7 meq/L, BSL 90 mg/dL.
Dx: CRF, citto HD Apa rencana farmasis terhadap kasus ini?
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CASE 3 Ny MS, 60 th, BB 55kg RP:DM, ESRD (routine on Dialysis) RO: Dexacap 3x25mg, Diltiazem 3x30mg,
Glurenorm1-0-0.Neurovit E 1x1tab,Allopurinol2x1tab
PC: Hyperglikemia, sesak napas, batuk kering,febris, hypertension ( 200/120mmHg)
Lab: Leukocyt 18000, Na 128 meq/dl,K 5,6 meq/dL, BSL 200mg/dl, Urat5,6mg/dl Cr PHD 7,5 mg/dl, BUN 89 mg/dl
Dx: CRF + febris,encephalopathy
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DIABETIK NEFROPATI Terjadi hampir 1/3 DM Tk albuminuria berhubungan dg tk gagal
ginjal Faktor resiko perkembangan DN: Kontrol
gula yg buruk, HT, intake protein Treatment: Insulin terapi, ACE inhibitor,
restriksi diet protein. Monitor: albuminuria, BP, komplikasi