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Bu Widy - Ginjal (Patofisiologi & Penatalaksanaan GGK)
Bu Widy - Ginjal (Patofisiologi & Penatalaksanaan GGK)
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)
PATOFISIOLOGI
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
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
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, confusioncoma
PENYEBAB CKD
Non-Diabet: Hipertensi, Renal Artery Stenosis Policystic kidney disease Glomerular disease Tubulointerstitial disease Obstructive Nephropathies Diabetes Mellitus
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
COMPLICATIONS
HYPERKALEMIA ACID-BASE DISORDER CARDIOVASCULAR HEMATOLOGIC NEUROLOGIC DISORDERS OF MINERAL METABOLISM ENDOCRINE DISORDERS GI DISORDER HYPERURICEMIA
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)
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
CARDIOVASCULAR
HYPERTENSION PERICARDITIS CONGESTIVE HEART FAILURE
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
Pericarditis
Cause: retention of metabolic toxins Symptoms & signs: chest pain, fever, pericardial effusion CO poor with distended Jugular Venous
PTH
Myocardial work
CHF
Atherosclerosis O2 demand
HEMATOLOGIC
ANEMIA COAGULOPATHY
ANEMIA
Characteristic: normochromic, normocytic Cause: erythropoetin production, Fe deficiency Low grade hemolysis Blood loss from platelet dysfunction HD
Coagulopathy
Platelet dysfunction Bleeding is prolong Platelet shows abnormal adhessiveness and aggregation Sign: petechiae, purpura
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)
OTHERS
GI DISORDERS include: nasea, vomiting, anoreksia, gastric/duodenal ulcer HYPERURICEMIA; impaired excretion of uric acid as renal function worsen
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
PHARMACOTHERAPY
Treating Reversible Causes of Renal Dysfunction Slowing the Progression of Renal Disease Treating Complications
1.
2. 3.
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
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, blocker Dietary Protein intake Protein restriction to 0,6g/kg/day in pt not on dialysis Glycemic control Strict glycemic control
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 13 x 325mg FeSO4 DISORDER OF MINERAL METABOLISM PTH, Ca Calcitriol, Ca CO3
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 amoniaurea Terapi: Antasid, H2-bloker, sukralfat
PHARMACEUTICAL CARE
TREATMENT OUTCOME
PREVENT PROGRESSION OF RENAL DISEASE PREVENT & MANAGE COMPLICATIONS
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
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
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
MONITORING
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
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?
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
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