Download - Presentasi Gout
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HIPERURISEMIA & GOUT
Oleh:Dinna Hanifah
I11111051
Pembimbing :dr. Fitri Fatimah
SMF ILMU KEDOKTERAN KOMUNITASUPTD PUSKESMAS KECAMATAN
PONTIANAK SELATANFAKULTAS KEDOKTERAN
UNIVERSITAS TANJUNGPURA2016
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PENDAHULUAN Purin (adenin & guanin) dan pirimidin
(sitosin, timin, urasil) mempunyai peran yang penting dalam:Replikasi materi genetikTranskripsi genSintesis proteinMetabolisme seluler
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PENDAHULUAN Asam urat adalah produk akhir dari
degradasi purin pada manusia Monosodium urat adalah bentuk ionisasi
dari asam urat, 98% predominasi di cairan plasma ekstraseluler dan cairan synovial.
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PENDAHULUAN Purin sebagai nukleotida disintesis dan
didegradasi di semua jaringan Asam urat di produksi hanya pada
jaringan yang mengandung xanthine oxidase, terutama pada hati dan usus halus
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PENDAHULUAN Normalnya 67-75% asam urat
dieksresikan oleh ginjal dan sisanya dieleminasi melalui usus
Konsentrasi asam urat: Anak: 3,0 – 4,0 mg/dl Laki-laki dewasa : 6,8 mg/dl Wanita premenopouse : 6,0 mg/dl
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HIPERURISEMIA Hiperurisemia didefinisikan sebagai
konsentrasi asam urat pada serum/plasma darah > 6,8 mg/dl.
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ETIOLOGI
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PATOGENESIS
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Evaluasi Keputusan untuk memberikan terapi
bergantung pada penyebab dan konsekuensi potensial dari hiperurisemia
Overproduksi/eksresi berkurang?Ekskresi asam urat laki-laki normal dengan purine free diet <3,6 mmol/d.
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GOUT
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DEFINISIGout adalah suatu gangguan metabolisme dari purin dengan karakteristik hiperuresemia, deposit kristal monosodium urate (MSU) pada sendi dan jaringan peri-articular dan adanya synovitis akut yang berulang.
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FAKTOR RISIKO
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EPIDEMIOLOGI Laki-laki : perempuan 20: 1 Insidensi >40 tahun Prevalensi simptomatik gout 1-10 dari 1000
orang, dapat meningkat sesuai dengan lifestyle dan pola makan
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Patofisiologi
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PENEGAKAN DIAGNOSIS
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Anamnesa Nyeri yang hebat selama beberapa jam Onset tiba-tiba Dapat dipicu oleh adanya trauma lokal, operasi,
latihan yang salah Biasanya lebih dari satu sendi Tersering pada sendi metatarsophalangeal ibu jari
kaki, siku, sendi jari tangan, dan olecranon Riwayat keluarga menderita gout Kebiasaan minum alkohol Mendapatkan obat-obatan seperti thiazide diuretik,
aspirin, warfarin, pirazinamid
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PEMERIKSAAN FISIK Kulit sekitar sendi
terlihat kemerahan dan mengkilat
Bengkak Sendi teraba panas
dan tegang
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PEMERIKSAAN FISIK
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Pemeriksaan laboratorium Kunci diagnosis menemukan kristal
monosodium urat didalam sel darah putih di cairan synovial
Kristal berbentuk jarum berwarna kuning dengan mikroskop cahaya terpolarisasi
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Athrocentesis
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Arthrocentesis Berbentuk seperti
jarum Kristal
extra/intraselular Negatif birefringence
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PEMERIKSAAN LABORATORIUM Hiperurisemia25-40% kadar asam urat pasien normal Peningkatan leukosit & LED
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Radiografi Fase awal
biasanya normal, dapat ditemukan pembengkakan soft tissue
Fase lambat- erosi tulang, kalsifikasi, tophi, penyempitan sendi, destruksi sendi
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DIAGNOSIS BANDING Artritis septik Haemartrosis CPPD (calcium pyrophosphate crystal
deposition)
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TATALAKSANA SERANGAN AKUT
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TATALAKSANA SERANGAN AKUT
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TATALAKSANA SERANGAN AKUT
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TATALAKSANA SERANGAN AKUT
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TATALAKSANA KRONIK Diet
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TATALAKSANA KRONIK Hindari dehidrasi dan obat-obatan yang
memicu hiperurisemia (thiazide, loop diuretics)
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TATALAKSANA KRONIK Antihiperurisemia:
AllupurinolFebuxostatProbenecid
Goal <6 mg/dl
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TATALAKSANA KRONIK
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TATALAKSANA KRONIK
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Antihiperurisemia
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PROFILAKSIS Profilaksis: colchicine (menurunkan
~50% serangan akut) atau NSAIDs (<< bukti efektif)
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TERIMA KASIH
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Uricosuric
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insulin Hyperuricemia reflects defects in insulin action on the renal tubular
reabsorption of uric acid, whereas the increase in asymmetric dimethylarginine,
an endogenous inhibitor of nitric oxide synthase, relates to endothelial
dysfunction. Microalbuminuria may also be caused by altered endothelial pathophysiology in
the insulin-resistant state