patogenesis,gejala& tanda dm (workshop boyolali 7082010)
DESCRIPTION
diabetes mellitusTRANSCRIPT
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Identitas: › Nama : Dr.Sugiarto .dr.SpPD. FINASIM.› Lahir : Surakarta, 22-Mei 1962.› Alamat : Banyuagung RT 05/ Rw 02.
Kadipiro, Banjarsari ,Surakarta.
› Pekerjaan : Subagian Endokrinologi dan Metabolik RSUD Dr Mowardi/ FK Sebelas Maret
Surakarta Pendidikan :
› Lulus Dokter umum (FK UNS 1988).› Lulus Spesialis Penyakit Dalam (FK UGM 2003).› Lulus Doktor (Pascasarjana UNAIR 2010).
Organisasi:› PAPDI.› IDI.› PERKENI.› Persadia.
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1.Definisi 2. Prevalensi. 3. Faktor risiko. 4. Tanda & gejala. 5. Klasifikasi. 6. Diagnosis. 7. Patogenesis. 8. Komplikasi. 9. Penatalaksanaan.
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Penyakit kronik disertai gangguan metabolik dengan berbagai penyebab yang
ditandai: hiperglikemia kronik dengan gangguan metabolisme karbohidrat, protein dan lemak
akibat : › Defek sekresi insulin› Defek aktifitas insulin atau › keduanya.
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Penyakit Kronik :› Perawatan dan Edukasi secara kontinue.
Tujuan terapi :› Mencegah komplikasi akut dan kronik.
Estimasi 7% Diabetes USA, 25 % penderita (USA) tidak terdiagnosis.
Indonesia (1980-2001) 0,8-12,8 %. A1c (Hb A1c) oleh American Diabetes
Association (ADA 2010) direkomendasikan untuk diagnosis.
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Negara 1995 (juta) Negara 2025 (juta)
Urutan 1 India 19.4 India 57.22 China 16.0 China 37.63 U.S. 13.9 U.S. 21.94 Russian Fed. 8.9 Pakistan 14.55 Japan 6.3 Indonesia 12.46 Brazil 4.9 Russian Fed. 12.27 Indonesia 4.5 Mexico 11.78 Pakistan 4.3 Brazil 11.69 Mexico 3.8 Egypt 8.810 Ukraine 3.6 Japan 8.5
Negara Lainnya 49.7 103.6
Total 135.3 300.0
Perkiraan Jumlah Pasien DM Dewasa Terbanyak, 1995 and 2025
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Ligaray, 2007.Last Update
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3.5 %5.7 %
1.6 %
6.1%
1.1% 1.4%
Rata-rata Prevalence DM di Indonesia
19921992
20012001
19821982
3.7%
20042004
14.7 %
9.2%
20032003
Padang
Jakarta
Singaparna
PekajanganMakassar
Surabaya
Bali
Manado
20052005 19841984
19981998
12.5 %
20052005
1.5 %
6.1%
12,3 % hiperglikemia
2006
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2000 5.6 milions people with DM 2020 8.2 milions people with DM
World 5th largest prevalence!!!
(International Diabetes Federation)
INDONESIA ?
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Hipertensi. Dislipidemia. Riwayat gestasional
diabetes. Riwayat bayi lahir
dengan berat badan >4000 mg.
Sindroma polikistik ovarium
Penyakit psikiatri
Riwayat keluarga diabetes.
Penyakit kardiovaskuler.
Overweight atau obese.
Suku bangsa. Gangguan toleransi
glukosa atau gangguan glukosa puasa.
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Gejala Klinis :› Asymptomatik.› Polyuria. › Polydipsia. › Polypagie. › BB yang tidak jelas
Tanda :› Ditemukan hiperglikemia.
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American Diabetes Association. American Association of Clinical
Endocrinologists
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DM Tipe 1.› Destruksi sel ß pancreas.› Defisiensi insulin absolut.
DM Tipe 2.› Defek sekresi insulin secara progresif.› Resistensi insulin
DM Tipe Lain.› Defek genetik funsi sel ß.› Defek genetik dari aksi insulin.› Penyakit eksokrin pancreas.› Karena obat atau bahan kimia
DM Gestasional.› Diabetes selama kehamilan.
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Diabetes tipe 1. Diabetes tipe 2. Diabetes gestasional.
Parkin, et al, 2007. Endocrine practice vol 13.
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Modi PCurrent Drug Discovery Technologies, 2007, Vol. 4, No. 1
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Glukosa darah puasa :100-125 mg/dL (Impared fasting glucose [IFG]).
Glukosa 2 jam post-prandial dengan 75 gr OGTT: 140 -199 mg/dL (impared glucose tolerance [IGT])
A1C (Hemoglobin A1C): 5,6-6,4%.
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A1C > 6,5% atau
Glukosa darah puasa ≥ 126 mg/dL atau
Glukosa darah 2 jam post-prandial ≥ 200 mg/dL selama OGTT (beban 75gr glukosa anhydrous)
atau Gejala klasik hiperglikemia atau krisis
hiperglikemia dengan glukosa darah sewaktu ≥ 200 mg/dL.
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Predisposisi Genetik.
Environment :› Obese &
lifestyle
Defek sekresi insulin.Resistensi insulin.
Diabetes Mellitus
Adapted from DeFronzo RA. Diabetes 1988; 37: 667–87.
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Gangguan fase pertama sekresi insulin selama rangsangan glukosa.
Hiperglikemia (glucotoxicity), free fatty acids (lipotoxicity), cytokines, dan agent inflammatory.
Autoimmune destruction. 80% DM tipe 2, adanya perlambatan
respon insulin pada fase sekunder sekresi insulin .
Mahler and Adler, The Journal of Clinical Endocrinology & Metabolism ,1999
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Defek Sekresi insulin
Kegagalan Sel beta Deposisi amiloid Obat 2 & hormon yang abnormal Malnutrisi in utero and early childhood Mutasi glukokinase Mutasi insulin Mutasi mitokondria DNA
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Penyebab : genetik & lingkungan. Hiperinsulinemia kronik dapat
menghambat baik sekresi & aksi insulin.
Hiperglikemia dan hiperinsulinemia menggangu sekresi insulin terhadap glukosa.
Obesitas ( abdominal obesitas). aktifitas sintesis glycogen.
Mahler and Adler, The Journal of Clinical Endocrinology & Metabolism ,1999
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Insulin signalling rangsangan aktifitas tyrosine kinase pada
resptorObesitas (obesitas abdominal)Diet tinggi karbohidrat & lemakPenyakit EndokrinKehamilanObat-obatMalnutrisi in utero and early
childhood Mutasi (jarang)
Reseptor insulinKomponen Post reseptor
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Resistensi insulin hepar. glucokinase and catalytic subtrat
glukosa. free fatty acid.
Mahler and Adler, The Journal of Clinical Endocrinology & Metabolism ,1999
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Normal glucose metabolism
Impaired glucose metabolism
Type 2 diabetes
Insulin sensitivity Insulin secretion
30%
70%
100%
50%
150%
100%
Diabetes Obes Metab 1999; 1(1): S1
IGT50% 70-100%
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Defek multiorgan:› Resistensi insulin (liver, adiposit dan otot):
Faktor genetik. Faktor environmental (Obesitas& Pola hidup)
› Penurunan sekresi insulin yang progresif.› Peningkatan produksi glukosa hepar.› Peningkatan produksi glukagon.› Penurunan produksi incretin.
Rodbard et al, Endocrine Practice, 2007)
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Hyperglycemia
Decreased Insulin secretion
Increased Lipolysis
Decreased Glucose Uptake
Increased Hepatic Glucose Production
Bays, et al,2004. J clin Endocrinol Metab 89 : 463-478
Adiposit , liver & muscle (cardiac & skeletal)
PANCREAS JARINGAN ADIPOSIT
JARINGAN OTOT
HEPAR
Increased Glucagon
Decreased Incretin secretion
Rodbard et al, Endocrine Practice, 2007)
GASTROINTESTINAL
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Years From Diagnosis
T2 DMphase I
T2 DMphase II
Perjalanan DM tipe 2Perjalanan DM tipe 2
Lebovitz, 2000
T2 DM phase III
-12 -10 -6 -2 0 2 6 10 14
100
75
50
25
0
Beta CellFunction
(%)IFG IGT/
PostpandrialHiperglycemi
T-2 DM phase IBeta Cell function 50 -60 %
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Makrovaskuler:› Kardiovaskuler.› serebrovaskuler.› Perifir arteri disease
Mikrovaskuler:› Nefropati.› Neuropati.› Retinopati.› Cardiomiopati.
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Resiko diabetes :
Komplikasi Relative risk› Blindness 20 x› End stage renal disease 25 x› Amputation 40 x› Myocardial infarction 2-5 x› Stroke 2-3 x
Donnely, et al, 2000. BMJ 320: 1062-1066)
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Atherosclerosis
Type 2 diabetesImpaired
glucose tolerance
Polycysticovary disease
Obesity (central)
Dyslipidemia Hypertension
Acanthosisnigricans
Hyperuricemia
Decreasedfibrinolytic activity
InsulinResistance
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Tujuan :› 1. Mencegah jangan menjadi diabetes.
Menghambat perkembangan Pre-Diabetes menjadi Diabetes.
› 2. Pencegahan dan terapi komplikasi diabetes Menghambat untuk menurunkan risiko
komplikasi diebetes. Meliputi :
› Deteksi awal.› Pencegahan.› Perawatan medik.
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A. Diabetes Mellitus Asymptomatik.1. Overweight atau Obese (BMI ≥ 25 kg/M2)2. Faktor risiko.3. Usia > 60 th tanpa faktor risiko.4. Jika hasil normal direkomendasikan ulang
setiap 3 tahun.
B. Diabetes Mellitus tipe 2 dengan faktor risiko
C. Diabetes Mellitus tipe 2 pada Anak.D. Diabetes Mellitus tipe 1. Pemeriksaan :
› A1c, Glukosa puasa & Glukosa Pos-prandial.
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1. IGT, IFG & A1c : 5,7-6,4 %.› BB (5-10 %).› aktifitas Fisik jalan kaki ( 15o menit/minggu
atau 30 menit/hari). 2. Konseling rutin
› mencegah Perkembangan Diabetes.› Pola Hidup dan terapi Metformin :› IFT,IGT,A1c >6 %,Hipertensi, Dislipidemia.› Riwayat keluarga diabetes, obese & usia >60 th.
3. Monitoring laboratorium setiap tahun.
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4. Studi UKPDS › Perubahan pola hidup selama 3 th dapat
mencegah Diabetes dari Pre-diabetes menurun 58%.
5. Obat pencegahan:› a. Direkomendasikan ADA 2010 : › Metformin
Indikasi usia < 60 th: IGT IFG. Obese. Faktor Risiko Diabetes.
› b. Not rekomended : α Glucosidase inhibitor c. Orlistat d. Thiazolidinediones .
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1. Evaluasi :› Klas Diabetes.› Komplikasi Diabetes› Mereview terapi diabetes sebelumnya› Rencana perawatan dan penatalaksanaan› Pemeriksaan Laboratorium
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2. Penatalaksanaan : Perlu kolaborasi dan integrasi team
› Physicians nurse practitioners› Physician’s assistants› Nurse› Dietitians› Pharmacists› Mental health professionals
Target :› Pasien.› Keluarga› Dokter› Team perawat kesehatan.
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Perencanaan meliputi :› Usia.› Kondisi tertentu ( Belajar atau Bekerja)› Aktifitas Fisik.› Kebiasaan Makan.› Faktor-faktor Sosial dan Kultural.› Komplikasi dan Kondisi tertentu.
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1. Pola hidup:› Aktifitas Fisik› Terapi Nutrisi Medik
2. Terapi Psikososial 3. Kontrol glikemia (self-monitoring
glucose) 4. Pencegahan dan Penatalaksanaan
Komplikasi Diabetes
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Meliputi :› Aktifitas Fisik ( exercise)› Terapi nutrisi medik.
Perubahan pola hidup Pendidikan yang terarah. Monitoring kadar glukosa mandiri. Penurunan berat badan. Membiasakan makan yang sehat. Berhenti merokok.
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• Mencegah faktor risiko Kardiovaskuler• Makrovaskuer :
– Berhenti merokok.– Aktifitas Fisik.– Diit.
• Mikrovakuler :– Berhenti merokok.
• Perubahan perilaku.• Persepsi tentang penyakit diabetes.
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Aktifitas fisik minimal 150 menit perminggu.
Pilih olah raga jenis aerobik ( maximum heart rate antara 50-70 %) ( grade A).
Manfaat :› Memperbaiki tekanan darah.› Menurunkan risiko penyakit
kardiovaskuler.› Menurunkan berat badan› Meningkatkan kesenangan.
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Penurunan berat badan pada penderita overweight atau obese (grade A)
Rendah karbohidrat dan lemak selama 1 tahun (grade A).
Latihan fisik dan modifikasi gaya hidup dalam penurunan berat badan (grade B).
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• Pengaruh faktor psikososial pada diabetes:– Gangguan makan.– Problem emosi pederita.– Problem keluarga.– Ansietas.– Depresi.
• Skrening adanya stress psikologi.• Intervensi psikologi terhadap keberhasilan
terapi diabetes.• Terapi terhadap stress psikologi.
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• Ada hubungan variabel psikologi dan sosial terhadap keberhasilan terapi diabetes.
• Management dirinya sendiri (self-management ) dan kepatuhan (adherence).
• Intervensi : – Behaviour modification, – Motivational interviewing (MotI),– Cognitive behavioural therapy (CBT), – Acceptance and commitment therapy (ACT), – Goal setting,– Guided self-determination (GSD)– Coping skills.
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A1c : › Target utama goal terapi.› 2 kali dalam setahun.› Goal terapi < 7 %/6,5%
Preprandial :› 70- 130 mg/dL.
Pos prandial :› <180 mg/dL.
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A1c < 6,5 %
Glukosa puasa < 110 mg/dL
2 Jam postprandial
< 140 mg/dL
AACE.2007
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A1c < 7 %
Tekanan Darah < 130 / 80 mmHg
LDL-kolesterol < 100 mg/dL
ADA, 2010.
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A. Penyakit Kardiovaskuler.› Kontrol Hipertensi.› Kontrol Dislipidemia.› Anti-Platelet agent.› Berhenti Merokok.
B. Terapi dan sekrining Nephropati. C. Terapi dan sekrining Neurophropati. D. Terapi dan sekrining Retinopati. E. Perawatan Kaki (Foot care)
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1. Jumlah pasien dengan < 7%.
2. Komplikasi akut (ketoacidosis, hyperosmolar coma, severe hypoglycemia).
3. Komplikasi kronik (retinopathy, nephropathy, vasculopathy, neuropathy).
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4. LDL < 100 mg/dL.
5. Blood Pressure <130/80 mm Hg.
6. pemakaian ACE inhibitors atau ARB's untuk pasien dengan microalbuminuria.
7. pemakaian aspirin pada pasien > 30 th dengan resiko tinggi kejadian kardiovaskuler.
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Diabetes disebabkan multipatologis yang melibatkan beberapa organ.
Komplikasi Diabetes Melitus menyebabkan mortalitas & morbiditas yang tinggi di masyarakat.
Perlu kolaborasi dan integrasi team untuk mengontrol glukosa.
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Perencanaan terapi meliputi : Pola hidup, Terapi Psikososial, Kontrol glikemia serta Pencegahan dan Penatalaksanaan Komplikasi Diabetes.
Penatalaksanaan penderita diabetes perlu memperhatikan goal terapi
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MATUR NUWUNTERIMA KASIH