kuliah dm 2015
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Kuliah DM 2015TRANSCRIPT
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KULIAH 2015
DIABETES MELLITUS
Krishna W. Sucipto
Divisi Endokrinologi & MetabolismeBag./SMF Penyakit Dalam
FK Unsyiah/ RSUZABanda Aceh
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Definisi Diabetes Mellitus
Suatu Sindroma kelainan metabolik, ditandai adanya hiperglikemia, akibat defek sekresi insulin, defek kerja insulin, atau kombinasi keduanya.
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Sudah dikenal sejak zaman Ebers Papyrus 1550 SM
Willis : mencatat ada rasa manis pada urine
Matthew Dobson : Rasa manis karena gula
1815 : Chevreul (ahli Kimia) membuktikan bahwa gula dalam urine adalah glucosa
1921 : Frederic Grant, Banting, Charles Best berhasil mengekstraksi insulin pertama kali dari pancreas anjing
11 Jan 1922 : Leonardo Thompson, remaja merupakan pasien pertama yang mendapat insulin di RS Toronto Kanada
1979 : Goedde menghasilkan human insulin dengan rekayasa genetik
Pendahuluan
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Faktor Resiko untuk Terjadinya DM
• Kelompok Usia > 45 tahun• Gemuk : BB > 120% BBI (IMT > 27 kg/m2)• Hypertensi• Riwayat Keluarga DM• Riwayat melahirkan bayi > 4 kg.• Riwayat DM pada waktu hamil (DM Gestasi)• Dislipidemia : HDL < 35 mg/dl, Trigliserida > 250
mg/dl• Pernah mengalami gangguan toleransi glukosa
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Pankreas• Terletak dibelakang lambung• Berat : 200 – 250 gram• Bentuk : Kerucut terbaring• Bagian yang lebar : Kepala (Caput)• Bagian yang kecil : Ekor (Cauda)• Terdapat kumpulan sel disebut pulau-pulau Langerhans yang
berisi sel Beta dan mengeluarkan hormon Insulin.• Disamping sel Beta terdapat sel Alfa yang mengeluarkan
Glukagon yang bekerja berlawanan dengan insulin yaitu meningkatkan kadar gula darah. Juga ada sel Delta yang mengeluarkan Somatostatin
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F A S E 1 F A S E - 2
Individu normal
Insulin
plasma
waktu3-5 mnt 50-60 menit
60 ng/ml
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Kerja Fisiologik Insulin• MEMASUKKAN GLUKOSA DARI DALAM DARAH KE:
– Hati• Glukosa di robah jadi glikogen (Glikogenesis)• Glikogen hati menjadi cadangan gula dalam tubuh
– Otot: • Glukosa di robah jadi Glikogen (Glikogenesis)• Glikogen otot dibakar menjadi sumber kalori.
– Adiposa• Glucosa dirobah (?) jadi trigliserida .• Mencegah pemecahan lemak (Antilipolisis)
– Mengaktifkan Lipoprotein Lipase di sel sel endotel P.darah– Jaringan lain: Meningkatkan sintesa protein dari A.Amino
• INSULIN MENURUNKAN KADAR GLUKOSA DARAH
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Bila insulin tidak ada sama sekali (DM tipe 1) atau :Insulin tidak cukup atau efisiensi kerjanya rendah (DM tipe 2)
PEMASUKAN GLUKOSA KE HATI, OTOT, ADIPOSA
AKAN TERGANGGUHIPERGLIKEMIA
GLUKOSURIA
GLIKOGENOLISIS &GLUKONEOGENESIS
TIDAK DIHAMBAT
GANGGUAN SINT.PROTEIN LIPOLISIS TAK DIHAMBAT
POLIURI POLIDIPSILEMAS /MUDAH LELAH
BERAT MAKIN MENURUN
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Etiologi• Herediter, diperlukan faktor lain yang disebut faktor
risiko atau faktor pencetus• Virus
– Pada DM tipe 1 dijumpai HLA gen yang rentan terhadap infeksi virus tertentu.
– Virus yang selalu menimbulkan insulitis adalah : Coxackie, Mumps, Rubella, Cytomegalovirus, Herpes, dll.
• Obesitas– Kadar Insulin cukup tetapi tidak efektif (Resistensi Insulin )
• Memakai obat-obatan yang menyebabkan Kadar Gula Darah meningkat
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Klasifikasi Diabetes Mellitus
• DM tipe-1 – Terjadi destruksi sel Beta (Autoimun atau Idiopatik)
defisiensi insulin absolut.• DM tipe-2
– Gemuk : Resistensi Insulin > Disfungsi sel ß – Tak gemuk : Disfungsi sel ß > Resistensi Insulin
• DM tipe lain– MODY (Maturity Onset Diabetic of the Young), Peny.
Eksokrin pancreas, Cushing Syndrome, dll.• DM Gestasi.
– Kalau hamil DM, tak hamil DM nya sembuh.
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Karakteristik D.M Tipe-1 & D.M Tipe-2
• D.M.TIPE-1 – Mudah terjadi ketoasidosis– Pengobatan harus dgn insulin– Onset nya akut– Biasanya kurus /Umur muda– Terkait dgn HLA-DR3 & DR4– ICA; GADA; & IAA selalu (+)– Riwayat keluarga (+) pd 10%– 30-50% kembar identik
terkena
• DM TIPE-2– Jarang ketoasidosis (HONK
bisa)– Tidak mesti diberi insulin– Onsetlambat (pelan pelan)– Gemuk atau tak gemuk / > 45
thn– Tak ada kaitan dengan HLA– Tak ada autoantibodi– Riwayat keluarga (+) pada
30% – ± 100% kembar identik
terkena
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Gejala Diabetes Mellitus
• Gejala Khas – Poliuria (banyak kencing)– Polidipsia (cepat haus)– Polifagia (banyak makan)– Penurunan berat badan– Lemas dan mudah lelah
• Gejala Tidak Khas– Kesemutan (Parestesi)– Mudah mengantuk– Gatal didaerah kemaluan– Bisul yang hilang timbul– K e p u t i h a n– Penglihatan kabur– Infeksi yang sukar
sembuh
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Kriteria Diagnosa DM• Gejala Klasik DM + Kadar Gula Darah Sewaktu > 200
mg/dl (11,1 mmol/dl)• Gejala Klasik DM + Kadar Gula Darah Puasa > 126
mg/dl (7,0 mmol/dl)• Kadar Gula Darah 2 jam TTGO > 200 mg/dl (11,1
mmol/L)
• Puasa diartikan tidak mendapat kalori tambahan sedikitnya 8 jam TTGO dengan standar WHO, menggunakan beban glukosa yang setara dengan 75 gram glukosa anhidrous yang dilarutkan dalam air
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Pilar Pengelolaan Diabetes Mellitus
• Edukasi• Perencanaan makan• Olah raga• Obat-obatan
– Oral– Injeksi
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Tujuan Pengelolaan Diabetes Mellitus
• Menghilangkan gejala• Mempertahankan rasa sehat• Memperbaiki kualitas hidup• Mencegah komplikasi (akut dan kronis)• Mengurangi laju komplikasi yang sudah ada• Menurunkan jumlah kematian
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Edukasi
Tujuan: • Pencegahan Primer• Pencegahan Sekunder• Pencegahan Tertier
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Perencanaan Makan
TB dan BB
BB Idaman = 90% x (TB-100)
BB dalam KG, TB dlm CMPria TB < 160, Wanita TB < 150
BB Idaman = TB - 100
BBR = (BB / TB – 100) x 100%(BB dlm KG; TB dlm CM)
Underweight = <90%Normoweight: 90-110%Overweight 110-120%
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Perencanaan Makan
KALORI BASAL Pria = BBI x 30 Kkal/hari Wanita = BBI x 25 Kkal/hari
KOREKSIUmur > 40 thn : - 5% KKB ( -0,5% pertahun)
Aktifitas ringan : + 10% KKB Aktifitas sedang : + 20% KKBAktifitas berat : + 30% KKB
Gemuk : - 20% KKBOverweight : - 10% KKB Underweight : + 20% KKBStress metabolik : + 10 sd 30% KKB
Hamil Trimester I /II : + 300 Kkal/hariHamil Trimester III /Laktasi : + 500 Kkal/hari
KEBUTUHAN TOTAL : ……… Kkal/hari
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Perencanaan Makan
Komposisi makananKarbohidrat 60-70%
Protein 10-15%
Lemak : 20-25%
Sarapan : 20% Snack 9.00 : 10%Makan siang : 25% Snack 16.00 : 10%Makan malam : 25% Snack 21.00 : 10%
Makanan Harus Dihabiskan
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Olah Raga• Prinsip Cripe :
– Continuous, Rhythmic, Interval, Progressive, Endurance
• Frekuensi : 3 – 5 kali/minggu• Lama : 0,5 – 1 jam/kali• Sasaran HR : 75 - 85 % Nadi maksimum
– Nadi Maksimum: 220 – Umur
• Pakai sepatu/alas kaki yang enak, sesuai, dan aman• Mulai dengan Pemanasan (5’),Latihan inti (15-20’),
Pendinginan (5’)
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Obat-obatan
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Obat Antidiabetik Oral
1. Insulin Secretagogues – Merangsang sel ß mengeluarkan insulin– Sulfonilurea (Glibenclamide, Glipizide, Gliclazide, Glikuidon , dan
Glimepiride)– Metiglinide (Repaglinide =Novonorm, Nateglinide = Starlix)
2. Metformin – Membantu insulin menghambat glukoneogenesis di hati/ mengurangi
resistensi insulin di hati – Glucophage dll
3. Thiazolidindione – Meningkatkan kepekaan (sensitifitas) jaringan peri feral terhadap
insulin = meningkatkan ambilan glukose oleh jaringan perifera; (otot, & adiposa)
– Troglitazone, Pyoglitazone4. Acarbose
– Menunda penyerapan glukosa dari saluran usus halus
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5. DPP-4 Inhibitor
Dipeptidyl peptidase 4 inhibitor-memperlambat inaktivasi GLP-1 dan GIP
Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin Sangat minim efek samping Paling efektif bila digunakan dengan
metformin
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Insulin Yang Beredar Di Indonesia
JENIS INSULIN ONSET PUNCAK LAMA KERJA• Insulin Regular 30’ sd 1 jam 2 - 4 jam 6 – 8 jam• Insulin NPH 1-2 jam 8 – 12 jam 18 = 24 jam• Premixed 30 /70 30’ sd 1 jam 2 – 4 jam 6 – 8 jam• Insulin & 1-2 jam & 8-12 jam & 18-24 jam• Insulin analog
Insulin Reguler: Warnanya jernih, yang lain warnanya keruh/seperti susu
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Indikasi Pemberian Insulin
• DM Tipe 1• Krisis Hiperglikemia
– KAD, HONK, AL.• BB turun sangat cepat (drastis) tanpa kausa lain yg jelas• Stress berat
– Infeksi sistemik, Pembedahan (> 3 jam)• Kontrol glikemik tak tercapai dengan OAD dosis maks.• Penggunaan OAD kontraindikasi• Hamil/DM gestasi tak terkontrol dengan diit.
DIABETES TERKENDALI ? : Berdasarkan HbA1cGULA DARAH TERKENDALI ? : Berdasarkan KGD
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Incretin Mimetics• Exenatide: diisolasi dari air liur Kadal • Meningkatkan sekresi insulin• Mengembalikan respon insulin fase pertama• Menekan sekresi glukagon • Memperlambat laju pengosongan lambung• BID injeksi• Efek samping mual utama / penurunan berat badan
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Tempat Injeksi Insulin
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Pharmacologic Targets of Current Drugs Used in the Treatment of T2DM
-glucosidase inhibitorsDelay intestinal carbohydrate absorption
TZDIncrease glucose uptake in skeletal muscle and decrease lipolysis in fat tissue
SulfonylureasIncrease insulin secretion from pancreatic -cells
GLP-1 mimeticsImproves glucose-dependent insulin secretion, suppresses glucagon secretion, slows gastric emptying
Biguanide (metformin)Decreases hepatic glucose production and increases glucose uptake
DDP-4=dipeptidyl peptidase-4; GLP-1=glucagon-like peptide-1; T2DM=type 2 diabetes mellitusAdapted from Cheng AY, Fantus IG. CMAJ. 2005; 172: 213–226.
GlinidesIncrease insulin secretion from pancreatic -cells
DPP-4 inhibitorsProlong GLP-1 action, stimulate insulin secretion, suppress glucagon release
SGLT2 inhibitor
Inhibit renal glucose reabsortion from tubular fluid
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Terdiagnosis DM Tipe 2
Perubahan Gaya Hidup
Cek Kadar Glukosa Darah
Kadar A1C (%)
>106,5-7 7-8 8-10< 6,5
Teruskan Terapi*:
·Metformin·AGI·TZDKeadaan Khusus·Meglitinides·SU·Rapid-ActingInsulin analog
Terapi Kombinasi Oral*:
·SU·Metformin·AGI·TZD·MeglitinidesKeadaan Khusus
·Rapid-ActingInsulin analogPre-MixedInsulin analog
Terapi Kombinasi Oral+Insulin*:
·Metformin·TZD·SU·Long-actinginsulin·Rapid-actingInsulin analog·Pre-MixedInsulin analog·NPH·Kombinasi lain yang diakui
Terapi Insulin*:
·Rapid-actingInsulin analog\
·NPH atau Long acting·Pre-MixedInsulin analogBeberapa pasienTertentu dengan nilai A1C>10% kombinasi OHO kemungkinan juga efektifTarget
tercapaiTarget tidak
tercapai
Teruskan terapi
Intensifikasi terapi atau
Target tercapai
Target tidak tercapai
Teruskan terapi
Intensifikasi terapi atau
Target tercapai
Target tidak tercapai
Teruskan terapi
Intensifikasi terapi atau
Target tercapai
Target tidak tercapai
Teruskan terapi
Intensifikasi terapi insulin basal+bolus
Algoritma pengobatan DM tipe 2 tanpa disertai dekompensasi metabolik
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Annual Lipid ProfileLDL < 100HDL > 40Trigs < 150 DM + CVD LDL < 70
Annual Lipid ProfileLDL < 100HDL > 40Trigs < 150 DM + CVD LDL < 70
Blood Pressure (every visit)Dx and Rx = 130/80
Blood Pressure (every visit)Dx and Rx = 130/80
Annual ScreeningNephropathyMicroalbumin ScreeningCalculated GFR RetinopathyDilated Retinal ExamNeuropathyNeuro and Foot exam
Annual ScreeningNephropathyMicroalbumin ScreeningCalculated GFR RetinopathyDilated Retinal ExamNeuropathyNeuro and Foot exam
Hospital Care Gestational DM Foot CareDental CareImmunizations
Hospital Care Gestational DM Foot CareDental CareImmunizations
Hemoglobin HbA1C Target <6.5 - 7.0%SMBGPre 70-120 mg/dL Post <160 mg/dL(~ 50% of readings)
Hemoglobin HbA1C Target <6.5 - 7.0%SMBGPre 70-120 mg/dL Post <160 mg/dL(~ 50% of readings)
Macrovascular Complications ASA, Tobacco, ACEI/ARB, Statin Macrovascular Complications ASA, Tobacco, ACEI/ARB, Statin
HypertensionHypertensionGlucoseGlucose LipidsLipids
Priorities of Care for Adults With Diabetes
Microvascular Complications
Microvascular Complications
Other Essentialsof Care
Other Essentialsof Care
Diabetes Self-Management Skills Diabetes Self-Management SkillsLifestyle Patient EducationBG Monitoring Medical Nutrition Physical Activity
Behavioral Health Emotional Assessment Distress, Depression, Complications Support Needs Family, Peers, Medical
Diagnosis - PreventionDiabetes
Pre Diabetes (IFG –IGT) Metabolic Syndrome
Diagnosis - PreventionDiabetes
Pre Diabetes (IFG –IGT) Metabolic Syndrome
© 2005 International Diabetes Center. All rights reserved. Staged Diabetes Management
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• Normal HbA1c <6.0%
• ADA target HbA1c <7.0%1
• AACE target HbA1c <6.5%2
1. ADA. Diabetes Care. 2002;25(suppl 1):S33-S49. 2. ACE Consensus Statement on Guidelines for Glycemic Control 2001. Endocrine Practice. 2002;8(suppl 1):6-11.
HbA1c Targets in Diabetes
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Hyperglycemic hyperosmolar state:common in elderlytriggered by underlying disorder(s)risk increased in elderly due to decreased thirst reflexoften complicated by delirium
Acute Complications of type 2 DM
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Hyperglycemic hyperosmolar state:serum osmolarity > 320 mosm/Lplasma glucose > 600mg/dLdehydrationno ketoacidosisunderlying disorder(s)
Acute Complications of type 2 DM
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Therapy:rehydration with hypotonic solutioninsulin infusion (initially)watch for signs of fluid overload/CHFmonitor potassiumtreat underlying cause (eg UTI, cellulitis)
Hyperosmolar State
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Hypoglycemia = plasma glycemia < 50mg/dL with or without symptoms
More common in type 1 DM and patients with significant renal or liver disease
Another reason for glucose monitoringTreated with po sugar (e.g. fruit juice or glucose tablets)
or IV dextrose 50% in water or IV glucagon or both
Hypoglycemia
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Chronic complications of diabetes mellitus include: MacrovascularMicrovascularNeuropathic
Complications of DM
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Macrovascularatherosclerosis/cardiovascular diseaseperipheral vascular disease
Complications of DM
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Microvasculardiabetic retinopathy: due to ischemia of retina; provokes neovascularization with vessels more fragile => leaking => scarring & fibrosis
diabetic nephropathy: common cause of ESRD;prevention via control of blood pressure and glycemia; earliest signs urine albumin 30mg/day or 20g/min; appears to benefit from ACE-I’s and ARB’s too
Complications of DM
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Diabetic Neuropathyperipheral sensory neuropathycardiovascular autonomic neuropathygastrointestinal autonomic neuropathyerectile dysfunctionmononeuropathydiabetic foot
Complications of DM
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Peripheral sensory neuropathyvariable presentationdysesthesiatingling painloss of pain sensation (risk of injury)
Complications of DM
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Cardiovascular Autonomic Neuropathy
orthostatic hypotensionlack of normal variation in heart rate with breathing, tachycardia
Complications of DM
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Gastrointestinal Autonomic Neuropathygastroparesis: nausea, bloating, vomiting (tx metoclopramide)diarrhea: often nocturnal
Complications of DM
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Erectile dysfunction:autonomic neuropathyabsent nocturnal and morning erectionsmore common than diagnosed
Complications of DM
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Mononeuropathyacute local paindistribution of a nervemay recede if treated early with improved glucose control (glucotoxicity)
Complications of DM
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Diabetic Footsensory deficit (skin, bone, ligament)fungal infectionwoundspulses (PVD)slow healingulcers
Complications of DM
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Terima Kasih
Andrista Nararya Khairul Anam