10businessmodelsofourtimebeta 100204180704-phpapp02-130915004644-phpapp02
diabetesmelitusdr-140427221257-phpapp02
-
Upload
frans-apandi -
Category
Documents
-
view
3 -
download
0
description
Transcript of diabetesmelitusdr-140427221257-phpapp02
Diabetes MelitusDM
MUHAMMMAD UMAR FERDIANSAH Amd.Kep
SMF Ilmu Penyakit DalamPoli Spesialis RS AL-Irsyad Surabaya
2014
Aetiological Classification of Disorders of Glycaemia
Type 1 (beta–cell destruction, usually leading to absolute insulin deficiency) : Autoimmune: Idiopathic
Type 2 (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with or without insulin resistance)
Other specific types
Genetic defects of beta–cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas Endocrinopathies
Drug– or chemical–induced Infections Uncommon forms of
immune–mediated diabetes
Other genetic syndromes sometimes associated with diabetes
Gestational diabetes
Other types of Diabetes
Genetic defects of beta–cell function
Chr’me 20, HNF4_ (MODY1)
Chr’me 7, glucokinase (MODY2)
Chr’me 12, HNF1_ (MODY3)
Chr’me 13, IPF–1 (MODY4)
Mitochondrial DNA 3243 mutation
Genetic defects in insulin action
Type A insulin resistance
Leprechaunism
Rabson–Mendenhall syndrome
Lipoatrophic diabetes & Others
Diseases of the exocrine pancreas
Fibrocalculous pancreatopathy
Pancreatitis
Trauma / pancreatectomy
Neoplasia
Cystic fibrosis
Haemochromatosis & Others
Endocrinopathies
Cushing’s syndrome
Acromegaly
Phaeochromocytoma
Glucagonoma
Hyperthyroidism
Somatostatinoma & Others
Diabetes Melitus
Diabetes melitus ----- Penyakit metabolik yang paling sering, yang ditandai hiperglikemia dan glukosuria disertai komplikasi pendek atau jangka panjang pada mata, ginjal, saraf dan beberapa vaskuler.Sebagai akibat kurangnya insulin efektif dalam tubuh
Klasifikasi DM (ADA 1997)
1. DM tipe 11. Autoimun2. idiopatik
2. DM tipe 21. Resistensi insulin/ def insulin relatif
3. DM tipe lain1. Defek genetik (MODY,DNA mitokondria)2. Defek genetik kerja insulin 3. P eksokrin pankreas (pankreatitis, tumor, pankreopati
fibrocalculus)4. Endokrinopati ( akromegali, S Cushing, feokromositoma,
hipertoroidism)5. Karena obat ( vacor, petamidin, glukorkortikoid, hormon tirod,
dinlatin dll)6. Infeksi (rubella kongenital, CMV)7. Imunologi ( antibodi anti insulin)8. Sindrom genetik lain (S Down,S Klinefelter,S Turner dll)
4. DM gestational
Types-continued
InfectionsCongenital rubellaCytomegalovirusOthers Uncommon forms of
immune–mediated diabetes
Insulin autoimmune syndrome (antibodies to insulin)
Anti–insulin receptor antibodies
“Stiff Man” syndromeOthers
Drug– or Chemical–induced Diabetes
Nicotinic acid Glucocorticoids Thyroid hormone Alpha–adrenergic agonists Beta–adrenergic agonists Thiazides Dilantin Pentamidine Vacor Interferon–alpha therapy Others
ADA diagnostic criteria (1997) Symptoms of diabetes & a casual glucose concentration
more than or equal to 200 mg/dl(11.1 mmol/l); Casual is defined as any time of day without regards to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia and unexplained weight loss
or FPG more than or equal to 126 mg/dl (7.0 mmol/l).
Fasting is defined as no caloric intake for at least 8 hours
or 2 hour PG more than or equal to 200mg/dl(11.1 mmol/l)
during an OGTT. The test should be performed as described by WHO, using a glucose load containing the equivalent of 75 gm anhydrous glucose dissolved in water
WHO diagnostic criteria
whole bloodplasma
Diabetes mellitus (fasting) > 6.1mmol/l > 7.0mmol/l
2 hour post glucose load > 10.0 mmol/l > 11.1mmol/l
IGT (fasting) < 6.1mmol/l < 7.0mmol/l
& &2 hr post glucose load > 6.7 mmol/l > 7.8
mmol/l IFG (fasting) > 5.6 mmol/l >
6.1mmol/l
& <6.1 mmol/l & <7.0mmol/l
2hr post glucose load <6.7 mmol/l <7.8 mmol/l
Type 1 diabetes
Previously known as IDDM(Insulin dependent diabetes)
Ketosis prone:Usually diagnosed in younger age group(<30 years) (Peak incidence 11-13 yr)
Prevalence highly variable but approximately 0.20% with an incidence of 15-20 per 100000 population aged less than 21
Highest rate in Finland and Sicily( 30 new cases per 100000) to lowest in Japan and Korea (1 new case per 100000)
Seasonal variation- with lowest rate in spring and summer
Type 1 diabetes Presentation of type 1 is acute with symptoms
of polyuria, polydipsia, lethargy weight loss, nausea, vomiting,abdominal cramps,blurred vision and superficial infection
This presentation is the end point of recent and continuing beta cell function resulting in near total loss of Insulin production
Hyperglycaemia itself begets further beta cell destruction as treatment with insulin often results in a “honeymoon” period where the patient can often manage without insulin
Type 2 diabetes Previously known as NIDDM Non ketosis prone: , diagnosis > 30 years Prevalence highly variable1-2%, with a slight
male excess 1 in 1000 population as new cases each year Rates in relation to age ; 15- 44 yrs 0.5%,45-
64-1.8%,>65- 4.0% Rural population <1%
(Papua,Solomon,Bantu)Euro/N Americans 1-10%( Urban Bantu)Indo Asians abroad 10-20%(Australia, Aborigines)Pima Indians >20% (Nauru)
What is type 2 diabetes?
A progressive metabolic disordercharacterised by:
Insulin resistance
-cell dysfunction
Type 2diabetes
1. Beck-Nielsen H, Groop LC. J Clin Invest 1994;94:1714–17212. Saltiel AR, Olefsky JM. Diabetes 1996;45:1661–1669
Treatment of Diabetes
Non Pharmacological Diet, Low in fat, low refined sugars,high
carbohydrate,high fibre, low calories if obese, spacing of meals (Healthy eating)
Low cholesterol and triglyceride diet if hyperlipidemia
Exercise and Education All Type 1 patients will require Insulin
and type 2 can be on diet only, tablets or insulin treated
Treatment of diabetes- Tablets
Sulphonylureas: Glibenclamide, gliclazide, Tolbutamide,Glimiperide, Repaglanide etc.
Biguanides:Metformin Alpha glucosidase inhibitor:Acarbose Thiazolidinedione derivatives:
Troglitazone, Rosiglitazone,Pioglitazone.
Three main profiles: human bio-engineered,pork or Bovine.Various regimens: twice daily soluble and isophane, thrice daily soluble (pre-meal) and evening isophane, rarely once daily
Diabetic Complications
Acute Complication:
hypoglycaemia,ketoacidosis often with coma (DKA),
Hyperosmolar state often with coma (HONK)
Micro vascular complications
Diabetic retinopathy,nephropathy and neuropathy
Macro vascular complication
cerebrovascular accidents, coronary artery disease,hypertension, peripheral vascular disease
Pregnancy with increased maternal and foetal morbidity
Patogenesis
DM tipe I ( kerusakan sel Beta Pankreas, Reseptor perifer cukup. )Sintesis dan sekresi insulin kualitas maupun kuantitas kurang.Predisposisi genetik ---- lingkungan ----- kerusakan sel ß autoimun ---- DM Genetik HLA DR 4 Lingkungan
DM tipe 2 ( kelainan sekresi insulin dan reseptor insulin ) Sekresi insulin terlambat Reseptor insulin kurang ( < 30.000) Kualitas reseptor jelek Kelainan post reseptor ( glikolisis terganggu) Campuran
MRDM Sel beta rusak ok HCN Defisiensi protein dan kalori Sebab lain.
Gejala klinis :
fase kompensasi : polifagi, polidipsi, BB naik
fase dekompensasi : polidipsi, poliuri, BB turun. Mual
kronik : lemah badan, semutan, difungsi seks,
Laboratorium : GDP < 110 mg/dl, 2JPP < 140 mg/dl metode : Hagedorn- Jensen,
Somogyi Nelson, Autoanalyser, Ensimatik
Urine : Reduksi 3 x sebelum makan (Fehling, Benidict, Stick) keton : (Gerhard/Rothera) atau ketostik
Diagnosis
Kriteria DM (Perkeni 1998)
Poliuri, Polidipsi, BB sebab tidak jelas plus :1. GDA > 200 mg/dl atau2. GDP (vena) ≥ 126 mg/dla atau3. TTGO 2 JPP ≥200 mg/dl
Kriteria Diagnosis MRDM Surabaya – Kobe 1989
Kriteria dugaan MRDM
Didapatkan 1,2,3,4 atau lebih :
1. DM usia 15 – 40 tahun ( dapat kurang atau lebih)
2. Ax atau ada tanda malnutrisi-undernutrisi : BBR < 80 % atau BMI < 19
3. Tx perlu Insulin dan ada resistensi insulin ( 1,5-2 /Kg BB/hari)
4. Resistensi ketoasidosis
5. Nyeri perut berulang
6. Tanda malabsrbsi
7. Kalsifikasi pankreas
Kriteria definitif1. Fibrocalculus Pancreatic DM
(FCPD)1. DM umur 15 – 40 th, tanda
malnutrisi (BBR< 80 %), Tx insulin, resistensi insulin, resistensi ketoasidosis, kalsifikasi pankreas dengan atau tidak disertai tanda malnutrisi.
2. Tes fungsi pankreas menurun :1. BT- PABA urine < 60 % dan
atau2. Isoenzyme amylase positif
2. Protein Deficient Pancreatic DM (PDPD)
1. DM umur 15-40 tah, BBR< 80 %, Tx insulin, resistensi insulin, R ketoasidosi, tanpa kalsifikasi Pankreas
2. Tes fungsi pankreas menurun
Keluhan klinis
Positit Negatif
GDPGDS
³ 126³ 200
< 126 200
Ulang GDS atau GDP
110 < 126
110 - 190
< 110
TTGO2J PP
GDPGDS
³ 126³ 200
< 126< 200
> 126 200
GDPGDS
200 140 - 190 < 140
GDPTD I A B E T E S M E L L I T U S Normal TGT
EVALUASI: GIZI, PENYULIT, PERENCANAAN MAKANNasihat umum, makanan, olahraga, BB idaman, obat -
Langkah Dx Diabetes Melitus
PENATALAKSANAAN
TERAPI PRIMER
1. Diit (21 macam). Diit B, B1, B puasa, B1 puasa, B2, B3, Be, M, M puasa, G, KV, H dan GL.
Mengikuti 3 J ( Jumlah kalori dihabiskan, Jadwal ditepati,Jenis gula pantang)Diit tepat diberikan. Kumur setelah makan.Diit B2 untuk px ND stad IIDiit B3 untuk px ND stad IIIDiit Be untuk px ND stad IV
2. Latihan fisik : primer dan sekunder1. Latihan primer : latihan 1 atau 1,5 jam setelah makan2. Latihan sekunder : terutama px obesitas, latihan setiap pagi, siang sore.
3. Penyuluhan kesehatan masyarakatPerorangan , TV, Kaset video, Disko, Poster, Leaflet dll.
TERAPI SEKUNDER
4. Obat hipoglikemia (OHO dan insulin)
5. Cangkok Pankreass
Penatalaksaan gizi dan kalori Kebutuhan kolori/hari :
1. BB normal (BBR 90-100%) = 30 kal/KG BB/hari2. BB lebih (BBR.110 %) = 20 kal/KGBB/hari3. BB kurang (BBR< 90 %) = 40-60 kal/KGBB/hari4. Gemuk (BBR> 120 %) = 15 kal/KGBB/hari
Indikasi DIIT B (68 % kal KH, 20 % kal lemak, 12 % kal protein)5. Kurang tahan lapar6. Hiperkolesterolemia7. Makroangiopati 8. Mikroangiopati 9. DM >15 tahun
Indikasi DIIT B1 (60 % kal KH, 20 % kal Lemak, 20 % kal protein)1. Makan biasa tinggi protein lemak normal2. Kurus 3. Patah tulang4. Hamil atau menyusui5. Hepatitis kronis atau SH6. Tb paru7. Gangren8. Morbus basedowi9. Kanker10. Infeksi dll
Obat Hipoglikemik(OHO)
Indikasi : DM tipe 2, MRDM teregulasi baik; MRDM belum teregulasi baik dengan TKOI
Klasifikasi Rasional
Kelas A. hipoglkemik kuat ( glibenklamide, klorpropamide, glipisid). Kelas B. kel hepar dan atau ginjal ( glukoidon glimepiride, glipizide GITS) Kelas C. angiopati (glikazide dan glimepiride) Kelas D. DM ringan atau gg post reseptor ( glipizide) Kelas E. DM dgn kel hepar/ginjal ( glimepiride) Kelas BG. Absorbsi glukose menurun dan uptake perifer meningkat ( metformin) Kelas SP. Spesifik (Acarbose, Troglitazone, Rosiglitazone, Proglitazone, Repaglinide,
Nataglinide) Cara kerja
Sulfonilurea1. Tolbutamide, Acetahesamide, Tolazamid, Carbutamide, glycodiazin, klorpropamide2. Glibornurid, Glipizid, Glipizide GITS, Glisoxepid, Glibenclamide, Gliclazid, Gliquidon3. Glimepiride Biguanide
Phenformin, Metformin, Buformin
Syarat OHO berhasil baik: diit dan latihan sesuai 3 J, diberikan pada px umur > 40 th, lama DM < 5 th, Tx insulin belum pernah, KAD belum pernah.
INSULIN Indikasi
1. DMTI2. MRDM3. DM-tipe X4. Koma diabetik5. DM tipe 2 : gagal sek OHO,hamil, gangren, kurus, fraktur,
hepatitis/sirosis hati, operasi
Cara pemberian Dosis rumatan.3 x (2 x n)/ subkutan. n=angka awal GDS. Regulasi cepat.
Indikasi : DM-sepsis pro op; GPDO; IMA; rawat inap RC intravena (rumus 1,2,3,4,5 dan rumus 4,6,8,10,12)
Rumus minus 1 (rumus1,2,3,4,5) Rumus kali 2 (rumus 4,6,8,10,12)
RC subkutan. Rumus kali 2/sub kutan/1 x (dosis awal ekstra) dilanjutkan dosis rumatan.
Insulin pada NPE-Diabetik Rumus 5 –1. 5 gr glukosa alkohol (maltose dll) diperlukan 1 U IR Rumus 2,5 – 1. 2,5 gr glukosa diperlukan 1 U IR
TKOI. PPS (pagi OHO, sore insulin) & PPP (pagi OHO & insulin)
Penanganan komplikasi akut Hipoglikemia Gejala : lapar, gemetar, keringat dingin, berdebar,pusing –
koma. Diagnosis : Gejala + glukosa darah < 30 – 60 mg/dl Terapi :
1. Pisang/roti/kh lain, bila gagal ---no 22. The gula, bila gagal --- no 33. Glukosa 40% i.v 25 ml ---- dilanutkan M 10 % atau D 10 %. Dapat
diulang sampai 6 kali selang 0,5 jamrumus 3 – 2 - 1
4. Efedrin 25 – 30 mg atau glukagon 1 mg i.m
Koma lakto asidosis (KLA) Patogensesa. Gagal merubah laktat menjadi bikarbonat. Faktor predisposisi
Infeksi, shok/gg vaksuler lainnya, gg hepar & ginjal, DM+pherformin,gg oksigenasi (PPOM, mikroangiopati dll)
Gejala Stupor – koma, hiperglikemia ringan Bikarbonat < 15 mEq/l. A laktat > 7 mMol/l Anion gap.( K+ Na) – (Cl+CO2) >20mEq atau Na – (Cl+CO2) >15
mEq Terapi: kausal
Penanganan KHONK ( Askandar 1991-1998,1999,2000)
Diagnosis Klinik. Tetralogi KHONK
1. Rw DM tidak ada; Dehidrasi berat, hipotensi – syok, tidak ada Kussmaul, gejala nerolgi, reduksi +++, tidak bau aseton, tidak ada ketonuria
2. Gukosa dasar >600 mg/dl; BIK > 15 mEq/l; pH normal, tidak ada ketonemia, glukosa darah relatif rendah bl ada nefropati
3. Faktor peunjang : pH>7,3; prerenal azoemia; hipernatremia; gg kesadaran; nerologi (kejang)
Pasti. Pentalogi KHONK ( 1 + 2 ) plus OSM darah > 325 – 350 mOSM/ L
Patogenesa Faktor presipitasi : Thiazide, glukose, infeksi, steroid, B
bolcker,phenotoin, cimitidine, clorpromazine Glukagon meningkat Relatif defisiensi insulin Hambatan lipolisis oleh insulin cukup
Terapimirip terapi KAD, tanpa BIK
1. NaCl 0,9 % bila Na < 150 mEq/l; NaCl 0.45 % bila Na >150 mEq/l2. IR seperti KAD3. Antibiotika sesuai indikasi
Penanganan Ketoasidosis Diabetik
KRITERIA KAD1. Klinik : poliuri, polidipsi, mual/muntah, Kussmaaul, lemah
dehidrasi, hipotensi – syok dan kesadaran terganggu.2. Darah : glukosa darah > 300 mg/dl (biasanya > 500);
bikarbonat < 20 mEq/l (dan pH< 7,35)3. Urine ; glukosuria dan ketonuria
KLASIFIKASI KADI. Ringan. pH 7,30 – 7,35 ; BIK 15 – 20 mEq/lII. Sedang. pH 7,20 – 7, 30 ; BIK 12 – 15 mEq/lIII. Berat. pH 6,90 – 7,20 ; BIK 8 – 12 mEq/lIV. Sangat berat. pH < 6,90 ; BIK < 8 mEq/l
PATOGENESA1. Hiperglikemia 2. hiperketogenesis
TERAPI3. Fase I (gawat)4. Fase II (fase rehabilitasi) Dengan batas kedua fase glukosa darah 250 mg/dl
ADA Recommendations for Glycemic Control
Goal Take ActionPreprandial glucose mg/dl
80-120 <80>140
Bedtime glucose mg/dl
100-140 <100>160HbA1c % <7 >8
ADA Diabetes Care 2000
Terima kasih