This document discusses the classification and treatment of diabetes mellitus. It describes the main types of diabetes as type 1, type 2, and other specific types. Type 1 is characterized by beta-cell destruction leading to insulin deficiency, while type 2 involves insulin resistance with relative insulin deficiency or a secretory defect. The document then discusses the pharmacological and non-pharmacological treatment and management of diabetes, including medications, diet, exercise and patient education. It also covers diabetes complications if not properly managed.

1. Diabetes Melitus
DM
MUHAMMMAD UMAR FERDIANSAHAmd.Kep
SMF Ilmu Penyakit Dalam
Poli Spesialis RS AL-Irsyad Surabaya
2014

2. 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

3. 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

4. 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 1
1. Autoimun
2. idiopatik
2. DM tipe 2
1. Resistensi insulin/ def insulin relatif
3. DM tipe lain
1. 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

5. Types-continued
 Infections
Congenital rubella
Cytomegalovirus
Others
 Uncommon forms of immune–
mediated diabetes
Insulin autoimmune syndrome
(antibodies to insulin)
Anti–insulin receptor antibodies
“Stiff Man” syndrome
Others
 Drug– or Chemical–induced
Diabetes
 Nicotinic acid
 Glucocorticoids
 Thyroid hormone
 Alpha–adrenergic agonists
 Beta–adrenergic agonists
 Thiazides
 Dilantin
 Pentamidine
 Vacor
 Interferon–alpha therapy
 Others

6. 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 byWHO, using a
glucose load containing the equivalent of 75 gm anhydrous glucose
dissolved in water

7. WHO diagnostic criteria
whole blood plasma
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

8. 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

9. 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

10. 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)

11. What is type 2 diabetes?
A progressive metabolic disorder
characterised by:
Insulin
resistance
-cell
dysfunction
Type 2
diabetes
1. Beck-Nielsen H, Groop LC. J Clin Invest 1994;94:1714–1721
2. Saltiel AR, Olefsky JM. Diabetes 1996;45:1661–1669

12. 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
 AllType 1 patients will require Insulin and type 2
can be on diet only, tablets or insulin treated

13. Treatment of diabetes-
Tablets
 Sulphonylureas: Glibenclamide, gliclazide,
Tolbutamide,Glimiperide, Repaglanide etc.
 Biguanides:Metformin
 Alpha glucosidase inhibitor:Acarbose
 Thiazolidinedione derivatives:
Troglitazone, Rosiglitazone,Pioglitazone.

14. 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

16. 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

17. 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.

18. 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

19. Diagnosis
 Kriteria DM (Perkeni 1998)
Poliuri, Polidipsi, BB sebab tidak jelas plus :
1. GDA > 200 mg/dl atau
2. GDP (vena) ≥ 126 mg/dla atau
3. TTGO 2 JPP ≥200 mg/dl

20. 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 definitif
1. 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
atau
2. 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

21. Keluhan klinis
Positit Negatif
GDP
GDS
 126
 200
< 126
 200
Ulang GDS atau GDP
110 < 126
110 - 190
< 110
TTGO
2J PP
GDP
GDS
 126
 200
< 126
< 200
> 126
 200
GDP
GDS
 200 140 - 190 < 140
GDPTD I A B E T E S M E L L I T U S NormalTGT
EVALUASI: GIZI, PENYULIT, PERENCANAAN MAKAN
Nasihat umum, makanan,
olahraga, BB idaman, obat -
Langkah Dx Diabetes Melitus

22. 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 II
Diit B3 untuk px ND stad III
Diit Be untuk px ND stad IV
2. Latihan fisik : primer dan sekunder
1. Latihan primer : latihan 1 atau 1,5 jam setelah makan
2. Latihan sekunder : terutama px obesitas, latihan setiap pagi, siang sore.
3. Penyuluhan kesehatan masyarakat
Perorangan , TV, Kaset video, Disko, Poster, Leaflet dll.
TERAPI SEKUNDER
4. Obat hipoglikemia (OHO dan insulin)
5. Cangkok Pankreass

23. Penatalaksaan gizi dan kalori
Kebutuhan kolori/hari :
1. BB normal (BBR 90-100%) = 30 kal/KG BB/hari
2. BB lebih (BBR.110 %) = 20 kal/KGBB/hari
3. BB kurang (BBR< 90 %) = 40-60 kal/KGBB/hari
4. Gemuk (BBR> 120 %) = 15 kal/KGBB/hari
Indikasi DIIT B (68 % kal KH, 20 % kal lemak, 12 % kal protein)
1. Kurang tahan lapar
2. Hiperkolesterolemia
3. Makroangiopati
4. Mikroangiopati
5. DM >15 tahun
Indikasi DIIT B1 (60 % kal KH, 20 % kal Lemak, 20 % kal protein)
1. Makan biasa tinggi protein lemak normal
2. Kurus
3. Patah tulang
4. Hamil atau menyusui
5. Hepatitis kronis atau SH
6. Tb paru
7. Gangren
8. Morbus basedowi
9. Kanker
10. Infeksi dll

24. 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
 Sulfonilurea
1. Tolbutamide, Acetahesamide, Tolazamid, Carbutamide, glycodiazin, klorpropamide
2. Glibornurid, Glipizid, Glipizide GITS, Glisoxepid, Glibenclamide, Gliclazid, Gliquidon
3. 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.

25. INSULIN
 Indikasi
1. DMTI
2. MRDM
3. DM-tipe X
4. Koma diabetik
5. 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)

26. 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 2
2. The gula, bila gagal --- no 3
3. Glukosa 40% i.v 25 ml ---- dilanutkan M 10 % atau D 10 %. Dapat
diulang sampai 6 kali selang 0,5 jam
rumus 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

27. 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
 Terapi
mirip terapi KAD, tanpa BIK
1. NaCl 0,9 % bila Na < 150 mEq/l; NaCl 0.45 % bila Na >150 mEq/l
2. IR seperti KAD
3. Antibiotika sesuai indikasi

28. KRITERIA KAD
1. 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 KAD
I. Ringan. pH 7,30 – 7,35 ; BIK 15 – 20 mEq/l
II. Sedang. pH 7,20 – 7, 30 ; BIK 12 – 15 mEq/l
III. Berat. pH 6,90 – 7,20 ; BIK 8 – 12 mEq/l
IV. Sangat berat. pH < 6,90 ; BIK < 8 mEq/l
PATOGENESA
1. Hiperglikemia
2. hiperketogenesis
TERAPI
1. Fase I (gawat)
2. Fase II (fase rehabilitasi)
Dengan batas kedua fase glukosa darah 250 mg/dl

29. ADA Recommendations for Glycemic
Control
Goal Take Action
Preprandial
glucose mg/dl
80-120 <80
>140
Bedtime
glucose mg/dl 100-140
<100
>16
0HbA1c % <7 >8
ADA Diabetes Care 2000

30. Terima kasih