D iabetes M elitus

DM
MUHAMMMAD UMAR FERDIANSAH
Amd.Kep
SMF Ilmu Penyakit Dalam
Poli Spesialis RS AL-Irsyad Surabaya
2014

A etiologicalClassif c
iation
of D specific
isorders
of
Other
types
G lycaem ia
Genetic defects of betacell
Type 1 (betacell

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)

function

Genetic defects in insulin

action

Diseases of the exocrine

pancreas Endocrinopathies

Drug or chemicalinduced

Infections

Uncommon forms of
immunemediated diabetes

Other genetic syndromes

sometimes associated with
diabetes

Gestational diabetes

O ther types ofD iabetes

Genetic defects of beta

cell function

Chrme 20, HNF4_ (MODY1)

Chrme 7, glucokinase (MODY2)
Chrme 12, HNF1_ (MODY3)
Chrme 13, IPF1 (MODY4)
Mitochondrial DNA 3243
mutation

Genetic defects in insulin

action

Type A insulin resistance

Leprechaunism
RabsonMendenhall syndrome
Lipoatrophic diabetes & Others

Diseases of the exocrine

pancreas
Fibrocalculous pancreatopathy
Pancreatitis
Trauma / pancreatectomy
Neoplasia
Cystic fibrosis
Haemochromatosis & Others
Endocrinopathies
Cushings 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.
2.
3.

DM
1.
2.
DM
1.
DM
1.
2.
3.
4.
5.
6.
7.

tipe 1
Autoimun
idiopatik
tipe 2
Resistensi insulin/ def insulin relatif
tipe lain
Defek genetik (MODY,DNA mitokondria)
Defek genetik kerja insulin
P eksokrin pankreas (pankreatitis, tumor, pankreopati
fibrocalculus)
Endokrinopati ( akromegali, S Cushing, feokromositoma,
hipertoroidism)
Karena obat ( vacor, petamidin, glukorkortikoid, hormon tirod,
dinlatin dll)
Infeksi (rubella kongenital, CMV)
Imunologi ( antibodi anti insulin)

Types-continued
Infections

Congenital rubella
Cytomegalovirus
Others
Uncommon forms of
immunemediated
diabetes
Insulin autoimmune
syndrome (antibodies to
insulin)
Antiinsulin receptor
antibodies
Stiff Man syndrome
Others

Drug or Chemical
induced Diabetes
Nicotinic acid
Glucocorticoids
Thyroid hormone
Alphaadrenergic agonists
Betaadrenergic agonists
Thiazides
Dilantin
Pentamidine
Vacor
Interferonalpha therapy
Others

AD A 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

W H O 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
2hr post glucose load
<7.8 mmol/l

& <7.0mmol/l
<6.7 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%,4564-1.8%,>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)

W hat is type 2 diabetes?

A progressive metabolic disorder

characterised by:

Insulin
resistance

Type 2
diabetes

-cell
dysfunction

1. Beck-Nielsen H, Groop LC. J Clin Invest 1994;94:17141721

2. Saltiel AR, Olefsky JM. Diabetes 1996;45:16611669

Treatm ent ofD iabetes

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

Treatm ent ofdiabetes-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 (premeal) and evening isophane, rarely once daily

D iabetic Com plications

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

Patogenesis

DM tipe I ( kerusakan sel Beta Pankreas, Reseptor perifer cukup. )

Sintesis dan sekresi insulin kualitas maupun kuantitas kurang.
Predisposisi genetik ---- lingkungan ----- kerusakan sel 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
seks,

: lemah badan, semutan, difungsi

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 atau
2. GDP (vena) 126 mg/dla atau
3. TTGO 2 JPP 200 mg/dl

Kriteria Diagnosis MRDM Surabaya Kobe 1989

Kriteria dugaan MRDM

Kriteria definitif

Didapatkan 1,2,3,4 atau lebih :

1.

1.

DM usia 15 40 tahun ( dapat

kurang atau lebih)

2.

Ax atau ada tanda malnutrisiundernutrisi : 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

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

Langkah Dx Diabetes Melitus

Keluhan klinis

Positit

GDP
GDS

Negatif

126
200

GDP
GDS

< 126
200

126
200

110 < 126

< 110

110 - 190
Ulang GDS atau GDP

GDP
GDS

> 126
200

< 126
< 200

TTGO
2J PP

200

D IAB E TE S

MELLITUS

EVALUASI: GIZI, PENYULIT, PERENCANAAN MAKAN

140 - 190

TGT

< 140

GDPT

Normal

Nasihat umum, makanan,

olahraga, BB idaman, obat -

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.
2.

3.

Latihan primer : latihan 1 atau 1,5 jam setelah makan

Latihan sekunder : terutama px obesitas, latihan setiap pagi, siang sore.

Penyuluhan kesehatan masyarakat

Perorangan , 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/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)
5.
Kurang tahan lapar
6.
Hiperkolesterolemia
7.
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 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

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

1.
2.
3.
.

Sulfonilurea
Tolbutamide, Acetahesamide, Tolazamid, Carbutamide, glycodiazin, klorpropamide
Glibornurid, Glipizid, Glipizide GITS, Glisoxepid, Glibenclamide, Gliclazid, Gliquidon
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.
2.
3.
4.
5.

DMTI
MRDM
DM-tipe X
Koma diabetik
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)
.
.

RC subkutan. Rumus kali 2/sub kutan/1 x (dosis awal ekstra)

dilanjutkan dosis rumatan.

Insulin pada NPE-Diabetik

.
.

Rumus minus 1 (rumus1,2,3,4,5)

Rumus kali 2 (rumus 4,6,8,10,12)

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)

Hipoglikemia

Penanganankomplikasiakut

Gejala : lapar, gemetar, keringat dingin, berdebar,pusing

koma.
Diagnosis : Gejala + glukosa darah < 30 60 mg/dl
Terapi :
1.
2.
3.

4.

Pisang/roti/kh lain, bila gagal ---no 2

The gula, bila gagal --- no 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
Efedrin 25 30 mg atau glukagon 1 mg i.m

Koma lakto asidosis (KLA)

Patogensesa. Gagal merubah laktat menjadi bikarbonat.

Faktor predisposisi
.

Gejala
.
.
.

Infeksi, shok/gg vaksuler lainnya, gg hepar & ginjal,

DM+pherformin,gg oksigenasi (PPOM, mikroangiopati dll)
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.
2.
3.

Pasti. Pentalogi KHONK

..

( 1 + 2 ) plus OSM darah > 325 350 mOSM/ L

Patogenesa

Rw DM tidak ada; Dehidrasi berat, hipotensi syok, tidak ada

Kussmaul, gejala nerolgi, reduksi +++, tidak bau aseton, tidak ada
ketonuria
Gukosa dasar >600 mg/dl; BIK > 15 mEq/l; pH normal, tidak ada
ketonemia, glukosa darah relatif rendah bl ada nefropati
Faktor peunjang : pH>7,3; prerenal azoemia; hipernatremia; gg
kesadaran; nerologi (kejang)

Faktor presipitasi : Thiazide, glukose,

bolcker,phenotoin, cimitidine, clorpromazine
Glukagon meningkat
Relatif defisiensi insulin
Hambatan lipolisis oleh insulin cukup

infeksi,

steroid,

Terapi
mirip terapi KAD, tanpa BIK
1.
2.
3.

NaCl 0,9 % bila Na < 150 mEq/l; NaCl 0.45 % bila Na >150 mEq/l
IR seperti KAD
Antibiotika sesuai indikasi

KRITERIA KAD
1.
2.
3.

Klinik : poliuri, polidipsi, mual/muntah, Kussmaaul, lemah

dehidrasi, hipotensi syok dan kesadaran terganggu.
Darah : glukosa darah > 300 mg/dl (biasanya > 500);
bikarbonat < 20 mEq/l (dan pH< 7,35)
Urine ; glukosuria dan ketonuria

KLASIFIKASI KAD
I.
II.
III.
IV.

Ringan. pH 7,30 7,35 ; BIK 15 20 mEq/l

Sedang. pH 7,20 7, 30 ; BIK 12 15 mEq/l
Berat. pH 6,90 7,20 ; BIK 8 12 mEq/l
Sangat berat. pH < 6,90 ; BIK < 8 mEq/l

PATOGENESA
1.
2.

Hiperglikemia
hiperketogenesis

TERAPI
3.
Fase I (gawat)
4.
Fase II (fase rehabilitasi)
Dengan batas kedua fase glukosa darah 250 mg/dl

AD A Recom m endations for G lycem ic

Control

Goal

Take Action
Preprandial
<80
80-120
glucose mg/dl
>140
Bedtime
<100
100-140
glucose
>1
mg/dl
60
HbA1c %
<7
>8
ADA Diabetes Care 2000

Terima kasih