APAKAH DIABETES ITU ?

Faktor Faktor
keturunan lingkungan Gaya hidup
berisiko:
Makan
berlebihan
Kurang sport
Stres
Insulin kurang jumlahnya
Insulin kurang baik kerjanya

DIABETES =
Gula (glukosa) darah meningkat
Bagaimana Terjadinya Diabetes?

Sel otot tidak

Kekurangan bisa
Insulin menggunakan
insulin

Hiperglikemi
DeFronzo RA.Diabetes.37:667,1988
Saltiel J.Diabetes.45:1661-1669,1996
Robertson RP.Diabetes.43:1085,1994
Tokuyama Y.Diabetes 44:1447,1995
 Organs Involved with Glucose Homeostasis
Pancreas
Liver Kidneys
Sulfonylureas
Glinides, GLP-1RA
DPP-4 Inhibitors
Metformin
SGLT2
TZDs
Inhibitors
 Hyperglycemia
-glucosidase inhibitors
Adipose TZDs GLP-1RA, Colesevelam
Insulin GLP-1RA
Bromo-
criptine Gut

Muscle
Brain
Holst JJ, Ørskov C. Diabetes. 2004;53:S197-S204.
5
Lebovitz HE. Diabetes Rev. 1999;7:139-153.
 A. Apa tanda-tanda diabetes?
Gejala khas
1. Klinis

poliuria
(sering Poliphagia polidipsia
kencing) (cepat lapar)(sering haus) lemas
berat badan
turun

Gatal di
kemaluan
gatal-gatal mata kabur impotensia (wanita) kesemutan

Gejala lain
 Prevalensi DM di Indonesia

5
7

International Diabetes Federation 2014

.
International Diabetes Federation 2013
. 7
8
 Diabetes Mellitus Classification
β-cell destruction, usually leading to absolute
Type 1 DM insulin deficiency, autoimmune, ideopathic

Varied, ranging from dominant insulin resistance

Type 2 DM accompanied by relative insulin deficiency to a
predominantly insulin secretory defect with
insulin resistance

Any degree of glucose intolerance with onset or

Gestational first recognition during pregnancy
DM

9
Rudianto et al. Indonesian Society of Endocrinology’s Summary Article of DM National Clinical Practice Guidelines. JAFES. May 2011 26(1)
 Differences of
Type 1 and Type 2 Diabetes
Type 1 Type 2
Pathophysiology Range: Insulin resistance
β-cell destruction, absolute with insulin deficiency to
insulin deficiency insulin secretory defect with
insulin resistance
Age Any >30 years

Weight Usually lean Obese

Onset of
Abrupt Gradual
signs/symptoms
Symptoms Hyperglycemia, ketosis Few classic symptoms

Treatments Insulin therapy May require Insulin therapy

10
 Clinical Presentation
T1DM T2DM
Frequent urination Any of the Type 1 symptoms
Usual thirst Frequent infections
Extreme hunger Blurred vision
Unusual weight loss Cuts/bruises that are slow to heal
Extreme fatigue and irritability Tingling/numbness in the hands/feet
Recurring skin, gum,
or bladder infections

11
http://www.diabetes.org/diabetes-basics/symptoms/?loc=DropDownDB-symptoms
T2DM is a Progressive Disease Characterized by
Insulin Deficiency and Insulin Resistance
Inherited/acquired factors Overweight, inactivity
(inherited/acquired)

Insulin deficiency Insulin resistance

FFA
Glucose Glucose
uptake production
Gluco- in the liver
lipotoxicity

Hyperglycemia

Yki-Järvinen H.
In: Textbook of Diabetes 1, third edition. T2DM 12
Oxford, UK: Blackwell; 2003: p22.122.19.
 Kelompok Risiko Tinggi

• Kelompok dengan berat badan lebih (Indeks Massa Tubuh [IMT] ≥23
kg/m2) yang disertai dengan satu atau lebih faktor risiko sebagai berikut:
1. Aktivitas fisik yang kurang.
2. First-degree relative DM
3. Kelompok ras/etnis tertentu.
Kelompok risiko
4. Riwayat tinggi
dengan bayidengan hasil
BB >4 kg atau pemeriksaan
GDM.
glukosa5. plasma
Hipertensi normal sebaiknya diulang setiap 3
(≥140/90 mmHg)
tahun 6. HDL <35 mg/dL dan atau trigliserida >250 mg/dL.
(E),
7. Wanita dengan sindrom polikistik ovarium.
kecuali8.pada
Riwayatkelompok
prediabetes. prediabetes pemeriksaan
diulang9. tiap
Obesitas berat, akantosis
1 tahun (E). nigrikans.
10. Riwayat penyakit kardiovaskular.

• Usia >45 tahun tanpa faktor risiko di atas.

 Kadar Glukosa Darah Sewaktu dan Puasa Sebagai Patokan
Penyaring dan Diagnosis DM di Indonesia
Bukan Belum Pasti DM
DM DM
Plasma vena <100 100-199 ≥ 200
Kadar glukosa
darah sewaktu Darah kapiler <90 90-199 ≥ 200
(mg/dL)
Kadar glukosa Plasma vena <100 100-125 ≥126
darah puasa
(mg/dL)
Darah kapiler <90 90-99 ≥100
15
 pada

Diabetes Melitus
 PADA DIABETES, ADALAH:

= A1C
= BLOOD PRESSURE (TEKANAN DARAH)
= CHOLESTEROL
 A1c
A1C ADALAH GLUKOSA YANG
TERIKAT PADA SEL DARAH
MERAH
Kadar A1c didalam darah
menggambarkan kadar gula darah
rata-rata selama 3 bulan

Kadar normal A1c <7%

http://www.metrika.com/3medical/hemoglobin-m.html
 Target of Treatment
Risk CVD (-)
BMI (kg/m2) 18.5 – <23

Blood Glucose
• Pre Prandial Glucose (mg/dL) 80-130

• Post Prandial BG (mg/dL) <180

A1C (%) <7.0

Systolic Blood Pressure (mmHg) <140

Diastolic Blood Pressure (mmHg) < 90

Triglyceride (mg/dL) <150

HDL Cholesterol (mg/dL) >40 / >50

LDL Cholesterol (mg/dL) <100/<70

19
PERKENI GUIDELINES 2015
• Edukasi
• Terapi Gizi Medis
• Latihan Jasmani
• Obat-obatan dan insulin
• Prinsip pengaturan makan  SEIMBANG sesuai dengan
kebutuhan kalori dan zat gizi.

• Tepat 3J : Jadwal, Jenis dan Jumlah

• BNI : Batasi-Nikmati-Imbangi

Makanan seimbang : Karbohidrat, protein, dan lemak

• Karbohidrat : 60-70%
• Protein : 10-15%
• Lemak : 20-25%
• Latihan jasmani dilakukan secara teratur (3-4x seminggu
selama kurang lebih 30 menit), diluar kegiatan sehari-hari.
• Latihan jasmani yang dianjurkan adalah yang bersifat aerobik,
seperti jalan kaki, bersepeda santai, jogging dan berenang.
• Hindari kebiasaan hidup yang kurang gerak dan bermalas-
malasan.
23
 Oral Diabetes Drugs in Indonesia
Daily
Duration of Freq/d A1C
Class Generic Mg/tab dose Time FBG vs. PPG
action (hr) ay reduction
(mg)

Glibinclamide 2.5-5 2.5-15 12-24 1-2 Before 1.5 FBG

meals
Glipizid 5-10 5-20 12-16 1
Sulfonylureas Gliklazid 30,60,80 30-320 24 1-2
Glikuidon 30 30-120 6-8 2-3
Glimepiride 1,2,3,4 0.5-6 24 1
Repaglinid 1 1.5-6 3 1-1.5 Both
Glinid
Nateglinid 120 360 3 0.5-0.8 PPG

Pioglitazone 15-30 15-45 18-24 1 Indep of 0.5-1.4 FBG

TZD meals

Acarbose 50-100 100- 3 With 1st 0.5-0.8 PPG

α-glucosidase 300 food
inhibitor

24
 Oral Diabetes Drugs in Indonesia
Daily dose Duration of Freq/ A1C FBG vs.
Class Generic Mg/tab Time
(mg) action (hr) day reduction PPG

Metformin 500-850 500-3000 6-8 1-3 With or 1.5 FBG

Biguanides after meals
Metformin XR 500-750 500-2000 24 1

Vildagliptin 50 50-100 12-24 1-2 Indep of 0.6-0.8 Both

meals
DPP-IV inhibitors Sitagliptin 25,50,100 25-100 24 1
Saxagliptin 5 5 24 1
Metformin+ 25-500/ Glib max 20 12-24 1-2 With or
Glibenclamide 1.25-5 mg/day after meals
Glimepiride + 1-2/ 2-4/ 2
metformin 250-500 500-1000
Fixed dose
Pioglitazone+ 15-30/ Piog max 45 18-24 1
combination
metformin 500-850 mg/day
drug
Sitagliptin + 50/ Sita max 100 1
metformin 500-1000 mg/day
Vildagliptin + 50/ Vilda max 12-24 2
metformin 500-1000 100 mg/day

25
 Insulin in Indonesia
Awal Kerja Puncak Kerja Lama Kerja
Sediaan Insulin Kemasan
(Onset) (Peak) (Duration)
Insulin Prandial (Meal Related)
Insulin Short Acting
Reguler (Actrapid®, Humulin® R) 30-60 menit 30-90 menit 3-5 jam Vial, pen/cartridge
Insulin Analog Rapid Acting
Insulin Lispro (Humalog®) 5-15 menit 30-90 menit 3-5 jam Pen/cartridge
Insulin Glulisine (Apidra®) 5-15 menit 30-90 menit 3-5 jam Pen
Insulin Aspart (Novorapid®) 5-15 menit 30-90 menit 3-5 jam Pen, Vial
Insulin Intermediate Acting
NPH (Insulatard®, Humulin® N) 2-4 jam 4-10 jam 10-16 jam Vial, Pen/cartridge
Insulin Long Acting
Insulin Glargine (Lantus®) 2-4 jam No Peak 18-26 jam Pen
Insulin Detemir (Levemir®) 2-4 jam No Peak 22-24 jam Pen
Insulin Campuran
70% NPH 30% Reguler
30-60 menit Dual 10-16 jam Pen/cartridge
(Mixtard®, Humulin® 30/70)
70% Insulin Aspart Protamin
10-20 menit Dual 15-18 jam Pen
30% Insulin Aspart (Novomix® 30)
75% Insulin Lispro Protamin
5-15 menit Dual 16-18 jam Pen/cartridge 26
30% Insulin Lispro (HumalogMix® 25)
American Diabetes Association:
Standards of Care 2015 in people with Diabetes

27
American Diabetes Association. Diabetes Care 2015;38(Suppl. 1):S49–S57
 28

I N S U L I N
INSULIN INJECTION TECHNIQUE
 KEY BARRIERS TO INSULIN INITIATION

More than 50% of patients are very worried about

starting on Insulin

More than 50% of patients believe that starting on Insulin

mean that they have failed to manage their disease

Only 20% believe

that Insulin can help
them manage their
disease

More than 33% of HCPs postpone Insulin

until “absolutely essential”

67% use Insulin as a threat for their patients

Rubin RR et al. Diabetes Care 2006;29:1249–55.

Blood vessels penetrate
each layer of skin
But BLOOD FLOW differs considerably
from one layer to another

• Dermis : small but swift flow and highly

variable

• Subcutaneous : slow flow and very stable

• Muscle : large, swift flow and highly

Injection Sites
 Adults

 Studies have shown that IM Injections occur

in 12 -34 % of injections depending on :
Injection site
Body habitus of patient
Length of needle
Use of pinch or not
How long pinch held and when realesed
Teknik Penyuntikan Insulin
 Tutup vial diusap dengan alkohol 70%, untuk
melarutkan tidak dikocok tetapi digulingkan
 Setelah masuk pada alat suntik, periksa
gelembung udara, ketuk  buang gelembung
 Suntikan pada subkutan setelah desinfektan,
tegak lurus (pen), sudut 45 derajat bila dengan
spuit agar tidak kena muskuler
 Bila insulin campuran sendiri (bukan premixed),
ambil dulu insulin reguler, kemudian insulin
menengah  agar tidak tercemar yang keruh
 Tempat Penyuntikan
Ideal untuk insulin aksi pendek atau campuran pagi hari:
 Perut dibawah pusar
Ideal untuk insulin aksi menengah, aksi panjang atau
campuran malam hari:
 Lengan atas bagian luar
 Glutea
 Paha atas bagian luar
Sebaiknya berpindah tempat untuk mencegah insulin lipodistrofi
atau jaringan sikatrik yang luas
Regio satu berpindah ke regio lain sekitar 2 minggu
Absorpsi insulin dipengaruhi:
 Persiapan insulin (premixed, aksi panjang, aksi
pendek dll)
 Cara pemberian (s.c., i.m. atau i.v.)
 Lokasi (regio, ada lipoatrofi/lipohipertrofi)
 Temperatur
 Olah raga/latihan
 Pijat
 Obat vasoaktif
Thickness of SC in mm
LOKASI PENYUNTIKAN INSULIN
(berpindah tiap 2 minggu)
-

- -

- -

- -
Injection Site Rotation
PEN INJECTION TECHNIQUE
INJECTION TECHNIQUES
How is the correct Pinch Up?
Angle of Needle with a pinch
SUMMARY
 Cara Menyimpan Insulin
 Penyimpanan insulin dalam suhu 20 – 80 C (Insulin akan
stabil sampai dengan masa kadaluarsa )
 Umur insulin yang belum digunakan sampai dengan masa
kadaluarsa adalah 2,5 tahun
 Insulin yang sudah dipakai, disimpan pada suhu kamar ( <
300) dan akan stabil sampai dengan 6 minggu
 Hindari terpapar cahaya matahari langsung
 Bila insulin dingin diputar-putar di telapak tangan atau
ditaruh dalam suhu kamar dahulu
 Karena perbedaan suhu insulin jangan diletakkan di mobil
atau bagasi pesawat
 Insulin beku atau menggumpal, berubah warna, jernih jadi
keruh  jangan dipakai
Efek Samping Penyuntikan Insulin

LYPODYSTROPHY
&
LYPOHYPERTROPHY
 Lipohypertrophy

• Sites should be inspected by the HCP at very visit

• Making two ink marks at opposites edges of the
lipohypertrophy
• Patients should not inject into areas of lipohypersthrophy
until the abnormal tissue returns to normal
• Switching injections from lipohyperthropy to normal tissue
• The best current presentative and therapeutic strategies
for lipohypertrophy

Patients feels less pain when injecting in the lipohypertrophy

Slide 49
 Tips of Making Injection Less Painful

• Keep insulin in use at room temperature

• If using alcohol, injecting only when the alcohol has
fully dried
• Avoid injecting at hair roots
• Using shorter length and smaller dismeter needle
• Using new needle at each injection
Pen Injection Technique
 PEN INJECTION TECHNIQUE
RE-SUSPENSION REQUIRED FOR PRE-MIX
AND INTERMEDIATE ACTING INSULIN
Gulung Pena Insulin Gerakkan pena insulin
diantara kedua telapak keatas dan ke bawah
tangan sampai dengan 10 x sebanyak 10 x

&
PEN INJECTION TECHNIQUE
REMOVING THE OUTER CAP
 PEN INJECTION TECHNIQUE
ENSURE THAT NO AIR BUBBLES ARE
PRESENT IN THE PEN
Pen Solostar Lantus & Apidra harus dengan
Jarum BD

5mm (3/16”) x 31G Tersedia di

Catalog No. 320470 ecatalog LKPP

4mm (5/32”) x 32G

Catalog No. 320472
 PENUTUP
Untuk bisa hidup sehat, bahagia dan
sejahtera dengan diabetes perlu :
• Memahami apa itu diabetes
• Kemampuan dan ketrampilan
mengendalikan diabetes (mandiri) dan
penatalaksanaan penggunaan insulin
• Kemampuan mengendalikan problem
kejiwaan/emosi optimis
• B N I – S, Batasi – Nikmati – Imbangi
Syukuri
 Criteria for the Diagnosis (Perkeni, 2015)
FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at
least 8 h.*
OR
2-h PG ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should be
performed as described by the WHO, using a glucose load containing the
equivalent of 75 g anhydrous glucose dissolved in water.*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis,
a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
OR
A1C ≥6.5%. The test should be performed in a laboratory using a method
that is NGSP certified and standardized to the DCCT assay.*

59
Impaired: Fasting Glucose & Glucose Tolerance

• Impaired Fasting Glucose (IFG):

– A condition in which the blood glucose level
is between 100 mg/dL to 125mg/dL after an
8- to 12-hour fast.

• Impaired Glucose Tolerance (IGT):

– A condition in which the blood glucose level
is between 140 and 199 mg/dL at 2 hours during an
oral glucose tolerance test (OGTT).

60
 Keuntungan Terapi Insulin
• Pengobatan yang digunakan sejak lama, dengan pengalaman klinis yang
lebih banyak

• Paling efektif menurunkan glukosa darah

• Dapat menurunkan kadar HbA1c pada keadaan apapun

• Tidak ada dosis maksimum insulin

• Efek menguntungkan pada trigliserida dan HDL

Nathan DM, et al. Diabetes Care 2009;32 193-203.

61
 Indikasi Insulin Dini
1. Gula Darah Puasa (FPG) >250 mg/dL;
2. Gula Darah Acak >300 mg/dL;
3. HbA1C >10%;
4. Ketonuria; atau
5. Gejala jelas diabetes polyuria, polydipsia, dan BB turun.[1,2]

1. Nathan DM, Buse JB, Davidson MB, et al. Management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy.
Diabetes Care. 2006;29:1963-1972. Abstract
2. Hirsch IB, Bergenstal RM, Parkin CG, et al. A real-world approach to insulin therapy in primary care practice. Clin Diabetes. 2005;23:78-86.
Memulai Terapi Insulin

Insulin mana yang digunakan?

 Insulin jangka panjang yang ideal?

• 1 injeksi/hari mencakup 24 jam

• “Peakless” (tanpa puncak)
• Angka kejadian hipoglikemia rendah
• Kontrol gula darah yang baik
• Kenaikan berat badan minimal
• Dapat diprediksi
• Mudah digunakan

– Dapat injeksi di berbagai tempat

– Dapat diinjeksi pada waktu yang
berbeda
– Tidak perlu mencampur / cairan
bening
• Tingkat kepuasan dan penerimaan terapi yang baik
 KAPAN MEMULAI TERAPI INSULIN?
sedikitnya 3 bulan
terapi GHS + 2 OHO:
• A1c >7 % dan
Glukosa Puasa>100

Glukosa Darah

A1c > 9 %

GHS: Gaya Hidup Sehat

Konsensus Perkeni 2011
Teknik Injeksi
Teknik Injeksi (2)
 Jika gula darah puasa • Gunakan insulin basal
meningkat

Jika gula darah sesudah • Gunakan insulin bolus

makan meningkat

Jika gula darah puasa dan • Gunakan insulin premix

sesudah makan meningkat • Atau tambahkan insulin
basal pada terapi OAD
• Atau mulai terapi basal
bolus

Perkeni, Petunjuk praktis terapi insulin pada pasien diabetes, 2011

Lokasi Injeksi Insulin
 Summary
• Screening for risk factors for development of DM helps identify
patients early
• T1DM & T2DM can be distinguished by age onset, weight, and
progression of signs and symptoms
• Each have different underlying pathophysiology and thus require
different treatment and management strategies
• There are several different classes of anti-hyperglycemia
medications available
– Biguanides, sulfonylureas, thiazolidinediones, alpha-glucosidase
inhibitors, DPP-IV inhibitors and GLP-1 receptor agonists
• Each class differs in their target site, pharmacology, efficacy and
safety profile
• Treatment algorithms aid in choosing which medication to use for
each patient
70
 Summary

• Assessing a patient’s cardiometabolic risk is important in the

prevention of CVD and T2DM

71
 Insulin Deficiency is Often Already
Established when T2DM is Diagnosed
DIAGNOSIS
20
Postprandial
15
glucose
Glucose
(mmol/l)

Fasting
10 glucose

250
Relative -cell
function (%)

200 Insulin resistance

150
100 Insulin
level
50 -cell failure
0

MACROVASCULAR CHANGES
Clinical
features
MICROVASCULAR CHANGES

Years 10 5 0 5 10 15 20 25 30
72
Adapted from Rhodes CJ. Science. 2005;307:380-4.