Diabetes Mellitus

The Disease and Its Management

Oleh :
Abdur Rahman
• DIABETESDIPERMASALAHKAN KARENA :
• 1. Diabetes berbahaya karena komplikasinya
hebat
• 2. Jumlah pengidapnya setiap tahun makin
• meningkat
• 3. Banyaknya ketidaktahuan tentang kapan
harus
• berobat dan tentang pentingnya
pengendalian
• 4. Diabetes dapat dijinakkan
DIABETES: A GROWING EPIDEMIC
Definisi
Diabetes mellitus is a group of metabolic
diseases characterized by hyperglycemia
resulting from defects in insulin secretion,
insulin action, or both
(Expert Committee on the Diagnosis and Classification of Diabetes mellitus 2002)

Long-term damage, dysfunction, and failure

of various organs especially the eyes, kidneys,
nerves, heart, and blood vessels
 Risk Factors for Endothelial Dysfunction

Verringerte Oxidative Athero- Increased

Hyperglycaemia
NO-Synthase- NO- Synthetase Platelet-
Stress sclerosis
Aktivität aggregation

Hyper- Cardiac--
Neuro- Hypertension
cholesterol- Smoking
hormones insufficiency
emia

endothelial function

5
 Macrovascular complications of diabetes

Cerebrovascular circulation
Stroke (22%*)

Coronary arteries
Angina

MI (34.7%*)
Sudden death
Renal arteries Renal damage

Peripheral vascular disease

Peripheral arteries
Gangrene
and amputation (2.7%*)

6
 Hyperglycemia

postprandial glucose total glucose impact (HbA1c)

microangiopathy macroangiopathy

acute glucose toxicity chronic glucose toxicity

endothelial damage

Diabetic late complications

7
Patofisiologi:

DM tipe 1:
Proses autoimunrusak pankreas
sel ß pankreas produksi insulin
berkurang/tidak ada
DM tipe 2:
Produksi insulin normal or berkurang
tp tdk efektif gangg. penyerapan dan
pemakaian glukosa di sel
 Kelainan Fungsi /
Jumlah Sel  Genetik

Tipe I (Autoimun)
Faktor Lingkungan
Virus
Sistim imun INSUFISIENSI Diet
(Ab anti pankreas) INSULIN Obesitas
Hamil

Marker :
Insulin auto Ab Kelainan Aktifitas Insulin
Islet cell auto Ab o.k. Reseptor
Glutamic acid
dicarbosaflase
Au Ab (GAD. Abs)

Ideopatik
Symptoms :
Polyuria
Polydipsia
Weight loss
Sometimes polyphagia
Blurred vision
Diagnosis
Symptoms
Symptoms of
of diabetes
diabetes plus
plus glucose
glucose >> 200
200 mg/dl
mg/dl

or
or

Fasting
Fasting plasma
plasma glucose
glucose >> 126
126 mg/dl
mg/dl

or
or

2-h
2-h plasma
plasma glucose
glucose >> 200
200 mg/dl
mg/dl during
during an
an OGTT
OGTT
The glycemic targets for GDM should be at the
following levels :
1. Fasting Plasma Glucose (FPG)  105 mg/dl.
2. 1-h Postprandial Plasma Glucose (1-h PP) < 155
mg/dl.
3. 2-h Postprandial Plasma Glucose (2-h PP) < 130
mg/dl.
 DIABETES vs PRE-DIABETES

Fasting 2 hours post

Blood prandial (mg/dl)
Glucose
Normal < 100 * < 140
Pre-Diabetes 100 * – 125 140 – 199

Diabetes  126  200

If
If FBG
FBG is
is >> 100,
100, have
have a 10-15%
10-15% chance
chance of
of
developing
developing DM DM in
in next
next 7 years.
Fig. 1. Proposed sequence of the key pathological features of type 2 diabetes as
discussed in this review.

Mark N. Feinglos, md, cm

M. Angelyn Bethel, md
 III. Klasifikasi Etiologis DM
1. Diabetes Tipe-1 (destruksi
(destruksi D.
D. Endokrinopati
Endokrinopati
sel beta) Acromegali,
Acromegali, sindroma
sindroma Cushing,
Cushing,
Autoimun
Autoimun Feokromositoma,
Feokromositoma,
hipertiroidisme
hipertiroidisme
Idiopatik
Idiopatik
E.
E. Karena
Karena obat/zat
obat/zat kimia
kimia
2. Diabetes Tipe-2 (( resistensi
resistensi Vacor,
Vacor, pentamidin,
pentamidin, asamasam nikotinat,
nikotinat,
insulin disertai defek sekresi Glukokortikoid,
Glukokortikoid, hormontiroid,
hormontiroid,
insulin atau sebaliknya) tiazid,
tiazid, Dilantin,
Dilantin, interferon
interferon alfa
alfa
3. Diabetes Tipe lain F.
F. Infeksi
Infeksi :: rubellakongenital,
rubellakongenital, CMVCMV
A.
A. Defek
Defek genetik
genetik fungsi
fungsi sel
sel beta
beta G.
G. Sebab
Sebab imunologi
imunologi yangyang jarang
jarang ::
MODY
MODY 1,2,3.
1,2,3. DNA
DNA Antibodi
Antibodi anti
anti insulin
insulin
mitokondria
mitokondria H.
H. Sindroma
Sindroma genetik
genetik lain:
lain:
B.
B. Defek
Defek genetik
genetik kerja
kerja insulin
insulin Sindroma
Sindroma Down,Down, Klinefelter,
Klinefelter,
C.
C. Penyakit
Penyakit eksokrin
eksokrin pankreas;
pankreas; Turner
Turner dll.
dll.
Pankreatitis,
Pankreatitis, tumor
tumor pankreas,
pankreas,
pankreatektomi,
pankreatektomi, pankreopati
pankreopati 4. Diabetes Gestasional
fibrokalkulus
fibrokalkulus
Pola Sekresi Insulin DM Tipe I

Sekresi insulin tergantung sisa masa sel 

Glycemic Control
 Management
Management
A.
A. Aim
Aim

Short Longer
Longer term
term ::
Short term
term ::
Eliminate Prevent
Prevent complications
complications
Eliminate symptoms
symptoms
Maintain Reduce
Reduce morbidity
morbidity
Maintain general
general well
well being
being
and
and mortality
mortality

Strategy
Strategy ::
Normalizing
Normalizing glucose,
glucose,
lipid,
lipid, and
and insulin
insulin levels
levels

Activities
Activities ::
Management with holistic
Management with holistic
approach and self
approach and self care
care
principles
principles
 Treatment Modalities

• Diet/Medical nutrition therapy

• Exercise
• Anti hyperglycemic agents
• Education
• Pancreas transplantation
• Cloning treatment (experiment)
 Education
Tujuan :
• Perubahan perilaku pasien dan keluarganya
Cara :
• Berikan dukungan dan nasehat positif
• Berikan informasi secara bertahap
• Mulai dengan hal hal yang sederhana
• Gunakan alat bantu
• Lakukan pendekatan dan simulasi
• Berikan pengobatan sesederhana mungkin
• Jangan terlalu memaksakan kehendak kita
• Berikan motivasi, penghargaan dan diskusikan hasil
pengelolaan
 Diet/Nutrition Therapy/Meal planning
Nutrient
Nutrient Composition
Composition of
of Diabetic
Diabetic Diet
Diet

PERKENI
PERKENI A
ADDA
A and
and B
BDDA
A
(Indonesian
(Indonesian Soc.of
Soc.of Endoc.)
Endoc.)
10-15% 10-15%
20-25% 30%

60-70%
55%
 PERENCANAAN MAKAN
KOMPOSISI :
• Karbohidrat : 60 – 70 %
• Protein : 10 – 15 %
• Lemak : 20 – 25 %
JUMLAH KALORI :
• Hitung BMI ( IMT ) = BB ( kg ) / TB ( m )2
• IMT wanita ( normal ) = 18,5 – 23,5 kg/ m2
• IMT laki ( normal ) = 22,5 – 25 kg / m 2
• Status gizi : BB Idaman = ( TB – 100 ) – 10%
• BB kurang : < 90% BBI
• BB Normal : 90 – 120% BBI
• BB lebih : 110 – 120 % BBI
• Gemuk : > 120% BBI
Exercise

30 minutes: 3 - 4 times / week

Continuous
Rhytmical
Interval
Progressive
Endurance training
 Anti Diabetic Agents

Hypoglycemic Agents

Anti Hyperglycemic Agents

 1A.
INSULIN

Insulin
Insulin actions
actions include
include ::
•• Ability
Ability of
of insulin
insulin to
to lower
lower circulating
circulating glucose
glucose
concentrations
concentrations
 Suppress
Suppress glucose
glucose production
production :: liver
liver
 Stimulate
Stimulate glucose
glucose utilization
utilization :: muscle
muscle plus
plus fat
fat

•• Additional
Additional metabolic,
metabolic, vascular
vascular &
& mitogenic
mitogenic actions
actions
 PRINCIPLES OF INSULIN
TREATMENT

Insulin regiment mimicking normal

(endogenous) physiologic insulin
secretion
Insulin Preparation

Basal Insulin
Prandial Insulin
(Pre)mixed Insulin
 Berdasar lama kerja, insulin terbagi menjadi empat jenis,
yakni:

 insulin kerja cepat (rapid acting insulin)

 insulin kerja pendek (short acting insulin)
 insulin kerja menengah (intermediate acting
insulin)
 insulin kerja panjang (long acting insulin)
 Insulin campuran
 Complications :
Infeksi
Acute : Chronic
Neuropathy

Microangiopathy Macroangiopathy

Ketoacidosis
Retinopathy CAD
Nonketotic Hyperosmolar
Nephropathy PVD
syndrome
Neuropathy Stroke
Lactic asidosis
Hypoglikemi/koma.
 Diabetes: A malignant vascular disorder
Most common Stroke
cause of 2-4 x risk for stroke
blindness in and coronary heart
younger people Diabetic disease *)
Retinopathy

Cardiovascular
disease

Diabetic
Myocardiac infarct
Nephropathy
*) Most common
Most common Diabetic
cause of death in
diabetics
cause of renal Neuropathy
failure → Dialysis

Most common cause of

lower limb amputation
National Diabetes Information Clearinghouse. Diabetes Statistics–Complications of Diabetes.
http://www.niddk.nih.gov/health/diabetes/pubs/dmstats/dmstats.htm#comp.
Penyulit Menahun KOMPLIKASI DM

33
Blood Flow Decrease by Smoking
Before smoking After smoking

(Photograph from Dr. Matsuo)

Oxidative Damage
How have these foot lesions possibly developed in
this woman with neglected type 2 diabetes?
KOMPLIKASI AKUT DM
HIPOGLIKEMI
HIPOGLIKEMI
 Kadar gula darah < 60 mg/dl
 Koma gula darah < 30 mg/dl

Penyebab Hipoglikemi pada

DM :
 OHA induce
 Insulin induce
Gejala dan Tanda Hipoglikemi :

1. Neuroglikopeni :

Daya berpikir menurun

Sulit berbicara
 Nyeri kepala
 Mata kabur
 Kesadaran menurun sampai koma
 Kejang
Gejala dan Tanda Hipoglikemi :

2. Adanya Rangsangan Adrenergik :

 Takhikardi
 Palpitasi
 Gemetar
 Berkeringat dan pucat
 Rasa lapar
 Mual
 Cemas
Hipoglikemi dibagi 3 derajat :

I. Ringan

II. Sedang

III. Berat
 TERAPI HIPOGLIKEMI

1. Pisang / roti / KH lain

2. gula , tetesi gula kembali atau madu dibawah lidah

3. Injeksi D 40% i.v 25 cc dilanjutkan infus D 10% atau

Martos 10% dapat diulang tiap 1/2 jam sampai sadar

4. Injeksi efedrin 25 - 50 mg atau glukagon 1 mg i.m.

Bila kadar gula darah diketahui

Kadar gula darah D 40%

<30 mg/dl 3 f

30 - 60 mg/dl 2 f

60 - 100 mg/dl 1f

(Askandar Tj., 1996)

KETO ASIDOSIS
METABOLIK
PENCETUS KAD :

 Infeksi
 Penghentian insulin atau terapi insulin
yang tidak adekuat
 Penderita baru
 IMA
 Obat steroid
 20% tidak diketahui
KRITERIA DIAGNOSIS KAD

1. Klinik : Poliuria, polidipsia, mual / muntah,

pernafasan kussmaul (dalam dan frekuen),
lemah, dehidrasi, hipotensi sampai syok,
kesadaran terganggu sampai koma.

2. Darah : hiperglikemi lebih dari 300 mg/dl

(biasanya melebihi 500 mg/dl), bikarbonat
kurang dari 20 mEg/l (dan pH<7.35), ketonemia

3. Urin : glukosuria dan ketonuria

KLASIFIKASI KAD

Stadia KAD Macam KAD PH darah Bikarbonat darah

I. Ringan KAD ringan 7.30-7.35 15-20 mEq/l

II. Sedang Prekoma diabetik 7.20-7.30 12-15

III. Berat Koma diabetik 6.90-7.20 8-12

IV. Sangat berat Koma diabetik berat < 6.90 <8

TERAPI KAD

Protokol terapi KAD terdiri dari 2 fase yaitu : Fase I (fase gawat)
Fase II (fase rehabilitasi)
Dengan batas kadar glukosa darah antara kedua fase tersebut sekitar 250 mg/dl.

FASE I :
1. Rehidrasi : Na cl 0.9% atau RL 2 liter/2 jam pertama, lalu 80 tetes/menit
selama 4 jam, lalu 30-50 tetes/menit selama 18 jam (4-6 liter/24 jam),
diteruskan sampai 24 jam berikutnya.
2. Insulin dosis rendah intravena : 4-8 unit/jam I.v sampai fase II.
3. Infus K : 75 mEq (bila K <2.5 mEq/l), 50 mEq (K = 2.5 -3.0 mEq/l) dan 25 mEq (K
= 3.0 - 3.5 mEq/l) per 24 jam
4. Infus bikarbonat : bila pH <7.20 atau bikarbonat <12 mEq/l : 50-100 mEq
langsung drip dalam 2 jam, bolus 50-100 mEq diberikan bila pH kurang dari
7.0
5. Antibiotika up to date dan dosis adekuat.
TERAPI KAD
FASE II :

1. Maintenance : Nacl 0.9%, atau potakol R (IR 4-8 U),

maltosa 10% (IR 8-12 U) bergantian 20 tetes/menit

2. Kalium : p.e (bila K < 4 mEq/l) atau per os (air tomat

atau kaldu 1-2 gelas)

3. Insulin reguler : 3 x 8-12 U s.c

4. Makanan lunak Karbohidrat kompleks peroral

HIPER OSMOLAR NON
KETOTIK
KOMA HIPEROSOMOLER NON KETOTIK (KHONK)

 Hiperglikemi
 Dehidrasi berat
 Tanpa asidosis metabolik dan ketosis
 Privalensi lebih jarang 1/5 - 1/6 KAD
 DM tipe-2 usia tua
 Mortalitas 30.4% kasus KHONK
Faktor Pencetus :

Faktor pencetus KHONK yang paling penting adalah

infeksi dan penyakit kardiovaskuler.
Namun dapat juga disebabkan o.k. iatrogenik seperti
hiperalimentasi parenteral, peritoneal dialysis
hipertonik, pembedahan dan pemberian obat-
obat kortikosteroid dan diuretic.

(Kuzuya T, 1999)
 KRITERIA DIAGNOSIS KHONK

Diagnosis klinik KHONK bila didapatkan :

1. Glukosa darah >800 mg/dl

2. Anamnesis DM tidak ada atau meragukan
3. Pernafasan Kussmaul tidak ada
4. Ketonuri dan ketonemia negatif atau positif
ringan.
KRITERIA DIAGNOSIS KHONK

Faktor penunjang diagnosis klinik HONK

1. pH darah >7.3
2. Adanya prerenal azotemia
3. Hipernatremi (>150 mEq/l)
4. Gangguan kesadaran
5. Gejala neurologik (konvulsi)

Diagnosis Pasti KHONK : Diagnosis klinik + Osmolaritas

> 325.

Osm/l = 2X (Na + K) + Glukosa (mg/dl) + BUN

18 2.8
TERAPI

 = KAD
 Bila Na <150 mEq/l cairan Nacl 0.9%
 Na > 150 mEq/l cairan hipotonik
 Tanpa Nabic.
LACTIC ACIDOSIS
ESS DX :
Severe acidosis with hyperventilation
pH darah < 7.30
Serum bicarbonat < 15 meq/l
Anion gap > 15 meq/l
Absent serum keton
Serum lactat > 5 mmol/l

ANION GAP N = (Na+ + K+) – (Cl– + HCO3–) = 16  7

(unnaeasua red anion)

pH rumus Henderson – Hasselbach :

CO2 content meq/L

pH = 6.10 + Log
pCO2 mmHg x 0,03
Normal sumber asam lactat :
• Erithrosit
• Otot
• Kulit
• Otak
Hati
Asam Lactat Glukose
Ginjal

Symtom and Sign :

 Terutama hiperventilasi, bila penyebab
hipoksia/kolap vaskuler, klinis variabel ~ penyulit
dasar.
 Tensi normal, sirkulasi perifer baik, sianosis (-).
Pencegahan Diabetes Mellitus

1. Primer, untuk orang yang resiko tinggi.

2. Sekunder, mencegah/menghambat
komplikasi.
3. Tertier, mencegah kecacatan
 Monitor Pengelolaan Diabetes Terbaik

1. HbA1c (A1C)
2. Fructosamine
Correlation Between AIC level and
Mean Plasma Glucose
AIC (%) Mean Plasma Glucose
mg% mmol/L
6 133 7.5
7 170 9.9
8 205 11.5
9 240 13.5
10 275 15.5
11 310 17.5
12 345 19.5

Rohlfing CL et al. Diabetes Care 25; 275:, 2002

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