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Definition
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)
3
Status of diabetes management
Symptoms :
Polyuria
Polydipsia
Weight loss
Sometimes polyphagia
Blurred vision
50% of type 2 diabetes patients have
complications at the time of diagnosis
MICROVASCULAR MACROVASCULAR
Retinopathy, Cerebrovascular
glaucoma or disease
cataracts
Coronary
Nephropathy
heart
disease
Peripheral
Neuropathy vascular
disease
FPG
< 100 mg/dl (5.6 mmol/l) normal fasting glucose
100–125 mg/dl (5.6–6.9 mmol/l) impaired fasting glucose
126 mg/dl (7.0 mmol/l) diabetes
or
OGTT 2-h post-load glucose
< 140 mg/dl (7.8 mmol/l) normal glucose tolerance
140–199 mg/dl (7.8–11.1 mmol/l) impaired glucose tolerance
200 mg/dl (11.1 mmol/l) diabetes
LIVER
GLYCOGENOLYSIS
-
HGP +
+ GLUCOSE G L UC O S E
GLUCONEO FFA
GENESIS
LIPOLYSIS Lactic Acid
ADIPOSE TISSUE
Management
A. Aim
Strategy :
Normalizing glucose,
lipid, and insulin levels
Activities :
Management with holistic
approach and self care
principles
Prinsip Dasar Terapi Diabetes Mellitus
1 2 3
4 5
Continuous
Rhytmical
Interval
Progressive
Endurance training
Diet/Nutrition Therapy/Meal planning
Nutrient Composition of Diabetic Diet
PERKENI A D A and B D A
(Indonesian Soc.of Endoc.)
10-15% 10-15%
20-25% 30%
60-70%
55%
-
HGP +
GLUCOSE N
+
3. Metformin
GLUCONEO 4. Acarbose + TZD
GENESIS +
Expected HbA1c
(time allotted)
―1 to 2%
Monotherapy (1―3 months)
―1 to 2% fall per
Combination oral therapy additional OHA
(1―3 months)
*Individualise
Adapted from Bergenstal RM. In: De Fronzo RA, et al (eds). International Textbook of Diabetes Mellitus.
3rd ed. Chichester, New York: John Wiley & Sons; 2004:995―1015.
New treatment paradigms for
type 2 diabetes
Stepwise treatment
Early aggressive
combination therapy
Sulphonylureas
• Have been a mainstay of type 2 diabetes treatment
for > 40 years
• Bind to an SU receptor (SUR) on the -cell which
leads to depolarisation of -cell membrane and
stimulates insulin secretion
• First generation : chlorpropamide
• Second generation : glibenclamide, glipizide,
gliclazide
• Third generation : glimepiride
• Attention : Hypoglycemia (less in glipizide GITS and
glimepiride)
Mode of Action of Sulphonylureas
Depola- Ca 2+ Voltage Dependent
ATP Sensitive risation Ca 2+Channel (VDCC)
K+ Channel
SU Islet cell
SUR Open
Closed
Ca 2+
ATP
ADP
Glucose Glucokinase
Proinsulin
Metabolism INSULIN
Insulin
-
HGP
GLUCOSE N
GLUCONEO
GENESIS
ADIPOSE TISSUE
The Stimulation of Glucose Uptake
Pancreas
LIVER
GLYCOGENOLYSIS
Insulin
G LYCOGEN
- +
HGP
GLUCOSE N G L UC O S E
Glucose
Uptake
GLUCONEO
GENESIS
ADIPOSE TISSUE
The Stimulation of Lipogenesis in Adipose Tissue
Pancreas
LIVER
GLYCOGENOLYSIS
Insulin
G LYCOGEN
- +
HGP
GLUCOSE N G L UC O S E
Glucose
FFA Uptake
GLUCONEO
GENESIS
+
Lipogenesis
ADIPOSE TISSUE
ADA Treatment Goals for Glycemic Control
Adapted from the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus
Diabetes Care 1999;22:S32-S41
Current ADA treatment targets
• HbA1c < 7%
• Blood pressure < 130/80 mmHg
• LDL-cholesterol < 100 mg/dl (2.6 mmol/l)
• HDL-cholesterol
Men > 40 mg/dl (1.1 mmol/l)
Women > 50 mg/dl (1.3 mmol/l)
• Triglycerides < 150 mg/dl (1.7 mmol/l)
Microvascular Macrovascular
disease disease
Control of Insulin Resistance
Hyperglycemia
Intervention/Control
Dyslipidemia
Obesity
Pro-coagulant State
DIAGNOSIS
1. Klinis
- Dehidrasi, koma, hipotensi-syok.
- Beda dengan ketoasidosis, oleh karena tanpa asidosis
tidak ada Kussmaul
- Orang tua > 60 tahun
2. Laboratorium
- Hiperglikemi, GDS > 400 mg/dl
- Osmolalitas plasma >= 315 mmol/kg
KOMA HIPERGLIKEMIK
HIPEROSMOLER NON-KETOTIK (KHHNK) (2)
PENATALAKSANAAN
1. Cairan
Sama dengan ketaosidosis, hanya biasanya penderita
dalam keadaan syok sehingga perlu pemberian NaCl 0.9%
cepat. Untuk seterusnya diberikan cairan NaCl 0.45%
2. Insulin sama dengan ketoasidosis
3. Potassium
4. Antibiotik kalau perlu
HIPOGLIKEMI (1)
Pada DM reaksi hipoglikemi terjadi bila GDS
< 50 mg/dl
Penyebab : Insulin berlebihan, OHO berlebihan,
gagal ginjal kronik mendapat OHO
Gambaran klinis
Keringat dingin, takhikardi, rasa lapar, pusing,
penglihatan kabur, kesadaran menurun sampai
koma
HIPOGLIKEMI (2)
PENATALAKSANAN
1. Segera hentikan insulin atau OHO
2. Bila masih sadar segera berikan teh gula
3. Dalam keadaan koma berikan Dextrose 40% sebanyak
50 ml i.v langsung
4. Dilanjutkan dengan infus Dextrose 10% selama 48 jam
KOMPLIKASI KRONIK
Komplikasi vaskuler
Makrovaskular
Penyakit jantung koroner, strok, pembuluh darah perifer
Mikrovaskular
Retinopati,nefropati
Komplikasi neuropati
Neuropati sensorimotorik,Neuropati otonomik
Gastroparesis, diare diabetik, buli-buli neurogenik, Impotensi,
gangguan refleks kardiovaskular
Campuran vaskuler-neuropati
Ulkus kaki
Komplikasi pada kulit
RETINOPATI
DIABETIK (1)
Dikenal empat bentuk yaitu :
1. Tipe background
2. Tipe pre-proliferatif
3. Tipe proliferatif
4. Makulopati
2. Transplantasi ginjal
We are not getting
older