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A.
Metabolisme Karbohidrat
& Diabetes Melitus
Oral Glucose Tolerance Test (OGTT)
0
50
100
150
200
250
300
0 0,5 1 1,5 2 2,5 3 3,5 4
Jam
Glu
ko
sa (
mg
/dl)
Insulin receptors glucose transporter
SRI HARTINI KS KARIADI,2007
INSULIN RESISTANCE
Genetic
Environment
Obesity TNF- Adiponectin
FPG
IFG
FFA TG
HDL
GeneticFetal Malnutrition
Pancreas
Hyperglycaemia
Hyperinsulinaemia
ED CVD
Decompensation I
Decompensation II
METABOLIC
SYNDROME - cell compensation
LiverMuscle
Hypertension
Hyperinsulinemia
Hyperinsulinemia
Modified from WHO consultation Report: Definition, Diagnosis and
Classification of Diabetes Mellitus and its Complications (1999)
GEJALA DIABETES
KLASIK
Poliuria Polidipsi Polifagi BB Tenaga
GEJALA KOMPLIKASI
KUALITASHIDUP
Faktor genetik
Kegemukan
Kurang gerak
Umur
Komplikasi akut
Diabetes yang tidak dikelola baik
mudah terkena infeksi
Infeksi menjadi berat dan sukar sembuh
apabila tidak diatasi
Turunnya kesadaran
yang dapat berakhir dengan kematian
Koma
KOMPLIKASI MENAHUN
Penebalan dinding pembuluh darah
Penyempitan pembuluh darah
Pembuluh darahkecil
Retina Saraf Ginjal
Kebutaan Kesemutan Disfungsi
ereksi
Cuci darah
Pembuluh darahbesar
(Aterosklerosis)
Jantung Otak Tungkai
Seranganjantung
Stroke Borok
ABDOMINAL OBESITY INCREASES THE
RISK OF DEVELOPING TYPE 2 DIABETES
96.3
24
20
16
12
8
4
0
Rela
tive
ris
k
Waist circumference (cm)
Carey et al 1997
HbA1C rata-rata gula darah dalam 2-3 bulan
HBA1c
* Average Blood Glucose Concentration
= 33,3 X HBA1c (%) 86 mg/dl
Nathan & Singer Equation.-
Mechanism of Oxidative Stress
in Diabetes Mellitus.-
1. Autoxidative Glycosylation
Superoxide, H2O22. Lipid Peroxidation
F2-isoprostane, GPx, SOD3. Reduced Anti-oxidant Defence
TAOS (TRAP)
DIABETES MONITORING
Laboratory Tests.-
Blood Glucose(Home (self) -Monitoring)
Blood Glucose
Fasting + 2 hr pp
HBA1c or Fructosamine
Lipid Profile
Ureum, Kreatinin
Microalbuminuria
Fibrinogen
PAI-1
TAOS or OX-LDL