Object-Oriented Programming Polymorphism Session 07 Mata kuliah: M0874 – Programming II Tahun: 2010.
Kuliah DM Semester 8 Tahun 2007
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Transcript of Kuliah DM Semester 8 Tahun 2007
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Dr. PANDJI MOELJONO, Sp.PD
SUBDEP PENYAKIT DALAMFK. UNIV. HANG TUAH
RUMKITAL Dr. RAMELAN
Diabetes Mellitus
The Disease and Its Management
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Definisi
Diabetes mellitus is a group of metabolicdiseases 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
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INSUFISIENSI
INSULIN
Kelainan Fungsi /
Jumlah Sel Genetik
Kelainan Aktifitas Insulin
o.k. Reseptor
Faktor Lingkungan
Virus
Diet
Obesitas
Hamil
Tipe I(Auto imun)
Sistim imun(Ab ant i pankreas)
Marker :
Insulin auto Ab
Islet cell auto Ab
Glutamic aciddicarbosaflase
Au Ab (GAD. Abs)
Ideopatik
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Symptoms :
Polyuria
Polydipsia
Weight lossSometimes polyphagia
Blurred vision
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Diagnosis
Symptoms of diabetes plus glucose > 200 mg/dl
or
Fasting plasma glucose > 126 mg/dl
or
2-h plasma glucose > 200 mg/dl during an OGTT
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TableDiagnosis of GDM with a 100 g Oral Glucose Load (ADA-
2003)
mg/dl mmol/l
Fasting 95 5.3
1-h 180 10.0
2-h 155 8.63-h 140 7.8
Two or of the venous plasma concentrations must be met or exceeded
for a positive diagnosis. The test should be done in the morning after
an overnight fast of between 8 and 14 h and after least 3 days of
unrestricted diet (150 g carbohidrate per day) and unlimitedphysical activity. The subject should remain seated and should not
smoke throughout the test.
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TableDiagnosis of GDM with a 75 g Oral Glucose Load
(ADA-2003)
mg/dl mmol/l
Fasting 95 5.3
1-h 180 10.0
2-h 1558.6
Two or of the venous plasma concentrations must be met or
exceeded for a positive diagnosis. The test should be done in the
morning after an overnight fast of between 8 and 14 h and after
least 3 days of unrestricted diet (150 g carbohidrate per day)and unlimited physical activity. The subject should remain seated
and should not smoke throughout the test.
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DIABETES vs PRE-DIABETES
Fasting
Blood
Glucose
2 hours post
prandial (mg/dl)
Normal < 100 * < 140
Pre-Diabetes 100 *125 140199
Diabetes 126 200
If FBG is > 100, have a 10-15% chance of
developing DM in next 7 years.
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Dual Defect of T2DM (IR and Impaired AIR) :Treating a Moving Target
-cellDysfunction
InsulinResistance T2DM
Euglycaemia
Insulin
Concentration
-Cell Failure
Insulin
Action
Normal IGT+Obesity or IFG Dx T2DM Progression to T2DM
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Insulin Resistance
Coronary heartdisease
Hyperinsulinemia
Glucoseintolerance
Increasedtriglyceride
Increased bloodpressure
Decreased HDL -Cholesterol
Small dense LDL
cholesterol
Increased
Uric acid
Increased
PAI - 1
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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.
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Keluhan Klinis Diabetes
Keluhan klasik + Keluhan klasik -
GDP >126 126 110-126 200 200 140-200
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III. Klasifikasi Etiologis DM
1. Diabetes Tipe-1 (destruksisel beta)
Auto imun
Idiopatik
2. Diabetes Tipe-2 ( resistensiinsulin disertai defek sekresiinsulin atau sebaliknya)
3. Diabetes Tipe lainA. Defek genet ik fun gsi sel beta
MODY 1,2,3. DNA
mitokondria
B. Defek genet ik ker ja insu l in
C. Penyakit eksok r in pankreas;
Pankreatitis, tumor pankreas,pankreatektomi, pankreopati
fibrokalkulus
D. Endokr inop ati
Acromegali, sindroma
Cushing, Feokromositoma,
hipertiroidisme
E. Karena obat/zat kim ia
Vacor, pentamidin, asam
nikotinat, Glukokortikoid,hormontiroid, tiazid, Dilantin,
interferon alfa
F. Infeksi : rubellakon geni tal, CMV
G. Sebab imunolog i yang jarang :
Antibodi anti insulinH. Sindroma genet ik lain:
Sindroma Down, Klinefelter,
Turner dll.
4. Diabetes Gestasional
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FASTING GLUKOSA BERBEDA SECARA
METABOLIK HORMONAL DENGAN
PRANDIAL
Insulin
puasa
Glukosa
puasa
Glukagon
Glukosa darah puasa
Insulin prandial
(glukosa uptake/utilzation
Glukosa
prandial
Makanan
Glukosa darah prandial
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SEKRESI INSULIN NORMAL
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Sekresi Insulin Pada DM Tipe II
Gambar. Variabilitas
responsi insulin
terhadap OGTT
pada NIDDM
Untuk mengatasi resistensi insulin, sel harus mampu
sekresi insulin lebih banyak dan sepanjang mampu DM,
GTG (-) maka DM tipe II sekresi insulin bervariasi
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Pola Sekresi Insulin DM Tipe I
Sekresi insulin tergantung sisa masa sel
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Glycemic Control
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Longer term :Prevent complications
Reduce morbidityand mortality
anagement
Short term :Eliminate symptoms
Maintain general well being
Strategy :
Normalizing glucose,
lipid, and insulin levels
Activities :Management with holistic
approach and self careprinciples
A. Aim
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Treatment Modalities
Diet/Medical nutrition therapy
Exercise
Anti hyperglycemic agents Education
Pancreas transplantation
Cloning treatment (experiment)
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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 hasilpengelolaan
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Nutrient Composition of Diabetic Diet
PERKENI A D A and B D A(Indonesian Soc.of Endoc.)
Carbohydrate Fat Protein
20-25%10-15%
60-70%
Diet/Nutrition Therapy/Meal planning
Carbohydrate Fat Protein
30%10-15%
55%
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PERENCANAAN MAKANKOMPOSISI :
Karbohidrat : 6070 %
Protein : 1015 %
Lemak : 2025 %
JUMLAH KALORI :Hitung BMI ( IMT ) = BB ( kg ) / TB ( m )2
IMT wanita ( normal ) = 18,523,5 kg/ m2
IMT laki ( normal ) = 22,525 kg / m2
Status gizi : BB Idaman = ( TB100 )10%
BB kurang : < 90% BBI
BB Normal : 90120% BBI
BB lebih : 110120 % BBI
Gemuk : > 120% BBI
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Exercise
30 minutes: 3 - 4 times / week
Continuous
Rhytmical
Interval
Progressive
Endurance training
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Anti Diabetic Agents
Hypoglycemic Agents
Anti Hyperglycemic Agents
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Pilihan Terapi DM Tipe 2
Berdasarkan Target Organ
PANKREAS
SEKRESI INSUL INSulfonylureas
Meglitinides ; RepaglinideInsulin
ABSORBSI
GLUKOSA
alpha-glucosidase inhibitorsSAL. CERNA
Sonnenberg and Kotc hen. Curr Opin Nephrol Hypertens1998;7(5):5515
OTOT
AMBILAN GLUKOSAPERIFER
ThiazolidinedionesBiguanides
(Metformin)
JARINGAN
LEMAK
PRODUKSI
GLUKOSA
Biguanides
(Metformin)
Thiazolidinediones
HATI
Sites of Action of Antihyperglycemic Agents
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Adipose tissue
Sites of Action of Antihyperglycemic AgentsPancreas
1. Insulin
GLUCOSE
GLUCONEO
GENESIS
HGP-
N
Intestine
2. Insulin
secretagogue
4. Acarbose
3. Metformin
TZD
3. Metformin
TZD
+
GLYCOGENOLYSIS
+
-
+
+
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1a. Insulin
Insulin actions include :
Ability of insulin to lower circulating glucose
concentrations
Suppress glucose production : liver
Stimulate glucose utilization : muscle plus fat
Additional metabolic, vascular & mitogenic actions
h S i ti Gl d ti
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LIVER
ADIPOSE TISSUE
The Suppression Hepatic Glucose ProductionPancreas
Insulin
GLUCOSE
GLUCONEO
GENESIS
HGP
GLYCOGENOLYSIS
-
N
Th Sti l ti f Li i i Adi Ti
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LIVER
ADIPOSE TISSUE
The Stimulation of Lipogenesis in Adipose TissuePancreas
Insulin
GLUCOSE
GLUCONEO
GENESIS
HGP-
GLYCOGENOLYSIS
G LYCOGEN
G L UC O S E
+
GlucoseUptake
Lipogenesis+
N
FFA
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Indications of Insulin Treatment
Indication for the use of insulin inType 2 DM
In severe metabolic decompensation
Ketoacidosis
Hyperosmolar non ketotic coma Lactic acidosis
Severe stress :
Systemic infection
Major surgery Weight loss within a short period of time
Pregnancy if diet does not succeed to control
glycemia
OHA failure or contra-indication of OHA
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The Pharmacology of Insulin
Lispro Aspart
Regular
NPH
LenteUltra lente
Glargine
0.10-0.25
0.10-1.0
1.0-3.0
1.5-4.02-6
2-4
0.75-2.0
1.0-4.0
5.0-7.0
4.0-8.08.0-12
None
4.0-5.0
4.0-10
13-18
13-2018-30
-24
Yes w RI
+/- w lispro
+/-+/-
NO !!!
precipitate
Minimal
Moderate
High
HighVery High
Moderate to
high
Onset(h)
Peak(h)
Duration(h)
Miscibility withLispro or
Reg. insulin
Variability inabsorption
Pre-mixed (70/30,50/50,lispro mix 75/25) equivalent to sum of above components
Buse BB Diabetes Spectrum 2000
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Insulin available in Indonesia
Short acting insulin Long acting insulin
Actrapid Human U 40, U100 PZI U40
Humulin R U40, U100 Ultratard U100
Regular Insulin U40
Intermediate acting insulin Penfil
Monotard U40, U100 Actrapid penfil
Insulatard U40, U100 Insulatard penfil
Humulin N U40, U100 Mixtard 30/40 penfil
NPH U40 Humulin R penfil
Humulin 30/70 penfil
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1 b. Insulin Analogues
Genetic engineering
Main aim : Solubility reduction
Substitution/addition of amino acid residue ofinsulin
Short acting :
Lispro: B28-lysine, B29-proline
X14 : B28-aspartateLong acting:
B31-B32arginine, A21-glycine
Immunogenicity
Proactive management of glycemia:
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OAD
+ basal insulin OAD + multiple daily
insulin injections
OAD
monotherapy
OAD
combinations
Proactive management of glycemia:
early combination approach
OADsuptitration
7
6
9
8
10
Diet
and exercise
Duration of diabetes
HbA1c= 7%
*OAD = oral antidiabetic
HbA1c= 6.5%
Del Prato S, et al. Int J Clin Pract2000; 7:625631.
HbA1c
(%)
OHO
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OHO
(Obat Hipoglikemic Oral)
2. Insulin Secretagogues Induce insulin secretion
Potentiate nutrient-induced insulin
secretion
Antagonize inhibitors of insulin secretion
Calcium, Cyclic AMP and Adrenoreceptor
Manipulator
Other Insulin secretagogues
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Insulin Secretagogues (cont.)
ATP-sensitive Potassium Channel Inhibitors
Long acting:Sulphonylureas
Short acting :
Repagl inide : Benzoic acid derivative
Nategl inide : Phenyl alanine derivative
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Sulphonylureas
Have been a mainstay of type 2 diabetes treatmentfor > 40 years
Bind to an SU receptor (SUR) on the-cell whichleads to depolarisation of -cell membrane andstimulates insulin secretion
First generation : chlorpropamide
Second generation : glibenclamide, glipizide,gliclazide
Third generation : glimepiride
Attention : Hypoglycemia (less in glipizide GITS andglimepiride)
Mode of Action of S lphon l reas
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Depola-
risation Ca2+
Voltage DependentCa 2+Channel (VDCC)
Proinsulin
Closed
ATP SensitiveK+ Channel
SS 01
Islet cell
Open
Ca 2+
INSULIN
C-PEPTIDE
SU
SUR
ATP
ADP
ATP
ADP
Glucose
Am. acid
Glucokinase
Metabolism
Mode of Action of Sulphonylureas
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3. Insulin Sensitizers (1)
Metformin Anti hyperglycemic not hypoglycemic
Do not target -cell
Suppress HGP (hepatic glucose production)
Enhance tissue sensitivity to insulin topromote uptake of glucose into muscle
Cardioprotective effect on obesepatients(UKPDS)
Often used in combination with Sus Little effect on post prandial hyperglycemia
Gastrointestinal discomfort
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Thiazolidinediones
Anti hyperglycemic not hypoglycemic
Increase expression of transmembrane glucose
transporters (GLUT 1 and GLUT 4) Increase insulin-stimulated glucose disposal
Increase insulin-stimulated glucose uptake andmetabolism by muscle and fat
Suppression of hepatic glucose production Reduce plasma triglycerides
Pioglitazone
Rosiglitazone
Insulin Sensitizers (2)
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4. Inhibition of CHO digestion
and absorption Alpha glucosidase inhibitors
acarbose Plant fibre supplements
guar gum
bran
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Ingested with meals
Delay the digestion of complexcarbohydrate
Competitive inhibition of alpha
glucosidase in the intestine
Blunting postprandial glucose spikes
Gastrointestinal side effects
Alpha Glucosidase Inhibitors
(Acarbose)
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C bi ti Th i T2DM
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Combination Therapy in T2DM:
Insulin Plus Oral Hypoglycemic Agents
Insulin Plus Sulphonylurea - BIDSSome insulin is endogenous, with natural
secretory pattern
Biguanide Plus Insulin
Reduces hepatic insulin resistance
May achieve better control with less insulin
Can reduce weight gain
Alpha Glucosidase Inhibitor Plus Insulin
Reduces posotprandial glucose level
Thiazolidinedione Plus InsulinReduces peripheral insulin resistance
Reduces insulin requirement
Must balance TZD and insulin carefully to minimize
weight gain
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O l H l i D A il bl i I d i
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Oral Hypoglycemic Drugs Available in Indonesia
Initial dose Maximal dose Frequency of
mg/day mg/day administration /day
Sulphonylurea
Glibenclamide 2,5 15-20 1-2 X
Gliclazide 80 240 1-2 X
Glipizide : 5 20 2-3 X
Glipizide GITS 5 20 1-2 XGliquidone 30 120 1 X
Chlorpropamide 50 500 1 X
Glimepiride 0,5 6 1 X
Megl i t in ide
Repaglinide 1.5 mg 8 mg 3XNateglinide 120 mg 360 mg 3X
Metformin 500 3000 1-3 X
Alpha glucosidase inhibitor
Acarbose 50 300 3 X
ADA Treatment Goals for Glycemic Control
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ADA Treatment Goals for Glycemic Control
Glycemia Normal Goal Further Action
Required*
Average Preprandial
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Proposed New Treatment Paradigm
for Type 2 Diabetes
Medical Nutrition Therapy, Exercise , Education and SMBG
HbA1c< 7 % HbA1c7- 8 % HbA1c > 8 %
Consider oral
monotherapy
Add
insulin sensitizer
or secretagoque
Add
insulin sensitizer
and secretagoque
Target not Met Target not Met Target not Met
Start Insulin or
add Third oral agent
Full Insulin therapy
With Or without Oral agent(s)
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PADA DM TIDAK TERKONTROL
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Stres Oksidatif EndothelHYPERGLYCEMIA
Polyol
Pathway
Antioxidant
Defence
Glucose
Autoxidation Polyol
Pathway
Oxidative
Factors
Oxidative Stress
O2/ NO
LDL
Oxidation
NOdependent Vasolidation
Ca2+
VSMC Proliferation
Hemorheologic alternations Coagulation activation
Hipoxia
NVC
Endoneural
Blood Flow
Heparan
Sulphate
Vasculopathy Retinopathy Neuropathy Nephropathy
Hiperglikemia
Oxidative Stress
Komplikasi vaskular menahun(Giugliano et al 1996, Modifikasi)
R dik l B b & Di b t M llit
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Radikal Bebas & Diabetes Mellitus
DIABETES MELLITUS
HYPERGLYCEMIA
D I R C G O S
Efek Toksik Hiperglikemia : 2 Trisula dan 1 Tombak
Rangkuman : Askandar Tjokroprawiro 1999
Keterangan :
D : Direct Effect G : Glycation C : Cytokines
I : Immunology O : Oxidants
R : Rheology S : Sorbitol
f iTidak Suntik Insulin
iPatogenesis
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Lemak (Lipolisis)
Pelepasan FFA
Menuju hepar
Esterifikasi
Hiper-
Trigliseridemia
Oksidasi
Partial
Ketoanemia
Ketosuria
Muntah
Asidosis
Pernafasan
Kussmaul
Defisiensi insulin akut
Karbohidrat
Pembakaran glukosa turun
Glukoneogenesis
hiperglikemia
Glukosuria
Diurese Osmotik -
Poliuiria
Dehidrasi
Ekskresi H+
Protein
(Proteolisis)
Pelepasan A.A
Menuju hepar
Ureum naik
Syok
InfeksiTidak Suntik Insulin
Tipe IDiet bebasKetoacidosis
Diabetik
AA : Asam Amino
G : Glukosa
FFA : Free Fatty Acid
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STAGE DESCRIPTION CLINICAL FEATURES
At in creased risk Diabetes Mellitus, HBP, family history
12 Kidney Damage Microalbuminuria :
Diabetes duration 510 years, retinopathy,
rising BP
Albuminuria :
Diabetes duration 1015 years, retinopathy,
HBP
34 Decreased GFR HBP, retinopathy, CVD, other diabetic
complications
5 Kidney Failure Retinopathy, CVD, other diabetic
complications, uremia
Stages and Clinical Features of Diabetic Kidney Disease
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KOMA PADA DM
1. Hipoglikemi o.k. over Tx. Insulin, OHO.
2. Hipoglikemi
Severe defisiensi insulin Ketoasidosis
Mild / moderate hiperglikemi, hiper osmolar.
Laktik asidosis pada severe infekti,
cardiovaskuler collaps.
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DIABETIK KETOASIDOSIS
Essentials of Dx :
Hyperglycemia > 250 mg/dl.
Acidosis with blood pH < 7,3
Serum bicarbonat < 15 meq/L
Serum (+) for ketones.
Symtom + Sign :
3 P and marked fateque, nausea, vomiting
mental stupor
coma.
Dehydrasi, stupor, rapid deep breathing
Fruity breath odor of acitone.
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Tx :
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Tentukan osmolality (N = 280300 m Osm/kg)
Fluid and electrolyte replacement
- NaCl 0,9%
45 liter (o.k. dehidrasi)
- pH darah 7,1 Bikarbonat kontra indikasi
- pH darah 6,97 Bikarbonat 1 amp (+ 200 cc
steril aqua dalam 1 jam)
- pH darah < 6,9 2 amp Bikarbonat (+ 400 cc
steril aqua 2 jam)
= 2 (Na+) + Glucose (mg/dL)18
Setiap penambahan 1 amp bicarbonat ditambahkan
pula 15 mEq/L KCl selama K+tidak lebih dari 5,5 mEq/L.
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Setelah glukose < 250 mg/dL
D5 (dengan insulin tetap R/)
Untuk pertahankan glucose
200300 mg/dL
Cegah hipoglikemi
cerebral edema.
Insulin :
Regular insulin
bolus 0,1 unit/kg dilanjutkan 0,1 unit/kg/jam
infus/i.m.
Bila resistensi insulin (+)
dosis dapat dinaikkan
2 x setiap 2-4 jam
Antibiotika ~ dengan indikasi
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HYPERGLYCEMIC HYPEROSMOLAR STATE ( CHO )
ESS DX : Hyperglikemia > 600 mg/dL
Serum osm > 310 mOsm/kg
Acidosis (-) pH > 7,3
Serum bicarbonat > 15 meq/L
Normal aniopgam (< 14 eq/L)
Symtom and Sign :
3P, ***, vomiting
Lethargy, confusion
convulsion,
deep coma tanpa Kusmaull resp.
LACTIC ACIDOSIS
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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 HendersonHasselbach :
pH = 6.10 + LogCO2content meq/L
pCO2mmHg x 0,03
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Normal sumber asam lactat :
Erithrosit
Otot Kulit
Otak
Asam LactatHati
GinjalGlukose
Symtom and Sign :
Terutama hipervent i lasi, bila penyebabhipoksia/kolap vaskuler, klinis variabel ~ penyulit
dasar.
Tensi normal, sirkulasi perifer baik, sianosis (-).
Treatment Priority
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Treatment Priority
of Type 2 DM
Glucose control as
near to normal asreasonably possible
Microvasculardisease
Control of Insulin resistance:
Hyperinsulinemia, Obesity,
Glucose intolerance,
Dyslipidemia, Hypertension,Procoagulant state
Macrovasculardisease
Control of Insulin Resistance
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Insulinresistance
PAI-1,Factor VII, Fibrinogen
Hyperglycemia
Hypertension
Pro-coagulant State
Obesity
Dyslipidemia
Cardiovasculardisease
Intervention/Control
Control of Insulin Resistance
Tabel. Definitions of the Metabolic Syndrome
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ATP III (American Heart
Association) (2005)
World Health
Organisation 1999
International Diabetes Federation
(2005)
Minimal
requirements
Any 3 or mor of the
following criteria
Diabetes, IFG, IGT, or
insulin resistance + any2 or more of the
following criteria
Central obesity (see under) + any 2
or more of the following criteria
Waist
circumference
In men < 102 cm
In women < 88 cm
In men 94 cm
In womwn 80 cm
Waist to hip
ratio
< 0,90 in men
< 0,85 in womwn
Reduced HDL
cholesterol
< 1.00 mmol/l in men
< 1.30 mmol/l in women
< 0.90 mmol/l in men
< 1.00 mmol/l in women
< 1.03 mmol/l (40 mg/dl) in men
< 1.29 mmol/l (50 mg/dl) in women
Elevated
Triglycerides
> 1.70 mmol/l > 1.70 mmol/l
1.70 mmol/l (150 mg/dl)
Elevated Blood
Pressure
> 130 / >85
140 /
90
130 /
85
Urinary Albumin
Excretion
> 20 mg/min
Serum glucose 6.1 (5.6) mmol/l 5.6 mmol/l (100 mg/dl)
ATP III (Expert panel etc, 2001)
American Heart Association (Grundy et al, 2005)
World Health Organisation (World Health Organisation, 1999)International Diabetes Federation (Alberti et al, 2005)
Modified NCEP ATP III 2001
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Modified NCEP-ATP III 2001
80 cm
90 cm 150mg/dL
< 50mg/dL
< 40mg/dL
130/85mmHg
110mg/dL. (sekarang > 100)
1.Lingkar perut
wanita
pria2. Trigliserida
3.HDLkolesterol
wanita
pria
4. Tekanan Darah
5.Gula Darah Puasa
3 Kriteria dari variabel dibawah ini
"The Cumulative Metabolic Syndrome"
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Insulin ResistanceHyperinsulinemia2
1
Visceral Obesity
"The Black Goat"
4 Atherogenic Dyslipidemia
TriglyceridesHDL-CholesterolApolipoprotein-BSmall Dense LDL
Inflammatory Markers
(CRP, TNF, IL - 1, IL - 6)
8
Hyperuricemia 9
7Vascular Abnormalities
- Urinary Albumin Excretion- Endothelial Dysfunction
IFGIGT DM3
5
Hypertension
LVHCHF
Prothrombotic State
PAI-1 (Esp. Omental Fat)Factor VIIFibrinogenvWF
Adhesion Molecules
6
ACTH, Cortisol( Salivary Cortisol)
10
VISCERALADIPOSE TISSUE
GABRA-6 ?
The Cumulative Metabolic Syndrome A Cluster of 10 Possible Metabolic and CV Risk Factors
(Visceral Obesity is the Culprit)(Summarized : Tjokroprawiro 2002, 2003)
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Pencegahan Diabetes Mellitus
1. Primer, untuk orang yang resiko tinggi.
2. Sekunder, mencegah/menghambat
komplikasi.
3. Tertier, mencegah kecacatan
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