R. Bowo Pramono R. Bowo Pramono Endocrinology Subdivision of Endocrinology Subdivision of Internal Medicine Department Internal Medicine Department Faculty of Medicine Faculty of Medicine Gadjah Mada University Gadjah Mada University YOGYAKARTA YOGYAKARTA Recent Update Diabetes Mellitus Recent Update Diabetes Mellitus Management Management
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R. Bowo PramonoR. Bowo Pramono
Endocrinology Subdivision of Endocrinology Subdivision of
Internal Medicine DepartmentInternal Medicine Department
• DM is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
• The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.
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By 2030, By 2030, 7 of the 107 of the 10 Countries with the Countries with the Most Diabetic Patients Will Be in AsiaMost Diabetic Patients Will Be in Asia
DeFronzo et al. Diabetes Care 1992;15:318-68DeFronzo et al. Diabetes Care 1992;15:318-68
Diabetes mellitus is a group of metabolic Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia diseases characterized by hyperglycemia
resulting fromresulting from defect of insulin action, defect of insulin action, insulin secretion or bothinsulin secretion or both
PATHOGENESIS OF TYPE 2 DIABETESPATHOGENESIS OF TYPE 2 DIABETES
CRITERIA FOR THE DIAGNOSIS OF CRITERIA FOR THE DIAGNOSIS OF DIABETES MELLITUSDIABETES MELLITUS
or or 2. 2. Fasting plasma glucose Fasting plasma glucose >> 126 mg/dl. 126 mg/dl. FPG, no caloric intake for at least 8 hourFPG, no caloric intake for at least 8 hourss
oror 3. 3. 2-h post-OGTT 2-h post-OGTT >> 200 mg/dl 200 mg/dl 75 gram glucose dissolved in water75 gram glucose dissolved in water
Natural History of Type 2 Diabetes
IR phenotypeAtherosclerosisobesityhypertensionHDL,TG,HYPERINSULINEMIAEndothelial dysfunctionPCO,ED
Envir.+ Other Disease
Obesity (visceral)Poor Diet Inactivity
Insulin Resistance
Risk of Dev. Complications
ETOHBPSmoking
EyeNerveKidney
Beta Cell Secretion
Genes
BlindnessAmputationCRF
Disability
Disability
MICVAAmp
Age 0-15 15-40+ 15-50+25-70+
Macrovascular Complications
IGT/IFG Type II DM
Microvascular Complications
DEATHFBS>5.5,ppg>7.8
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Type 2 diabetes is NOT a mild disease
DiabeticRetinopathyLeading causeof blindnessin working ageadults1
DiabeticNephropathyLeading cause of end-stage renal disease2
CardiovascularDisease
Stroke2 to 4 fold increase in cardiovascular mortality and stroke3
DiabeticNeuropathyLeading cause of non-traumatic lower extremity amputations5
8/10 diabetic patients die from CV events4
1 Fong DS, et al. Diabetes Care 2003; 26 (Suppl. 1):S99–S102. 2Molitch ME, et al. Diabetes Care 2003; 26 (Suppl. 1):S94–S98. 3 Kannel WB, et al. Am Heart J 1990; 120:672–676. 4Gray RP & Yudkin JS. In Textbook of Diabetes 1997.
5Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl. 1):S78–S79.
Target on Management of DM
• A : HbA1c• B : Blood Pressure• C : Ch0lesterol
PERKENI 2011
04/17/23 Page 14
ADA/EASD: Metabolic Management of Type 2 Diabetes
Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203
* Check HbA1c every 3 months until HbA1c <7%, and then at least every 6 months.** Preferred based on effectiveness and expense.
Add basal insulin(most effective)
Add sulfonylurea(least expensive)
Add TZD(no hypoglycemia)
If HbA1c> 7%*
Add basal or intensify insulin
Add TZDIntensify insulin**
Add basal insulin**
Add sulfonylurea
Intensive insulin + metformin +/- TZD
If HbA1c > 7%
If HbA1c > 7%
ADA/EASD CONCENSUS…Lifestyle intervention and metformin
Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203
• Tight glycemic control• Age• Duration of diabetes• History of hypoglycemia• Sleeping• Alcoholism• Fasting• Increased insulin sensitivity: fitness, body weight• Clearance/metabolism of drugs: renal or hepatic
insufficiency
Mechanisms by which drugs increase the hypoglycemic effect of sulfonilureas
• Increase in half-life due to inhibition of metabolism or excretion rate:
• Mild hypoglycemia when self treatment with oral carbohydrate suffices
• Sever hypoglycemia when external help is required to effect recovery
Management of hypoglycemia: Prevention
1. Early familiarization with the symptoms of hypoglycemia2. Do reviewing at intervals3. Explain the relationship between insulin administration,
timing of meals, and exercise4. Explain methods of self-treating hypoglycemia5. Choose appropriate insulin regimens, dose schedules with
appropriate therapeutic goals
Management of hypoglycemia: Treatment
• Mild hypoglycemia: oral glucose 15-20 g, wait 10-15 min then check blood glucose. If glucose level does not increase ≥18 mg/dl, give oral glucose again
• Severe hypoglycemia: solution 50 ml of dextrose 50% given intravenously, check blood glucose in 20 min. If it is still hypoglycemia administrate once again
• Glucagon 1.0 mg s.c/i.m/i.v. adverse effects include nausea, vomiting, and headache. Contraindicated to sulfonylureas-induced hypoglycemia. Ineffective in patient who is anorectic, or with protracted hypoglycemia
PATOFISIOLOGI KAD & HHS
Sign & symptom of DKA
• Deep, rapid breathing• Sweet, fruity smell on breath• Loss of appetite• Nausea • Vomiting• Fever• Stomach pain• Weight loss
• Fatigue• Weakness• Confusion• Drowsiness
Clinical presentation
• Lost more than 5% body weight• More than 35 breaths a minute• Can’t control blood sugar• Become confused• Nausea and vomiting
What should you do?
• Check ketones if feeling especially stressed or blood sugar persistently above 240mg/dL
• High ketones in blood ketones excreted in urine.
• High ketones in urine must treatment & stay in hospital
• DKA can lead into coma and posibly death.
Treatment
• Replenishing lost fluids through i.v. line• Insulin combined with glucose, injected into iv
stop making ketones• Gradually blood sugar level back to normal, if
quickly can produce swelling in the Brain
HHS
• Blood sugar reaches such a high level that blood become thick and syrupy (level >600 mg/dL)
• Cells can’t absorb much blood sugar, the sugar passed from blood to urine draws tremenous amounts of fluid from body and produces dehydration
• Common in type 2 DM, especially who don’t monitor blood sugar and who don’t know have DM