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MBS2 K1-K2

DIABETES MELITUS
(EPIDEMIOLOGY,PATHOPHYSIOLOGY
,DIAGNOSIS,MANAGEMENT)

Division Of Endorinology & Diabetes


Departemen of Internal Medicine FK-
USU/Adam Malik Hosptal
The Prevalence of DM at Provinces
in Indonesia*
12,0
11,1 11,1
10,4

10,0

8,0
No. 14 7,7 7,8
8,1
8,5 8,6

6,8
6,6
6,2
6,0
6,0 5,7
5,4 5,5
5,2 5,3 5,3
5,0
4,8
4,5 4,6
4,1 4,1 4,2
4,0 3,7 3,8
3,4
3,2 3,3
3,0 3,0

2,0 1,7 1,8

0,0

(Riskesdas 2007)
Increasing DM
Prevalence in Indonesia

NATIONAL
6.9%
5.7%

1.7%

1985 2007 2013


WHO, Study Group 1985
RISKESDAS, 2007; RISKESDAS, 2013
Diabetes around the world

Dunia: 415 juta


Diabetesion
(46,8% undiagnosed)

International Diabetes Federation (IDF), 2015


Diabetes Care Volume 39, February 2016
Pathophysiological Hyperglycaemia:
The ‘Ominous Octet’

Islet b-cell

Decreased
Incretin Effect
Increased
Impaired Lipolysis
Insulin Secretion

Islet a-cell

Hyper-
glycaemia

Increased Increased Glucose


Glucagon Secretion Reabsorption

Increased
Decreased Glucose
HGP
Uptake
Neurotransmitter
Dysfunction
Genetic and environmental risk factors impact
inflammation, autoimmunity, and metabolic
stress are leading to hyperglycemia

Diabetes Volume 66, February 2017


Clinical Spectrum of DMT2
DIAGNOSIS Glukosa
20 Postprandial
15 Glukosa
(mmol/l)
Glukose

10
Puasa
5

0
Resistensi
250
Insulin
Fungsi sel 
Relatif (%)

200
150
100 Tingkat Insulin
50 Kegagalan sel  (~ - 50%)
0

PERUBAHAN MAKROVASCULAR
Gambaran
Klinis
PERUBAHAN MIKROVASCULAR

Tahun 10 5 0 5 10 15 20 25

Adapted from Rhodes CJ. Science. 2005;307:380-4.


Insulin Resistance and -Cell Dysfunction
Produce Hyperglycemia in Type 2
Diabetes
-Cell Dysfunction Insulin Resistance
Increased
Pancreas Lipolysis

Elevated
Liver Plasma FFA

Islet -Cell Degranulation;


Reduced Insulin Content
+ -
Muscle Adipose Tissue
Increased Glucose Output

Reduced
Plasma Insulin
Decreased Glucose Transport
& Activity (expression) of GLUT4
Hyperglycemia

Courtesy of S. Smith, GlaxoSmithKline


Role of Free Fatty Acids in Hyperglycemia

Adipose tissue
insulin
resistance
ADIPOSE TISSUE

MUSCLE
 Lipolysis LIVER

Muscle  FFA mobilization


insulin
resistance Liver insulin
resistance
 FFA oxidation  FFA oxidation

 Glucose utilization  Gluconeogenesis

Hyperglycemia

Boden G. Proc Assoc Am Physicians. 1999;111:241-248.


Insulin Resistance: An Underlying
Cause of Type 2 Diabetes
Aging
Obesity and Medications
inactivity

Genetic Rare
abnormalities disorders
INSULIN
RESISTANCE
Type 2
diabetes PCOS

Hypertension Atherosclerosis
Dyslipidemia
Reaven GM. Physiol Rev. 1995;75:473-486
Clauser, et al. Horm Res. 1992;38:5-12.
-cell dysfunction
• Reduced ability of -cells to secrete
insulin
• Impaired ability of -cells to
compensate for insulin resistance
• Genetic and environmental
pathophysiology

DeFronzo RA et al. Diabetes Care 1992; 15: 318–54.


Diabetes Care Volume 39, February 2016
Karakteristik Pasien Diabetes di Asia
Sales

20% 50%
Normoweight
30% Underweight
Obesity

The New Fact of Type 2 Diabetes in Asia


1. Beta Cell Failure
2. Increased of Adipocity
3. Renal complication
Juliana Chan. Beijing. China, March 2013
Profile T2DM in India

NATURE REVIEWS ENDOCRINOLOGY; VOLUME 12 , JUNE 2016


Criteria for the diagnosis of diabetes
Classic symptoms/ Complications Symptoms
(Polyuria,Polydipsia,Poliphagia,Decrease Body weigth)
+
Criteria for testing for diabetes or
prediabetes in asymptomatic adults
1. Testing should be considered in
overweight or obese (BMI$25 kg/m2
or$23 kg/m2 in Asian
Americans) adults who have one or
more of the following risk factors:
 A1C 5.7% (39 mmol/mol), IGT, or
IFG on previous testing
 first-degree relative with diabetes
 high-risk race/ethnicity (e.g., African
American, Latino, Native American,
Asian American, Pacific Islander)
 women who were diagnosed with
GDM
 history of CVD
 hypertension ($140/90 mmHg or on
therapy for hypertension)
 HDL cholesterol level ,35 mg/dL
(0.90 mmol/L) and/or a triglyceride
level .250 mg/dL (2.82 mmol/L)
 women with polycystic ovary
syndrome
 physical inactivity
 other clinical conditions associated
with insulin resistance (e.g., severe
obesity, acanthosis nigricans).
2. For all patients, testing should
begin at age 45 years.
3. If results are normal, testing
should be repeated at a minimum of 3-
year intervals, with consideration of
more frequent testing depending on
initial results (e.g., those with
prediabetes should be tested yearly)
and risk status.
Diabetes
Risk Test
Management for the
Treatment of Type 2 Diabetes
Education: leflet, advice, seminar

Diet nutrition

Physical activity/Exercise/Sport

Pharmacologic Oral

Insulin: Basal and Prandial

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