Epidemilogi, Patogenesis & Diagnosis DM

7/28/2019 Epidemilogi, Patogenesis & Diagnosis DM

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EPIDEMIOLOGY, PATHOGENESIS ANDDIAGNOSIS OF DIABETES MELITUS


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Definition of diabetes

Characterized by hyperglycaemia

Defects in insulin production

Autoimmune or otherdestruction of beta cells

Insulin insensitivity

Impaired action of insulin ontarget tissues


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Definition of diabetes

Chronic hyperglycaemia associatedwith long-term damage to:

Eyes

Kidneys

Nerves

Heart and blood vessels


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The diabetes epidemic

230 million affected in 2006

350 million within 20 years

Most rapid in Indian and Asiansubcontinents

IDF Diabetes Atlas


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Worldwide prevalence of diabetesmellitus

Harrisons Principles of Internal Medicine, 17th


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2000 2030

Ranking Country People with

diabetes(millions)

Country People with

diabetes(millions)

1 India 31.7 India 79.4

2 China 20.8 China 42.3

3 US 17.7 US 30.34 Indonesia 8.4 Indonesia 21.3

5 Japan 6.8 Pakistan 13.9

6 Pakistan 5.2 Brazil 11.3

7 Russia 4.6 Bangladesh 11.1

8 Brazil 4.6 Japan 8.9

9 Italy 4.3 Philippines 7.8

10 Bangladesh 3.2 Egypt 6.7

Diabetes in clinical reality Global


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Prevalence of centralobesity, IFG, DM and

Metabolic Syndrome

Population study in Bali involving 1840 adult subjects at 7 villages.

Suastika K et al. 2010. Data was presented at ADA 2010.


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Adults: 50% x 3 million = 1.5 million

DM: 5.3% x 1.5 million = 80.000

Diagnosed: 50% x 80.000 = 40.000

Treated: 50% x 40.000 = 20.000


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Classification

Type 1 diabetes

autoimmune

LADA

idiopathic

Type 2 diabetes


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Other specific types

MODY

Defects in insulin action Diseases of the pancreas

Endocrine disorders

Drug- or chemical-induced Infections

Classification


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Uncommon forms of immune-mediated diabetes

Other genetic syndromes

Gestational diabetes

Classification


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Insulin

GluconeogenesisGlycogenolysis

Glycogen synthesis

Glucose uptakeGlycogensynthesis

Blood glucose

Insulin and glucose disposal

Free fatty acid release


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Glucose uptake

Glycogenolysis

Gluconeogenesis (amino acids)

Ketone production (fatty acids)

Glucose uptakeProtein degradation amino acids

Blood glucose

Insulin deficiency intype 1 diabetes

Triglyceride degradation fatty acids


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Glucose uptake

Glycolysis


Glucose uptake

Protein degradation amino acids

Blood glucose

Insulin insensitivity intype 2 diabetes


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Blood glucose

Glucose uptake

Insensitivity to insulin intype 2 diabetes

Glucose uptake

Glycolysis


Glucose uptake



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Blood glucoseConverted to triglycerides

Effect of insulin resistance intype 2 diabetes

Glucose uptake

Glycolysis


Glucose uptake


Glucose uptake


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Idiopathic type 1 diabetes

Non-autoimmune type 1 diabetes

No autoimmune markers

Permanent insulinopenia

Ketoacidosis

People of African and Asian origin


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Type 2 diabetes

90%-95% of people withdiabetes

Insulin insensitivity andrelative insulin deficiency

Obesity or overweight

Complications often presentat diagnosis


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Pathogenesis of type 2 diabetes

Multiple genes involved

Hyperinsulinaemia

Poor fetal nutrition beta-cellformation

Low birth weight/weight change

7% beta-cell loss


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Age (years)

Endogenousinsulin

Insulinrequirements

Beta-cell loss

The natural history oftype 2 diabetes

Insulin

requirementswith age

Primaryfailure


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Age (years)

Endogenousinsulin

Insulinrequirements

Secondaryfailure

The natural history oftype 2 diabetes

Effect oforal drugs

Insulin

requirementswith age

Beta-cell loss

Hyper-

insulinaemia

Insulininsensitivity


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Epidemiology of type 2 diabetes

Dramatic increase

Aging population

Disturbing trends parallel obesityepidemic

Especially in adolescents andminority groups

Increasing in young people


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Risk factors for type 2 diabetes

Age > 40 years

First-degree relative with diabetes

Member of high risk population History of impaired glucose tolerance,

impaired fasting glucose

Vascular disease

History of gestational diabetes

History of delivery of macrosomicbaby


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Hypertension

Dyslipidaemia

Abdominal obesity

Overweight

Polycystic ovary disease

Risk factors for type 2 diabetes


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Polydipsia

Polyuria

Nocturia

Visual disturbance

Fatigue Weight loss

Infections

Signs and symptoms


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Diagnosing diabetes

Normal Impaired fasting glucose*

Impaired glucosetolerance**

Diabetes

FPG


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Impaired glucose toleranceImpaired fasting glucose

Intermediate states

Increased risk of developingdiabetes

Prevention strategies to prevent

or delay progression Increased risk of cardiovascular

disease


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Uncertain diagnosis:Oral glucose tolerance test

75 g glucose load after 8 hours

fasting

Readings taken in fasting state

and at 1 and 2 hours

Possible problems

l h h


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ADA/EASD algorithm for themanagement of T2DM (2008)

At diagnosis:

Lifestyle + Metformin


+ Basal insulin


+ Sulfonylureasa


+ Intensive insulin

Tier 1: well-validated therapies

STEP 1 STEP 2 STEP 3

Tier 2: Less well validated therapies

Lifestyle + metformin

+ Pioglitazone+ Sulfonylurea


+ Basal insulin


+ GLP-1 agonistbNo hypoglycaemia

Weight loss

Nausea/vomit ing

Lifestyle + Metformin+ PioglitazoneNo hypoglycaemia

Oedema/CHF

Bone loss

Nathan D, et al. Diabetes Care 2009;32:193203.

Reinforce lifestyle interventions at every visit and check A1C every 3 months until A1C is 7% andthen at least every 6 months. The interventions should be changed if A1C is 7%. aSulfonylureasother than glybenclamide (glyburide) or chlorpropamide. bInsufficient clinical use to be confidentregarding safety


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Summary

Type 1 diabetes

Results from progressive beta-

cell destruction

People with type 1 diabetes needinsulin therapy to live


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Type 2 diabetes

Often characterized by insulin

insensitivity and relative ratherthan absolute insulin deficiency

A progressive condition

Most people with type 2 diabeteswill need insulin within 5 to 10years of diagnosis

Summary


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Epidemilogi, Patogenesis & Diagnosis DM

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