1_1 Diagnosis, Classification and Prevention

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Diagnosis, classification andprevention of diabetes

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Curriculum Module II – 1 | Diagnosis, classification andpresentation of diabetes



Diagnosis and typesCurriculum Module II-1

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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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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

GluconeogenesisGlycogenolysisGlycogen synthesis

Glucose uptakeGlycogensynthesis

Blood glucose

Insulin and glucose disposal

Free fatty acid release




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Glucose uptakeGlycogenolysisGluconeogenesis (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

Gluconeogenesis (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






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Blood glucoseConverted to triglycerides

Effect of insulin resistance intype 2 diabetes

Glucose uptake

Glycolysis



Glucose uptake




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Pathogenesis of type 1 diabetes

• Immunological activation

• Progressive beta-cell destruction

• Insufficient beta-cell function

• Dependent on exogenous insulin

• Risk of ketoacidosis




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• Genetic susceptibility

• Immune factors

– other autoimmune disease– antigen-specific antibodies

• Environmental trigger– viruses– bovine serum albumin– nitrosamines: cured meats– chemicals: vacor (rat poison),

streptozotin




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Beta-cellmass


Time (months - years)

Trigger

Genetic

Pre-diabetes „Honeymoon‟

Chronicphase

Clinicaldiabetes

Immunologicalabnormalities




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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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Epidemiology of type 1 diabetes

• Increasing in recent years

• Geographic variation

• Relative affluence

• Lack of treatment

IDF Diabetes Atlas




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• Age of onset peaks

– preschool– puberty

• Autumn/winter peaks





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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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• Multiple genes involved

• Hyperinsulinaemia

• Poor fetal nutrition beta-cellformation

• Low birth weight/weight change

• “Thrifty gene”

• 7% beta-cell loss




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Age (years)

Endogenousinsulin

Insulinrequirements

Beta-cell loss

The natural history of type 2 diabetes

Insulin

requirementswith age

Primaryfailure




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Age (years)

Endogenousinsulin

Insulinrequirements

Secondaryfailure

The natural history of type 2 diabetes

Effect of oral drugs

Insulin

requirementswith age

Beta-cell loss

Hyper-

insulinaemia

Insulininsensitivity




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• Dramatic increase

• Aging population

• Disturbing trends parallel obesityepidemic

• Especially in adolescents andminority groups

• Increasing in young people

d




Slide 25 of 48ACTIVITY


• What are the most common riskfactors for type 2 diabetes for

people in your country?

• Are any of these risk factorsmodifiable?

Di i d




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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

CDA 2003

Di i d




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• Hypertension

• Dyslipidaemia

• Abdominal obesity

• Overweight

• Polycystic ovary disease

• Acanthosis nigricans

• Schizophrenia

Risk factors for type 2 diabetes

Di i d




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• Polydipsia

• Polyuria

• Nocturia

• Visual disturbance

• Fatigue

• Weight loss

• Infections

Signs and symptoms

Di i d t




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Diagnosing diabetes

Normal Impaired fasting glucose*

Impaired glucosetolerance**

Diabetes

FPG <6.1mmol/L

<110mg/dL

6.1 to 6.9mmol/L*

110 to 126mg/dL

≥7.0mmol/L

≥126mg/dL

2hr PG <7.8mmol/L

<126mg/dL

7.8 to 11mmol/L**

126 to 200mg/dL

≥11.1mmol/L

≥200mg/dL

CDA 2003, ADA 2004, WHO 2002

Di g i d t




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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

Diagnosis and t pes




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Uncertain diagnosis:Oral glucose tolerance test

• 75 g glucose load after 8 hours

fasting

• Readings taken in fasting stateand at 1 and 2 hours

• Possible problems

Diagnosis and types




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• Urinary ketones

• Antibodies

• C-peptide

Tests for differential diagnosis

Diagnosis and types




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Metabolic syndrome

• Cluster of risk factors or syndrome

• Type 2 diabetes

• Different criteria

• Three-fold increase in heartdisease and stroke

• Two-fold increase in cardiovasculardisease deaths

Diagnosis and types




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Prevention of type 1 diabetes

• Early exposure to cows milkprotein

• Nicotinamide

Diagnosis and types




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Insulin

• Diabetes Prevention Trial

• Diabetes Prediction andPrevention Project

Diagnosis and types




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Lifestyle modification

• Da Qing Study

• Finnish Diabetes Prevention Study

Diagnosis and types




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Lifestyle vs medication

• Diabetes Prevention Program

• STOP-NIDDM

Diagnosis and types




Slide 38 of 48ACTIVITY


Type 2 diabetes can be delayed inpeople with IGT

Lifestyle modification is mosteffective

What do you think could be done at

community level to prevent or delaydiabetes?

Diagnosis and types




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Summary

Type 1 diabetes

• Results from progressive beta-cell destruction

• People with type 1 diabetes needinsulin therapy to live

Diagnosis and types




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Type 2 diabetes

• Often characterized by insulininsensitivity and relative ratherthan absolute insulin deficiency

• A progressive condition

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

Summary

Diagnosis and types




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Review question

1. The pathogenesis for type 2 diabetesincludes:

a. Insulin deficiency and insulininsensitivity

b. Insensitivity to insulin andautoimmune beta-cell destruction

c. Autoimmune beta-cell destructionand glucagon deficiency

d. Insulin deficiency and glucagondeficiency

Diagnosis and types




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Review question

2. A person with type 2 diabetes, recentlystarted on insulin, asks if there is a wayto measure if he/she is still producing anyinsulin. The correct response would be:

a. Islet cell antibody tests

b. C-peptide test

c. HbA 1c test

d. Serum insulin test

Diagnosis and types




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Review question

3. The Diabetes Prevention Program (DPP):

a. Included people with type 1diabetes

b. Included only people with IGT

c. Tested the value of exercise

d. Included people with type 2diabetes

Diagnosis and types




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Review question

4. Type 1 diabetes is usually caused by:

a. Injury to the pancreas

b. An autoimmune reaction

c. Insulin insensitivity in the cells

d. Hypersensitivity to insulin

Diagnosis and types



g ypCurriculum Module II-1

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Answers

1. a

2. b

3. b

4. b

Diagnosis and types




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References

1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. DiabetesCare 2004; 27(suppl 1): S5-S10.

2. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. CanadianDiabetes Association 2003 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diab 2003; 27(suppl 2).

3. Chiasson JL, Josse RG, Gomis R, et al. Acarbose for prevention of type 2 diabetes mellitus:The STOP-NIDDM randomized trial. Lancet 2002; 346: 393-403.

4. Delahanty LM and Halford BN. The role of Diet Behaviours in Achieving improved glycaemiccontrol in intensively treated patients in the Diabetes Control and Complications Trial.Diabetes Care 1993; 16(11): 1453-58.

5. Diabetes Control and Complications Trial Research Group. Effect of intensive diabetestreatment on the development and progression of long-term complications in adolescents withinsulin dependent diabetes mellitus: Diabetes Control and Complications Trial. The Journal of Paediatrics 1994; 125(2): 177-88.

6. Diabetes Control and Complications Trial/epidemiology of diabetes interventions and

complications research group intensive diabetes therapy and carotid intima-media thickness intype 1 diabetes mellitus. New Engl J Med 2003; 348: 2294-303.

7. Diabetes Control and Complications Trial: The effect of intensive treatment of diabetes on thedevelopment and progression of long-term complications in insulin-dependent diabetesmellitus. N Engl J Med 1993; 329: 977-86.

Diagnosis and types




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References

8. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults:findings from the third National Health and Nutrition Examination Survey. JAMA 2002; 297:356-59.

9. Diabetes Atlas 2006. Brussels: International Diabetes Federation, 2006.

10. Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated withthe metabolic syndrome. Diabetes Care 2001; 24(4): 683-9.

11. Pan X, Li G, Hu Y, et al. Effects of diet and exercise in preventing NIDDM in people with

impaired glucose tolerance: The Da Qing IGT and Diabetes Study. Diabetes Care 1997; 20(4):537-44.

12. Report of a WHO Consultation. Laboratory Diagnosis and monitoring of Diabetes Mellitus.World Health Organisation 2002. http://whqlibdoc.who.int/hq/2002/9241590483.pdf citedApril 30, 2005.

13. Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus bychanges in lifestyle among subjects with impaired glucose tolerance. N Eng J Med 2001; 344:1343-50.

14. The Diabetes Prevention Program Research Group. The diabetes prevention Program (DPP).Diabetes Care 2002; 23(12): 2165-71.

15. UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulpfonylureas orinsulin compared with conventional treatment and risk of complications in patients with type 2diabetes. Lancet 1998; 352: 837-53.

Diagnosis and types

http://whqlibdoc.who.int/hq/2002/9241590483.pdf

http://whqlibdoc.who.int/hq/2002/9241590483.pdf




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References

16. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes UKPDS 38. BMJ 1998; 317: 703-13.

17. IDF Clinical Guidelines Task Force. Global Guideline for Type 2 Diabetes. Brussels:International Diabetes Federation, 2005.

18. Harris SB, Ekoe JM, Zdanowicz Y, Webster-Bogaert S. Glycemic Control andmorbidity in the Canadian primary care setting (results of the diabetes in Canadaevaluation study). Diab Research and Clin Pract 2005; 70: 90-7.

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