5491 Diabetes

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DIABETESDr. Padghan Dilip

M.D.(Medicine)Padghan Hospital

Shrirampur

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Diabetes Education Part

Dr. Dilip Padghan (M.D.Med)

Padghan hospital, Sakhar kamgarhospital, Shrirampur

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World2007 = 246 million2025 = 380 million

Increase +55%Diabetes Atlas, 3rd edition, IDF 2006

28.340.5+43%

16.232.7+102%

10.418.7+80%

53.264.1+21%

24.544.5

+81%

67.099.4

+48%

46.580.3+73%

Global projections for

diabetes (millions)2007-2025

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The Top 10s(number of people with diabetes)

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Prevalence of Diabetes

European Countries Urban Indians

(USA- UK)

6% 12-15%

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1971

1972

1979

1979

1984

1986

1988

1989

19891992

1996

2000

1.2(Urban)

2.3(Urban)

0.5(Urban)

3.0(Urban)

1.3(Rural)4.7(Urban)

3.8(Urban)

5.0(Urban)

2.2(Rural)

1.6(Rural)8.2(Urban)

2.4(Rural)

11.6(Urban)

12.1(Urban)

Tripathy et al

Ahuja et al

Johnson et al

Gupta et al

Murthy et al

Patel

Ramachandran et al

Kodali et al

Rao et alRamachandran et al

Ramachandran et al

Ramachandran et al

Cuttack

New Delhi

Madurai

Multicentre

Tenali

Bhadran

Kudremukh

Gangavathi

EluruMadras

Madras

Six metros

Year Author Place Prevalence(%)

Steadily Rising Prevalence

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Classification of DiabetesType 1 7.6%Type 2 90.6%Others 1.9%

Demographics

Age Groups

0

25

50

70

Current Age Distribution

Current Mean Age 53.4 13.0 (n= 2269)

Mean Age at Onset of Diabetes 43.6 12.2 (n= 2251)

Mean Diabetes Duration 10.0 6.9 (n= 2251)

DiabCare Asia India

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Why are We Concerned about

Diabetes?Every 24 hours... 3,600 new cases of diabetes are diagnosed

580 people die of diabetes-related complications

225 people have a diabetes-related amputation

120 people with diabetes progress to end-stagerenal disease

55 people with diabetes become blind

ADA -2002

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Magnitude of the Problem

Diabetic retinopathy: most common

cause of blindness before age 65

Nephropathy: most common cause of

ESRD

Neuropathy: most common cause of non-

traumatic amputations

2-3 fold increase in cardiovascular

disease

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Risk Factors for Diabetes

Mellitus Family history of diabetes (i.e., parent or sibling with type 2 diabetes. Obesity (BMI > 25 kg/m2)

Physical inactivity

Mental Stress Race/ethnicity (e.g., African American, Latino, Native American, Asian

American, Pacific Islander)

Previously identified with IFG, IGT, or an A1C of 5.76.4%

History of GDM or delivery of baby >4 kg (9 lb)

Hypertension (blood pressure 140/90 mmHg)

HDL cholesterol level 250 mg/dL (2.82 mmol/L)

Polycystic ovary syndrome or acanthosis nigricans

History of cardiovascular disease

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Diabetes Mellitus- Genetics

Risk of Diabetes

- F/H/O Diabetes

- One parent diabetic

- One parent diabetic and

other from a diabetic family

Family History

20 %

40 %

70 %

V Mohan & KGMM Alberti

International Textbook of Diabetes Mellitus,1992,178.

Family history significant predictor of Diabetes

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More Risk Factors

Overweight (Abdominal)

Over 45 years old

Sedentary Lifestyle

Non-White Race Family History of DB

Family History of High BP

History of High BP (self)

High Cholesterol History of Gestational DB

Delivered a baby > 9 lbs.

Goals:

Women < 35Men < 40

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WEIGHT

100 105 110 115 120 125 130 135 140 145 150 155 160 165 170 175 180 185 190 195 200 205 210 215 220 225 230 235 240 245 250

HEIGHT 5'0" 20 21 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49

5'1" 19 20 21 22 23 24 25 26 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 43 44 45 46 47

5'2" 18 19 20 21 22 23 24 25 26 27 27 28 29 30 31 32 33 34 35 36 37 37 38 39 40 41 42 43 44 45 46

5'3" 18 19 19 20 21 22 23 24 25 26 27 27 28 29 30 31 32 33 34 35 35 36 37 38 39 40 41 42 43 43 44

5'4" 17 18 19 20 21 21 22 23 24 25 26 27 27 28 29 30 31 32 33 33 34 35 36 37 38 39 39 40 41 42 43

5'5" 17 17 18 19 20 21 22 22 23 24 25 26 27 27 28 29 30 31 32 32 33 34 35 36 37 37 38 39 40 41 42

5'6" 16 17 18 19 19 20 21 22 23 23 24 25 26 27 27 28 29 30 31 31 32 33 34 35 36 36 37 38 39 40 40

5'7" 16 16 17 18 19 20 20 21 22 23 23 24 25 26 27 27 28 29 30 31 31 32 33 34 34 35 36 37 38 38 39

5'8" 15 16 17 17 18 19 20 21 21 22 23 24 24 25 26 27 27 28 29 30 30 31 32 33 33 34 35 36 36 37 38

5'9" 15 16 16 17 18 18 19 20 21 21 22 23 24 24 25 26 27 27 28 29 30 30 31 32 32 33 34 35 35 36 37

5'10" 14 15 16 17 17 18 19 19 20 21 22 22 23 24 24 25 26 27 27 28 29 29 30 31 32 32 33 34 34 35 36

5'11" 14 15 15 16 17 17 18 19 20 20 21 22 22 23 24 24 25 26 26 27 28 29 29 30 31 31 32 33 33 34 35

6'0" 14 14 15 16 16 17 18 18 19 20 20 21 22 23 23 24 24 25 26 26 27 28 29 29 30 31 31 32 33 34 34

6'1" 13 14 15 15 16 16 17 18 18 19 20 20 21 22 22 23 24 24 25 26 26 27 28 28 29 30 30 31 32 32 33

6'2" 13 13 14 15 15 16 17 17 18 19 19 20 21 21 22 22 23 24 24 25 26 26 27 28 28 29 30 30 31 31 32

6'3" 12 13 14 14 15 16 16 17 17 18 19 19 20 21 21 22 22 23 24 24 25 26 26 27 27 28 29 29 30 31 31

6'4" 12 13 13 14 15 15 16 16 17 18 18 19 19 20 21 21 22 23 23 24 24 25 26 26 27 27 28 29 29 30 30

BODY MASS INDEX

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Diabetes+Obesity=

Diabesity

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Diabetes Mellitus The name diabetes mellitus means

sweet urine. It stems from ancient

times when physicians would taste a

patients urine as a part of a diagnosis.

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What is Diabetes?

A condition in which

the body cannotmake or cannot use

insulin properly

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INDIAN SCENARIOHigh prevalence

Life style changes further accentuate the high genetic predisposi

Under diagnosed due to low awareness

Perhaps occurs a decade earlier

Non obese/lean Type II fairly common

Treated less seriously as considered Mild Disease

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Pancreas The pancreasfunctions as both an exocrine and an

endocrine gland

Exocrine function is associated with the digestivesystem .

Endocrine Function: produces two importanthormones in Islets of Langerhans, insulinandglucagon

Glucagon

-Insulin -Somatostatin

PP-Pancreatic polypeptide

-Gastrin

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Normal Insulin Metabolism

Insulin

Produced by the cells in the islets of

Langherans of the pancreas

Facilitates normal glucose range of

80mg120 mg/dl.

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DIABETES

Dr Padghan Dilip R

M.D. Medicine

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Insulin Secretion

Fig. 47-1

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NORMALCONDITION

DIABETICCONDITION

Body is able to convert glucose into

energy due to the action of insulin

(carrier of glucose)

Body is unable to utilize glucose because of

impaired action/lack of insulin & glucose

concentration in blood raises.

MOUTH

STOMACH

PANCREAS

BLOOD STREAMBLOOD STREAM

Blockage

Fat Accumulation

Food consumed

Food gets converted

into glucose

Pancreas make

insulin

Pancreas make

little or no insulin

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Promotes glucose transport from the

bloodstream across the cellmembrane to the cytoplasm of the

cell

Analogous to a key that unlocksthe cell door to allow glucose in

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Insulin after a meal: Stimulates storage of glucose as

glycogen

Inhibits gluconeogenesis

Enhances fat deposition in adiposetissue

Increases protein synthesis

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Fasting state

Counter-regulatory hormones (especially

glucagon) stimulate glycogen glucose When glucose unavailable during fasting

state

Lipolysis (fat breakdown)Proteolysis (amino acid breakdown)

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What goes wrong in Diabetes ?

Multitude of mechanisms

Insulin

Regulation Secretion

Uptake or breakdown

Beta cells

damage

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ALTERED CHO METABOLISM

Insulin

Glucose Utilization+Glycogenolysis

Hyperglycemia

Glucosuria (osmotic diuresis)

Polyuria*(and electrolyte imbalance)

Polydipsia*

* Hallmark symptoms of diabetes

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ALTERED PROTEIN METABOLISM

Insulin

Protein Catabolism

Gluconeogenesis(amino acids glucose)

HyperglycemiaWeight Loss and Fatigue

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ALTERED PROTEIN METABOLISM

Insulin

Protein Catabolism

Gluconeogenesis(amino acids glucose)

HyperglycemiaWeight Loss and Fatigue

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ALTERED FAT METABOLISM

Insulin

Lipolysis

Free fatty acids + ketones

Acidosis + Weight Loss

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Types of Diabetes Mellitus

Type 1

Type 2

Gestational DM

Other
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Type 1 Diabetes Mellitus

Formerly known as juvenile onset or

insulin dependent diabetes

Most often occurs in people under 30

years of age, but may occur at any age.

Peak onset between ages 11 and 13

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Etiology and Pathophysiology

Progressive destruction of pancreatic

cells

Autoantibodies cause a reduction of 80%

to 90% of normal cell function before

manifestations occur

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Etiology and Pathophysiology

Causes:

Genetic predisposition

Exposure to a virus

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Onset of Disease

Manifestations develop when the

pancreas can no longer produce insulin

Rapid onset of symptoms

Present at ER with impending or

actual ketoacidosis

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Onset of Disease

Weight loss Polydipsia (excessive thirst)

Polyuria (frequent urination)

Polyphagia (excessive hunger) Weakness and fatigue

Ketoacidosis

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Onset of Disease

Diabetic ketoacidosis (DKA)

Life-threatening complication of Type 1

DM

Occurs in the absence of insulin

Results in metabolic acidosis

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Formerly known as adult onset or

Non insulin dependent Diabetes.

Accounts for >90% of patients with

diabetes

Usually occurs in people over 30 yearsold

80-90% of patients are overweight

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Pathology of Type 2 Diabetes

Insulin resistance Beta-cell function

Blood glucose

Insulin response

Euglycemia Type 2 diabetes

Adequate Inadequate

Obesity Sedentary lifestyle Aging Genetics Glucotoxicity FFA levels

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Insulin Resistance

Occurs when tissues do not respond to insulin

and glucose is not taken up by cells

To compensate, (initially) more insulin is

produced

Euglycemia initially

A main etiologic factor in IGT, DM 2

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Insulin Resistance

AcanthosisNigricans

Skin Tags

Wh H i T 2 DM
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What Happens in Type 2 DM

Liver puts toomuch sugar

into the blood

Muscle cells and other tissues

are

resistant to insulin

Pancreas cant makeenough insulin

Stomach empties 50%faster than normal

Type 2

Diabetes

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Progression of Insulin Resistance

Insulin resistance

Insulin production

Glucose level

Time

Non-

diabetes

Pre-

diabetes

Type 2

diabetes

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Progression Of Beta Cell Failure

in Type 2 Diabetes

Progressive -cell defectin type 2 diabetes

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Onset of Disease

Gradual onset

Person may go many years with undetected

hyperglycemia

Marked hyperglycemia (27.655.1

mmol/L)

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Clinical Manifestations


Non-specific symptoms

Fatigue

Recurrent infections

Prolonged wound healing

Visual changes

Cl ifi ti f Di b t

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Classification of DiabetesType I DM Type II DM

Aetiology Autoimmune

(- cell destruction)

Insulin resistance and -celldysfunction

Peak age 12 years 60 years

Prevalence 0.3% 6% (>10% above 60 years)

PresentationOsmotic symptoms, weight

loss (days to weeks), DKA

Patient usually slim

Osmotic symptoms, diabetic

complications (months to years).

Patient usually obese

Treatment Diet and insulin Diet, exercise (weight loss), oralhypoglycemics, Insulin later

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Gestational Diabetes

Develops during pregnancy

Detected at 24 to 28 weeks of gestation

Associated with risk for cesarean delivery,perinatal death, and neonatal complications

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Secondary Diabetes

Results from another medical condition or

due to the treatment of a medical conditionthat causes abnormal blood glucose levels

Cushing syndrome (e.g. steroid administration)

HyperthyroidismParenteral nutrition

Auto-Immunity

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Auto Immunity

Latent Auto immune diabetes in young

(LADA)

Presence of autoimmunity to islet protein is the

feature of IDDM.

However there are some pts over 30 yrs of agepresent with diabetic symptoms and require

insulin therapy within one to two yrs, many of

these pts. Have auto antibodies to islet protein.

They are called as LADA

About 10-15% have ICA (Islet cell antibody)

and / or Glutamic acid decarboxylase antibody

(GADA)

Maturity Onset Diabetes of

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Maturity Onset Diabetes of

the young (MODY)

Result from mutations in a singlegene

Occurs in the young (under 25 yrs ofage)

Resembles type 2 diabetes, responds

to oral hypoglycemic agents

Presence of complications is rare

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DIAGNOSIS

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Diabetes Types

Type 1 diabetes

Type 2 diabetes

Other specific types

Gestational DM

Prediabetes

Impaired glucose regulation (IFG & IGT)

Criteria for the Diagnosis of Diabetes

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A1C 6.5%OR

Fasting plasma glucose (FPG)

126mg/dl

OR

Two-hour plasma glucose 200 mg/dl during an

OGTT

OR

A random plasma glucose 200 mg/dl

ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 2.


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A1C 6.5%

The test should be performed in a laboratory using

an NGSP-certified method standardized to the

DCCT assay*

*In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing.



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Fasting plasma glucose (FPG)126mg/dl (7.0 mmol/l)

Fasting: no caloric intake for

at least 8 h*

*In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing.



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Two-hour plasma glucose 200 mg/dl (11.1mmol/l) during an OGTT

The test should be performed as described by the

World Health Organization, using a glucose load

containing the equivalent of 75 g anhydrous glucose

dissolved in water*

*n the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing.

ADA. I. Classification and Diagnosis. Diabetes Care2011;34(suppl 1):S13. Table 2.


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In a patient with classic symptoms ofhyperglycemia or hyperglycemic crisis,

a random plasma glucose 200 mg/dl (11.1mmol/l)


Prediabetes: IFG IGT Increased A1C

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Prediabetes: IFG, IGT, Increased A1C

Categories of increased risk for diabetes (Prediabetes)*

FPG 100-125 mg/dl (5.6-6.9 mmol/l): IFG

or

2-h plasma glucose in the 75-g OGTT140-199 mg/dl (7.8-11.0 mmol/l): IGT

or

A1C 5.7-6.4%

*For all three tests, risk is continuous, extending below the lower limit of a range and becoming disproportionately greater at

higher ends of the range.


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Revised Diagnostic Criteria

FPG

mg/dl

OGTT

2 hr

mg/dl

Casual PG

mg/dl

Normal 140 and

126 >200 >200 +

symptoms

Standards of Medical Care in Diabetes--2007.Diabetes Care30:S4-S41, 2007

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What is pre-diabetes?

Impaired Fasting Glucose

Impaired Glucose Tolerance

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Impaired Fasting Glucose

Defined as a fasting plasma blood glucose

of >/= to 110 but < 126 Increased risk for DM

Must educate regarding risks and need for

lifestyle modifications

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Impaired Glucose Tolerance

Defined as a plasma blood glucose of >/= to 140but < 200 after a 2 hour 75 gram glucose

tolerance test 25 % risk of developing DM 2

Increased risk for macrovascular diseases Must educate regarding risks and need for

lifestyle modifications

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Is pre-diabetes dangerous?

Yes. Around 40-50 % of pre-diabetics eventually

progress to develop DM at the end of 5 yrs. Hence

it is recommended to act at this stage itself in

order to prevent DM.

Pre-diabetes may also be associated with ongoing

vascular damage and hence increased risk of

micro/macro-vascular complications of DM evenbefore the setting in of high blood sugars.

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CLINICAL PRESENTATION

If you have any of the following

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If you have any of the following

symptoms you can be a DIABETIC

Excessive Thirst (POLYDIPSIA)

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Excessive Hunger

(POLYPHAGIA)

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Excessive Urination

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WEIGHT

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FATIGUE

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Additional Symptoms

Blurred Vision

Tiredness; Sleepiness

Weight Changes

Headaches

Frozen Shoulder

Skin Infections

Slow Healing

Yeast Infections Urinary Infections

Dry Skin; Itching

Numbness; Tingling

Feeling / Acting Evil

High Blood Pressure

Cholesterol Problems

Does the course of DM vary from

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Does the course of DM vary from

patient to patient?

Yes. Some patients may have an aggressive course

with retinopathy, nephropathy and neuropathy

complications whereas others may neverdevelop any.

Also cardiac and vascular complications may

develop in some.Thus the course of DM varies from patient to

patient sparing some a debilitating life but

kinder to others.

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Medical History

Symptoms

Eating patterns, nutritional status, and weight history

Exercise history

Medications

History for Diabetes Complications

Risk factors for atherosclerosis

smoking, hypertension, obesity, dyslipidemia, and familyhistory

Physical Examination

Head to toe

Clinical Evaluation

Components of the Comprehensive DiabetesEvaluation

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Evaluation

ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

Physical examination (1)

Height, weight, BMI waist circumferance

Blood pressure determination, including orthostatic

measurements when indicated

Fundoscopic examination*

Oral- Gum,dental

Systemic Exam-CVS,RS,PACNS Ankle jerk

Skin Exam genitalia Foot Exam -web spaces callosities ulcers monofilamemt

*See appropriate referrals for these categories.

Components of the Comprehensive

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Components of the ComprehensiveDiabetes Evaluation


*See appropriate referrals for these categories.

Physical examination

Comprehensive foot examination

Inspection

Palpation of dorsalis pedis and posterior tibial pulses

Presence/absence of patellar and Achilles reflexes

Determination of proprioception, vibration, and monofilamentsensation

Components of the ComprehensiveDiabetes Evaluation

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Referrals

Annual dilated eye exam

Family planning for women of reproductive age

Registered dietitian for MNT

Diabetes self-management education

Dental examination

Mental health professional, if needed


Diabetes Evaluation

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LaboratoryInvestigations

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Who Should be tested?

All persons >45 years; repeat every 3 years High risk persons: screen at younger age

and more frequently

Overweight (BMI >25) First-degree relative with diabetes High-risk ethnic population Delivered baby >9 lb or diagnosed GDM

Hypertensive

HDL 200 Prediabetes Polycystic ovary syndrome

In Diabetes

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Initial Laboratory Evaluation Blood sugars Hemoglobin A1C

Fasting lipids

U/A

Microalbuminuria (yearly) BUN/Cr (Yearly)

TSH (Yearly)

EKG (Yearly)

Anti-GAD antibodies (Once) (Type 1 DM)

C-peptide level (yearly for 5 years)

Every Visit Labs FBS

A1C every 3 months or fructosamine every 2-3 weeks

U/A

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Urine Tests

URINE "GLUCOSE"

lacks sensitivity = positivity in disease

poor specificity = negativity in health Problems

renal threshold variable 6 to 15 mmol/L

interferences : Clinitest / Glucose oxidase stripsIF URINE TEST POSITIVE

A CONFIRMATORY BLOOD TEST

IS NEEDED

Mon itor ing o f Ur ine Sugar

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Urine Testing Positive only when blood sugar is high > 180 mg/dl.

not accurate but non invasive and less expensive

Not useful to detect and document hypoglycemia

Not useful in DM with nephropathy. Concentrated urine

False positive ,Concentrated Urine

What is needed Test tube to collect urine

Test strips

Steps Collect urine in test tube (second void preferable for urine

sugar)

Dip test strip in urine and do as per instructions

Note and record result

Mon itor ing o f Ur ine Sugar

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Urine Ketone Test

Monitoring is important particularlyin type 1 diabetic patients

All urine samples corresponding toblood glucose >250 mg/dl should betested for ketones

Should be tested during pregnancy

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MICROALBUMINURIA

Microalbuminuria (MAU)

Denied as the urinary excretion of human in therange of 20 200g mm or 30-300 mg/day

At the earliest detectable

It is a reversible condition

Methods

Radio on immunoassay of urinary albuminImmunotubridimetric assays

Micral

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Blood Sugar

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Blood Tests

Glucose

whole blood 10-15% lower than plasma

venous 10% lower than capillary PP

Venous blood = Capillary for fasting

BSLThere is no decrease within 24 h in the

presence of sodium fluoride

M it i f B l d S

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Moni tor ing of B lood Sugar

Check when and how often to monitor -

suggested times include Fasting, before lunch and dinner

2 hrs after breakfast, lunch and dinner

3 AM

Test more often

When not well Suspect hypoglycemia

During pregnancy

When changing treatment or not in control

Test at Alternating Timesf h D

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of the Day

Before or 2 Hours After Eating

XXWed.

XXTues.

XXMon.

BedtimeDinnerLunchBreakfastDay of

the week

HbA1c: the blood test with a memory

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HbA1c: the blood test with a memory

What is HbA1c?

Hemoglobinis a protein that makes

your red blood cells red-colored.

When hemoglobin picks up glucosefrom your bloodstream, the hemoglobin

becomes glycosylated.

Glycosylated hemoglobinis HbA1c.

The HbA1c test measures thepercentage of HbA1c in your blood

a number that corresponds to your

average blood glucose for the previous

3 months.

HbA1c in your bloodstream.

GLYCOSYLATED HB

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GLYCOSYLATED HB

Glycosylated hemoglobin (HbA1c) Is formed due to non-enzymatic glycation of hemoglobin

It percentage is proportional to the mean blood glucoseconcentration

HbA1c reflects glycemic status in the preceding 2-3months

Significance of HbA1C

To assess the long term glycemic control is diabetes

patients To predict risk for development of chronic complications

in diabetes

To guide treatment of diabetes more effectively

Correlation of A1C with Estimated AverageGlucose (eAG)

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Glucose (eAG)

Mean plasma glucose

A1C (%) mg/dl mmol/l

6 126 7.0

7 154 8.6

8 183 10.2

9 212 11.8

10 240 13.4

11 269 14.9

12 298 16.5


These estimates are based on ADAG data of ~2,700 glucose measurements over 3 months per A1C measurement in 507 adults with

type 1, type 2, and no diabetes. The correlation between A1C and average glucose was 0.92. A calculator for converting A1C results

into estimated average glucose (eAG), in either mg/dl or mmol/l, is available at

http://professional.diabetes.org/GlucoseCalculator.aspx.

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Plasma insulin or C peptide

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Plasma insulin or C-peptide

measurement These estimations are not required in routine

clinical practice

However they are useful in research in clinical

situations such as recurrent hypoglycemia and

when clinical classification is difficult

Can be done only in specialized laboratories

Laboratory evaluation (frequency

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Laboratory evaluation (frequency

of test) Test Frequency Plasma Glucose as per requirement

HbA1C Quarterly

Lipid profile Annually / more frequently while

monitoring hyperlipidaemia

Urine Albumin with catch blood glucose measurement

Microalbuminiria In long term cases, if albuminuria is

negative by common laboratory test

Sett ing b lood Sugar targets

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Sett ing b lood Sugar targets

Optimal blood sugar levels are :

Blood

Sugar

Good Borderline Poor

Fasting

mg/dl

80-110 111-140 > 140

PostPrandial

mg/dl

80-144 145-180 > 180

Recommended Goals of Diabetes

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Treatment

Glycemic control

HbA1c

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A blood sugar range that works for someone elsemay not work for you.

Ask your doctor about your best range.

Checklist for a Diabetic

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In Conclusion

Diabetes is a very complicated disease. It is

easy to diagnosis and it is difficult to treatLaboratory plays an important part in the

diagnosis and care of diabetic patients

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5491 Diabetes

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