DIABETES

Dr. Padghan Dilip M.D.(Medicine) Padghan Hospital Shrirampur

Diabetes Education Part

Dr. Dilip Padghan (M.D.Med) Padghan hospital, Sakhar kamgar hospital, Shrirampur

Global projections for diabetes (millions)

2007-2025
53.2 64.1 28.3 40.5

+21 %

+43 %

24.5 44.5

+81 %

67.0 99.4 46.5 80.3

+48 %

+102 %

16.2 32.7

10.4 18.7

+80 %

+73 %

Diabetes Atlas, 3rd edition, IDF 2006

World 2007 = 246 million 2025 = 380 million Increase +55%

The Top 10s

(number of people with diabetes)

Prevalence of Diabetes
European Countries (USA- UK) 6% Urban Indians 12-15%

Steadily Rising Prevalence

Year Author Place Prevalence(%)

1971 1972 1979 1979 1984 1986 1988 1989 1989 1992 1996 2000

Tripathy et al Ahuja et al Johnson et al Gupta et al Murthy et al Patel Ramachandran et al Kodali et al Rao et al Ramachandran et al Ramachandran et al Ramachandran et al

Cuttack New Delhi Madurai Multicentre Tenali Bhadran Kudremukh Gangavathi Eluru Madras Madras Six metros

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)

Demographics
Current Age Distribution
50
25 0 <15 15-30 30-45 45-55 55-70 >70 Classification of Diabetes Type 1 7.6% Type 2 90.6% Others 1.9%

Age Groups

Current Mean Age Mean Age at Onset of Diabetes Mean Diabetes Duration

53.4 13.0 (n= 2269) 43.6 12.2 (n= 2251) 10.0 6.9 (n= 2251)
DiabCare Asia India

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-stage renal disease 55 people with diabetes become blind

ADA -2002

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 nontraumatic amputations 2-3 fold increase in cardiovascular disease

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 <35 mg/dL (0.90 mmol/L) and/or a triglyceride level >250 mg/dL (2.82 mmol/L) Polycystic ovary syndrome or acanthosis nigricans History of cardiovascular disease

Diabetes Mellitus- Genetics

Family history significant predictor of Diabetes
Family History Risk of Diabetes 20 % 40 % 70 %

- F/H/O Diabetes - One parent diabetic - One parent diabetic and other from a diabetic family

V Mohan & KGMM Alberti International Textbook of Diabetes Mellitus,1992,178.

More Risk Factors

Goals: Women < 35 Men < 40

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.

BODY MASS INDEX

HEIGHT WEIGHT 100 105 5'0" 20 21 5'1" 19 20 5'2" 18 19 5'3" 18 19 5'4" 17 18 5'5" 17 17 5'6" 16 17 5'7" 16 16 5'8" 15 16 5'9" 15 16 5'10" 14 15 5'11" 14 15 6'0" 14 14 6'1" 13 14 6'2" 13 13 6'3" 12 13 6'4" 12 13 110 21 21 20 19 19 18 18 17 17 16 16 15 15 15 14 14 13 115 22 22 21 20 20 19 19 18 17 17 17 16 16 15 15 14 14 120 23 23 22 21 21 20 19 19 18 18 17 17 16 16 15 15 15 125 24 24 23 22 21 21 20 20 19 18 18 17 17 16 16 16 15 130 25 25 24 23 22 22 21 20 20 19 19 18 18 17 17 16 16 135 26 26 25 24 23 22 22 21 21 20 19 19 18 18 17 17 16 140 27 26 26 25 24 23 23 22 21 21 20 20 19 18 18 17 17 145 28 27 27 26 25 24 23 23 22 21 21 20 20 19 19 18 18 150 29 28 27 27 26 25 24 23 23 22 22 21 20 20 19 19 18 155 30 29 28 27 27 26 25 24 24 23 22 22 21 20 20 19 19 160 31 30 29 28 27 27 26 25 24 24 23 22 22 21 21 20 19 165 32 31 30 29 28 27 27 26 25 24 24 23 23 22 21 21 20 170 33 32 31 30 29 28 27 27 26 25 24 24 23 22 22 21 21 175 34 33 32 31 30 29 28 27 27 26 25 24 24 23 22 22 21 180 35 34 33 32 31 30 29 28 27 27 26 25 24 24 23 22 22 185 36 35 34 33 32 31 30 29 28 27 27 26 25 24 24 23 23 190 37 36 35 34 33 32 31 30 29 28 27 26 26 25 24 24 23 195 38 37 36 35 33 32 31 31 30 29 28 27 26 26 25 24 24 200 39 38 37 35 34 33 32 31 30 30 29 28 27 26 26 25 24 205 40 39 37 36 35 34 33 32 31 30 29 29 28 27 26 26 25 210 41 40 38 37 36 35 34 33 32 31 30 29 29 28 27 26 26 215 42 41 39 38 37 36 35 34 33 32 31 30 29 28 28 27 26 220 43 42 40 39 38 37 36 34 33 32 32 31 30 29 28 27 27 225 44 43 41 40 39 37 36 35 34 33 32 31 31 30 29 28 27 230 45 43 42 41 39 38 37 36 35 34 33 32 31 30 30 29 28 235 46 44 43 42 40 39 38 37 36 35 34 33 32 31 30 29 29 240 47 45 44 43 41 40 39 38 36 35 34 33 33 32 31 30 29 245 48 46 45 43 42 41 40 38 37 36 35 34 34 32 31 31 30 250 49 47 46 44 43 42 40 39 38 37 36 35 34 33 32 31 30

Diabetes

Obesity = Diabesity

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.

Definition

Hyperglycemia due to Absolute or relative deficiency of insulin.

What is Diabetes?

A condition in which the body cannot make or cannot use insulin properly

INDIAN SCENARIO
High 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

Pancreas

The pancreas functions as both an exocrine and an endocrine gland Exocrine function is associated with the digestive system . Endocrine Function: produces two important hormones in Islets of Langerhans, insulin and glucagon

Glucagon -Insulin -Somatostatin PP-Pancreatic polypeptide -Gastrin

Normal Insulin Metabolism

Insulin Produced by the cells in the islets of Langherans of the pancreas Facilitates normal glucose range of 80mg 120 mg/dl.

DIABETES
Dr Padghan Dilip R M.D. Medicine

Insulin Secretion

Fig. 47-1

NORMAL CONDITION

Food consumed

MOUTH

DIABETIC CONDITION

STOMACH Food gets converted into glucose Pancreas make insulin

BLOOD STREAM PANCREAS

Pancreas make little or no insulin Fat Accumulation

BLOOD STREAM

Blockage
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.

Normal Insulin Metabolism

Promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell Analogous to a key that unlocks the cell door to allow glucose in

Normal Insulin Metabolism

Insulin after a meal:
Stimulates storage of glucose as glycogen Inhibits gluconeogenesis Enhances fat deposition in adipose tissue Increases protein synthesis

Normal Insulin Metabolism

Fasting state
Counter-regulatory hormones (especially glucagon) stimulate glycogen glucose

When glucose unavailable during fasting state

Lipolysis (fat breakdown) Proteolysis (amino acid breakdown)

What goes wrong in Diabetes ?

Multitude of mechanisms
Insulin
Regulation Secretion Uptake or breakdown

Beta cells
damage

ALTERED CHO METABOLISM

Insulin Glucose Utilization + Glycogenolysis Hyperglycemia Glucosuria (osmotic diuresis) Polyuria* (and electrolyte imbalance) Polydipsia* * Hallmark symptoms of diabetes

ALTERED PROTEIN METABOLISM

Insulin Protein Catabolism Gluconeogenesis (amino acids glucose) Hyperglycemia Weight Loss and Fatigue

ALTERED PROTEIN METABOLISM

Insulin Protein Catabolism Gluconeogenesis (amino acids glucose) Hyperglycemia Weight Loss and Fatigue

ALTERED FAT METABOLISM

Insulin Lipolysis Free fatty acids + ketones Acidosis + Weight Loss

Types of Diabetes Mellitus

Type 1
Type 2 Gestational DM Other

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

Type 1 Diabetes Mellitus

Etiology and Pathophysiology
Progressive destruction of pancreatic cells Autoantibodies cause a reduction of 80% to 90% of normal cell function before manifestations occur

Type 1 Diabetes Mellitus

Etiology and Pathophysiology
Causes: Genetic predisposition Exposure to a virus

Type 1 Diabetes Mellitus

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

Type 1 Diabetes Mellitus

Onset of Disease
Weight loss Polydipsia (excessive thirst) Polyuria (frequent urination) Polyphagia (excessive hunger) Weakness and fatigue Ketoacidosis

Type 1 Diabetes Mellitus

Onset of Disease
Diabetic ketoacidosis (DKA) Life-threatening complication of Type 1 DM Occurs in the absence of insulin Results in metabolic acidosis

Type 2 Diabetes Mellitus

Formerly known as adult onset or Non insulin dependent Diabetes. Accounts for >90% of patients with diabetes Usually occurs in people over 30 years old 80-90% of patients are overweight

Pathology of Type 2 Diabetes

Obesity Sedentary lifestyle Aging Genetics Glucotoxicity FFA levels

Insulin resistance

Beta-cell function

Blood glucose

Adequate

Inadequate

Insulin response

Euglycemia

Type 2 diabetes

Islet Dysfunction Leads to Hyperglycaemia in T2DM

T2DM pancreatic islet

Fewer -cells

-cell hypertrophy

Insufficient insulin +

Excess glucagon

Less effective glucose uptake

Glucose
HGO

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

Insulin Resistance

Skin Tags

Acanthosis Nigricans

What Happens in Type 2 DM

Pancreas cant make enough insulin

Stomach empties 50% faster than normal

Type 2

Diabetes
Liver puts too much sugar into the blood Muscle cells and other tissues are resistant to insulin

Progression of Insulin Resistance

Time

Insulin resistance

Insulin production
Glucose level

Nondiabetes

Prediabetes

Type 2 diabetes

Progression Of Beta Cell Failure in Type 2 Diabetes

Progressive -cell defect in type 2 diabetes

Type 2 Diabetes Mellitus

Onset of Disease
Gradual onset Person may go many years with undetected hyperglycemia Marked hyperglycemia (27.6 55.1 mmol/L)

Clinical Manifestations
Type 2 Diabetes Mellitus
Non-specific symptoms Fatigue Recurrent infections Prolonged wound healing Visual changes

Classification of Diabetes
Type I DM
Aetiology
Autoimmune (- cell destruction) 12 years

Type II DM
Insulin resistance and -cell dysfunction 60 years

Peak age

Prevalence

0.3%

6% (>10% above 60 years)

Presentation

Osmotic symptoms, weight loss (days to weeks), DKA Patient usually slim Diet and insulin

Osmotic symptoms, diabetic complications (months to years). Patient usually obese Diet, exercise (weight loss), oral hypoglycemics, Insulin later

Treatment

Gestational Diabetes
Develops during pregnancy Detected at 24 to 28 weeks of gestation Associated with risk for cesarean delivery, perinatal death, and neonatal complications

Secondary Diabetes
Results from another medical condition or due to the treatment of a medical condition that causes abnormal blood glucose levels Cushing syndrome (e.g. steroid administration) Hyperthyroidism Parenteral nutrition

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 age present 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 the young (MODY)

Result from mutations in a single gene
Occurs in the young (under 25 yrs of age) Resembles type 2 diabetes, responds to oral hypoglycemic agents Presence of complications is rare

DIAGNOSIS

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

A1C 6.5%
OR

Fasting plasma glucose (FPG) 126 mg/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.

Criteria for the Diagnosis of Diabetes

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

Criteria for the Diagnosis of Diabetes

Fasting plasma glucose (FPG) 126 mg/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. ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 2.

Criteria for the Diagnosis of Diabetes

Two-hour plasma glucose 200 mg/dl (11.1 mmol/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 Care 2011;34(suppl 1):S13. Table 2.

Criteria for the Diagnosis of Diabetes

In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose 200 mg/dl (11.1 mmol/l)

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

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 OGTT 140-199 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.

ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 3.

Revised Diagnostic Criteria

FPG mg/dl Normal Prediabetes Diabetes <100 >100 and < 126 >126 OGTT 2 hr mg/dl <140 >140 and <200 >200 >200 + symptoms Casual PG mg/dl

Standards of Medical Care in Diabetes--2007. Diabetes Care 30:S4-S41, 2007

What is pre-diabetes?
Impaired Fasting Glucose Impaired Glucose Tolerance

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

Impaired Glucose Tolerance

Defined as a plasma blood glucose of >/= to 140 but < 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

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 even before the setting in of high blood sugars.

CLINICAL PRESENTATION

If you have any of the following symptoms you can be a DIABETIC

Excessive Thirst (POLYDIPSIA)

Excessive Hunger (POLYPHAGIA)

Excessive Urination

WEIGHT

FATIGUE

Additional Symptoms
Skin Infections Slow Healing Yeast Infections Urinary Infections Dry Skin; Itching Numbness; Tingling Feeling / Acting Evil High Blood Pressure Cholesterol Problems

Blurred Vision Tiredness; Sleepiness Weight Changes Headaches Frozen Shoulder

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 never develop 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.

Clinical Evaluation
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 family history

Physical Examination
Head to toe

Components of the Comprehensive Diabetes Evaluation

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

Components of the Comprehensive Diabetes Evaluation

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 monofilament sensation
*See appropriate referrals for these categories. ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.

Components of the Comprehensive Diabetes Evaluation

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

Laboratory Investigations

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 <35 mg/dl or TG >200 Prediabetes Polycystic ovary syndrome

In Diabetes
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

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 strips IF URINE TEST POSITIVE A CONFIRMATORY BLOOD TEST IS NEEDED

Monitoring of Urine Sugar

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

Urine Ketone Test

Monitoring is important particularly in type 1 diabetic patients
All urine samples corresponding to blood glucose >250 mg/dl should be tested for ketones

Should be tested during pregnancy

MICROALBUMINURIA
Microalbuminuria (MAU)
Denied as the urinary excretion of human in the range of 20 200g mm or 30-300 mg/day At the earliest detectable It is a reversible condition

Methods
Radio on immunoassay of urinary albumin Immunotubridimetric assays Micral

Blood Sugar

Blood Tests
Glucose
whole blood 10-15% lower than plasma venous 10% lower than capillary PP Venous blood = Capillary for fasting BSL There is no decrease within 24 h in the presence of sodium fluoride

Monitoring of Blood 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 Times of the Day Before or 2 Hours After Eating

Day of the week Mon. Breakfast Lunch X Dinner X Bedtime

Tues.

Wed.

HbA1c: the blood test with a memory

What is HbA1c?
Hemoglobin is a protein that makes your red blood cells red-colored. When hemoglobin picks up glucose from your bloodstream, the hemoglobin becomes glycosylated. Glycosylated hemoglobin is HbA1c. The HbA1c test measures the percentage 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
Glycosylated hemoglobin (HbA1c) Is formed due to non-enzymatic glycation of hemoglobin It percentage is proportional to the mean blood glucose concentration HbA1c reflects glycemic status in the preceding 2-3 months 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 Average Glucose (eAG)

A1C (%) Mean plasma glucose mg/dl mmol/l

6 7 8 9 10 11 12

126 154 183 212 240 269 298

7.0 8.6 10.2 11.8 13.4 14.9 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. ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S18. Table 9.

Serum Fructosamine
Reflects the state of glycemic control for LAST 2 weeks. Also known as: Glycated Serum Protein; GSP; Glycated Albumin . Glycation of albumin and other plasma proteins A reference range of serum fructosamine is between 1.61 2.68 mmol/L Useful for monitoring of glycemic control in GDM patient

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 of test)

Test
Plasma Glucose HbA1C Lipid profile Urine Albumin Microalbuminiria

Frequency
as per requirement Quarterly Annually / more frequently while monitoring hyperlipidaemia with catch blood glucose measurement In long term cases, if albuminuria is negative by common laboratory test

Setting blood Sugar targets

Optimal blood sugar levels are :

Blood Sugar Fasting mg/dl Post Prandial mg/dl

Good

Borderline Poor

80-110

111-140

> 140

80-144

145-180

> 180

Recommended Goals of Diabetes Treatment

Glycemic control HbA1c <7.0% Preprandial plasma glucose 90-100 mg/dl Postpradial plasma glucose <180 mg/dl Blood pressure Lipids 130.80 mmHg

LDL
Triglyceride HDL

<100 mg/dl
150 mg >40 mg/dl

A blood sugar range that works for someone else may not work for you. Ask your doctor about your best range.

Checklist for a Diabetic

Checklist for a Diabetic

Checklist for a Diabetic

In Conclusion
Diabetes is a very complicated disease. It is easy to diagnosis and it is difficult to treat Laboratory plays an important part in the diagnosis and care of diabetic patients