DR.V.SEKARDR.V.SEKAR

COIMBATORE COIMBATORE DIABETES DIABETES

FOUNDATIONFOUNDATION

HYPERGLYCEMIA IS THEHYPERGLYCEMIA IS THE

HALLMARK HALLMARK OF DIABETESOF DIABETESHYPERGLYCEMIA IS THE HYPERGLYCEMIA IS THE

HALLMARK OF DIABETESHALLMARK OF DIABETES

HYPERGLYCEMIA IS THEHYPERGLYCEMIA IS THE

HALLMARK HALLMARK OF DIABETESOF DIABETES

DIABETES TREATMENT IS DIABETES TREATMENT IS BASED ON THE BASED ON THE

NUMBER IN MILLIGRAMSNUMBER IN MILLIGRAMS

BEFORE WE DECIDE WHETHER BEFORE WE DECIDE WHETHER BLOOD SUGAR IS BLOOD SUGAR IS

NORMAL , HIGH OR LOWNORMAL , HIGH OR LOW

HYPERGLYCEMIA IS THEHYPERGLYCEMIA IS THE

HALLMARK HALLMARK OF DIABETESOF DIABETES

HOW THE BOOLD SUGAR IS HOW THE BOOLD SUGAR IS

DERIVED FROM DERIVED FROM WHERE,WHATWHERE,WHAT

METHOD IS CRITICALMETHOD IS CRITICAL

HYPERGLYCEMIA IS THEHYPERGLYCEMIA IS THE

HALLMARK HALLMARK OF DIABETESOF DIABETES

THE MOST CRITICAL ISSUE THE MOST CRITICAL ISSUE IS CLINICAL CORELATIONIS CLINICAL CORELATION

BLOOD SUGAR SHOULD BLOOD SUGAR SHOULD NOT BE TREATEDNOT BE TREATED

THE PERSON WITH BLOOD THE PERSON WITH BLOOD SUGAR SHOULD BE SUGAR SHOULD BE

TREATEDTREATED

SOURCE OF BLOODSOURCE OF BLOOD

CAPILLARY OR VENOUS PLASMAWHAT METHOD?

WHICH MACHINE?

MANUAL,SEMI AUTOMATED,FULLY AUTOMATED

STEPS FOR STEPS FOR INTERPRETATING BLOOD INTERPRETATING BLOOD

SUGAR VALUESUGAR VALUE

•PRE ANALYSIS

•ANALYSIS

•POST ANALYSIS

PRE ANALYSISPRE ANALYSIS

•BLOOD COLLECTION•LABELLING•ANTI COAGULANT•CENTRIFUGE

BLOOD BLOOD COLLECTIONCOLLECTION

ANTI COAGULANTANTI COAGULANT

LABELLINGLABELLING

CENTRIFUGATIONCENTRIFUGATION VIDEO

PLASMA

PIPETINGPIPETING

1 ML OF REAGENT1 ML OF REAGENT10 MICRO LITER OF PLASMA10 MICRO LITER OF PLASMA

TYPES OF MACHINETYPES OF MACHINE

•TOTALLY MANUAL•SEMI AUTOMATED•FULLY AUTOMATED

ANALYSISANALYSIS

TYPES OF TESTINGTYPES OF TESTING

GLUCOSE OXIDATES DEHYDROGENASE METHOD (GOD)

HEXOKINASE METHOD

TYPE OF REAGENTSTYPE OF REAGENTS

1. END POINT METHOD

2. KINETIC METHOD

TESTINGTESTING VIDEO

TIME OF TESTINGTIME OF TESTING

BLOOD COLLECTION TIME

TESTING TIME

REPORT RELEASING TIME

IS MORE IMPORTANT

EVERY ONE HOUR THERE IS A EVERY ONE HOUR THERE IS A FALL FALL

OF 10 – 15 MILLIGRAMSOF 10 – 15 MILLIGRAMS

SAMPLE SAMPLE STORAGESTORAGE

ONLY FOR 24 ONLY FOR 24 HRSHRSATAT

2 – 8 DEGREE2 – 8 DEGREE

POST ANALYSISPOST ANALYSIS

REPORT RELEASINGREPORT RELEASING

VERIFICATION

RECHECKING

CLINICAL CORRELATION

CALIBERATIONCALIBERATIONQUALITY CONTROLQUALITY CONTROL

WHY FASTING IS HIGH ?WHY FASTING IS HIGH ?Basal Insulin Deficiency:Pre Dinner / Post Dinner Blood Sugar Abnormality:

CHO Load: High Low MediumGlycaemic Index: High Low Fibre Content of Food: High Low MediumTime of Food: Untimely Food Timely Food

Somyogi:Dawn Phenomenon:

Medication:Check Insulin Vial Clear Turbid Expiry CheckedStorage Area Refrigerator Room TempCheck Syringe U 40 U100Check OHA Less dose Correct dose High doseTime of Insulin Correct Time UntimeInsulin Meal Mismatch:

WHY POST PRANDIAL IS WHY POST PRANDIAL IS HIGH ?HIGH ?

Basal Insulin Deficiency:Pre Dinner / Post Dinner Blood Sugar Abnormality:CHO Load: High Low MediumGlycaemic Index: High Low Fibre Content of Food: High Low MediumTime of Food: Untimely Food Timely Food Somyogi:Dawn Phenomenon:Medication:

Check Insulin Vial Clear Turbid Expiry Checked Storage Area Refrigerator Room Temp

Check Syringe U 40 U100Check OHA Less dose Correct dose

High doseTime of Insulin Correct Time UntimeInsulin Meal Mismatch:

PERSISTANTLY PERSISTANTLY A1C A1C 1.Diet factor:

High CHO Load

Glycaemic index High, Low

Fibre content of the food High, Low, Medium

Time of Food Timely food, Untimely food

2. Exercise :Frequency IntensityTimeType Aerobics gym yoga exercise

6. Co morbid conditions:HT MAU LIPIDS BDR

7. Complication: IHD PDR NEPHROPATHY NEUROPATHY DFS

PVD

8.Doctor factor:Clinical InertiaSelection of drugDosage

CONT’CONT’

HBA1C MAJESTIC IN THE MANAGEMENT OF DIABETESHBA1C MAJESTIC IN THEHBA1C MAJESTIC IN THE

MANAGEMENT OF DIABETESMANAGEMENT OF DIABETES

DIABETES MEANS CHRONIC HYPERGLYCEMIA

WHAT WE TREAT IS ONLY ACUTE HYPERGLYCEMIA?

DIABETES MEANS DIABETES MEANS CHRONIC HYPERGLYCEMIACHRONIC HYPERGLYCEMIA

WHAT WE TREAT IS ONLY WHAT WE TREAT IS ONLY ACUTE HYPERGLYCEMIAACUTE HYPERGLYCEMIA

BLOOD SUGAR TELLS YOU THE DAY TO DAY VARIATION

HBA1C IDENTIFIES THE OVER ALL FLUCCATION OF

BLOOD SUGAR

BLOOD SUGAR TELLS YOU BLOOD SUGAR TELLS YOU THE DAY TO DAY VARIATIONTHE DAY TO DAY VARIATION

HBA1C IDENTIFIES THE OVER HBA1C IDENTIFIES THE OVER ALL FLUCCUATION OF BLOOD ALL FLUCCUATION OF BLOOD SUGARSUGAR

CLINICAL CASE STUDY

MR.SANKARANARAYANAN 60YRS C/O SWELLING IN LEGS

HIS HBA1C IS 11.0% CREA 2.4 WITH BDR ON THE DAY OF TESTING

CLINICAL CASE STUDY

MRS.PADMINI 60 YRS ON THE DAY

OF TESTING HAD BREAKFAST IN

HOTEL HER FASTING WAS 140

POST PRANDIAL 260 & HBA1C 6.0%

HBA1C HELPS TO DECIDE ABOUT DIABETES IS UNDER CONTROL OR NOT

PREDICTS FUTURE COMPLICATIONS

HELPS TO DECIDE THE DIABETES MANAGEMENT

BLOOD SUGAR IS DYNAMIC KEEPS CHANGING

WITH EACH MEAL BLOOD SUGAR GOES UP

3 TIMES A DAY 90 TIMES IN A MONTH

WE CHECK BLOOD SUGAR ONCE IN A MONTH / FEW MONTHS &

DIABETES IS TREATED ON PARTICULAR VALUE UNSCIENTIFIC NOT LOGIC

ROLE OF HBA1C

•CONTROL < 7 %

•NOT UNDER CONTROL > 7 %

•PREDICTS FUTURE COMPLICATION

DCCT , UKPDS STUDY DECIDE ABOUT THE DIABETES MANAGEMENT

< 7 % UNDER CONTROL

> 7 % NOT UNDER CONTROL

7 – 8 % NEEDS ACTION

> 8 % CHANGING THE MEDICATION OR ADDING THE DOSE

>10 % MAY REQUIRE INSULIN

LEVEL OF DECREASE IN HBA1C

LIFE STYLE MODIFICATION

0.5 – 1

METFORMIN 1 – 1.5SULFONYLUREA 1 – 1.5GLITAZONES 0.5 – 1.0SITAGLIPTIN 0.5 – 1.0INSULIN ANY NUMBER

CLINICAL DECESION MAKING

1.SYMPTOMS

2.COMPLICATIONS

3.DURATION OF DIABETES

4.AGE

5.HBA1C

6.TYPE 1 OR TYPE 2

7.INSULIN DEFECIENCY OR INSULIN RESISTANCE

8.WHICH BLOOD SUGAR IS HIGH FASTING OR POST PRANDIAL

9.DIFFERENCE BETWEEN FASTING AND PP

10.DIABETES + OBESITY

11.DIABETES + HYPERTENSION

12.DIABETES + DYSLIPIDEMIA

13.PSYCO – SOCIO STATUS ,ECONOMIC STATUS

14.CO-OPERATION OF THE PERSON AND HIS FAMILY

SYMPTOMSCLINICAL SYMPTOMS ARE THE MOST

IMPORTANT PARAMETER IN DECIDING THETREATMENT PATHWAY

Eg: POLYURIA,POLYPHYGIA,POLYDYPSIA,WT LOSSINDICATES A DECOMPENSATED SYMPTOMATIC

DIABETES STATUS – NEEDS INSULIN THERAPY

SEVERE NEUROPATHY – THE CHOICE IS INSULIN

COMPLICATIONSBASED ON THE MICRO OR MACRO VASCULAR

COMPLICATION THE TREATMENT DECESION MAY DIFFER

DURATION OF DIABETESAT DIAGNOSIS 50 % OF BETA CELL IS LOST LONGER THE DURATION MORE LIKELY REQUIRE

INSULIN THERAPYProgressive Beta Cell FailureProgressive Beta Cell Failure

85 %

70 %

50 % Beta Cell Lossat Detection

100 %Betamass IGT PPBS DIABETES 35 %

PHASE III

I I I

-12 -6 0 6 10 14Y EARS

AGE• YOUNG AGE ONSET• MIDDLE AGE ONSET / CLASSICAL ONSET• OLD AGE ONSET

YOUNG AGE ONSET MAY REQUIRE A TIGHT CONTROL

HBA1CINDICATES A CHRONIC HYPERGLYCEMIA

HBA1C > 10% MAY REQUIRE INSULIN THERAPY

INSULIN RESISTANCE OR INSULIN DEFECIENCYWHICH IS PREDOMINANT ?

FASTING OR POST PRANDIAL WHICH BLOOD SUGAR IS HIGH?

WHAT IS THE DIFFERENCE BETWEEN FASTING AND POST PRANDIAL?

Eg: BASAL INSULIN TO CONTROL THE FASTINGBOLUS TO CONTROL THE POST PRANDIAL

CO – MORBID CONDITIONS

• HYPER TENSION• OBESITY• DYSLIPIDEMIA

PSYCO-SOCIAL, ECONOMICAL STATUS