UPDATE ON CLASSIFICATION AND DIAGNOSIS OF DIABETES MELLITUSTYPE

UPDATE ON CLASSIFICATION AND DIAGNOSIS OF DIABETES MELLITUS

TYPE 1 DIABETES MELLITUS PREVIOUS NAMES: 1. JUVENILE D.M. 2. IDDM

COMPLETE DESTRUCTION OF -Cells

AUTOIMMUNE, CELL - MEDIATED -Cell DESTRUCTION

MARKERS OF AUTOIMMUNE DESTRUCTION ISLET CELL ANTIBODIES (ICAS). INSULIN ANTIBODIES (IAAS). GLUTAMIC ACID DECARBOXYLASE ANTIBODIES (GAD). TYROSINE PHOSPHATE ANTIBODIES.

ONE OR MORE IS PRESENT IN 85-90% OF CASES WHEN FASTING HYPERGLYCEMIA IS INITIALLY DETECTED.

INVIRONMENTAL FACTORS NOT WELL DEFINED - VIRUSES - TOXINS

PRESENTATION RATE OF -CELL DESTRUCTION IS VARIABLE:- 1- RAPID IN SOME ESP.: INFANTS & CHILDREN 2- SLOW ESP.: ADULTS

MAY PRESENT INITIALLY WITH DKA. OTHERS MAY PRESENT WITH MODEST HYPERGLYCEMIA, & MAY DECOMPENSATE TO DKA WHEN THERE IS INFECTION OR OTHER STRESS.

OTHERS (esp. ADULTS): MAY RETAIN SOME RESIDUAL B-CELL FUNCTION, TO PREVENT DKA, FOR YEARS!. YEARS LATER, THEY EVENTUALLY END UP WITH COMPLETE B-CELL DESTRUCTION.

IDIOPATHIC DIABETES A MINORITY OF TYPE 1 D.M. AFRICAN OR ASIAN ORIGIN. NO EVIDENCE OF AUTOIMMUNITY. NOT HLA ASSOCIATED. STRONGLY INHERITED. ABSOLUTE REQUIREMENT FOR INSULIN THERAPY MAY COME & GO!

TYPE 2 DIABETES MELLITUS PREVIOUS NAMES: - NIDDM - ADULT ONSET DM.

ETIOLOGY INSULIN RESISTANCE & RELATIVE INSULIN DEFECIENCY

SPECIFIC ETIOLOGIES: NOT CLEARLY KNOWN, BUT: NO AUTOIMMUNE DESTRUCTION OF -CELLS. OBESITY CENTRAL OR VISCERAL FAT DESTRIBUTION. AGE LACK OF EXERCISE

DKA DOES NOT OCCUR BUT, IF IT OCCURS:- LOOK FOR MAJOR STRESS! e.g. 1. M.I 2. INFECTION BE VERY CAREFULL!!

STRONG GENETIC PREDISPOSITION THE GENETICS: ARE COMPLEX & NOT CLEARLY DEFINED

NEW CRITERIA FPG > 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h. Or 2-h PG > 200 mg/dl (11.1 mmol/l) during an OGTT. The test should be performed as described by WHO, using a glucose load containing the equivalent of 75-g anhydrous glucose dissolved in water.

CRITERIA FOR THE DIAGNOSIS OF DIABETES MELLITUS Normoglycemia IFG D.M FPG <110mg/dl FPG>110mg/dl & FPG>126mg/dl <126mg/dl (IFG) 2-h PG+<140mg/dl 2-h PG+>140mg/dl 2-h PG+>200mg/dl & <200mg/dl (IGT) --- --- Symptoms of DM & casual plasma glucose concentration >200mg/dl

Or Symptoms of diabetes plus casual plasma glucose concentration > 200mg/dl (11.1 mmol/l). Casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyria, polydipsia, and unexplained weight loss.

THE NEW DIAGNOSTIC CRITERIA FOR DIABETES MELLITUS WERE LARGELY BASED ON CLINICAL CONSIDERATIONS: AROUND FASTING PLASMA GLUCOSE OF 110 MG% (6.1 MMOL/1) THE EARLY PHASE OF INSULIN SECRETION STARTS TO BE IMPAIRED.

AROUND FASTING PLASMA GLUCOSE OF 126 mg% (7.0 mmol/1), THE RISK OF MICROVASCULAR COMPLICATIONS INCREASES SIGNIFICANTLY. THERE IS STRONG ASSOCIATION BETWEEN THE FOLLOWING PARAMETERS IN CAUSING MICROAGNIOPATHY: FPG. 2 HR PLASMA GLUCOSE. HbAic

LOWERING BLOOD GLUCOSE BELAYED THE ONSET, AND SLOWED THE PROGRESSION, OF MICROVASCULAR COMPLICATIONS

IS TIGHT CONTROL OF BLOOD GLUCOSE DANGEROUS ??

1- HYPOGLYCEMIA BE CAREFUL FREQUENT PG MONITORING ADJUSTMENT OF INSULIN DOSE, TIMING AND FREQUENCY ADJUSTMENT OF MEALS, CONTENT & TIMING ADJUSTMENT OF EXERCISE/ACTIVITY

FOR EVERY 1% DECREASE IN HbAIC (e.g. FROM 9 TO 8%): THERE WAS A 25% REDUCTION IN DIABETES - RELATED DEATHS.

DIABETES & B.P OPTIMUM B.P 120/80. SYSTOLIC B.P SHOULD BE: < 130 mmHg DIASTOLIC B.P SHOULD BE: < 80 mmHg ------------------- SYSTOLIC B.P: 130-139 OR DIASTOLIC B.P: 80-90

Rx: 3 MONTH TRIAL OF :-LIFESTYLE/BEHAVIORAL THERAPY (LBT). IF TARGET NOT ACIEVED: ---> ADD PHARMACOTHERAPY

LBT DIET:  SODIUM  BODY WEIGHT D/C ALCOHOL D/C SMOKING INCREASE PHYSICAL ACTIVITY.

SYSTOLIC B.P > 140 OR DIASTOLIC B.P > 90 SHOULD RECEIVE DRUG THERAPY IN ADDITION TO (LBT). USE 1,2,3 OR MORE ANTIHYPERTENSIVE DRUGS AS NEEDED TO CONTROL B.P

INDICATIONS FOR INITIAL TREATMENT & GOALS FOR ADULT HYPERTENSIVE DIABETIC PATIENTS Systolic Diastolic Goal (mmHg) <130 <80 Behavioral therapy alone 130-139 80-89 (maximum 3 months) then add pharmacologic treatment Behavioral therapy + >140 >90 pharmacologic treatment

DIABETES & LIPID MANAGEMETN LOWERING LDL CHOLESTEROL. LOWERIND TGD & INCREASING HDL CHOLESTEROL: IS ASSOCIATED WITH A REDUCTION IN CARDIOVASCULAR EVENTS.

LDL GOAL: < 100 mg/dl (2.6 mmol/l) LDL 100-129 mg/dl AGGRESSIVE DIET, EXERCISE TO  Wt. + STATIN

HDL < 45 mg/dl IN MALES < 55 mg/dl IN FEMALES EXERCISE Wt. REDUCTION STOP SMOKING ? FIBRIC ACID ? NIACIN

TGD: GOAL: < 150 mg/dl DIET,  Wt., CONTROL D.M DRUGS: FIBRIC ACID

CATEGORY OF RISK BASED ON LIPOPROTEIN LEVELS IN ADULTS WITH DIABETES LDL HDL Risk cholesterol cholesterol* Triglyceride High >130 <35 >400 Borderline 100-129 35-45 200-399 Low <100 >45 <200 Data given in milligrams per deciliter. *For women, the HDL cholesterol values should be increased by 10mg/dl.

DIABETES & ASPIRIN ASPIRIN BLOCKS THROMBOXANE SYNTHESIS BY ACETYLATING PLATELET CYCLO-OXYGENASE  30%  M.I  20%  IN STROKES DOSAGE: 75-325 mg/day

USE IN ALL ADULTS WITH D.M & MACROVASCULAR DISEASE. FOR PRIMARY PREVENTION: IN PATIENT WITH D.M: > 40 YEARS WITH ONE OR MORE OTHER CARDIOVASCULAR RISK FACTORS.

CORONARY HEAR DISEASE SCREENING IN D.M TO IDENTIFY THE PRESENCE OF CHD IN DIABETIC PATIENTS WITH NO SYMPTOMS OF CHD.

NEPHROPATHY SCREENING AND D.M DIABETIC NEPHROPATHY OCCURS IN 20-40% IN DIABETICS THE SINGLE LEADING CAUSE OF END-STAGE RENAL DISEASE (ESRD) MICROAIBUNINURIA: 30-299 mg/24hr.: THE EARLIEST STAGE OF DIABETIC NEPHROPATHY. ALSO A MARKER FOR CVD.

PERFORM A TEST FOR MICROAIBUMENURIA ANNUALLY, IN:- 1- TYPE 1 DIABETICS > 5 YEARS AFTER Dx. 2- TYPE 2 DIABETICS: AT Dx. USE ACE INHIBITORS OR/AND ARBS

DEFINITIONS OF ABNORMALITIES IN ALBUMIN EXCRETION 24-h collection Spot collection Category (mg/24h) (µg/mg creatinine) -------------------------------------------------------------------------- Normal <30 <30 Microalbuminuria 30-299 30-299 Clinical albuminuria >300 >300

RETINOPATHY & D.M DIABETIC RETINOPATHY: THE MOST FREQUENT CAUSE OF BLINDNESS IN AGES 20-74 YEARS. PREVALANCE OF DIABETIC RETINOPATHY: IS STRONGLY RELATED TO THE DURATION OF DIABETES.

AIM OF SCREENING: EARLY DISCOVERY EARLY MANAGEMENT VALUE OF EARLY LASER PHOTOCOAGULATION IN PREVENTING VISUAL LOSS

OPTIMAL GLYCEMIC CONTROL. OPTIMAL B.P CONTROL. CAN REDUCE PROGRESSION OF DIABETIC RETINOPATHY

SCREENING RECOMMENDATIONS TYPE 1 DIABETICS: INITIAL DILATED & COMPREHENSIVE FUNDUS EXAM. BY AN OPHTHALMOLOGIST WITHIN 3-5 YEARS AFTER Dx. TYPE 2 DIABETICS: SHORTLY AFTER Dx. IS MADE SUBSEQUENT EXAMS: ANNUALLY EXCEPT ?! WHEN RETINOPATHY IS PROGRESSING

PREVENTION OF TYPE 1 D.M ALL RESEARCH ! -IN FIRST- DEGREE RELATIVES OF TYPE 1 DIABETICS BECAUSE WE NOW HAVE THE ABILITY TO PREDICT DEVELOPMENT OF TYPE 1 D.M IN SOME PEOPLE: INVESTIGATIONS ARE GOING ON TO HALT OR EVEN PREVENT B-CELL DESTRUCTION.

PANCREAS & ISLET CELL TRANSPLANTATION FOR TYPE 1 D.M PANCREAS & KIDNEY TRANSPLANTS PANCREAS ONLY TRANSPLANTS ISOLATED ISLET CELL TRANSPLANTATION: RESEARCH ONLY.