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Diabetes in saudi

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Some reports suggest that the Kingdom spends approximately SR 30 billion every year on the treatment of diabetes. A patient’s treatment costs the government SR 5,000 per year, if there are no …

Some reports suggest that the Kingdom spends approximately SR 30 billion every year on the treatment of diabetes. A patient’s treatment costs the government SR 5,000 per year, if there are no complications. Those would increase the cost considerably. The treatment of one common diabetes complication, renal failure, costs the government between SR 98 and 180 thousand per year for the dialysis of only one patient.

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  • 1. DIABETES MELLITUSDIABETES MELLITUS
  • 2. DIABETES MELLITUSDIABETES MELLITUS- DIABETES MELLITUS AND ITSCOMPLICATIONS ARE NOW THETHIRD LEADING CAUSE OFMORTALITY IN SAUDI ARABIAAND THE SECOND LEADINGCAUSE OF BLINDNESS.
  • 3. -ESTIMATED PREVALENCE INU.S.A 3 - 6 % AND INCREASINGRAPIDLY-ESTIMATED PRVALENCE INSAUDI ARABIA to 200318-24%
  • 4. -STROKE, M1 AND END – STAGE RENALDISEASE ARE FREQUENT CAUSESOFMORTALITY.-THE DISEASE IS FOUNDTHROUGHOUT THE WORLD ATVARYING PRVALENCE RATE.- IN PIMA INDIANDS PREVALENECRATE AT 50 %
  • 5. NIDDM IS MAJOR CAUSE OFMORBIDITY AND MORTALITYPREVAILING FROM,MACROVASCULARDISEASE , BUT ALSO FROM SPECIFICCOMPLICATIONS OF DISABETES ,RETINOPATHY , NEPHROPATHY ANDNEUROPATHY.
  • 6. DIABETES MELLITUS IS ADISEASECOMPLEX CHARACTERISED BY RELATIVE ORABSOLUTE INSUFFICIENCY OF INSULINSECRETION AND A CONCMMITANTINTENSITIVITY OR RESISTANCE TO THEMETABOLIC ACTION INSULIN TARGETTISSUE.
  • 7. NON INSULIN DEPENDENTDABETES ( NIDDM ) IS by FARTHE MOST PREVALENT FORMOF DIABETES WORLD –WIDE , FORMING MORE THAN95 % OF ALL DIABETES INMANY DEVELOPINGCOUNTRIES .
  • 8.  Genetic FactorsHLA class 2 antigens in DR + DQ regions =>90% Caucasian patients have eitherDR3 or DR4 , DR2 is protective. Environmental Factors:No Specific factors have been identified
  • 9.  VirusesThe risk greater for children bornbetween February-SeptemberIgM antibodies against conxsackievirusfound in25-30% of new cases suggesting recentinfection( cont . )
  • 10. Coxsackievirus B RNA has been detectedin 65% of children under the age of 7 yearswith newly diagnosed IDDM compared with4% of controls which is consistent withrecent Infection..
  • 11. (CONT)Dietary FactorsCow,s mild feeding fist 4 monthsindicated risk of subsequent IDDM,whilst breast feeting appeared protective.Case controlled studies in Sweden haveindicated a positive association betweenIDDM ,high protein intake and frequencyof consumption of foods containingnitrosamine.
  • 12. (CONT)Loss of first- phase insulinsecretion in response to intravenousglucose is highly Predictive of earlyonset of diabetes .
  • 13.  Islet cell antibodies in ICA are present in80% of children at the time of diagnosis andhave been detected up to 15 years beforediagnosis of IDDM. Long- term follow up has shown thatfamily members with ICA are at greatlyincreased risk of progression to diabetes andthis risk is directly related to persistence andstrength of the ICA reaction.
  • 14. Other antibodies include: insulin autoantibodies ( IAA)antibodies to GAD ( Glutamate decarboxylase )Protein tyrosine phosphatase IA-2 The presence of ICA together with 2 ormore markers indicate a greater than 80%risk of progressing for insulin treatment inotherwise healthy family members .( cont.)
  • 15. 050100RELEASE“HONEYMOON”PERIODOVERTDIABETESPROGRESSIVE IMPAIRMENT ININSULIN RELEASENORMAL INSUILNTIME(YR)BETA-CELLMASS(%OFMAX)0BIRTHIMMUNOLOGIC ABNORMALITESGENETIC PREDISPOSITIONNATURAL HISTORY OF BETA-CELL DEFECT
  • 16. DUE TO BETA-CELL RESERVEINSULIN REQUIREMENT DECREASEDLASTS FOR UP TO 1 YRPATIENT ALWAYS RELAPSESTREATMENT PROPOSED TO EXTENDHONEYMOON PERIOD STILLEXPERIMENTAL
  • 17. RELATIONSHIPS OF TYPE I WITH OTHERAUTOIMMUNE DISEASESASSOCIATION BETWEEN HLA GENES ANDDIABETESPRESENCE OFANTI-ISULET AND/OR ANTI-INSULIN ANTIBIESPRESENCE OF INFLAMMATORY CELLSAROUND ISLETSEVIDENCE OF IMMUNE SYSTEM ACTIVATION
  • 18. 050Slow B cell failureLess insulitisGAD antibodies/ICA HLAassociations+YearsAcute B cell failureInsulitis1AA/1A-2 antibodies/1CA/GAD antibodies HLAassociations +++The spectrum of autoimmune diabetes
  • 19. 050Years? LADASlow type 1Classic type 1Type 1 in infancyClinical spectrum
  • 20. The clinical and immunogeneticcharacteristics of insulindependent diabetes mellituschange according to age atpresentation1AA,insulin auto-antibodies:1A-2,protein1A-2:GAD,glutamatedecarboxylase;ICA,islet cellantibodies,LADA, latentautoimmune diabetes in the adult
  • 21. DR2TYPE I DR3DR4A 2 ---------- BW51--------------- DR4B8-------------B15 GENERALLY LOWIN POPULATION
  • 22. W.H.O. CLASSIFICATIONTYPE I ( INSULIN DEPENDET DIABETES MLLITUSIDDM)HAVE LITTLE OR NO ENDOGENOUSINSULINONSET OF DISEASE IS CLNICALLYABRUPTWITH : MARKED POLYURIA, POLYDIPSIAPOLYPHAGIA WEIGHT LOSS, FATIGUE.THESE PATIENTS ARE HIGHLY PRONE TOKETOSTSTHEY FREQUENT ARE PRESNT IN AND
  • 23. GENERALLY HAVE WEIGHT LOSS AND AREFREQUENTLY AT OR BELOW IDEAL WEIGHTAND ARE THEREFORE PARTICULARYSENSITIVE TO INSULIN (ESPECIALLY REGULAROR SOLUBLE INSULIN). CAN OCCUR AT ANY AGE , BUT PEAKS INTHEMIDDLE OF THE FIST DECADE AND AGAINAT THETIME OF GROWTH ACCELERATION OFADOLESCENCE.TYPE I CONTD . .
  • 24. A PRODOMAL PHAE OF POLYUREA ,POLYDYPSIA AND WEIGH LOSS MAYPRECEDE THE DEVELOPMENT OFKETOACIDOSIS BY A PERIOD OFMONTHS ( MOST COMMONLY 2 - 4WEEKS ). GENETIC PREDISPOSISTION ( FAMILYHISTORY LESS STRONGLY ASSOCIATEDTHAN WITH TYPE II ). ASSOCIATED WITH SOME HLAHITOCMPATIBILTY ANTIGENS EG . B8,TYPE I CONTD…
  • 25.  ASSOCIATED WITH ISLET CELLANTIBODIES VIRUS AETIOLOGY IS IMPLICATEDESPECIALLY COXACKIE B4 AND MUMPS. SIGNIFICANT ASSOCIATION WITH CERTAINAUTOIMMUNE DISORDERS - ADDISON ‘ S ,HASHIMOTO’S TYROIDITS,HYPOPARATHYROIDISM, PERNICIOUSANAEMIATYPE I CONTD .. .
  • 26. 100908070605040302010COMA5%WEIGHTLOSSDKA25%%POLYURIA75%
  • 27. 100908070605040302010PH< 7.220%HYPERGLYCEMIAAND/ ORGLYCOSURIA 100%KETONURIA85%HCO3<1860%%
  • 28. NIDDM IS ALMOSTCERTAINLY AHETEOGENOUS MIXTURE OFCONDITIONSCHARACTERISEDBYHYPERGLYCAEMIA , OFINSULIN RESISTANCE ANDINSULIN HYOP-SECRETION ANDLACK OF DEPENDENCE ONEXOGENOUS INSULIN TOMAINTAIN LIFE
  • 29. FOR MAJOR ABNORMLITIES APPEAR TOACCOUNTFOR THE INAPPROPRIATE HYPERGLYCMIA SEEINTYPE II ( NIDDM) PATIENTS1- DESCREASE IN QUANTITY INSULIN SECRETE2- DELAY IN THE TIME OF RELEASE OF INSULIN3- IMPAIRMET OF THE EFFCTS OF INSULIN ONTHE PEREPHERAL TISSUES( INSULIN RESISTANCE )TYPE II ( NIDDM )
  • 30. DIABETES MELLITUSTYPE I ( IDDM )TYPE II ( NIDDM)- OBESE- NONBESEGESTATIONAL DIABETESOTHER TYPESIMPAIRED GLUCOSE TOLERANCE ( IGT)
  • 31.  Due primarily to a Beta cell defect resultingin inadequate insulin secretion for a givenblood glucose level . There is no significant increase in insulinresistance. Various mutations in the giucokinase geneonchromosomes 7p, probably account for 10-50% of cases of MODY . Giucokinase – Mody is characterized byearly onset ( often less than 18 months ofage ) mild hyperglycaemia which is usually
  • 32. Autosmal DominantDiagnostic Criteria• Diagnosis before 25 years of age inatleast 2 family member .•No requirement of insulin treatment 5years after diagnosis and/or C- Peptidepositivity.•Convincing vertical transmission of type IDiabetes mellitus through at least threegenerations.•Accounts upto 1% of Diabetes Mellitus
  • 33. 11 22 33 44 55Gene defect HNF4a GCK HNF1a 1PF1 HNF1BPrevalence(%) 5 15 70 <1 2GlycaemiaProgressivedeteriorationin glycaemiaMild stablehyperglycaemia Progressive deterioration in glycaemiaAge of onset(years)12-35 Birth 12-28 14-40 12-28Other features Low glucose riseon OGTTSulphonylureasensitivityCystic renalChronic renalfailureComplications Yes Very rare Common ? YesTreatmentProgressiveincrease inrequirementsUsually noneexcept inpregnancyProgressiveincrease inrequirementsSulphonylureafirst-line after diet?ProgressiveincreaserequirementsMODY
  • 34. GENETICS :( STRONG FAMILY AGGREGATESALMOST 100% CONCORDANCERATE IN IDENTICAL TWINS ( PYKEET AL )RACE :( DIABETES IN MIGRANT INDIANS)
  • 35. OBSITY :(PIMA INDIANS NAURANS)PHYSICAL INACTIVITYLONGIVITY :(DIABETES PREVALENCEINCREASESWITH AGE E .G . PREVALENCERATE > 30 % IN ELDERLY IN
  • 36. Two genes have been implicated so far : NIDDM 1and NIDDM2MODY (Autosomal Dominant )-MODY 1, (HNF-4) extremely uncommon)-MODY 2, (Glucokinase gene-impairs B-cell glucosesensing)-MODY 3, ( Hepatocyte Nuclear factor 1- ( HNF-1) aremore commonMaternally inherited diabetes with deafness ( MIDD)Late onset IDDM
  • 37. SYNDROME CLINICAL FEATURESProgressive conedystrophy Colour blindness Liver disease Deafiness Mental etardationTurner,s  45,xo kayotype Short stature Gonadal dysgenesisThalassaemia  Iron overlandTable 22.5
  • 38. SYNDROMESYNDROME CLINICALCLINICALFEATURESFEATURESAlstrom• Retinitis pigmentosa• Deafness• ObesityLaurence-Moon-Biedl• Retinits pigmentosa• Obesity• Polydactyly• HypogonnadismPseudo-Refsum• Retinitis pigmentosa• AtaxiaGenetic syndromes associated with an early onset NIDDM
  • 39. SYNDROMESYNDROME CLINICALCLINICALFEATURESFEATURESWerner’s  Premature senility CataractsPrader-Willi Obesity Short stature Mental retardation Micropenis
  • 40. TYPE II CONTD . . . THE CLINICALPRESENTATION VARIESGREATLY:I . THEY MAY MANIFEST DM AFTER THDEVELOPMENT OF COMPLICTIONS ( E.G.RETIOPATHY ) .II . MAY HAVE SIGNIFICANT POLYRIA ,POLYDIPSIA ,EASY FATIGUABILITY ETIII . MAY BE FOUND BY CHANCE ON ROUTIN
  • 41. MILDTO AMRKED OBES IS PRESENT IN80% TYPE II AT THE TIME OF DIAGNOSIS .OBESITY IS A MAJOR RISK FACTORRROBABLY DUE TO THE DECREASEINSULIN RECEPTOR DENSITY ANDABNORMAL COUPLING OF RECEPTOR TOMETABOLIC PROCESS THAT OCCUR INTHE OBESE STATETYPE II CONTD. . .
  • 42. MOSTPATIENTS ARE DIAGNOSEDAFTERTHE AGE OF 40 YEARSOLD NAME - MANTURIY ONSETD.M .
  • 43. A GTT IS DOME FOR THOSE IN THEIMPAIRED TOLERANCE RANGECOMMON CAUSES OF TRANSIENTCARBOHYDRTE INTOLERANCES :PHYSICAL OR EMOTIONALSTRESSINFECTIONUNDER NUTRITIONBED REST
  • 44. NONOREGNANTADULITS
  • 45. PLASMA OTHERCRITERIAGLUCOSE ( mg/dI)RANDOM > 200 CLASSICSIGNS ANDSYMPTOMSORFASTING >126 ON ATLEST 2 OCCASIONSORFASTING < 126 SUSTAINEDELEVATED LASMA
  • 46. OGTT SAMPLE PLASMA GLUCOSEVALUES (mg/dI)FASTING < 1262 HOUR 126- 199INTERVENING >200*NONPREGANTDx OF IMPAIRED GLUCOSETOLERANCE IN ADULTS*
  • 47. WHODIABETICDIABETIC IMPAIRED GTIMPAIRED GTASTINGASTING >> 8 MMOL8 MMOL// LLHRSHRS >>11 MMOL11 MMOL // LL6- 8 MMOL / L6- 8 MMOL / L8 – 11 MMOL / L8 – 11 MMOL / L
  • 48. Diabetes mellitus in olderadults is the commonestmetabolic disorder inmainstream clinical practiceThe disorder present aninterplay between metabolicdysfunction, vasculopathyand the ageing processKey Points
  • 49. cardinal features withenable clinicians to focusdiabetes risk associated withfunctional decline, visualcognitive disorderdepression, and vulnerabilityto hypoglycemia
  • 50. Interventions based on bothvascular and rehabilitationmodels complement themetabolic approach torestructuring diabetes carefor elderly
  • 51. Diabetes is suspectedMeasure FPG or RPGIf FPG >7.8 orRPG > 11.1If FPG 5.5-7.7 orRPG 7.8-11.0If FPG < 5.5orRPG< 7.8Perform OGTT ( 75g)If FPG >7.8and/or2hPG > 11.1If FPG <7.8 and2hPG 7.8-11.0If FPG <7.8 and2hPG< 7.8Normal Impaired glucosetoleranceDiabetes
  • 52. 20181614121086420Fasting 0.5 1.0 1.5 2.0DiabeticImpairedglucose toleranceNormalTime after oral glucose ( hours)Plasmaglucose(mmol/litre)Examples of the oral glucosetolerance test curve
  • 53. GLUCOSE INTOLERANCE DEVELOPSDURING PREGNANCYOCCURS IN 2% OF PRENGNANTWOMENONSET USUALLY IN 2nd OR 3rdTRIMESTERINCREASED FEATAL SIZE ANDMORBIDITYGTT USUALLY RETURNS TO NORMAL
  • 54. Dx TESTINDICATEDCRIERION FOR POSITIVE SCREEN1HOUR PLASMA GLUCOSE > 140 mg / dIIf POSITIVESCREEN
  • 55. 1.DISEASES PRODUCING ANTI –INSULIN HOSRMONES.PHAEOCHROMOCYTOMACUSHING ‘SACHROMEGALYGLUCAGONOMATHROTOXICOSIS
  • 56. 2. DRUGSTHIAZIDE DIURETICSFRUSOMIDE ( LASIX )STEROIDSTHYROID HORMONESORAL CONTRACETIVES
  • 57. COMPLICATIONS OF MANAGEMENT-HYPOGLYCAEMIA-KETOACIDOSIS-LACTICACIDOSISOTHER COMPLICATIONS-INFECTIONS-SOCIAL ETCTREATEMENT-DIET-ORAL HYPOGLYCAEMICS-INSULIN
  • 58. 3.ASSOCIATED WITH MANY OTHER DISEASEG . MUSLAR DYSTROPHIESDOWN ‘SKLEINFELTER’STURNER ‘SFREDERICK’ S ATAXIAGLYCOGEN STORAGE DISEASE
  • 59. CLINICALFEATURESTYPE IJUVENILE ONSTTYPE IIMATURITYONSETKETOSISOBESITYONSETUSUALUNCOMMONACUTE OR SUBACUTERAREFREOUENTOFTEN INSIDOUSEPIDEMIOLOGYINCIDENCEAGE ATONSETPATHOLOGYISLETMASSBETACELLMAPEAK AGE 12 - 14MOSTLY < 40 YRS< 10 %< 10 %FREQUENTRISES UNTIL 8THDECADEMOSTLY > 40 YRSMODERATE RED.MODERATE RED.
  • 60. IMMUNOLOGYANTIPANCRETICCELL MEDIATEDIMMUNITYANTIPANCREATICCELL HUMORALIMMUNITY35– 50 % ATONSET60 – 85 %< 5 %APPROX . 5 %GENETICSCONCRODANCEWITHIDENTICAL TWITNSASSOCIATED EITHHLA< 50 %PRESENTMOSTLY INVARPRESENT
  • 61. THE PRESENCE OF COMMONLYASSOCIATAED CONDITIONSSHOULDBE EVALUATED EG:-•OBESITY• HYPERTENSION• HYPERLIPIDAEMIA• MACROVASCULARDISEASE
  • 62. AT DIAGNOSIS , A COMPLETEHISTORY AND PHYSICALEXAMINATION ARE ANDATORY ASMACROVASCLUAR ISEASE , ANDSOMETIONS MICROVASCULARCOMPLICATIONS ARE RESENTAT DIAGNSIS OF NIDDM
  • 63. HETEROGENEOUS DISORDERCHARACTERIZED BY :DEFICIENT INSULINSECRETION INSULIN RESISTANCE
  • 64. •* Mature onset diabetes of theyoung is inherited in anautsomal dominant manner andassociated with 8 celldysfunction.* Environmental factorsimportant for NIDDM includephysical inactivity, excessiveconsumption of food leading toobesity stress and some drugs
  • 65. •* Non-insulin dependentdiabetes mellitus ( NIDDM ) is aheterogeneous disease in whicha number of genetic andenvironmental factors interact tocause diabetes•* Maternally inhented diabetesand deafness is a distinctPractice points
  • 66. Fasting plasma glucose(mM(4 6 8 10 12060801004020MeanpiasmainsulinresponseguringOGTT(U/ml(Relationship between fasting glucose and insulin secretion
  • 67. HETEROGENEOUS DISORDERCHARACTERIZED BY : DEFICIENT INSULINSECRETIONINSULIN RESISTANCE
  • 68. 10090807060504030201000 1 2 3 4 5 6 7 8 9 101 marker2 markers>3 markersFollow – up(years(IDDM-freesurvival(%(