糖尿病基礎(chǔ)知識英文課件

DiabetesMellitusDr.RashaSalamaPhDPublicHealth,SuezCanalUniversity,EgyptDiabetesMSc,CardiffUniversity,UnitedKingdomDiabetesMellitusDr.RashaSalDiabetesmellitus(DM)isagroupofdiseasescharacterizedbyhighlevelsofbloodglucoseresultingfromdefectsininsulinproduction,insulinaction,orboth.Thetermdiabetesmellitusdescribesametabolicdisorderofmultipleaetiologycharacterizedbychronichyperglycaemiawithdisturbancesofcarbohydrate,fatandproteinmetabolismresultingfromdefectsininsulinsecretion,insulinaction,orboth.Theeffectsofdiabetesmellitusincludelong–termdamage,dysfunctionandfailureofvariousorgans.Whatisdiabetes?

Diabetesmellitus(DM)isagrDiabetesmellitusmaypresentwithcharacteristicsymptomssuchasthirst,polyuria,blurringofvision,andweightloss.Initsmostsevereforms,ketoacidosisoranon–ketotichyperosmolarstatemaydevelopandleadtostupor,comaand,inabsenceofeffectivetreatment,death.Oftensymptomsarenotsevere,ormaybeabsent,andconsequentlyhyperglycaemiasufficienttocausepathologicalandfunctionalchangesmaybepresentforalongtimebeforethediagnosisismade.DiabetesDiabetesmellitusmaypresentThelong–termeffectsofdiabetesmellitusincludeprogressivedevelopmentofthespecificcomplicationsofretinopathywithpotentialblindness,nephropathythatmayleadtorenalfailure,and/orneuropathywithriskoffootulcers,amputation,Charcotjoints,andfeaturesofautonomicdysfunction,includingsexualdysfunction.Peoplewithdiabetesareatincreasedriskofcardiovascular,peripheralvascularandcerebrovasculardisease.DiabetesLong-termEffectsThelong–termeffectsofdiabeThedevelopmentofdiabetesisprojectedtoreachpandemicproportionsoverthenext10-20years.InternationalDiabetesFederation(IDF)dataindicatethatbytheyear2025,thenumberofpeopleaffectedwillreach333million–90%ofthesepeoplewillhaveType2diabetes.InmostWesternsocieties,theoverallprevalencehasreached4-6%,andisashighas10-12%among60-70-year-oldpeople.Theannualhealthcostscausedbydiabetesanditscomplicationsaccountforaround6-12%ofallhealth-careexpenditure.BurdenofDiabetesThedevelopmentofdiabetesisType1DiabetesMellitusType2DiabetesMellitusGestationalDiabetesOthertypes:LADA(MODY(maturity-onsetdiabetesofyouth)SecondaryDiabetesMellitusTypesofDiabetes

Type1DiabetesMellitusTypesWaspreviouslycalledinsulin-dependentdiabetesmellitus(IDDM)orjuvenile-onsetdiabetes.Type1diabetesdevelopswhenthebody’simmunesystemdestroyspancreaticbetacells,theonlycellsinthebodythatmakethehormoneinsulinthatregulatesbloodglucose.Thisformofdiabetesusuallystrikeschildrenandyoungadults,althoughdiseaseonsetcanoccuratanyage.Type1diabetesmayaccountfor5%to10%ofalldiagnosedcasesofdiabetes.Riskfactorsfortype1diabetesmayincludeautoimmune,genetic,andenvironmentalfactors.Type1diabetesWaspreviouslycalledinsulin-Waspreviouslycallednon-insulin-dependentdiabetesmellitus(NIDDM)oradult-onsetdiabetes.Type2diabetesmayaccountforabout90%to95%ofalldiagnosedcasesofdiabetes.Itusuallybeginsasinsulinresistance,adisorderinwhichthecellsdonotuseinsulinproperly.Astheneedforinsulinrises,thepancreasgraduallylosesitsabilitytoproduceinsulin.Type2diabetesisassociatedwitholderage,obesity,familyhistoryofdiabetes,historyofgestationaldiabetes,impairedglucosemetabolism,physicalinactivity,andrace/ethnicity.AfricanAmericans,Hispanic/LatinoAmericans,AmericanIndians,andsomeAsianAmericansandNativeHawaiiansorOtherPacificIslandersareatparticularlyhighriskfortype2diabetes.Type2diabetesisincreasinglybeingdiagnosedinchildrenandadolescents.Type2diabetesWaspreviouslycallednon-insu糖尿病基礎(chǔ)知識英文課件糖尿病基礎(chǔ)知識英文課件Aformofglucoseintolerancethatisdiagnosedinsomewomenduringpregnancy.GestationaldiabetesoccursmorefrequentlyamongAfricanAmericans,Hispanic/LatinoAmericans,andAmericanIndians.Itisalsomorecommonamongobesewomenandwomenwithafamilyhistoryofdiabetes.Duringpregnancy,gestationaldiabetesrequirestreatmenttonormalizematernalbloodglucoselevelstoavoidcomplicationsintheinfant.Afterpregnancy,5%to10%ofwomenwithgestationaldiabetesarefoundtohavetype2diabetes.Womenwhohavehadgestationaldiabeteshavea20%to50%chanceofdevelopingdiabetesinthenext5-10years.GestationaldiabetesAformofglucoseintoleranceOtherspecifictypesofdiabetesresultfromspecificgeneticconditions(suchasmaturity-onsetdiabetesofyouth),surgery,drugs,malnutrition,infections,andotherillnesses.Suchtypesofdiabetesmayaccountfor1%to5%ofalldiagnosedcasesofdiabetes.OthertypesofDMOtherspecifictypesofdiabetLatentAutoimmuneDiabetesinAdults(LADA)isaformofautoimmune(type

1diabetes)whichisdiagnosedinindividualswhoareolderthantheusualageofonsetoftype1diabetes.Alternatetermsthathavebeenusedfor"LADA"includeLate-onsetAutoimmuneDiabetesofAdulthood,"SlowOnsetType1"diabetes,andsometimesalso"Type1.5Often,patientswithLADAaremistakenlythoughttohavetype

2diabetes,basedontheirageatthetimeofdiagnosis.LADALatentAutoimmuneDiabetesinLADA(cont.)LADA(cont.)About80%ofadultsapparentlywithrecentlydiagnosedType2diabetesbutwithGADauto-antibodies(i.e.LADA)progresstoinsulinrequirementwithin6years.Thepotentialvalueofidentifyingthisgroupathighriskofprogressiontoinsulindependenceincludes:theavoidanceofusingmetformintreatmenttheearlyintroductionofinsulintherapyLADA(cont.)About80%ofadultsapparentlyMODY–MaturityOnsetDiabetesoftheYoungMODYisamonogenicformofdiabeteswithanautosomaldominantmodeofinheritance:Mutationsinanyoneofseveraltranscriptionfactorsorintheenzymeglucokinaseleadtoinsufficientinsulinreleasefrompancreatic?-cells,causingMODY.DifferentsubtypesofMODYareidentifiedbasedonthemutatedgene.Originally,diagnosisofMODYwasbasedonpresenceofnon-ketotichyperglycemiainadolescentsoryoungadultsinconjunctionwithafamilyhistoryofdiabetes.However,genetictestinghasshownthatMODYcanoccuratanyageandthatafamilyhistoryofdiabetesisnotalwaysobvious.MODYMODYMODY(cont.)MODY(cont.)WithinMODY,thedifferentsubtypescanessentiallybedividedinto2distinctgroups:glucokinaseMODYandtranscriptionfactorMODY,distinguishedbycharacteristicphenotypicfeaturesandpatternonoralglucosetolerancetesting.GlucokinaseMODYrequiresnotreatment,whiletranscriptionfactorMODY(i.e.Hepatocytenuclearfactor-1alpha)requireslow-dosesulfonylureatherapyandPNDM(causedbyKir6.2mutation)requireshigh-dosesulfonylureatherapy.MODY(cont.)WithinMODY,thedifferentsubSecondarycausesofDiabetesmellitusinclude:Acromegaly,Cushingsyndrome,Thyrotoxicosis,PheochromocytomaChronicpancreatitis,CancerDruginducedhyperglycemia:AtypicalAntipsychotics-Alterreceptorbindingcharacteristics,leadingtoincreasedinsulinresistance.Beta-blockers-Inhibitinsulinsecretion.CalciumChannelBlockers-Inhibitssecretionofinsulinbyinterferingwithcytosoliccalciumrelease.Corticosteroids-Causeperipheralinsulinresistanceandgluconeogensis.Fluoroquinolones-InhibitsinsulinsecretionbyblockingATPsensitivepotassiumchannels.Naicin-Theycauseincreasedinsulinresistanceduetoincreasedfreefattyacidmobilization.Phenothiazines-Inhibitinsulinsecretion.ProteaseInhibitors-Inhibittheconversionofproinsulintoinsulin.ThiazideDiuretics-Inhibitinsulinsecretionduetohypokalemia.Theyalsocauseincreasedinsulinresistanceduetoincreasedfreefattyacidmobilization.SecondaryDMSecondarycausesofDiabetesmPrediabetesisatermusedtodistinguishpeoplewhoareatincreasedriskofdevelopingdiabetes.Peoplewithprediabeteshaveimpairedfastingglucose(IFG)orimpairedglucosetolerance(IGT).SomepeoplemayhavebothIFGandIGT.IFGisaconditioninwhichthefastingbloodsugarleveliselevated(100to125milligramsperdecilitreormg/dL)afteranovernightfastbutisnothighenoughtobeclassifiedasdiabetes.IGTisaconditioninwhichthebloodsugarleveliselevated(140to199mg/dLaftera2-houroralglucosetolerancetest),butisnothighenoughtobeclassifiedasdiabetes.Prediabetes:Impairedglucosetoleranceandimpairedfastingglucose

PrediabetesisatermusedtoProgressiontodiabetesamongthosewithprediabetesisnotinevitable.Studiessuggestthatweightlossandincreasedphysicalactivityamongpeoplewithprediabetespreventordelaydiabetesandmayreturnbloodglucoselevelstonormal.Peoplewithprediabetesarealreadyatincreasedriskforotheradversehealthoutcomessuchasheartdiseaseandstroke.Prediabetes:Impairedglucosetoleranceandimpairedfastingglucose(cont.)ProgressiontodiabetesamongDiagnosisofDiabetesMellitusDiagnosisofDiabetesMellitusValuesofDiagnosisofDiabetesMellitusValuesofDiagnosisofDiabeteResearchstudieshavefoundthatlifestylechangescanpreventordelaytheonsetoftype2diabetesamonghigh-riskadults.ThesestudiesincludedpeoplewithIGTandotherhigh-riskcharacteristicsfordevelopingdiabetes.Lifestyleinterventionsincludeddietandmoderate-intensityphysicalactivity(suchaswalkingfor21/2hourseachweek).IntheDiabetesPreventionProgram,alargepreventionstudyofpeopleathighriskfordiabetes,thedevelopmentofdiabeteswasreduced58%over3years.Preventionordelayofdiabetes:

Lifestylemodification

ResearchstudieshavefoundthStudieshaveshownthatmedicationshavebeensuccessfulinpreventingdiabetesinsomepopulationgroups.IntheDiabetesPreventionProgram,peopletreatedwiththedrugmetforminreducedtheirriskofdevelopingdiabetesby31%over3years.Treatmentwithmetforminwasmosteffectiveamongyounger,heavierpeople(those25-40yearsofagewhowere50to80poundsoverweight)andlesseffectiveamongolderpeopleandpeoplewhowerenotasoverweight.Similarly,intheSTOP-NIDDMTrial,treatmentofpeoplewithIGTwiththedrugacarbosereducedtheriskofdevelopingdiabetesby25%over3years.Othermedicationstudiesareongoing.InadditiontopreventingprogressionfromIGTtodiabetes,bothlifestylechangesandmedicationhavealsobeenshowntoincreasetheprobabilityofrevertingfromIGTtonormalglucosetolerance.Preventionordelayofdiabetes:MedicationsStudieshaveshownthatmedicaManagementofDiabetesMellitusManagementofDiabetesMellituThemajorcomponentsofthetreatmentofdiabetesare:ManagementofDMADietandExerciseBOralhypoglycaemictherapyCInsulinTherapyThemajorcomponentsofthetrDietisabasicpartofmanagementineverycase.Treatmentcannotbeeffectiveunlessadequateattentionisgiventoensuringappropriatenutrition.Dietarytreatmentshouldaimat:ensuringweightcontrolprovidingnutritionalrequirementsallowinggoodglycaemiccontrolwithbloodglucoselevelsasclosetonormalaspossiblecorrectinganyassociatedbloodlipidabnormalitiesA.DietDietisabasicpartofmanageThefollowingprinciplesarerecommendedasdietaryguidelinesforpeoplewithdiabetes:Dietaryfatshouldprovide25-35%oftotalintakeofcaloriesbutsaturatedfatintakeshouldnotexceed10%oftotalenergy.Cholesterolconsumptionshouldberestrictedandlimitedto300mgorlessdaily.Proteinintakecanrangebetween10-15%totalenergy(0.8-1g/kgofdesirablebodyweight).Requirementsincreaseforchildrenandduringpregnancy.Proteinshouldbederivedfrombothanimalandvegetablesources.Carbohydratesprovide50-60%oftotalcaloriccontentofthediet.Carbohydratesshouldbecomplexandhighinfibre.Excessivesaltintakeistobeavoided.Itshouldbeparticularlyrestrictedinpeoplewithhypertensionandthosewithnephropathy.A.Diet(cont.)ThefollowingprinciplesarerPhysicalactivitypromotesweightreductionandimprovesinsulinsensitivity,thusloweringbloodglucoselevels.Togetherwithdietarytreatment,aprogrammeofregularphysicalactivityandexerciseshouldbeconsideredforeachperson.Suchaprogrammemustbetailoredtotheindividual’shealthstatusandfitness.Peopleshould,however,beeducatedaboutthepotentialriskofhypoglycaemiaandhowtoavoidit.ExercisePhysicalactivitypromotesweiTherearecurrentlyfourclassesoforalanti-diabeticagents:i.Biguanidesii.InsulinSecretagogues–Sulphonylureasiii.InsulinSecretagogues–Non-sulphonylureasiv.α-glucosidaseinhibitorsv.Thiazolidinediones(TZDs)B.OralAnti-DiabeticAgents

TherearecurrentlyfourclassIfglycaemiccontrolisnotachieved(HbA1c>6.5%and/or;FPG>7.0mmol/Lor;RPG>11.0mmol/L)withlifestylemodificationwithin1–3months,ORALANTI-DIABETICAGENTshouldbeinitiated.Inthepresenceofmarkedhyperglycaemiainnewlydiagnosedsymptomatictype2diabetes(HbA1c>8%,FPG>11.1mmol/L,orRPG>14mmol/L),oralanti-diabeticagentscanbeconsideredattheoutsettogetherwithlifestylemodification.B.1OralAgentMonotherapy

B.1OralAgentMonotherapy

Asfirstlinetherapy:Obesetype2patients,consideruseofmetformin,acarboseorTZD.Non-obesetype2patients,considertheuseofmetforminorinsulinsecretagoguesMetforministhedrugofchoiceinoverweight/obesepatients.TZDsandacarboseareacceptablealternativesinthosewhoareintoleranttometformin.Ifmonotherapyfails,acombinationofTZDs,acarboseandmetforminisrecommended.Iftargetsarestillnotachieved,insulinsecretagoguesmaybeaddedB.1OralAgentMonotherapy(cont.)Asfirstlinetherapy:B.1OralCombinationoralagentsisindicatedin:NewlydiagnosedsymptomaticpatientswithHbA1c>10Patientswhoarenotreachingtargetsafter3monthsonmonotherapyB.2CombinationOralAgents

CombinationoralagentsisindIftargetshavenotbeenreachedafteroptimaldoseofcombinationtherapyfor3months,consideraddingintermediate-acting/long-actinginsulin(BIDS).Combinationofinsulin+oralanti-diabeticagents(BIDS)hasbeenshowntoimproveglycaemiccontrolinthosenotachievingtargetdespitemaximalcombinationoralanti-diabeticagents.Combininginsulinandthefollowingoralanti-diabeticagentshasbeenshowntobeeffectiveinpeoplewithtype2diabetes:Biguanide(metformin)Insulinsecretagogues(sulphonylureas)Insulinsensitizers(TZDs)(thecombinationofaTZDplusinsulinisnotanapprovedindication)α-glucosidaseinhibitor(acarbose)InsulindosecanbeincreaseduntiltargetFPGisachieved.B.3CombinationOralAgentsandInsulin

IftargetshavenotbeenreachDiabetesManagementAlgorithm糖尿病基礎(chǔ)知識英文課件OralHypoglycaemicMedicationsOralHypoglycaemicMedicationsInelderlynon-obesepatients,shortactinginsulinsecretagoguescanbestartedbutlongactingSulphonylureasaretobeavoided.Renalfunctionshouldbemonitored.Oralanti-diabeticagentsarenotrecommendedfordiabetesinpregnancyOralanti-diabeticagentsareusuallynotthefirstlinetherapyindiabetesdiagnosedduringstress,suchasinfections.InsulintherapyisrecommendedforboththeaboveTargetsforcontrolareapplicableforallagegroups.However,inpatientswithco-morbidities,targetsareindividualizedWhenindicated,startwithaminimaldoseoforalanti-diabeticagent,whilereemphasizingdietandphysicalactivity.Anappropriatedurationoftime(2-16weeksdependingonagentsused)betweenincrementsshouldbegiventoallowachievementofsteadystatebloodglucosecontrolGeneralGuidelinesforUseofOralAnti-DiabeticAgentinDiabetes

Inelderlynon-obesepatients,Short-termuse:Acuteillness,surgery,stressandemergenciesPregnancyBreast-feedingInsulinmaybeusedasinitialtherapyintype2diabetesinmarkedhyperglycaemiaSeveremetabolicdecompensation(diabeticketoacidosis,hyperosmolarnonketoticcoma,lacticacidosis,severehypertriglyceridaemia)Long-termuse:IftargetshavenotbeenreachedafteroptimaldoseofcombinationtherapyorBIDS,considerchangetomulti-doseinsulintherapy.Wheninitiatingthis,insulinsecretagoguesshouldbestoppedandinsulinsensitiserse.g.MetforminorTZDs,canbecontinued.C.InsulinTherapy

Short-termuse:C.InsulinTherThemajorityofpatientswillrequiremorethanonedailyinjectionifgoodglycaemiccontrolistobeachieved.However,aonce-dailyinjectionofanintermediateactingpreparationmaybeeffectivelyusedinsomepatients.Twice-dailymixturesofshort-andintermediate-actinginsulinisacommonlyusedregimen.

Insomecases,amixtureofshort-andintermediate-actinginsulinmaybegiveninthemorning.Furtherdosesofshort-actinginsulinaregivenbeforelunchandtheeveningmealandaneveningdoseofintermediate-actinginsulinisgivenatbedtime.Otherregimensbasedonthesameprinciplesmaybeused.Aregimenofmultipleinjectionsofshort-actinginsulinbeforethemainmeals,withanappropriatedoseofanintermediate-actinginsulingivenatbedtime,maybeused,particularlywhenstrictglycaemiccontrolismandatory.Insulinregimens

ThemajorityofpatientswillOverviewofInsulinandActionOverviewofInsulinandAction糖尿病基礎(chǔ)知識英文課件Patientsshouldbeeducatedtopracticeself-care.Thisallowsthepatienttoassumeresponsibilityandcontrolofhis/herowndiabetesmanagement.Self-careshouldinclude:BloodglucosemonitoringBodyweightmonitoringFoot-carePersonalhygieneHealthylifestyle/dietorphysicalactivityIdentifytargetsforcontrolStoppingsmokingSelf-Care

PatientsshouldbeeducatedtoNationalDiabetesFactSheet2003,DEPARTMENTOFHEALTHANDHUMANSERVICESCentresforDiseaseControlandPreventionWorldHealthOrganization.Definition,DiagnosisandClassificationofDiabetesMellitusanditsComplications.ReportofWHO.DepartmentofNon-communicableDiseaseSurveillance.Geneva1999AcademyofMedicine.ClinicalPracticeGuidelines.Managementoftype2diabetesmellitus.MOH/P/PAK/87.04(GU),2004NHS.Diabetes-insulininitiation-UniversityHospitalsofLeicesterNHSTrustWorkinginpartnershipwithPCTsacrossLeicestershireandRutland,May2008.ReferencesNationalDiabetesFactSheet2

ThankYou

ThankYouDiabetesMellitusDr.RashaSalamaPhDPublicHealth,SuezCanalUniversity,EgyptDiabetesMSc,CardiffUniversity,UnitedKingdomDiabetesMellitusDr.RashaSalDiabetesmellitus(DM)isagroupofdiseasescharacterizedbyhighlevelsofbloodglucoseresultingfromdefectsininsulinproduction,insulinaction,orboth.Thetermdiabetesmellitusdescribesametabolicdisorderofmultipleaetiologycharacterizedbychronichyperglycaemiawithdisturbancesofcarbohydrate,fatandproteinmetabolismresultingfromdefectsininsulinsecretion,insulinaction,orboth.Theeffectsofdiabetesmellitusincludelong–termdamage,dysfunctionandfailureofvariousorgans.Whatisdiabetes?

Diabetesmellitus(DM)isagrDiabetesmellitusmaypresentwithcharacteristicsymptomssuchasthirst,polyuria,blurringofvision,andweightloss.Initsmostsevereforms,ketoacidosisoranon–ketotichyperosmolarstatemaydevelopandleadtostupor,comaand,inabsenceofeffectivetreatment,death.Oftensymptomsarenotsevere,ormaybeabsent,andconsequentlyhyperglycaemiasufficienttocausepathologicalandfunctionalchangesmaybepresentforalongtimebeforethediagnosisismade.DiabetesDiabetesmellitusmaypresentThelong–termeffectsofdiabetesmellitusincludeprogressivedevelopmentofthespecificcomplicationsofretinopathywithpotentialblindness,nephropathythatmayleadtorenalfailure,and/orneuropathywithriskoffootulcers,amputation,Charcotjoints,andfeaturesofautonomicdysfunction,includingsexualdysfunction.Peoplewithdiabetesareatincreasedriskofcardiovascular,peripheralvascularandcerebrovasculardisease.DiabetesLong-termEffectsThelong–termeffectsofdiabeThedevelopmentofdiabetesisprojectedtoreachpandemicproportionsoverthenext10-20years.InternationalDiabetesFederation(IDF)dataindicatethatbytheyear2025,thenumberofpeopleaffectedwillreach333million–90%ofthesepeoplewillhaveType2diabetes.InmostWesternsocieties,theoverallprevalencehasreached4-6%,andisashighas10-12%among60-70-year-oldpeople.Theannualhealthcostscausedbydiabetesanditscomplicationsaccountforaround6-12%ofallhealth-careexpenditure.BurdenofDiabetesThedevelopmentofdiabetesisType1DiabetesMellitusType2DiabetesMellitusGestationalDiabetesOthertypes:LADA(MODY(maturity-onsetdiabetesofyouth)SecondaryDiabetesMellitusTypesofDiabetes

Type1DiabetesMellitusTypesWaspreviouslycalledinsulin-dependentdiabetesmellitus(IDDM)orjuvenile-onsetdiabetes.Type1diabetesdevelopswhenthebody’simmunesystemdestroyspancreaticbetacells,theonlycellsinthebodythatmakethehormoneinsulinthatregulatesbloodglucose.Thisformofdiabetesusuallystrikeschildrenandyoungadults,althoughdiseaseonsetcanoccuratanyage.Type1diabetesmayaccountfor5%to10%ofalldiagnosedcasesofdiabetes.Riskfactorsfortype1diabetesmayincludeautoimmune,genetic,andenvironmentalfactors.Type1diabetesWaspreviouslycalledinsulin-Waspreviouslycallednon-insulin-dependentdiabetesmellitus(NIDDM)oradult-onsetdiabetes.Type2diabetesmayaccountforabout90%to95%ofalldiagnosedcasesofdiabetes.Itusuallybeginsasinsulinresistance,adisorderinwhichthecellsdonotuseinsulinproperly.Astheneedforinsulinrises,thepancreasgraduallylosesitsabilitytoproduceinsulin.Type2diabetesisassociatedwitholderage,obesity,familyhistoryofdiabetes,historyofgestationaldiabetes,impairedglucosemetabolism,physicalinactivity,andrace/ethnicity.AfricanAmericans,Hispanic/LatinoAmericans,AmericanIndians,andsomeAsianAmericansandNativeHawaiiansorOtherPacificIslandersareatparticularlyhighriskfortype2diabetes.Type2diabetesisincreasinglybeingdiagnosedinchildrenandadolescents.Type2diabetesWaspreviouslycallednon-insu糖尿病基礎(chǔ)知識英文課件糖尿病基礎(chǔ)知識英文課件Aformofglucoseintolerancethatisdiagnosedinsomewomenduringpregnancy.GestationaldiabetesoccursmorefrequentlyamongAfricanAmericans,Hispanic/LatinoAmericans,andAmericanIndians.Itisalsomorecommonamongobesewomenandwomenwithafamilyhistoryofdiabetes.Duringpregnancy,gestationaldiabetesrequirestreatmenttonormalizematernalbloodglucoselevelstoavoidcomplicationsintheinfant.Afterpregnancy,5%to10%ofwomenwithgestationaldiabetesarefoundtohavetype2diabetes.Womenwhohavehadgestationaldiabeteshavea20%to50%chanceofdevelopingdiabetesinthenext5-10years.GestationaldiabetesAformofglucoseintoleranceOtherspecifictypesofdiabetesresultfromspecificgeneticconditions(suchasmaturity-onsetdiabetesofyouth),surgery,drugs,malnutrition,infections,andotherillnesses.Suchtypesofdiabetesmayaccountfor1%to5%ofalldiagnosedcasesofdiabetes.OthertypesofDMOtherspecifictypesofdiabetLatentAutoimmuneDiabetesinAdults(LADA)isaformofautoimmune(type

1diabetes)whichisdiagnosedinindividualswhoareolderthantheusualageofonsetoftype1diabetes.Alternatetermsthathavebeenusedfor"LADA"includeLate-onsetAutoimmuneDiabetesofAdulthood,"SlowOnsetType1"diabetes,andsometimesalso"Type1.5Often,patientswithLADAaremistakenlythoughttohavetype

2diabetes,basedontheirageatthetimeofdiagnosis.LADALatentAutoimmuneDiabetesinLADA(cont.)LADA(cont.)About80%ofadultsapparentlywithrecentlydiagnosedType2diabetesbutwithGADauto-antibodies(i.e.LADA)progresstoinsulinrequirementwithin6years.Thepotentialvalueofidentifyingthisgroupathighriskofprogressiontoinsulindependenceincludes:theavoidanceofusingmetformintreatmenttheearlyintroductionofinsulintherapyLADA(cont.)About80%ofadultsapparentlyMODY–MaturityOnsetDiabetesoftheYoungMODYisamonogenicformofdiabeteswithanautosomaldominantmodeofinheritance:Mutationsinanyoneofseveraltranscriptionfactorsorintheenzymeglucokinaseleadtoinsufficientinsulinreleasefrompancreatic?-cells,causingMODY.DifferentsubtypesofMODYareidentifiedbasedonthemutatedgene.Originally,diagnosisofMODYwasbasedonpresenceofnon-ketotichyperglycemiainadolescentsoryoungadultsinconjunctionwithafamilyhistoryofdiabetes.However,genetictestinghasshownthatMODYcanoccuratanyageandthatafamilyhistoryofdiabetesisnotalwaysobvious.MODYMODYMODY(cont.)MODY(cont.)WithinMODY,thedifferentsubtypescanessentiallybedividedinto2distinctgroups:glucokinaseMODYandtranscriptionfactorMODY,distinguishedbycharacteristicphenotypicfeaturesandpatternonoralglucosetolerancetesting.GlucokinaseMODYrequiresnotreatment,whiletranscriptionfactorMODY(i.e.Hepatocytenuclearfactor-1alpha)requireslow-dosesulfonylureatherapyandPNDM(causedbyKir6.2mutation)requireshigh-dosesulfonylureatherapy.MODY(cont.)WithinMODY,thedifferentsubSecondarycausesofDiabetesmellitusinclude:Acromegaly,Cushingsyndrome,Thyrotoxicosis,PheochromocytomaChronicpancreatitis,CancerDruginducedhyperglycemia:AtypicalAntipsychotics-Alterreceptorbindingcharacteristics,leadingtoincreasedinsulinresistance.Beta-blockers-Inhibitinsulinsecretion.CalciumChannelBlockers-Inhibitssecretionofinsulinbyinterferingwithcytosoliccalciumrelease.Corticosteroids-Causeperipheralinsulinresistanceandgluconeogensis.Fluoroquinolones-InhibitsinsulinsecretionbyblockingATPsensitivepotassiumchannels.Naicin-Theycauseincreasedinsulinresistanceduetoincreasedfreefattyacidmobilization.Phenothiazines-Inhibitinsulinsecretion.ProteaseInhibitors-Inhibittheconversionofproinsulintoinsulin.ThiazideDiuretics-Inhibitinsulinsecretionduetohypokalemia.Theyal