Diabetes Mellitus

DiabetesMellitusPhysiologyofEnergyMetabolismAllbodycellsuseglucoseforenergy.Tomaintainthisconstantsourceofenergy,bloodglucoselevelsmustbekeptbetween3.3-6.1mmol/L.Severalhormones,helptomaintainthislevelbetween3.3-6.1mmol/L,includeinsulin,glucagon.Theinsulinandtheglucagontogethermaintainaconstantlevelofglucoseinthebloodbystimulatingthereleaseofglucosefromtheliver.Theglucagonisreleasedwhenbloodglucoselevelsdecreased(e.g.betweenmealsandoverthenight)andstimulatethelivertoreleasestoredglucose.InsulinDiabetesisadiseasewhichdealswithinsulin.Ahealthypancreasreleases40-50unitsofinsulindaily,stillkeepingseveralhundredunitsavailableinstoragetobereleasedifthebloodglucoselevelsrise.Wheninsulinentersthebloodstream,itbindstoinsulinreceptorsonthemembranesoftheliver,muscle,andfatcells.Inthesecells,insulinencouragesglucoseuptakebycausingashiftofanotherinsulinsensitiveglucosetransporter,GLUT4,tothesurfaceofcells.PathophysiologyofDiabetesMellitusDiabetesmellitusisnotasinglediseasebutacomplexsyndromecharacterizedbyhyperglycemiaresultingfromalteredcarbohydrate,fat,andproteinmetabolism.Thisalteredmetabolismissecondarytoinsulininsufficiency,insufficientinsulinactivity,orboth.Becauseofthealteredfuelmetabolism,diabetesischaracterizedbyvascularandneurologicchangesthroughoutthebody.Absenceofinsulinorineffectiveinsulinactivitypreventsglucosefromenteringliver,muscleandfatcellsPathophysiologyofDiabetesMellitusAsthebloodglucoselevelapproaches10mmol/L,theabilityofthekidneytoreabsorbglucoseissurpassed,andglucoseisexcretedintotheurine.Becauseitisanosmoticdiuretic,glucosecausestheosmosisoflargeamountsofwaterandelectrolytesintothetubules,causingfrequenturinationinlargequantities(polyuria),notablyatnight(nocturia).Dehydration,hunger,andfatiguefollow.ClassicalmanifestationsofdiabetesPolyuria–increasedurinationPolydispia–increasedthirst,whichoccursasaresultofexcesslossoffluidassociatedwithosmoticdiuresis.Polyphagia–increasedappetitewhichresultsfromthecatabolicstateinducedbyinsulindeficiencyTypesofdiabetesTypeITypeIIGestationaldiabetesTypeIThisischaracterizedbythedestructionofthepancreaticbetacellsandearlyonsetThedestructionofthebetacellsresultsindecreasedinsulinproduction,uncheckedglucoseproductionbytheliverandfastinghyperglycemia.Glucosederivedfromfoodisnotstoredintheliverbutremainsinthebloodstreamandcontributestopostprandial(aftermeals)hyperglycemia.S&SIncreasedthirstFrequenturinationFatigueExcessiveweightlossNauseaandvomitingHavingdry,itchyskinFeelingofnumbnessandtinglinginthefeetBlurryeyesightConstanthungerAbdominalpainifDKA(DiabeticKetoacidosis)haveoccurredTypeIIThisthemostcommonformofdiabetes,oftenassociatedwitholderage,obesity,familyhistoryofdiabetese.t.c.Intype2diabetes,thepancreasisusuallyproducingenoughinsulin,butforunknownreasonsthebodycannotusetheinsulineffectively,aconditioncalledinsulinresistance.Afterseveralyears,insulinproductiondecreases.SothusglucosebuildsupinthebloodandthebodycannotmakeefficientuseofitsmainsourceoffuelThesepatientsarenotpronetothedevelopmentofDKA.S&SFatigueFrequenturinationIncreasedthirstandhungerBlurredvisionGestationaldiabetesGestationaldiabetesisatypeofdiabetesthatoccursinnon-diabeticwomenduringpregnancy.Itisanydegreeofglucoseintolerancewithitsonsetduringpregnancyorlateinpregnancy.Thisformofdiabetesusuallydisappearsafterthebirthofthebaby.RiskfactorsofgestationaldiabetesOvertheageof30ObesityFamilyhistoryofdiabetesHavingpreviouslygivenbirthtoaverylargechild(over9pounds,14ounces),havingpreviouslygivenbirthtoastillbornchildorachildwithabirthdefectHavingtoomuchamnioticfluidHavinggestationaldiabetesinapreviouspregnancyHavinghighbloodpressureS&SGenerally,gestationaldiabetesmaynotcauseanysymptoms;however,thewomanmayexperienceExcessiveweightgain,Excessivehungerorthirst,ExcessiveurinationRecurrentvaginalinfectionsDiagnosisofdiabetesDMisindicatedbytypicalS&Sandconfirmedbymeasurementofplasmaglucose.Fastingplasmaglucose(FPG):measurementafteran8-12hfast.Oralglucosetolerancetesting(OGTT):2hafteringestionofaconcentratedglucosesolution.OGTTismoresensitiveforDxDMandimpairedtolerancebutismoreexpansiveandlessconvenientandreproduciblethanFPG.Itisrarelyusedroutinely,exceptforDxofgestationalDM.HbA1c:testingforglycosylatedhemoglobin.HbA1clevelsreflectglucosecontroloverthepreceding2-3months.HbA1cisnotconsideredasreliableasFPGorOGTTtestingforDxDMandusedmainlyformonitoringDMcontrol.Diagnosisofdiabetes(con’t)DiagnosticcriteriaforDMandimpairedglucoseregulationTestNormalImpairedglucoseregulationDiabetesCBG3.3-6.1mmol/LFPG5.6mmol/L5.6-6.9mmol/L7.0mmol/LOGTT7.7mmol/L7.7-11.0mmol/L11.1mmol/LHbA1c3%-6%7%HbA1cGlucosestickstothehaemoglobintomakea‘glycosylatedhaemoglobin’molecule,calledhaemoglobinA1corHbA1c.Themoreglucoseintheblood,themorehaemoglobinA1corHbA1cwillbepresentintheblood.Redcellslive120daysbeforetheyarereplaced.BymeasuringtheHbA1Citcantellyouhowhighyourbloodglucosehasbeenonaverageoverthelast8-12weeks.Anormalnon-diabeticHbA1Cis3.5-5.5%.Indiabetesabout6.5%isgood.TheHbA1Cte