HannahChouinard

KNH411
CaseStudy#15Presentation
Type1DiabetesMellitusintheAdult
1. WhatarethedifferencesamongT1DM,T2DM,andLADA?
T1DMisthegradualdestructionofthecellsofthepancreascausedbyacellmediated
autoimmuneresponse.Individualsareinherentlymoresusceptibleprimarilydueto
polymorphismsintheHLAregiononchromosome6,whichaccountfor4050%ofthe
geneticriskofdevelopingT1DM(Nelms,481).ThosewithT1DMcharacteristically
haveabsoluteinsulindeficiencythatoftenresultsinketoacidosisandfasting
hyperglycemia.Duetothisdeficiency,insulinisusuallystartedimmediatelyafter
diagnosis.
T2DMisapolygenic(multiplefactor)conditioncausedbypreventableenvironmental
factorssuchaspoornutrition,physicalinactivity,andoverweight/obesity.UnlikeT1DM,
individualswithT2DMstillproduceinsulinbuttheirtissuesareinsulinresistantdueto
abnormalinsulinsecretionandinsulinresistance,sothepancreasincreasesproduction,
whichcannotbesustainedatsuchhighlevelsovertime(Nelms,483).
LADA(latentautoimmunediabetesinadults)isavariationoftype1DMthatslowly
progresses.LADAisoftenreferredtoastype1.5diabetes,becauseitscharacteristicsfall
betweenT1DMandT2DM.AlthoughLADAcanbeclassifiedasamoreslowly
progressingvariationofT1DM,itisoftenmisdiagnosedasT2DM(Gebel,2010).Those
withLADAshowpresenceofautoantibodiescomparabletothosewithT1DM,however
progressiontoinsulindependenceusuallyoccursovermonthsandyearsinsteadofwithin
days/weeksofdiagnosis.Thereisalsosomesignofinsulinresistancesimilartothose
withT2DM,andtypicalageofonsetoccursinadulthood.

2. Whatarethestandarddiagnosticcriteriaforeachofthesediagnoses?
T1DM:symptomsofpolyuria,polydipsia,andunexplainedweightlossaccompaniedby
presenceofautoantibodies,anA1Cgreaterthanorequalto6.5%bystandardized
laboratorymeasuresORfastingplasmaglucoseofgreaterthanorequalto126mg/dL
(7.0mmol/L)ORsymptomsofdiabetesplusrandomplasmaglucoseconcentration
greaterthanorequalto200mg/dL(11.1mmol/L)OR2hourpostprandialglucose
greaterthanorequalto200mg/dL(11.1mmol/L)duringanoralglucosetolerancetest
(OGTT)(Nelms,481).
T2DM:Proveninsulinresistancealongwithprevalenceofmultipleriskfactorsusually
determinesDiagnosticcriteria.ThosewithaBMIof25orhigherespeciallythosewith
centralbodyadiposityaremorelikelytodevelopT2DM.Laboratoryevaluations
showingdyslipidemia,abnormalmedicalhistoriesofCVD,CHD,PADorHTN,and
previousIGTorIFGallincreasethelikelihoodofT2DM.Otherfactorsincludefamily
historyofDM(includinggestational),impairedglucosemetabolism,physicalinactivity,
andpoornutrition.AlthoughweareseeingmorechildrenbeingaffectedbyT2DM,
prevalenceusuallyincreaseswithage,whichiswhyitisoftenreferredtoasadultonset
diabetes.Peopleofcolorarealsodisproportionatelyaffected,withthehighestincidence
of18.7%forallnonHispanicblacksage20orolder(Nelms,483).
LADA:PresenceofautoantibodiescomparabletothosewithT1DM,however
progressiontoinsulindependenceusuallyoccursovermonthsoryearsinsteadofwithin
days/weeksofdiagnosis.Thereisalsosomesignofinsulinresistancesimilartothose
withT2DM.Typicalageofonsetoccursinadulthood.
3. WhydoyouthinkhewasoriginallydiagnosedwithT2DM?WhydoestheMDnow
suspecthemayactuallyhaveT1DMorLADA?

Armandowasoriginallydiagnosedprobablyduetohisage.Adultonsetinmost

commoninT2DM,whilediagnosisinchildhoodismorecommonforT1DMpatients.
HismotheralsohadT2DM,whichincreaseshisriskofgettingT2DM.However,the
MDisnowabletodiagnoseArmandomoreaccuratelywithT1DMorLADAbecause
althoughitwaslateonsetoccurringinhisadulthood(characteristicofLADA),heis
fairlythinandhasahealthyBMI.MetforministypicallyproducedforT2DMpatients;
thereforehemaynothavebenefitingasmuchinusingit,resultinginaplethoraof
worsenedsymptomsfromhisinsulindeficiency.Thefactthatautoantibodieswere
presentinhisbloodlabresultsalsoindicatesT1DMorLADA.
4. DescribethemetaboliceventsthatledtoArmandossymptomsandsubsequent
admissiontotheER(polyuria,polydipsia,polyphagia,fatigue,andweightloss),
integratingthepathophysiologyofT1DMintoyourdiscussion.

Bythetimeclinicalsymptomsoccur,6080%ofBcellshavebeendestroyed.This
destructionofBcells,whichareresponsibleforinsulinproductioninthepancreas,
resultsinglucosenotbeingabletoenterthecells.Thiscausesplasmaglucoselevelsto
rise(hyperglycemia)andthestarvationofcellsbecausetheyarenotreceivingglucose
theprimarysourceofenergyforcells.Whencellsarenotproperlyfueledtheyresorttoa
stateofemergencyandpolyphagiaoccursinanattempttogetglucoseintothebody.
Signalsarealsosentthatincreasegluconeogenesisintheliverandstimulate
glycogenolysis,whichfurthersuppliestothehyperglycemicstate.Tocounteractthehigh
levelsofglucoseinthebloodstream,excessglucoseisdisposedofbytheurine
(glycosuria)andcausespolyuria.Becausesomuchfluidisbeinglostbyfrequent
urination,thethirstmechanismistriggeredwhichresultsinpolydipsiaandeventually
dehydration.Ketoacidosis,alongwithhypervolemiaandmusclecatabolism,causethe
unexplainedweightlossmanyDMpatientsstrugglewith,whichcanbeconfusingwith
theirincreasedcaloricconsumptionduetotheirpolyphagia.(Nelms,481482).
5. Describethemetaboliceventsthatresultinthesignsandsymptomsassociatedwith
DKA.WasArmandointhisstatewhenhewasadmitted?Whatprecipitatingfactors

mayleadtoDKA?
Diabeticketoacidosis,DKAischaracterizedbyincreasedketoneconcentrationwithinthe
bloodthatcausesanacidbaseimbalance.Thebodywillstarttoturntoalternative
sourcesofenergyandbreakdownfatstoresinadiposetissueasinsulindeficiency
persists.ThistransformsFFAintoketoacidsintheliver,whicharedisposedfromthe
bodyasketonebodieswithintheurine.Asthiscyclepersists,bicarbonateconcentration
intheblooddecreasesandketoacidosisoccurs.Symptomsofketoacidosisincludenausea
and/orvomiting,stomachpain,fruity(acetone)breath,heavy(Kussmaul)breathing,and
achangeinmentalstatus.Armandowasmostlikelyinthisstatewhenhewasadmitted.
Thisisindicatedbythefactthathewasfoundunconsciouspriortohisarrival.Metabolic
acidosisoccursfollowingketosis,whichifleftuntreatedcanresultinadiabeticcomaand
evendeath.(Nelms482,488).
6. ArmandowillbestartedonacombinationofNovologpriortomealsandsnacks
withglarginegiveninthea.m.andp.m.Describetheonset,peak,anddurationfor
eachofthesetypesofinsulin.

Novolog:
Type: rapidactinganalog
Onset: 515(minutes)
Peak: 3090(hours)
Duration:35(hours)
Note:canbeusedinpumptherapy
Glargine:(Lantus)
Type: extendedlongactinganalog
Onset: 24(hours)
Peak: none
Duration:2024(hours)

note:cannotbetakenwithotherinsulin
(Nelms,491)

7. Usinghiscurrentweightof165lbs,determinethedischargeofglargineaswellasan
appropriateICRforArmandotostartwith.

Dischargedoseofglargine=0.6units/kg(75kg)=45units.
ICR=500/45units=11.1gCHO/unitinsulin.(Nelms,491).
8. Intensiveinsulintherapyrequiresfrequentbloodglucoseselfmonitoring.Whatare
someofthebarrierstosuccessforpatientswhobeginthistypeoftherapy?Give
suggestionsonhowyoumightworkwithArmandotosupporthiscompliance.

ThetoptenbarriersforpatientsrequiringSMBGaccordingtoWilliamPolonskyinhis
bookDiabetesBurnoutareasfollows:
1.Theirmetermakesthemfeelbadaboutthemselves
2.Monitoringseemspointlessbecausetheyfeeltheirbloodglucoseresultsareoutof
theircontrol.
3.Checkingbloodglucoseremindsthemoftheirdiabetes.
4.Metermakesitseemliketheirlifeisoutofcontrol.
5.Servesasanopportunityforfriendsandfamilytobotherthem.
6.Thinkthathealthcareprovidersdontdoanythingwiththeresults.
7.Itispainful.
8.Itisinconvenient.
9.Itisexpensive.
10.Lifeistoobusyordemanding;lackoftime.
MayoClinicsuggestshelpingclientstoovercomethesepersonalbarriersbypointingout

toclientsthat:
Theirreadingsarenotmeanttobeasourceofjudgment;theyshouldbethought
ofasacheck,notatest.
Theirhealthcareproviderwillworkasateamwiththemandusetheirresultsin
ordertoevaluatetheeffectivenessoftheirdiabetescareplan.
Glucoselevelsarenotalwaysgoingtobewithinthetargetrange;thereforethey
shouldnotbediscouragedbyreadingsoutsideofthisrange.
Theirreadingswillbehowtheysuccessfullymanagetheirdiabetes.Itwill
allowadjustmentsoftheirdietplanandmedicationsthatwillhelpthemtomeet
theirbloodglucosegoals.
Davidson,N.,&Moreland,P.(2009,February10).Diabetes.RetrievedNovember19,
2015,fromhttp://www.mayoclinic.org/diseasesconditions/diabetes/expertblog/blood
glucose/bgp20056587
9. Armandotellsyouthatheisveryfrightenedofhavinghisbloodsugardroptoolow.
Whatishypoglycemia?Whatarethesymptoms?Whatinformationwouldyougive
Armandotomakesureheiswellpreparedtopreventortreathypoglycemia?

Hypoglycemiaiswhenbloodsugarlevelsareabnormallylow(sometimesreferredtoas
insulinreaction/shock).Symptomsofhypoglycemiamayinclude:anxiety,sweating,
irritability,confusion(includingdelirium),rapidheartbeat,hungerandnausea,fatigue,
headaches,moodswings,blurredorimpairedvision,tinglingandnumbnessofthelips
and/ortongue,andlackofcoordination.Severehypoglycemiacouldresultsinseizures
andunconsciousness(AmericanDiabeticAssociation,Hypoglycemia(LowBlood
Glucose).
Inordertopreventhyperglycemiafromoccurring,Armandoneedstobeinformedabout
whatcausesittohappen.Factorsthatwouldcauseahypoglycemicstatecouldbeexcess
orinappropriatetimingofmedications.Inthiscase,hecouldmakeadjustmentstothe

amountofthemedicationafterconsultingwithhisdoctor,and/ortrytocoordinatethe
timeshetakeshismedicinearoundmealtimesandphysicalactivity.Notenoughfood
and/orCHOcouldbeaproblem,soheshouldbeawareofconsumingappropriate
amountsofbothaswellastheappropriateamountofinsulinheshouldbetaking.Eating
mealsontimeorsnackingbetweenmealswillbeanotherusefultipinpreventinglow
bloodsugar.Anotherimportantfactorheshouldbeknowledgableaboutisdrugnutrient
interactionsthatspecificallyapplytothemedicationheistaking(Nelms,488).
10. ArmandosmotherhasT2DM.Sheiscurrentlyhavingproblemswithvisionand
burninginherfeet.Whatisshemostlikelyexperiencing?Describethe
pathophysiologyofthesecomplications.Youcantellthatheisworriednotonly
abouthismotherbutalsoabouthisownhealth.Explain,usingthefoundation
researchoftheDiabetesControlandComplicationsTrial(DCCT)aswellasany
otherpertinentresearchdata,howhecanpreventthesecomplications.
Armandosmothermaybesufferingfromadiabeticneuropathy;nervedamagethat
developsinDMpatientsafterprolongedexposertohighbloodglucoselevels.Sheis
mostlikelyfeelingtheburningsensationinherfeetfromperipheralneuropathy,whichis
themostcommontypeofdiabeticneuropathyandaffectsthetoes,feet,legs,hands,and
arms(NIDDK,DiabeticNeuropathies:TheNerveDamageofDiabetes).Accordingto
theDCCT,intensivetreatmentpreventedtheriskofnervedamageby60%(2008).
Hismotherisalsomostlikelysufferingfromdiabeticretinopathy.Accordingtothe
NationalEyeInstitute,diabeticeyediseasecanaffectvariouspartsoftheeyeincluding
theopticnerve,macula,retina,andlens.Diabeticretinopathyisthemostcommoncause
ofvisionproblem,characterizedbyaffectingtheretina.Studieshavefoundstrong
correlationsrelatedtochronichighbloodsugarofthosewithDM.Amongworkingage
adults,itistheleadingcauseofvisionimpairmentandblindness.Diabeticretinopathy
damagesbloodvesselsfoundwithintheretina,causingthemtoleakfluidorbleedwhich
causesthevisionimpairment.TheDCCTfoundthatintensivetherapyreducedtherisk
ofdiabeticeyediseaseby76%,andslowedtheprogressionby54%(2008).

FactsAboutDiabeticEyeDisease.(2015,September1).RetrievedNovember19,2015,
fromhttps://nei.nih.gov/health/diabetic/retinopathy
TheDCCTlistselementsofintensivemanagementas:
testingbloodglucoseatleast4x/day
injectionofinsulinatleast3x/daywithinsulinpump
adjustinginsulindosetofoodintakeandphysicalactivity
monthlyvisitstohealthcareteamcomposedofphysician,

nurse,educator,RD,andbehavioraltherapist

InformationClearinghouse(NDIC),DCCTandEDIC:TheDiabetesControl
ComplicationTrialandFollowupStudy).
11. OutlinethebasicprinciplesforArmandosnutritiontherapytoassistincontrolof
hisDM.
1.Attainindividualizedglycemic,bloodpressure,andlipidgoals.
2.Delayorpreventcomplicationsofdiabetes.
3.Toaddressindividualnutritionneeds.
4.Tomaintainthepleasureofeatingbyprovidingpositivemessagesaboutfoodchoices
whilelimitingfoodchoicesonlywhenindicatedbyscientificevidence.
5.Toprovidetheindividualwithdiabeteswithpracticaltoolsfordaytodaymeal
planningratherthanfocusingonindividualmacronutrients.
Evert,A.(2013,November1).NutritionTherapyRecommendationsfortheManagement
ofAdultsWithDiabetes.RetrievedNovember19,2015,from
http://www.professional.diabetes.org/admin/UserFiles/0Sean/dc132042FINAL.pdf?
utm_source=Offline&utm_medium=Print&utm_content=nutritionguidelines&utm_camp

aign=DP&s_src=vanity&s_subsrc=nutritionguidelines
12. AssessArmandosheightandweight.CalculatehisBMI.
a.)

ArmandohasaBMIof23,whichfallswithinthenormal/healthyrangeforhis

currentweightandheight.
Calculations:
Weight:
165lbs(75kg)
165/2.2=75
Height:
511(71inor1.8m)

BMI:
(wt.inkg)/(ht.inm)2

75/(1.8)2=23
13. Identifyanyabnormallaboratoryvaluesmeasureduponhisadministration.
ExplainhowtheymayberelatedtohisnewlydiagnosedDM.
Ref.Range

Armando7/1178

RelationtoDMDiagnosis

Chemistry
Sodium(mEq/L)

136145

130(low)

CO2(mEq/L)
Glucose(mg/dL)

2330
70110

31(borderline)
683(high!)

Phosphate,inorganic(mg/dL)
Osmolality(mmol/kg/H2O)

2.34.7
285295

2.1(low)
306(high)

Cholesterol(mg/dL)

120199

210(high)

Triglycerides(mg/dL)

40160M

175(high)

Totalbodywaterlossr/t
polyuria(frequenturination)
Mayindicateketoacidosis
Fastinghyperglycemiar/t
inabilitytoproduceinsulin
Waterlossr/tpolyuria
Highamountofchemicalsin
bloodserumr/twaterloss&
highbloodsugar;couldindicate
kidneydamageduetourea
buildupintheblood
r/tdietaryconsumptionor
familyhistory
Increasedbreakdownofadipose
tissueandreleaseofFFAinthe
bloodduetoincreased
hormonesr/tinsulindeficiency

A1C(%)

3.95.2

12.5(high!)

Cpeptide(ng/mL)

0.512.72

0.09(low)

ICA

GADA

IAA

Urinalysis
pH

57

4.9(borderlinelow)

Protein(mg/dL)

Neg

+1(high)

Glucose(mg/dL)

Neg

+3(high)

Ketones
Protchk

Neg
Neg

+4(high)
tr

ArterialBloodGases(ABGs)
pH
HCO3(mEq/L)

7.357.45
2428

7.31(borderlinelow)
22(low)

Averageglucoseconcentration
forprevious23monthsishigh
r/tprolongedhyperglycemia
(DMdiagnosisif>6.5)
Indicatesdeficiencyofinsulin
production
Presenceofcytoplasmic
autoantibodies;indicatorfor
T1DM
Presenceofautoantibodiesr/t
chronicdestructionofBcell;
indicatorforT1DM
Presenceofinsulin
autoantibodiesr/tchronic
destructionofBcells;indicator
forT1DM
DKAcausesmetabolicacidosis;
pHdropsduetoexcretionof
acidicketonesandincreased
bicarbonateproduction;first
signofT1DM.
Indicatesdecreasedfluid
volumer/tpolyuria
Excessglucoseproducesasa
resultofattemptingto
counteracthyperglycemiaislost
throughurine
IndicatesDKA
Proteinlossr/tkidneysbeing
overworked;proteinnotbeing
absorbedinbodytherefore
excessissecretedinurine

Indicatorofketoacidosis
Respiratoryrateincreases
(Kussmaulbreathing)r/t
metabolicacidosisfromDKA
14. DetermineArmandosenergyandproteinrequirement.Besuretoexplainwhat
standardsyouusedtomakethisestimation.Wouldyourecommendthathegainor
loseweightinthefuture?
ArmandosBMIis24,whichiswithinthenormalrangeforahealthyweightforheight

thereforeheshouldtrytomaintainhisweight.Inordertodoso,heneedsatleast2000
kcal/day.Iwouldrecommend2200kcal/daybasedoffhiscurrentfoodconsumptionand
toaccountforanypossibleincreaseinphysicalactivityimplementedbyhisdiabetes
managementplan.For15%ofhistotaldailycaloriescomingfromprotein,his
requirementswouldbegPRO/day.
IusedtheMifflinSt.Jeorformulatocalculatehisdailyenergyrequirements,takinginto
accounthislowphysicalactivitylevel(PAL1.2).

Calculations:
BMR=(10x75kg)+(6.25x180cm)(5x32y)+5=1721kcal/day
REE=1721x1.2(PAL)=2065kcal/day
PRO:15%of2200totalkcal=330kcal/4=83gPRO/day

15. PrioritizetwonutritionproblemsandcompletethePESstatementforeach.
Selfmonitoringdeficit(NB1.4)r/tnoncompliancewithmedicationrecommendations
forSMBGasevidencedbyirregularuseofmetforminsincediagnosisoneyearagodue
tofeelingthatitreallywasntnecessary.
Insulindeficiencyr/tproperdiagnosisofT1DM/LADAasevidencedbysymptomsof
polyuria,polyphagia,polydipsiaandfatiguealongwithserumglucoselevelof610
mg/dL,fastingglucoseof683mg/dL,A1Cof12.5%,Cpeptideof0.09ng/mL,and
testingpositiveforICA,GADA,andIAA.
16. DetermineArmandosinitialCHOprescriptionusinghisdietrecordfromhomeas
aguideline,aswellasyourassessmentofhisenergyrequirements.Whatnutrition
educationmaterialwouldyouusetoteachArmandoCHOcounting?

2200kcal/dayx0.5(50%totalkcalfromCHO)=1100/4g=275/3meals=

92gCHO/mealOR6CHOchoices/meal
OR
1100/4g=275/6meals=46g/15=3CHOchoices/meal
InordertoeffectivelyteachArmandoCHOcounting,Iwouldgooverthebasicsby
tellinghimwhatCHOcountingisandhowithelpstomanageDMbycontrollingblood
glucose.Iwouldalsoprovidehimwithtipsonhowtobestcontrolhisbloodsugarusing
CHOcountingbygoingoverhisindividualcarbohydrategoalswithhim.Iwouldexplain
tohimthateatingthreemealsaday(roughly46hoursapart),noskippingmeals,and
tryingtoconsistentlyeatthesameamountofcarbohydrateateachmewouldhelptobest
controlhisbloodsugar(USCF,CountingCarbohydrates).Iwouldalsoprovidehim
withADAcarbohydrateexchangelistsaswellasgoingoverhowtoreadnutritionlabels,
howtotrackhiscarbohydrateintakeviaafoodjournalorelectronictrackingsystem,and
howtoweighhisfood.Attheendofoursession,Icouldprovideaselfassessmentquiz
inordertoassesstheinformationhehasretained.

17. Armandosusualbreakfastconsistsof2slicesoftoast,butter,2tbspjelly,2
scrambledeggs,andorangejuice(~1c).UsingtheICRthatyoucalculatedin
question#7,howmuchNovologshouldhetaketocoverthecarbohydrateinthis
meal?

HiscalculatedICRis11gCHOper1unitofinsulin.Armandosbreakfasthasabout65g
CHO,sohisinsulinrequirementforNovologwillbe6units.
18. UsingtheADAguidelines,whatwouldbeappropriatefastingandpostprandial
glucoselevelsforArmando?
ADAsuggestsafastingglucoserangeof8130mg/dL(takenbeforeameal)and
postprandialglucoselevelslessthan180mg/dL(taken12hoursafterbeginningofa

meal)(ADA,CheckingYourBloodGlucose).
19. WriteanADIMEnoteforyourinitialnutritionassessment.
A

A: Wt. 165 lbs. Ht. 511 BMI: 23 IBW: 166 lbs.

%IBW: 99%
B: fasting glucose 683 mg/dL, A1C 12.5%, Cpeptide 0.09 ng/mL, glucose +3mg/dL, ketones +4,
positive for ICA, GADA, IAA, C: 32-year old Hispanic
male, daily alcohol use, smoker 1 ppd x 10yr.
diagnosis of T1DM/LADA after found
unconsciousness (GCS 13) resulting from DKA.
Diagnosed with T2DM 1 y ago; family history of
T2DM (mother). Prescribed to metformin but states
does not use appropriately.
D: 2200 kcal diet- 50% CHO, 30% FAT, 15% PRO
83 g PRO/day
73 g FAT/day, <10% saturated
275 g CHO/day 3 meals 4-6 hours apart @ 92 g
CHO/meal (6 CHO choices)
Novolog prior to meals 11g CHO/1 unit insulin.
Daily dose Lantus = 45 units taken at bedtime

Selfmonitoringdeficit(NB1.4)r/tnoncompliancewith
medicationrecommendationsforSMBGasevidencedby
irregularuseofmetforminsinceDMdiagnosisoneyearagodue
tofeelingitreallywasntnecessary.
Insulindeficiencyr/tproperdiagnosisofT1DM/LADAas
evidencedbysymptomsofpolyuria,polyphagia,polydipsiaand
fatiguealongwithserumglucoselevelof610mg/dL,fasting

glucoseof683mg/dL,A1Cof12.5%,Cpeptideof0.09ng/mL,
andtestingpositiveforICA,GADA,andIAA.
Diabetesselfmanagementeducation

3to4meetingsover46monthswithRDfor4590minfor
MNT;discussdietplan,CHOcountingandSMBG
Behavioraltherapytohelpassistinsmokingcessationand
decreaseinalcoholconsumption
M&E

Increasephysicalactivity
RDtomonitorweightandevaluatesuccessofselfmanagement
throughfoodandexercisejournal
AnnualfollowupsessionwithRDtomonitorhealthoutcomes
anddeterminewhetheradditionalsessionsareneeded
Assesssymptomsofpolyuria,polydipsia,polyphagia,and
fatigue
AssesslabvaluesincludingA1C,FPG,serumglucoseaswell
aslipidprofile,ketone,urineanalysis
MNTgoals:A1Clessthan7%,BPlessthan140/80mgHg,
LDL<100mg/dL,TGlessthan150mg/dL,HDLgreaterthan40

mg/dL
20. Armandocomesbacktotheclinic2weeksafterhisdiagnosis.Listtheimportant
questionsyouwillaskhiminordertoplanthenextstepsforprovidingthe
additionaleducationthathemightneed.
Haveyoubeensuccessfulinselfmonitoringyourglucose?
AreyoucomfortablewithCHOcounting?
Doyoufeelanychangesneedtobemadetoyourdietorinsulin?
Howhaveyoubeenkeepingupwithyourinsulin?
Doyouhaveanysymptomsoffrequenturination,abnormalhungerorthirst?
Howaboutfeelingoverlyfatigued?Dizzy?
Haveyouhadanymoreinstancesofunconsciousness?

21. Armandostatesthathewouldliketostartexercisingagainasheisfeelingbetter.
Heisusedtoplayingtennisseveraltimesperweekaswellascyclingatleast2days
perweekforover20mileseachtime.Again,heexpresseshisconcernregardinglow
bloodsugar.HowwouldyoucounselArmandoregardinghisphysicalactivity,his
diet,andhisbloodglucosemonitoring?

IfArmandoplanstostartimplementingphysicalexercisebackintohisdailyroutine,this
couldbeverybeneficialtohimintermsofhelpingtocontrolhisT1DM.Physical
activitycouldleadtohypoglycemiaduetonaturaldropsinglucoselevelsduring
exercise.Ifheisappropriatelyfollowinghisdietandinsulinplanandaccuratelycarb
countingbeforeappropriatelyspacedoutmealsandsnacks,heshouldbeabletomaintain
hisglucoselevels.Heshouldmakesuretoeatpriortoexerciseaswell,andmonitorhis
glucoselevelsbeforephysicalactivity.Easilyaccessedcarbohydratedensesnackswill
begoodtokeeponhandincaseofasuddendropinbloodsugar.
22. Armandostatesthatoneofhisfriendshastalkedaboutusingtheglycemicindexas
awaytomanagehisdiabetes.Hesaysthathehasalsoseemsomenutrition
programsadvertisetheirfoodproductsasbeinglowglycemicindexonTV.
Explainglycemicindex,glycemicload,andhowhemightusethisinformation
withinhisnutritiontherapyplans.
Theglycemicindex(GI)measureshowamuchacarbohydratecontainingfoodwillraise
glucoselevelsintheblood.Glucoseorwhitebreadareusedasreferencefoods,whileall
otherfoodsarebasedonhowtheycompareinraisingglucoselevelstothesereference
foods.HighGIfoodswillincreasebloodglucoselevelsmoresothanthosewitha
mediumorlowGI.Glycemicload(GL)simplyestimateshowmuchthesefoodswill
raisethebloodglucoseafterconsumption;oneunitGL=effectofconsumingonegram
ofglucose.GLcanbecalculatedusingtheformulaGL=GI/100xNetCarbs.
ArmandomayuseGIwithhisdiabetesinordertomealplan.Hecanbalancehismeals
basedoffofGIbycombininglowGIfoodswithhighGIfoods.Duetothefactthatthis

isbasicallyanotherformofCHOcounting,usingtheGImaybehelpfulinfinetuning
bloodglucosemanagementforthosewhodontmindextramonitoringoftheirfood
choices(ADA,GlycemicIndexandDiabetes).

REFERENCES
CheckingBloodGlucose.(2015,June17).RetrievedNovember19,2015,from
http://www.diabetes.org/livingwithdiabetes/recentlydiagnosed/wheredoi
begin/checkingbloodglucose.html
CountingCarbohydrates.(n.d.).RetrievedNovember19,2015,from
http://dtc.ucsf.edu/livingwithdiabetes/dietandnutrition/understanding
carbohydrates/countingcarbohydrates/
DCCTandEDIC:TheDiabetesControlandComplicationTrialFollowupStudy.(2008,
May1).RetrievedNovember19,2015,fromhttp://www.niddk.nih.gov/about
niddk/researchareas/diabetes/dcctedicdiabetescontrolcomplicationstrialfollowup
study/Documents/DCCTEDIC_508.pdf

Davidson,N.,&Moreland,P.(2009,February10).Diabetes.RetrievedNovember19,
2015,fromhttp://www.mayoclinic.org/diseasesconditions/diabetes/expertblog/blood
glucose/bgp20056587
DiabeticNeuropathies:TheNerveDamageofDiabetes.(2013,November26).Retrieved
November19,2015,fromhttp://www.niddk.nih.gov/healthinformation/health
topics/Diabetes/diabeticneuropathiesnervedamagediabetes/Pages/diabetic
neuropathiesnervedamage.aspx
Evert,A.(2013,November1).NutritionTherapyRecommendationsforthe
ManagementofAdultsWithDiabetes.RetrievedNovember19,2015,from
http://www.professional.diabetes.org/admin/UserFiles/0Sean/dc132042FINAL.pdf?
utm_source=Offline&utm_medium=Print&utm_content=nutritionguidelines&utm_cam
paign=DP&s_src=vanity&s_subsrc=nutritionguidelines
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