糖尿病英文版.pptx

糖尿病英文版.pptx

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MAN212PATHOPHYSIOLOGICALCONCEPTS,Bilibili我有小菜你要不要2020/6/21,CONTENTS,Definition,Epidemiology,Mechanism,Pathophysiology,Etiology,Diagnosis,Signsandsymptoms,Treatment,Riskfactors,Nursingmanagement,Definition,Classification,AmericanDiabetesAssociation,2020,Classificationanddiagnosisofdiabetes:

standardsofmedicalcareindiabetes:

43

（1）,14,Main4typesofdiabetes,Epidemiology,Toptencountriesfornumberofpeopleaged2079yearswithdiabetesin2018,Chinahasthelargestnumberofpeoplewithdiabetes.,Adultswithdiabetes,In2018Almost11.6%,114.4millionadultshaddiabetesinChina,11.6%,NewsRxHealthTheLancetDiabetes&Endocrinology:

1in4peoplewithdiabetesworldwideliveinChina12

（1）,21-23,Etiology,-celldestruction,usuallyleadingtoabsoluteinsulindeficiency.a.Immune-mediatedb.Idopathic,Unknowetiology.Acombinationofinsulinsecretorydefectwithinsulinresistance（relativeinsulinedeficiency）,Type1diabetes,Type2diabetes,EtiologicclassificationofdiabetesmellitusbasedontheAmericanDiabetesAssociation（rareetiologieswerenotincluded）.,Astateofincreasedinsulinresistancesuperimposedonanalreadyexistingstateof-celldysfunctionorloss,Gestationaldiabetes,a.Monogenicdefectsof-cellfunction:

MODY1-8:

MutationinNHF-1,NHF-4.glucokinase,andothers.Transientneonatal:

MutationinZAC/HYAMIb.geneticdefectsininsulinactionc.diseaseoftheexocrinepancreas,Others,f.drugorchemicalinduced（diazoxide,cyclosporine,tacrolimus,others）g.infectionsh.othergeneticsyndromesassociatedwithdiabetes（Down,PW,others）,d.endocrinopathies:

-Insulinresistance（hypersomatotropism,hypercortisolism,others）-decreasedinsulinsecretion（somatostatinoma,others）e.Uncommonformsofimmune-mediateddiabetesmellitus.（Anti-insulinreceptorantibodies,stiff-mansyndrome,others）,Areyouriskfortype2diabetes?

DiabetesRisktests:

1.Howoldareyou?

lessthan40years（0pints）40-49years（1points）50-59years（2points）60yearsorolder（3points）2.Areyouamanorawoman?

Man（1point）Women（0points）3.Ifyouareawomen,haveyoueverbeendiagnosedwithgestationaldiabetes?

Yes（1point）No（0points）4.Doyouhaveamother,father,sisterorbrotherwitdiabetes?

yes（1point）No（0points）5.Haveyoueverbeendiagnosedwithhighbloodpressure?

yes（1point）No（0points）,WriteYourscoreinthebox,Height,Weight（Ibs）,6.Areyouphysicallyactive？

Yes（0points）No（1point）7.Whatisyourweightcategory?

seechartatright.,ADDUPYOURSCORE,LOWERYOURRISKThegoodnewsisyoucanmanageyourriskfortype2diabetes,smallstepsmakeabigdiffereneinhelpingyoulivealongerhealthierlife.ifyouareathighrisk,yourfirststepistovisityourdoctortoseeifadditionaltestingisneeded.visitdiabetes.orgorcall1-800-diabetes（800-342-2383）forinformation,tipsongettingstarted,andideasforsimple,samllstepsyoucantaketohelploweryourrisk,youareatincreasedriskforhavingdiabetes.however,onlyyourdoctorcantellforsureifyoudohavetype2diabetesorprediabetes,aconditioninwhichbloodglucoselevelsarehigherthannormalbutnotyerhighenoughtobediagnosedasdiabetes.talktoyourdoctortoseeifadditionaltestingisneeded.Type2diabetesismorecommoninAfricanAmericans,Hispanics/Latinos,nativeamericans,asianamericansandnativehawailansandpacificislanders.higerbodyweighincreaseddiabetesriskforeveryone.AsianAmericansareatincreaseddiabetesriskatlowerbodyweihtthantherestofthegenralpublic（about15poundslower）,Learnmoreatdiabetes.org/risktest,Ifyouscored5orhigher,Areyouriskfortype2diabetes?

Histologyofnormalpancreas,HE,Islet,Intralobularduct,Fatcell/MuscleCell,Insulinreceptor,Insulin,IsletofLangerhans,cell（onthecenterofislets）,Pancreas,cell（ontheperipheryofislets）,Glucose,Glucagon,Insulin,BloodVessel,liver,Insulin,Glucose,Glycogen,Pyruvate,Fattyacids,Insulinreceptor,Lipidmetabolism,Na+K+ATPase,Na/KATPase,InsulinIncreasetheactivityofNa+K+ATPase,Insulin,1,2,3,4,5,Insulinalsoincreasesthepermiabilityofmanycellstopotassium,magnesiumandphosphateions.Insulinactivatessodium-potassiumATPasesinmanycells,causingafluxofpotassiumintocells.,InsulinactivatesNa+K+ATPaseincells,Insulininhibitsbreakdownoffatinadiposetissue,Insulininhibitsbreakdownoffatinadiposetissuebyinhibitingtheintracellularlipasethathydrolyzestriglyceridestoreleasefattyacids.,Insulinfacilitatesentryofglucoseintoadipocytes,andwithinthosecells,glucosecanbeusedtosynthesizeglycerol.Thisglycerol,alongwiththefattyacidsdeliveredfromtheliver,areusedtosynthesizetriglyceridewithintheadipocyte.Bythesemechanisms,insulinisinvolvedinfurtheraccumulationoftriglycerideinfatcells.,PhysiologicEffectsofInsulin,Insulin,Glucagon,GlucoseoxidationGlycogensynthesisFatsynthesisProteinsynthesis,GlycogenolysisGluconeogenesisKetogenesis,Fedstate:

insulindominates,Fastedstate:

glucagondominates,Glucagon,Insulin,G:

glucoseFFA:

freefattyacids,Energymetabolisminthefedstate,Glucose（providebyingestedfood）,Gastrointestinalhormone,InhibitgastricemptyingSuppressglucagonreleaseInducesatiety,InhibitstheproductionofglucosebyliverGlucoseintoadiposeandmuscletissue,Glycolysis,insulin,Amylin,（producedbypancreas）,Provideenergyneedofcell,Energymetabolisminthefastingstate,Insulin,Freefattyacids,Breakdownofstoreglycogen,Aminoacidsandother,Provideenergyneedofcell,Glucagon,G:

glucoseFFA:

freefattyacids,Lipolysis,Glycogenolysis,Gluconeogenesis,Nodigestedfoodprovideglucose,Wholebloodglucose,Normalbloodsugar,Normalfastingwholebloodglucose：

3.9-6.1mmol/L70-110mg/dL）,Type1diabetes,RecognizeforeignmoleculesMaintainingself-tolerance,Muscletissuebreakdownproteins,Renalglucosethreshold（180mg/dL）,Glycosuria,Polyuria,Polydipsia,Glucose,Noinsulin,NoGlucoseIncell,Freefattyacids,ketonebodies,Acetoaceticacid,hydroxybutyricacid,Provideenergyforcell,DiabeticKetoacidosis（DKA）,Increasetheacidityofthebody,Movecarbondioxideoutoftheblood,DKA,Type2diabetes,cellproducemoreinsulin,Hyperplasiaandhypertrophyofcell,Bloodglucoselevelskeepnormal（normoglycemia）,cellbecomeDysfunctionalHypotrophyHypoplasia,Insulinlevels,Glucoselevels,PolyphagiaGlycosuriaPolyuriaPolydipsia,Gestationaldiabetesmellitus（GDM）,Theplacentasuppliesagrowingfetuswithnutrientsandwater,andalsoproducesavarietyofhormonestomaintainthepregnancy.Someofthesehormones（estrogen,cortisol,andhumanplacentallactogen）canhaveablockingeffectoninsulin.Thisiscalledcontra-insulineffect,whichusuallybeginsabout20to24weeksintothepregnancy.Astheplacentagrows,moreofthesehormonesareproduced,andtheriskofinsulinresistancebecomesgreater.,GDMisaconditioninwhichahormonemadebytheplacentapreventsthebodyfromusinginsulineffectively.Glucosebuildsupinthebloodinsteadofbeingabsorbedbythecells.,Characteristics,Thecharacteristicsoftype1andtypes2diabetes,SignsandSymptoms,Signsandsymptoms,Chroniccomplication,Acutecomplication,Metabolicdisturbance,Chroniccomplications,Diabetesneuropathy,Diabetesmicroangiopathy,DiabetesFoot,Atherosclerosis,Nephropathy,Cardiomyopathy,Retinopathy,Ucler,Diabetesmacroangiopathy,Charcot,Gangrene,Atherosclerosis,Crosssectionofthevessel,Atherosclerosis,Diabeticnephropathy,Havinghighbloodglucoselevelscaninterferewiththefunctionoftheglomerulus.Thefilteringfunctionofthekidneysdoesntworkproperlyandproteinsstarttoleakfromthebloodintotheurine.Highbloodglucoselevelscanalsocausescarringoftheglomerulus（calledglomerulosclerosis）.Asthescarringgetsworse,thekidneysstopbeingabletofilterwasteproductsfromtheblood.Whenenoughglomerulihavebeendamaged,kidneyfailureresults.,Nephronsisresponsibleforprocessingwasteproductsandexcesswaterfromthebloodstreamandexcretethemintheformofurine.Glomerulusisthemajorstructureinthenephronwhichactsasafilter.,Glycemiainterferethefunctionofkidney,DiabeticRetinopathy,Earlydiabeticretinopathy:

Toomuchsugarinbloodleadtotheblockageofthetinybloodvesselsthatnourishtheretina,cuttingoffitsbloodsupplyAdvanceddiabeticretinopathy:

thennew,abnormalbloodvesselsgrowintheretina,andcanleakintotheclear,jelly-likesubstancethatfillsthecenterofeyes（vitreous）.,Highbloodsugardamagethetingvesselineyes,Cardiomyopathy,Diabeticcardiomyopathyisadisorderoftheheartmuscleinpeoplewithdiabetes.Itcanleadtoinabilityofthehearttocirculatebloodthroughthebodyeffectively,astateknownasheartfailure,withaccumulationoffluidinthelungs（pulmonaryedema）orlegs（peripheraledema）.Mostheartfailureinpeoplewithdiabetesresultsfromcoronaryarterydisease.diabeticcardiomyopathyisonlysaidtoexistifthereisnocoronaryarterydiseasetoexplaintheheartmuscledisorder.,Diabetescausetheenlargedventricles,Diabetesneuropathy,Thistypeofneuropathymayalsobecalleddistalsymmetricperipheralneuropathy.Itsthemostcommontypeofdiabeticneuropathy.Itaffectsthefeetandlegsfirst,followedbythehandsandarm.,NumbnessorreducedabilitytofeelpainortemperaturechangesTinglingorburningsensationSharppainsorcrampsIncreasedsensitivitytotouchforsomepeople,evenabedsheetsweightcanbepainfulSeriousfootproblems,suchasulcers,infections,andboneandjointpain,Symptomsofperipheralneuropathy,DiabeticFoot,Adiabeticfootisanypathologythatresultsdirectlyfromperipheralarterialdisease（PAD）and/orsensoryneuropathyaffectingthefeetindiabetesmellitus.Duetoadvancedperipheralnervedysfunctionassociatedwithdiabetes（diabeticneuropathy）,patientsfeethaveareducedabilitytofeelpain.Thismeansthatminorinjuriesmayremainundiscoveredforalongwhi