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Adult health 1

by: Anne Owusu

Adult health 1 NUR 304

Anne Owusu
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diabetes, respiratory
Adult Health I
Prof. Robillard
Class Notes




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This 108 page Class Notes was uploaded by Anne Owusu on Sunday February 28, 2016. The Class Notes belongs to NUR 304 at Augusta State University taught by Prof. Robillard in Winter 2016. Since its upload, it has received 233 views. For similar materials see Adult Health I in Nursing and Health Sciences at Augusta State University.

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Date Created: 02/28/16
2/4/2016 Nursing Management of Diabetes Chapter 49 Beth Melvin, MA, RD, LD, CDE, CHES CoordinatorDiabetes Education St. Mary’s Health Care System LearningOutcomes • Describethepathophysiologyand clinicalmanifestations of diabetesmellitus • Differentiatebetweentype1 and type2 diabetesmellitus. • Describethecollaborativecareofthepatientwithdiabetes mellitus. • Describetheroleofnutritionand exerciseinthemanagement of diabetes mellitus. • Discussthe nursingmanagement ofapatientwithdiabetes mellitus. • Relatethe pathophysiologyofacuteand chroniccomplicationsof diabetesmellitusto theclinicalmanifestations. AnAmerican Epidemic • 7 Leading cause ofdeath • Many unaware theyhave it • Costly 1 2/4/2016 26 million with Diabetes 79 million with Pre-Diabetes Diabetes 101: • A chronicmultisystemdiseaserelatedto abnormal insulin production,impairedinsulinutilization,orboth • Notjust a “sugar” problem • Major contributingfactor – Heart disease – Stroke – Hypertension • The complications,not just the diagnosisofdiabetes,cause the problems True or False Diabetes is the leading causeof adultblindness, amputation, and kidneyfailure? 2 2/4/2016 Etiology and Pathophysiology • CombinationofCausative Factors Genetic Autoimmune Environmental Absent/Insufficientinsulinand/or poorutilizationofinsulin Etiology and Pathophysiology • Normalinsulinmetabolism – Producedby -cellsin isletsof Langerhans – Releasedcontinuouslyinto bloodstreaminsmall incrementswith larger amountsreleasedafter food – Stabilizesglucoselevelin range of70 to 120 mg/dL Normal Insulin Secretion 3 2/4/2016 Etiology and Pathophysiology • Insulin –Promotesglucosetransport inskeletalmuscleand adipose tissue –Storageofglucoseas glycogen –Inhibitsgluconeogenesis –Enhances fat deposition –Increases proteinsynthesis –Notnecessaryforglucosetransportin brain, liver,bloodcells Etiology and Pathophysiology • Counterregulatoryhormones –Glucagon,epinephrine,growthhormone,cortisol –Opposeeffectsofinsulin –Stimulateglucoseproductionby liver –Decreasemovementof glucoseintocell –Helpmaintainnormal bloodglucoselevels Types ofDiabetes • Type1 • Type2 • Gestational • Other specifictypes 4 2/4/2016 Type 1 Diabetes Mellitus • Formerlyknownas juvenile-onsetorinsulin-dependent diabetes • Accountsfor5% ofall cases ofdiabetes • Onset in peopleyoungerthan 40years • Incidenceincreasing Morefrequentlyinyoungerchildren • Autoimmunedestructionof β-cells • Totalabsenceof insulin Type 1 Diabetes Mellitus Onset ofDisease • Autoantibodiesare presentfor monthsto years before symptomsoccur • Manifestationsdevelopwhenpancreas can no longerproduce insulin—thenrapid onsetwith ketoacidosis • Necessitatesinsulinfor life • Patient may have temporaryremissionafter initialtreatment Type 1 Diabetes Mellitus ClassicSymptoms: • Polydipsia • Polyuria • Polyphagia May have historyofrecent and suddenweightloss 5 2/4/2016 Type 2 Diabetes Mellitus • Formerlyknown as adult-onsetdiabetes(AODM) or non– insulin-dependentdiabetes(IDDM) • Most prevalenttype(90%to 95%) • Riskfactors:overweight,obesity,advancing age,family history • Increasing prevalenceinchildren • Greaterprevalenceinethnicgroups Type 2 Diabetes Mellitus Etiology and Pathophysiology • Pancreas continuesto producesome endogenousinsulin • Insulininsufficientorpoorlyutilized • Multipleetiologicfactors – Obesityis greatestrisk factor(especiallyabdominal) – Geneticcomponentincreasesinsulinresistanceand obesity Type 2 Diabetes Mellitus Etiology and Pathophysiology • 4 major metabolic abnormalities 1. Insulinresistance 2. Decreasedinsulinproductionby pancreas 3. Inappropriatehepaticglucoseproduction 4. Alteredproductionofhormonesand cytokinesby adipose tissue(adipokines) 6 2/4/2016 Type 2 Diabetes Mellitus Etiology and Pathophysiology Metabolicsyndrome (3of the 5) increasesrisk for type 2 diabetes • Elevatedglucoselevels • Abdominalobesity • Elevatedbloodpressure • Highlevelsof triglycerides • DecreasedlevelsofHDLs Type 2 Diabetes Mellitus Onset ofDisease • Gradual onset • Hyperglycemiamay gomany years withoutbeingdetected • Many timesdiscoveredwith routinelaboratory testing • May requireinsulinduring periodsof stresssuchas illnessor surgery Altered Mechanisms in Type 1 andType 2 Diabetes 7 2/4/2016 Clinical Manifestations Comparisontable 49-1 Type 1 Type 2 Classic symptoms Nonspecificsymptoms Polyuria(frequenturination) Type 2Tyop Recurrentinfection Polydipsia(excessivethirst) Polyphagia(excessive Recurrentvaginal yeast or hunger) candidal infection • Weightloss • Weakness Prolongedwound healing Visualchanges • Fatigue Prediabetes • Individualsat riskfortype2 diabetes • Impairedglucoseintolerance(IGT) Two-houroral glucosetolerancetest(OGTT): 140 to 199 mg/dL • Impairedfasting glucose(IFG) Fasting glucoselevel:100 to 125 mg/dL Prediabetes • Asymptomaticbut long-termdamage already occurring • Patient teachingimportant Undergoscreening Manage riskfactors Monitorfor symptomsof diabetes Maintain healthyweight,exercise,healthydiet 8 2/4/2016 Gestational Diabetes • Developsduringpregnancy • Increases riskofneed for cesareandeliveryand ofperinatal complications • Screenhigh-riskpatientsfirst visit;othersat 24 to 28 weeks ofgestation • Usuallyglucoselevelsnormal 6 weeks postpartum • At risk fordevelopingtype2 diabetes OtherSpecificTypes of Diabetes • Resultsfrom damageto, injuryto, interferencewith,or destructionofβ-cellfunctionin thepancreas • From medicalconditionsand/or medications(steroids) • Resolveswhenunderlyingconditionis treatedor medicationis discontinued 4 Methodsof Diagnosis 1. A1C level:6.5% orhigher 2. Fasting plasmaglucoselevel:higherthan 126mg/dL 3. Two-hourplasmaglucoselevelduringOGTT: 200mg/dL (with glucoseload of75 g) 4. Classicsymptomsofhyperglycemiawith random plasma glucoselevelof 200mg/dLorhigher 9 2/4/2016 DiagnosticStudies HemoglobinA1C test – Reflectsglucoselevelsoverpast 2 to 3 months – Used to diagnose,monitorresponseto therapy,and screen patientswith prediabetes – Goal:less than6.5% to 7% – Does not reflectdaily control HbA1ccompared to Blood glucose CollaborativeCare Goals of diabetes management – Decreasesymptoms – Promotewell-being – Preventacute complications – Delay onsetand progressionof long-termcomplications Needto maintainbloodglucoselevelsas near to normal as possible 10 2/4/2016 CollaborativeCare Patient teaching Nutritionaltherapy Medicationtherapy Exercise Self-monitoringof bloodglucose • Diet,exercise,and weightloss may be sufficientfor patients with type2 diabetes • All patientswithtype 1require insulin Insulin Exogenousinsulin • Insulinfrom an outsidesource • Requiredfortype1 diabetes • Prescribedforpatientswith type2 diabeteswho cannot controlbloodglucoseby othermeans Insulin Administration ofinsulin • Usuallyavailableas U100 insulin(1 mLcontains 100U of insulin) • Syringesmarked forunits:varioussizes • Only user recaps syringe • Inject at 45- to 90-degreeangle 11 2/4/2016 Insulin Typesofinsulin • Rapid-acting:Lispro(Humalog) Aspart (Novolog) glulisine(Apidra) • Short-acting:Regular(Clear) • Intermediate-acting:NPH (Cloudy) • MixedInsulin: Short+ NPHorRapid + NPH • Long-acting:Glargine(Lantus) detemir(Levemir) U – 500RegularInsulin • Used forpatientswith extremeinsulinresistance(TDI > 200units) • 1 mLcontains 500units of insulin(5XStronger) • A tuberculinsyringeis recommendedfor administration • Onset – 30 minutes • Peak– 2 – 5 hours • Duration– 24 hours InsulinComparison,Fig 49-3 12 2/4/2016 Insulin Regimens Basal-bolusregimen (intensive insulin therapy) Most closelymimicsendogenousinsulinproduction Goal:achievenear normal glucoseof70-130md/dLbefore meals Rapid-or short-acting(bolus)insulinbeforemeals Intermediate-orlong-acting(basal) backgroundinsulin once ortwicea day Requiresmultipleinjections and frequent BS monitoring Less intense regimes may alsobe be used Mealtime Insulin (Bolus) Controlpostprandialbloodglucoselevels Timinginrelationto meals crucial – Rapid-acting (bolus) • Injected 0 to 15 minutes before meal • Onset of action 15 minutes – Short-acting (bolus) • Regular • Injected 30 to 45 minutes before meal • Onset of action 30 to 45 minutes (Basal)BackgroundInsulin Used to controlglucoselevelsinbetweenmeals and overnight Long-acting(basal) -CLEAR Insulinglargine(Lantus) and detemir(Levemir) Releasedsteadilyand continuouslywithno peakaction Administeredonceor twicea day Do not mix withany otherinsulinorsolution 13 2/4/2016 (Basal)BackgroundInsulin Intermediate-actinginsulin-CLOUDY NPH (HumulinN,NovolinN) Duration12 to 18 hours Peak4 to 12 hours Can mixwith short-and rapid-actinginsulins Cloudy;must agitateto mix Combination InsulinTherapy -CLOUDY Can mixshort-or rapid-actinginsulinwith intermediate-actinginsulininsame syringe Providesmealtimeand basal coverage in one injection Commerciallypremixedorself-mix or Aspart Example: Novolin70/30 Regularwith NPH Novolog70/30 Mix Insulin – Long-acting (basal) • Typically injected once a day at bedtime or in the morning (Can be needed twice a day) • Released steadily and continuously • No peak action • Cannot be mixed with any other insulin or solution – Intermediate-acting insulin • Injected twice a day; at breakfast and at bedtime • Cloudy 14 2/4/2016 Insulin Storage ofinsulin Do not heat/freeze In-use vials may be left at room temperatureup to 4 weeks Extrainsulinshouldbe refrigerated Avoidexposureto directsunlight,extremeheat or cold Storeprefilledsyringesuprightfor1 weekiftwo insulintypes; 30 days forone Insulin • Administrationofinsulin • Fastest absorptionfrom abdomen,followedby arm, thigh,and buttock – Abdomenis the preferredsite. – Rotateinjectionswithinone particularsite. – Do not inject insite to be exercised. Insulin Pen 15 2/4/2016 Insulin Pump • Continuous subcutaneousinfusion • Battery-operateddevice • Connectedviaplastic tubingto a catheter insertedinto subcutaneoustissuein abdominalwall • Potentialfortight glucosecontrol Problems with InsulinTherapy • Hypoglycemia • Allergicreaction • Lipodystrophy • Somogyieffect • Dawn Phenomena Somogyi Effect • overdose of insulin causes hypoglycemia • Usually during hours of sleep • Counterregulatory hormones released • Rebound hyperglycemia and ketosis may occur. • Tx: May require less insulin • Danger if BS measured in am and found to be high, PCP may increase insulin 16 2/4/2016 Dawn Phenomenon Characterized byhyperglycemia presenton awakening in the morning Due to release of counterregulatory hormones in predawn hours Growth hormone/cortisol possible factors administration time if BS elevated between 2-4amin It isdifferent from Somogyi rebound in thatdawnphenomenon is notassociated withnocturnal hypoglycemia Oral and Noninsulin InjectableAgents Workonthree defectsof type2 diabetes Insulinresistance Decreasedinsulinproduction Increased hepaticglucoseproduction Can be used incombination OralandNoninsulinInjectableAgents • Biguanides • Sulfonylureas • Dipeptidyl peptidase-4 (DDP-4) inhibitor • Non-Sulfonylurea Insulin Secretagogues • α-Glucosidase inhibitors • Thiazolidinediones 17 2/4/2016 Biguanides (Metformin) – Reduceglucoseproductionby liver – Increase insulinsensitivityat tissues – Improveglucosetransportinto cells – May cause weightloss – Used to preventType2 inpre-diabetes – First drug ofchoiceformostpeoplewithType2 – Withholdifcontrast mediumis used Day ortwo beforeand atleast48 hours after Monitorserum creatinine Sulfonylureas • ↑ insulinproductionfrompancreas • 10%experiencedecreasedeffectivenessafter prolonged use • Highriskof hypoglycemia,especiallywithpoorpo intake and renal insufficiency • Examples Glipizide(Glucotrol) Glimepiride(Amaryl) Glyburide(Micronase,DiaBeta,Glynase) Meglitinides • ↑ Insulinproductionfrom pancreas • Rapid onset: ↓ hypoglycemia • Taken 30 minutesto just beforeeachmeal • Shouldnot be taken ifmeal skipped • Examples Repaglinide(Prandin) Nateglinide(Starlix) 18 2/4/2016 α-glucosidaseinhibitors “Starch blockers” • Slowdownabsorptionofcarbohydratein smallintestine • Take withfirst biteofmeal – Example Acarbose(Precose) Thiazolidinediones • Most effectiveinthosewith insulinresistance • Improveinsulinsensitivity,transport,and utilizationat target tissues • Examples Pioglitazone(Actos) Rosiglitazone(Avandia) Rarely usedbecause ofadverseeffects Dipeptidyl peptidase-4(DDP-4)inhibito r • Blocksinactivationof incretin hormones – ↑ Insulinrelease – ↓Glucagonsecretion – ↓ Hepaticglucoseproduction • Examples(gliptins) Sitagliptin(Januvia) Saxagliptin(Onglyza) Linagliptin(Tradjenta) 19 2/4/2016 Dopamine ReceptorAgonist • Bromocriptine(Cycloset) • Mechanismofactionunknown • Thoughtthat patientswith type2 diabeteshave lowlevelsof dopamine • Increases dopaminereceptoractivity • Alone orincombination Incretin mimetic – injectable (SQ) • Simulateglucagon-like peptide–1 (GLP-1) • Increase insulin synthesis and release • Inhibit glucagon secretion • Decrease gastric emptying • Increases satiety • Musttake oral meds 1 hour before injecting  Exenatide (Byetta)  Liraglutide(Victoza) AmylinAnalog - injectable (SQ) • Slowsgastricemptying,reducespostprandialglucagon secretion,increasessatiety • Used concurrentlywithinsulin • Subcutaneouslyin thighor abdomenbeforemeals • Watchfor hypoglycemia Pramlintide(Symlin) 20 2/4/2016 Drug Interactions • -adrenergicblockers – Mask symptoms of hypoglycemia – Prolong hypoglycemic effects of insulin • Thiazide/loopdiuretics – Can potentiate hyperglycemia • By inducing potassium loss Diabetes NutritionalTherapy • Cornerstoneofcare forpersonwithdiabetes • Most challengingformany people • Recommendedthat diabeteseducatorand registereddietitian with diabetesexperienceshouldbe membersofteam • Considerfoodpreferences,lifestyle,usual eating times,and culturaland ethnicbackground Diabetes NutritionalTherapy • No “diabeticdiet” or“ADA diet”– all individualized • No forbiddenfoods • Many mythsand misconceptions 21 2/4/2016 Diabetes NutritionalTherapy • Type1 diabetesmellitus • Type2 diabetesmellitus – Meal plan is based on – Emphasisis based on individual’susual food achievingglucose,lipid, intake and is balanced and bloodpressuregoals. with insulinand exercise – Caloriereduction patterns. – Insulinregimenis managed day to day. Diabetes NutritionalTherapy • Carbohydrates • Protein – Sugars, starches, andfiber – Contribute 15% to 20%of total calories consumed – Carbohydrateallowanceis a minimum of130g/day. – 50-60% of calories • Fats • Fiber – Less than 200mg/dayof - 25g daily fatsesterol and limited trans • <7% from saturated fats• Sweeteners Diabetes NutritionalTherapy • Alcohol Limitto moderate amount – Highin calories – No nutritivevalue Consumewithfood to reduceriskofnocturnal – Promotes hypoglycemiaifusing hypertriglyceridemia insulinor insulin – Detrimentaleffectson secretagogues liver ConsumewithCHO to reducehypoglycemia,but – Can cause severe thenwatch for hypoglycemia hyperglycemiafromCHOs 22 2/4/2016 CarbCounting –Why? • Carbohydrateis thenutrient infood that raisesbloodglucosethe most • Amount ofcarbohydrateeaten determineshowhighbloodglucosewillrise after a meal Basicsof a Diabetic Diet MAIN POINTS: • Eat 3 mealsa day withsnacks as needed • Knowwhichfoodsmake bloodsugargo up (CARBS) • Knowhowmuchof thosefoods you shouldeat at each meal and snack (CARBCOUNTING) Carbohydrates • Includes: Starches,Fruits,Diary (milkand yogurt),andOther CarbohydratesorSweets • Amount ofcarbohydrateis always individualized! • What about otherfoodgroups? 23 2/4/2016 Diabetes NutritionalTherapy Dietitianinitiallyprovidesinstruction • Carbohydratecounting Servingsize is 15 g ofCHO Typically45 to 60 g per meal Insulindosebased on numberofCHOs consumed Patient teachingessential Plate Method Amount ofCarbohydratein Foods  StarchGroup  MilkGroup ◦ 1 sliceof bread orsmallroll ◦ 1 cupmilk ◦ 1/3 cup cookedrice orpasta ◦ ¾ cup lightyogurt ◦ ½ cup beans, corn,peas ◦ 1 med.(4oz)baked potato  Sweets ◦ 6 saltines ◦ ½ cup icecream ◦ 2 small cookies  FruitGroup ◦ 1Tbsp.jam or jelly ◦ 1 smallfruit (4oz) ◦ ½ cup canned fruit orjuice 1 carb choice = 15 grams carb 24 2/4/2016 CarbCounting: How many grams of carb? 7 oz apple = 4 oz apple= 15 gmcarb, 26 gm carb, ~ 105 calories ~ 60 calories 1 carbchoice 2 carb choices • Count carbs correctly Food recall Glycemic Index • Termused to describerise inbloodglucoselevelsafter carbohydrate-containingfood is consumed • Highglycemicindexfoods increaseglucoselevelsfaster • Misleading FoodLabels SugarFreeCookies o Sorbitolhols* Other sugar substitutes o Lactitol o Maltitol 25 2/4/2016 “Sugar-Free”Can Be Misleading • Comparelikefoods for“TotalCarbs” • Checkfat and calories • Usuallynot a “free”food • More costly • Sideeffects Diabetes Exercise Type/amount • clearancelyafter medical Minimum 150minutes/week aerobic • Monitorbloodglucosebefore, duringand afterwards Resistance training three times/week • Glucose-loweringeffectupto Benefits 48hoursafter exercise • Exercise1hourafter a meal ↓ Insulin resistanceand bloodglucose • 15g carbsnack priorto Weight loss preventhypoglycemia • Do not exercise if blood ↓Triglycerides andLDL , ↑ HDL glucoselevel exceeds 250 Improve BP andcirculation presentinurineonesare Self-Monitoring of blood glucose(SMBG) – Enablespatient to make self-managementdecisions regardingdiet,exercise,and medication – Important fordetectingepisodichyperglycemiaand hypoglycemia – Patient trainingis crucial. – Suppliesimmediateinformationabout bloodglucoselevels – Frequencyof testingvaries 26 2/4/2016 Self-Monitoring of BloodGlucose (SMBG) Patient teaching Howto use,calibrate • Whento test Beforemeals Two hoursafter meals Whenhypoglycemiais suspected During illness Before,during,and after exercise ContinuousGlucose Monitor BloodSugarTargets • Daily MonitoringofBloodSugar – Morning (fasting)= 70 –130 – 2 Hours after meals = 140 – 180 – Bedtime= 120– 150 mg/dl • Howoftento check? 27 2/4/2016 3AcuteComplications • Diabeticketoacidosis(DKA) • Hyperosmolarhyperglycemicsyndrome(HHS) • Hypoglycemia Hypoglycemia • Checkbloodglucoselevel –If lessthan 70 mg/dL,begintreatment –If morethan 70 mg/dL,investigatefurtherforcause of signs/symptoms –If monitoringequipmentnot available,treatmentshouldbe initiated Hypoglycemia • Bloodglucoselevelless than70 mg/dL • Neuroendocrinehormonesreleased • Autonomicnervoussystemactivated • Causes –Toomuchinsulinororal hypoglycemicagents –Toolittlefood –Delayingtimeofeating –Toomuchexercise • Symptomscan also occurwhenhighglucoselevelfalls too rapidly 28 2/4/2016 Hypoglycemia • Commonmanifestations • Alteredmental functioning –Shakiness –Difficultyspeaking –Palpitations –Visualdisturbances –Nervousness –Stupor –Diaphoresis –Confusion –Anxiety –Coma –Hunger • Untreated hypoglycemiacan –Pallor progressto loss of consciousness,seizures, coma,and death Hypoglycemia (Able to takepo) • Treatment:rule of 15 1.Consume15 g ofa simplecarbohydrate • Fruit juiceorregularsoft drink, 4 to 6 oz 2.Recheckglucoselevelin15 minutes • Repeatif stillless than70 gm/dL 3.Avoidfoods withfat • Decreaseabsorptionofsugar 4.Avoid overtreatment 5.GivecomplexCHO after recovery Hypoglycemia (Unable to takepo) • Treatment –In acute care settings • Fifty percentdextrose,20to 50 mL,IV push • Glucagon,1 mg,IM orsubcutaneously • Explorereasonwhy occurred 29 2/4/2016 Diabetic Ketoacidosis(DKA) • Caused by profounddeficiencyof insulin • Characterizedby –Hyperglycemia –Ketosis(Ketones) –Acidosis(metabolic) –Dehydration • Most likelyto occurintype1 diabetes Diabetic Ketoacidosis(DKA) • Precipitatingfactors –Illness –Infection –Inadequate insulindosage –Undiagnosedtype1 diabetes –Poor self-management –Neglect Diabetic Ketoacidosis(DKA) • Clinical manifestations –Abdominalpain, anorexia, Dehydration –Kussmaulrespirations (attempt • Poor skin turgor to blowoffCO2) • Dry mucous membranes –Sweet, fruitybreath odor • Tachycardia (acetone) • Orthostatichypotension –Bloodglucoselevel of250 –Lethargy andweakness early (hyperglycemia) –and sunkenndloose;eyes soft –BloodpH lowerthan 7.30(acidosis) –Serum bicarbonatelevel lower than 16 mEq/L –Moderateto high ketone levels in urine or serum (ketosis) 30 2/4/2016 Diabetic Ketoacidosis(DKA) • Hospitalizeforseverefluidand electrolyteimbalance, fever,nausea/vomiting,diarrhea,alteredmental state • Ensure patent airway; administerO 2 • EstablishIV access;beginfluidresuscitation –NaCl,0.45%or0.9% –Add 5% to 10%dextrosewhenbloodglucoselevel approaches250 mg/dL • Continuousregularinsulindrip may be required • Potassiumreplacementas needed Hyperosmolar HyperglycemicSyndrome (HHS) • Life-threateningsyndrome • Occurs withtype 2 diabetes • Precipitatingfactors –UTIs, pneumonia,sepsis –Acuteillness –Newlydiagnosedtype2 diabetes –Impairedthirstsensationand/orinabilityto replace fluids Hyperosmolar HyperglycemicSyndrome (HHS) • Enoughcirculatinginsulinto • Medicalemergency preventketoacidosis • Highmortalityrate • Fewersymptomsleadto higher • Therapysimilar tothat for glucoselevels(>600mg/dL) DKA • More severe neurologic –infusionsand NaCl manifestations because of ↑ –Morefluidreplacement serumosmolality needed –Monitorserum • bloodand urineor minimal in potassiumand replace as needed • Correct underlying precipitatingcause 31 2/4/2016 DKA/HHS Nursing Management • Monitor – IV fluids –Insulintherapy –Electrolytes • Assess –Renal status –Cardiopulmonarystatus –Levelofconsciousness ChronicComplications ChronicComplications Angiopathy • Damage to bloodvesselssecondarytochronic hyperglycemia • Leading cause ofdiabetes-relateddeath • Macrovascularand microvascular • Tightglucosecontrolcan preventorminimize complications 32 2/4/2016 ChronicComplications MacrovascularAngiopathy • Diseasesoflarge and medium-sizedbloodvessels • Greater frequencyand earlieronset in patientswith diabetes • Cerebrovasculardisease • Cardiovasculardisease • Peripheralvasculardisease ChronicComplications MacrovascularAngiopathy • Decreaseriskfactors (yearlyscreening) –Obesity –Smoking –Hypertension –Highfat intake –Sedentarylifestyle • Screenfor and treat hyperlipidemia ChronicComplications MicrovascularAngiopathy • Thickeningofvesselmembranesin capillariesand arterioles • Specificto diabetesand includes –Retinopathy –Nephropathy –Dermopathy • Usuallyappear10 to 20years after diagnosis 33 2/4/2016 ChronicComplications Diabetic Retinopathy • Microvasculardamage to retina • Most commoncauseof newcases of adultblindness • Nonproliferative:more common • Proliferative:more severe • Initiallyno changes invision • Annual eyeexaminationswithdilationto monitor • Maintain glycemiccontroland manage hypertension ChronicComplications Diabetic Nephropathy • Damage to smallbloodvesselsthat supplythe glomeruliof the kidney • Leading cause ofend-stagekidneydisease • Riskfactors –Hypertension –Genetics –Smoking –Chronichyperglycemia ChronicComplications Diabetic Nephropathy • Annual screening • If albuminuriapresent,drugs to delayprogression: –ACE inhibitors –AngiotensinII receptorantagonists • Controlofhypertensionand tightbloodglucose control:imperative 34 2/4/2016 ChronicComplications Diabetic Neuropathy • Nervedamage due to metabolicderangementsof diabetes • Of patientswith diabetes,60%to 70% have some degreeofneuropathy • Reducednerveconductionand demyelinization • Sensory –Loss ofprotective sensationin lower extremities –Majorrisk for amputation • Autonomic Bowel incontinence, urinary retention, gastroparesis, silent MI, ED ChronicComplications Diabetic Neuropathy • Distalsymmetricpolyneuropathy –Most commonform –Affectshands and/orfeet bilaterally –Loss ofsensation,abnormal sensations,pain, and paresthesias Neuropathy:NeurotrophicUlceration 35 2/4/2016 ChronicComplications FootComplications • Microvascularand macrovasculardiseasesincreasesrisk forinjuryand infection • Sensoryneuropathyand PADare majorriskfactors for amputation • Also clottingabnormalities,impairedimmunefunction, autonomicneuropathy • Smokingincreasesrisk ChronicComplications FootComplications • Sensoryneuropathy→loss ofprotectivesensation→ unawareness ofinjury – Monofilamentscreening • Peripheralartery disease – ↓ Bloodflow, ↓ wound healing,↑risk forinfection ChronicComplications FootComplications • Patient teachingto preventfootulcers –Properfootwear –Avoidanceoffoot injury –Skinand nail care –Daily inspectionof feet –Prompttreatmentofsmall problems • Diligentwound care forfootulcers • Neuropathicarthropathy(Charcot’sfoot) 36 2/4/2016 NecroticToe Before andAfterAmputation ChronicComplications Diabetic Neuropathy • Treatmentforsensoryneuropathy –Tightbloodglucosecontrol –Drug therapy • Topicalcreams • Tricyclicantidepressants • Selectiveserotoninand norepinephrinereuptake inhibitors • Antiseizuremedications ChronicComplications Diabetic Neuropathy • Autonomicneuropathy –Can affect nearly all bodysystems –Gastroparesis • Delayedgastricemptying –Cardiovascularabnormalities • Posturalhypotension,restingtachycardia,painless myocardialinfarction 37 2/4/2016 ChronicComplications Diabetic Neuropathy • Autonomicneuropathy –Sexualfunction • Erectiledysfunction • Decreasedlibido • Vaginal infections –Neurogenicbladder →urinaryretention • Emptyfrequently,useCredé’smaneuver • Medications • Self-catheterization ChronicComplications Skin Problems • Diabeticdermopathy –Most common –Red-brown,round or oval patches • Acanthosisnigricans –Velvetylightbrown to blackskin • Necrobiosislipoidicadiabeticorum –Red-yellowlesions Necrobiosis LipidoidicaDiabeticorum 38 2/4/2016 ChronicComplications Infection • Defectin mobilizationofinflammatorycellsand impairedphagocytosis • Recurringorpersistentinfections • Treat promptlyand vigorously • Patient teachingforprevention –Hand hygiene –Flu and pneumoniavaccine GerontologicConsiderations • Increased prevalenceand mortality • Glycemiccontrolchallenging –Increased hypoglycemicunawareness –Functionallimitations –Renal insufficiency • Dietand exercise:main treatment • Patient teachingmust be adapted to needs 39 2/16/2016 Chapter27 Managementof PatientsWith UpperRespiratoryTract Disorders Presentedby: PriscilaHartley,DNP,RN Objectives  Describe nursing management ofpatients with upper airway disorders.  Compare and contrastthe upper respiratory problems according to cause,incidence, clinicalmanifestations, management, and the significanceofpreventive health care.  Use the nursing process as a frameworkfor care ofpatients with upper airwayinfection.  Describe nursing management ofthe patient with epistaxis.  Use the nursing process as a frameworkfor care ofpatients with head andneck cancer. Problemsof NoseandParanasal Sinuses  Deviatedseptum  CongenitalorTraumatic  Septoplasty  Nasal fracture  Epistaxis, Ecchymosis,CSF, Facial Fractures  Maintain airway, Keepupright,ice,xray  Rhinoplasty  Collaborativecare 1 2/16/2016 Nursingmanagement:Nasalsurgery  Pre-op NoASA (Aspirin,NSAIDS for2 weeks)  Post-op: MaintainAirway Assess Respiratory Assess forBleeding Assess forEdema/Bruising Assess forInfection Epistaxis  Hemorrhagefrom the nose  Anteriorseptum,mostcommonsite  Seriousproblem,may resultin airway compromiseor significantbloodloss Epistaxis Causes: Nursing Interventions/Medical  Trauma Management:  FB (ForeignBody)  Uprightposition  Pinch  Steroids  NasalSprayAbuse  Leanforward  Ice  Drugs(street,OTC,prescribed)  Hypertension  VS  Cauterization/Packing  Irritation  Anticoagulation  Balloon  DeterminationofCause 2 2/16/2016 Controlof Epistaxis—Packingof NasalCavityorBalloonCatheter EpistaxisNursingManagement  Airway, breathing,circulation  Vitalsigns  Reduceanxiety  Patient teaching:  Avoidnasal trauma, forcefulblowing,spicyfoods, tobacco,exercise  Adequate humidificationto preventdryness AllergicRhinitis Clinical manifestations Triggers Releaseofhistamine,leukotrienes Nursing and collaborativemanagement: AvoidTriggers Pharmacology: Table27-2,pg501 3 2/16/2016 AcuteViralRhinitis “Cold”  Rest,fluids,properdiet,antipyretics,and analgesics are therecommendedmanagementof acuteviral rhinitis.  During thecoldseason, advisepatientswith a chronic illnessora compromisedimmunestatusregarding measuresto decreasethe riskofacquiringa cold. RhinitisTreatment  Dependson thecause  Viral rhinitis-medicationsto relievesymptoms  Allergicrhinitis-allergytestperformedto determine allergen,avoid triggers  Bacterialinfection-antimicrobial  Nasal deformitiesor polyps-referto ENT Influenza  Clinical manifestations  Abrupt onset  Systemicsymptoms  Rapid Flu andStrepScreen  Nursing and collaborativemanagement:  Antivirals(Tamiflu)  SupportiveCare  FluVaccine  Complications:Pneumonia 4 2/16/2016 Sinusitis  Clinical manifestations: pain overthe affectedsinus,purulent nasal drainage,nasal obstruction,congestion,fever,and malaise.  Accumulatingsecretionsprovidea richmediumforgrowthof bacteria,viruses,and fungi,all ofwhichmay cause infection.  Nursing and collaborativemanagement: Symptomrelief,antibiotics,oral ortopicaldecongestants,nasal corticosteroids,and antihistamines. Locationof thesinuses Obstructionof theNoseand ParanasalSinuses Polyps Foreignbodies 5 2/16/2016 AcutePharyngitis …acuteinflammationofthe pharyngeal walls that may includethe tonsils,palate,and uvula.  Clinical manifestations Symptomsrange in severityfrom complaintsof a “scratchy throat”to painso severethat swallowingis difficult.Bothviral and strep infectionsappearas a red and edematouspharynx, with orwithoutpatchyyellowexudatesso appearanceis not always diagnostic.  Goals: infectioncontrol,symptomaticrelief,and preventionofsecondary complications. Pharyngitis Treatment  Viral pharyngitis-supportivemeasureto manage symptoms  Severesorethroat painrelievedby analgesic  Bacterialpharyngitis-Antibiotic10 days Penicillinis treatmentof choice If allergicto penicillin,cephalosporinsand macrolides  Soft diet  Coolbeverageor warm liquids 6 2/16/2016 PeritonsillarAbscess Sincea peritonsillarabscess—acomplicationof acute pharyngitis—maythreatenthe airway, needle aspiration,drainage,or surgeryis indicated LaryngealPolyps  Polypson thevocalcords developas a resultof vocalabuse or irritation.  The mostcommonsymptomis hoarseness.  hydration.eatedconservativelywith voicerest and adequate  Surgicalremovalmay be indicatedfor largepolyps,whichmay cause dyspnea. Head& NeckCancer  Usuallysquamous cell  Riskfactors  Age > 50 years  Male gender2-5x  Smokingoralcohol–prolongeduse**(most common)orsmokelesstobacco  Vegetable/fruitdeficientdiet  Human papillomavirus(HPV)infection 7 2/16/2016 HeadandNeckCancer SignsandSymptoms Early: Later:  Hoarseness Dysphagia,dyspnea  Ulcer Nasal obstruction  Hemoptysis Persistenthoarseness  Sore throatorburninPersistentulceration throat Foul breath  Raspy voice,lowerpiWeightloss  Lump inneck DiagnosticStudies  Historyand physical  Laryngoscopy  Biopsy  Barium swallowstudy  Endoscopy,CT,MRI, PET scan  Tumorsgrade and stage byTNM system(Tumor, Nodes,Metastasis) CollaborativeManagement HeadandNeckCancer StagesI and II StagesIII and IV  Radiationtherapy Radiationtherapy  Larynx sparing surgChemotherapy  Potentiallycurable Cordectomy Totallaryngectomy 8 2/16/2016 RadicalNeckSurgery ChangesinAirflowWithTotal Laryngectomy PostoperativeNursingCare  Maintain patent airway, controlsecretions  Reduceanxiety  Supportalternative communication  Promoteadequate nutritionand hydration  Promotepositivebodyimage,self-esteem  Self-caremanagement 9 2/16/2016 UpperRespiratory: NursingProcess:Assessment  Healthhistory  Physicalassessment  Nutrition,BMI, albumin,glucose,electrolytes  Literacy,hearing,and vision;may impact communicationafter surgery  Copingskillsand availablesupportsystemsforpatient and familyafter surgery UpperRespiratory: NursingProcess: Diagnosis  Ineffectiveairway clearance  Impairedverbal communication  Imbalanced nutrition  Disturbedbodyimage  Anxiety,depression  Self-caredeficit  Knowledgedeficit UpperRespiratory: CollaborativeProblems/Potential Complications  Respiratorydistress  Hemorrhage  Infection  Wound breakdown  Aspiration  Tracheostomalstenosis 10 2/16/2016 CaseStudy Mary Par, 44 years of age, is a female patient who presents to the emergency department with epistaxis. She has a bath towel saturated with bright red blood and small clots. She is breathing through her mouth as she has her head tilted forward and has direct pressure applied to the soft outer portion of the nose against the midline septum using her thumb and index finger. She applied direct pressure for over 15 minutes and her nose will not stop bleeding. (Learning Objective 4) a. What nursing management is needed for the patient? b. What measures may be used to treat the epistaxis? c. Once the bleeding is controlled and the underlying cause is identified, if able and treated, what instructions should the nurse provide the patient? Whatnursing management is needed forthe patient?  Assess airway patency and vital signs ongoing until stabilized.  Assessment of cardiac status via cardiac monitoring, if indicated, in the emergency department.  Assess oxygenation using pulse oximetry.  Assess if the patient had a traumatic event leading to the epistaxis or a history of bleeding or clotting problems in the past, and if the patient is taking anticoagulants, such as aspirin or warfarin, or any herbal treatments, or if she has high blood pressure.  Provide emesis basin so the patient may expectorate excess blood into it.  Provide ongoing emotional support.  Assist the emergency department physician in controlling the bleeding.  Provide ordered interventions. The interventions may include hemoglobin and hematocrit and platelet count, PT, and PTT.The orders may include an IV infusion of normal saline; replacement of platelets if the patient has thrombocytopenia; replacement of clotting factors, if low; and replacement of blood, if low. Whatmeasuresmaybeusedtotreat theepistaxis?  Use of illumination to determine the site of bleeding. Apply direct pressure if bleeding is from anterior portion of nose.  Assist patient to tilt head forward and pinch soft outer portion of nose against septum for 5 to 10 minutes to prevent aspiration and swallowing of blood.  Application of nasal decongestant to act as a vasoconstrictor.  Cauterization with silver nitrate or electrocautery, if visible bleeding sites are found that do not respond to above treatments.  Use of Surgicel orGelfoam patch to stop bleeding.  Cotton tampon may be used to stop the bleeding by direct occlusion of localized vessels.  Packing the nose with gauze with petroleum or antibiotic ointment to decrease bleeding if unable to identify the bleeding vessel. A balloon inflated catheter may also be used.The packing may remain in place 3 to 4 days, if needed. 11 2/16/2016 Answerscontinued  Once the bleedingis controlled andthe underlying causeis identified,ifableand treated, what instructions shouldthe nurse provide the patient?  Avoid vigorous exercise or bending over with head downfor the next several days.  Avoid hot or spicy foodsor tobaccoproducts becausethese products willleadto increased risk for bleeding.  Avoid forcefulnose blowingor straining or high altitudesor nasaltrauma.  If a nosebleedoccurs in the future, apply direct pressure to your noseas youdidwhen youpresented to the emergency department and, if the bleeding does not stopafter 15 minutes, then seek prompt medicalattention. Q & A 12 Lower Respiratory Problems Chapter 28 Priscilla Hartley, DNP, RN Learning Outcomes  Prioritize thenursing managementof the patient with lowerrespiratory problems.  Describethe etiology,clinical manifestations, and nursing and collaborative managementof patients with lowerlung disordersincludingPneumonia,TB, Lung Cancer, and Pulmonary Embolus  Describethe pathogenesis, classification, clinical manifestations, complications, diagnostic abnormalities, and nursing and collaborative managementof patients with lowerrespiratory problems Acute Bronchitis  Inflammation of the bronchiresulting from viral or bacterialupper respiratory infection(URI)  Symptoms: Hackingcough, Fever, Dyspnea, malaise  Usually self-limiting condition;treatment is supportive.  NSAIDS,Bronchodilators, Cough Suppressants, Antibiotics 1 Pertussis  Highly contagious infection.  Although immunization is available, incidencerates are rising possiblybecauseof waningimmunity.  Symptoms:cough that has a “whooping”sound.  Treatment:antibiotics (Erythromycin/Zithromax) and supportive care. Pneumonia  Acute infectionoflung caused by bacteria, viruses,fungi, parasites,and chemicals  Pneumoniaisa leadingcause of deathinthe US th  Pneumonia/Flu,6 leadingcause ofdeathin ages >65 years. 6 2 Etiology  Mucociliarymechanismimpaired Pollution Cigarette smoking Upperrespiratory infections Trachealintubation Aging 7 Etiology  3 waysorganisms reach lungs: Aspiration from nasopharynxor oropharynx Inhalation of microbessuch as Mycoplasma pneumoniae Hematogenousspreadfrom primary infection elsewherein body 8 Community-acquired pneumonia (CAP) Lower respiratory infectionof lung occurringfirst 2daysof hospitalization Onset incommunity Highest incidenceinmidwinter Smokingimportant risk factor Refer to Table28-1for Risk Factors 9 3 Community-acquired pneumonia (CAP)  Three-stepapproachto treatment Assess ability to treat at home. Calculate PORT (PneumoniaPatient Outcomes Research Team). Empiricantibiotic therapyshould bestarted as soon as possible even if a definitivediagnosis has not bemade. 10 MCAP: HAP, VAP, HCAP Hospital AcquiredPneumonia(HAP): Occurring48 hours or longer after admission andnot incubatingat time of hospitalization Ventilator AcquiredPneumonia(VAP): Occurringmore than 48 hours after endotrachealintubation HealthcareAssociated Pneumonia(HCAP) 11 HAP  Risk factors for HAP Immunosuppressive therapy Generaldebility Endotrachealintubation 12


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