NUR 317 Med Surg 1 Exam 3 Study Guide- Ch. 48, 49, 32, 37: Diabetes; Thyroid; Adrenal Gland; Hyper/hypotension; Vascular Disorders
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NUR 317 Med Surg 1
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NUR 317 Med Surg 1
NUR 317 Med Surg 1 Exam 3 Study Guide- Ch. 48, 49, 32, 37: Diabetes; Thyroid; Adrenal Gland; Hyper/hypotension; Vascular Disorders
NUR 317 EXAM 3 Lewis Chapter 48/ Diabetes: 1. Describe the prevalence and incidence of diabetes mellitus. ● Diabetes mellitus is the seventh leading cause of d...
NUR 317 Med Surg 1 Exam 3 Study Guide - Ch., 49, 32, 37: Diabetes; Thyroid; Adrenal Gland; Hyper/hypotension; Vascular Disorders NUR 317 EXAM 3 Lewis lChapter l48/ lDiabetes: 1. Describe lthe lprevalence land lincidence lof ldiabetes lmellitus. ● Diabetes lmellitus lis lthe lseventh lleading lcause lof ldeath lin lthe lU.S., lbut lit lis llikely lto lbe lunderreported land lunderdiagnosed. l 2. What lare lthe lmajor lorgans laffected lby lthe llack lof ltight lglucose lcontrol land lhow lare lthey laffected lnegatively? ● Tight lglucose lcontrol: lreduced ltheir lrisk lfor lthe ldevelopment lof lretinopathy land lnephropathy. l ○ Treatment lgoals lto lmaintain lblood lglucose llevels las lnear lto lnormal las lpossib le l(keep lA1C lless lthan l7) ○ 9 lis lnot lwell lcontrolled l ● Lack lof ltight lglucose lcontrol leffects: leyes, lkidneys, land lblood lvessels l 3. Review lthe lpathophysiology, lrisk lfactors, lmanifestations lof ltype l1 land ltype l2 ldiabetes. l ● Type lI l ○ Caused lby lautoimmune ldestruction lof lthe lpancreatic lB-cells l ■ B-Cells: lsite lof linsulin lproduction ○ Results lin lTOTAL labsence lof linsulin lproduction ○ Generally ldiscovered l<30 lyears lold l ○ Manifestations: lpolyuria, lpolydipsia, lpolyphagia l ■ Polyuria l→ lglucose l(increased lin lthe lbloodstream) l ● osmotic leffect l(increased lurination land lthirst) ■ Polydipsia l(increased lthirst) l→ ldue lto ldehydration ■ Polyphagia l→ lIncreased lhunger ● Consequence lof lcellular lmalnourishment l ● Glucose lcan’t lget linto lcells land lbe lused lso lthe lbody luses lfats land lprotein lfor lenergy l ■ Weight lloss, lfatigue, lfrequency lof linfections, lrapid lonset l ■ Late, lautoantibodies lto lthe lislet lcells lcause la lreduction lof l80% lto l90% lof lnormal lfunction. l ● Type lII l ○ The lMOST lprevalent l ○ Pancreas lproduces linsulin l→ lbut lnot lenough l(beta lcells lbecome lfatigued lafter lmass lis llost) l ○ Insulin lis lpoorly lused lby lthe ltissues, laltered lglucose, land lfat lmetabolism l ○ Defective linsulin lreceptors lunresponsive land linsufficient l ■ (decreased luptake= lincreased lglucose linto lcirculation l= lhyperglycemia) ○ Risk lFactors l ■ Obesity, lsedentary llifestyle l ■ Age, lethnicity l→ lAsian, lAfrican lAmerican, lNative lAmericans, lor lfamily lhx l ■ Diagnosed l→ lgradually lfind lwith lblood ltest lA1C l l 4. Identify lthe ldiagnostics ltests lused lfor lscreeni ng, ldiagnosis, land lmonitoring ldiabetes. ● Pancreatic lstudies l(Fasting lBlood lGlucose l(FBG) ● Oral lGlucose lTolerance lTest l(OGTT) ● Hemoglobin lA1C l(Hb lA1C) ○ This ltest loffers lthe lBEST linformation labout lglucose lcontrol l ○ Measures lamount lof lglucose lthat lis lattached lto lhemoglobin l(RBC) ■ 9 lis lnot lcontrolled l ○ Shows lglucose lcontrol lover l2-3 lmonths l(90 ldays) linstead lof lsnapshot l ● Microalbuminuria ○ Yearly lurine lscreening l ○ Spilling lout lalbumin linto lurine lbecause lglomeruli lare ldamaged l ● Urine lglucose ● Ketones ○ Acids lfrom lbreakdown lof lfat l→ lcause lacidosis ○ Ketones lare lacidic lby-products lof lfat lmetabolism ● Ketonuria lis la lprocess lthat loccurs lwhen lketone lbodies lare lexcreted lin lthe lurine l 5. Identify lvarious loral lantidiabetic lmedication lclassifications, lhow lthey lwork land lan lexample lof leach. l(those lnames llisted lon lPP lslides). ● Thiazolidinediones l(pioglitazone) ○ Decrease lendogenous lglucose lproduction, lincreases linsulin lsensitivity l ○ Watch lfor lcardiac levent l ○ Do lNOT lcause lhypoglycemia lwhen lused lalone l ● a-Glucosidase lInhibitors : l(acarbose, lmiglitol) ○ Slow ldown labsorption lof lcarbohydrate lin lsmall lintestine l ○ Reduces lpost lmeal lhyperglycemia ○ GI lupset l* ● DPP4 -Inhibitors l ○ Increase linsulin lsynthesis land lrelease, ldecrease lhepatic lglucose lproduction ○ Lower lthe lpotential lfor lhypoglycemia l(because lthey lare lglucose ldependent) l ○ GI lupset l a. What lis limportant lto lremember lwhen lcaring lfor la lclient ltaking lsulfonylureas lor lmeglitinides? ● Sulfonylureas : l(glipizide, lglimepiride, lglyburide) l ○ Stimulates linsulin lrelease lfrom lpancreas * l→ ldecreased lBG l ○ Increase ltissue lsensitivity lto linsulin l ○ Side leffects: lHypoglycemia l→ lcommon l* ○ Beta-blockers lcan lmask l(signs lof lhypoglycemia)* ○ Take l30 lminutes lprior lto lmeals l ○ Avoid lalcohol l ● Meglitinides l(repaglinide, lnateglinide) l ○ Stimulates linsulin lrelease lfrom lpancreas l* ○ Administer l15-30 lmin lbefore lmeal* ○ Omit ldose lif lmeal lis lskipped l→ lprevent lhypoglycemia* l ○ SE: lhypoglycemia; lless llikely lthan lsulfonylureas l* b. What lis limportant lto lremember lwhen lcaring lfor la lclient ltaking lthe lbiguanide: lmetformin lregarding ldiagnostic ltests. ● Biguanide l(Metformin): l ○ IV lcontrast liodine l→ lrisk lfor lacute lkidney linjury l ■ Stop lit l2 ldays lbefore land lwait l2 ldays lafter ○ Reduce lglucose lproduction lby lliver l ○ Increases ltissue lsensitivity lto linsulin l ○ Slows lcarb. lAbsorption lin lintestine l ○ Improve lglucose ltransportation linto lcells l ○ May lcause lmoderate lweight lloss l ○ LACTIC lACIDOSIS l ○ First-choice ldrug lfor lmost ltype l ○ Not lused lwith lkidney ldisease l ○ Take lwith lfood l ○ D/c lbefore lprocedure lwith lcontrast lmedium l→ luntil l48 lhours lafterward l* ○ First lchoice ldrug lfor lmost lpeople lwith ltype l2 ldiabetes 6. Discuss lthe lonset, lpeak, land lduration lof lthe lfollowing ltypes lof linsulins: l(use lATI lpharm lbook las lyour lreference) a. Rapid -acting : llispro l(Humalog)/aspart l(Novolog) ● Most lrapid lonset lof laction l(15-30 lminutes) ● Peaks lin l1-3 lhours l ● DOA: l3-6 lhours l ● MUST lbe ladministered lwithin l5 lminutes lbefore la lmeal* ● Clear l b. Short -acting : lregular l(Humulin lor lNovulin) lreplace lmeal ● Onset: l30-60 lminutes l ● Peak: l1-5 lhours ● DOA: l6-10 lhours l ● ONLY lone lyou lcan lgive lIV lbolus, lIV linfusion, lor lIM* ● Clear l c. Intermediate : lNPH/humulin lN ● Onset: l1-2 lhours ● Peak: l6-14 lhours ● DOA: l16-24 lhours l ● Cloudy l ○ Never lshake lthem, ldecrease lability lto labsorb, lroll lthem l d. Long -acting : lglargine l(Lantus) ● Onset: l70 lminutes l ● Peak: lNONE* ● Duration: l24 lhours l ○ Administered lonce la lday l(SAME ltime leach lday) ○ CAN lNOT lbe lmixed lwith lother linsulin s l 7. Why lis lit limportant lfor lnurses lto lknow lonset, lpeak, land lduration lof leach ltype lof linsulin? ● Onset lof laction ltells lyou lwhen lthe lpatient lhas lto leat l ● The lpeak lis lwhen lthe lpatient lis lat lgreatest lrisk lfor lhypoglycemia l 8. Describe lthe lsites land ladministration ltechniques lfor linsulin linjection. l lWhat llocal lskin lcomplications lcan loccur lwith lthe luse lof l“pork” linsulin, lnot lrotating lsites lor
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