Minor Case Study of Diabetic Ketoacidosis and Type 2 Diabetes Mellitus

Alexandra Shear Minor Case Study 2 2/18/14

Introduction: atient T!"! is a #$ year%old fe&ale! She is ' feet # inches tall( and her ad&ittin) *ei)ht is 188 lbs! T!"! *as ad&itted *ith a pri&ary proble& of nausea( +o&itin)( polydipsia( and polyuria! This patient *as chosen for the study because she *as recently dia)nosed *ith type 2 diabetes &ellitus ,T2DM- and *as a )reat candidate for diet education! The study be)an 2/1#/14 and ended 2/14/14! The focus of this study is on diabetic .etoacidosis and type 2 diabetes &ellitus! Social History: T!"! is sin)le! She is currently e&ployed( and she is insured throu)h Medicaid! She does not ha+e any children and li+es *ith her &other! T!"! is a current s&o.er! She has s&o.ed 1 pac. per day for the past 12 years! She reports social alcohol use! Normal Anatomy and Physiology of Applicable Body Functions: Durin) nor&al &etabolis&( excess ener)y put into the body durin) &eals is stored for later use! /ner)y use in the body in constant( but ener)y inta.e is not( *hich &eans ener)y &ust be stored( so it &ay be used *hen there is no ener)y inta.e!1 1'$$ .cals are stored as carbohydrates in the for& of )lucose in the blood strea& and )lyco)en in the li+er and &uscle! 0f there is &ore than 1'$$ .cals of carbohydrate( the rest is con+erted to tri)lycerides and stored as fat in adipose tissue and the blood strea&! After &eals( nutrients are absorbed and enter the blood strea&! This is referred to as the fed state( and )lucose is used as the &ain source of ener)y! 1n a+era)e( it ta.es about 4 hours for a typical &eal to be absorbed!1 2hen there are no nutrients in the 30 tract to be absorbed( ener)y stores are used for ener)y! This is called the fastin) state! Stored for&s of protein and fat are bro.en do*n for )lucose for&ation and ener)y production!1 The pancreas is located in the abdo&inal ca+ity! The cells *ithin the pancreas are classified into t*o difference functions4 exocrine and endocrine! The exocrine cells are responsible for secretion of fluid and di)esti+e en5y&es( *hich tra+el +ia the pancreatic duct to the duodenu&1! The endocrine cells &a.e up a s&all portion of the pancreas and include4 Alpha cells4 secrete )luca)on and )luca)on%li.e peptide ,36 %1-

7eta cells4 secrete insulin Delta cells4 secrete so&atostatin 8 cells4 secrete pancreatic polypeptide

0nsulin and )luca)on are the &ain hor&ones used to control and &aintain nor&al blood )lucose! 0nsulin is initially secreted as a pro%hor&one( called pro%insulin! 0t is acti+ated by the re&o+al of a peptide se9uence and disulfide bondin) bet*een t*o peptide chains! The acti+e insulin then enters the blood strea& throu)h the portal +ein! 0nsulin has a half%life of ' &inutes( so it de)rades 9uic.ly bac. to t*o peptide chains!1 0nsulin is considered an anabolic hor&one( *hich &eans it controls the &etabolis& of carbohydrates( proteins( and lipids! 0t pro&otes the upta.e of )lucose into hepatic( &uscle( and adipose tissue and the sti&ulation of )lyco)en( tri)lycerides( and protein synthesis!1 0nsulin secretion is sti&ulated by an increased le+el of blood )lucose and action of counter%re)ulatory hor&ones( such as )ro*th hor&one! Transport &olecules( called 36:T%1 throu)h '( are used to absorb )lucose( fructose( and )alactose into the cell! The type of transporter a+ailable on the cell reflects the cell re9uire&ent for food! Most cells need &ore than one transport &olecule to absorb ade9uate nutrients!1 The 36:T%4 transport &olecule is insulin depended! 0t is present in s.eletal and cardiac &uscle cells and adipocytes! 0nsulin allo*s translocation of 36:T%4 fro& inside the cell to the cell &e&brane( so it can transport the )lucose into the cell! The brain( li+er( and *or.in) &uscle cells do not need insulin and are readily per&eable to )lucose( but &ost tissues depend on insulin for transportation of )lucose into the cell!1 0nsulin pro&otes )lucose oxidation( )lyco)en and tri)lyceride stora)e( acti+e transport of a&ino acids fro& blood into &uscle and other tissues( protein synthesis *ithin the cells( and it produces a positi+e nitro)en balance! 3luca)on is released *hen blood )lucose is belo* a nor&al le+el! 0t sti&ulates the brea.do*n of stored )lyco)en and production of ne* )lucose fro& a&ino acids! 0t also sti&ulates lipolysis( *hich pro+ides additional &aterial to &eet the body;s ener)y needs! 36 %1 and 2 are &ade fro& a precursor of )luca)on and sti&ulate the action of insulin and inhibit the action of )luca)on!1

Past Medical History: /lecti+e abortion Type 2 Diabetes Mellitus( dia)nosed 1/8/14

Present Medical Status and Treatment: 0n T2DM( the body produces insulin( but the tissues are insulin resistant( and cannot utili5e the insulin as they nor&ally *ould! The insulin resistance is caused by a defect in the cell%receptors! The )lucose transporters do not &o+e to the outer cell &e&brane and are unable to ta.e )lucose into the cells! 7ecause the cells aren;t recei+in) )lucose( the li+er produces &ore )lucose( *hich causes hyper)lyce&ia! This increases the need for insulin( so the pancreas increases insulin production! /+entually( the pancreas burns out and is unable to produce insulin!1 Diabetes is dia)nosed usin) a he&o)lobin A1c lab test! 0f t*o separate tests results are )reater than <!'=( diabetes is indicated! A rando& blood su)ar le+el )reater than 2$$ &)/d6 or a fastin) blood su)ar le+el )reater than 12< &)/d6 also indicates diabetes! An oral )lucose tolerance test( *hich re9uires fastin) o+erni)ht( &easurin) fastin) blood )lucose( then consu&in) a su)ary li9uid and testin) blood su)ar periodically for t*o hours can also be done! A blood )lucose le+el )reater than 2$$ &)/d6 t*o hours after in)estin) the li9uid also indicates diabetes!2 0ndi+iduals *ith T2DM &ay be asy&pto&atic for so&e ti&e and present only *ith co&plications associated *ith diabetes!1 Diabetic .etoacidosis is a life%threatenin) proble& caused by hyper)lyce&ia! 0t is al*ays the result of inade9uate insulin for )lucose use! Characteristics of DKA include hyper)lyce&ia( &etabolic acidosis( and .eto)enesis! The hyper)lyce&ia results fro& the inade9uate insulin( *hich lea+es the )lucose in the blood! 7ecause the cells are not recei+in) )lucose to produce ener)y( fat is used and .etones are for&ed! The acidosis occurs because of the increased production and decreased use of acetoacetic acid and #% beta%hydroxybutyric acid fro& the fatty acids! The excess .etones then spill into the urine! DKA is dia)nosed by the a&ount of .etones in the urine( blood acidity( and ele+ated blood )lucose!# DKA occurs &ost often in T1DM patients and ne*%onset T2DM patients( *ho are obese and ha+e i&paired insulin secretion and action! 0llnesses( such as

the flu( colds( +o&itin)( and diarrhea can lead to DKA if they are not treated properly! Sy&pto&s of DKA include4 olyuria olydipsia 2ei)ht loss >o&itin) Abdo&inal pain Dehydration ,loss of s.in tur)or( dry &ucous &e&branes( tachycardia( hypotensionAcetone breath Kuss&al respirations T2DM is &ana)ed usin) a co&bination of nutrition therapy( physical acti+ity( and &edications( *hen re9uired! The opti&al &ethod is tar)eted blood )lucose control( *here indi+iduals .no* and atte&pt to achie+e blood )lucose )oals usin) feedbac. fro& self% &onitorin) blood )lucose ,SM73- and routine labs! Medications used to treat T2DM include4 Alpha%)lucosidase inhibitors4 delay intestinal absorption of )lucose A&ylin analo)s4 delay )astric e&ptyin)( decrease postprandial )luca)on release( suppresses appetite 7i)uanides4 decrease hepatic )lucose production( increase insulin upta.e in &uscles 0ncretin &e&etics4 &i&ic )lucose%dependent insulin secretion( suppress ele+ated )luca)on secretion( delay )astric e&ptyin) Me)litinides4 sti&ulate insulin secretion in presence of )lucose Sulfonylurea a)ents4 sti&ulate insulin secretion Thia5olindinediones4 decrease insulin resistance 0nsulin4 replaces endo)enous insulin4

0f left untreated( DKA can lead to co&a and death!1

hysical acti+ity is )enerally reco&&ended for e+eryone *ith T2DM! /xercise increases blood )lucose upta.e in the &uscles durin) and after acti+ity and also i&pro+es insulin sensiti+ity! #$%4' &inutes of &oderate intensity exercise #%' days per *ee. is su))ested( *ith no &ore than 2 consecuti+e days *ithout acti+ity! 1 ?esistance exercises that tar)et &a@or &uscle )roups # ti&es per *ee. are also ad+ised! 0ndi+iduals ta.in) insulin or insulin secreta)o)ues should &onitor blood su)ar before exercise to pre+ent hypo)lyce&ia! 0f blood )lucose is belo* 1$$ &)/d6( 1' ) of carbohydrate should be in)ested!1 Treat&ent )oals for nutrition therapy are based on chan)es that the patient is *illin) to &a.e! The ulti&ate )oal is to Asupport and facilitate lifestyle and beha+ior &odifications that result in i&pro+ed &etabolic control!B1 A decrease in ener)y inta.e to pro&ote *ei)ht loss is often reco&&ended! 3ra&s of carbohydrates are &onitored by exchan)es or carbohydrate countin)! 6ess than 1#$ ) of carbohydrate per day is not reco&&ended! Typically( protein inta.e should not exceed $!8 )/.) per day or 1$= of total calories( and inta.e abo+e 2$= of total calories &ay be a ris. factor for neuropathy! Total fat should not exceed 2'%#'= of daily calories( and saturated fat should not be abo+e C= of ener)y inta.e! Trans fat should be &ini&al! A +ariety of fiber%rich foods are reco&&ended! 8oods *ith increased a&ounts of )u&s( beta%)lucans( psylliu&( resistant starches( and pectin ha+e a positi+e effect on blood )lucose le+els because they slo* absorption of the )lucose fro& the s&all intestine! These can be found in le)u&es( fruits( +e)etables( and oats! 8or indi+iduals under '$( #8 ) of fiber per day is reco&&ended for &en( and 2' ) of fiber per day for *o&en! 1 Treat&ent for DKA includes hospitali5ation for ad&inistration of 0> fluids and supple&ental insulin! Seru& electrolytes are also assessed and replaced( if needed!1 7ecause DKA can be caused by illness( patients need to .no* the precautions to ta.e *hen sic.! To &aintain )lucose in the )oal ran)e and pre+ent .etosis( about 1'$ to 2$$ ) of carbohydrate per day should be in)ested and &edication should be ad@usted accordin)ly!# Ade9uate a&ounts of li9uid should also be consu&ed *hen ill! T!"!;s sy&pto&s upon ad&ission *ere nausea( +o&itin)( polyuria( and polydipsia! "yper)lyce&ia can often cause diuresis( *hich leads to excessi+e urination and dehydration! The dehydration causes the patient to be +ery thirsty!

6aboratory findin)s can be found in Appendix A! Medications can be found in Appendix 7!' The patient *as not seen by nutrition i&&ediately after ad&ission( but often patients are lethar)ic and tired *hen first ad&itted! 0t is difficult to discuss nutrition education *ith the patient in this state! T!"! *as eatin) brea.fast durin) the first +isit! She stated she *as no lon)er feelin) nauseous and had an appetite! Durin) the second +isit( T!"! *as preparin) for dischar)e and said she *as feelin) li.e her nor&al self a)ain! Medical treat&ent included4 2/12/144 0> fluids and insulin started in /D 2/1#/144 D' in *ater s*itched to D' D ESF 1$$ &6 2/1#/144 0> insulin discontinued o Started on 6antus G "u&alo) 2/14/144 Dischar)ed ho&e *ith ho&e health care on Metfor&in and 6antus

There *ere no sur)ical procedures done! Medical Nutrition Therapy: T!"! stated she doesn;t eat brea.fast or lunch! Eor&ally( her first &eal of the day is bet*een # and 'p&( *hen she )ets off *or.! "er &other does all the coo.in) and shoppin)! T!"! said her &other is also diabetic( so she is fa&iliar *ith a diabetic diet! She also said they don;t typically a+oid any foods in her house! She eats *hate+er her &o& &a.es for dinner! The patient said she had been +ery sic. for the past 24 hours( so she really hadn;t eaten &uch! T!"!;s current prescribed diet is a Diabetic Mediu& diet( *hich pro+ides 1<$$% 1H$$ .cals/day and 1H'%24$ ) carbohydrate/day! This diet also li&its total fat to 2'%#'= of .cals( cholesterol to less than 2$$ &)/day( sodiu& to #%4 )/day( and controls carbohydrate inta.e *ith each &eal! T!"!;s esti&ated nutritional needs *ere calculated usin) 22%2C .cal/.)( $!8%1 ) protein/.)( and 1 &6/.cal fluid! 7ecause T!"!;s 1 inta.e *as )ood *hile ad&itted( this diet should &eet her esti&ated nutritional needs! T!"! *as &ade E 1 in the /? on 2/12! "er diet *as ad+anced to clear li9uids on 2/1#! She then re9uested her diet to be ad+anced to solid foods( so a soft ,30- diet *as 7

ordered! The ?E put AdiabeticB in the co&&ent section of the order( *hich does not interface *ith the diet office orders( so T!"! *as not recei+in) any carbohydrate restriction! After brea.fast on 2/1#( T!"!;s diet *as further ad+anced to a Diabetic Mediu& diet! The ob@ecti+es of this dietary treat&ent *ere to li&it the a&ount of carbohydrate( in hopes of i&pro+in) the patient;s blood )lucose! 2hen discussin) carbohydrates and her diet( T!"! initially stated she *asn;t Aallo*ed to eat anythin)!B She *as a little sad that should *ould not be able to drin. re)ular soda( and she see&ed a little o+er*hel&ed by the diet infor&ation! As the con+ersation pro)ressed( she see&ed a little &ore co&fortable *ith countin) carbohydrates and her diet at ho&e! T!"! *as pro+ided *ith handouts fro& the Acade&y of Dietetics and Eutrition on carbohydrate countin) and label readin)! She *as also )i+en a Diabetes Sur+i+al S.ills boo.let and infor&ation on the Diabetes 2ellness Center in Middleto*n! 0nfor&ational +ideos on diabetes &ana)e&ent *ere loaded onto the patient;s tele+ision for her +ie*in)! Durin) the second +isit( the patient had loo.ed o+er &uch of the infor&ation and *as feelin) confident about her success *ith the diet at ho&e! /S State&ents4 8ood and nutrition%related .no*led)e deficit related to DM as e+idenced by patient state&ent! Altered nutrition%related lab +alues related to DM as e+idenced by 1C )lucose and ")b A1c of 1#!<! T!"!;s present nutritional status is )ood! "er 7M0 is ##!4( *hich is considered )rade 1 obese! There is no concern for &alnutrition! She does not ta.e a &ulti+ita&in at ho&e( but she *ould benefit fro& one! T!"! has no difficulties che*in) or s*allo*in)( so there is no need for alternati+e feedin) &ethods! 0t is difficult to e+aluate her food or nutrient inta.e *ithout a detailed diet history! "o*e+er( T!"! stated she eats a lot of pasta at ho&e! 0t is possible her diet relies hea+ily on si&ple carbohydrates and processed con+enience foods! :pon dischar)e( T!"! had an appoint&ent *ith a local CE and had a referral for the Diabetes 2ellness Center! Contact infor&ation for the ?D *as also pro+ided on the patient;s handouts to call *ith any 9uestions or concerns re)ardin) her diet!

Prognosis: T!"!;s pro)nosis is )ood! She see&ed to understand the carbohydrate countin) infor&ation and *as able to repeat &ultiple carbohydrate foods and her carbohydrate allo*ance for each &eal! She *ill need diet reinforce&ent and further education( *hich can hopefully be pro+ided at the Diabetes 2ellness Center! Summary and onclusion: 0 chose this patient for &y last case study because 0 *as able to do so&e diet education and co&pare &y patient interaction and education s.ills *ith &y first case study patient! Eo*( 0 find it easier to tal. to patients about their diets( *hich 0 thin. &a.es the education better! This patient *as also youn)er and easier to education than &y first case study patient( *hich &ade thin)s a little si&pler! "opefully( the education &aterial pro+ided and discussion *ill help her to follo* her diet *hile she;s at ho&e and pre+ent further read&issions!

Bibliography 1- Eel&s M( Sucher K( ?oth S6! Eutrition Therapy and athophysiolo)y! 2nd ed! Cen)a)e 6earnin)I 2$$<! 2- Type 2 Diabetes4 Tests and Dia)nosis! Mayo Clinic!http4//***!&ayoclinic!or)/ diseases%conditions/type%2%diabetes/basics/tests%dia)nosis/C1E%2$$#1H$2! Accessed 8ebruary 1<( 2$14! #- 6! Kathleen Mahan MS ?D CD/( Syl+ia /scott%Stu&p MA ?D 6DE( Janice 6 ?ay&ond MS ?D CD! KrauseKs 8ood and the Eutrition Care rocess! 1#th ed! St! 6ouis( M14 SaundersI 2$12! 4- /scott%Stu&p S! Eutrition and Dia)nosis%?elated Care! Cth ed! 7alti&ore MD4 6ippincott 2illia&s G 2il.insI 2$$8! '- rons.y LM( Cro*e J ! 8ood Medication 0nteractions! 1Cth ed! 7irchrun+ille( A4 8ood%Medication 0nteractionsI 2$12!

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