NR 507 PATHOPHYSIOLOGY WEEK 5 TD1 Alterations in Endocrine Function Discussion Part One (NR507)

Exam (elaborations) NR 507 PATHOPHYSIOLOGY WEEK 5 TD1 Alterations in Endocrine Function Discussion Part One (NR507) Week 5: Alterations in Endocrine Function - Discussion Part One Loading... This week's graded topics relate to the following Course Outcomes (COs). 1 Analyze pathophysiologic mechanisms associated with selected disease states. (PO 1) 2 Differentiate the epidemiology, etiology, developmental considerations, pathogenesis, and clinical and laboratory manifestations of specific disease processes. (PO 1) 3 Examine the way in which homeostatic, adaptive, and compensatory physiological mechanisms can be supported and/or altered through specific therapeutic interventions. (PO 1, 7) 4 Distinguish risk factors associated with selected disease states. (PO 1) 5 Describe outcomes of disruptive or alterations in specific physiologic processes. (PO 1) 6 Distinguish risk factors associated with selected disease states. (PO 1) 7 Explore age-specific and developmental alterations in physiologic and disease states. (PO 1, 4) Discussion Discussion Part One (graded) Responses Lorna Durfee 5/29/2016 8:58:33 AM Discussion Part One dMrisn. kB dlaukrein igs tahni so tlidmere .a Sduhlet hwaist ha dhiiasbtoerteys o afn Tdy hpaes Ib deieanb etoteos .i ll to get out of bed for two days. She has had a severe cough and has been unable to eat or On admission, her laboratory values show: PATIENT VALUES Sodium (Na+) 156 mEq/L Potassium (K+) 4.0 mEq/L Chloride (Cl–) 115 mEq/L Arterial blood gases (ABGs) pH- 7.30; Pco2-40; Po2-70; HCO3-20 NORMAL VALUES Normal values Sodium (Na+) 136-146 mEq/L Potassium (K+) 3.5-5.1 mEq/L Chloride (Cl–) 98-106 mEq/L Arterial blood gases (ABGs) pH- 7.35-7.45 Pco2- 35-45 mmHg Po2-80-100 mmHg HCO3–22-28 mEq/L • List five (5) reasons on why she may have become bed ridden? • Based on these reasons what tests would you order? • Describe the molecular mechanism of the development of ketoacidosis The patient is an older adult and has been ill for two days. She has a severe cough and not able to eat or drink. She has type I diabetes. Labs: Sodium is 156 mEq/L, normal is: 136-146, Chloride 115 mEq/L, normal is: 98-106, pH 7.30, normal is 7.35-7.45, little low, normal 80-100, HC03 low at 20, normal 22-28. Po2- 70, is low, The patient has: High sodium at 156, high chloride at 115. Low Ph 7.30, Low, Po2 (partial pressure of oxygen) is 70, HC03 (bicarbonate) is 20, low. Doctor Brown and Class: aKciisdhoosries .( 2H0e1 4a)l seox epxlapilnasi ntsh atht adti aDbKetAic okcectouarsc imdoossitsl yis i na tcyopme p1l idciaatbioente osf m deiallbietutess ( DchMar)a pctaetrieiznetds. b Wy hhyepne ar gplaytcieemnti ha,a sh ykpeetorkaectiodnoesims,i ath, eayn dc amne etxabhoibliict nausea, cvoonmfiirtimnged, awndit ha bddeotemctiinoanl poaf ihny. p Ietr ikse ato vneermy isae arinodu sa ncioonnd gitaiopn m theatat bcoalnic l eaacdid toos icse rweibtrha hl yedpeemrgaly acnedm ciao.m aB aesc awueslel tahsi sd epaatthie. n Tt hise idlli,a igt ncoasni sb oe fo DneK oAf tihs e stressors that can trigger DKA (Kishore, 2014). dMecvCelaonpcse a, sB ara rsehseurlst ,o Hf uae dtheefirc aienndc Ry oobf eirnts Eul iJno naensd (a2n0 1in4c)r teealsl eu isn t hthaet Dleivaeblest oicf kinestoualicni dcoosuins t(eDr-KreAgu) liast oa rsye rhioorums ocnoemsp (lMiccaCtioann coef edti.a able.,t e2s0 m14e lpl.i t7u4s.4 D). KItA is emsopsetc ciaolmlym a opnaltyie fnotu wndit hin d piaabtieetnetss twypiteh I t ydpiaeb Ie tdicia kbeettoeas cbiudto ssiosm ceatnim bee sa f soeurniodu isn ptryopbel eIIm d. i aTbheete asu. t hWohrse nal aso p raetileantet thhaast awnh iennte trhceurrer eisn ta inl linnetsesr rourp itniofenc otifo n, insulin administration can also result in DKA (McCance, Huether, Brashers, & Rote, 2014, p. 744). GWHhe. n T thheesree hiso irnmsounliens daenftiacgieonnciyze t hines cuoliunn bteyr -irnecgruelaastionrgy ghlourcmosoen ep rcoodnuccetniotrna ttihounss dienccrreeaassien. g T tihsosusee huoserm oof ngelus caorese c. a tWecihtho laa mdeifniecsie, nccoyrt iosfo iln, sgululicna tghoant ,i as nd gplruocfoounneodg, ethneersei si sa na dd ekcerteoagseende sgilsu. c oWseit hu pintackree.a s Aedls gol,u tchaegreo nis l eavne ilnsc trheearsee dis faa tc monettraibbuotliiosmn two itthhe t hacet irvealetiaosne ooff tfhaett yg laucciodns eaongde nacicc ealnedra kteedto genic liver pKaetthownaesy sa.r eB uesceadu sbey tthheer eti isss uinessu alsin s oduefricceise ntoc yr etgheen oevraetrep rtohde ubcitciaornb oonf ahteep. a Wtich Ben-h kyedtroonxeysb aurtey froatuen adn tdh eayc eatcota tcoe tbica laacnicdes tchaeu lsoinssg oinf cbriecaasrebdo nkaetteo.n es. nHoytp oecrckuerto, ntheem piaa tmienayt dbeev ae lroepssu lmt oetfa ibmopliaci ramciednots iins (thMec uCsaen ocfe keet taoln.,e 2s 0b1y4 t,i sps.u 7e4s5, ) this allows organic acids to circulate. If bicarbonate buffering does cDoiratbiseotilc, gKroetwotahc ihdoorsmiso rnees.u lTtsh ien e rfefdeuctcse do fi nhsourmlino nleavl eallst earnadti oenlesv aarteio; na cocfe cleoruantitoenr- roefg gulluactoornye ohgoermneosnise sa.n Tdh gel yhcoorgmeonnoelys sairse a cnadt eac hdoeclarmeaisnee isn, gglluuccaogsoen , uwthiliiczha taioren cboyn tvheer tpeedr itpoh keertaol nteis sbuoedsi etsh aint wthiell lrievseurl, ta innd h tyhpiso glelyadces mtoi ak,e atnodn eamn iian. c rTehaesree i nis laiplsool yasnis i nrecsruealtsien gin i np rion-cirnefalsaemdm parotodruyc ctiyotno koifn fer eaen dfa pttryo -acids, coagulation factor levels (Dynamed, 2016). iWnfeesctteirobne.r gT (h2e0 d1e3f)i c aielsnoc yin sftoimrmusl autes st hthaet DelKevAa trieosnu oltfs cino uinnsteurlrieng duelafitcoireyn chyo rfmroomne isn s (uWline snteornbceormg,p 2li0a1n3c,e p, .a 3n3d7 i)n.c rWeahseend tihnesruel iins nneoe adb bileictya utose u osfe glucose tohfe a bdoipdoys en eteisdssu ea naontdh ethr es ofurerec ef aotft ye naecridgsy .c oLnivpearste t hacet iavciettyy wl ciolle innzcyremaes eA a nfodr ceanuesregsy a p broredaukcdtioownn. oTfh aed riepmosaein tdisesru ies tbhraotk fernee dso fwatnty i natcoid kse. t oTnhees .b rTehake dboowdyn tuhseerse k ies tao nperso mfoor teionne rigny h. yHpoewrgelvyecre,m thiae ya nadcc luemadusl atote a rna poisdmlyo.t i Gc dlyiucoregseins tahnadt rpersouteltisn sin a dree hcyadtarbaotiloizne, dm aentadb foolrimc a gcliudcoossise .a nWd ihthy pthereo psrmoodluacrt isotant eo f glucose, (Westerberg, 2013, p. 338). aTnhde rteh ea rceo amt pleliacsatt (io5n) sf itvhea tr eaarsisoen ws fiothr tthhies pcaotniednitti obnei.n gA sb ewderi ddod enno. t Bkneocawu sthee t hmee pdaitciaetniot nhsa ss haen rienqfeucirteiosn w aen dd os hneo ti sk dnioawbe itfi cs,h iet hcaans mseet dthicea tsitoang e for DKA cboe mdephliyadnrcaet.e dM. Sedhiec aaltsioon hsa csa bne aclosmo ein wfleuaekn cbee cmaeutsaeb sohliec ips rnoocte sesaetisn. g T ohre d priantikeinntg a. pApgeaairns, two eh aavree na olta ccke rotafi anp wpehtaitt ei nasnudl iins snhoet mdrainyk bine gr eoqru eiaritningg, aanndd can lpeetrhhaarpgsy .s h Seh hea ms nayo th taavkee np rhoebrl ienmsus lwini tcho brrreecattlhyi.n gH, earn md esnhtea cl osutaltdu sh amvaey p bneecuommoen d due to dehydration. Because of her illness, she also may have oTrhdee rte wstosu tlhda tb ne eseedru tmo oebletacitnroedly aterse, oBuUtliNn,e dan bdy c Kreiasthionrine e(,2 g0l1u4c)o. s eT,h kee atountheos,r oinsmfoormlarsi tuys. oSfh teh ne eneedesd a t ou reivnael tueastte f hoer rk seetrounmes .g lIufc tohsee .k eAtodndeisti oarnea lp toessittsiv teo tghleunc oAseB aGn dm keeatsounreesm aernet .p oWsiittihv eD wKeA c a tnh eprree sisu mane ,a srtheer ihaal dp HD K< A7..3 0 W wiitthh h aenri opnre gseanpt >il l1n2e,s asn, dsh see raulsmo kneeteodnse asp ipnr tohper ipartees setnucdei eosf (hcyuplteurrgelsy, ciemmaigai.n gIf) urine (MKIi sahnodr ed,e 2te0r1m4i)n. e S ahben worimll anleiteieds a i nc hseesrtu xm- rKay. fWore h sehr ocuoludg mhienags utore r uplheo ospuht aptnee aunmdo mniaag onre soituhmer, pliavtehro elongzyy.m Sesh,e C sBhoCu lwdi thha vdeif faenr eEnCtiGal ,t oH sbcAre1ecn ( fDoyr naacmuteed , 2016). Further investigation is urgently needed. References DynaMed [Internet]. Ipswich, MA: EBSCO Information Services. 1995-. Record No. , Diabetic ketoacidosis (DKA) in adults; [updated 2016 May 06]; Available from direct=true&db=dnh&AN=&site=dynamed-live&scope=site. Registration and login required Kishore, P. (2014). Diabetic Ketoacidosis (DKA). In Merck Manual online. Retrieved from metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/diabetic-ketoacidosis-dka Jones, R.E, (2014). Alterations in Hormonal Regulation. In McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (Eds.), Pathophysiology: The biologic basis for disease in adults and children (7th ed., pp. 744, 745). St. Louis, MO: Mosby. Westerberg, D. P. (2013). Diabetic ketoacidosis; evaluation and treatment. American Family Physician, 87(5), 337-346. 5/Rechel DelAntar 29/2016 10:43:07 PM Differential Diagnoses Hello professor and Class, Differential Diagnoses This is a case of an adult female with a history of Type I diabetes who has been too sick to get out of bed for 2 days. This accompanied by symptoms of severe cough, inability to eat or drink during this time. Admission labs show Sodium (Na+)=156mEq/L, Potassium (K+)=4.0mEq/L, Chloride (Cl-) =115mEq/L. ABG shows pH=7.30, pCO2=40, pO2=70 and HCO3=20. From these initial labs, of elevated Sodium level, low pH and an elevated anion gap (21) the patient appears to have some dehydration and metabolic acidosis. In this case, the patient may be exhibiting signs of diabetic ketoacidosis. DKA is common in type 1 diabetes as this form of diabetes is associated with an absolute lack of insulin production by the islets of Langerhans. In type 2 diabetes, insulin production is present but is insufficient to meet the body's requirements as a result of end-organ insulin resistance. Usually, these amounts of insulin are sufficient to suppress ketogenesis. Diabetic ketoacidosis can occur in response to stress, in the case of this patient having severe cough and can occur in 24 hours (Klocker, A.A., et. al., 2013). As the body mounts a stress response, it releases glucagon, growth hormone and adrenaline, which begins to breakdown muscle, fat, liver cells into glucose and fatty acids into fuel in the absence of insulin. The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration (American Diabetes Association, 2013). Five reasons why this patient may be bedridden: 1. Dehydration = DKA can causes dehydration due to increase urination. Osmotic diuresis leads to dehydration and a potential hypovolemic state from fluid loss and inadequate fluid intake making the patient weak and bedridden. 2. Hypernatremia = Hyperosmolality is a common result of hypernatremia. Because sodium is largely in the extracellular compartment, increases in the concentration of sodium cause intracellular dehydration and hypervolemia. Sodium has a vital role in the maintenance of Fluid balance and is responsible for plasma osmolarity. The effects of cellular dehydration are seen principally in the CNS, where stretching of shrunken neurons and alteration of membrane potentials from electrolyte flux lead to ineffective functioning and altered mental status (McLafferty, E., Johnstone, C., Hendry, C. and Farley, A., 2014). 3. Presence of severe cough = although she may not have any fever at this time however she may be at the initial stage of having a URI. This severe cough may have caused her to be short of breath and not having enough oxygenation as manifested in her ABG pO2=70. 4. Hypotension = In this case, the patient is dehydrated from DKA with an inadequate fluid intake causing hypovolemia from fluid loss causing weakness and altered consciousness (Klocker, A.A., et. al., 2013). 5. Lactic acidosis = Lactic acidosis is more common in DKA than traditionally appreciated and is associated with change in mental status. The positive correlation of lactate with glucose causes lactic acidosis in DKA may be due to hypoperfusion and also to altered glucose metabolism causing confusion and in some cases being obtunded (Cox. K., et. al., 2012). References: American Diabetes Association. (2013). DKA and Ketones. Retrieved from ?referrer= Cox, K., Cocchi, M.N., Salciccioli, J.D., Carney, E., Howell, M. and Donnino, M.W. (2012). Prevalence and Significance of lactic acidosis in diabetic ketoacidosis. Journal of Critical Care. 27(2). 132-137. Klocker, A.A., Phelan, H., Twigg, S.M. and Craig, M.E. (2013). Blood B-hydroxybutyrate vs. urine acetoacetate testing for the prevention And management of ketoacidosis in Type I diabetis; a systemic review Diabetic Medicine. 30(7). 818-824. McLafferty, E., Johnstone, C., Hendry, C. and Farley, A. (2014). Fluid and Electrolyte Balance. Nursing Standard. 28(29). 42-49. Jennifer Roth reply to Rechel DelAntar 6/1/2016 12:30:58 PM RE: Differential Diagnoses Hi Rechel, Great post! Lab values are imperative to the diagnosis of this patient. Laboratory values should be assessed as indicated by the patient's presentation and history of present illness for an accurate diagnosis. Important lab values to assess when DKA is suspected are: CBC, CMP, ABGs, Jennifer Roth reply to Jennifer Roth 6/1/2016 12:50:02 PM RE: Differential Diagnoses Hi Rechel, Great post! Lab values are imperative to the diagnosis of this patient. Laboratory values should be assessed as indicated by the patient's presentation and history of present illness for an accurate diagnosis. Important lab values to assess when DKA is suspected are: CBC, CMP, ABGs, serum lactic acid, glycosylated hemoglobin, serum amylase, serum lipase, and anion gap (Lenahan & Holloway, 2015). Diagnostic criteria for DKA are based on several lab values including plasma glucose, arterial pH, serum bicarbonate, urine and serum ketones, effective serum osmolality, and anion gap accompanied by mental status (Lenahan & Holloway, 2015). Plasma glucose levels in individuals with DKA are typically greater than 250 mg/dL. Arterial pH can range from 7.25 in mild DKA to less than 7.00 in severe DKA. Urine and serum ketones are present with DKA and serum osmolality is variable but typically less than 320 mOsm/kg. Serum bicarbonate can range from 15 to 18 mEq/L in mild DKA, 10 to 15 mEq/L in moderate DKA, and less than 10 mEq/L in severe DKA. In individuals with DKA, the anion gap, which is a difference of the serum cations sodium and potassium and the serum anions chloride and bicarbonate, can range from greater than 10 mEq/L in mild DKA to greater than 12 mEq/L in moderate to severe DKA (Lenahan & Holloway, 2015). Mental status can range from alert in mild DKA to alert or drowsy in moderate DKA, to stupor or coma in persons with severe DKA (Lenahan & Holloway, 2015). The presence of a plasma glucose level greater than 250 mg/dL, an arterial pH less than 7.3, and the presence of urine and/or serum ketones are considered diagnostic criteria for DKA (Lenahan & Holloway, 2015). Jennifer Roth Reference Lenahan, C.M. & Holloway, B. (2015). Differentiating between DKA and HHS. Journal of Emergency Nursing, 41(3), 201-207. doi: 10.1016/.2014.08.015 Rechel DelAntar reply to Jennifer Roth 6/1/2016 7:05:05 PM RE: Differential Diagnoses Hello Jennifer, I'm glad you found the post informative. In this case, the patient being diabetic. compounded with what seem to be early signs of URI progressed his illness to DKA. DKA can be caused having an uncontrolled hyperglycemic therapy,severe infection or other illness, becoming severely dehydrated, or some combination of these things and may occur in a span of 2 days. With prompt treatment it can be easily corrected, but if left untreated may become induce coma and become life threatening. Diabetic ketoacidosis is distinguished from other diabetic emergencies by the presence of large amounts of ketones in blood and urine, and marked metabolic acidosis. comapred to HONK - Hyperosmolar non-ketotic state which occurs among type II diabetics. Ketoacidosis is not always the result of diabetes. It may also result from starvation which in this case the patient has had a poor intake for what was described as "some time now" (Misra, S. and Oliver, N.S., 2015). This case shows us that one factor alone did not cause ketoacidosis but multiple factors played a role either separately or in conjunction with each other. Reference: Misra, S. and Oliver, N.S. (2015). Utility of ketone measurement in the prevention, diagnosis and management of ketoacidosis. Diabetic Medicine: A Journal of the British Diabetic Association. 32(1), 14-23. Lanre Abawonse 5/30/2016 11:21:52 PM Discussion Part One TAh)isD piaatbieentitc m keigtohat cbied obseids ridden because she has BC)) RHeynpaolt efanisliuorne ED)) DFaietitgaurye /dGeefniceireanlcizye/d S wtaervakatnieosns ketosis In the event that diabetic ketoacidosis is happening the patient might have generalized weakness (Lieu & Goldberg, 2015) resulting in inability to do anything and any of the listed symptoms will be occurring as well. Based on these reasons what tests would you order? In analyzing the patient’s lab results, it is suggested that the patient might be experiencing metabolic acidosis. Chen and Abramowitz (2014) described metabolic acidosis as a common complication of chronic kidney disease, which results in a gain in acids or a loss of bases from the plasma. Chronic metabolic acidosis may have various adverse effects in patients with CKD, including altered skeletal metabolism, insulin resistance, proteinenergy wasting, and accelerated progression of kidney disease. In epidemiologic studies, low serum bicarbonate levels have been associated with high mortality. Therefore, the test that would be ordered is based on the history that we know on the patient and the current assessment. This patient might be in diabetic ketoacidosis as she is unable to eat or drink and possibly has not been able to check her blood sugar. Lieu and Goldberg (2015) stated that diabetic ketoacidosis is a true medical emergency secondary to severe insulin deficiency and characterized by hyperglycemia, ketosis, and metabolic acidosis. This patient’s blood sugar must be check immediately. They also suggest that the patient’s CBC, electrolytes, BUN, creatinine, and A1C help determine history of diabetic control. Anion gap must be checked. This patient has an Anion gap that is above normal: Na – (Cl + Hco3) = 21. Other test will be useful as well to determine the level of this patient severity of illness. Describe the molecular mechanism of the development of ketoacidosis. In ketoacidosis there is continual deficiency and other hormonal influences. Lieu and Goldberg (2015) stated that there is a deficiency of insulin, exacerbated by an increase in counterregulatory hormones (e.g., catecholamines, cortisol, glucagon, and growth hormone) leading to a hyperglycemic crisis, osmotic diuresis, and ketosis. The insulin is unable to get inside the cell membrane as a result and is not able to bind with glucose to create glycolysis and inhibiting pyruvate to form, therefore resulting in no energy for the patient with ketoacidosis. This patient will have a lot of palmitoyl CoA. As explained above, there is no insulin production and there is no inhibition of fatty acid to transport matrix into the mitochondria causing a lot of beta oxidation leading to ketone bodies, which then manifests as acidosis, thus reflecting in anion gap acidosis. The potassium is also increased due to exchange within the cell between protons (up in serum) and potassium (up in cell). The glucose level increases, dehydration (increase in creatine) kicks in, osmotic diuresis follows, and then total body phosphate depletes. Reference. Chen, W., & Abramowitz, M. K. (2014). Metabolic acidosis and the progression of chronic kidney disease. BMC Nephrology, 1555. doi:10.1186/1471- Lieu, C., & Goldberg, E. (2015). Diabetic Ketoacidosis (DKA) In F. J. Domino (Ed.), The 5-minute clinical consult 2015 [electronic resource].Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Jaimie Buckner reply to Lanre Abawonse 6/4/2016 8:24:38 PM RE: Discussion Part One Lanre, Diabetes in general is becoming more common in the United States with DKA being on rog the most serious acute complications (Fusco, Gonzales, & Siu, 2015). DKA is typically characterized by hyperglycemia over 250mg/dL, Bicarbonate level less than 18mEq/L and pH less than 7.30, with ketonemia and ketonuria (Hamdy et. al., 2015). Another test that can be added to the list of tests that you have mentioned is a urinalysis. When the blood glucose levels are too high in the blood it spills over into the urine and is excreted (Hamdy et. al., 2015). A urinalysis can determine if there is glucose and ketones in the urine. Protein can also be found in the urine all leading to diagnosis of DKA. Its amazing how many areas of the body DKA affects. Great post! Reference Fusco, N., Gonzales, J., & Siu, Y. (2015). Evaluation of the treatment of diabetic ketoacidosis in the medical intensive care unit. American Journal Of Health-System Pharmacy, 72S177-S182. doi:10.2146/sp Hamdy, O., Khardori, R., Bessen, H., Brenner, B., Raghavan, V., Rucker, D., Schade, D., Schalch, D., & Schraga, E. (2015). Diabetic ketoacidosis. Medscape. Alice Jeffries 5/31/2016 2:52:50 AM Discussion Part One Dr. Brown and class, Saonmeme ioa,f hthyep errekaasloenmsi aI ,b deeliehvyed rsahteio mn,a gya hstarvoein bteeestni nbaeld trriadcdte (nG Ii)n tcrlaucdke :d disioarbdeetric: ketoacidosis, since she is a type 1 diabetic, metabolic acidosis, diarrhea, Ikfe at opneerss,o wn hisinch’t aarbel ea ctoid uics (eM thcCe agnluceco, sHeu ient htheer, bBlroaosdh,e trhse, a bnodd Ry owteil,l b20re1a3k) .d Wowhne nli ptihdes ktoet uosnee as sa eren eerxgcyre atnedd ain b uyrpinroed, uecletc otfr othlyet elisp aidre m aelstoa blooslits man ids a hpaesrs koind nceayn dbiesecoasmee a ds eahny odlrdaetre da daunldt. thirsty (McCance et al., 2013). Type one usually starts at a younger age, which means that the patient probably S3o5m% eo fe xthpee rptes obpelleie hvaev teh acht rao dneicc lkiniden ieny k didisneeays efu (nCcKtDio)n ( Disr aaw nzo, rBmaabli npeaartu o, af nadgi nRga hfomra mn,a 2n0y1 p2e)o. Tphlee, edveecnre tahsoesde r wenhaol afuren cntoiotn d ciaabne lteica,d a tnod f mluiodr ea nthda n leoleacdtirnogl,y lteea idminbga ltaon mcee,t aanbdo ltihc ea cdiedcorseisa s(De rianw tuz beut laalr. ,a 2b0s1o2rp).t iAodnd oitfi opnhaolslyp,h eoldroeurlsy, wdeitchr eCaKsDed a reex carte htiiognh eorf raisckid f oinr rceasrpdoiancs ceo tmo pthlicea atmionm, ownhiuicmh mchaloyr aidlseo be caonndt erilbeucttrinogly ttoe timheb ianlaanbcileit,y w toh igchet c oouutl do af lbseod c afours etw woe daakyn.e Tshs.e patient may also have a GI tract disorder, which could lead to diarrhea, dehydration, fTleusidtss Ia wt 0o.u9l%d onrodremr ainl csalulidnee apneinodni ngagp b,l oHo&dH g, lcuhceocske floerv eklest. oLnoewse, rb lpoloasdm galu bciocsaer bleovnealt, ea nadn da bhdigohmerin aanl iuolntr gaaspo uanred bfoior mGIa trrkaecrks dfoisro mrdeetar.b oI lwico aucldid sotsaisrt IV (Mandel, Curhan, Hu, and Taylor, 2012). Ikfe at opneerss,o wn hisinch’t aarbel ea ctoid uics Me tchCea nglcuec,o Hsuee inth tehre, Bbrlaosohde, rtsh, ea nbdo dRyo wtei,l l2 b0r1e3a)k. dWowhenn l itphide