2 Caso Clinico Ingles

8/3/2019 2 Caso Clinico Ingles

1/13

UniversidadLaSalle.

ExtensionCoursefortheNationalExamPreparation

FortheMedicineResidencyAspirers.

ClinicalCase.

DistantLearningSystem.

Maleof20yearsoldwhoissenttotheemergencyroomaccompaniedbyhisfamily,peoplewith

diabetesmellitussinceage13isanirregulartreatmentwithdietandintermediateacting insulin.

Family referred to, that in recent days he has shown fatigue, weakness, anorexia, nausea and

some vomiting gastrobiliar content, polyuria, diffuse abdominal pain located in mesogastrio

gnawing. In the last two days has been drinking alcohol and suspended insulin injections. The

patiententryisinitiatedinanstuporousstateclearlyappreciated.

Withtheseclinicaldataisveryprobablethatamongtheselabstudieselaboratedtothepatienttherewillbefound:

A. NormalPlasmaticOsmolarity.B. Hyponatraenia.C. Leucopaenia.D. Hypoglouconemia.

Concept:

Hyponatremia is the plasma concentration of Na +


2/13

Symptomsandseveritydependontherapidityofonsetandthedecreaseinplasmaconcentration

ofNa+.Aslowertheconcentration,youwillobserve:

Nausea,vomiting

Musclemanifestations(weakness,cramps,ileus)

AsitdescendstheconcentrationofNa+inplasma,symptomswillworsen,appearing:

Headache

Lethargy

Confusion

Drowsiness

OnlyiftheplasmaNaconcentrationsare


3/13

Diagnosticalgorithmforhyponatremia

Bibliography:

Rose BD, Post TW. Hyponatremia hypoosmolaritysituations. In: Rose BD, PostTW,eds.Electrolytedisordersandacidbase,MarbanSLBooks,2001,697745.

JCAys.Disordersofbodyfluidsosmolarity:changesofsodium. In:L.Hernandoeds.ClinicalNephrology,2nded,Panamericana,2003,4655.

BerlT,J.VerbalPathophysiologyofWaterMetabolism. In:BrennerBM,edsTheKidney,7thedition,Saunders,2002,857919.

2. Itismorelikelythattheclinicalframeworkcorrespondsto:

a)LacticacidosistypeB.

b)Diabeticketoacidosis.

c)Alcoholicketoacidosis.

d)Hypoglycemiaandacutealcoholism.

DEFINITION

While Lebovitz inhis1995 reviewmentioned that there isno consensusdefinition,we can

consider that the definition published in 1996 by the American Diabetes Association for

HospitalAdmissionsindiabeticpatients.OnepatienthadanepisodeofCADwhen:

Thebloodglucoseisabove250mg/dl(>14mM/l)ThearterialpHislessthan7.35,venouspHislessthan7.30orserumbicarbonatelessthan15

mEq/l.Thereisthepresenceofketonuriaand/orketonemia.

Diabetic ketoacidosis (DKA) is one of the most serious acute metabolic complications of

diabetes mellitus caused by a relative or absolute deficiency of insulin and a concomitant


4/13

increaseofcontrainsularshormones.Itischaracterizedbyamarkedcatabolicdisturbancein

themetabolismofcarbohydrates,proteinsand lipids,classicallypresentingwith thetriadof

hyperglycemia,ketosisandacidosis.

PATHOPHYSIOLOGY

HORMONEACTIONONTHEINTERMEDIATEMETABOLISMThe CAD is caused primarily by an absolute or relative deficiency of insulin, a hypoglycemic

hormone.Intheregulationofbloodsugarhormonesareinvolvedagroupofantihyperglycemicor

regulatory action, that can be fast (adrenaline and glucagon) or slower (somatotropin,

glucocorticoids,prolactinandthyroxine),whoseincreasehasaroleinthepathophysiologyofDKA

and nonketotic hyperosmolar state (EHNC), which some authors regard as the ends of a

pathophysiological state of common5 DKA. It will predominate in insulin deficiency and EHNC,

increasedonbackregulatorhormones.

Amongmanyfunctionsofinsulin,itemphasizestheroleofpromotingentryofglucoseintotarget

tissuesbystimulatingtheconveyor.Thisfeatureallowsclassificationoftissuein: InsulinSensitive:Cannotuseglucoseforenergy intheabsenceof insulin,suchas liver,muscle

andadiposetissue,amongothers.

InsulinInsensitive:Canuseglucoseforenergyintheabsenceofinsulin,suchasbraintissueand

erythrocytes.Insulinosensibletissuesarewhereimportantmetabolicchangesoccurduetoinsulindeficiency.

Althoughtheyarecloselyrelatedconsiderationswewillseparatetheintermediatemetabolismin:Changesinthemetabolismofcarbohydrates

TypicalhyperglycemiaofCADismainlyduetotwomainmechanisms:

1. Inallinsulinosensibletissuesthereisadecreaseintheentryandsubsequentutilizationofglucoseand


5/13

2.Intheliverarea,anincreasemainlyglycogenolysisandgluconeogenesis,thusincreasingthe

levelofcirculatingglucose.

Alterationsinlipidmetabolismandsourceofketonebodies.

Increased counterregulatory hormones play here more prominent role next to the insulin

deficiency.Ononehandincreasedlipolysisleadingtoincreasedfreefattyacids.Thesefattyacids

aremetabolizedbytheoxidationincompleteastheKrebscycleisblockedandgenerateketone

bodies in the mitochondria of hepatocytes. This mechanism called Ketogenesis gives rise to

acetoacetic acid and Hydroxybutyric and Acetone. In turn, this also decreased peripheral

utilizationofketonebodies,whichiswhymaintainingandincreasingitscirculatinglevel.

Alterationsinproteinmetabolism

Proteolysisisincreasedoriginatingaminoacidsintheliver,usedasprecursorsingluconeogenesis.

Interrogationandphysicalexamination

Althoughthesymptomsofpoorlycontrolleddiabetesmellitusmaybepresentfromseveraldaysearlier,themetabolicalterationstypicalofCADusuallydevelopquickly(usuallywithin24hours.)

The clinicalpicture includesahistoryofpolyuria,polydipsia,weight loss,nausea, vomitingand

decreasedappetite.Thisrelativeanorexia is importantbecauseitisthefirstmanifestationofthe

transition fromsimplehyperglycemia toketosis.Occasionally, itappears in theadultabdominal

pain(morecommoninchildren),whichcansimulateanacutesurgicalabdomen;thecauseofthis

painisnotfullyelucidatedandisattributedtodehydrationofmuscletissue,gastricdilatationand

paralytic ileus (secondary to electrolyte disturbance and metabolic acidosis). Another theory

relatesittochangesinthePG.

The metabolic diagnosis of acute abdomen can only be accepted when theres no other

reasonable causeabdominalpain, thepH is lowand the symptoms improvewith correctionof

acidosis; therefore, if there is no improvement in pain, it should exclude other diagnostic

possibilities such as mesenteric thrombosis and acute pancreatitis (secondary to severe

hypertriglyceridemiamayaccompanyCAD).


6/13

Thealteredstateofconsciousness,mainlylethargyandsleepiness,areoftenofdelayedonsetand

may progress to coma in untreated patients. A small number of cases occur in coma. Other

symptomsincludegeneralweakness,fatigueandtiredeasily.

3. Aphysiologicalphenomenonthatoftenoccursinthesecasesis:

a)Increasedproductionofpyruvate.

b)Excessofglucagoninplasma.

c)Decreasedliverfattyacids.

d)Removaloftheactionofcarnitineacyltransferase.


7/13

GLUCAGON

Glucagon release is stimulated when insulin is unable to provide the cells needed glucose for

energy.Glucagonincreasestheamountofglucoseinthebloodstreambythecatabolismofstored

glucose (glycogenolysis) and the conversion of carbohydrate molecules to glucose

(gluconeogenesis).ThebloodglucoseconcentrationsinpatientswithCADtypicallyrangebetween

300 and 800mg/dl blood. The CAD cannot be diagnosed only in terms of blood glucose

concentrations,astheketoacidosisisalsoafactor.


8/13

Bibliography

1. WagnerA,RisseA,BrillHLetat.TherapyofSeverediabeticketoacidosis.DiabetesCare1999,22:674677.

2. DelaneyMF,ZismanA,KettyleWM.Diabeticketoacidosisandhyperosmolarnonketoticsyndrome.EndocrinolMetabClinNorthAm2000;29(4):683705.

3. KitabchiAE,WallBM.Managementofdiabeticketoacidosis.AmFamPhysic1999;60:455464.4. Umpierrel GE, Khajavi M, Kitabchi AE. Review: Diabetic ketoacidosis and hyperglycemic

hyperosmolarnonketoticsyndrome.AmJMedSci1996;311:225233.

5. KitabchiAE,WallBM.Diabeticketoacidosis.MedClinNorthAm1995;79(1):937.6. RuckerDW.Diabeticketoacidosis.MedicineJournal2001;2(4)7. AmericanDiabetesAssociation.Hyperglycemic crises inpatientswithdiabetesmellitus.Diabetes

Care2001;24(Suppl1):S83S90.

8. Magee MF, Bhatt BA. Management of descompensated diabetes. Diabetic ketoacidosis andhyperglycemichyperosmolarsyndrome.CriticalCareClinics2001;17(1):75106.

9. KitabchiAE,UmpierrelGE,MurphyMB,BarrettEJ,KreisbergRA,MaloneJI,WallBM.Managementof hyperglycemic crises in patients with diabetes (technical review). Diabetes Care 2001; 24(1):

131153.

10. GarberAJ.DiabetesMellitus.In:SteinJH(EditorinChief).InternalMedicine.FourthEdition.Mosby;1994,13911424.

4 Inrelationshiptothepathogenesisofinsulindependentdiabetes,thisisaprocess:

a)Purelygenetic.

b)Dependingontheenvironment.

c)Abnormalinsulinsecretion.

d)Resistancetoinsulinaction.

DiabetesmellitustypeIoralsoknownasjuvenilediabetesorinsulindependentdiabetesmellitus

isametabolicdisordercharacterizedbyselectivedestructionofpancreatic cellscausingabsolute

insulin deficiency. It differs from type 2 diabetes mellitus because it is a type of diabetes

characterizedbyearlyageoccursinlife,usuallybeforeage30.Only1in20peoplewithdiabetes

havetype Idiabetes,whichoccursmostoften inyoungchildren.Theadministrationof insulin inthesepatients isessential.Type1diabetes isclassifiedasautoimmunecases,themostcommon

form, and idiopathic cases. . Type 1 diabetes mellitus is a chronic autoimmune disease whose

primary pathophysiologic event is based on a "insulinitas", which is characterized by an

inflammatory infiltrate of inflammatory pancreatic acini with a predominance of CD8 T

lymphocytesandavariablenumberofCD4.Thedestruction isselectivetowards cells,resulting


9/13

in cell death 80% of these cells to the onset of symptoms. Their chronic sequelae because of

microangiopathyandneuropathyproducehighmorbidityandmortalityinpatientswhohaveit.

1.JeanLouisChiasson,Diagnosisandtreatmentofdiabeticketoacidosis;andthehyperglycemichyperosmolarstate;CMAJ2003;168(7):85966.

2.Todd,J.A.,Bell,J.I.&McDevitt,H.O.HLADQbetagenecontribuyestosusceptibilityandresistanceto

insulindependentdiabetesmellitus.Nature1987;329:599604.3.McDevitt,H.O.&Tyan,M.L.Geneticcontroloftheantibodyresponseininbredmice.

Transfertoresponsebyspleencellsandlinkagetothemayorhistocompatibility(H2)

locus.JExpMed1968;128(1):111.4.InsulinodependientDiabetesMellitus.ILADIBA.January1995:148.

5.FrazerdeLlado,T.E.,GonzlezdePijem&Hawk,B.IncidentofIDDMinchildrenlivinginPuertoRico.

PuertoRicoIDDMCoalition.DiabetesCare1998;21(5):7446.6.Carrasco,E.,Prez,F.,Calvillan,M.,Lpez,G.,Wolf,C.,Castano,A.&GarcadelosRos,

M.IncidentofinsulindependentdiabetesmellitusinSantiago,Chile(19901993).

RevistaMdicadeChile1996;124(5):5616.7.Ferreira,S.R.,Franco,L.J.,Vivolo,M.A.,Negrato,C.A.,Simoes,A.C.&Ventureli,C.R.Populationbased

incidentofIDDMinTheStateofSaoPaulo,Brazil.DiabetesCare1993;16(5):7014.8.Bach,J.F.Predictivemedicineinautoimmunediseases:fromtheidentificationofgeneticpredisposition

andenvironmentalinfluencetoprecociousimmunotherapy.ClinImmunol,Immunopathol1994;72:156161

5. Thefollowingclinicaldataisverycharacteristicofthisdisease:

a)KussmaulBreathing.

c)Absenceofbrainstemreflexes.

d)SignofBabinski.

e)Tetany.

Physicalexaminationshowedsignsofdehydration(lossofskinturgor,drymucousmembranes,tachycardia

andhypotension)thatcanreachthehypovolemicshock.Youcanseeatypicalbreathingpattern(Kussmaul

breathing)withdeepbreathing,slowregularandperceivedanodorcharacteristic,badapplesintheexhaled

air..KussmaulbreathingappearswhenthepHislessthan7.20to7.10,soistheclinicalsignsappearwhen

thepatienthasgone fromastateofketosis tooneofketoacidosis.WhenthepH isvery low (6.9)may

disappearduetoinvolvementofbulbarcenter,whichisasignofpoorprognosis.


10/13

JeanLouisChiasson,Diagnosisandtreatmentofdiabeticketoacidosis;andthehyperglycemichyperosmolarstate;CMAJ

2003;168(7):85966.

6. Themostlikelycauseofcardiacarrestinthispatientduringthefirsthoursofhospitalization

wouldbe:

a)Hyperkalemia.

b)Iatrogenichypoglycemia.

c)Persistentmetabolicacidosis.

d)Cerebraledema.

Serum potassium concentrations are high due to the movement of intracellular potassium into the

extracellularspacecausedbyacidemia,hypertonicityandinsulindeficiency.Shouldbecloselymonitoredfor

treatmentvalueforitdropsrapidly(initial levels


11/13

Hyperkalaemia:

PeakedTwaves(QTintervalnormalorslightlyreduced)

PRintervalprolongationwithSTdepression

ProgressivedisappearanceofthePwave

Progressiveheartblock

Ventriculararrhythmias

Cardiacarrest

PeakedTwavesaretheECGdatainthemostconsistentinhyperkalemia.

REFERENCES

Brenner, BM, Rector FC, eds. The Kidney. W B Saunders, Philadelphia, 1991.

Massry, SG, Glassock, RJ, eds. Textbook of nephrology. 3rd ed. Williams &

Wilkins,Baltimore,1995.

Narins, RG, ed. Clinical Disorders of fluid and electrolyte metabolism. 5th ed.

McGraw Hill,NewYork,1994.

"Washington Manual of medical therapeutics. " 9th. edition. Ed Masson

"Principles of Internal Medicine Harrison. " 13th. edition. Inter

McGrawHill.

7. Theinitialtreatmentforthisconditionis:

a)Measureplasmalactateandpyruvate.

b)Generalmeasuresandliquidi.v.

c)measuringserumandurineosmolarity.

d)Toadministerinsulinandtodetermineaniongap.

8. Aftertheadministrationofinsulinandmonitoringbloodglucoselevelseverytimeitdetects

thatnofigureshavebeenreachedbetween50and70mg/dl,thenyoudecide:

a)Increasethe amountoffluid

b)Doublingthedoseorgivingbowlingi.v.(10u.)

c)Wait12hourstoobtaingoals

d)Administerbolusof0.5U.


12/13

9. Whenweappreciateglucoselevelsbelow250mg/dl,normalNaandmildhypotension,we

decidedtocontinuewiththenextsolutionparenterally

a)Hartman1000ml/4hrs

b)5%glucosesaline(0.45%)to150or250mL/h

c)Continuewithphysiologicalsol1000ml/hr.

d)MixedSol1000ml/8hrs

Answerstoquestions7,8and9.


13/13

Bibliography:

1. WagnerA,RisseA,BrillHLetal.Therapyofseverediabeticketoacidosis.DiabetesCare1999,22:674677,

2. DelaneyMF,ZismanA,KettyleWM.Diabeticketoacidosisandhyperosmolarnonketoticsyndrome.EndocrinolMetabClinNorthAm2000;29(4):683705

3. KitabchiAE,WallBM.Managementofdiabeticketoacidosis.AmFamPhysic1999;60:455464

4. UmpierrelGE,KhajaviM,KitabchiAE.Review:Diabeticketoacidosisandhyperglycemichyperosmolarnonketoticsyndrome.AmJMedSci1996;311:225233

5. KitabchiAE,WallBM.Diabeticketoacidosis.MedClinNorthAm1995;79(1):9376. RuckerDW.Diabeticketoacidosis.MedicineJournal2001;2(4)7. AmericanDiabetesAssociation.Hyperglycemiccrisesinpatientswithdiabetesmellitus.

DiabetesCare2001;24(Suppl1):S83S90

8. MageeMF,BhattBA.Managementofdescompensateddiabetes.Diabeticketoacidosisandhyperglycemichyperosmolarsyndrome.CriticalCareClinics2001;17(1):75106

2 Caso Clinico Ingles

Documents

Transcript of 2 Caso Clinico Ingles