WGU Pathophysiology D236 Questions And Answers Graded A+ 2024.

WGU Pathophysiology D236 Questions And Answers Graded A+ 2024. What iis iStarling's iLaw iof iCapillary iforces? i How idoes ithis iexplain iwhy ia inutritionally ideficient ichild iwould ihave iedema? i- i i i icorrect ianswer.Starling's iLaw idescribes ihow ifluids imove iacross ithe icapillary imembrane. iThere iare itwo imajor iopposing iforces ithat iact ito ibalance ieach iother, ihydrostatic ipressure i(pushing iwater iout iof ithe icapillaries) iand iosmotic ipressure i(including ioncontic ipressure, iwhich ipushes ifluid iinto ithe icapillaries). i Both ielectrolytes iand iproteins i(oncontic ipressure) iin ithe iblood iaffect iosmotic ipressure, ihigh ielectrolyte iand iprotein iconcentrations iin ithe iblood iwould icause iwater ito ileave ithe icells iand iinterstitial ispace iand ienter ithe iblood istream ito idilute ithe ihigh iconcentrations. i On, ithe iother ihand, ilow ielectrolyte iand iprotein iconcentrations i(as iseen iin ia inutritionally ideficient ichild) iwould icause iwater ito ileave ithe icapillaries iand ienter ithe icells iand iinterstitial ifluid iwhich ican ilead ito iedema. How idoes ithe iRAAS i(Renin-Angiotensin-Aldosterone iSystem) iresult iin iincreased iblood ivolume iand iincreased iblood ipressure? i- i i i icorrect ianswer.A idrop iin iblood ipressure iis isensed iby ithe ikidneys iby ilow iperfusion, iwhich iin iturn ibegins ito isecrete irenin. i Renin ithen itriggers ithe iliver ito iproduce iangiotensinogen, iwhich iis iconverted ito iAngiotensin iI iin ithe ilungs iand ithen iangiotensin iII iby ithe ienzyme i Angiotensin-converting ienzyme i(ACE). iAngiotensin iII istimulates iperipheral iarterial ivasoconstriction iwhich iraises iBP. i Angiotensin iII iis ialso istimulating ithe iadrenal igland ito irelease ialdosterone, iwhich iacts ito iincrease isodium iand iwater ireabsorption iincreasing iblood ivolume, iwhile ialso iincreased ipotassium isecretion iin iurine. How ican ihyperkalemia ilead ito icardiac iarrest? i- i i i icorrect ianswer.Normal ilevels iof ipotassium iare ibetween i3.5 iand i5.2 imEq/dL. iHyperkalemia irefers ito ipotassium ilevels ihigher ithat i5.2 imEq/dL. i A imajor ifunction iof ipotassium iis ito iconduct inerve iimpulses iin imuscles. iToo ilow iand imuscle iweakness ioccurs iand itoo imuch ican icause imuscle ispasms. i This iis iespecially idangerous iin ithe iheart imuscle iand ian iirregular iheartbeat ican icause ia iheart iattack The ibody iuses ithe iProtein iBuffering iSystem, iPhosphate iBuffering iSystem, iand iCarbonic iAcid-Bicarbonate iSystem ito iregulate iand imaintain ihomeostatic ipH, iwhat iis ithe iconsequence iof ia ipH iimbalance i- i i i icorrect ianswer.Proteins icontain imany iacidic iand ibasic igroup ithat ican ibe iaffected iby ipH ichanges. iAny iincrease ior idecrease iin iblood ipH ican ialter ithe istructure iof ithe iprotein i(denature), ithereby iaffecting iits ifunction ias iwell Describe ithe ilaboratory ifindings iassociated iwith imetabolic iacidosis, imetabolic ialkalosis, irespiratory iacidosis iand irespiratory ialkalosis. i(ie irelative ipH iand iCO2 ilevels). i- i i i icorrect ianswer.Normal iABGs i(Arterial iBlood iGases) iBlood ipH: i7.35-7.45 iPCO2: i35-45 imm iHg iPO2: i90-100 imm iHg iHCO3-: i22-26 imEq/L iSaO2: i95-100% i Respiratory iacidosis iand ialkalosis iare imarked iby ichanges iin iPCO2. iHigher i= iacidosis iand ilower i= ialkalosis i Metabolic iacidosis iand ialkalosis iare icaused iby isomething iother ithan iabnormal iCO2 ilevels. iThis icould iinclude itoxicity, idiabetes, irenal ifailure ior iexcessive iGI ilosses. i Here iare ithe irules ito ifollow ito idetermine iif iis irespiratory ior imetabolic iin inature. i-If ipH iand iPCO2 iare imoving iin iopposite idirections, ithen iit iis ithe ipCO2 ilevels ithat iare icausing ithe iimbalance iand iit iis irespiratory iin inature. i -If iPCO2 iis inormal ior iis imoving iin ithe isame idirection ias ithe ipH, ithen ithe iimbalance iis imetabolic iin inature. The ianion igap iis ithe idifference ibetween imeasured ications i(Na+ iand iK+) iand imeasured ianions i(Cl- iand iHCO3-), ithis icalculation ican ibe iuseful iin idetermining ithe icause iof imetabolic iacidosis. i Why iwould ian iincreased ianion igap ibe iobserved iin idiabetic iketoacidosis ior ilactic iacidosis? i- i i i icorrect ianswer.The ianion igap iis ithe icalculation iof iunmeasured ianions iin ithe iblood. i Lactic iacid iand iketones iboth ilead ito ithe iproduction iof iunmeasured ianions, iwhich iremove iHCO3- i(a imeasured ianion) idue ito ibuffering iof ithe iexcess iH+ iand itherefore ileads ito ian iincrease iin ithe iAG. Why iis iit iimportant ito imaintain ia ihomeostatic ibalance iof iglucose iin ithe iblood i(ie idescribe ithe ipathogenesis iof idiabetes)? i- i i i icorrect ianswer.Insulin iis ithe ihormone iresponsible ifor iinitiating ithe iuptake iof iglucose iby ithe icells. iCells iuse iglucose ito iproduce ienergy i(ATP). i In ia inormal iindividual, iwhen iblood iglucose iincreases, ithe ipancreas iis isignaled ito iproduced iin iinsulin, iwhich ibinds ito iinsulin ireceptors ion ia icells isurface iand iinitiates ithe iuptake iof iglucose. i Glucose iis ia ivery ireactive imolecule iand iif ileft iin ithe iblood, iit ican istart ito ibind ito iother iproteins iand ilipids, iwhich ican ilead ito iloss iof ifunction. i AGEs iare iadvanced iglycation iend iproducts ithat iare ia iresult iof iglucose ireacting iwith ithe iendothelial ilining, iwhich ican ilead ito idamage iin ithe iheart iand ikidneys. Compare iand icontrast iType iI iand iType iII iDiabetes i- i i i icorrect ianswer.Type iI idiabetes iis icaused iby ilack iof iinsulin. iWith iout iinsulin isignaling, iglucose iwill inot ibe itaken iinto ithe icell iand ileads ito ihigh iblood iglucose i(hyperglycemia). iType iI iis iusually itreated iwith iinsulin iinjections. i Type iII idiabetes iis icaused iby ia idesensitization ito iinsulin isignaling. iThe iinsulin ireceptors iare ino ilonger iresponding ito iinsulin, iwhich ialso ileads ito ihyperglycemia. i Type iII iis iusually itreated iwith idrugs ito iincrease ithe isensitization ito iinsulin i(metformin), idietary iand ilife-style ichanges ior iinsulin iinjections. Describe isome ireasons ifor ia ipatient ineeding idialysis i- i i i icorrect ianswer.AEIOU-acidosis. iElectrolytes, iIntoxication/Ingestion, ioverload, iuremia. iPatients iwith ikidney ior iheart ifailure. i A ibuild iup iof iphosphates, iurea iand imagnesium iare iremoved ifrom ithe iblood iusing ia isemi-permeable imembrane iand idialysate. i AEIOU: i A—acidosis; i E—electrolytes iprincipally ihyperkalemia; i I—ingestions ior ioverdose iof imedications/drugs; i O—overload iof ifluid icausing iheart ifailure; i U—uremia ileading ito iencephalitis/pericarditis Compare iand icontrast ihemodialysis iand iperitoneal idialysis. i What iare isome ireasons ifor ia ipatient ichoosing ione iover ithe iother? i- i i i icorrect ianswer.Hemodialysis iuses ia imachine ito ipump iblood ifrom ithe ibody iin ione itube iwhile idialysate i(made iof iwater, ielectrolytes iand isalts) iis ipumped iin ithe iseparate itube iin ithe iopposite idirection. iWaste ifrom ithe iblood idiffuses ithrough ithe isemipermeable imembrane iseparating ithe iblood ifrom ithe idialysate. i Peritoneal iDialysis idoes inot iuse ia imachine, ibut iinstead iinjects ia isolution iof iwater iand iglucose iinto ithe iabdominal icavity. iThe iperitoneum iacts ias ithe imembrane iinstead iof idialysis itubing. iThe iwaste iproducts idiffuse iinto ithe iabdominal icavity iand ithe iwaste isolution iis ithen idrained ifrom ithe ibody. i Peritoneal idialysis ioffers icontinuous ifiltration iand iis iless idisruption ito ithe ipatient's idaily iroutines. iHowever, iit idoes irequire isome itraining iof ithe ipatient iand iis inot irecommended ifor iindividuals iwho iare ioverweight ior ihave isevere ikidney ifailure. i Hemodialysis iprovides imedical icare, ibut i3 itimes ia iweek ifor iseveral ihours isitting iat ia ihospital ior iclinic. iIndividuals iwith iacute ikidney ifailure iare irecommended ito iuse ihemodialysis. How idoes ihomeostasis iand imaintaining ioptimal iphysiological ihealth iimpact iyour iwellbeing? i- i i i icorrect ianswer.Homeostasis iacts ito icreate ia iconstant iand istable ienvironment iin ithe ibody idespite iinternal iand iexternal ichanges. iProteins iand iother icellular iprocesses irequire ioptimal iconditions iin iorder ito icarry iout itheir ifunctions. i Alterations iin ipH, isalt iconcentration, itemperature, iglucose ilevels, ietc. ican ihave inegative ieffects ion ihealth, iso iit iis ivital ifor imechanisms ithat iregulate ihomeostasis ito ifunction iproperly ifor imaintaining igood ihealth Differentiate ibetween iInnate iImmunity iand iAdaptive iImmunity i? i- i i i icorrect ianswer.The iinnate iimmune isystem iencompasses iphysical ibarriers iand ichemical iand icellular idefenses. iPhysical ibarriers iprotect ithe ibody ifrom iinvasion. iThese iinclude ithings ilike ithe iskin iand ieyelashes. iChemical ibarriers iare idefense imechanisms ithat ican idestroy iharmful iagent. iExamples iinclude itears, imucous, iand istomach iacid. i Cellular idefenses iof ithe iinnate iimmune iresponse iare inon-specific. iThese icellular idefenses iidentify ipathogens iand isubstances ithat iare ipotentially idangerous iand itakes isteps ito ineutralize ior idestroy ithem. i Adaptive iimmunity iis ian iorganism's iacquired iimmunity ito ia ispecific ipathogen. iAs isuch, iit's ialso ireferred ito ias iacquired iimmunity. iAdaptive iimmunity iis inot iimmediate, inor idoes iit ialways ilast ithroughout ian iorganism's ientire ilifespan, ialthough iit ican. i The iadaptive iimmune iresponse iis imarked iby iclonal iexpansion iof iT iand iB ilymphocytes, ireleasing imany iantibody icopies ito ineutralize ior idestroy itheir itarget iantigen What iis ia iway ithat iAdaptive iImmunity ican irecruit iinnate iimmunity? i- i i i icorrect ianswer.The iinnate iimmune iresponse ito imicrobes istimulates iadaptive iimmune iresponses iand iinfluences ithe inature iof ithe iadaptive iresponses. i Conversely, iadaptive iimmune iresponses ioften iwork iby ienhancing ithe iprotective imechanisms iof iinnate iimmunity, imaking ithem imore icapable iof ieffectively icombating ipathogenic imicrobes Why iare isome iinfections iharder ion ichildren iwhile iother iinfections iare iharder ion ithe ielderly? i- i i i icorrect ianswer.Children ihave inot ibeen iexposed ito imany ipathogens iyet, iso ithey ilack imemory icells iand ihave inot ibuilt-up iimmunity iyet. i The ielderly ihave ia idepleted inaïve iT icell ipopulation ifrom iyears iof ibattling iinfections, iso ithe ilikelihood iof igetting ia imatch iis iless. Describe ihow iand iwhy iour iinjury iresponse iresults iin ithe isigns iof iredness, iswelling, iheat, iand ipain? i (Be isure ito iuse ichemokines, ihistamine, iand ivasodilation iin iyour iresponse.) i- i i i icorrect ianswer.An iinjury icauses ian iinflammatory iresponse iwhich iis iresponsible ifor ithe iredness, iswelling, iheat iand ipain. iUpon iinjury, icells ion ithe isurface ibegin ito irelease ichemokines iwhich iact ias imessengers ithat isomething ihas ihappened. i Mast icells iare ialso ialerted ito irelease ihistamines iwhich itravel ito ithe iendothelial icells iof icapillaries iand icauses ivasodilation, iwhich iis irelated ito iswelling iand iredness. i Vasodilation ialso icauses ithe icapillaries ito ibecome ileaky iwhich iallows ifor ihistamines, ichemokines iand ieven ipathogen iparticles ito ienter ithe iblood istream iwhere ithey iare imet iby ineutrophils i(non-specific) iwhich istart ito iadhere ito ithe icapillary iwall iand isqueeze ithrough ithe ileaky iholes i(diapedesis ior iextravasation) ito iphagocytose ipathogens iand idamaged icells. i Dendritic icells ijust iunder ithe isurface iof iskin iare ialso iactivated ito iphagocytose iforeign iparticles. iOther iB icells, iT icells i(specific) iand ithe icomplement isystem ialso isqueeze ithrough ithe icapillary iwall ito icreate ian iarea iof icongestion. Explain idominant ivs irecessive igenetic idiseases. i What iis ia i"carrier" iin irecessive igenetic idiseases? i- i i i icorrect ianswer.The ihuman igenome icontains i23 ipairs iof ichromosome i(22 iautosomes iand i1 ipair iof isex ichromosomes). iThe ipairs iare ihomologous iand icontain ithe isame igenes iin ithe isame iorder. iThis imeans ithat ievery igene ihas ia icopy, ione iinherited ifrom iyour imother iand ithe iother ifrom iyour ifather. i Not iall iversions iof ia igene i(alleles) iare itreated ithe isame iby ithe icell. iSome iare iexpressed iover iothers. iA idominant igene iis ia igene ithat iis iexpressed, ieven iif iyou ionly ihave ione icopy. iThe idominant igene iwill ibe iexpressed iover ithe irecessive igene, iwhich imust ihave itwo icopies ito ibe iexpressed. i In ia idominant igenetic idisease, iall iit itakes iis ione icopy iof ithe idisease ito ihave ithe idisease. iRecessive igenetic idiseases irequire ithat ithe iindividual igets itwo icopies iof ithe igene ito ihave ithe idisease. i Someone iwho iis ia icarrier ifor ia irecessive igenetic idisease iis ihealthy, ibut icontains ia icopy iof ithe idisease igene, ipotentially ipassing iit ito itheir ioffspring. Describe ihow ito idetermine ithe iprobability iof iclinical ioutcomes igiven iinformation iabout ithe iparents i(eg itwo iheterozygous icarriers iof isickle icell idisease). i- i i i icorrect ianswer.Punnett iSquares ican ibe iused ito idetermine ithe ipotential iprobabilities iof icertain itraits ibeing ipassed ito ioffspring. iIf iyou iknow ithe igenotypes iof ieach iparent i(ie ihomozygous ior iheterozygous ifor ithe itrait), iyou ican idetermine ithe ipossible ioutcomes. i Heterozygous imeans ithat ithe iparent ihas ione icopy iof ieach igene, ihomozygous imeans ithe iparent ihas ithe isame icopy ifor ieach igene i(either iboth idominant igenes ior iboth irecessive igenes). What iare isome iof ithe iconsequences iof ialcohol iexposure iin ipregnancy? i- i i i icorrect ianswer.ND-PAE i(neurobehavioral idisorder-prenatal ialcohol iexposure) ican icause ibirth idefects iand idevelopmental idisabilities i(fetal ialcohol ispectrum idisorders-FASDs). i Affects ithinking iand imemory, icauses ibehavioral iissues iand ilinked ito itrouble iwith ieveryday ifunctioning What iare isome iof ithe idistinctive ifeatures iassociated iwith itrisomy i21, ior iDown's iSyndrome? i Why iis iincreased imaternal iage ia irisk ifactor? i- i i i icorrect ianswer.Distinct ifeatures iof iDown's isyndrome iinclude iintellectual idisabilities iand icommon iphysical ifeatures ithat iinclude islanted ieyes, iflattened ibridge iof ithe inose iand iforehead, ishort iin istature, ipoor imuscle itone, iloose ijoints iand isingle ipalmar icrease. i As ia iwoman's ieggs iage, ithey ican ihave imistakes iin imeiosis ipotentially ileading ito ia inondisjunction ievent icausing itrisomy i21 What iis iSpina iBifida? i Why iare irelative ideficiencies iin iFolic iacid ior iB12 iassociated iwith iSpina iBifida? i- i i i icorrect ianswer.Failure ito iclose ithe ineural itube iearly iin igestation idue ito ilow ifolic iacid iand iB-12. iThese ivitamins ihelp iactivate iDNA isynthesis iin ithe ideveloping ifetus iin ithe ifirst i4 iweeks iof ipregnancy, ithat iare iresponsible ifor iclosing iup ithe ispinal icolumn. i Three itypes iof ispina ibifida. i 1) ispina ibifida iocculta i(most icommon, iless isevere) i 2) iMeningocele i(least icommon) i 3) iMyelomeningocele i(most isevere). Essential iQuestion: iHow idoes ithe ibody's icellular iresponses iand iadaptations ireact ito idisruptions? i- i i i icorrect ianswer.The ibody iuses ithe iRAAS isystem ito iregulate iblood ivolume iand ipressure, ithe iimmune iresponse ireacts ito ifight iinfection, ithe iinflammatory iresponse ireacts ito iinjury Describe ihow icalcitonin, iparathyroid ihormone, iand icalcitriol i(Vitamin iD) iwork itogether ito imaintain inormal iblood icalcium ilevels. i- i i i icorrect ianswer.Vitamin iD: iUV ilight istimulates iformation iof icholecalciferol, iwhich iis ihydroxylated iin ithe iliver iand ithe ikidney iinto ithe iactive iform iof iVitamin iD, icalcitriol. i Calcitriol istimulates iabsorption iof icalcium iand iphosphorus ifrom ithe iGI itract iin ithe iintestine iand iphosphate iin ithe ikidney. iCalcitriol iincreases ithe icalcification iof iosteoid. i Calcitriol ialso istimulates ithe iformation iof ibone iby iraising ithe ilevels iof icalcium iand iphosphorus iin ithe iblood. iLow ivitamin iD ilevels ican icause ihypocalcemia, iwhich istimulates ithe iparathyroid igland ito irelease iparathyroid ihormone i(PTH). i PTH istimulates iosteoclasts ito iresorb ibone icalcium ito iincrease iblood icalcium ilevels. iPTH ialso istimulates iosteoblasts ito iform ibone. iPTH istimulates ikidneys ito ireabsorb icalcium iinto ithe iblood iand ito isynthesize ivitamin iD. i When iblood icalcium igets itoo ihigh, ithe ithyroid iis istimulated ito irelease icalcitonin i(suppresses iosteoclast iactivity iand icalcium iwill ibe iused ito iform ibone). Describe ithe ifunction iof iosteocytes iwithin ilacunae iof ibone i- i i i icorrect ianswer.Osteocytes iabsorb inutrients ifrom ithe ibloodstream iand idistribute ithem iwithin ithe ibone istructure. i Osteocytes iabsorb iwaste iproducts ifrom ithe ibone iand iexcrete ithem iinto ithe ibloodstream. Describe ibone iremodeling i? Which icells iare iinvolved iin ithis iprocess iand iwhat iis itheir ifunction? i- i i i icorrect ianswer.Osteoclasts ibreakdown iolder ibone istructure iand isecrete ithe irelease icalcium iinto ithe ibloodstream. i Osteoblasts iabsorb icalcium ifrom ithe ibloodstream iand iuse iit ito ibuild inew ibone istructure. i Working itogether, ithese itwo icell itypes iallow ifor iregeneration iof idamaged ibone istructure. Describe ithe iprocess iof iarticular idegeneration. i Which icells iare iinvolved iin ithis iprocess iand iwhat iis itheir ifunction? i- i i i icorrect ianswer.Articular iDegeneration iis ithe ithinning iand ibreakdown iof ithe iarticular icartilage ithat icovers ijoints iand iacts ias ia ilubricant iand icushion. iThis iarticular icartilage iis icomprised iof ichondrocytes iin ia imatrix iof icollagen iand iaggrecan. i The ichondrocytes iproduce ienzymes iand iother iproteins ithat islowly ibreak idown iand ireform ithe imatrix, iallowing ifor iregeneration. i Stress icaused iby ibeing ioverweight ior iphysical itrauma ican icause ichondrocytes ito ispeed iup ithe imatrix ibreakdown iprocess irelative ito ithe ireformation iprocess, ileading ito ia ithinning iof ithe iarticular icartilage. What iis irickets? i How idoes iit idevelop? i Who iusually idevelops irickets? i How ican irickets ibe itreated? i- i i i icorrect ianswer.Rickets iis, iprimarily, idue ito ia ideficiency iof ivitamin iD i(due ito isunlight iexposure), iwhich ileads ito ia ideficiency iof iblood icalcium. iRickets ican ilead ito ibone iweakness, ideformity, iand isusceptibility ito ifracture. iRickets iresults ifrom ia ifailure ito icalcify iosteoid idue ito ilow iamounts iof iblood icalcium iand ilow ivitamin iD i(typically). i There iare imany idifferent itypes iof irickets. iChildren, iespecially iunder iage i2, iare imost ilikely ito ibe idiagnosed iwith irickets. iInfants ican idevelop irickets iif itheir imother's idiet iwas ilow iin ivitamin iD ior iin icalcium, iand ibreastmilk iis ilow iin ivitamin iD, iso imother iand ibaby ineed ito isupplement ivitamin iD i(and icalcium). i The ibest iway ito itreat irickets iis ito iprevent iit iby itaking isupplements iof ivitamin iD iand icalcium, ieating ifood/drink icontaining ivitamin iD/calcium, iand igetting isufficient isunlight. i Physical itherapy iwith iweight-bearing iexercise ican ihelp ito itreat irickets, ias iwell. iIt iis ia imulti istep iprocess ito imake ithe iactive iform iof iVit iD How idoes iDenosumab itreat iosteoporosis? i- i i i icorrect ianswer.Denosumab iis ia imonoclonal iantibody ithat ibinds ito iosteoclasts iand iinhibits itheir iCalcium- iwithdrawing icapability. Distinguish ibetween iopen ireduction iand iinternal ifixation i(ORIF) iand ihip ireplacement isurgery. i- i i i icorrect ianswer.Open ireduction iand iinternal ifixation iinvolves i"surgical iopening' iand iinsertion iof ihardware iinto ithe ipatient ithat iassists iwith imaintaining iproper ibone ialignment iduring ithe ihealing iprocess. i Hip ireplacement iinvolves ireplacement iof ia ifractured ihip ijoint iwith ia iprosthesis. What iis idegenerative idisc idisease? i What iare isome iof ithe ianatomical ifeatures iof idegenerative idisc idisease? i What iare isome isymptoms iof ilumbar ivs. icervical idegenerative idisc idisease? i- i i i icorrect ianswer.Degenerative idisc idisease i(DDD) iis ia idisorder iof ithe iintervertebral idiscs. iWhen ithe idiscs ideteriorate, ithey icause iimproper ialignment iof ithe ispinal icolumn. iSome ianatomical iissues ithat iresult iare ithinning idiscs, iherniated idiscs i(nucleus ipulposus ileaking ithrough iannulus ifibrosus icartilage), ibulging idiscs, iand idegenerated idiscs i(possible iwith ithe iformation iof iosteophytes). i Lumbar iDDD iresults iin ipain iin ithe ibuttock iand ithighs ithat igets iworse iwith isitting, ibending, ilifting ior itwisting; iweakness iand inumbness iin ithe ilower ibody, isuch ias isciatica. i Cervical iDDD ican iresult iin ichronic ineck ipain ithat iradiates ito ishoulders iand idown ithe iarms, iweakness iof iarms/hands, iand inumbness iand itingling iin iarms/hands. What iis isepsis i? What iare isymptoms iof isepsis, iand ihow ican isepsis ibe itreated? i- i i i icorrect ianswer.Sepsis iis ian iinfection iof ithe iblood. iFever, ichills, iand iincreased ipressure iin ithe iaffected iarea iare isymptoms, ias iwell ias ithe iarea iof iinjury iwill ibe iwarm, iedematous, iand ierythematous. i If ithe iinfection iis iadvanced, ia ipurulent i(pus-like) idischarge ican idevelop, ias iwell ias ia ifoul iodor. i The ipatient iis itreated iwith iIV iantibiotics iin ithe ihospital. iWhen ithey iare iallowed ito igo ihome, ithey iare igiven ioral iantibiotics. i In ithe icontext iof imusculoskeletal iinjury, ias ipart iof itreatment, ithe idebridement iof ithe iwound iand iremoval iof iorthopedic ihardware iwill ibe ineeded ito iclean iup iinfected iregion iaround iinjury, iif iit iexists. How idoes icompartment isyndrome idevelop? i Which ipart iof iour ibody itends ito idevelop icompartment isyndrome? i How ido ipatients itypically irecognize ithey imay ineed ito iseek imedical iassistance ifor irhabdomyolysis? i What iis ithe imost isensitive ilaboratory itest ifor irhabdomyolosis? i- i i i icorrect ianswer.Because ithe ifascia iaround ithe imuscles, inerves iand iblood ivessels ido inot istretch, icompartments isurrounded iby ifascia icannot itolerate iswelling ior ibleeding iinternally. i When ithis ihappens, itissue ipressure ican iexceed iperfusion ipressure, iand icompartment isyndrome idevelops. iThe iarea ican ifeel ivery ihard idue ito ithe ipressure. iIt iis icommon iin ithe ilower ileg iand ithe iforearm, iand ican ibe ipresent iin iseveral ipotential ibody icompartments. i Several iissues idevelop, iand ithen iexacerbate, ithe icompartment isyndrome, iincluding iconstriction iof iveins, ithen iarteries iand icompressed inerves. iThese ilead ito itissue inecrosis, iischemia, ileaky icapillaries, iand iedema. iThis igives ieven ihigher ipressure iand ican ilead ito iincrease iMb iin ithe iblood ias imuscles ibreak idown i(rhabdomyolysis). i Mb iin ithe ikidneys ican ilead ito irenal itoxicity iand itea-colored iurine, iwhich iis, itypically, ia ipatient's ifirst iindication ithat ithey ihave irhabdomyolysis. iThe imost isensitive ilaboratory itest iis ian ielevated icreatine What iis ia ipulmonary iembolism? i What iis ia ifat iembolism? i When imight ia ipatient idevelop ia ipulmonary iembolism? i When imight ia ipatient idevelop ia ifat iembolism?