WGU pathophysiology D236 questions and answers well illustrated. What lis lStarling's lLaw lof lCapillary lforces? l How ldoes lthis lexplain lwhy la lnutritionally ldeficient lchild lwould lhave ledema? l- l lcorrect lanswer. l l lStarling's lLaw ldescribes lhow lfluids lmove lacross lthe lcapillary lmembrane. lThere lare ltwo lmajor lopposing lforces lthat lact lto lbalance leach lother, lhydrostatic lpressure l(pushing lwater lout lof lthe lcapillaries) land losmotic lpressure l(including loncontic lpressure, lwhich lpushes lfluid linto lthe lcapillaries). l Both lelectrolytes land lproteins l(oncontic lpressure) lin lthe lblood laffect losmotic lpressure, lhigh lelectrolyte land lprotein lconcentrations lin lthe lblood lwould lcause lwater lto lleave lthe lcells land linterstitial lspace land lenter lthe lblood lstream lto ldilute lthe lhigh lconcentrations. l On, lthe lother lhand, llow lelectrolyte land lprotein lconcentrations l(as lseen lin la lnutritionally ldeficient lchild) lwould lcause lwater lto lleave lthe lcapillaries land lenter lthe lcells land linterstitial lfluid lwhich lcan llead lto ledema. How ldoes lthe lRAAS l(Renin -Angiotensin -Aldosterone lSystem) lresult lin lincreased lblood lvolume land lincreased lblood lpressure? l- l lcorrect lanswer. l l lA ldrop lin lblood lpressure lis lsensed lby lthe lkidneys lby llow lperfusion, lwhich lin lturn lbegins lto lsecret e lrenin. l Renin lthen ltriggers lthe lliver lto lproduce langiotensinogen, lwhich lis lconverted lto lAngiotensin lI lin lthe llungs land lthen langiotensin lII lby lthe lenzyme l Angiotensin -converting lenzyme l(ACE). lAngiotensin lII lstimulates lperipheral larterial lvasoconstrictio n lwhich lraises lBP. l Angiotensin lII lis lalso lstimulating lthe ladrenal lgland lto lrelease laldosterone, lwhich lacts lto lincrease lsodium land lwater lreabsorption lincreasing lblood lvolume, lwhile lalso lincreased lpotassium lsecretion lin lurine. How lcan lhyperkalemia llead lto lcardiac larrest? l- l lcorrect lanswer. l l lNormal llevels lof lpotassium lare lbetween l3.5 land l5.2 lmEq/dL. lHyperkalemia lrefers lto lpotassium llevels lhigher lthat l5.2 lmEq/dL. l A lmajor lfunction lof lpotassium lis lto lconduct lnerve limpulses lin lmuscles. lToo llow land lmuscle lweakness loccurs land ltoo lmuch lcan lcause lmuscle lspasms. l This lis lespecially ldangerous lin lthe lheart lmuscle land lan lirregular lheartbeat lcan lcause la lheart lattack The lbody luses lthe lProtein lBuffering lSystem, lPhosphate lBuffering lSystem, land lCarbonic lAcid-Bicarbonate lSystem lto lregulate land lmaintain lhomeostatic lpH, lwhat lis lthe lconsequence lof la lpH limbalance l- l lcorrect lanswer. l l lProteins lcontain lmany lacidic land lbasic lgroup lthat lcan lbe laffected lby lpH lchanges. lAny lincrease lor ldecrease lin lblood lpH lcan lalter lthe lstructure lof lthe lprotein l(denature), lthereby laffecting lits lfunction las lwell Describe lthe llaboratory lfindings lassociated lwith lmetabolic lacidosis, lmetabolic lalkalosis, lrespiratory lacidosis land lrespiratory lalkalosis. l(ie lrelative lpH land lCO2 llevels). l- l lcorrect lanswer. l l lNormal lABGs l(Arterial lBlood lGases) lBlood lpH: l7.35-7.45 lPCO2: l35-45 lmm lHg lPO2: l90-100 lmm lHg lHCO3 -: l22-26 lmEq/L lSaO2: l95-100% l Respiratory lacidosis land lalkalosis lare lmarked lby lchanges lin lPCO2. lHigher l= lacidosis land llower l= lalkalosis l Metabolic lacidosis land lalkalosis lare lcaused lby lsomething lother lthan labnormal lCO2 llevels. lThis lcould linclude ltoxicity, ldiabetes, lrenal lfailure lor lexcessive lGI llosses. l Here lare lthe lrules lto lfollow lto ldetermine lif lis lrespiratory lor lmetabolic lin lnature. l-If lpH land lPCO2 lare lmoving lin lopposite ldirections, lthen lit lis lthe lpCO2 llevels lthat lare lcausing lthe limbalance land lit lis lrespiratory lin lnature. l -If lPCO2 lis lnormal lor lis lmoving lin lthe lsame ldirection las lthe lpH, lthen lthe limbalance lis lmetabolic lin lnature. The lanion lgap lis lthe ldifference lbetween lmeasured lcations l(Na+ land lK+) land lmeasured lanions l(Cl- land lHCO3 -), lthis lcalculation lcan lbe luseful lin ldetermining lthe lcause lof lmetabolic lacidosis. l Why lwould lan lincreased lanion lgap lbe lobserved lin ldiabetic lketoacidosis lor llactic lacidosis? l- l lcorrect lanswer. l l lThe lanion lgap lis lthe lcalculation lof lunmeasured lanions lin lthe lblood. l Lactic lacid land lketones lboth llead lto lthe lproduction lof lunmeasu red lanions, lwhich lremove lHCO3 - l(a lmeasured lanion) ldue lto lbuffering lof lthe lexcess lH+ land ltherefore lleads lto lan lincrease lin lthe lAG. Why lis lit limportant lto lmaintain la lhomeostatic lbalance lof lglucose lin lthe lblood l(ie ldescribe lthe lpathogenesis lof ldiabetes)? l- l lcorrect lanswer. l l lInsulin lis lthe lhormone lresponsible lfor linitiating lthe luptake lof lglucose lby lthe lcells. lCells luse lglucose lto lproduce lenergy l(ATP). l In la lnormal lindividual, lwhen lblood lglucose lincreases, lthe lpancreas lis lsignaled lto lproduced lin linsulin, lwhich lbinds lto linsulin lreceptors lon la lcells lsurface land linitiates lthe luptake lof lglucose. l Glucose lis la lvery lreactive lmolecule land lif lleft lin lthe lblood, lit lcan lstart lto lbind lto lother lproteins land llipids, lwhich lcan llead lto lloss lof lfunction. l AGEs lare ladvanced lglycation lend lproducts lthat lare la lresult lof lglucose lreacting lwith lthe lendothelial llining, lwhich lcan llead lto ldamage lin lthe lheart land lkidneys. Compare land lcontrast lType lI land lType lII lDiabetes l- l lcorrect lanswer. l l lType lI ldiabetes lis lcaused lby llack lof linsulin . lWith lout linsulin lsignaling, lglucose lwill lnot lbe ltaken linto lthe lcell land lleads lto lhigh lblood lglucose l(hyperglycemia). lType lI lis lusually ltreated lwith linsulin linjections. l Type lII ldiabetes lis lcaused lby la ldesensitization lto linsulin lsignaling. lThe linsulin lreceptors lare lno llonger lresponding lto linsulin, lwhich lalso lleads lto lhyperglycemia. l Type lII lis lusually ltreated lwith ldrugs lto lincrease lthe lsensitization lto linsulin l(metformin), ldietary land llife-style lchanges lor linsulin linjections. Describe lsome lreasons lfor la lpatient lneeding ldialysis l- l lcorrect lanswer. l l lAEIOU -acidosis. lElectrolytes, lIntoxication/Ingestion, loverload, luremia. lPatients lwith lkidney lor lheart lfailure. l A lbuild lup lof lphosphates, lurea land lmagnesium lare lremoved lfrom lthe lblood lusing la lsemi -
permeable lmembrane land ldialysate. l AEIOU: l A—acidosis; l E—electrolytes lprincipally lhyperkalemia; l I—ingestions lor loverdose lof lmedications/drugs; l O—overload lof lfluid lcausing lheart lfailure; l U—uremia lleading lto lencephalitis/pericarditis Compare land lcontrast lhemodialysis land lperitoneal ldialysis. l What lare lsome lreasons lfor la lpatient lchoosing lone lover lthe lother? l- l lcorrect lanswer. l l lHemodialysis luses la lmachine lto lpump lblood lfrom lthe lbody lin lone ltube lwhile ldialysate l(made lof lwater, lelectroly tes land lsalts) lis lpumped lin lthe lseparate ltube lin lthe lopposite ldirection. lWaste lfrom lthe lblood ldiffuses lthrough lthe lsemipermeable lmembrane lseparating lthe lblood lfrom lthe ldialysate. l Peritoneal lDialysis ldoes lnot luse la lmachine, lbut linstead linjects la lsolution lof lwater land lglucose linto lthe labdominal lcavity. lThe lperitoneum lacts las lthe lmembrane linstead lof ldialysis ltubing. lThe lwaste lproducts ldiffuse linto lthe labdominal lcavity land lthe lwaste lsolution lis lthen ldrained lfrom lthe lbody. l Peritoneal ldialysis loffers lcontinuo us lfiltration land lis lless ldisruption lto lthe lpatient's ldaily lroutines. lHowever, lit ldoes lrequire lsome ltraining lof lthe lpatient land lis lnot lrecommended lfor lindividuals lwho lare loverweight lor lhave lsevere lkidney lfailure. l Hemodialysis lprovides lmedical lcare, lbut l3 ltimes la lweek lfor lseveral lhours lsitting lat la lhospital lor lclinic. lIndividuals lwith lacute lkidney lfailure lare lrecommended lto luse lhemodialysis. How ldoes lhomeostasis land lmaintaining loptimal lphysiological lhealth limpact lyour lwellbeing? l- l lcorrect lanswer. l l lHomeo stasis lacts lto lcreate la lconstant land lstable lenvironment lin lthe lbody ldespite linternal land lexternal lchanges. lProteins land lother lcellular lprocesses lrequire loptimal lconditions lin lorder lto lcarry lout ltheir lfunctions. l Alterations lin lpH, lsalt lconcentration, ltemp erature, lglucose llevels, letc. lcan lhave lnegative leffects lon lhealth, lso lit lis lvital lfor lmechanisms lthat lregulate lhomeostasis lto lfunction lproperly lfor lmaintaining lgood lhealth Differentiate lbetween lInnate lImmunity land lAdaptive lImmunity l? l- l lcorrect lanswer. l l lThe linnate limmune lsystem lencompasses lphysical lbarriers land lchemical land lcellular ldefenses. lPhysical lbarriers lprotect lthe lbody lfrom linvasion. lThese linclude lthings llike lthe lskin land leyelashes. lChemical lbarriers lare ldefense lmechanisms lthat lcan ldestroy lharmful lagent. lExamples linclude ltears, lmucous, land lstomach lacid. l Cellular ldefenses lof lthe linnate limmune lresponse lare lnon-specific. lThese lcellular ldefenses lidentify lpathogens land lsubstances lthat lare lpotentially ldangerous land ltakes lsteps lto lneutralize lor ldestroy lthem. l Adaptive limmunity lis lan lorganism's lacquired limmunity lto la lspecific lpathogen. lAs lsuch, lit's lalso lreferred lto las lacquired limmunity. lAdaptive limmunity lis lnot limmediate, lnor ldoes lit lalways llast lthroughout lan lorganism's lentire llifespan, lalthough lit lcan. l The ladaptive limmune lresponse lis lmarked lby lclonal lexpansion lof lT land lB llymphocytes, lreleasing lmany lantibody lcopies lto lneutralize lor ldestroy ltheir ltarget lantigen What lis la lway lthat lAdaptive lImmunity lcan lrecruit linnate limmunity? l- l lcorrect lanswer. l l lThe linnate limmune lresponse lto lmicrobes lstimulates ladaptive limmune lresponses land linfluences lthe lnature lof lthe ladaptive lresponses. l Conversely, ladaptive limmune lresponses loften lwork lby lenhancing lthe lprotective lmechanisms lof linnate limmunity, lmaking lthem lmore lcapable lof leffectively lcombating lpathogenic lmicrobes Why lare lsome linfections lharder lon lchildren lwhile lother linfections lare lharder lon lthe lelderly? l- l lcorrect lanswer. l l lChildren lhave lnot lbeen lexposed lto lmany lpathogens lyet, lso lthey llack lmemory lcells land lhave lnot lbuilt-up limmunity lyet. l
