NR 507 FINAL EXAM REVIEW
i i i i
Peripheral ivascular idisease:
PATHOPHYSIOLOGY iOF iDEEPiVEIN iTHROMBOSIS:
Deep ivenous ithrombosis i(DVT) iis iclotting iof iblood iin ia ideep ivein iof ian iextremity i(usually icalfior
ithigh) ior ithe ipelvis. iDVT iis ithe iprimary icause iof ipulmonary iembolism. iDVT iresults ifrom
iconditions ithat iimpair ivenous ireturn, ilead ito iendothelial iinjury ior idysfunction, ior icause
ihypercoagulability.
Lower iextremity iDVT imost ioften iresults ifrom iimpaired ivenous ireturn i(eg, iin iimmobilized
ipatients), iendothelial iinjury ior idysfunction i(eg, iafter ileg ifractures), ihypercoagulability
Upper iextremity iDVT ioccasionally ioccurs ias ipart iof isuperior ivena icava i(SVC) isyndrome ior
iresults ifrom ia ihypercoagulable istate ior isubclavian ivein icompression iat ithe ithoracic ioutlet. iThe
icompression imay ibe idue ito ia inormal ior ian iaccessory ifirst irib ior ifibrous iband i(thoracic ioutlet
isyndrome) ior ioccur iduring istrenuous iarm iactivity i(effort ithrombosis, ior iPaget-Schroetter
isyndrome, iwhich iaccounts ifor i1 ito i4% iof iupper iextremity iDVT icases).
Deep ivenous ithrombosis iusually ibegins iin ivenous ivalve icusps. iThrombi iconsist iof ithrombin,
ifibrin, iand iRBCs iwith irelatively ifew iplatelets i(red ithrombi); iwithout itreatment, ithrombi imay
ipropagate iproximally ior itravel ito ithe ilungs.
VICHOW’S iTRIAD
Three ifactors iare iknown ias iVirchow’s
• Blood iflow
• The ivessel iwalls
• Blood icomponents
i The ifeatures iof iVirchow’s itriad
• Circulatory istasis i– iabnormalities iof ihemorheology iand iturbulence iat ivessel ibifurcations
iand istenotic iregions
• Vascular iwall iinjury i– iabnormalities iin ithe iendothelium, isuch ias iatherosclerosis iand
iassociated ivascular iinflammation
• Hypercoagulable istate i– iabnormalities iin icoagulation iand ifibrinolytic ipathways iand iin
iplatelet ifunction iassociated iwith ian iincreased irisk iof iVTE iand iother icardiovascular
idiseases i(including iCAD iand iheart ifailure, iand istroke iin ipatients iwith iAF)
Shock:
CAUSES iOF iHYPOVOLEMIC iSHOCK
, Hypovolemic ishock iresults ifrom isignificant iand isudden iblood ior ifluid ilosses iwithin iyour ibody.
iBlood iloss iof ithis imagnitude ican ioccur ibecause iof:
• bleeding ifrom iserious icuts ior iwounds
• bleeding ifrom iblunt itraumatic iinjuries idue ito iaccidents
• internal ibleeding ifrom iabdominal iorgans ior iruptured iectopic ipregnancy
• bleeding ifrom ithe idigestive itract
• significant ivaginal ibleeding
• Endometriosis
In iaddition ito iactual iblood iloss, ithe iloss iof ibody ifluids ican icause ia idecrease iin iblood ivolume.iThis
ican ioccur iin icases iof:
• excessive ior iprolonged idiarrhea
• severe iburns
• protracted iand iexcessive ivomiting
• excessive isweating
Blood icarries ioxygen iand iother iessential isubstances ito iyour iorgans iand itissues. iWhen iheavy
ibleeding ioccurs, ithere iis inot ienough iblood iin icirculation ifor ithe iheart ito ibe ian ieffective ipump.
iOnce iyour ibody iloses ithese isubstances ifaster ithan iit ican ireplace ithem, iorgans iin iyour ibody ibegin
ito ishut idown iand ithe isymptoms iof ishock ioccur. iBlood ipressure iplummets, iwhich ican ibe ilife-
ithreatening.
HOW iTHE iBODY iMAINTAINS iGLUCOSE iLEVELS iDURING iSHOCK
Our ibody imaintain iglucose ilevel iduring ishock iby ibreaking idown iprotein ito ifuel igluconeogenesis.
iThe ineuroendocrine iresponse ito istress iis icharacterized iby iexcessive igluconeogenesis,
iglycogenolysis iand iinsulin iresistance. iStress ihyperglycemia, ihowever, iappears ito ibe icaused
ipredominantly iby iincreased ihepatic ioutput iof iglucose irather ithan iimpaired itissue iglucose
iextraction. iThe imetabolic ieffects iof icortisol iinclude ian iincrease iin iblood iglucose iconcentration
ithrough ithe iactivation iof ikey ienzymes iinvolved iin ihepatic igluconeogenesis iand iinhibition iof
iglucose iuptake iin iperipheral itissues isuch ias ithe iskeletal imuscles. iBoth iepinephrine iand
inorepinephrine istimulate ihepatic igluconeogenesis iand iglycogenolysis; inorepinephrine ihas ithe
iadded ieffect iof iincreasing ithe isupply iof iglycerol ito ithe iliver ivia ilipolysis. iInflammatory
imediators, ispecifically ithe icytokines iTNF-α, iIL-1, iIL-6, iand iC-reactive iprotein, ialso iinduce
iperipheral iinsulin iresistance. iIn iaddition, ithe ialtered irelease iof iadipokines i(increased izinc-alpha2
iglycoprotein iand idecreased iadiponectin) ifrom iadipose itissue iduring iacute iillness iis ithought ito
iplay ia ikey irole iin ithe idevelopment iof iinsulin iresistance
Acid/Base:
CAUSES iOF iRESPIRATORY iALKALOSIS
Respiratory ialkalosis iis ia idisturbance iin iacid iand ibase ibalance idue ito ialveolar ihyperventilation.
iAlveolar ihyperventilation ileads ito ia idecreased ipartial ipressure iof iarterial icarbon idioxide
i i i i
Peripheral ivascular idisease:
PATHOPHYSIOLOGY iOF iDEEPiVEIN iTHROMBOSIS:
Deep ivenous ithrombosis i(DVT) iis iclotting iof iblood iin ia ideep ivein iof ian iextremity i(usually icalfior
ithigh) ior ithe ipelvis. iDVT iis ithe iprimary icause iof ipulmonary iembolism. iDVT iresults ifrom
iconditions ithat iimpair ivenous ireturn, ilead ito iendothelial iinjury ior idysfunction, ior icause
ihypercoagulability.
Lower iextremity iDVT imost ioften iresults ifrom iimpaired ivenous ireturn i(eg, iin iimmobilized
ipatients), iendothelial iinjury ior idysfunction i(eg, iafter ileg ifractures), ihypercoagulability
Upper iextremity iDVT ioccasionally ioccurs ias ipart iof isuperior ivena icava i(SVC) isyndrome ior
iresults ifrom ia ihypercoagulable istate ior isubclavian ivein icompression iat ithe ithoracic ioutlet. iThe
icompression imay ibe idue ito ia inormal ior ian iaccessory ifirst irib ior ifibrous iband i(thoracic ioutlet
isyndrome) ior ioccur iduring istrenuous iarm iactivity i(effort ithrombosis, ior iPaget-Schroetter
isyndrome, iwhich iaccounts ifor i1 ito i4% iof iupper iextremity iDVT icases).
Deep ivenous ithrombosis iusually ibegins iin ivenous ivalve icusps. iThrombi iconsist iof ithrombin,
ifibrin, iand iRBCs iwith irelatively ifew iplatelets i(red ithrombi); iwithout itreatment, ithrombi imay
ipropagate iproximally ior itravel ito ithe ilungs.
VICHOW’S iTRIAD
Three ifactors iare iknown ias iVirchow’s
• Blood iflow
• The ivessel iwalls
• Blood icomponents
i The ifeatures iof iVirchow’s itriad
• Circulatory istasis i– iabnormalities iof ihemorheology iand iturbulence iat ivessel ibifurcations
iand istenotic iregions
• Vascular iwall iinjury i– iabnormalities iin ithe iendothelium, isuch ias iatherosclerosis iand
iassociated ivascular iinflammation
• Hypercoagulable istate i– iabnormalities iin icoagulation iand ifibrinolytic ipathways iand iin
iplatelet ifunction iassociated iwith ian iincreased irisk iof iVTE iand iother icardiovascular
idiseases i(including iCAD iand iheart ifailure, iand istroke iin ipatients iwith iAF)
Shock:
CAUSES iOF iHYPOVOLEMIC iSHOCK
, Hypovolemic ishock iresults ifrom isignificant iand isudden iblood ior ifluid ilosses iwithin iyour ibody.
iBlood iloss iof ithis imagnitude ican ioccur ibecause iof:
• bleeding ifrom iserious icuts ior iwounds
• bleeding ifrom iblunt itraumatic iinjuries idue ito iaccidents
• internal ibleeding ifrom iabdominal iorgans ior iruptured iectopic ipregnancy
• bleeding ifrom ithe idigestive itract
• significant ivaginal ibleeding
• Endometriosis
In iaddition ito iactual iblood iloss, ithe iloss iof ibody ifluids ican icause ia idecrease iin iblood ivolume.iThis
ican ioccur iin icases iof:
• excessive ior iprolonged idiarrhea
• severe iburns
• protracted iand iexcessive ivomiting
• excessive isweating
Blood icarries ioxygen iand iother iessential isubstances ito iyour iorgans iand itissues. iWhen iheavy
ibleeding ioccurs, ithere iis inot ienough iblood iin icirculation ifor ithe iheart ito ibe ian ieffective ipump.
iOnce iyour ibody iloses ithese isubstances ifaster ithan iit ican ireplace ithem, iorgans iin iyour ibody ibegin
ito ishut idown iand ithe isymptoms iof ishock ioccur. iBlood ipressure iplummets, iwhich ican ibe ilife-
ithreatening.
HOW iTHE iBODY iMAINTAINS iGLUCOSE iLEVELS iDURING iSHOCK
Our ibody imaintain iglucose ilevel iduring ishock iby ibreaking idown iprotein ito ifuel igluconeogenesis.
iThe ineuroendocrine iresponse ito istress iis icharacterized iby iexcessive igluconeogenesis,
iglycogenolysis iand iinsulin iresistance. iStress ihyperglycemia, ihowever, iappears ito ibe icaused
ipredominantly iby iincreased ihepatic ioutput iof iglucose irather ithan iimpaired itissue iglucose
iextraction. iThe imetabolic ieffects iof icortisol iinclude ian iincrease iin iblood iglucose iconcentration
ithrough ithe iactivation iof ikey ienzymes iinvolved iin ihepatic igluconeogenesis iand iinhibition iof
iglucose iuptake iin iperipheral itissues isuch ias ithe iskeletal imuscles. iBoth iepinephrine iand
inorepinephrine istimulate ihepatic igluconeogenesis iand iglycogenolysis; inorepinephrine ihas ithe
iadded ieffect iof iincreasing ithe isupply iof iglycerol ito ithe iliver ivia ilipolysis. iInflammatory
imediators, ispecifically ithe icytokines iTNF-α, iIL-1, iIL-6, iand iC-reactive iprotein, ialso iinduce
iperipheral iinsulin iresistance. iIn iaddition, ithe ialtered irelease iof iadipokines i(increased izinc-alpha2
iglycoprotein iand idecreased iadiponectin) ifrom iadipose itissue iduring iacute iillness iis ithought ito
iplay ia ikey irole iin ithe idevelopment iof iinsulin iresistance
Acid/Base:
CAUSES iOF iRESPIRATORY iALKALOSIS
Respiratory ialkalosis iis ia idisturbance iin iacid iand ibase ibalance idue ito ialveolar ihyperventilation.
iAlveolar ihyperventilation ileads ito ia idecreased ipartial ipressure iof iarterial icarbon idioxide
