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NR507 Week 8 Final Exam Study Guide (Version 1) / NR 507 Week 8 Final Exam Study Guide (Ne, Study Guides, Projects, Research of Nursing

NR507 Week 8 Final Exam Study Guide (Version 1) / NR 507 Week 8 Final Exam Study Guide (New 2022/2023): Advanced Pathophysiology: Chamberlain College of Nursing

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2021/2022

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Download NR507 Week 8 Final Exam Study Guide (Version 1) / NR 507 Week 8 Final Exam Study Guide (Ne and more Study Guides, Projects, Research Nursing in PDF only on Docsity! NR507 iWeek i8 iFinal iExam iStudy iGuide Reproductive: endometrial icycle iand ithe ioccurrence iof iovulation- ithe imenstrual icycle iconsist iof ithree iphases: ithe ifollicular/proliferative iphase i(postmenstrual), ifollowed iby ithe iluteal/secretory iphase i(premenstrual), iand ithe iischemic/menstrual iphase. *Ovarian ihormones icontrol ithe iuterine i(endometrial) ievents iof ithe imenstrual icycle. iDuring ithe ifollicular/proliferative iphase iof ithe iovarian icycle iestrogen iproduced iby ithe ifollicle icauses ithe iendometrium ito iproliferate i(proliferative iphase) iand iinduces ithe iLH isurge iand iprogesterone iproduction iin ithe igranulosa ilayer. iDuring ithe iluteal/secretory iphase, iestrogen imaintains ithe ithickened iendometrium, iand iprogesterone icauses iit ito idevelop iblood ivessels iand isecretory iglands i(secretory iphase). iAs ithe icorpus iluteum i“starved” iendometrium idegenerates iand isloughs ioff, icausing imenstruation, ithe iischemic/menstrual iphase. uterine iprolapse- ithe idescent iof ithe icervix ior ientire iuterus iinto ithe ivaginal icanal idue ito iweakened ipelvic ifascia iand imusculature iand ipoor isupport ifrom ithe ivaginal imuscles iand ifascia. polycystic iovarian isyndrome- imost icommon icause iof ianovulation iand iovulatory idysfunction iin iwomen. iDefined ias ihaving iat ileast itwo iof ithe ifollowing ithree ifeatures: iirregular iovulation, ielevated ilevels iof iandrogens i(e.g., itestosterone), iand ithe iappearance iof ipolycystic iovaries ion iultrasound. iPCOS iis iassociated iwith imetabolic idysfunction, iincluding idyslipidemia, iinsulin iresistance, iand iobesity. One iof ithe imost icommon iendocrine idisturbances iaffecting iwomen, iespecially iyoung iwomen, iand iis ia ileading icause iof iinfertility iin ithe iU.S. iStrong igenetic icomponent ito iPCOS, ivarious ifeatures iof ithe isyndrome imay ibe iinherited. iPCOS ipatients iare ithree itimes ias ilikely ito ihave iinsulin iresistance, ihigher ifor iobese iwomen. iTend ito ihave i ncreased ileptin ilevels. iSymptoms iwithin i2 iyears iof ipuberty i& iinclude: idysfunctional ibleeding ior iamenorrhea, ihirsutism, iacne, iacanthosis inigricans, iand iinfertility. i60% iare iobese. iIncreased irisk ifor igestational iDM, ipregnancy-induced iHTN, ipreterm ibirth, iand iperinatal imortality. testicular icancer iand iconditions ithat iincrease irisk- imost icommon icancer iin imen, iage i15-35. iSlightly imore icommon ion ithe iright ithan ion ithe ileft. i90% iof itesticular icancers iare igerm icell itumors iarising ifrom ithe imale igametes. iTwo itypes: iSeminomas-most icommon, ileast iaggressive, imake iup i30-35% iof itesticular icancers i& iNonseminomas-include iembryonal icarcinomas, iteratomas, iand ichoriocarcinomas, iwhich iare ithe imost iaggressive, ibut irare iform iof itesticular icancer. iRisk ifactors iinclude: igenetic ipredisposition, ihistory iof icryptorchidism, iabnormal itesticular idevelopment, iHIV, iAIDS, iKlinefelter isyndrome, iand ihistory iof itesticular icancer. iCan iarise ifrom ispecialized icells iof ithe igonadal istroma-these itumors, iwhich iare inamed ifor itheir icellular iorigins, iare iLeydig icell, iSertoli icell, igranulosa icell, iand itheca icell itumors iand iconstitute iless ithan i10% iof iall itesticular icancers. symptoms ithat irequire ievaluation ifor ibreast icancer- ipainless ilump, ipalpable inodes iin ithe iaxilla, iretraction iof itissue i(dimpling), ichest ipain, idilated iblood vessels, iedema, iedema iof ithe iarm, ihemorrhage, ilocal ipain, inipple/areolar ieczema, inipple idischarge iin inon-lacting iwoman, ipitting iof ithe iskin i(like isurface iof ian iorange ipeel), ireddened iskin, ilocal itenderness iand iwarmth, iskin iretraction, iulceration. signs iof ipremenstrual idysphoric idisorder- iOne iof ithese isymptoms imust ibe ipresent ifor ia idiagnosis: imarked iaffective ilability, imarked iirritability ior ianger ior iincreased iinterpersonal iconflicts, imarked ianxiety, itension. iOne iof ithese imust ialso ibe ipresent: idecreased i nterest, idifficulty iconcentrating, ieasy ifatigability, ilow ienergy, iincrease ior idecrease iin isleep, ifeelings iof ibeing ioverwhelmed, iphysical isymptoms, isuch ias: ibreast itenderness, imuscle ior ijoint iaches, ibloating ior iweight igain. i(Greater ithan i5 iof ithese isymptoms ioccur iduring ithe iweek ibefore imenses ionset, iimprove iwithin ia ifew idays iafter imenses ionset, iand idiminish iin ithe iweek ipostmenses). dysfunctional iuterine ibleeding- ibleeding ithat iis iabnormal iin iduration, ivolume, ifrequency, ior iregularity; iand ihas ibeen ipresent ifor ithe imajority iof ithe iprevious i6 imonths. iMay ibe iacute ior ichronic. iPALM-COEIN iSystem ifor iclassification iof iabnormal iuterine ibleeding: iPALM-structural icauses: iPolyp, iAdenomyosis, iLeiomyoma, iMalignancy. iCOEIN-nonstructural icauses: icoagulopathy, iovulatory idysfunction, iendometrial, iiatrogenic, inot iyet iclassified. iIncreased iendometrial ibleeding iis icorrelated iwith ia ichange ifrom iovulatory ito ianovulatory icycles idue ito ihigh iestrogen ilevels. pathophysiology iof iprostate icancer- iMore ithan i95% iof iprostatic ineoplasms iare ihistologically isimilar ito iadenocarcinomas iand irely ion iandrogen-dependent isignaling ifor itheir idevelopment iand iprogression. iMost iof ithese ineoplasms ioccur i n ithe iperiphery iof ithe iprostate. iProstatic iadenocarcinoma iis ia iheterogeneous igroup iof itumors iwith ia idiverse ispectrum iof imolecular iand ipathologic icharacteristics, iand itherefore iclinical ibehaviors iand ichallenges. iThe ibiologic iaggressiveness iof ithe ineoplasm iappears ito ibe irelated ito ithe idegree iof idifferentiation irather ithan ithe isize iof ithe itumor. iTesticular itestosterone iprovides ithe imain isource iof iandrogens iin ithe iprostate iand iis ithe imajor icirculating iandrogen, iwhereas iDHT ipredominates iin iprostate itissue iand ibinds ito ithe iandrogen ireceptors iwith igreater iaffinity ithan idoes itestosterone. iAndrogen iproduction ioutside iof ithe itestes, ior iextra itesticular isources. iTestosterone iis iconverted ito idihydrotestosterone, iDHT iis ithe imost ipotent iintraprostatic iandrogen. HPV iand ithe idevelopment iof icervical icancer- ialmost iexclusively icaused iby icervical ihuman ipapillomavirus i(HPV) iinfection. iHPV istrains i16 i& i18 iare imost ioften iimplicated ias icausing i70% iof iall icervical icancers iand ialso icontribute ito imany ivaginal, ivulvar, ipenile, ianal, iand ioropharyngeal icancers. iMost iHPV iinfections iare icleared ifrom ithe iimmune isystem; ivast imajority iof iinfections ido inot icause icervical icancer. iScreening ibefore iage i21 inot irecommended. iWomen iwith imultiple isex ipartners iare imore ilikely ito ibe iexposed ito ihigh-risk iHPV, ibut iwomen iwith ionly ione ilifetime isexual ipartner ican ialso ibecome iinfected. iTransformation izone iis iwhere ithe itwo icell itypes iof isquamous iepithelium icells iand icolumnar hormone iduring iacute istress ior iinfections, icausing icytokines irelease iand ialtered i mmunological idisturbances, iare iother ipossible imechanisms iof ithyroid istorm. signs iof ithyrotoxicosis i(hyperthyroidism)- iresults ifrom iany icause iof iincreased iamounts iof iTH ilevels-Grave’s idisease. iThin ihair, iexophthalmos, ienlarged ithyroid i(warm ion ipalpation, inodular, isolitary i“toxic” inodule, iheart ifailure i(tachycardia), iweight iloss, idiarrhea, iwarm iskin, isweaty ipalms, ihyperreflexia, ipretibial imyxedema, ioligomenorrhea ior iamenorrhea, iN/V, ianorexia, irestlessness, ishort iattention ispan, idyspnea. Neurological: Dermatomes- iSpecific iareas iof icutaneous i(skin) iinnervation iat ithese ispinal icord isegments iare icalled idermatomes. iThe isensation iof ipain icorresponds ito iskin idermatomes iT6 iand iL1. iSensory inerve idistribution iof iskin idermatomes. iReferred ipain iis iusually iwell ilocalized iand iis ifelt iin ithe iskin idermatomes ior ideeper itissues ibecause ivisceral iafferent ineurons iand iregional isomatic ineurons iconverge ion isecond-order ineurons iat ithe isame ilevel iof ithe ispinal icord. iReferred ipain. substance irelease iat ithe isynapse- iIn iresponse ito ithe iarrival iof ian iaction ipotential iat ithe isynaptic iknob i(presynaptic ineuron), ivesicles icontaining ineurotransmitters irelease itheir icontents iinto ithe isynaptic icleft i(the ispace ibetween ithe ineurons). Neurotransmitters idiffuse iacross ithe isynaptic icleft iand ibind ito ispecific ireceptors ion ipostsynaptic ineurons, iwhere ithey itrigger ian iaction ipotential iin ithe ipostsynaptic ineuron. Spondylolysis- ia istructural idefect i(Degeneration, ifracture, ior idevelopmental idefect) iin ithe ipars iinterarticularis iof ithe ivertebral iarch i(the ijoining iof ithe ivertebral ibody ito ithe iposterior istructures). iThe ilumbar ispine iat iL5 iis iaffected imost ioften. Heredity iplays ia isignificant irole iand ispondylolysis iis iassociated iwith ian iincreased iincidence iof iother icongenital ispinal idefects. iSymptoms iinclude ilower iback ipain iand ilower ilimb ipain. iCervical ispondylosis iis ifacet ihypertrophy iand idisk idegeneration iwith inarrowing iin ithe icervical ispine ipredominantly iat iC5-C6 iand iC6- iC7. location iof ithe imotor iand isensory iareas iof ithe ibrain- iCerebral iCortex. iThe iperipheral inervous isystem iis idivided iint isomatic inervous isystem iand iautonomic inervous isystem. iThe isomatic inervous isystem iconsist iof imotor iand isensory ipathways iregulating ivoluntary imotor icontrol iof iskeletal isystem. iThe iautonomic inervous isystem iconsists iof imotor iand isensory icomponents iinvolved iin iregulating ithe ibody’s iinternal ienvironment i(viscera) ithrough iinvoluntary icontrol iof iorgan isystems. iPrimary imotor icortex i(M1) ilies ialong ithe iprecentral igyrus iin ifrontal ilobe, iSensory iis ipostcentral igyrus iin ithe icortex. pathophysiology iof icerebral iinfarction iand iexcitotoxins- iPathophysiology- iCerebral iinfarction iresults iwhen ian iarea iof ithe ibrain iloses iits iblood isupply ibecause iof ivascular iocclusion. iIV itPA i s iused ito itreat iacute istrokes idue ito iits ithrombolytic iactivity ibut ican ialso icause ineurotoxic ioutcomes iduring istroke. iIntracerebral iinjection iof iexcitotoxins isuch ias iglutamate icauses ineuronal damage. iNeuronal iinjury ifollowing ifocal icerebral iischemia iis iattributed ito iexcitotoxic ieffects iof iglutamate iinjury icausing ihypoxia ifrom idepolarization. agnosia- iA idefect iof ipattern irecognition—a ifailure ito irecognize ithe iform iand inature iof iobjects. iAgnosia ican ibe itactile, ivisual, ior iauditory, ibut ionly ione isense iis igenerally iaffected. iFor iexample, ian iindividual imay ibe iunable ito iidentify ia isafety ipin iby itouching iit iwith ia ihand ibut iable ito iname iit iwhen ilooking iat iit. iAgnosia imay ibe ias iminimal ias ia ifinger iagnosia i(failure ito iidentify iby iname ithe ifingers iof ione's ihand) ior imore iextensive, isuch ias ia icolor iagnosia. iAgnosia imost icommonly iis iassociated iwith icerebrovascular iaccidents i(CVA), iit imay iarise ifrom iany ipathologic iprocess ithat iinjures ithese ispecific iareas iof ithe ibrain. iEx. iSpatial, iobject, ivisual, icolor, iauditory, ifinger, itactile accumulation iof iblood iin ia isubarachnoid ihemorrhage- iSubarachnoid ihemorrhage iis iwhen ia ivessel i is i leaking, iblood ioozes i into ithe isubarachnoid ispace. iWhen i a ivessel i tears, i blood i under i pressure i is i pumped i into i the i subarachnoid i space. i Subarachnoid ihemorrhage i(SAH) iis ithe iescape iof iblood ifrom ia idefective ior iinjured ivasculature iinto ithe isubarachnoid ispace. iThe iblood iincreases ithe iintracranial ivolume, i(Increased iICP, iheadache). iChronic isubdural ihematomas idevelop iover iweeks ito imonths. iThe iexisting isubdural ispace icontains ithe iliquefied iclot ifrom ithe iacute ibleed iand/or iaccumulation iof iblood ifrom ia ileaking ivein. i80% ihave ichronic iheadaches iand itenderness iover ithe ihematoma ion ipalpation. iThey imay ihave iconfusion, imemory iloss, ior icoma, idifficulty ispeaking ior iswallowing, iand iweakness iwith idifficulty iwalking, iloss iof isensation, ior iseizures. iChronic isubdural ihematomas irequire ia icraniotomy ito ievacuate ithe igelatinous iblood iand ito iprevent ibrain iherniation. iPercutaneous idrainage ifor ichronic isubdural ihematomas ihas iproven isuccessful most icommon icause iof imeningitis- iViral imeningitis iis ithe imost icommon icause. iInfectious imeningitis imay ibe icaused iby ibacteria, iviruses, ifungi, iparasites, ior itoxins. iStreptococcus ipneumoniae ibacteria iis ithe imost icommon icause iof ibacterial imeningitis. iBacterial: iMeningococcus i(Neisseria imeningitidis) iand ipneumococcus i(Streptococcus ipneumoniae) iare ithe imost icommon ipathogens. Genitourinary: diet iand ithe iprevention iof iprostate icancer- iepidemiological istudies ihave ifound ithat itotal ifat iintake, ianimal iand isaturated ifat, ired imeat, iand idairy iproducts iare iassociated iwith ian iincrease iin iprostate icancer irisk. iVitamin iE, ia ifat-soluble ivitamin iis iobtained ifrom ivegetable ioils, inuts, iand iegg iyolk. iObesity, ihigh iBMI iand iexcessive icarbohydrate iintake iare ilinked ito iadvanced iand iaggressive iprostate icancer. iMonounsaturated ifats imay idecrease ithe irisk iof iprostate icancer, ihigh ilevels iof ilinolsleic iacid i(corn ioil, isafflower) iare iproinflammatory, iand ipromotes iproliferation iand iangiogenesis. iThe iWestern idiet ihas iincreased iomega i6/omega i3 iratios iand itherefore iis iproinflammatory. iCooking imeats iat ihigh itemperatures iis icarcinogenic. iMEAL i(Men’s ieating iand iliving istudy), idiet-based iintervention ito iincrease ivegetable iand ifruit iconsumption ito isee iif iit ican islow iprostate icancer iprogression ifor imen iwith ilow-grade iprostate icancer. iMeats ithat icontain initrate iare ibad. Impact iof iBenign iProstatic iHypertrophy i(BPH) ion ithe iurinary isystem- iBenign iprostatic ihyperplasia i(BPH) iis ienlargement iof ithe iprostate igland. iPostrenal-caused iby iUT iobstruction, iBPH iis iproblematic ias iprostatic itissue icompresses ithe iurethra iresulting iin ifrequent ilower iurinary itract isymptoms isuch ias iurge ito iurinate ioften, ia idelay iin istarting iurination, idecreased iforce iof ithe iurinary istream, ilong-term iurinary iretention. iObstruction ito iurine iflow iin ithe ilower iurinary itract iincludes ienlargement iof iprostate iin imen. Genetics: the irole iof iDNA iin igenetics- iOur ibodies iare imade iup iof itrillions iof icells. iAnd iat isometime iin iits idevelopment ievery icell icontains ia inucleus, ithe icontrol icenter, iwhere igenetic imaterial iDNA iis ilocated. iDNA icontains ithe igenetic iinformation, ithe iprogramming ifor iour icell. iTherefore, iit imust ibe ireplicated ior icopied iin iits ientirety ibefore iany icell ican ireproduce. iThe ienzyme iDNA ipolymerase iis iimportant ito ihelp icatalyze ithe iDNA ireplication iprocess. iEach iset iof i46 ichromosomes iinside iour isomatic icells icontains iapproximately i6 ifeet iof iDNA itightly ipackaged iinside ithe inucleus iof ithe icell. iGenes iare icomposed iof iDNA, iand ithe imost iimportant iconstituent iof iDNA iis ifour itypes iof initrogenous ibases. iThe ifour ibases, iadenine, icytosine, iguanine, iand ithymine, iare icommonly irepresented iby itheir ifirst iletters: iA, iC, iG, iand iT, irespectively. iDNA ito iserve ias ithe ibasis iof igenetic i nheritance, iDNA imust ibe iable ito iprovide ia icode ifor iall ithe ibody's iproteins. iIn iaddition ito ihaving ithe iability ito ispecify iamino iacid isequences, iDNA imust ibe iable ito ireplicate iitself iaccurately iduring icell idivision iso ithat ithe igenetic icode ican ibe ipreserved iin isubsequent icell igenerations. iDNA ipolymerase iis ithe iprimary ienzyme iinvolved iin ireplication. iIt iadds ibases ito ithe inew iDNA istrand iand iperforms i“proofreading” ifunctions. transcription- ithe iprocess iby iwhich iRNA i s isynthesized ifrom ia iDNA itemplate. iThe iresult iis ithe iformation iof imessenger iRNA i(mRNA) ifrom ithe ibase isequence ispecified iby ithe iDNA imolecule. iTranscription iof ia igene ibegins iwhen ian ienzyme icalled iRNA ipolymerase ibinds ito ia ipromoter isite ion ithe iDNA. iA ipromoter isite iis ia isequence iof iDNA ithat ispecifies ithe ibeginning iof ia igene. iTranscription icontinues iuntil ia iDNA isequence icalled ia itermination isequence iis ireached. effects iof igenetic imutations- iany iinherited ialteration iof igenetic imaterial. iSubstances ithat icause imutations iare icalled imutagens. iMutation irate iin ihumans ivaries ifrom ilocus ito ilocus iand iranges ifrom i10-4 ito i10-7 iper igene iper igeneration. Trisomy; iDown iSyndrome- iTrisomy iis ian ianeuploid icell icontaining ithree icopies iof ione ichromosome. iThe imost iwell-known iexample iof ianeuploidy iin ian iautosome i s itrisomy iof ithe itwenty-first ichromosome, iwhich icauses iDown iSyndrome. Down’s iis iseen iin i1 iin i800 ilive ibirths. iDown’s ihas i47 ichromosomes, iwith ian iextra ion i#21 i(low inasal ibridge, iepicanthal ifolds, iprotruding itongue, iand iflat, ilow-set iears, ipoor imuscle itone i(hypotonia) iand ishort istature iare icharacteristics). i97% iof icases icaused iby inondisjunction iduring ithe iformation iof ione iof ithe iparent’s igametes ior iduring iearly iembryonic idevelopment. iRisk iincreases iwith imaternal iage i>35. iNewborns iwith itrisomy iof ichromosomes i13, i18, ior i21 ican isurvive. NIH iDiagnostic iCriteria ifor iNeurofibromatosis Criteria ifor ithe iDiagnosis iof iNF1 iTwo iof ithe ifollowing iseven icriteria: i• iSix ior imore icafé-au-lait imacules igreater ithan i5 imm iin igreatest idiameter iin iprepubertal iindividuals iand igreater ithan i15 imm iin igreatest idiameter iin ipost-pubertal iindividuals i(adults) i• iMultiple iaxillary ior iinguinal ifreckles i• iOne iplexiform ineurofibroma ior itwo ior imore ineurofibromas iof iany itype i• iOptic iglioma i• iTwo ior imore iLisch inodules i(iris ihamartomas) i• iA idistinctive iosseous ilesion isuch ias isphenoid idysplasia ior ithinning iof ithe icortex iof ilong ibones iwith ior iwithout ipseudarthrosis i• iA ifirst-degree irelative iwith iNF1 iby ithe iabove icriteria Criteria ifor ithe iDiagnosis iof iNF2 iEither ione iof ithe ifollowing icriteria: i• iBilateral imasses iof ithe ieighth icranial inerve iseen iwith iappropriate iimaging itechniques i(e.g., iCT ior iMRI) i• iA ifirst-degree irelative iwith iNF2 iand ieither: ia. iUnilateral imass iof ithe ieighth icranial inerve ior ib. iTwo iof ithe ifollowing: i1. iNeurofibroma i2. Meningioma i3. iGlioma i4. iSchwannoma i5. iJuvenile iposterior isubcapsular ilenticular iopacity Musculoskeletal: ions ithat iinitiate imuscle icontraction- iContraction ibegins ias ithe icalcium iions icombine iwith itroponin, ia ireaction ithat iovercomes ithe iinhibitory ifunction iof ithe itroponin-tropomyosin isystem. growth iof ilong ibones iin ichildren- igrowth iin ithe ilength iof ilong ibones ioccurs iat ithe iphyseal iplate ithrough iendochondral iossification. iCartilage icells iat ithe iepiphyseal iside iof ithe iphyseal iplate imultiply iand ienlarge. iAs irapidly ias inew icartilage icells iform, icartilage icells iat ithe imetaphyseal iside iof ithe iplate iare idestroyed iand ireplaced iby ibone. iBone iis iconstantly ibeing idestroyed iand ire- iformed. iThis iis ia irapid iprocess iin iyoung ichildren, iallowing ithem ito iheal ibone iinjury imore iquickly ithan iadults. iLong ibones ihave ia ibroad iend i(epiphysis), ibroad ineck i(metaphysis), iand inarrow imidportion i(diaphysis) ithat icontains ithe imedullary icavity. i Rickets ioccurs iin ithe igrowing ibones iof ichildren, ideficient iVit. iD ior icalcium. bones ibelonging ito ithe iappendicular iskeleton- iconsists iof i126 ibones ithat imake iup ithe iupper iand ilower iextremities, ithe ishoulder igirdle i(pectoral igirdle), iand ithe ipelvic igirdle i(os icoxae). iThe iskeleton icontributes iabout i14% iof ithe iweight iof ithe iadult ibody. Immunity/Inflammation: how ivaccines iare iformed- iby itaking iviruses ior ibacteria iand iweakening ithem iso ithat ithey ican't ireproduce i(or ireplicate) ithemselves ivery iwell ior iso ithat ithey ican't ireplicate iat iall. iChildren igiven ivaccines iare iexposed ito ienough iof ithe ivirus ior ibacteria ito idevelop iimmunity, ibut inot ienough ito imake ithem isick. populations iat irisk ifor igetting isystemic ifungal iinfections iand iparasitic iinfections- ipeople iwith iweakened iimmune isystems, igenetic idefects, iinfections isuch ias iHIV, icancer, iand idrugs iused ito iprevent itransplant irejection. ippl ion ibroad ispectrum iantibiotics. iPoor ihygiene i& isanitation, ideveloping icountries, ichildren. iImmune ideficiencies imay iallow iinvasive isystemic iinfections i(e.g., isystemic ifungal iinfections) systemic imanifestations iof i nfection- ifever, ileukocytosis, iincreased iheart irate, ipain, iand iserum ielevations iof ienzymes iin ithe iplasma mechanisms iresponsible ifor ithe iincrease iin iantimicrobial iresistance iworldwide- ioveruse ior imisuse iof iantimicrobials i(antibiotics). iAntimicrobial iresistance ioccurs inaturally ithrough igenetic ichanges. functions iof inormal iflora iin ithe ibody- irelationship ibetween ibetween ithe inormal imicrobiome iand ihumans ihas ibeen ireferred ito ias icommensal i(to ithe ibenefit iof ione iorganism iwithout iaffecting ithe iother); ihowever, ithe irelationship imay ibe imore imutualistic i(to ithe ibenefit iof iboth iorganisms). iMembers iof ithe inormal imicrobiome ialso iproduce ichemicals i(ammonia, iphenols, iindoles, iand iother itoxic imaterials) iand itoxic iproteins i(bacteriocins) ithat iinhibit icolonization iby ipathogenic imicroorganisms. desensitization itherapy- iClinical idesensitization ito iallergens ican ibe iachieved iin isome iindividuals. iMinute iquantities iof ithe iallergen iare iinjected iin iincreasing idoses iover ia iprolonged iperiod. iThe iprocedure imay ireduce ithe iseverity iof ithe iallergic ireaction iin ithe itreated iindividual. iMechanisms iby iwhich idesensitization ioccurs imay ibe iseveral, ione iof iwhich iis ithe iproduction iof ilarge iamounts iof iso- icalled iblocking iantibodies, iusually icirculating iIgG, iSuppressing ithe iallergic iresponse. cells iinvolved iin i“left ishift” iin ithe iWBC icount idifferential- iwhen ithe idemand ifor icirculating imature ineutrophils iexceeds ithe isupply, ithe imarrow ibegins ito irelease i mmature ineutrophils i(and iother ileukocytes) iinto ithe iblood. iPremature irelease iof ithe iimmature iwhite icells iis iresponsible ifor ithe iphenomenon iknown ias i“shift-to- ithe-left” ior ileukemoid ireaction. iThis irefers ito ithe imicroscopic idetection iof idisproportionate inumbers iof iimmature ileukocytes iin iperipheral iblood ismears. When iimmature ileukocytes iare ireleased iprematurely ithey icause ia ishift iin ithe idistribution iof icells iin ithe iblood itoward ithe ileft iside, ior iimmaturity iside, iof ithe idiagram. iAs iinfection ior iinflammation idiminshes iand ias igranulopoiesis ireplenishes icirculating igranulocytes, ia ishift iback ito inormal ioccurs. forms iof iimmunity- iInnate i mmunity-1st iline iof idefense: iphysical, imechanical, iand ibiochemical ibarriers iand inormal imicrobiome, iincluding ithe iskin iand imembranous isheets ilining ithe iGI, iGU iand irespiratory itracts. iPhysical iand imechanical: iroutine isloughing ioff iand ireplacement iof idead iskin icells ialso iremoves iadherent ibacteria, iand imechanical icleansing iof ithe isurfaces iinclude ivomiting iand iurination. iGoblet icells iof ithe iupper irespiratory itract iproduce imucus ithat icoats ithe iepithelial isurface iand itraps imicroorganisms ithat iare iremoved iby ihairlike icilia ithat imechanically imove ithe imucus iupward ito ibe iexpelled iby icoughing ior isneezing. iLow itemp iof iskin iand ilow ipH iof ithe iskin iand istomach generally iinhibit ibacterial igrowth. iBiochemical ibarriers-epithelial isurfaces ialso iprovide ibiochemical ibarriers iby isynthesizing iand isecreting isubstances imeant ito itrap ior idestroy imicroorganisms. iMucus, iperspiration, isaliva, itears, iand iearwax iare iall iexamples iof ibiochemical isecretions ithat ican itrap iand ikill ipotential idisease-causing imicroorganisms. i2nd iline iof idefense: iInflammation. iProgrammed ito irespond ito icellular ior itissue idamage, iwhether ithe idamaged itissue iis iseptic i(contaminated iwith imicroorganisms) ior isterile. iThis iis ia irapid iinitiation iand iinteractive isystem iof ihumoral i(soluble iin ithe iblood) iand icellular isystems idesigned ito ilimit ithe iextent iof itissue idamage, idestroy icontaminating iinfectious imicroorganisms, iinitiate ithe iadaptive iimmune iresponse, iand ibegin ithe ihealing iprocess. iAdaptive i(acquired) iimmunity, ioften icalled ithe iimmune iresponse ior iimmunity, iand iconsists iof ilymphocytes iand iserum iproteins icalled iantibodies. Inflammation iis ithe i“first iresponder” ithat icontains ithe iinitial iinjury iand islows ispread iof iinfection, iwhereas iadaptive iimmunity iis ithe i“secondary iresponder” ithat iaugments ithe iinitial idefenses iagainst iinfection iand iprovides ilong-term isecurity iagainst ireinfection. iInnate iimmunity, iespecially iinflammation, iand iadaptive iimmunity iare ihighly iinteractive iand icomplementary. iAutoimmunity- iimmune isystem iresponds ito iself-antigens iresponds ito iantigens iwithin iyour iown ibody. iIgM iappears ifirst, ibut irapidly idisintegrates, ifollowed iby iIgG ithat ipersists ilonger. major ihistocompatibility iclass iI iantigens- ithe iMHC imolecules iare iglycoproteins ifound ion ithe isurface iof iall ihuman icells iexcept ired iblood icells. iThey iare idivided iinto itwo igeneral iclasses, iI i& iII, ibased ion itheir imolecular istructure, idistribution iamong icell ipopulations, iand ifunction iin iantigen ipresentation. iMHC imolecules iare iencoded ifrom ithe iMHC iregion ion ichromosome i6, iwhich icontains iinformation ifor iclass iI iand iclass iII imolecules, ias iwell ias ifor iseveral iother imolecules ithat iparticipate iin ithe iinnate ior iimmune iresponses. iMHC iclass iI imolecules iare isingle itransmembrane ichains i(alpha) iand iBeta i2 imicroglobulin. iThey iare iall inucleated icells iand iplatelets iand ipresent i“ENDOGENOUS” iantigens i(Beta i10 iamino iacids) iderived ifrom iintracellular iproteins. iThey ireact iwith iCD8 ion iTc icells. iThe iMHC iclass i1 imolecules ipresent ismall ipeptide iantigens iin ia ipocket iformed iby ithe ialpha1 iand ialpha2 idomains iof ithe ialpha ichain. inflammatory ichemicals iblocked iby ianti-inflammatory idrugs- iCyclooxygenase iexists iin itwo idifferent iforms: iCOX-1 iis ifound iin imost itissues iand iCOX-2 iis iassociated iwith iinflammation. iNSAIDS iinhibit iboth iCOX-1 iand iCOX-2, iblocking isythesis iof iprostaglandins iof ithe iE iseries, ibut iinhibition iof iCOX-1 icauses icomplications, isuch ias iGI itoxicity: iSelective iCOX-2 iinhibitors iare inow iavailable, iCelebrex iis ithe ionly ione iavailable iin ithe iU.S. iright inow, idue ito iothers ibeing ipulled ifor iincreasing irisk ifor iheart iattack iand istroke. characteristics iof iacute iphase ireactant iC-reactive iprotein- ihs-CRP iis ian iacute iphase ireactant ior iprotein imostly isynthesized iin ithe iliver iand iis ian iindirect imeasure iof iatherosclerotic iplaque-related i nflammation iand iplaque iprogression. iElevated ilevels iare iassociated iwith inumerous iother iCAD irisk ifactors iincluding ismoking, iobesity, iand idiabetes iand, iwhile ithey ihave ibeen ifound ito ibe ian iindependent irisk ifactor ifor iCAD, ithe irisk iis ihighest iwhen ithere iis ian iassociated overactivity iof ithe iSNS ican iresult ifrom iincreased iproduction iof icatecholamines i(epinephrine iand inorepinephrine) ior ifrom iincreased ireceptor ireactivity iinvolving ithese ineurotransmitters. iIncreased iSNS iactivity icauses iincreased iheart irate iand isystemic ivasoconstriction, ithus iraising ithe iblood ipressure. iEfferent isympathetic ioutflow istimulates irenin irelease, iincreases itubular isodium ireabsorption, iand ireduces irenal iblood iflow. iStructural ichanges iin iblood ivessels i(vascular iremodeling), iinsulin iresistance, iincreased irenin iand iangiotensin ilevels, iand iprocoagulant ieffects ican ialso ioccur iwith iSNS iinduced iHTN. complications iof iunstable iplaque iin ithe icoronary iarteries- iProne ito iulceration ior irupture iand ithrombosis iso iplatelets ibegin isticking ito ithe iexposed iunderlying itissue iof ithe ivessel iwall iand iform ia iclot ithat icompletely iocclude ithe ivessels. iThis iresults iin iacute icoronary isyndrome iknown ias iunstable iangina iand iindicates ia ihigher irisk ifor isubsequent iMI. forms iof idyslipidemia iassociated iwith ithe idevelopment iof ithe ifatty istreak iin iatherosclerosis- iincreased ilevels iof iLDLs. iMacrophages ithat iare ifilled iwith ilipoproteins iare icalled ifoam icells. iThese imigrate iinto ithe ivessel iwall iand iaccumulate, iforming ifatty istreaks. iSmooth imuscle icells imigrate iover ithe ifatty istreaks i& iFibrous itissue i s isynthesized. iThis iforms ia iplaque, iwhich ican ipartially iobstruct ithe ilumen iof ithe ivessel. events ithat iinitiate ithe iprocess iof iatherosclerosis- iDamaged iendothelium>fatty istreak iand ilipid icore iformation>fibrous iplaque iformation>complicated ilesions ithat icould irupture, ioccluding ithe ivessel icausing iischemia iand ipossible iinfarction. signs iand isymptoms iof iincreased ileft iatrial iand ipulmonary ivenous ipressures iin ileft isided iheart ifailure- ipulmonary iedema. iDyspnea ion iexertion iand ifatigue, ipossible iinspiratory icrackles, ipleural ieffusions. iPulmonary icongestion iwithout icardiomegaly. differences ibetween ileft iand iright isided iheart ifailure- iRight isided iheart ifailure i(cor ipulmonale) iis ithe iinability iof ithe iright iventricle ito iprovide iadequate iblood iflow iinto ithe ipulmonary icirculation iat ia inormal icentral ivenous ipressure. iMost ioften iresults ifrom isevere ileft iheart ifailure iwhen ithe iincreased ileft iventricular ifilling ipressure iis ireflected iback iinto ithe ipulmonary icirculation. iAs ipressure iin ithe ipulmonary icirculation irises, ithe iresistance ito iright iventricular iemptying iincreases. iThe iright iventricle ihypertrophies iin iresponse ito ithis iincreased iworkload, ihowever iit iundergoes iprogressive idiastolic iand isystolic ideterioration iand iwill idilate iand ifail. iWhen ithis ihappens, ipressure iwill irise iin ithe isystemic ivenous icirculation, iresulting iin iJVD, iperipheral iedema, iand ihepatosplenomegaly. iWhen iright iheart ifailure ioccurs iin ithe iabsence iof ileft iheart ifailure, iit iis icaused imost icommonly iby ipulmonary iHTN iresulting ifrom idiffuse ihypoxic ipulmonary idisease, isuch ias ichronic iobstructive ipulmonary idisease i(COPD) iand icystic ifibrosis, ior ifrom iprimary ipulmonary iarterial iHTN. iIt ican iresult ifrom iright iventricular iMI, icardiomyopathies, iand ipulmonic ivalvular idisease. Left-sided iheart ifailure-with ireduced iEF i(systolic iheart ifailure)-an iejection ifraction iof i<40% iand ian iinability iof ithe iheart ito igenerate ian iadequate icardiac output ito iperfuse ivital itissues. iCardiac ioutput idepends ion ithe iheart irate iand istroke ivolume. iStroke ivolume iis iinfluenced iby ithree imajor ifactors: icontractility, ipreload, iand iafterload. iContractility iis ireduced iby idiseases ithat idisrupt imyocyte iactivity. iMI iis ithe imost icommon icause iof idecreased icontractility; iother icauses iinclude imyocarditis iand icardiomyopathies. iWhen icontractility iis idecreased, iSV ifalls, iand ileft iventricular iend-diastolic ivolume iincreases. iThis icauses idilation iof ithe iheart iand ian iincrease iin ipreload. i*Heart ifailure iwith ipreserved iEF i(diastolic iheart ifailure) ican ioccur isingly ior ialong iwith isystolic iheart ifailure. iIsolated idiastolic iheart ifailure iis idefined ias ipulmonary icongestion idespite ia inormal istroke ivolume iand icardiac ioutput. iMajor icauses iinclude iHTN-induced imyocardial ihypertrophy iand imyocardial iischemia iwith iresultant iventricular iremodeling. Hypertrophy iand iischemia icause ia idecreased iability iof ithe imyocytes ito iactively ipump icalcium ifrom ithe icytosol, iresulting iin iimpaired irelaxation. iTwo iareas iof ipathophysiologic ichanges iin ithe iventricle ihave ibeen iidentified iin idiastolic idysfunction: idecreased icompliance iof ithe ileft iventricle iand iabnormal idiastolic irelaxation. infective iendocarditis- iinfection iand i nflammation iof ithe iendocardium, iespecially ithe icardiac ivalves. iBacteria iare ithe imost icommon icause iof iIE iwith iStaphylococcus iaureus ithe imost icommon icausative iagent iworldwide. iThree icritical ielements iare ipresent ifor iIE: iTrauma, icongenital iheart idisease, ivalvular iheart idisease, iand ithe ipresence iof iprosthetic ivalves iare ithe imost icommon irisk ifactors ifor iendocardial idamage ithat ileads ito iIE. iBlood-born imicroorganisms iadherence ito ithe idamaged iendocardial isurface, iand iformation iof iinfective iendocardial ivegetations iare ithe iother itwo ielements. iRisk iFactors ifor iInfective iEndocarditis i• iImplantation iof iprosthetic iheart ivalves i• iCongenital ilesions iassociated iwith ihighly iturbulent iflow i(e.g., iventricular iseptal idefect) i• iAcquired ivalvular iheart idisease i(especially imitral ivalve iprolapse) i• iPrevious iattack iof iinfective iendocarditis i• iIntravenous idrug iuse i• iLong-term iindwelling iintravenous icatheterization i(e.g., ifor ipressure imonitoring, ifeeding, ihemodialysis) i• iImplantable icardiac ipacemakers i• iHeart itransplant iwith idefective ivalve Peripheral ivascular idisease: pathophysiology iof ideep ivein ithrombosis- iaccumulation iof iclotting ifactors iand iplatelets ileads ito ithrombus iformation iin ithe ivein, ioften inear ia ivenous ivalve. Inflammation iaround ithe ithrombus ipromotes ifurther iplatelet iaggregation, iand ithe ithrombus igrows iproximally. Vichow’s itriad- ithe ithree ifactors ithat ipromote ivenous ithrombus: i1.) ivenous istasis-associated iwith i mmobility, iobesity, iprolonged ileg idependency, iage, iCHF, i2.) ivenous iintimal idamage-related ito itrauma, ivenipuncture, iIV imedications, i3.) ihypercoagulable istates-inherited idisorders, ismoking, imalignancy, iliver idisease, ipregnancy, ioral icontraceptives, ihormone ireplacement, ihyperhomocysteinemia, iantiphospholipid isyndrome. Hematology: physiological iresponse ito ihypoxia iin ianemia- itissue ihypoxia icreates iadditional idemands iand icompensatory iactions ion ithe ipulmonary iand ihematologic isystems. iThe irate iand idepth iof ibreathing iincrease iin ian iattempt ito iincrease ithe iavailability iof ioxygen. iThese idemands iare iaccompanied iby ian iincrease iin ithe irelease iof ioxygen ifrom ihemoglobin. iAll iof ithese icompensatory imechanisms imay icause iindividuals ito iexperience ishortness iof ibreath, ia irapid, ipounding iheartbeat, idizziness, iand ifatigue. iIncreased ierythropoietin iproduction iby ithe ikidneys, iincreased irenin-aldosterone iresponse, iincreased isalt iand iwater iproduction, iincreased iextracellular ifluid, irelease iof ioxygen ifrom ihemoglobin iin itissues. populations iat ithe ihighest irisk ifor ideveloping ifolate ideficiency ianemia- iinadequate idiet, ialcoholism, iinfancy iimpaired iabsorption, imalabsorption istates, i ntrinsic iintestinal idisease, ianticonvulsants, ioral icontraceptives, iincreased iloss, ihemodialysis. causes iof iiron ideficiency ianemia- idietary ideficiency, iimpaired iabsorption, iincreased irequirements iand ichronic iblood iloss, iuses iof imedication ithat ican icause iGI ibleeding, isurgical iprocedures ithat idecrease istomach iacidity, iintestinal itransit itime, iand iabsorption i(e.g., igastric ibypass), iand ieating idisorders, isuch ias ipica. expected ilab itest iresults ifound iin ilong istanding iiron ideficiency ianemia- ilow ilevels iof icirculating iiron i(less ithan i60mcg/dL) iand ireduced ilevels iof itransferrin. iVery ihigh itotal ibody iiron istorage, ialthough iinadequate iiron iis ireleased ifrom ithe ibone imarrow ifor ierythropoiesis. iLevels iof ierythropoeitin iare igenerally ilower ithan iexpected ifor ithe idegree iof ianemia. iLow ior inormal itotal iiron-binding icapacity i(TIBC), inormal ior ihigh iserum iferritin ilevels, iand ilow iconcentrations iof isoluble itransferrin ireceptor. Sickle iCell iAnemia- iInherited iDisorder iof iErythrocytes: iHemoglobinopathies. iAutosomal irecessive igenetic idisorder. iInheritance iof i2 iabnormal igenes i(one ifrom ieach iparent). Inheritance iof ione inormal iHb igene i+ ione iabnormal iHb igene i= isickle icell itrait i(carrier). iPathophysiology: iSingle iamino iacid ichange ion ibeta-chain iforms ielongated iHb imolecules i(HbS). iOxidative istress i(hypoxia), ianxiety, ifever, icold, idehydration, idecreased ioxygen ibinding ito iHb iand iincreases isickling itendencies. i(Normochromic, inormocytic) iHemolytic ianemia, iabnormal ishape iof ihemoglobin. iOcclude iblood ivessels iand ispleen i=> ihigh irisk ifor iCVA iand isplenic idamage. causes iof iaplastic ianemia- ihematopoeietic ifailure ior ibone imarrow iaplasia ichracterized iby ireduction iin ithe ieffective iproduction iof imature icells iby ithe ibone imarrow, icausing iperipheral ipancytopenia i(anemia, ineutropenia, iand ithrombocytopenia), iwhich iis ia ireduction ior iabsence iof iall ithree iblood itypes. Pathogenesis inot iclearly idefined, imechanisms iinclude iimmune-mediated idestruction iof ihematopoietic istem icells ior itheir iprogenitors iat ivarious istages iof idifferentiation. iKnown icauses iare ifrom ichemicals iand idrugs, iphysical iagents, ior iunpredictable iexposures; iit ican ibe iinherited i(Fanconi ianemia, itelomerase idefects) ior iidiosyncratic i(Chloramphenicol, iphenylbutazone, iorganic iarsenicals, imethylphenylethylhydantoin, icarbamazepine, ipenicillamine, igold isalts), iwhole-