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

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  • April 5, 2022
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NR507 Week 8 Final Exam Study Guide
i i i i i i




Reproductive:
endometrial icycle iand ithe ioccurrence iof iovulation- i the 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 iincreased ileptin ilevels. iSymptoms iwithin i2 iyears iof ipubertyi&

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, ipalpableinodes
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 iinterest, 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

iin 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

, epithelial icells icome itogether iand ithis iis iwhere icarcinoma iin isitu iis imost ilikely ito
idevelop. iPAP itest ior iHPV iscreening inecessary ifor iearly idetection; i90% ican ibe

idetected iby ithese. iViral iDNA ibecomes iintegrated iinto ithe igenomic iDNA iof ithe

iinfected ibasal icell iof ithe icervix iand idirects ithe ipersistent iproduction iof iviral

ioncogenes. iPersistence iof iinfection iwith ihigh-risk iHPV iis ia iprerequisite ifor ithe

idevelopment iof icervical iintraepithelial ineoplasia, ilesions, iand iinvasive icervical

icancers.



Endocrine:
body’s iprocess ifor iadapting ito ihigh ihormone ilevels- iFeedback isystems. iMost
ihormone ilevels iare iregulated iby inegative ifeedback, iin iwhich itropic ihormone

isecretion iraises ithe ilevel iof ia ispecific ihormone. iThe ielevated ilevel iof ithe ispecific

ihormone ithen icauses inegative ifeedback, idecreasing isecretion iof ithe itropic

ihormone. iPositive ifeedback isystems, iin iwhich ielevated ihormone ilevels iincrease ia

iresponse iwhich ithen ifurther iincreases ihormone isecretion, iis iseen imost ioften iin

ireproductive ihormones. iNegative ifeedback iis ithe imost icommon i& ioccurs iwhen ia

ichemical, ineural, ior iendocrine iresponse idecreases ithe isubsequent isynthesis iand

isecretion iof ia ihormone. iPositive ifeedback ioccurs iwhen ia ineural, ichemical, ior

iendocrine iresponse iincreases ithe isynthesis iand isecretion iof ia ihormone. iPositive

ifeedback ialso ioccurs iwhen ian iincreased ihormone ilevel ifurther iincreases ithe

isynthesis iand isecretion iof ithat isame ihormone. iThe isensitivity ior iaffinity iof ithe

itarget icell ito ia iparticular ihormone iis irelated ito ithe iconcentration iof ireceptors iper

icell: ithe imore ireceptors, ithe ihigher ithe iaffinity ior ithe imore isensitive ithe icell iis ito

ithe istimulating ieffects iof ithe ihormone. iThus ithe icell ican iadjust iits isensitivity ito

ithe iconcentration iof ithe isignaling ihormone. ihormone iis idistributed ithroughout

ithe ibody, ionly itarget icells iwith ispecific ireceptors ifor ithat ihormone iare iaffected.

Target icell iresponse idepends ion iblood ilevels iof ithe ihormone, ithe iconcentrationiof
itarget icell ireceptors, iand iaffinity iof ithe ireceptor ifor ithe ihormone. iHormone

ireceptors iof ithe itarget icell ihave itwo imain ifunctions: i(1) ito irecognize iand ibind iwith

ihigh iaffinity ito itheir iparticular ihormones iand i(2) ito iinitiate ia isignal ito iappropriate

iintracellular ieffectors. iSee iChapter i1 ifor icell isignaling ipathways, iparticularly.



Cushing’s iSyndrome- ithe iclinical imanifestations iresulting ifrom ichronic iexposure
ito iexcess iendogenous icortisol iand iis imore icommon iin iwomen. iCushing’s idisease

iis iexcess iendogenous isecretion iof iACTH. iACTH idependent ihypercortisolism

i(about i80%) iresults ifrom ioverproduction iof ipituitary iACTH iby ia ipituitary iadenoma

i(most icommon iand ican ioccur iat iany iage) ior iby ian iectopic isecreting inonpituitary

itumor, isuch ias ia ismall icell icarcinoma iof ithe ilung i(more icommon iin iolder iadults).

iACTH-independent ihypercortisolism i(about i20%) iis icaused iby icortisol isecretion

ifrom ia irare ibenign ior imalignant itumor iof ione ior ibothiadrenal i glands i (more

i common i in ichildren). iA iCushing-like isyndrome i may idevelop ias ia iside ieffect iof

ilong-term ipharmacologic iadministration iof iglucocorticoids. iWith iACTH-

dependent ihypercortisolism, ithe iexcess iACTH istimulates iexcess iproduction iof
icortisol iand ithere iis iloss iof ifeedback icontrol iof iACTH isecretion. iWhatever ithe

icause, itwo iobservations iconsistently iapply ito iindividuals iwith iCushing’s

isyndrome: i1.) iThey idon’t ihave idiurnal ior icircadian

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