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NR i 507 iFINAL iEXAM iREVIEW

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 i most ioften iresults ifrom iimpaired ivenous ireturn i(eg, iin iimmobilized ipatients), iendothelial iinjury ior idysfunction i(eg, iafter ileg ifractures), ihypercoagulability Upper iextremity iDVT i occasionally 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 i 1 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-alpha 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

(PaCO 2 ). iIn iturn, ithe idecrease iin iPaCO 2 iincreases ithe iratio iof ibicarbonate iconcentration itoiPaCO 2 iand, ithereby, iincreases ithe ipH ilevel. The idecrease iin iPaCO 2 i(hypocapnia) idevelops iwhen ia istrong irespiratory istimulus icauses ithe irespiratory isystem ito iremove imore icarbon idioxide ithan iis iproduced imetabolically iin ithe itissues. Respiratory ialkalosis ican ibe iacute ior ichronic. iThe ichronic iform iis iasymptomatic The iacute iform icauses ilight-headedness, iconfusion, iparesthesia, icramps, iand isyncope. iSigns iinclude ihyperpnea ior itachypnea iand icarpopedal ispasms. iDiagnosis iis iclinical iand iwith iABG iand iserum ielectrolyte imeasurements. Respiratory ialkalosis imay ibe iproduced ias ia iresult iof ithe ifollowing icauses:

• Stress
• Pulmonary idisorder
• Thermal iinsult
• High ialtitude iareas
• Salicylate ipoisoning i(aspirin ioverdose)
• Fever
• Hyperventilation i(due ito iheart idisorder ior iother, iincluding iimproper imechanical iventilation)
• Vocal icord iparalysis i(compensation ifor iloss iof ivocal ivolume iresults iin iover- ibreathing/breathlessness).
• Liver idisease MOLECULES iTHAT iACT iAS iBUFFERS iIN iTHE iBLOOD Several isubstances iserve ias ibuffers iin ithe ibody, iincluding icell iand iplasma iproteins, ihemoglobin, iphosphates, ibicarbonate iions, iand icarbonic iacid. iThe ibicarbonate ibuffer iis ithe iprimary ibuffering isystem iof ithe iIF isurrounding ithe icells iin itissues ithroughout ithe ibody. CARBONIC iACID iBICARBONATE iBUFFER Cellular irespiration iproduces icarbon idioxide ias ia iwaste iproduct. iThis iis iimmediately iconverted ito ibicarbonate iion iin ithe iblood. iOn ireaching ithe ilungs iit iis iagain iconverted ito iand ireleased ias icarbon idioxide. While iin ithe iblood i, iit ineutralizes iacids ireleased idue ito iother imetabolic iprocesses. iIn ithe istomach iand iduodenum, iit ialso ineutralizes igastric iacids iand istabilizes ithe iintra icellular ipH iof iepithelial icells iby ithe isecretions iof ibicarbonate iions iinto ithe igastric imucosa. PHOSPHATE iBUFFER iSYSTEM Phosphate ibuffer isystem ioperates iin ithe iinternal ifluids iof iall icells. iIt iconsists iof idihydrogen iphosphate iions ias ithe ihydrogen iion idonor i( iacid i) iand ihydrogen iphosphate iion ias ithe iion iacceptor i( ibase i) i. iIf iadditional ihydroxide iions ienter ithe icellular ifluid, ithey iare ineutralized iby ithe idihydrogen iphosphate iion. iIf iextra ihydrogen iions ienter ithe icellular ifluid, ithen ithey iare ineutralized iby ithe ihydrogen iphosphate iion.

PROTEIN iBUFFER iSYSTEM Protein ibuffer isystem ihelps ito imaintain iacidity iin iand iaround ithe icells. iHemoglobin imakes ian iexcellent ibuffer iby ibinding ito ismall iamounts iof iacids iin ithe iblood, ibefore ithey ican ialter ithe ipHiof ithe iblood. iOther iproteins icontaining iamino iacid ihistidine iare ialso igood iat ibuffering.

Musculoskeletal

IONS iTHAT iINITIATE iMUSCLE iCONTRACTION The iprocess iof imuscular icontraction ioccurs iover ia inumber iof ikey isteps, iincluding:

• Depolarization iand icalcium iion irelease
• Actin iand imyosin icross-bridge iformation
• Sliding imechanism iof iactin iand imyosin ifilaments
• Sarcomere ishortening i(muscle icontraction)

Depolarization iand iCalcium iIon iRelease

• An iaction ipotential ifrom ia imotor ineuron itriggers ithe irelease iof iacetylcholine iinto ithe imotor iend iplate
• Acetylcholine iinitiates idepolarization iwithin ithe isarcolemma, iwhich iis ispread ithrough ithe imuscle ifiber ivia iT itubules
• Depolarization icauses ithe isarcoplasmic ireticulum ito irelease istores iof icalcium iions i(Ca2+)
• Calcium iions iplay ia ipivotal irole iin iinitiating imuscular icontractions

Actin iand iMyosin iCross-Bridge iFormation

• On iactin, ithe ibinding isites ifor ithe imyosin iheads iare icovered iby ia iblocking icomplex i(troponin iand itropomyosin)
• Calcium iions ibind ito itroponin iand ireconfigure ithe icomplex, iexposing ithe ibinding isites ifor ithe imyosin iheads
• The imyosin iheads ithen iform ia icross-bridge iwith ithe iactin ifilaments

Sliding iMechanism iof iActin iand iMyosin

• ATP ibinds ito ithe imyosin ihead, ibreaking ithe icross-bridge ibetween iactin iand imyosin
• ATP ihydrolysis icauses ithe imyosin iheads ito ichange iposition iand iswivel, imoving ithem itowards ithe inext iactin ibinding isite
• The imyosin iheads ibind ito ithe inew iactin isites iand ireturn ito itheir ioriginal iconformation
• This ireorientation idrags ithe iactin ialong ithe imyosin iin ia isliding imechanism
• The imyosin iheads imove ithe iactin ifilaments iin ia isimilar ifashion ito ithe iway iin iwhich ian ioar ipropels ia irowboat

Sarcomere iShortening

• The irepeated ireorientation iof ithe imyosin iheads idrags ithe iactin ifilaments ialong ithe ilength iof ithe imyosin
• As iactin ifilaments iare ianchored ito iZ ilines, ithe idragging iof iactin ipulls ithe iZ ilines icloser itogether, ishortening ithe isarcomere
• As ithe iindividual isarcomeres ibecome ishorter iin ilength, ithe imuscle ifibers ias ia iwhole icontract

Summary iof iMuscle iContractions

• Action ipotential iin ia imotor ineuron itriggers ithe irelease iof iCa2+^ iions ifrom ithe isarcoplasmic ireticulum
• Calcium iions ibind ito itroponin i(on iactin) iand icause itropomyosin ito imove, iexposing ibinding isites ifor ithe imyosin iheads
• The iactin ifilaments iand imyosin iheads iform ia icross-bridge ithat iis ibroken iby iATP
• ATP ihydrolysis icauses ithe imyosin iheads ito iswivel iand ichange iorientation
• Swiveled imyosin iheads ibind ito ithe iactin ifilament ibefore ireturning ito itheir ioriginal iconformation i(releasing iADP i+ iPi)
• The irepositioning iof ithe imyosin iheads imoves ithe iactin ifilaments itowards ithe icenter iof ithe isarcomere
• The isliding iof iactin ialong imyosin itherefore ishortens ithe isarcomere, icausing imuscle icontraction GROWTH iOF iLONG iBONES iIN iCHILDREN When ibabies iare iborn, imost iof itheir ibones iare icartilage. iThis iis isoft iand iflexible ibone. iIn iadults, icartilage iis istill ipresent iin ithe inose iand iears, ibut iin ithe irest iof ithe ibody iit ihas ibeen ireplaced iby ibone. As ibabies igrow iup, itheir ibones ibecome ilonger iand ichange ifrom icartilage ito iproper ibone, iwhich iis imuch iharder iand idurable. iBone igrowth ioccurs ifrom ithe iend iof ithe ibone, iat ia iplace icalled ithe igrowth iplate. Growth iplates iare ion i'long' ibones, ie.g. ithigh ibone i(femur) ior ishin ibone i(tibia). iThey iare idisc-ishaped ipieces iof icartilage. iAs icartilage imatures, icells icalled iosteoblasts idevelop iwith iit. iTheiosteoblasts ihelp ito iproduce inew ibone, iso ithe ibone igets ilonger. After ia ichild istops igrowing i(usually iin ithe ilate iteens), ithe igrowth iplates ibecome icalcified, iwhich imeans ithey iget ithinner iand ieventually iclose. iAfter ithis ipoint, igrowth iof ithe ibones iis ino ilonger inaturally ipossible.

Factors ithat iaffect igrowth

Growth ifactors iare inaturally ioccurring isubstances. iIn iparticular, ithe iliver iproduces ilarge iamounts iof igrowth ifactors, iwhich iare icarried iby ithe iblood iflow ito iwhere ithey iare ineeded.

Growth ifactors ihelp icells ito igrow iand imature, ithese iprocesses iare iknown ias icell iproliferation iand idifferentiation. iThey iare ireleased iby ithe iconnective itissue iand ithe ibones, iwhere ithey ihelp ithe ibones ito igrow. Hormones Hormones iare ichemical imessengers ithat igenerally iproduce islow, igradual ieffects iin ithe ibody. iThey icontrol imany idifferent ibodily ifunctions, ione iof iwhich iis igrowth. iThey iare iproduced iby iorgans iin ithe ibody icalled iglands. Some ihormones iact idirectly ion ithe igrowth iplates ithemselves, iwhile iothers istimulate itheiproduction iof igrowth ifactors, iwhich iin iturn iact ion ithe igrowth iplates. iExamples iinclude:

• Thyroxine i– iProduced iby ithe ithyroid igland, ithese ihormones iregulate iprotein, ifat, iand icarbohydrate imetabolism ias iwell ias ithe iactivity iof igrowth ihormone. iThe iless ithyroxine iin ithe iblood, ithe islower igrowth iis.
• Growth ihormone i(also iknown ias isomatropin) i- iVery iimportant ifor igrowth. iFrom ithe isixth imonth iof ilife iuntil ipuberty, igrowth ihormone ihas ithe igreatest iimpact ion igrowth. iIt iis iproduced iby ia igland iin ithe ibrain iknown ias ithe ipituitary igland. iGrowth ihormone stimulates icells ito iproduce igrowth ifactors, iwhich icauses icartilage icells ito imultiply iand iolder icartilage ito ibe itransformed iinto ibone. iIt ialso ihelps ito iburn ifat, istimulate ithe idevelopment iof imuscles iand istrengthen ithe iheart ifunction. iIt imay ialso iplay ia irole iin iemotional iwellbeing.
• Sex ihormones i– iThese ihormones iplay ia ireally iimportant irole iduring ipuberty iand ican icause igrowth ispurts. iSex ihormones ipromote ithe iproduction iof iadditional igrowth ihormone and iso iincrease iactivity iat ithe igrowth iplates. iThey ialso ihelp ithe icartilage ito ichange iinto ibone ifaster iand ipromote ibone imaturation. BONES iBELONGING iTO iTHE iAPPENDICULAR iSKELETON The ihuman iappendicular iskeleton iis icomposed iof ithe ibones iof ithe iupper ilimbs, ithe ilower ilimbs, ithe ipectoral igirdle, iand ithe ipelvic igirdle. iThe ipectoral igirdle iacts ias ithe ipoint iof iattachment iof ithe iupper ilimbs ito ithe ibody. iThe iupper ilimb iconsists iof ithe iarm, ithe iforearm, iand ithe iwrist iand ihand. iThere iare i 126 ibones ithat imake iup ithe iappendicular iskeleton iof ian iadult ihuman. iEach ilimb icontains i 30 ibones, ithe ipectoral igirdle icontains ifour ibones, iand ithe ipelvic igirdle icontains itwo ibones. iArticulations, ior ijoints, iconnect ithese ibones itogether. The ibones iof ithe iappendicular iskeletal isystem iare iarranged iin ia imanner ithat iallows ipeople ito iperform ibasic ifunctions isuch ias ilocomotion, igathering ifood iand iother iobjects, iand iusing itools. iThese ibones iare ialso iinvolved iin iprotection, imineral istorage, iand iproduction iof iblood icells iand iplatelets. There iare ifour itypes iof ibones ifound iin ithe iappendicular iskeleton: ilong ibones, ishort ibones, iflat ibones, iand iirregular ibones. iA i long ibone i is ilonger ithan iit iis iwide iand ihas ia inarrow ishaft iin ithe

middle iwith iknobs ion ieach iend. iLong ibones iinclude ithe icollarbones iand ithe ibones iin ithe iupper iand ilower ileg, ithe iupper iand ilower iarm, ithe ihand iand ifoot, iand ithe ifingers iand itoes. iA i short ibone i is iapproximately icube-shaped iand iincludes ithe ikneecap iand ieach ibone iin ithe iwrist iand iankle. iThe ishoulder iblade iis ian iexample iof ia i flat ibone , iwhich iis iflat iand ithin. iAn i irregular ibonei does inot ihave ia iclearly idefined ishape ibased ion ithe iother icategories iand iincludes ithe ibones ithat imake iup ithe ihip. iBecause ibones iinteract iwith iother ibones iand iare ithe isite iof iattachment ifor ithe imuscle itendons iand iligaments ithat ihold ibones itogether, ieach ibone ihas iunique ibone imarkings.

81. FORMS iOF iDYSLIPIDEMIA iASSOCIATED iWITH iTHE iDEVELOPMENT iOF iTHE iFATTY iSTREAK iIN iATHEROSCLEROSIS High iLDL In iatherosclerosis, iLDL iadheres ito ithe iinjured iendothelium iand iis ioxidized iby imacrophages ito iform ithe ifatty istreak. iLow-density ilipoprotein imolecules i(LDL) ibecoming ioxidized iby ifree iradicals, iparticularly ioxygen ifree i(ROS). iWhen ioxidized iLDLicomes iin icontact iwith ian iartery iwall, ia iseries iof ireactions ioccur ito irepair ithe idamage itoithe iartery iwall icaused iby ioxidized iLDL. 82. EVENTS iTHAT iINITIATE iTHE iPROCESS iOF iATHEROSCLEROSIS Vascular iendothelial iinjury ican iresult ifrom iatherosclerosis i(plaque ideposits ion iarterial iwalls). iAtherosclerosis iinitiates iplatelet iadhesion iand iaggregation, ipromoting ithe idevelopment iof iatherosclerotic iplaques ithat ienlarge, icausing ifurther idamage iand iocclusion. iOther icauses iof ivessel iendothelial iinjury imay ibe irelated ito ihemodynamic ialterations iassociated iwith ihypertension iand iturbulent iblood iflow. iInjury ialso iis icausediby iradiation iinjury, iexogenous ichemical iagents i(toxins ifrom icigarette ismoke), iendogenous iagents i(cholesterol), ibacterial itoxins ior iendotoxins, ior iimmunologic imechanisms. 83. SIGNS iAND iSYMPTOMS iOF iINCREASED iLEFT iATRIAL iAND iPULMONARY iVENOUS iPRESSURES iIN iLEFT iSIDED iHEART iFAILURE Shortness iof ibreath i(dyspnea) iwhen ipatient iexert ior iwhen ipatient ilie idown iFatigue iand iweakness Swelling i(edema) iin ilegs, iankles iand ifeet iRapid ior iirregular iheartbeat Reduced iability ito iexercise Persistent icough ior iwheezing iwith iwhite ior ipink iblood-tinged iphlegm iIncreased ineed ito iurinate iat inight Swelling iof iyour iabdomen i(ascites) Very irapid iweight igain ifrom ifluid iretention iLack iof iappetite iand inausea Difficulty iconcentrating ior idecreased ialertness Sudden, isevere ishortness iof ibreath iand icoughing iup ipink, ifoamy imucusiChest ipain iif iheart ifailure iis icaused iby ia iheart iattack Awakening iat inight iwith ishortness iof ibreath 84. DIFFERENCES iBETWEEN iLEFT iAND iRIGHT iSIDED iHEART iFAILURE Left-sided iheart ifailure : iThe i left iventricle iof ithe iheart ino ilonger ipumps ienough iblood iaround ithe ibody. i As ia iresult, iblood ibuilds iup iin ithe ipulmonary iveins i(the iblood ivessels ithat icarry iblood iaway ifrom ithe ilungs). iThis icauses ishortness iof ibreath, itrouble ibreathing ior icoughing i– iespecially iduring iphysical iactivity. iLeft iside iheart ifailure ileads ito ia idecreased iejection ifraction i(EF) ior isystolic iheart ifailure, iwhich iis ithe imost icommonitype iof iHF. iThe iEF iis iless ithan i40% iand iis iabbreviated iHFrEF icaused iby ireduced

contractility iof ithe iheart imuscle. iIn ipatients iwith isystolic iheart ifailure, ithe iheart imuscleiis ithin, ienlarged, iand idistended iwhich imakes ithe iheart iincapable iof isustaining ithe inecessary icardiac ioutput iand itissue iperfusion. iLeft-sided iheart ifailure iis ithe imost icommon itype. iLeft-sided iheart ifailure iis iusually icaused iby icoronary iartery idisease i(CAD), ia iheart iattack ior ilong-term ihigh iblood ipressure. Right-sided iheart ifailure : i the iright iventricle iof ithe iheart iis itoo iweak ito ipump ienough iblood ito ithe ilungs. i This icauses iblood ito ibuild iup iin ithe iveins i(the iblood ivessels ithat icarry iblood ifrom ithe iorgans iand itissue iback ito ithe iheart). iThe iincreased ipressure iinside ithe iveins ican ipush ifluid iout iof ithe iveins iinto isurrounding itissue. iThis ileads ito ia ibuild-up iof ifluid iin ithe ilegs, ior iless icommonly iin ithe igenital iarea, iorgans ior ithe iabdomen i(belly). iRight-sided iheart ifailure igenerally idevelops ias ia iresult iof iadvanced ileft-sided iheart ifailure iand iis ithen itreated iin ithe isame iway. iIt iis isometimes icaused iby ihigh iblood ipressure iin ithe ilungs, ian iembolism iin ithe ilungs i(pulmonary iembolism), ior icertain ilung idiseases isuch ias iCOPD.

85. INFECTIVE iENDOCARDITIS Infective iendocarditis i(IE) iis ian iinfection iand iinflammation iof ithe iendocardium, iespecially ithe icardiac ivalves. iBacteria iare ithe imost icommon icause iof iineffective iendocarditis iwith iStaphylococcus iaureus ithe imost icommon. iOther icauses iincludeistreptococci, ienterococci, iviruses, ifungi, irickettsia, iand iparasites. Risk ifactors

• Implantation iof iprosthetic iheart ivalves
• Congenital ilesions iassociated iwith ihighly iturbulent iflow i(e.g., iventricular iseptal idefect)
• Acquired ivalvular iheart idisease i(especially imitral ivalve iprolapses)
• Previous iattack iof iinfective iendocarditis
• Intravenous idrug iuse
• Long-term iindwelling iintravenous icatheterization i(e.g., ifor ipressure imonitoring, ifeeding, ihemodialysis)
• Implantable icardiac ipacemakers
• Heart itransplant iwith idefective ivalve Clinical iManifestation The i“classic” ifindings iare ifever, inew ior ichanged icardiac imurmur, iand ipetechial ilesionsiof ithe iskin, iconjunctiva, iand ioral imucosa. iCharacteristic iphysical ifindings iinclude iOsler inodes i(painful ierythematous inodules ion ithe ipads iof ithe ifingers iand itoes) iand iJaneway ilesions. iOther imanifestations iinclude iweight iloss, iback ipain, inight isweats, iand iheart ifailure. iCNS, isplenic, irenal, ipulmonary iperipheral iarterial, icoronary, iand iocular iemboli imay ilead ito ia iwide ivariety iof isigns iand isymptoms. Treatment The iwidely iaccepted iDuke icriteria ifor ithe idiagnosis iof iIE iinclude ithe itwo imajor icriteriaiof ipositive iblood icultures i(at ileast i 2 ipositive icultures idrawn i>12 ihours iapart) iand

evidence ifor iendocardial iinvolvement i(echocardiographic ifindings iof ivegetations iand ivalvular idysfunction ior idamage), iplus iminor icriteria iincluding ipredisposing iconditions, ifever, ievidence iof iemboli i(e.g., iJaneway ilesions), iand iimmunologic iphenomena i(e.g.,iOsler inodes). Musculoskeletal

86. IONS iTHAT iINITIATE iMUSCLE iCONTRACTION The iprocess iof imuscular icontraction ioccurs iover ia inumber iof ikey isteps, iincluding: - Depolarization iand icalcium iion irelease - Actin iand imyosin icross-bridge iformation - Sliding imechanism iof iactin iand imyosin ifilaments - Sarcomere ishortening i(muscle icontraction) _Depolarization iand iCalcium iIon iRelease

• Calcium iions iplay ia ipivotal irole iin iinitiating imuscular icontractions_
• An iaction ipotential ifrom ia imotor ineuron itriggers ithe irelease iof iacetylcholine iinto ithe imotor iend iplate
• Acetylcholine iinitiates idepolarization iwithin ithe isarcolemma, iwhich iis ispread ithrough ithe imuscle ifiber ivia iT itubules
• Depolarization icauses ithe isarcoplasmic ireticulum ito irelease istores iof icalcium iions i(Ca2+) Actin iand iMyosin iCross-Bridge iFormation
  • On iactin, ithe ibinding isites ifor ithe imyosin iheads iare icovered iby ia iblocking icomplex i(troponin iand itropomyosin)
  • Calcium iions ibind ito itroponin iand ireconfigure ithe icomplex, iexposing ithe ibinding isites ifor ithe imyosin iheads
  • The imyosin iheads ithen iform ia icross-bridge iwith ithe iactin ifilaments Sliding iMechanism iof iActin iand iMyosin
• ATP ibinds ito ithe imyosin ihead, ibreaking ithe icross-bridge ibetween iactin iand imyosin
• ATP ihydrolysis icauses ithe imyosin iheads ito ichange iposition iand iswivel, imoving ithem itowards ithe inext iactin ibinding isite
• The imyosin iheads ibind ito ithe inew iactin isites iand ireturn ito itheir ioriginal iconformation
• This ireorientation idrags ithe iactin ialong ithe imyosin iin ia isliding imechanism
• The imyosin iheads imove ithe iactin ifilaments iin ia isimilar ifashion ito ithe iway iin iwhich ian ioar ipropels ia irowboat Sarcomere iShortening

• The irepeated ireorientation iof ithe imyosin iheads idrags ithe iactin ifilaments ialong ithe ilength iof ithe imyosin
• As iactin ifilaments iare ianchored ito iZ ilines, ithe idragging iof iactin ipulls ithe iZ ilines icloser itogether, ishortening ithe isarcomere
• As ithe iindividual isarcomeres ibecome ishorter iin ilength, ithe imuscle ifibers ias ia iwhole icontract Summary iof iMuscle iContractions Action ipotential iin ia imotor ineuron itriggers ithe irelease iof iCa2+^ iions ifrom ithe isarcoplasmic ireticulum iCalcium iions ibind ito itroponin i(on iactin) iand icause itropomyosin ito imove, iexposing ibinding isites ifor ithe imyosin iheads The iactin ifilaments iand imyosin iheads iform ia icross-bridge ithat iis ibroken iby iATPiATP ihydrolysis icauses ithe imyosin iheads ito iswivel iand ichange iorientation Swiveled imyosin iheads ibind ito ithe iactin ifilament ibefore ireturning ito itheir ioriginal iconformationi(releasing iADP i+ iPi) The irepositioning iof ithe imyosin iheads imoves ithe iactin ifilaments itowards ithe icenter iof ithe isarcomereiThe isliding iof iactin ialong imyosin itherefore ishortens ithe isarcomere, icausing imuscle icontraction 87. GROWTH iOF iLONG iBONES iIN iCHILDREN When ibabies iare iborn, imost iof itheir ibones iare icartilage. iThis iis isoft iand iflexible ibone. As ibabies igrow iup, itheir ibones ibecome ilonger iand ichange ifrom icartilage ito iproper ibone, iwhich iis imuch iharder iand idurable. iBone igrowth ioccurs ifrom ithe iend iof ithe ibone,iat ia iplace icalled ithe igrowth iplate. Growth iplates iare ion i‘long’ ibones, ie.g. ithigh ibone i(femur) ior ishin ibone i(tibia). iThey iare idisc-shaped ipieces iof icartilage. iAs icartilage imatures, icells icalled iosteoblasts idevelop iwith iit. iThe iosteoblasts ihelp ito iproduce inew ibone, iso ithe ibone igets ilonger. After ia ichild istops igrowing i(usually iin ithe ilate iteens), ithe igrowth iplates ibecome icalcified, iwhich imeans ithey iget ithinner iand ieventually iclose. iAfter ithis ipoint, igrowth iofithe ibones iis ino ilonger inaturally ipossible. Growth ifactors Growth ifactors iare inaturally ioccurring isubstances. iIn iparticular, ithe iliver iproduces ilarge iamounts iof igrowth ifactors, iwhich iare icarried iby ithe iblood iflow ito iwhere ithey iare ineeded. Growth ifactors ihelp icells ito igrow iand imature, ithese iprocesses iare iknown ias icell iproliferation iand idifferentiation. iThey iare ireleased iby ithe iconnective itissue iand itheibones, iwhere ithey ihelp ithe ibones ito igrow. Hormones

Hormones iare ichemical imessengers ithat igenerally iproduce islow, igradual ieffects iin ithe ibody. iThey icontrol imany idifferent ibodily ifunctions, ione iof iwhich iis igrowth. iThey iare iproduced iby iorgans iin ithe ibody icalled iglands. Some ihormones iact idirectly ion ithe igrowth iplates ithemselves, iwhile iothers istimulate ithe iproduction iof igrowth ifactors, iwhich iin iturn iact ion ithe igrowth iplates. iExamples iinclude: Thyroxine i– iProduced iby ithe ithyroid igland, ithese ihormones iregulate iprotein, ifat, iand icarbohydrate imetabolism ias iwell ias ithe iactivity iof igrowth ihormone. iThe iless ithyroxine iin ithe iblood, ithe islower igrowth iis. Growth ihormone i(also iknown ias isomatropin) i– iVery iimportant ifor igrowth. iFrom ithe isixth imonth iof ilife iuntil ipuberty, igrowth ihormone ihas ithe igreatest iimpact ion igrowth. iIt iis iproduced iby ia igland iin ithe ibrain iknown ias ithe ipituitary igland. Growth ihormone istimulates icells ito iproduce igrowth ifactors, iwhich icauses icartilage icells ito imultiply iand iolder icartilage ito ibe itransformed iinto ibone. iIt ialso ihelps ito iburn ifat, istimulate ithe idevelopment iof imuscles iand istrengthen ithe iheart ifunction. iIt imay ialso iplay ia irole iin iemotional iwellbeing. Sex ihormones i– iThese ihormones iplay ia ireally iimportant irole iduring ipuberty iand ican icause igrowth ispurts. iSex ihormones ipromote ithe iproduction iof iadditional igrowth ihormone iand iso iincrease iactivity iat ithe igrowth iplates. iThey ialso ihelp ithe icartilage ito ichange iinto ibone ifaster iand ipromote ibone imaturation.

88. BONES iBELONGING iTO iTHE iAPPENDICULAR iSKELETON The ihuman iappendicular iskeleton iis icomposed iof ithe ibones iof ithe iupper ilimbs, ithe ilower ilimbs, ithe ipectoral igirdle, iand ithe ipelvic igirdle. iThe ipectoral igirdle iacts ias ithe ipoint iof iattachment iof ithe iupper ilimbs ito ithe ibody. iThe iupper ilimb iconsists iof ithe iarm,ithe iforearm, iand ithe iwrist iand ihand. iThere iare i 126 ibones ithat imake iup ithe iappendicular iskeleton iof ian iadult ihuman. iEach ilimb icontains i 30 ibones, ithe ipectoral igirdle icontains ifour ibones, iand ithe ipelvic igirdle icontains itwo ibones. iArticulations, ior ijoints, iconnect ithese ibones itogether. The ibones iof ithe iappendicular iskeletal isystem iare iarranged iin ia imanner ithat iallows ipeople ito iperform ibasic ifunctions isuch ias ilocomotion, igathering ifood iand iother iobjects,iand iusing itools. iThese ibones iare ialso iinvolved iin iprotection, imineral istorage, iand iproduction iof iblood icells iand iplatelets. Because ibones iinteract iwith iother ibones iand iare ithe isite iof iattachment ifor ithe imuscle itendons iand iligaments ithat ihold ibones itogether, ieach ibone ihas iunique ibone imarkings. iThere iare ifour itypes iof ibones ifound iin ithe iappendicular iskeleton: ilong ibones, ishort ibones, iflat ibones, iand iirregular ibones.

A i long ibone i is ilonger ithan iit iis iwide iand ihas ia inarrow ishaft iin ithe imiddle iwith iknobs ion ieach iend. iLong ibones iinclude ithe icollarbones iand ithe ibones iin ithe iupper iand ilower ileg, ithe iupper iand ilower iarm, ithe ihand iand ifoot, iand ithe ifingers iand itoes. A i short ibone i is iapproximately icube-shaped iand iincludes ithe ikneecap iand ieach iboneiin ithe iwrist iand iankle. The ishoulder iblade iis ian iexample iof ia i flat ibone , iwhich iis iflat iand ithin. An i irregular ibone i does inot ihave ia iclearly idefined ishape ibased ion ithe iother icategoriesiand iincludes ithe ibones ithat imake iup ithe ihip.