Laboratuvar

Alfa 1 antitripsin eksikliği

<= span style=3D'font-size:63%'>lAAT in gör= evi: proteaz inhibitörüdür. Elastaz, tripsin, = kolojenaz ve lökosit proteaz ların= 05; inhibe eder.

<= span style=3D'font-size:63%'>lEksikliğin= de:

<= span style=3D'font-size:64%'>–Akciğ= erde-- elastin giderek düşer ve erken amfizem gelişir.

<= span style=3D'font-size:64%'>–Karaci= 7;erde -- defektif proteinlerin atılaması ve birikmesi ile <= /span>hasar oluşur

l75 çe= 51;it AAT alelinden pi MM -- normal, pi ZZ ise en fazla eksikliği gösterendir. Pi ZZ den sonr= a piSS de en öok se= rum düzeyi düşük bulunur.

lPi ZZ lerinde tümünde hastalık oluşmaz (12% sinde KC rahatsızlığı, %75 inde ise amfizem olur).

<= span style=3D'font-size:63%'>l1/2000 oran= 5;nda rastlanır.

<= span style=3D'font-size:63%'>lBozuk gene chr = 14 de dir. 342 . Pozisyonda lizin yerine glutamik asid gelir. Proteinin katlanmasın= da gerekli Sialik as= id eksikliğine sebep olur. bozukluğuna yol açar

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= a 1 AT eksikliği-KLİNİK I

lKronik kc hastalığı

–Çocukluk kolestazından siroza kadar değişik tablo olabilir.

–Çocuklarda bilyer atreziden sonra ikinci= en sık kc tx ne= denidir.

–HCC gelişebilir
–Kc hastalığı sık olarak PiZZ formunda görülür. Pi ZZ formuna sahip çocukların %11 inde karaciğer hastalığı görülürken. %75 inde transaminaz yüksekliği görülür.

–En sık görülen klinik infantil kolestaz dır. 6 ayda geriler, ancak %10 vakada kalıcı ve hızlı ilerleyici olabilir.

–Otoimmun hepatiti benzeri tablo gösterebil= ir- yüksek gam= aglobülin ve immun markerlar vardı= ;r-

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= a 1 AT eksikliği-KLİNİK II

lAmfizem <= /b>

–Erişkinde amfizem var ise solunum sıkıntısı görülür. Özellikle sigara durumu kötüleştirir. <= /span>

–Kc hastalığına göre daha er= ken yaşta ve erk= eklerde daha sıktır.

lDiğer= 3;

lGlomerülonefrit

lPannicülit

lReaktif hava yolu hastalığı

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= a 1 AT eksikliği-TANI

<= span style=3D'font-size:75%;color:yellow;mso-color-index:7'>lA1AT serum d&uum= l;zeyi ve tiplendirilmesi

<= span style=3D'font-size:64%'>–tanıda ikiside bakılması daha iyi olur.

<= span style=3D'font-size:64%'>–Serum düzeyi homozigot larda %40 lara kadar düşebilir. <= /span>

–Heterozigo= t ve karaciğer hastalığı olan vakalard bazen normal düzeyler görülebilir. Bu durumda tipin belirlenmesi katkıda bulunacaktır.

<= span style=3D'font-size:75%;color:yellow;mso-color-index:7'>lHİSTOPATOLO= JİK TANI:
<= span style=3D'font-size:64%'>–PAS- diast= ase + globüller Z tip A1AT periportal hepatositlerde görülür. <= /div>
<= span style=3D'font-size:64%'>–Benzer gobüller PBS de ve HCC dede görülebilir ancak onlarda A1AT eksikliği görülmez.

<= span style=3D'font-size:64%'>–PIQo tipin= de hiçbir A1AT yapılmayacağından globüllerin <= /span>görülmeyeceği akılda tutulmalıdır.

<= span style=3D'font-size:64%'>–İnfant hastalarda histopatoloji bilyer atreziyi taklit edebilir. <= /span>

<= span style=3D'font-size:67%'>lSafra yolu proliferasyonu

<= span style=3D'font-size:67%'>lDeğiş= en derecelerde fibroziz görülüt.

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= a 1 AT eksikliği-TEDAVİ

lDestek tedavisi&= #13;

lVit K

–Kolestazı sürenlerde önemlidir.

–İnfantile kolestazda vit K eksikliğine bağlı intrakraniyal kanama en sı= ;k ölüm sebebidir.

lkc nakli

–Kür sağlar

lgen tedavisi = ;

–Deneysel aşamada

lRECOMBİNAN = A1AT ÜRETİLDİ. Özellikle amfizem gelişmiş hastalarda baz&#= 305; kriterlere uygun şekilde kullanılabiliyor.

l

–

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Z24tc3BlY2lhbDpiYXNlbGluZTsNCgltc28tYW5zaS1sYW5ndWFnZTpUUjt9DQphOmxpbmsNCgl7 Y29sb3I6I0ZGMDAzMyAhaW1wb3J0YW50O30NCmE6YWN0aXZlDQoJe2NvbG9yOiMzMzY2RkYgIWlt cG9ydGFudDt9DQphOnZpc2l0ZWQNCgl7Y29sb3I6eWVsbG93ICFpbXBvcnRhbnQ7fQ0K ------=_NextPart_01C970EC.2DD534F0 Content-Location: file:///C:/24DAE4F0/ALFA1ANTITRIPSINEKSIKLIGI_dosyalar/script.js Content-Transfer-Encoding: quoted-printable Content-Type: application/javascript; charset="us-ascii" function LoadSld() { var sld=3DGetObj("SlideObj") if( !g_supportsPPTHTML ) { =09 sld.style.visibility=3D"visible" return } if( MakeNotesVis() ) return runAnimations =3D _InitAnimations(); =09 if( IsWin("PPTSld") ) parent.SldUpdated(GetSldId()) g_origSz=3DparseInt(SlideObj.style.fontSize) g_origH=3Dsld.style.posHeight g_origW=3Dsld.style.posWidth g_scaleHyperlinks=3D(document.all.tags("AREA").length>0) if( g_scaleHyperlinks ) InitHLinkArray() if( g_scaleInFrame||(IsWin("PPTSld") && parent.IsFullScrMode() ) ) document.body.scroll=3D"no" _RSW() if( IsWin("PPTSld") && parent.IsFullScrMode() ) FullScrInit(); =09 MakeSldVis(); ChkAutoAdv() if( runAnimations ) { if( document.all("NSPlay") ) document.all("NSPlay").autoStart =3D false; if( sld.filters && sld.filters.revealtrans ) setTimeout( "document.body.start()", sld.filters.revealtrans.duration * = 1000 ); else document.body.start(); } } function MakeSldVis()=20 { var fTrans=3Dg_showAnimation && SldHasTrans() if( fTrans )=09 { if( g_bgSound ) { idx=3Dg_bgSound.indexOf(","); pptSound.src=3Dg_bgSound.substr( 0, idx ); pptSound.loop=3D -(parseInt(g_bgSound.substr(idx+1))); } SlideObj.filters.revealtrans.Apply()=09 } SlideObj.style.visibility=3D"visible" if( fTrans ) SlideObj.filters.revealtrans.Play() } function MakeNotesVis()=20 { if( !IsNts() ) return false=20 SlideObj.style.display=3D"none" nObj =3D document.all.item("NotesObj") parent.SetHasNts(0) if( nObj ) {=20 nObj.style.display=3D"" parent.SetHasNts(1) } return 1 } function ChkAutoAdv() { if(SldHasTrans()) SlideObj.onfilterchange=3DAutoAdv else AutoAdv() } function AutoAdv() { if(!IsWin("PPTSld") || !gUseSldTimings )return var sld=3DGetCurSld() if( (sld.mAdvDelay>0) && !parent.IsFramesMode() ) setTimeout("parent.GoToNextSld()",sld.mAdvDelay) } function GetObj(id) { if(g_supportsPPTHTML) return document.all(id); else return document.getElementById(id); } function SldHasTrans() { return SlideObj.style.filter !=3D ""; } function GetSldId() { return sId=3Dlocation.href.substring(location.href.la= stIndexOf('/')+1) } function HideMenu() { if( frames["PPTSld"] && PPTSld.document.all.item("ctx= tmenu") && PPTSld.ctxtmenu.style.display!=3D"none" ) { PPTSld.ctxtmenu.styl= e.display=3D'none'; return true } return false } function IsWin( name ) { return window.name =3D=3D name } function IsNts() { return IsWin("PPTNts") } function IsSldOrNts() { return( IsWin("PPTSld")||IsWin("PPTNts") ) } function SupportsPPTAnimation() { return( navigator.platform =3D=3D "Win32"= && navigator.appVersion.indexOf("Windows")>0 ) } function SupportsPPTHTML() { var appVer=3Dnavigator.appVersion, msie=3DappVer.indexOf("MSIE "), ver=3D0 if( msie >=3D 0 ) ver=3DparseFloat( appVer.substring( msie+5, appVer.indexOf(";",msie) ) ) else ver=3DparseInt(appVer) return( ver >=3D 4 && msie >=3D 0 ) } function _RSW() { if( !g_supportsPPTHTML || IsNts() || ( !g_scaleInFrame && (!IsWin("PPTSld") || !parent.IsFullScrMode()) ) ) return var padding=3D0; if( IsWin("PPTSld") && parent.IsFramesMode() ) padding=3D6 cltWidth=3Ddocument.body.clientWidth-padding cltHeight=3Ddocument.body.clientHeight-padding factor=3D(1.0*cltWidth)/g_origW if( cltHeight < g_origH*factor ) factor=3D(1.0*cltHeight)/g_origH newSize =3D g_origSz * factor if( newSize < 1 ) newSize=3D1 s=3DSlideObj.style s.fontSize=3DnewSize+"px" s.posWidth=3Dg_origW*factor s.posHeight=3Dg_origH*factor s.posLeft=3D(cltWidth-s.posWidth+padding)/2 s.posTop=3D(cltHeight-s.posHeight+padding)/2 if( g_scaleHyperlinks ) ScaleHyperlinks( factor ) } function _InitAnimations() { animRuntimeInstalled =3D ''+document.body.localTime !=3D 'undefined'; isFullScreen =3D (window.name =3D=3D "PPTSld") && !parent.IsFramesMode(); g_animUseRuntime =3D g_showAnimation && animRuntimeInstalled && !(isFullSc= reen && parent.IsSldVisited()); if( g_animUseRuntime ) { collSeq =3D document.all.tags("seq"); if( collSeq !=3D null ) { for(ii=3D0;ii numSlds ) gSldJumpIdx =3D numSlds; if ( gSldJumpIdx >=3D 0 ) { if ( gSldJumpIdx =3D=3D 0 ) gSldJumpIdx =3D 1; var jumpTo =3D parseInt(gSldJumpIdx); gSldJump =3D 0; gSldJumpIdx =3D ""; win.GoToSld( parent.GetSldList().mList[jumpTo-1].mSldHref ) } } } function _KDH() { if( event.keyCode =3D=3D 8 ) { event.returnValue =3D 0; parent.GoToPrevSld(); } }function DocumentOnClick() { if( IsNts() || parent.HideMenu() ) return; if( ( g_allowAdvOnClick && (window.name=3D=3D"PPTSld") && !parent.IsFrames= Mode() ) || (event && event.keyCode=3D=3D32) ) { =09 if( g_animUseRuntime && g_animMainSequence && g_animMainSequence.cangonex= t ) return; parent.GoToNextSld(); } } var g_supportsPPTHTML =3D SupportsPPTHTML(), g_scaleInFrame =3D 1, gId=3D""= , g_bgSound=3D"", g_scaleHyperlinks =3D false, g_allowAdvOnClick =3D 1, g_showInBrowser = =3D 0, gLoopCont =3D 0, gUseSldTimings =3D 1; var g_showAnimation =3D g_supportsPPTHTML && SupportsPPTAnimation() && ( (w= indow.name=3D=3D"PPTSld" && !parent.IsFramesMode()) || g_showInBrowser );va= r g_animManager =3D null; var g_animUseRuntime =3D false; var g_animItemsToHide, g_animInteractiveItems, g_animSlideTime; var g_animMainSequence =3D null; var ENDSHOW_MESG=3D"Slayt gösterisi bitti, çıkmak iç= ;in tıklatın.", SCREEN_MODE=3D"Frames", gIsEndShow=3D0, NUM_VIS_S= LDS=3D6, SCRIPT_HREF=3D"script.js", FULLSCR_HREF=3D"fullscreen.htm"; var gCurSld =3D gPrevSld =3D 1, g_offset =3D 0, gNtsOpen =3D gHasNts =3D gO= tlTxtExp =3D 0, gHasNarration =3D 0, gOtlOpen =3D true window.gPPTHTML=3DSupportsPPTHTML() var gMainDoc=3Dnew Array(new hrefList("slide0003.htm",1,-1,1),new hrefList(= "slide0053.htm",1,-1,1),new hrefList("slide0054.htm",1,-1,1),new hrefList("= slide0063.htm",1,-1,1),new hrefList("slide0064.htm",1,-1,1),new hrefList("s= lide0065.htm",1,-1,1)); /********************************************* Frameset functions These functions control slide navigation and state of the frameset. **********************************************/ function FullScrInit() { g_allowAdvOnClick =3D GetCurSld().mAdvOnClk document.body.style.backgroundColor=3D"black" document.oncontextmenu=3Dparent._CM; document.onkeydown =3D _KDH; document.ondragstart=3DCancel document.onselectstart=3DCancel self.focus() } function Redirect( frmId ) {=09 var str=3Ddocument.location.hash,idx=3Dstr.indexOf('#'), sId=3DGetSldId() if(idx>=3D0) str=3Dstr.substr(1); if( window.name !=3D frmId && ( sId !=3D str) ) { obj =3D GetObj("Main-File") window.location.href=3Dobj.href+"#"+sId return 1 } return 0 } var MHTMLPrefix =3D CalculateMHTMLPrefix();=20 function CalculateMHTMLPrefix() { if ( document.location.protocol =3D=3D 'mhtml:') {=20 href=3Dnew String(document.location.href)=20 Start=3Dhref.indexOf('!')+1=20 End=3Dhref.lastIndexOf('/')+1=20 if (End < Start)=20 return href.substring(0, Start)=20 else=20 return href.substring(0, End)=20 } return ''; } function GetTags(base,tag) { if(g_supportsPPTHTML) return base.all.tags(tag); else return base.getElementsByTagName(tag); } function UpdNtsPane(){ if(frames["PPTNts"]) PPTNts.location.replace( MHTMLP= refix+GetHrefObj( gCurSld ).mNtsHref ) } function UpdNavPane( sldIndex ){ if(gNavLoaded) PPTNav.UpdNav() } function UpdOtNavPane(){ if(gOtlNavLoaded) PPTOtlNav.UpdOtlNav() } function UpdOtlPane(){ if(gOtlLoaded) PPTOtl.UpdOtl() } function SetHasNts( fVal ) { if( gHasNts !=3D fVal ) { gHasNts=3DfVal UpdNavPane() } } function ToggleOtlText() { gOtlTxtExp=3D!gOtlTxtExp UpdOtlPane() } function ClearMedia() { // Clear any sounds playing before launching another browser window. Other= wise, // in fullscreen mode, you'll continue to hear the sound in the frames mod= e. if (PPTSld.pptSound) PPTSld.pptSound.loop =3D 0; } function FullScreen() {=20 if ( PPTSld.g_animUseRuntime ) PPTSld.document.body.pause(); ClearMedia(); var href =3D ( document.location.protocol =3D=3D 'mhtml:') ? FULLSCR_HREF = : FULLSCR_HREF+"#"+GetHrefObj(gCurSld).mSldHref; if(PPTNav.event.ctrlKey) { var w =3D (window.screen.availWidth * 1.0) / 2.0 var h =3D w * (PPTSld.g_origH * 1.0) / PPTSld.g_origW win =3D window.open( MHTMLPrefix+href,null,"toolbar=3D0,resizable=3D1,top= =3D0,left=3D0," + "width=3D"+ w + ",height=3D" + h ); if( win.document.body && PPTSld.g_animUseRuntime ) win.document.body.PPTSldFrameset=3Dwindow; } else { win =3D window.open( MHTMLPrefix+href,null,"fullscreen=3Dyes" ); if( win.document.body && PPTSld.g_animUseRuntime ) win.document.body.PPTSldFrameset=3Dwindow; } } function ToggleVNarration() { rObj=3DPPTSld.document.all("NSPlay") if( rObj && !PPTSld.g_animUseRuntime ) { if( (rObj.playState =3D=3D 1)||(rObj.playState =3D=3D 0) ) rObj.Play() else if( rObj.playState =3D=3D 2 ) rObj.Pause() else return; } else if( PPTSld.g_animUseRuntime ) { narObj =3D PPTSld.document.all("narrationID") if( narObj ) narObj.togglePause() } } function GetCurSldNum() { =20 obj=3DGetHrefObj(gCurSld) if( obj.mOrigVis =3D=3D 1 ) return obj.mSldIdx else =20 return gCurSld } function GetNumSlds() { =20 if( GetHrefObj(gCurSld).mOrigVis =3D=3D 1 ) return GetSldList().mNumVisSlds; else return GetSldList().mList.length } function GetSldNum( href ) { for(ii=3D0; ii 1 ) PopSldList(); else if( !IsFramesMode() ) { if( gLoopCont ) GoToFirst() else EndShow() } } function GoToPrevSld() { ii=3DgCurSld-1 if( ii > 0 ) { obj=3DGetHrefObj(ii) while ( obj && ( obj.mVis =3D=3D 0 ) && ( ii>0 ) ) obj=3DGetHrefObj(--ii) if( ii =3D=3D 0 ) ii=3D1 GoToSldNum(ii) } } function GoToFirst(){ GoToSld( GetHrefObj(1).mSldHref ) } function GoToLast() { ii=3DGetSldList().mList.length if( ii !=3D gCurSld ) GoToSld( GetHrefObj(ii).mSldHref ) } function GoToSldNum( num ) { if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue obj =3D GetHrefObj( num ) obj.mVis=3D1 gPrevSld=3DgCurSld gCurSld =3D num; PPTSld.location.replace(MHTMLPrefix+obj.mSldHref) if( IsFramesMode() ) { UpdNavPane(); UpdOtlPane(); UpdNtsPane() } } function GoToSld( href ) { if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue GetHrefObj( GetSldNum(href) ).mVis=3D1 PPTSld.location.replace(MHTMLPrefix+href) } function SldUpdated( id ) { if( id =3D=3D GetHrefObj(gCurSld).mSldHref ) return gPrevSld=3DgCurSld gCurSld=3DGetSldNum(id) if( IsFramesMode() ) { UpdNavPane(); UpdOtlPane(); UpdNtsPane() } } function PrevSldViewed(){ GoToSld( GetHrefObj(gPrevSld).mSldHref ) } function HasPrevSld() { return ( gIsEndShow || ( gCurSld !=3D 1 && GetHrefO= bj( gCurSld-1 ).mVis =3D=3D 1 )||( GetCurSldNum() > 1 ) ) } function HasNextSld() { return (GetCurSldNum() !=3D GetNumSlds()) } function CloseWindow() { if( HideMenu() ) return; =09 var event =3D PPTSld.event; if( !IsFramesMode() && event && (event.keyCode=3D=3D27 || event.keyCode=3D= =3D32 || event.type=3D=3D"click" ) ) window.close( self ); CatchNumKeys( self, event ); } function Unload() { gIsEndShow=3D0; } function SetupEndShow() { gIsEndShow=3D1; PPTSld.document.body.scroll=3D"no"; PPTSld.document.onkeypress=3DCloseWindow; PPTSld.document.onclick=3DCloseWindow; PPTSld.document.oncontextmenu=3D_CM; } function EndShow() { if( IsFramesMode() ) return if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue doc=3DPPTSld.document var dir =3D doc.body.dir if( dir !=3D "rtl" ) dir =3D "ltr"; doc.open() doc.writeln('

' + ENDSHOW_MESG + '
') doc.close() } function SetSldVisited(){ GetSldList().mList[gCurSld-1].mVisited=3Dtrue } function IsSldVisited(){ return GetSldList().mList[gCurSld-1].mVisited } function hrefList( sldHref, visible, advDelay, advClk ) { this.mSldHref=3D this.mNtsHref =3D sldHref this.mOrigVis=3D this.mVis =3D visible this.mVisited=3D false this.mAdvDelay=3D advDelay this.mAdvOnClk=3D advClk } function SldList(arr,curSld,fEnd) { this.mCurSld =3D curSld; this.mList =3D new Array(); var idx =3D 1; for(ii=3D0;ii 0) { PushSldList(sldList,fEnd); gCurSld =3D 1; } else if( PPTSld.event ) PPTSld.event.cancelBubble=3Dtrue } function PushSldList(arr,fEnd) { var ii =3D gSldStack.length; gSldStack[ii] =3D new SldList(arr,gCurSld,fEnd); GoToSld( gSldStack[ii].mList[0].mSldHref ); } function PopSldList() { if (gSldStack[gSldStack.length-1].fEndShow) EndShow() else { gCurSld =3D gSldStack[gSldStack.length-1].mCurSld; gSldStack[gSldStack.length-1] =3D null; gSldStack.length--; var sldList =3D gSldStack[gSldStack.length-1]; GoToSld( sldList.mList[gCurSld - 1].mSldHref ); } } var custShowList=3Dnew Array(); /********************************************* Navigation button implementation There are 2 types of buttons: ImgBtn, TxtBtn implemented as function objects. They share a similiar interface so the event handlers can call SetActive, for example, on a button=20 object without needing to know exactly=20 what type of button it is. **********************************************/ //---------------------------------- function ImgBtn( oId,bId,w,action ) //---------------------------------- { var t=3Dthis t.Perform =3D _IBP t.SetActive =3D _IBSetA t.SetInactive=3D _IBSetI t.SetPressed =3D _IBSetP t.SetDisabled=3D _IBSetD t.Enabled =3D _IBSetE t.ChangeIcon =3D null t.UserAction =3D action t.ChgState =3D _IBUI t.mObjId =3D oId t.mBorderId=3D bId t.mWidth =3D w t.mIsOn =3D t.mCurState =3D 0 } function _IBSetA() { if( this.mIsOn ) { obj=3Dthis.ChgState( gHiliteClr,gShadowClr,2 ) obj.style.posTop=3D0 } } function _IBSetI() { if( this.mIsOn ) { obj=3Dthis.ChgState( gFaceClr,gFaceClr,1 ) obj.style.posTop=3D0=20 } } function _IBSetP() { if( this.mIsOn ) { obj=3Dthis.ChgState( gShadowClr,gHiliteClr,2 ) obj.style.posLeft+=3D1; obj.style.posTop+=3D1 } } function _IBSetD() { =20 obj=3Dthis.ChgState( gFaceClr,gFaceClr,0 ) obj.style.posTop=3D0=20 } function _IBSetE( state ) { var t=3Dthis GetObj( t.mBorderId ).style.visibility=3D"visible" if( state !=3D t.mIsOn ) { t.mIsOn=3Dstate if( state ) t.SetInactive() else t.SetDisabled() } } function _IBP() { var t=3Dthis if( t.mIsOn ) { if( t.UserAction !=3D null ) t.UserAction() if( t.ChangeIcon ) { obj=3DGetObj(t.mObjId) if( t.ChangeIcon() ) obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-4)*t.mWidth else obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-0)*t.mWidth } t.SetActive() } =20 } function _IBUI( clr1,clr2,nextState ) { var t=3Dthis SetBorder( GetObj( t.mBorderId ),clr1,clr2 ) obj=3DGetObj( t.mObjId ) obj.style.posLeft=3Dobj.style.posLeft+(t.mCurState-nextState)*t.mWidth-obj= .style.posTop t.mCurState=3DnextState return obj } //----------------------------------------- function TxtBtn( oId,oeId,action,chkState ) //----------------------------------------- { var t=3Dthis t.Perform =3D _TBP t.SetActive =3D _TBSetA t.SetInactive=3D _TBSetI t.SetPressed =3D _TBSetP t.SetDisabled=3D _TBSetD t.SetEnabled =3D _TBSetE t.GetState =3D chkState t.UserAction =3D action t.ChgState =3D _TBUI t.mObjId =3D oId t.m_elementsId=3D oeId t.mIsOn =3D 1 } function _TBSetA() { var t=3Dthis if( t.mIsOn && !t.GetState() ) t.ChgState( gHiliteClr,gShadowClr,0,0 ) } function _TBSetI() { var t=3Dthis if( t.mIsOn && !t.GetState() ) t.ChgState( gFaceClr,gFaceClr,0,0 ) } function _TBSetP() { if( this.mIsOn ) this.ChgState( gShadowClr,gHiliteClr,1,1 ) } function _TBSetD() { =20 this.ChgState( gFaceClr,gFaceClr,0,0 ) this.mIsOn =3D 0 } function _TBSetE() { var t=3Dthis if( !t.GetState() ) t.ChgState( gFaceClr,gFaceClr,0,0 ) else t.ChgState( gShadowClr,gHiliteClr,1,1 ) t.mIsOn =3D 1 } function _TBP() { var t=3Dthis if( t.mIsOn ) {=20 if( t.UserAction !=3D null ) t.UserAction() if( !t.GetState ) return if( t.GetState() ) t.SetPressed() else t.SetActive() } =20 } function _TBUI( clr1,clr2,lOffset,tOffset ) { SetBorder( GetObj( this.mObjId ),clr1,clr2 ) Offset( GetObj( this.m_elementsId ),lOffset,tOffset ) } function Offset( obj, top, left ){ obj.style.top=3Dtop; obj.style.left=3Dle= ft } function SetBorder( obj, upperLeft, lowerRight ) { s=3Dobj.style; s.borderStyle =3D "solid" s.borderWidth =3D 1=20 s.borderLeftColor =3D s.borderTopColor =3D upperLeft s.borderBottomColor=3D s.borderRightColor =3D lowerRight } function GetBtnObj(){ return gBtnArr[window.event.srcElement.id] } function BtnOnOver(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetActive() } function BtnOnDown(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetPressed() } function BtnOnOut(){ b=3DGetBtnObj(); if( b !=3D null ) b.SetInactive() } function BtnOnUp() { b=3DGetBtnObj() if( b !=3D null ) b.Perform() else Upd() } function GetNtsState(){ return parent.gNtsOpen } function GetOtlState(){ return parent.gOtlOpen } function GetOtlTxtState(){ return parent.gOtlTxtExp } function NtsBtnSetFlag( fVal ) { s=3Ddocument.all.item( this.m_flagId ).style s.display=3D"none" if( fVal ) s.display=3D"" else s.display=3D"none" } function _BSetA_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S= etActive() } function _BSetI_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S= etInactive() } function _BSetP_Border(){ b =3D gBtnArr[this.mObjId]; if( b !=3D null ) b.S= etPressed() } function _BSetA_BorderImg() {=20 b =3D gBtnArr[this.mBorderId]=20 if( b !=3D null && this.mIsOn && !b.GetState() ) { obj=3Dthis.ChgState( gHiliteClr,gShadowClr,2 ) obj.style.posTop=3D0 } } function _BSetI_BorderImg() {=20 b =3D gBtnArr[this.mBorderId] if( b !=3D null && this.mIsOn && !b.GetState() ) { obj=3Dthis.ChgState( gFaceClr,gFaceClr,1 ) obj.style.posTop=3D0 } } var gHiliteClr=3D"THREEDHIGHLIGHT",gShadowClr=3D"THREEDSHADOW",gFaceClr=3D"= THREEDFACE" var gBtnArr =3D new Array() gBtnArr["nb_otl"] =3D new TxtBtn( "nb_otl","nb_otlElem",parent.ToggleOtlPan= e,GetOtlState ) gBtnArr["nb_otlElem"] =3D new TxtBtn( "nb_otl","nb_otlElem",parent.ToggleOt= lPane,GetOtlState ) gBtnArr["nb_nts"] =3D new ImgBtn( "nb_nts","nb_ntsBorder",10,parent.ToggleN= tsPane ) gBtnArr["nb_nts"].SetActive =3D _BSetA_BorderImg; gBtnArr["nb_nts"].SetInactive =3D _BSetI_BorderImg; gBtnArr["nb_ntsBorder"] =3D new TxtBtn( "nb_ntsBorder","nb_ntsElem",parent.= ToggleNtsPane,GetNtsState ) gBtnArr["nb_ntsElem"] =3D new TxtBtn( "nb_ntsBorder","nb_ntsElem",parent.To= ggleNtsPane,GetNtsState ) gBtnArr["nb_prevBorder"] =3D gBtnArr["nb_prev"]=3D new ImgBtn( "nb_prev","n= b_prevBorder",30,parent.GoToPrevSld ) gBtnArr["nb_nextBorder"] =3D gBtnArr["nb_next"]=3D new ImgBtn( "nb_next","n= b_nextBorder",30,parent.GoToNextSld ) gBtnArr["nb_sldshw"]=3D new ImgBtn( "nb_sldshw","nb_sldshwBorder",18,parent= .FullScreen ) gBtnArr["nb_sldshwBorder"] =3D new TxtBtn( "nb_sldshw","nb_sldshwBorder",pa= rent.FullScreen,null ) gBtnArr["nb_sldshwBorder"].SetActive =3D _BSetA_Border; gBtnArr["nb_sldshwBorder"].SetInactive =3D _BSetI_Border; gBtnArr["nb_sldshwText"] =3D new TxtBtn( "nb_sldshw","nb_sldshwText",parent= .FullScreen,null ) gBtnArr["nb_sldshwText"].SetActive =3D _BSetA_Border; gBtnArr["nb_sldshwText"].SetInactive =3D _BSetI_Border; gBtnArr["nb_voice"] =3D gBtnArr["nb_voiceBorder"] =3D new ImgBtn( "nb_voice= ","nb_voiceBorder",18,parent.ToggleVNarration ) gBtnArr["nb_otlTxtBorder"] =3D gBtnArr["nb_otlTxt"]=3D new ImgBtn( "nb_otlT= xt","nb_otlTxtBorder",23,parent.ToggleOtlText ) gBtnArr["nb_ntsBorder"].m_flagId=3D "nb_nts" gBtnArr["nb_ntsBorder"].SetFlag =3D NtsBtnSetFlag gBtnArr["nb_otlTxt"].ChangeIcon=3D GetOtlTxtState /********************************************* Context menu implementation _CM() is the function that's hooked up to the oncontextmenu event. Once we're asked to show the menu, we first build it by creating DIVs on-the-fly. Then we position it=20 within the screen area so it doesn't get clipped. Creating the DIVs using createElement() means we don't have to write out any extra HTML into the slide HTML files. **********************************************/ var sNext=3D"Sonraki",sPrev=3D"Önceki",sEnd=3D"Gösteriyi Bitir",s= Font=3D"Arial",sArrow=3D"Ok",sFreeform=3D"Serbest Form",sRect=3D"Dikdö= rtgen",sOval=3D"Oval" function ShowMenu() { BuildMenu(); var doc=3DPPTSld.document.body,x=3DPPTSld.event.clientX+doc.scrollLeft,y= =3DPPTSld.event.clientY+doc.scrollTop m =3D PPTSld.document.all.item("ctxtmenu") m.style.pixelLeft=3Dx if( (x+m.scrollWidth > doc.clientWidth)&&(x-m.scrollWidth > 0) ) m.style.pixelLeft=3Dx-m.scrollWidth m.style.pixelTop=3Dy if( (y+m.scrollHeight > doc.clientHeight)&&(y-m.scrollHeight > 0) ) m.style.pixelTop=3Dy-m.scrollHeight m.style.display=3D"" } function _CM() { if( !parent.IsFullScrMode() ) return; if(!PPTSld.event.ctrlKey) { ShowMenu() return false } else HideMenu() } function BuildMenu() { if( PPTSld.document.all.item("ctxtmenu") ) return var mObj=3DCreateItem( PPTSld.document.body ) mObj.id=3D"ctxtmenu" mObj.style.visibility=3D"hidden" var s=3DmObj.style s.position=3D"absolute" s.cursor=3D"default" s.width=3D"120px" SetCMBorder(mObj,"menu","black") var iObj=3DCreateItem( mObj ) SetCMBorder( iObj, "threedhighlight","threedshadow" ) iObj.style.padding=3D2 CreateMenuItem( iObj,sNext,M_GoNextSld,M_True ) CreateMenuItem( iObj,sPrev,M_GoPrevSld,M_HasPrevSld ) =09 CreateSeparator( iObj ) CreateMenuItem( iObj,sEnd,M_End,M_True ) mObj.style.visibility=3D"visible" } function Cancel() { window.event.cancelBubble=3Dtrue; window.event.returnVa= lue=3Dfalse } function Highlight() { ChangeClr("activecaption","threedhighlight") } function Deselect() { ChangeClr("threedface","menutext") } function Perform() { e=3DPPTSld.event.srcElement if( e.type=3D=3D"menuitem" && e.IsActive() ) e.Action() else PPTSld.event.cancelBubble=3Dtrue } function ChangeClr( bg,clr ) { e=3DPPTSld.event.srcElement if( e.type=3D=3D"menuitem" && e.IsActive() ) { e.style.backgroundColor=3Dbg e.style.color=3Dclr } } function M_HasPrevSld() { return( parent.HasPrevSld() ) } function M_GoNextSld() { if( gIsEndShow ) M_End(); else GoToNextSld() } function M_GoPrevSld() { if( gIsEndShow ) { gIsEndShow=3D0; history.back();= PPTSld.event.cancelBubble=3Dtrue; } else GoToPrevSld() } function M_True() { return true } function M_End() { window.close( self ) } function CreateMenuItem( node,text,action,eval ) { var e=3DCreateItem( node ) e.type=3D"menuitem" e.Action=3Daction e.IsActive=3Deval e.innerHTML=3Dtext if( !e.IsActive() ) e.style.color=3D"threedshadow" e.onclick=3DPerform e.onmouseover=3DHighlight e.onmouseout=3DDeselect s=3De.style; 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No= tlar

Slayt Gösterisi

Anahat

1

AİBÜ Düzce TIP Fakültesi Gastroenteroloji Bilim Dalı=

ALFA-1 ANTİTRİPSİN EKSİKLİĞİ

Doç. Dr Yusuf AKCAN

2

Alfa 1 antitrips= in eksikliği

AAT in görevi: proteaz inhibitörüdür. Elastaz, tripsin, kolojenaz ve lökosit proteaz larını inhibe e= der.

Eksikliğinde:

Akciğerde-- elastin giderek düşer ve erken amfizem gelişir.

Karaciğerde -- defektif proteinlerin atılaması ve birikmesi ile hasar oluşur

75 çeşit AAT alelinden pi MM -- normal, pi ZZ ise en faz= la eksikliği gösterendir. Pi ZZ den sonra piSS de en öok serum düzeyi düşük bulunur.

Pi ZZ lerinde tümünde hastalık oluşmaz (12% sind= e KC rahatsızlığı, %75 inde ise amfizem olur).

1/2000 oranında rastlanır.

Bozuk gene chr 14 de dir. 342 . Pozisyonda lizin yerine glutamik asid gelir. Proteinin katlanmasında gerekli Sialik asid eksikliğ= ;ine sebep olur. bozukluğuna yol açar

3

a 1 AT eksikliği-KLİNİK I

Kronik kc hastalığı

Çocukluk kolestazından siroza kadar değişik t= ablo olabilir.

Çocuklarda bilyer atreziden sonra ikinci en sık kc tx nedenidir.

HCC gelişebilir

Kc hastalığı sık olarak PiZZ formunda görülür. Pi ZZ formuna sahip çocukların = %11 inde karaciğer hastalığı görülür= ken. %75 inde transaminaz yüksekliği görülür.
En sık görülen klinik infantil kolestaz dır. 6 = ayda geriler, ancak %10 vakada kalıcı ve hızlı ilerleyici olabilir.

Otoimmun hepatiti benzeri tablo gösterebilir- yüksek gamaglobülin ve immun markerlar vardır-

4

a 1 AT eksikliği-KLİNİK II

Amfizem

Erişkinde amfizem var ise solunum sıkıntısı görülür. Özellikle sigara durumu kötüleştirir.

Kc hastalığına göre daha erken yaşta ve erkeklerde daha sıktır.

Diğer

Glomerülonefrit

Pannicülit

Reaktif hava yolu hastalığı

5

a 1 AT eksikliği-TANI

A1AT serum düzeyi ve tiplendirilmesi

tanıda ikiside bakılması daha iyi olur.

Serum düzeyi homozigot larda %40 lara kadar düşebili= r.

Heterozigot ve karaciğer hastalığı olan vakalard bazen normal düzeyler görülebilir. Bu durumda tipin belirlenmesi katkıda bulunacaktır.

HİSTOPATOLOJİK TANI:

PAS- diastase + globüller Z tip A1AT periportal hepatositlerde görülür.

Benzer gobüller PBS de ve HCC dede görülebilir ancak onlarda A1AT eksikliği görülmez.

PIQo tipinde hiçbir A1AT yapılmayacağından globüllerin görülmeyeceği akılda tutulmalıdır.

İnfant hastalarda histopatoloji bilyer atreziyi taklit edebili= r.

Safra yolu proliferasyonu

Değişen derecelerde fibroziz görülüt.

6

a 1 AT eksikliği-TEDAVİ

Destek tedavisi

Vit K

Kolestazı sürenlerde önemlidir.

İnfantile kolestazda vit K eksikliğine bağlı intrakraniyal kanama en sık ölüm sebebidir.

kc nakli

Kür sağlar

gen tedavisi

Deneysel aşamada

RECOMBİNAN A1AT ÜRETİLDİ. Özellikle amfizem gelişmiş hastalarda bazı kriterlere uygun şekilde kullanılabiliyor.

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1	AİBÜ Düzce TIP Fakültesi Gastroenteroloji Bilim Dalı= ALFA-1 ANTİTRİPSİN EKSİKLİĞİ Doç. Dr Yusuf AKCAN
2	Alfa 1 antitrips= in eksikliği AAT in görevi: proteaz inhibitörüdür. Elastaz, tripsin, kolojenaz ve lökosit proteaz larını inhibe e= der. Eksikliğinde: Akciğerde-- elastin giderek düşer ve erken amfizem gelişir. Karaciğerde -- defektif proteinlerin atılaması ve birikmesi ile hasar oluşur 75 çeşit AAT alelinden pi MM -- normal, pi ZZ ise en faz= la eksikliği gösterendir. Pi ZZ den sonra piSS de en öok serum düzeyi düşük bulunur. Pi ZZ lerinde tümünde hastalık oluşmaz (12% sind= e KC rahatsızlığı, %75 inde ise amfizem olur). 1/2000 oranında rastlanır. Bozuk gene chr 14 de dir. 342 . Pozisyonda lizin yerine glutamik asid gelir. Proteinin katlanmasında gerekli Sialik asid eksikliğ= ;ine sebep olur. bozukluğuna yol açar
3	a 1 AT eksikliği-KLİNİK I Kronik kc hastalığı Çocukluk kolestazından siroza kadar değişik t= ablo olabilir. Çocuklarda bilyer atreziden sonra ikinci en sık kc tx nedenidir. HCC gelişebilir Kc hastalığı sık olarak PiZZ formunda görülür. Pi ZZ formuna sahip çocukların = %11 inde karaciğer hastalığı görülür= ken. %75 inde transaminaz yüksekliği görülür. En sık görülen klinik infantil kolestaz dır. 6 = ayda geriler, ancak %10 vakada kalıcı ve hızlı ilerleyici olabilir. Otoimmun hepatiti benzeri tablo gösterebilir- yüksek gamaglobülin ve immun markerlar vardır-
4	a 1 AT eksikliği-KLİNİK II Amfizem Erişkinde amfizem var ise solunum sıkıntısı görülür. Özellikle sigara durumu kötüleştirir. Kc hastalığına göre daha erken yaşta ve erkeklerde daha sıktır. Diğer Glomerülonefrit Pannicülit Reaktif hava yolu hastalığı
5	a 1 AT eksikliği-TANI A1AT serum düzeyi ve tiplendirilmesi tanıda ikiside bakılması daha iyi olur. Serum düzeyi homozigot larda %40 lara kadar düşebili= r. Heterozigot ve karaciğer hastalığı olan vakalard bazen normal düzeyler görülebilir. Bu durumda tipin belirlenmesi katkıda bulunacaktır. HİSTOPATOLOJİK TANI: PAS- diastase + globüller Z tip A1AT periportal hepatositlerde görülür. Benzer gobüller PBS de ve HCC dede görülebilir ancak onlarda A1AT eksikliği görülmez. PIQo tipinde hiçbir A1AT yapılmayacağından globüllerin görülmeyeceği akılda tutulmalıdır. İnfant hastalarda histopatoloji bilyer atreziyi taklit edebili= r. Safra yolu proliferasyonu Değişen derecelerde fibroziz görülüt.
6	a 1 AT eksikliği-TEDAVİ Destek tedavisi Vit K Kolestazı sürenlerde önemlidir. İnfantile kolestazda vit K eksikliğine bağlı intrakraniyal kanama en sık ölüm sebebidir. kc nakli Kür sağlar gen tedavisi Deneysel aşamada RECOMBİNAN A1AT ÜRETİLDİ. Özellikle amfizem gelişmiş hastalarda bazı kriterlere uygun şekilde kullanılabiliyor.