{"id":1936,"date":"2023-02-06T21:32:59","date_gmt":"2023-02-06T21:32:59","guid":{"rendered":"https:\/\/www.karotidnahirurgija.com\/?page_id=1936"},"modified":"2023-02-25T13:57:34","modified_gmt":"2023-02-25T13:57:34","slug":"2-6-nespecificni-aorto-arteritis","status":"publish","type":"page","link":"https:\/\/www.karotidnahirurgija.com\/?page_id=1936","title":{"rendered":"2.6. NESPECIFI\u010cNI AORTO-ARTERITIS"},"content":{"rendered":"

\"\"<\/a><\/p>\n

<\/p>\n

ETIOPATOGENEZA KAROTIDNE BOLESTI<\/h1>\n

<\/a><\/h1>\n

\n

\n

2.6. NESPECIFI\u010cNI AORTO-ARTERITIS

<\/h3>\n<\/div>\n
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Vaskulitis je segmentno zapaljenje i nekroza zidova arterija pra\u0107ena okluzivnim promenama ili re\u0111e pojavom aneurizmi.<\/p>\n

Infektivni<\/b> <\/b>vaskuliti<\/b>s nastaje direktnim \u0161irenjem infekcije na arterije ili hematogenim putem (TBC, Lu,virusi, gljivice).<\/p>\n

Neinfektivni<\/b> <\/b>vaskulitis<\/b> <\/b>nastaje razli\u010ditim imunolo\u0161kim mehanizmima inflamacije.<\/p>\n

Vaskulitisi velikih arterija, koji nas interesuju u okviru supraaortalnih grana su: Takayasu arteritis, temporalni arteritis, Morbus Kawasaki i poliarteritis nodosa.<\/p>\n

Takayasu arteritis<\/strong> je hroni\u010dna, sistemska, nespecifi\u010dna, zapaljenjska arteriopatija koja zahvata aortu i njene velike grane dovode\u0107i do njihove stenoze ili okluzije.<\/p>\n

Bolest je prvi opisao japanski oftalmolog Takayasu 1908.godine, po njemu je nazvana: Idiopathic Arteritis of Takayasu. To je nespecifi\u010dni aortoarteritis (Nonspecific Aortoarteritis). Obzirom da je jedan od osnovnih simptoma ove bolesti odsustvo palpabilnog pulsa na velikim arterijama naziva se i bolest bez pulsa (Pulseless Disease). Po\u0161to je naj\u010de\u0161\u0107e prisutan u mladih \u017eena sa Istoka naziva se i arteritis mladih \u017eena orijenta (Young Oriental Female Arteritis). Ve\u0107ina obolelih poti\u010de iz azijskih i ju\u017enoameri\u010dkih zemalja, mada se i u Evropi javlja, ve\u0107inom kod mladih \u017eena.<\/p>\n

Etiopatogeneza<\/strong>: Infekcija predstavlja pokreta\u010d verovatnog autoimunog procesa. Genetski faktori, autoimuni procesi, i patolo\u0161ka reakcija na razne infektivne agense se naj\u010de\u0161\u0107e pominju kao uzro\u010dnici.<\/p>\n

Inicijalni doga\u0111aj je infiltracija arterijskog zida T-limfocitima aktivisanim lokalnim maskiranim ili modulisanim antigenima arterijskog zida.<\/p>\n

T-limfociti aktivi\u0161u makrofage koji prouzrokuju o\u0161te\u0107enja. Produkti oslobo\u0111eni od strane zapaljenjskih \u0107elijskih infiltrata i endotelnih \u0107elija (adhezivni molekuli) potenciraju proliferaciju \u0107elija medije i nastanak okluzivnih promena i posledi\u010dnih ishemijskih manifestacija.<\/p>\n

Patolo\u0161ka anatomija<\/strong>: Nespecifi\u010dni aortoarteritis zahvata aortu, supraaortalne grane, plu\u0107ne i bubre\u017ene arterije. Po\u010detne promene javljaju se obi\u010dno od 20-30 godina.<\/p>\n

    \n
  • Promene<\/span> <\/span>u<\/span> <\/span>medijalnom<\/span> <\/span>sloju arterijskog zida karakteristi\u010dne su za pro- dromalnu fazu bolesti.<\/li>\n
  • U hroni\u010dnoj fazi bolesti, dominantne su promene na intimi (stenoza, okluzija).<\/li>\n
  • Recidivantna inflamacija medije i adventicije i zavr\u0161ava difuznom ili nodu- larnom<\/span> <\/span>periarterijskom<\/span> <\/span>fi<\/span>brozom.<\/span><\/li>\n<\/ul>\n

    Te\u017eina lezija supraaortnih grana nije u korelaciji sa neurolo\u0161kom klini\u010dkom slikom. Ponekad okluzija svih supraaortnih grana (\u201cbald arch\u201d<\/strong>) ne mora da bude pra\u0107ena znacima mo\u017edane ishemije, jer je ostvarena kompenzacija kolateralama preko interkostalnih arterija iz grudne aorte.<\/p>\n

    Mogu\u0107a je te\u0161ka ishemije gornjih ekstremiteta i posteriornog sliva ako nisu dovoljno razvijene intrasistemske ili intersistemske kolaterale. Obi\u010dno se kao posledica razvija globalna asimptomatska ili simptomatska mo\u017edana ishemija sa najzna\u010dajnijim deficitima u irigacionom podru\u010dju srednje i zadnje cerebralne arterije.<\/p>\n

    Klini\u010dka slika<\/strong> zavisi od simptoma aktivne sistemske inflamacije, a u kasnijoj fazi pojavljuju se neurolo\u0161ke reperkusije ishemije.<\/p>\n

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    • \n

      Simptomi<\/b><\/span> <\/b><\/span>aktivne<\/b><\/span> <\/b><\/span>sistemske<\/b><\/span> <\/b><\/span>in<\/b><\/span>fl<\/b><\/span>amatorne<\/b><\/span> <\/b><\/span>bolesti<\/b><\/span> <\/b><\/span>su<\/span> <\/span>zamor,<\/span> <\/span>febrilnost,<\/span> <\/span>op\u0161ta<\/span> <\/span>slabost,<\/span> <\/span>gubitak<\/span> <\/span>u<\/span> <\/span>te\u017eini,<\/span> <\/span>artralgije,<\/span> <\/span>bolovi<\/span> <\/span>du\u017e<\/span> <\/span>karotidnih<\/span> <\/span>arterija<\/span> <\/span>(karotidinija).<\/span><\/p>\n<\/li>\n

    • \n

      Simptomi<\/b><\/span> <\/b><\/span>cerebralne<\/b><\/span> <\/b><\/span>ishemije:<\/b><\/span> <\/b><\/span>okluzivne<\/span> <\/span>lezije<\/span> <\/span>supraaortnih<\/span> <\/span>grana<\/span> <\/span>mani- festuju<\/span> <\/span>se<\/span> <\/span>simptomima<\/span> <\/span>i<\/span> <\/span>znacima<\/span> <\/span>ishemije<\/span> <\/span>mozga<\/span> <\/span>i<\/span> <\/span>oka<\/span> <\/span>(hroni\u010dna<\/span> <\/span>ishemijska<\/span> <\/span>oftalmopatija).<\/span><\/p>\n<\/li>\n<\/ul>\n

        \n
      • \n

        Ishemija<\/b> <\/b> <\/b>ekstremiteta<\/b> <\/b> <\/b>odra\u017eava se bolovima u rukama i nogama sa karakterom klaudikacija. Kasnije bolovi postaju permanentni do ishemijske nekroze.<\/p>\n<\/li>\n<\/ul>\n

        Glavobolja je \u010desta, za razliku od arterioskleroze, tranzitorni ishemijski ataci predstavljaju retkost dok mo\u017edani udar nastaje iznenadno bez upozoravaju\u0107ih klini\u010dkih ishemi\u010dkih incidenata. Tranzitorni ishemijski ataci u vertebrobazilarnom slivu su relativno \u010desti. Ishemi\u010dki infarkti mozga su obi\u010dno lakunarni ili \u201cwathershed\u201d tipa.<\/p>\n

        Ishemija bubrega i renalna hipertenzija se \u010desto javlja zbog simultane stenoze renalnih arterija. Koronarne arterije zahva\u0107ene su u oko 8 % obolelih, sa ili bez znakova angine pektoris. Okluzivne promene torakalne aorte prouzrokuju ste\u010deni oblik koarktacije aorte.<\/p>\n

        Kriterijumi za postavljanje dijagnoze su: obostrane lezije potklju\u010dnih arterija, povi\u0161ena sedimentacija eritrocita, gracilnost karotidnih arterija, hipertenzija, le- zije srednje tre\u0107ine leve zajedni\u010dke karotidne arterije, distalnog segmenta brahio- cefali\u010dnog stabla, torakalne i abdominalne aorte i renalnih arterija.<\/p>\n<\/div>\n


        \n<\/p>\n","protected":false},"excerpt":{"rendered":"

        ETIOPATOGENEZA KAROTIDNE BOLESTI 2.6. NESPECIFI\u010cNI AORTO-ARTERITIS Vaskulitis je segmentno zapaljenje i nekroza zidova arterija pra\u0107ena okluzivnim promenama ili re\u0111e pojavom aneurizmi. Infektivni vaskulitis nastaje direktnim \u0161irenjem infekcije na arterije ili hematogenim putem (TBC, Lu,virusi, gljivice). Neinfektivni vaskulitis nastaje razli\u010ditim imunolo\u0161kim mehanizmima inflamacije. Vaskulitisi velikih arterija, koji nas interesuju u okviru supraaortalnih grana su: Takayasu arteritis, […]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_acf_changed":false,"footnotes":""},"class_list":["post-1936","page","type-page","status-publish","hentry"],"acf":[],"yoast_head":"\n2.6. 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