{"id":1778,"date":"2023-02-06T18:27:17","date_gmt":"2023-02-06T18:27:17","guid":{"rendered":"https:\/\/www.karotidnahirurgija.com\/?page_id=1778"},"modified":"2023-02-24T10:08:17","modified_gmt":"2023-02-24T10:08:17","slug":"2-etiopatogeneza-karotidne-bolesti","status":"publish","type":"page","link":"https:\/\/www.karotidnahirurgija.com\/?page_id=1778","title":{"rendered":"2.1. KAROTIDNA ATEROSKLEROZA"},"content":{"rendered":"

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

\n

ETIOPATOGENEZA KAROTIDNE BOLESTI<\/h1>\n<\/h1>\n
\n

\n

2.1 KAROTIDNA ATEROSKLEROZA

<\/h3>\n<\/div>\n
\n

Patogeneza<\/b><\/span> <\/b><\/span>ateroskleroze<\/b><\/span>:<\/span> <\/span>po\u010detna<\/span> <\/span>lezija<\/span> <\/span>endotelne<\/span> <\/span>barijere<\/span> <\/span>pripisuje<\/span> <\/span>se<\/span> <\/span>povi\u0161enoj<\/span> <\/span>koncentraciji<\/span> <\/span>lipoproteina<\/span> <\/span>LDL<\/span> <\/span>u<\/span> <\/span>plazmi,<\/span> <\/span>posebno<\/span> <\/span>u<\/span> <\/span>slu\u010daju<\/span> <\/span>da<\/span> <\/span>je<\/span> <\/span>nivo<\/span> <\/span>HDL<\/span> <\/span>sni\u017een.<\/span> <\/span>Kontroverze<\/span> <\/span>izme\u0111u<\/span> <\/span>lipometaboli\u010dke,<\/span> <\/span>tromboti\u010dke,<\/span> <\/span>endokrine,<\/span> <\/span>hemodinamske,<\/span> <\/span>imunolo\u0161ke,<\/span> <\/span>in<\/span>fl<\/span>amatorne<\/span> <\/span>i<\/span> <\/span>drugih<\/span> <\/span>teorija<\/span> <\/span>aterogeneze,<\/span> <\/span>obi\u010dno<\/span> <\/span>se<\/span> <\/span>prevazilaze<\/span> <\/span>zaklju\u010dkom<\/span> <\/span>da<\/span> <\/span>se<\/span> <\/span>radi<\/span> <\/span>o<\/span> <\/span>multifaktorijelno<\/span> <\/span>uslovljenom<\/span> <\/span>procesu.<\/span><\/p>\n

Aterogeneza<\/b><\/span> <\/b><\/span>podrazumeva:<\/span> <\/span>nakupljanje<\/span> <\/span>lipoproteina,<\/span> <\/span>posebno<\/span> <\/span>holesterola<\/span> <\/span>i<\/span> <\/span>njegovih<\/span> <\/span>estara<\/span> <\/span>u<\/span> <\/span>intimi;<\/span> <\/span>celularnu<\/span> <\/span>proliferaciju<\/span> <\/span>glatkih<\/span> <\/span>mi\u0161i\u0107nih<\/span> <\/span>\u0107elija<\/span> <\/span>medije<\/span> <\/span>koje<\/span> <\/span>migriraju<\/span> <\/span>u<\/span> <\/span>intimu,<\/span> <\/span>proliferaciju<\/span> <\/span>vezivnotkivnih<\/span> <\/span>elemenata<\/span> <\/span>(glukozaminoglikani<\/span> <\/span>i<\/span> <\/span>elastin),<\/span> <\/span>transformacija<\/span> <\/span>lokalnih<\/span> <\/span>monocita<\/span> <\/span>najpre<\/span> <\/span>u<\/span> <\/span>aktivne<\/span> <\/span>makrofage,<\/span> <\/span>a<\/span> <\/span>potom<\/span> <\/span>nagomilavanje<\/span> <\/span>fagocitovanoih<\/span> <\/span>lipoproteina<\/span> <\/span>i<\/span> <\/span>nastanak<\/span> <\/span>\u00bbpenastih<\/b><\/i><\/span> <\/b><\/i><\/span>\u0107elija\u00ab<\/b><\/i><\/span>.<\/span><\/p>\n

\n<\/div>\n

\"\"<\/p>\n

\n

Po\u010detna faza aterogeneze sa formiranjem subin- timalne masne pruge i o\u010duvanim endotelom.<\/em><\/p>\n<\/div>\n

\n

Progresija<\/b> <\/b>aterogeneze<\/b> <\/b>se odvija kroz tri stadijuma:<\/p>\n

    \n
  • Lipidni depoziti (fatty streak),<\/li>\n
  • Fibroateromatozni plak,<\/li>\n
  • Komplikovane lezije.<\/li>\n<\/ul>\n

    Regresija karotidnog plaka<\/strong> je tako\u0111e opisana, tokom statinima indukovane zna\u010dajne eliminacije lipoproteina niske gustine (LDL) i holesterola iz plazme.<\/p>\n

    Simptomi cerebralne ishemije javljaju se zbog komplikovanih lezija.<\/p>\n

      \n
    • Komplikovane arteriosklerot\u010dne lezije;<\/li>\n
    • Kalcifikacija,<\/li>\n
    • Egzulceracija,<\/li>\n
    • Intraplakalna hemoragija,<\/li>\n
    • Tromboza – okluzija<\/li>\n<\/ul>\n<\/div>\n

      \"\"<\/p>\n

      \n

      Pove\u0107ana kapilarna propustljivost usled lezije endotelnih \u0107elija. To dovodi do migracije solubilnih medijatora imunosti i proinflamatornih \u0107elija u subendotelni prostor. Endotel postaje adherentan.<\/em><\/p>\n<\/p>\n

      \u00a0<\/em><\/p>\n<\/div>\n

      \"\"<\/p>\n

      \n

      Akumuliraju se makrofazi, koji postaju \u201epenaste \u0107elije\u201d. U centru nastaje nekroti\u010dno srce plaka, prekriveno slojem fibroznih \u0107elija, koje \u010dine fibroznu kapu.<\/em><\/p>\n

      \u00a0<\/em><\/p>\n<\/div>\n

      \"\"<\/p>\n

      \n

      Glatkomi\u0161i\u0107ne \u0107elije migriraju iz medije, menjaju svoj genotip i pretvaraju se u \u201epenaste \u0107elije\u201d. Nakupljanje \u201epenastih \u0107elija\u201d dovodi do aktivacije T-limfocita, monocita i trombocita.<\/em><\/p>\n<\/div>\n

      \"\"<\/p>\n

      \n

      Aktivirani makrofazi osloba\u0111aju metaloproteinaze, \u0161to dovodi do istanjivanja fibrozne kape i rupture plaka sa distalnom em- bolizacijom.<\/em><\/p>\n

      \u00a0<\/em><\/p>\n<\/div>\n

      \"\"<\/p>\n

      \n

      Patomorfologija karotidnog ateroskleroti\u010dnog plaka.<\/em><\/p>\n<\/div>\n

      \n

      Kalci<\/b><\/span>fi<\/b><\/span>kacija<\/b><\/span> <\/b><\/span>arterioskleroti\u010dnog<\/b><\/span> <\/b><\/span>plaka<\/b><\/span><\/p>\n

      Kalcifikacija<\/span> <\/span>podrazumeva<\/span> <\/span>prisustvo<\/span> <\/span>kalcijumskih<\/span> <\/span>depozita<\/span> <\/span>u<\/span> <\/span>mediji<\/span> <\/span>arterio-<\/span> <\/span>skleroti\u010dno<\/span>g<\/span>plaka<\/span>.<\/span> <\/span>Proce<\/span>s<\/span>kalci<\/span>f<\/span>i<\/span>kacij<\/span>e<\/span>po\u010dinj<\/span>e<\/span>ka<\/span>o<\/span>difuzn<\/span>o<\/span>deponovanj<\/span>e<\/span>kalcijum<\/span>a<\/span> <\/span>du\u017e<\/span> <\/span>vlakana<\/span> <\/span>elastina<\/span> <\/span>i<\/span> <\/span>kolagena.<\/span> <\/span>Nastavlja<\/span> <\/span>se<\/span> <\/span>do<\/span> <\/span>eventualne<\/span> <\/span>epizode<\/span> <\/span>intraplakalne<\/span> <\/span>hemoragije<\/span> <\/span>ili<\/span> <\/span>ishemi\u010dke<\/span> <\/span>nekroze.<\/span> <\/span>Po\u0161to<\/span> <\/span>kalcijumski<\/span> <\/span>depoziti<\/span> <\/span>menjaju<\/span> <\/span>elasti\u010dna<\/span> <\/span>svojstva<\/span> <\/span>plaka<\/span> <\/span>njihove<\/span> <\/span>hemodinamske<\/span> <\/span>posledice<\/span> <\/span>su<\/span> <\/span>zna\u010dajne.<\/span><\/p>\n<\/div>\n


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

      ETIOPATOGENEZA KAROTIDNE BOLESTI 2.1 KAROTIDNA ATEROSKLEROZA Patogeneza ateroskleroze: po\u010detna lezija endotelne barijere pripisuje se povi\u0161enoj koncentraciji lipoproteina LDL u plazmi, posebno u slu\u010daju da je nivo HDL sni\u017een. Kontroverze izme\u0111u lipometaboli\u010dke, tromboti\u010dke, endokrine, hemodinamske, imunolo\u0161ke, inflamatorne i drugih teorija aterogeneze, obi\u010dno se prevazilaze zaklju\u010dkom da se radi o multifaktorijelno uslovljenom procesu. Aterogeneza podrazumeva: nakupljanje lipoproteina, […]<\/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-1778","page","type-page","status-publish","hentry"],"acf":[],"yoast_head":"\n2.1. 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