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  • Pathway Carcinoma Nasofaring

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    Pathway Carcinoma Nasofaring can occur through several processes: (1) viral infection (such as SV-40 virus), (2) genetic mutations of oncogenes, and (3) disruption of mechanisms that control normal cell growth. Initially tumors may be benign (non-cancerous) but can become malignant (cancerous) over time as the cells grow less cohesively, more rapidly, and in an irregular pattern without encapsulation and with increased ability to metastasize to other organs. Late stage carcinoma can cause multiple organ failure, sepsis, shock, fever, and death.

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    Pathway Carcinoma Nasofaring can occur through several processes: (1) viral infection (such as SV-40 virus), (2) genetic mutations of oncogenes, and (3) disruption of mechanisms that control normal cell growth. Initially tumors may be benign (non-cancerous) but can become malignant (cancerous) over time as the cells grow less cohesively, more rapidly, and in an irregular pattern without encapsulation and with increased ability to metastasize to other organs. Late stage carcinoma can cause multiple organ failure, sepsis, shock, fever, and death.

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    62 views2 pages

    Pathway Carcinoma Nasofaring

    Uploaded by

    roos-Beatrix-wattimury-888
    Pathway Carcinoma Nasofaring can occur through several processes: (1) viral infection (such as SV-40 virus), (2) genetic mutations of oncogenes, and (3) disruption of mechanisms that control normal cell growth. Initially tumors may be benign (non-cancerous) but can become malignant (cancerous) over time as the cells grow less cohesively, more rapidly, and in an irregular pattern without encapsulation and with increased ability to metastasize to other organs. Late stage carcinoma can cause multiple organ failure, sepsis, shock, fever, and death.

    Copyright:

    © All Rights Reserved
    Download as DOC, PDF, TXT or read online from Scribd
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    Pathway Carcinoma Nasofaring

    Infeksi virus Mutasi gen Berfungsinya Gangguan


    pengendali onkogen mekanisme
    ( Virus SV 4)
    pertumbuhan ( Carsinogenic pengendalian
    Agent) pertumbuhan normal

    Perubahan epitel siliadan mukosa / ulserasi bronchus


    Tumor Paru ( Bronkogenik)

    Jinak (Epidermoid, sel Ganas/kanker (Sel kecil/oat


    besar, adeno carsinoma ) cell)
    - Kohesif - Kurang kohesif
    - Tumbuh lambat - Pertumbuhan cepat
    - Pola teratur Ketakutan - Pola tidak teratur
    - Berkapsul (Kecemasan) - Tidak berkapsul

    Lumen Proksimal Kompetisi Metastase


    Pemakaian Hematogen/Limfogen/Langsung
    distal
    Nutrisi,
    rangsangan
    Sumbatan organ viseral
    partial/total melalui Multiorgan failure
    transmitor H1, Sepsis
    Penekanan serotonin (5
    reseptor Pada HT3), Host
    lobus paru, Brokiekta Cytokine
    prostalagnin, sis
    serotonin, Syok Pening
    bradikinin,
    norefinefrin, ion Sepsis katan
    hidrogen, ion suhu
    kalium dan tubuh
    subtance P Ggn Pola nafas
    pertukara tidak
    n gas efektif

    Nyeri Resiko infeksi Ggn Nutrisi

    Kelemahan
    /Intoleransi
    aktivitas

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