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    Pathophysiology of Cervical Cancer: High Risk HPV (16, 18, 31)

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    Moses Gabriel Valledor
    1. High risk HPV (types 16 and 18) infects and integrates into the basal cells of the cervical squamous epithelium, blocking tumor suppressor genes p53 and pRB and causing abnormal cell growth. 2. This leads to cervical intraepithelial neoplasia (CIN) and squamous intraepithelial lesions (SIL) as mutated cells proliferate. 3. Without treatment, CIN/SIL can progress to invasive cervical cancer where the tumor fills the cervix and spreads to distant organs via lymphatic or blood vessels.

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    Pathophysiology of Cervical Cancer: High Risk HPV (16, 18, 31)

    Uploaded by

    Moses Gabriel Valledor
    165 views2 pages
    1. High risk HPV (types 16 and 18) infects and integrates into the basal cells of the cervical squamous epithelium, blocking tumor suppressor genes p53 and pRB and causing abnormal cell growth. 2. This leads to cervical intraepithelial neoplasia (CIN) and squamous intraepithelial lesions (SIL) as mutated cells proliferate. 3. Without treatment, CIN/SIL can progress to invasive cervical cancer where the tumor fills the cervix and spreads to distant organs via lymphatic or blood vessels.

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    patho cervical

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    1. High risk HPV (types 16 and 18) infects and integrates into the basal cells of the cervical squamous epithelium, blocking tumor suppressor genes p53 and pRB and causing abnormal cell growth. 2. This leads to cervical intraepithelial neoplasia (CIN) and squamous intraepithelial lesions (SIL) as mutated cells proliferate. 3. Without treatment, CIN/SIL can progress to invasive cervical cancer where the tumor fills the cervix and spreads to distant organs via lymphatic or blood vessels.

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    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    165 views2 pages

    Pathophysiology of Cervical Cancer: High Risk HPV (16, 18, 31)

    Uploaded by

    Moses Gabriel Valledor
    1. High risk HPV (types 16 and 18) infects and integrates into the basal cells of the cervical squamous epithelium, blocking tumor suppressor genes p53 and pRB and causing abnormal cell growth. 2. This leads to cervical intraepithelial neoplasia (CIN) and squamous intraepithelial lesions (SIL) as mutated cells proliferate. 3. Without treatment, CIN/SIL can progress to invasive cervical cancer where the tumor fills the cervix and spreads to distant organs via lymphatic or blood vessels.

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    of 2

    Pathophysiology of Cervical Cancer

    High risk HPV (16, 18, 31) Risk factors:


    Early age of coitus
    Invasion of the basal cell of the Multiple sexual partners
    squamous epithelium of the Unsafe sexual practices
    cervix

    Integration of viral DNA

    p53 and pRB tumor suppressor


    genes are blocked/deactivated Barrel-shaped
    cervix

    Mutation and cell proliferation

    CIN/SIL Tumor fills the entire


    Co-carcinogens
    Carcinoma in situ cervix

    Metastasis to distant body parts


    Invasive cancer Tissue necrosis and
    sloughing
    Increased tumor growth
    Lymph invasion
    Hypermetabolic Increased
    activitypressure to the surrounding tissues, nerves and bladder Fistula formation Hemorrhage Infection
    of cell proliferation and Enlargement of lymph
    increased tumor growth nodes
    needs Leakage of
    Metrorrhagia Foul-
    urine and
    Pelvic and back pain Venous and Ureteral Bleeding smelling
    Dysuria feces into the
    obstruction after coitus vaginal
    vagina
    Anorexia anemia discharge
    Weight
    Hydronephrosi Leg edema
    loss
    s

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