Predisposing factors for cervical cancer include increasing age and family history of cervical cancer. Key etiological factors are infection with HPV types 16, 18 or 31, which can lead to invasion of basal cells and integration of viral DNA. Precipitating factors are those that weaken immune response like HIV/AIDS, nutrition deficiencies, smoking, and having multiple sexual partners. Progression involves cellular changes like CIN/SIL, carcinoma in situ, invasion into surrounding tissues, and eventual metastasis to lymph nodes and distant organs.
Predisposing factors for cervical cancer include increasing age and family history of cervical cancer. Key etiological factors are infection with HPV types 16, 18 or 31, which can lead to invasion of basal cells and integration of viral DNA. Precipitating factors are those that weaken immune response like HIV/AIDS, nutrition deficiencies, smoking, and having multiple sexual partners. Progression involves cellular changes like CIN/SIL, carcinoma in situ, invasion into surrounding tissues, and eventual metastasis to lymph nodes and distant organs.
Predisposing factors for cervical cancer include increasing age and family history of cervical cancer. Key etiological factors are infection with HPV types 16, 18 or 31, which can lead to invasion of basal cells and integration of viral DNA. Precipitating factors are those that weaken immune response like HIV/AIDS, nutrition deficiencies, smoking, and having multiple sexual partners. Progression involves cellular changes like CIN/SIL, carcinoma in situ, invasion into surrounding tissues, and eventual metastasis to lymph nodes and distant organs.
Predisposing factors for cervical cancer include increasing age and family history of cervical cancer. Key etiological factors are infection with HPV types 16, 18 or 31, which can lead to invasion of basal cells and integration of viral DNA. Precipitating factors are those that weaken immune response like HIV/AIDS, nutrition deficiencies, smoking, and having multiple sexual partners. Progression involves cellular changes like CIN/SIL, carcinoma in situ, invasion into surrounding tissues, and eventual metastasis to lymph nodes and distant organs.
Age Infection with HPV 16, 18, or 31. Low socioeconomic status Family history of cervical cancer Having multiple sexual partners Having sexual partners who have had previous partners with cervical cancer Invasion of the basal cell of the squamous Sex with uncircumcised men epithelium or immature metaplastic Parity of three or more squamous cells of the cervix Early childbearing Metastasis to other body parts Nutritional deficiencies Overweight status Prolonged use of oral contraceptives Smoking and exposure to secondhand smoke Integration of viral DNA Having HIV/AIDS and other causes of immune deficiency Exposure to diethylstilbestrol (DES) in utero Increased growth of the tumor
p53 and pRB tumor suppressor genes
are blocked/deactivated Tumor fills the entire cervix Barrel- shaped cervix Hypermetabolic Increased pressure to activity of cell the surrounding Mutation and cell proliferation Tissue necrosis and sloughing proliferation and tissues, nerves, and increased tumor bladder growth needs
Cervical intraepithelial neoplasia
(CIN)/Squamous Intraepithelial Lesion Fistula Hemorrhage Infection (SIL)/Carcinoma in situ formation
Anorexia Pelvic, Dysuria
/Extreme back, and and pain emancipa leg pain after Invasive cancer tion coitus Urine and feces leakage Malodorous into the discharge Lymph invasion vagina
Lymph nodes enlargement Abnormal
bleeding after coitus or menopause, Hydrone Rectal bleeding, phrosis Venous and Ureteral obstruction Anemia and leg edema