Cervical neoplasia typically occurs at the transformation zone or squamocolumnar junction because the epithelium at this location undergoes constant cell division and metaplasia (ie, simple columnar endocervix transitioning to stratified squamous ectocervix).
| Risk factors | • Immunocompromised (eg, HIV, chronic glucocorticoid use) • Early onset of sexual activity • Multiple or high-risk sexual partners • Previous sexually transmitted infection • Tobacco use (oncogenic effects on the cervix through impaired immunity) • OCPs use • Low socioeconomic status | | --- | --- | | Pathogenesis | • HPV infection (types 16 & 18) | | Clinical manifestations | • Asymptomatic most commonly and detected by screening • Postcoital or intermenstrual bleeding • Increased vaginal discharge • Inguinal lymphadenopathy (painless) + metastatic • Pelvic or low back pain • Physical exam may show lesions suspicious for malignancy (eg, ulcerative, friable, raised) | | Diagnosis | • Cervical biopsy on colposcopy |
<aside> 💡 Progression from persistent HPV Infection to invasive cervical carcinoma takes many years
</aside>
exophytic cervical mass due to cervical cancer may cause heavy vaginal bleeding; however, the bleeding is typically irregular rather than cyclic as with menstruation.
<aside> 💡 In HIV-positive patients, cervical cancer is an AIDS-defining illness because it indicates severe immunocompromise. In immunocompromised patients, HPV can cause cervical dysplasia that rapidly progresses to cancer (eg, within months).
</aside>
Recurrent cervical cancer typically presents with abnormal bleeding from raised, friable cervical nodules