Description
This detailed academic presentation on cervical cancer provides a comprehensive overview of its etiology, pathophysiology, clinical presentation, diagnostic workup, and stage-based management. The material highlights the central role of persistent high-risk HPV infection (notably types 16, 18, and 45) in carcinogenesis, facilitated by viral proteins E6 and E7 that inactivate tumor suppressors p53 and Rb. Key risk factors include early sexual activity, multiple partners, immunosuppression (e.g., HIV), smoking, and lack of screening. Clinical features such as irregular vaginal bleeding, discharge, and pelvic pain are outlined, alongside diagnostic steps from Pap smear and colposcopy to imaging and biopsy. Treatment strategies range from local excision for early-stage disease to chemoradiation for advanced stages, with emphasis on HPV vaccination for prevention. This resource is essential for medical students, obstetrics and gynecology trainees, and practitioners in Zambia, offering structured, exam-focused content for understanding cervical cancer within a tertiary medical education context. Download these comprehensive notes for thorough preparation and clinical insights.
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University of Zambia School of Medicine CERVICAL CANCERPRESENTER : RUTH MTONGAMODERATOR : DR. MWANZA INTRODUCTION Cervical cancer is a malignant tumour/neoplasm deriving from cells of the cervix. It is the third most common cancer in women worldwide, and it remains a leading cause of cancer-related death for women in developing countries (second most common cancer). It develops slowly and begins with a precancerous condition known as dysplasia. Dysplasia is easily detected in a routine Papanicolaou (Pap) smear and is completely treatable Education about the benefit of HPV vaccination is also important but must be accompanied by the information that vaccination does not substitute for regular screening. AETIOLOGY Human papillomavirus (HPV) infection must be present for cervical cancer to occur. HPV infection occurs in a high percentage of sexually active women. However, approximately 90% of HPV infections clear on their own within months to a few years and with no sequelae. On average, only 5% of HPV infections will result in the development of CIN grade 2 or 3 lesions (the recognized cervical cancer precursor) within 3 years of infection. Only 20% of CIN 3 lesions progress to invasive cervical cancer within 5years, and only 40% of CIN 3 lesions progress to invasive cervical cancer in 30years Because only a small proportion of HPV infections progress to cancer, other factors must be involved in the process of carcinogenesis. Aetiology cont. /risk factors The following factors have been postulated to influence the development of CIN 3 lesions: The type and duration of viral infection, with high-risk HPV type and persistent infection predicting a higher risk for progression; low-risk types do not cause cervical cancer Host conditions that compromise immunity (eg, poor nutritional status, immunocompromise and HIV infection) Environmental factors (eg, smoking and vitamin deficiencies) Lack of access to routine cytology and screening Gynecologic factors which include early age of first intercourse and higher number of sexual partners Promiscuous male partners Hx of sexually transmitted diseases Genetic susceptibility i.e women who have an affected first degree biologic relative have a 2-fold relative risk of developing a cervical tumor compared with women who have a non-biological first degree relative with cervical tumor Human papillomavirus Comprises a heterogeneous group of viruses that contain closed circular double-stranded DNA The viral genome encodes 6 early open reading frame proteins (ie, E1, E2, E3, E4, E6 and E7), which funtion as regulatory proteins, and 2 late open reading frame proteins (ie L1 and L2), which make up the viral capsid. To date, more than 115 different genotypes of HPV have been identified and cloned. More than 90% of all cervical cancers worldwide are caused by 8 HPV types: 16, 18, 31, 33, 35, 45, 52 and 58. Three types-16, 18 and 45 cause 94% of cervical adenocarcinomas HPV 16 may pose a risk of cancer that is an order of magnitude higher than that posed by other high-risk HPV types. The HPVs that infect the human cervix fall into 2 broad risk categories. The low-risk types (eg, HPV 6 and 11) are associated with condylomata and a very number of low-grade squamous epithelial lesions (SILs) but never found in invasive cancer. The high-risk types(eg, HPV 16) vary in prevalence according to the cervical disease state. PATHOPHYSIOLOGY Upon integration into the human genome, the linearization of high-risk HPV DNA places the E6 and E7 genes in a position of enhanced replication. E7 binds and inativates the Rb protein while E6 binds p53 and directs its degradation, and the funtional loss of the TP53 and RB genes leads to resistence to apoptosis, causing uncensored cell growth after DNA damage. This ultimately results in progression to malignancy Clinical Presentation Symptomatic: Vaginal bleeding-irregular, intermenstrual, post-coital, postmenopausal Vaginal discharge- copius, purulent, malodorous Cachexia Micturition symptoms-dysuria, frequency, urinary incontinence from VVF Rectal symptoms- rectal pain Pedal oedama Pain- dyspareunia, low backache, deep pelvic ache, sciatica. Investigations Diagnostic: Pap smear (if no obvious lesion) Colposcopy Cervical Biopsy for histology (for obvious lesions) Pre-treatment: FBC Urinalysis E/U/Cr LFT Chest X-ray ECG Abd-pelvic USS CT/MRI-evaluate liver, urinary tract, bones, nodules sizes IVU-assesses renal, ureter position Positron emission tomograghy- lymph node metastasis, distant metastasis Cystoscopy-tumour invasion imto the bladder Proctosigmoidoscopy-tumour invasion into the rectum Examination under anesthesia- extent …
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