Management and prevention of cervical cancer.pptx

Cervical cancer

1. Current update on the prevention and management of cervical cancer Dr Muhammed Khadijat Ayo Department of histopathology Dalhatu Araf Specialist Hospital

2. Outline of presentation Introduction Risk factors Etiology Pathophysiology Prevention Management of precancerous Lesion Staging of cervical cancer Management Conclusion

3. Introduction Cervical cancer is the fourth most common malignancy in women worldwide . Cervical cancer is a public health problem all over the world, even though it is preventable. Its incidence, morbidity and mortality has significantly reduced in countries with organized, population-based routine prevention (both primary and secondary) programs. Most LMIC, including Nigeria, have not achieved this. The WHO has adopted the 90:70:90 strategy to eliminate cervical cancer as a public health problem by 2030.

4. Aetiology Oncogenic (High risk) types of the Human Papilloma Virus are (16, 18, 31, 33, 35, 39, 45, 51, 52, and 58). non-oncogenic or low-risk types (6, 11, 40, 42, 43, 44, and 54) that are associated with genital warts(Muñoz, 2003). HPV 16 is the most oncogenic, accounting for almost half of all cervical cancers

5. Aetiology HPV 16 and 18 together account for approximately 70% of cervical cancers HPV 6 and 11 are the most common strains associated with genital warts and are responsible for approximately 90% of these lesions. 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 5 years, and only 40% of CIN 3 lesions progress to invasive cervical cancer with 30 years.

6. Pathophysiology

7. Pathophysiology

8. Pathophysiology The viral genome encodes 6 early open reading frame proteins (ie, E1, E2, E3, E4, E6, and E7), which function as regulatory proteins, and 2 late open reading frame proteins (ie, L1 and L2), which make up the viral capsid. E7 binds and inactivates the Rb protein while E6 binds p53 and directs its degradation, and the functional loss of the P53 and RB genes leads to resistance to apoptosis, causing uncensored cell growth after DNA damage. This ultimately results in progression to malignancy.

9. Pathophysiology

10. Risk Factors Multiple sexual Early coitarche (pre-menarcheal: susceptible cervix) Early marriage Early age at first pregnancy Early age at first child birth High parity Low socio-economic status Cigarette smoking Immunosuppression

11. 5.3.1 American Cancer Society ACS recommends cervical cancer screening with an  HPV test  alone every 5 years for everyone with a cervix from age 25 until age 65. If HPV testing alone is not available, people can get screened with an  HPV/Pap cotest  every 5 years or a Pap test every 3 years. Screening Approaches American Cancer society