KANSER SERVIKS: PENGENALAN, PENYEBAB, GEJALA DAN RAWATAN
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KANSER SERVIKS: PENGENALAN, PENYEBAB, GEJALA DAN RAWATAN
- 2. Malaysia
- 3. Bilangan Kanser Di Kalangan Wanita, 2000 0 100 200 300 400 500 600 X 1000 cases Breasts Cervix Colorectum Lungs stomach Ovary Uterus Liver Esophagus Developing Countries Developed Countries
- 4. 10 Kanser utama wanita di Malaysia 2003 2.7 2.9 3.8 4.0 4.1 4.1 4.3 6.0 12.9 31.0 0 5 10 15 20 25 30 35 Percentage of all cancers OTHER SKIN STOMACH LUNG LEUKAEMIAS OVARY RECTUM CORPUS UTERI COLON CERVIX UTERI FEMALE BREAST
- 8. Malaysian National Cancer Registry 2003 12.9% daripada keseluruhan Kanser Wanita Kadar Umur Rata 19.2 /100,000 Cina ASR 28.8 per 100,000 India ASR 22.4 per 100,000 Melayu ASR 10.5 per 100,000 Kejadian tertinggi pada umur 60-69 Tahun
- 9. Cervix Uteri Age specific Cancer Incidence per 100,000 population, Peninsular Malaysia 2003 AgespecificCancerIncidenceper100000population 0-9 10-19 20-29 30-39 40-49 50-59 60-69 70+ 0.0 70.6
- 12. Teens adults elderly Transformation zone
- 13. Siapa yang berisiko? Memulakan hubungan seks di awal usia Berbilang pasangan Suami pernah berkahwin dan isteri lama penghidap kanser serviks Penyakit bawaan kelamin Suami menghidap penyakit bawaan kelamin Merokok
- 14. • > 135 Jenis,70 jenis menjangkiti manusia •35 jenis menjangkiti alat kelamin •HPV Jenis 16,18,31 and 45 menyebabkan 80 % kes Kanser serviks Punca- Human Papillomavirus (HPV)Punca- Human Papillomavirus (HPV)
- 15. HPV exposure PATHOGENESIS Squamous metaplasia Transformation zone cells SI
- 16. Penyumbang kearah jangkitan virus HPV? Merokok* [OR 3.0] Status Imuniti Faktor Pemakanan Taraf hidup rendah Hormon Pengaruh Individu Jumlah Virus yang terjangkit Jangkitan Alat Kelamin HPV berperanan sebagai pemula kepada proses kanser (oncogenesis) – memerlukan interaksi daripada faktor persekitaran untuk menyebabkan kanser * Can Detectn & Prev 2002; 26(2)
- 17. Bagaimana Virus HPV menyebabkan Kanser Serviks? Jangkitan HPV Jangkitan HPV Jangkitan HPV yang Berulang Jangkitan HPV yang Berulang Ketidakaturan SelKetidakaturan Sel Pembentukan Kanser Awal Pembentukan Kanser Awal Kanser Berbahaya Kanser Berbahaya Faktor ImunitiFaktor Imuniti Faktor PenyumbangFaktor Penyumbang
- 18. Cancerous cervix Persistent HPV infection
- 20. Gejala Tiada Gejala - CIN (Kanser Awal) ; 30-an Kanser ; - 50-an Pendarahan tak tentu Selalu keluar Lendir kekuningan Sakit semasa hubungan seks Sakit ketika buang air kecil Simptom perebakan kanser ke organ lain
- 21. CERVIX - CANCER
- 22. Perebakan Secara Terus :Rahim,Pundi Kencing,Salur Kencing,rectum,vagina Melalui Sistem Limfa – Stesen Pertama Paracervical Hypogastric Obturator External iliac Melalui Sistem Limfa – Stesen Kedua Sacral Common iliac Aortic Inguinal Melalui Darah : Paru-paru, Hati, Sum2 Tulang
- 23. PROGNOSIS Clinical stage Nodal status Tumour size Dept of invasion Parametrial involvement Endometrial extension Blood vessel invasion Microscopic grading/type Cell proliferative indices - eg angiogenesis etc
- 24. Jangkaan Hidup 5 Tahun 0 - 100% I - 80 - 90% II - 75% III - 35% IV - 10-15%
- 25. Screening- PAP SMEAR APA itu Pap smear? KENAPA mesti buat? BAGAIMANA mengambil sampel? SIAPA yang ambil sampel? BAGAIMANA membaca keputusan??
- 26. KENAPA..? Untuk mengenalpasti Tanda2 Kanser awal (ie,dysplasia/CIS,CIN, SIL)
- 27. Pap smear 30% pengurangan risiko jika 10 tahun sekali dilakukan 80% ------------------------------ 5 yrs 90% ------------------------------ 3 yrs 91% ------------------------------ 2 yrs 93% ------------------------------ 1 yr
- 28. Bagaimana ?..Dimana..? Wooden Ayer spatula Cytobrush Transformation zone : teens 20-50 postmenopausal
- 30. Vaksinasi HPV
- 31. Klinik Nur Sejahtera Sandakan Lot. 17, Bandar Maju, Batu 1 1/2, Jalan Utara, 90000 Sandakan, Sabah 089-221437 (Telefon) 088-252214 (Fax)
Editor's Notes
- Next, we examine the progression of HPV infection to cervical cancer. After exposure to HPV, events in the viral life cycle are initiated, with specific activity regulated by the factors responsible for the host’s immune response. HPV infection alone is not sufficient to induce an immediate carcinoma because malignant tumors develop only after HPV-induced lesions persist for several months or even years. There is a large reservoir of HPV infection in young women in their teens and twenties. Only a few of these women go on to develop persistent HPV infection. Progression depends on viral type, immunologic factors and possibly co-carcinogens. Persistent high-risk infections can lead to cellular deregulation. Over time, this cellular deregulation can cause high-grade cervical lesions and ultimately, cervical cancer. Oncogenic activity has been attributed to the viral oncoproteins E6 and E7, which are crucial for malignant transformation of HPV associated cancers. In non-malignant cells, inter- and intra- cellular signals suppress these oncogenes at the transcriptional level thus limiting malignant progression. The E6 and E7 viral proteins interfere with cellular proteins that are involved in cell cycle control. They cause the human cell to experience disturbed physiologic function and genetic instability. Mutations in cellular genes devoted to the intracellular surveillance of HPV infections, integration of viral DNA, and deletions or mutations of viral transcription control sequences lead to a significantly increased expression of the E6/E7 genes, which is a consistent characteristic of high-grade intraepithelial neoplasia and cancers.6