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Cervical cancer
Cervical cancer
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Cervical Cancer

Cervical Cancer is common worldwide , ranking 3rd among all malignancies for women.
Second leading cause of cancer death.
Most of these cancers stem from infection with the Human Pappiloma Virus (HPV).

Cervical Cancer is common worldwide , ranking 3rd among all malignancies for women.
Second leading cause of cancer death.
Most of these cancers stem from infection with the Human Pappiloma Virus (HPV).

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Cervical Cancer

  1. 1. CANCER CERVIX IS PREVENTABLE!!!
  2. 2. ANATOMY
  3. 3. INCIDENCE AND PREVALENCE  Cervical Cancer is common worldwide , ranking 3rd among all malignancies for women.  Second leading cause of cancer death  Most of these cancers stem from infection with the Human Pappiloma Virus (HPV)  Although screening programs in US are well established, it is estimated that 30% of the cervical cancer cases will occur in those women who never had a Papanicolaou (PAP) test.  The mean age of cervical cancer in United States was 47 yrs  Bimodal peak – 35 - 39 years and 60-64 years.  Incidence in developing countries was found to be 60%  Women in lower socio economic groups have the highest age- standardized death rates from this cancer, thought to result from financial and cultural characteristics affecting access to screening and treatment.
  4. 4.  Cervical cancer is ranked as the most common cancer in women in India.  In India, the incidence rises in 30-34 years of age and peaks at 55-65 years of age, with an average age of 38 years ( 21-67 years)  These estimates suggest that more than 80% of the sexually active women acquire genital HPV by 50 years of age.  The current estimates indicate approximately 132,000 new cases are being diagnosed and 74000 deaths occur annually in India, accounting to nearly 1/3rd of the global cervical cancer deaths.  Indian women face a 2.5% cumulative lifetime risk and 1.4% cumulative death risk from cervical cancer.
  5. 5.  HPV 16 and 18 account for nearly 76.7% of cervical cancer in India.  Warts have been reported in 2-25% of sexually transmitted disease clinic attendees in India. Hence, the advent of a vaccine against HPV has stirred much excitement as well as debate.
  6. 6. TERMINOLOGIES  DYSPLASIA- an abnormality of development ( alteration in size, shape and organization of cells)- replacement of a mature cell with a less mature cell.  HYPERPLASIA- Increase in the number of normal cells or tissues  METAPLASIA- Abnormal REVERSIBLE change in the cells or tissues.  NEOPLASIA- Abnormal growth and proliferation of abnormal cells or abnormal amounts of cells , which can be benign or malignant.  INSITU- sitting in place
  7. 7. Production of estrogen Vaginal epithelium fills up with glycogen Low PH Stimulates subcolumnar reserve cells to undergo metaplasia lactobacilli PHYSIOLOGY
  8. 8. RISK FACTORS Demographic risk factors • Ethnicity • Low socioeconomic status • Early Marriage • Increasing age Behavioral risk factors • Early coitarche • Multiple sexual partners • Tobacco smoking • Dietary deficiencies Medical risk factors • Cervical high risk HPV infection • Co infection with Chlamydia and Gonorrhoea • Exogenous hormones • Multiple pregnancies • Immunosuppression • Inadequate screening
  9. 9. DEFENCE FACTORS  Initially, the metaplastic cells are immature ultimately become mature which are resistant to oncogenic stimuli.  The window period till it matures is sensitive to infection ,trauma or any oncogenic stimuli.  The metaplastic process is very active at the time of menarche and during and after first pregnancy.These periods are of high estrogenic phase which lowers the vaginal pH. The acid pH probably is an important trigger for the metaplastic process. The prolonged effect of cancer causing agents can produce continuous changes in the immature cells which may lead to malignancy.  Natural Immunity
  10. 10. HUMAN PAPILLOMA VIRUS  HPV is simple double stranded DNA virus with protein capsid.  Georgios Nikolaou Papanikolaou was a Greek pioneer in cytopathology and cancer detection, and inventor of the Pap smear.
  11. 11.  In 1928 Papanikolaou told about the noninvasive technique of gathering cellular debris from the lining of the vaginal tract and smearing it on a glass slide for microscopic examination as a way to identify cervical cancer. That year he had undertaken a study of vaginal fluid in women, in hopes of observing cellular changes over the course of a menstrual cycle. In female guinea pigs, Papanicolaou had already noticed cell transformation and wanted to corroborate the phenomenon in human females. It happened that one of Papanicolaou's human subjects was suffering from uterine cancer.  The Romanian physician Aurel Babes made similar discoveries in the cytologic diagnosis of cervical cancer.[7] He discovered that if a platinum loop was used to collect cells from a woman's cervix, and the cells were then dried on a slide and stained, it could be determined if cancer cells were present. This was the first screening test to diagnose cervical and uterine cancer..
  12. 12.  More than 120 types of HPV viruses, with 30 of them primarily infecting the androgenital tract of men and women.  The percentage of intraepithelial neoplasia attributed to HPV infection approaches 90%,  ♦ High oncogenic risk—Types 16, 18, 31, 33, 35, 45, 56.  ♦ Low oncogenic risk—Types 6, 11, 42, 43  Since the introduction of Papanicolaou (Pap) test in the 1950s, cytology screening has been associated with a significant reduction in both the incidence and mortality rate from invasive cervical cancer (Saslow,2002)  In the vast majority of cases, the infection will clear in 9-15 months.  A small minority of women exposed to HPV develops persistent infection that may progress to CIN. Factors affecting it are smoking, contraceptive use, infection with other STDs or nutrition.
  13. 13. TRANSMISSION  These sexually-transmitted HPV viruses are spread through contact with infected genital skin, mucous membranes, or bodily fluids of a partner with either warts or subclinical HPV infection.  Congenital infection due to transmission from mother – rare  Infection during perinatal period.  Autoinnoculation
  14. 14. SYMPTOMS  Continous vaginal discharge, not responding to medical treatment  Genital warts  Postmenopausal bleeding  Postcoital bleeding
  15. 15. DIAGNOSTIC METHODS  Visual inspection with acetic acid (VIA): A speculum is introduced and acetic acid is applied to the cervix and visualized with naked eye. Those women with acetowhite lesions are considered for colposcopic examination and/or biopsy  Can be done in any clinical setting, commonly in rural areas where high end facilities like colposcopy are not available  Painless procedure  Not done during menses or when on treatment with vaginal pessaries
  16. 16. PAP SMEAR  Gold standard for screening, differentiates between High Risk and Low Risk cases  Done on OPD basis  Painless  NOT done during menstruation.  Treatment of any vaginal or cervical infection done before the test.
  17. 17.  HPV DNA TEST  Hybrid capture method can reliably detect the high risk HPV types within hours (99.7%)  Nearly 80 percent test positive women will clear the infection (HPV) by their own immune defense. Positive test result in elderly women (> 30 years) suggests colposcopic examination
  18. 18. COLPOSCOPY  Examines the lower genital tract with binocular microscope  It is not a substitute for cytology  It is used to identify invasive or preinvasive lesions and their targeted biopsies if needed and subsequent managements.  Indications  Those having abnormal cytology.  Those with grossly abnormal cervical lesions even if cytology is negative.  Those with post coital bleeding even if the smear is negative.
  19. 19. SCREENING FOR PAP SMEAR GUIDLINE AMERCIAN COLLEGE OF OBSTETRICIAN AND GYNECOLOGISTS INITIAL SCREENING • Age 21 or 3 yrs after the onset of sexual activity INTERVAL • Every year for either liquid-based PAP or conventional • Every 2-3 yrs after age 30 with 3 consecutive normal PAP smears • HIV positive women- twice first year, and then annually DISCONTINUE • After 65 yrs of age if unsymptomatic • After hysterectomy done for benign lesions
  20. 20. SCREENING FOR HPV-DNA TEST  In 2003, FDA approved testing of HPV along with cytology for primary cervical cancer screening in women aged 30 yrs or older.  When the results of both PAP smear and HPV DNA tests are negative, the woman does not have to be retested for 3 years.  In case cytology negative and HPV DNA test positive, both tests to be repeated after 1 year.  Colposcopy recommended for persistent HPV positive test results.  2009 American Society guidline for Colposcopy and Cervical Pathology- immediate colposcopy in HPV DNA positive test result patients with high risk factors.  HPV testing alone is approximately twice as sensitive as a single PAP test and leads to earlier detection of high grade lesions
  21. 21. VACCINES  Effective in prevention of 90% of cervical cancers  Safe and well tolerated.  These vaccines are expected to prevent approximately 70% of cervical cancers, but they will not protect against the approximately 30% caused by oncogenic HPV types not covered in the vaccine.  Vaccine induced neutralizing antibodies works locally (cervix) by preventing the attachment of the virus to the cervical epithelium  Impact is greater when given to those who have not been infected( efficacy 100%)  Started from 11-12 yrs of age till 26 years of age, in both males and females  6.5 yrs of protection is documented
  22. 22.  GARDASIL – protects against 4 virus strains- HPV- 6,11,16 and 18  CERVARIX- protects against 2 virus strains- HPV 16 and 18  GARDASIL 9- 6,11,16,18,31,33,45,52,58  Given at 0, 1st -2nd and 6th month  Given intramuscularly
  23. 23.  If a vaccine series is started and a patient then becomes pregnant, completion of the vaccine series should be delayed until that pregnancy is completed.  Lactating women can receive any HPV vaccine because inactivated vaccines like HPV do not affect the safety of breastfeeding for mothers or infants.  The presence of immunosuppression, like that experienced in patients with human immunodeficiency virus (HIV) infection or organ transplantation, is not a contraindication to HPV vaccination.  Vaccination is recommended regardless of sexual activity or exposure to HPV.  Although the vaccine may be less effective in sexually active individuals, it is expected that some benefit will be experienced because prior sexual exposure to all vaccine types is unlikely (16, 17).  Vaccination is recommended even if the patient is tested for HPV DNA and the results are positive. Testing for HPV DNA is not recommended before vaccination in any group.
  24. 24. PREVENTIVE MEASURES  To delay sexual exposure until the cervical epithelium, especially in the transformation zone, has attained physiological maturity.  To maintain a local hygiene and to treat vaginal infections.  To use condom specially during early sexual life.  To maintain penile hygiene as it may be the reservoir for high risk HPV.  Reducing or quitting smoking reduces chances of infection.  To maintain ideal body weight.  Estrogen use in non-hysterectomized women should be restricted. The combined estrogen-progestogen preparations reduce the risks than estrogen alone.
  25. 25. TO CONCLUDE..  The vaccine for cervical cancer is available , which is 90% effective , and 100% effective if taken before sexual exposure.  The vaccine lasts for 7 years.  Early detection of Cervical Cancer makes it curable.  Awareness about the risk factors such as smoking and multiple sexual partners will definitely reduce the incidence. We all are here to prevent and eradicate Cervical cancer, like we have eradicated small pox!

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