cervical and vulval cancer Flashcards
HPV infection
peak prevalence 15-25 yrs prevalence declines with age • Can cause other cancers o Anal cancer ♣ Higher incidence reported in MSM due to HPV related anal cancer
An abnormal growth of squamous cells detectable on smear is a squamous intraepithelial lesion (SIL).
Abnormal cells in the cervix detected by biopsy and histological examination are classified as cervical intraepithelial neoplasia (CIN
• CIN 1 lesions may regress, remain unchanged or progress to CIN 2, CIN 3 or cervical cancer.
• HPV subtypes are very specific to where they infect
o 16 & 18 cause cervical cancer (responsible for 70% of cervical cancers in Europe)
6 & 11 cause genital warts
• Most low-grade SIL are cleared within 6–12 months.
• A small percentage of infections, with or without clinically detected CIN 1, persist and progress to high-grade SIL (HSIL), which is associated with a CIN 2/3 at biopsy.
At this stage, progression to carcinoma is estimated to be 40%.
• Without surgical intervention, progression to squamous cell carcinoma can occur.
• UK HPV vaccination – Quadrivalent vaccine HPV 16/18/6/11
aims of cervical screening
1) Detect cervical dyskaryosis
2) Reduce the risk of cervical cancer
3) Detect CIN
4) Prevent Cervical Cancer
liquid base cytology
cervical cytology
o Abnormal cytology (dyskaryosis – abnormal nuclei):
♣ Abnormal cells may be few
♣ Nuclear features
• increased size and nuclear:cytoplasmic ratio
• variation in size, shape and outline
• coarse irregular chromatin
nucleoli
colposcopy
♣ Magnification and light to see cervix
♣ Exclude obvious malignancy
♣ Use of acetic acid +/- iodine:
• Acetic acid – helps visualise the transition zone
• Iodine – stains starch on normal cells. Non-stained cells are the abnormal ones. (lactobacilli in vagina convert glycogen into lactic acid to maintain vaginal acidity)
• Select biopsy site
• Define area to treat
• Histology of transformation zone
Glandular lining cells of exposed endocervical epithelium transformed into squamous cells (squamous metaplasia)
o Site of HPV infection
♣ Infects basal layer of cells
♣ As host cell matures, different viral genes expressed (oncogenes)
♣ HPV histology – koilocytosis
• Cells with wrinkled nucleus and perinuclear halo, multinucleation
histology of CIN
o Neoplastic cells or undifferentiated cells fill full thickness of epithelium, no normal differentiated cells seen = CIN3
o When undifferentiated cells occupy 2/3 of thickness and only top layers show maturation to medium size cells = CIN2
o If undifferentiated cells only occupy lowest 1/3 of epithelium and surface cells can mature to big flat cells = CIN1
risk factors
o Early age at first intercourse, multiple sexual partners, prolonged oral contraceptive use
o Cigarette smoking, STD’s, immunodeficiency
o Persistent HPV infection
• E6 protein product – inhibits cell death
• E7 protein product – prevents cell cycle arrest
treatment CIN
♣ LLETZ – large loop excision of the transition zone
• Excision of about 7mm of cervix via electricity
♣ Cold Coagulation
♣ Laser ablation
o Follow-up
♣ To confirm that treatment was effective
• Residual disease within 2 years
♣ To prevent invasive cancer
• Recurrent disease 5% after 3-5 years
♣ Detect occasional cancer
Cervical cancer
- Good cure rate if detected early but major cause of death in women in developing countries
- Peak age 45-55 years
• Risk factors: o o HPV related (16 & 18) o Multiple partners o Early age at first intercourse o Older age of partner o Increased likelihood of exposure to HPV o Cigarette smoking
• Symptoms: o Abnormal vaginal bleeding o *Post coital bleeding o Intermenstrual bleeding/PMB o Discharge – Offensive discharge (dead tumour tissue)
diagnosis:
clinical
screen
EUA examination under anaesthesia
management: radical hysterectomy: ♣ Removal of cancer with a border of healthy tissue ♣ Removal of: • Uterus, cervix, upper vagina • Parametria – connective tissue around uterus, etc • Pelvic nodes ♣ Ovaries conserved
o Beyond stage 2a or unfit for radical surgery
♣ Radiotherapy- External Beam x 20 fractions
♣ Chemotherapy- 5 cycles of cisplatin
♣ Caesium Insertion (24 hours)
• Brachytherapy radiotherapy dose to the site of tumour
vulva intraepithelial neoplasia and Vulval cancer
HPC related diseases
• Lower Genital Tract Intra-epithelial Neoplasia
o Decreasing age at presentation – 36 years
♣ Younger women multi-focal disease (multi-zonal vulva + anus), HPV positive
♣ Older women uni-focal disease, HPV negative
-slower progression compared to CIN
risk factors
- smoking
- other genital intra epithelial neoplasia
clinical appearance of VIN raised papular or plaques lesions erosions, nodules, warty sharp border discolouration o Differentiated VIN tends to be unifocal ulcer or plaque
Management of VIN
o Topical treatments ♣ Tissue preservation ♣ Multiple lesions ♣ Effect on sexual function not known ♣ Long term recurrence rates and risk of cancer are not known ♣ Imiquimod ♣ Photodynamic therapy ♣ 5FU, alpha-interferon, cidofivir -laser ablation
vulva cancer
mostly SCC associated with VIN can be Basal CC • Presentation: o pain o itch o bleeding o lump/ulcer • o Older women tend to present with pain/ulcer o Young women present with VIN
staging
lymph node involvement-inguinal and upper femoral
pelvic
management
o Surgery ♣ Radical local excision ♣ Unilateral or bilateral node dissection • Groin node dissection o Inguinal and upper femoral nodes o Separate node incisions o Staging and remove nodal disease o Associated with significant morbidity ♣ Wound infection ♣ Lymphocysts ♣ Nerve damage radio,chemo good prognosis