cervical and vulval cancer Flashcards

1
Q

HPV infection

A
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

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2
Q

aims of cervical screening

A

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

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3
Q

colposcopy

A

♣ 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

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4
Q

• Histology of transformation zone

A

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

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5
Q

histology of CIN

A

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

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6
Q

risk factors

A

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

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7
Q

treatment CIN

A

♣ 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

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8
Q

Cervical cancer

A
  • 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

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9
Q

vulva intraepithelial neoplasia and Vulval cancer

A

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
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10
Q

Management of VIN

A
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
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11
Q

vulva cancer

A
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

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12
Q

management

A
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
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