Chapter 47: Cervical Neoplasia and Carcinoma Flashcards
How common is cervical cancer
- 3rd most common gynecological cancer here in the U.S., more common in countries that don’t screen for it
- Second most common cancer worldwide, first is breast cancer, and the most common cause of mortaliaity from gynecologic malignancy, accounting for 250,000 deaths per year
How do we treat the precursor to cervical cancer, CIN?
- Txs for CIN o Cryotherapy o Laser Ablation o LEEP: Loop electrosurgical excision procedure) o Cold-knife cone biopsy
High grade strains of HPV
o High grade: 15 of em. 4 most common: 16,18,31,45
Low risk HPV not associated with cancer
o Low risk not associated with cancer: 6 and 11
Genital warts
LSIL
Where does HPV hit down in there?
o Hits at SCJ (squamocolumnar junction) 90% of the time where the nonkeratinized stratified squamous from outside meets the columnar mucus secreting cells inside
Location of SCJ based on age
Childhood: Just inside external os
Puberty = Acidification + hormones = metaplasia of columnar cells so that junction moves OUTWARD onto cervical surface
o Location between old SCJ and new SCJ = Transformation zone.
o Nabothian cysts can form where squamous cells overrun glands from old columnar cells
o TZ cells, which are new and metaplastic, are most susceptible to oncogenesis, especially during puberty and early reproductive years when the metaplasia rate is highest
Perimenopausal: Recedes to internal os out of view
HPV entering the genome vs not entering it
Most infection with HPV is transient, our body can kill it
If HPV does not enter our genome, it just turns the cell it hit into a koilocyte, a withering looking cell with a pathetic looking nucleus that we see on histo
If HPV does enter genome, we can get the gene changes that lead to transformation into pre-cancer or cancer
Smokers and cervical cancer
o 3.5x greater in smokers – Products of smoking found in the cervix
Common sense risk factors for cervical cancer (due to increase HPV, hint hint)
o More than one sex partner or a sex partner with more partners
o Intercourse younger than 18
o Male partner who has had a partner with cervical cancer
o HIV or other STDs
o Organ transplant, particularly kidney
o DES exposure (DURING pregnancy. We are beyond this now, those women are all in their 50’s now, but great test question)
o Infrequent PAP smears or history of HSIL/Cervical cancer
Discuss in general what the 2001 Bethesda criteria is
Divides into squamous lesions and glandular lesions, followed by pre-cancer and cancer.
CIN 1,2,3 is the old system, but is still used today with the 2001 Bethesda update. The older system before that used mild, moderate, and severe dysplasia.
Precancer vs Cancer squamos variety
Precancer:
- Atypical squamous cells. Two types: ASC-US: Undetermined significance and ASC-H: Cannot exclude high grade
- LSIL – HPV infection, CIN I, mild dysplasia and HSIL – CIN 2/3 (3 AKA carcinoma in situ or CIS) and moderate/severe dysplasia
Cancer: Invasive squamous carcinoma
Precancer vs cancer glandular variety
Precancer:
- Atypical (AGC) - (Endocervical, endometrial, or glandular cells)
- Atypical, favor neoplastic (AFN) - (Endocervical and glandular cells)
- Endocervical adenocarcinoma in situ (AIS)
Cancerous: Adenocarcinoma (Endocervical, endometrial, extrauterine, NOS (not otherwise specified))
After abnormal PAP:
- After abnormal PAP, correlate with bimanual and visual inspection. Get HPV testing/cotesting and proceed to Colpo
How does colpo work?
o Binocular stereomicroscope goes to 7-15x magnification. Green filter to help distinguish abnormal blood vessels. Easier to see changes/dysplasia and bx. Look for white areas, abnormal vasculature, punctate lesions
Why do we use acetic acid in colpo
Acetic acid 3-4% used to dehydrate cells, and those with big nuclei look white (big due to metaplasia, dysplasia or HPV infection). Wait 10-90 seconds.
Unsatisfactory Colpo. What next?
o If SCJ not visualized or entire lesion not fully demarcated, Colpo is unsatisfactory
Proceed with cervical conization and endocervical curettage as indicated
When do we do HPV testing?
- HPV testing done in women over 30 for high risk strains, non-adolescent LSIL patients, and anyone with ASC-US
Ablation treatment options and the general point of it all
Get rid of CIN, the precursor lesion
Only do after PAP and correlated colpo and bx
Do laser or cryo. Electrofulguration also possible, as well as cold coag.
Laser is rarely done anymore in the U.S. we tend to use Cryo. Discuss how this works
Used most commonly in outpatient clinic for persistent CIN I
o Cover SCJ and identified lesions with stainless steel probe, then supercooled with liquid nitrogen or compressed gas
o 3 minute freeze with 5 minute thaw and repeat freeze. First freeze kills superficial layers, thawing allows edema, second freeze freezes that mess getting deeper areas. Alow recovery for 4-5 weeks, may experience water discharge and passing of necrotic debris as the new cervical layer forms. Follow up PAP 12 weeks post-procedure
o Cure rate for CIN I approaches 90%
Now on to the excisional methods. Problems with LEEP?
• LEEP may not be the best in glandular changes due to thermal damage to deeper cells
Problems with CKC, LEEP, LLETZ in pregnancy
• CKC, LEEP, LLETZ all associated with 2nd trimester pregnancy loss secondary to cervical incompetence, pre-term labor, premature rupture of membranes, and cervical stenosis.
Advantage of excision?
You get tissue to look at
Biopsy/margin results from excision and what we do with them
If positive margin, repeat conization or close follow up
If positive margin with HSIL or CIS, hysterectomy if not wanting pregnancy. If wanting to remain fertile, colposcopy with ECC and HPV testing an acceptable management protocol
Consider excising if ECC is positive, unsatisfactory colpo, or substantial discrepancy between PAP and histology of ECC and biopsy
Follow up after ablation/excision
o Noninvasive abnormalities treated with excision or ablation need PAP follow up every 6 months for 2 years with return to routine screening thereafter
