GYN malignancy Flashcards
cervical cancer
general
Rates are decreasing due to surveillance and vaccines!
Bimodal distribution- 30s and 60s
Main cause: HPV
How is it found?
Asymptomatic screening
Post-coital bleeding (pre-menopausal)
Post-menopausal: dysfunctional bleeding
MAIN TYPE: SQUAMOUS CELL CARCINOMA
cervical cancer
RF
1 Cause: HPV
Smoking (2-3 x increase)
Immunosuppression
Chlamydia infection
Diet low in fruits and vegetables
Obesity
Oral Contraceptive use
Intrauterine device use
Multi-full term pregnancies
First pregnancy < 17 years
cervical cancer
HPV
Most common STD in U.S.
>6 million cases per year!!
Infects females and males
Most new infections occur between ages 15-24
80% of women will have had HPV infection by age 50
Over 100 Types!
High risk types and low risk types
Acquired through sexual and genital skin-to-skin contact
Persistent cervical infections with high grade HPV genotypes required for development of cervical cancer and the precancerous lesion, CIN3
Types 16 (55-60%), 18 (10%),31,33, 45
HPV…
a player in other cancers
Vulvar Cancers-69%
Vaginal Cancers-75%
Penile Cancers-63%
Anal Cancers-89% (M) /93% (F)
Oropharyngeal Cancers 63% (F)/ 72% (M)
Dysplasia to cancer
Dysplasia= abnormal cells that have lost the ability to self regulate
PAP Smear/Liquid based cytology
Low Grade (LGSIL) c/w mild CIN 1
High Grade (HGSIL) c/w moderate to severe CIN 2-3
Cervical Intraepithelial Neoplasia (CIN) on biopsy - HOW MUCH OF THE CERVICAL EPITHELIUM IS INVOLVED
mild= CIN 1
Moderate= CIN2
Severe= CIN3
Carcinoma in situ = “cancer in place” or cancer that has not spread beyond the epithelial layer
Invasive cancer= cancer has invaded tissue beyond the epithelial layer of cells
Can be ectocervical/endocervical
Treatment of dysplastic/precancerous lesions
Will be discussed in detail by Nicole Grange (1/22/24)
Based on a number of criteria
In general treatment involves local ablative therapy
Colposcopy with Loop Electrosurgical Excision Procedure(leep)
Colposcopy with cryotherapy
cervical cancer work-up
Biopsy (near the margin is best)
Physical exam
rectovaginal exam
parametrial or rectal involvement,
lymph node survey
Inguinal
supraclavicular
CXR
pulmonary nodules
CBC, BMP,LFT
Cystoscopy/anoscopy/IVP
CT can be used for substitution
Treatment of cervical cancer
Simple vs Radical Hysterectomy
Simple/t0tal hysterectomy: removal of uterus, cervix
Subtotal/partial hysterectomy: removal of uterus only, cervix remains
Radical hysterectomy: removal of uterus, Fallopian tubes, cervix, bilateral parametrium and upper vagina
cervical cancer
Prevention
Incidence and mortality have declined since introduction of the Papanicolaou (Pap) test in the mid-20th century and testing for high-risk types of HPV however….
50% of women with cervical cancer have never had a Pap smear
30% of cancers have occurred in women who have not been screened within the last 5 years.
25% of cases and 41% of deaths occur in women 65 years of age and older
Screening Window of Opportunity
The latency period from dysplasia to cancer of the cervix is variable, but with 3 normal paps, the odds are < 1/1,000,000
Single Pap false negative rate is 20%.
HPV
screening
90% HPV infections transient
Screening strategies aimed at identifying those cervical cancer precursors likely to progress versus those which are only transient infections
Three screening modalities
PAP SMEAR
Co-testing for high risk HPV with PAP smear
Primary HPV TEST
cervical cancer
PREVENTION - HPV Vaccines
Shown to protect against types which are responsible for 98% cervical cancers and 89 and 99% genital warts in males and females, respectively
Also shown to protect against 97% vaginal cancers and 97% vulvar cancers
CDC estimates that 30,700 cancers could be prevented in US with vaccination
Gardasil (Merck) 9-valent vaccine (9vHPV)
PROTECTS against HPV 6,11,16, 18, 31, 33, 45, 52, and 58.
2 DOSE SCHEDULE IF < 15 YEARS OF AGE (0, 6-12 MONTHS)
3 DOSE SCHEDULE IF > 15 YEARS OF AGE (0, 2, 6 MONTHS)
IN 2018 FDA APPROVED USE FOR AGES 27-45 YEARS OF AGE BUT NOT PART OF GUIDELINES YET.
VULVAR CANCER
general
Rare, not as rare as vaginal
PRESENTATION IS USUALLY PRUITIS/SKIN CHANGES
RULE OUT INFECTION OR INFLAMMATORY PROCESS
MANY DIFFERENTIALS FOR VULVAR LESIONS
Condylomata
Epithelial hyperplasia (hyperplastic dystrophy)
Lentigo
Contact dermatitis
Seborrheic keratosis
Acanthosis nigricans
Paget’s disease*
Lichen sclerosis and lichen planus
uterine cancer
Endometrial hyperplasia
Proliferation of endometrial glands causing Thickening of uterine lining
Categorized into two groups:
Hyperplasia without atypia
usually not neoplastic (4x more likely to develop cancer)
Changes due to prolonged estrogen exposure or anovulation
Hyperplasia with atypia
Neoplastic/ premalignant lesions on the endometrium
1/3 of women develop endometrial cancer in 1 year
Also referred to as Endometrial intraepithelial neoplasia (EIN)
Either group, especially EIN, can progress to endometrial cancer
Uterine Cancer
Types of endometrial cancer
Type i= endometrioid
Most common
Estrogen related
Endogenous
Exogenous
Younger, obese patients
Low grade
Precursor-endometrial hyperplasia
Type II papillary serous clear cell
Rare
Unrelated to estrogen
Older, thinner women
aggressive
Different etiology
Mutant P53 overexpression
uterine cancer
workup
For vaginal bleeding:
Physical Exam
EMB, D&C – office EMB false neg 10%
Ultrasound?
Not really that useful, need biopsy
Heredity and Endometrial Cancer
10% of Endometrial Cancer can be hereditary
Lynch syndrome/HNPCC
Endometrial, Colorectal, Ovarian, Breast
Mutation in DNA mismatch repair genes: MSH2, MSH6, MLH1, PMS2 or MSI
Uterine Sarcoma
general
About 1 in 12 of all uterine cancers
Classification
carcinosarcoma
Endometrial stromal sarcoma
Undifferentiated sarcoma or pure heterologous sarcoma
Leiomyosarcoma
Generally worse prognosis/more aggressive
Treatment: surgery+/- chemotherapy/RT
Gestational trophoblastic disease
Types of moles
Benign= hydatiform mole
Complete moles
Incomplete/partial moles
Malignant
Invasive molar disease
choriocarcinoma
