Hsr - Hpv & Cervical Ca Screening

Front 1

What is the most common STI? What % of women will have it in their lifetimes?

Back 1

HPV. 75%

Front 2

__ types of HPV are known to cause CA. __ others are suspected.

Back 2

15; 3

Front 3

HPV 6 & 11 cause __ __.

Back 3

Condyloma accuminata (genital warts)

Front 4

What age group is HPV most common in?

Back 4

18 - 25yo

Front 5

What is the median duration of new HPV infections?

Back 5

8m; 81% were no longer infected by 24m

Front 6

What do CIN ratings say regarding level of dysplasia? Which CIN's are associated w/ SIL's?

Back 6

CIN= Cervical Intraepithelial Neoplasia
SIL= Squamous Intraepithelial Lesion
CIN1: mild dysplasia; LSIL
CIN2: moderate dysplasia; HSIL
CIN3: severe dysplasia + carcinoma in-situ; HSIL

Front 7

HPV 16 & 18 are responsible for __ of cervical CA cases worldwide

Back 7

2/3

Front 8

Almost __ of women clear both HPV & SIL by 33m. HPV clearance preceded regression of cytology to nl by __ mo. 4 women in the study cleared HPV w/o clearing SIL, but none had CIN__.

Back 8

half; 3m; CIN3

Front 9

Describe the lifecycle in HPV latent infection.

Back 9

HPV enters epithelium at basal layer. The virus loses the capsid & exists as circular episome in basal cell nucleus, replicating in tandem with host DNA. Cells appear histologically and cytologically nl.

Front 10

What are 3 possible courses of HPV infection?

Back 10

1. Sustained remission: cell-mediated immune response contains infection. 2. Productive infection: In the presence of co-factors, HPV replicates independent of host DNA. 3. Malignant transformation: risk established by persistent infection.

Front 11

What are the identified co-factors that can create a productive infection in which HPV is replicating independent of host DNA?

Back 11

Certain STI's, Cigarette smoking, Nutritional factors, Immunosuppression

Front 12

Describe the life cycle in HPV productive infection

Back 12

HPV replicates in intermediate & superficial layers independent of host DNA, causing increased viral DNA. As infected cels mature & move toward the surface, the virus reacquires capsids, resulting in many intact virions in each cell (koilocytes). The virus is released as superficial cells are shed.

Front 13

What is the cytology related to productive infection?

Back 13

ASCUS or LSIL. Productive infection & koilocytes are often assoc w/ genital warts

Front 14

What is the life cycle in HPV malignant transformation?

Back 14

Integrity of the viral episome allows the virus to coexist w/ host for decades during the latent phase. Random mutation results in break up of episome at E1/E2 region, allowing expression of E6 & E7 region. E6 & E7 permit the viral DNA to integrate into host DNA & block tumor suppressor proteins p53 & pRb, promoting unregulated cell growth. Accumulation of random mutations over years allows neoplastic transformation.

Front 15

What are the criteria for mass screening programs?

Back 15

1. Important health problem w/ high prevalence in the community. 2. Available screening test that is simple to administer, accurate & reliable, and acceptable to the population. 3. Recognizable latent phase. 4. Definitive dx & effective tx. 5. Acceptable screening dx & treatment costs.

Front 16

What are the sensitivity and specificity of Paps?

Back 16

Sensitivity is 51-80%, depending on study & cytology method. Specificity is ~95%.

Front 17

What is the major problem w/ Paps?

Back 17

Reliability of cytology interpretation. There is low interobserver reproducibility.

Front 18

Part of a good screening test is having a recognizable latent phase. How does the length of the latent phase change depending on pt age?

Back 18

Progression from dysplasia to CA can take years to decades, but it takes longer in younger women & is quicker in older.

Front 19

Why do women still get squamous cell cervical CA if the Pap test is so good?

Back 19

50% never tested. 30% errors in sampling/interpretation. 10% >5y since last screening. 10% errors in follow up.

Front 20

When should Pap screenings start?

Back 20

3y after onset of vaginal intercourse or age 21

Front 21

How often should women get Paps?

Back 21

From onset to age 30, ACS says annually if conventional & q2y if liquid based cytology. ACOG says annually regardless of type. >30yo: both say q2-3y if 3 consecutive negative Paps or annually if CIN2/3 DES exposed in utero or immunosuppressed

Front 22

How often should HIV+ women be screened?

Back 22

2x in year after HIV dx, then annually if negative

Front 23

When should screening be DC'd?

Back 23

US Preventative Services Task Force recs against p 65yo if adequate recent screening & nl Pap & not otherwise at high risk for cervCA. ACS says 70+yo p 3+ documented consecutive - Paps & no abn Paps w/in 10y prior to 70yo if low risk & in good health.

Front 24

What are the recommendations for women w/ total hysterectomy for benign indications? Is this what women do?

Back 24

Screening can be dq'd. If prior CIN2/3, continue annual Paps until 3 consecutive negs. 69% still get Paps for benign indications.

Front 25

How do HPV DNA testing & cytology compare?

Back 25

HPV DNA is more sensitive, but less specific & it has a higher negative predictive value.

Front 26

Why is combined cytology + HPV DNA recommended for women >30? How often should this be repeated if both are neg?

Back 26

Most sensitive, but least specific combination. Has the highest negative predictive value. Repeat no sooner than 3y if both are neg.

Front 27

Why is this limited to women >30?

Back 27

Because while the prevalence of high risk HPV types decreases in this age group, CA rates increase.