Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

27 Cards in this Set

  • Front
  • Back
What is the most common STI? What % of women will have it in their lifetimes?
HPV. 75%
__ types of HPV are known to cause CA. __ others are suspected.
15; 3
HPV 6 & 11 cause __ __.
Condyloma accuminata (genital warts)
What age group is HPV most common in?
18 - 25yo
What is the median duration of new HPV infections?
8m; 81% were no longer infected by 24m
What do CIN ratings say regarding level of dysplasia? Which CIN's are associated w/ SIL's?
CIN= Cervical Intraepithelial Neoplasia
SIL= Squamous Intraepithelial Lesion
CIN1: mild dysplasia; LSIL
CIN2: moderate dysplasia; HSIL
CIN3: severe dysplasia + carcinoma in-situ; HSIL
HPV 16 & 18 are responsible for __ of cervical CA cases worldwide
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__.
half; 3m; CIN3
Describe the lifecycle in HPV latent infection.
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.
What are 3 possible courses of HPV infection?
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.
What are the identified co-factors that can create a productive infection in which HPV is replicating independent of host DNA?
Certain STI's, Cigarette smoking, Nutritional factors, Immunosuppression
Describe the life cycle in HPV productive infection
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.
What is the cytology related to productive infection?
ASCUS or LSIL. Productive infection & koilocytes are often assoc w/ genital warts
What is the life cycle in HPV malignant transformation?
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.
What are the criteria for mass screening programs?
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.
What are the sensitivity and specificity of Paps?
Sensitivity is 51-80%, depending on study & cytology method. Specificity is ~95%.
What is the major problem w/ Paps?
Reliability of cytology interpretation. There is low interobserver reproducibility.
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?
Progression from dysplasia to CA can take years to decades, but it takes longer in younger women & is quicker in older.
Why do women still get squamous cell cervical CA if the Pap test is so good?
50% never tested. 30% errors in sampling/interpretation. 10% >5y since last screening. 10% errors in follow up.
When should Pap screenings start?
3y after onset of vaginal intercourse or age 21
How often should women get Paps?
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
How often should HIV+ women be screened?
2x in year after HIV dx, then annually if negative
When should screening be DC'd?
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.
What are the recommendations for women w/ total hysterectomy for benign indications? Is this what women do?
Screening can be dq'd. If prior CIN2/3, continue annual Paps until 3 consecutive negs. 69% still get Paps for benign indications.
How do HPV DNA testing & cytology compare?
HPV DNA is more sensitive, but less specific & it has a higher negative predictive value.
Why is combined cytology + HPV DNA recommended for women >30? How often should this be repeated if both are neg?
Most sensitive, but least specific combination. Has the highest negative predictive value. Repeat no sooner than 3y if both are neg.
Why is this limited to women >30?
Because while the prevalence of high risk HPV types decreases in this age group, CA rates increase.