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24 Cards in this Set

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HPV high risk subtypes
16, 18, 45, 31 , 33
Cervical dysplasia transit time if neglected
– CIN 1 is 5 years
– CIN 2 is 3 years
– CIN 3 is 1 year
After satisfactory colposcopy for CIN I
– If tx selected, excisional preferred
– Test for HPV at 12 mos OR do 2 repeat paps at 6 and 12 mos
– If repeat ASC or more OR high risk HPV refer back to colpo
After unsatisfactory colpo for CIN I
– Dx excisional procedure (not ablative)
– In pregnant, adolescent, immunosuppressed women may be followed as above
After satisfactory colposcopy for CIN II & III
Excisional or ablative therapy that removes the entire transformational zone
After unsatisfactory colposcopy for CIN II & III
– do dx excisional conization
– up to 7% will have occult invasive cervical carcinoma
– Margins are risk factor for recurrence/persistent
Cervical dysplasia in pregnancy
– Follow with Pap/colposcopy each trimester
– Bx if suspect cancer
– Plan treatment 6 weeks postpartum
Tx for cervical carcenoma
– Stage I is Surgery or Simple hysterectomy
– Stage II is Surgery or Radical Hysterectomy (take LN’s and part of vagina)
– Stage III and IV is Radiation
False (-) pap
– Too few abnormal cells
– smears w/ obscuring inflamm or blood limiting evaluation
What defines a satisfactory pap
– in conventional, ³10% of slide has cells
– Thin preps, 5000 cells
– Epi or glandular abnormality even if there are less than adequate numbers of cells
What defines an unsatisfactory pap
– Specimen rejected (Improper pt identifiers, Slides received broken)
- Too few squamous cells
- poor preservation
- Totally obscured by blood
(-) for Intraepithelial Lesion or Malignancy pap classification
– benign cellular changes
– Endometrial cells if >40 yrs (May indicate an endometrial lesion like hyperplasia, carcinoma)
Condyloma (Koilocytes) histo
– Pathgnomonic for HPV (LGSIL in Bethesda)
– Clear cyto, well defined vacuole w/ enlarged, irregular and dark nucleus (binucleation common)
SC in situ histo
3D aggregates of cells w/ little cytoplasm and dark irregular nuclei
Cervical invasive SCC histo
– irregular chromatin clumping, prominent nucleoli
– Background may be necrotic
ASCUS histo
– Nuclear enlargement but no hyerchromasia
– Cytoplasmic vacuolization without nuclear abnormalities of HPV
– Inflammation induced nuclear enlargement
ASC-H histo
– Small cells with hyperchromatic nuclei too few in number for diagnosis of HSIL
– Atypical squamous metaplasia from endocervical canal
AGUS histo
– Nuclear enlargement w/ minimal hyperchromasia
– Inflamm associated reactive atypia
– Metaplasia w/ reactive atypia
– Thick clusters of endocervical cells difficult to classify (may be related to sampling device)
HPV-mediated carcinogenesis
– infects basal cells at
– integrates into host DNA
– viral oncogenes E6 and E7 over expressed and bind
– this -> destruction of proteins from p53 and Rb genes
– Proliferating cells acquire additional genetic errors
– Clonal selection leads to malignant phenotype
Lichen sclerosus
– vulvar dystrophy
– may be painful, pale white plaques, cause unknown
Squamous hyperplasia
– vulvar dystrophy
– may be pruritic and related to a wide variety of irritants
Paget’s disease
– Glandular tumor cells w/in epidermis that stain for mucin (indicative of their glandular origin)
– Most cases are NOT associated with an underlying adenocarcinoma
Nabothian cyst
benign mucinous cyst-like distension of endocervical glands 2o to obstruction from squamous metaplasia
Microglandular hyperplasia
benign prolif of endocervical glands, likely hormonally driven (P stimulation)