211b vulva, cervix path Flashcards
cervix
neck portion of uterus - protrudes into vagina
vagina
muscular tube
vulva
external genitalia
cervical maturation
2 zones - exposed to vagina = ecto; similar stratified squamous epi like vagina
endocervical canal - at birth is columnar epi (glandular, mucin producing) –>
at puberty - shape of cervix changes – canal pulges out into vagina with columnar, glandular epi –> acid changes epi (metaplasia) –> squamous epi change (transformation zone)
where does cervical path take place?
transition zone - squamous epi (metaplasia) from columnar epi that bulged out during puberty
cervical histo
submucosa - ct and vessels
epi on top w/ basal layer –> smaller with less cytoplasm (higher nuc to cyto ratio) –> proliferative compartment –> cells mature outward
mucosa different than skin – no sweat, no hair, no keratin layer
endocervix histo
single layer of columnar cells that produce mucin with endocervical glands of invaginations
transformation zone
endocervical mucosa that becomes squamous mucosa
endocervical glands invaginations that have squamous epithelium on top
features of both
cervical histo key points
squamous + glandular components
transformation from glandular to squamous at puberty –> where pathology occurs
cervical cancer - who gets it? risks?
younger, healthier women - 45 y/o multiple sexual partners** early sex** high parity** smoking
high risk HPV exposure risk factors
cervical cancer pathology
ectocervical face - yellow, tan mucosa is normal; orange mass –> cancer
epithelium cells infiltrate into the stroma (past the BM)
2 cancer types: squamous (80%) and adenocarcinoma (minority)
squamous cell carcinoma - how do we ID in cervical cancer?
keratinization - dense pink material in and outside of cells
intracellular bridges - thin connections between individual tumor cells (desmosomes)
adenocarcinoma cervical cancer id?
forms glands
mucin production - special stain
what causes all cervical cancer
high risk HPV infection (16,18,31,33)
what leads to cervical cancer (squamous)?
dysplasia - CIN (cervical intraepithelial neoplasia) –> 3 grades (CIN I, II, III)
what drives dysplasia?
high risk HPV
CIN vs invasive carcinoma
CIN much more common than invasive squamous cell carcinoma –> much cases will resolve spontaneously (only 1% of CIN leads to cancer)
CIN I–>III–> cancer takes years
CIN histo with HPV infection
surface - koilocytes (big epi cells with lots of cyto, infected with HPV, big dark nuclei, binucleation, perinuclear clearing –> halo)
dysplastic cell - nuclei are big, irregular with a high nuclear to cytoplasmic ratio
different - koilocytes at surface, dysplastic at basal later; koilocyters lots of cyto, dysplastic little cyto;
CIN vs carcinoma
carcinoma - invades BM
CIN I vs II/III
II/III extend to surface
when does CIN peak?
mid 20’s - HPV is STD so related to sexual active
HPV - high risk types
16, 18, 31, 33 –> integrate into host chromosomes
low risk are 6,11 –> don’t integrate
HPV mechanism
proteins
E6 - degrades p53 (guardian of genome - fixes damages, stops cell cycle, apoptosis if not fixable)
E7 - binds Rb gene (Rb binds E2F until P by CDK4/cyclin D; if E2F free –> upregulates p16 –> cell cycle)
pap test
screening, requires confirmation via biopsy, not 100% sensitive but repeating testing will probably catch due to long natural hx
