215. Pathology of Cervix, Vagina, Vulva Flashcards
Cervix:
- describe the changes that occur during menarche
- what is the ectocervix, endocervix, and transition zone?
Menarche: hormonal milieu causes glandular component to evert to ectocervix - metaplasia can occur due to inflammation/irritation to exposed glandular epithelium
Ectocervix: stratified squamous epithelium (cytoplasm expands with glycogen), basal layer is proliferative, replenishes epithelium; submucosa
Endocervix: simple columnar epithelium (mucin-filled = blue cytoplasm), glandular mucosa (connect to lumen or entrapped= cysts), submucosa
Transformation Zone: from ecto to endocervix; vulnerable to HPV (metaplastic squamous epithelium)
Cervical Cancer
- 4 risk factors
- most common kind (signs)
- 2nd most common kind
- most common etiology
- time course
- histo
- mild vs. moderate vs. severe dysplasia
RF: multiple sexual partners, early initiation of sexual activity, high parity, smoking
most common: SCC: large mass on cervix, tumor cells (nests of infiltrative glands into submucosa), keritinization and intracellular bridges (spines)
2nd most common: adenocarcinoma (infiltrative gland formation from endocervix)
HR HPV - in most cases of dysplasia, invasive carcinoma, most cases resolve spontaneously
time: takes ~10 YEARS from low grade to high grade, and more years to then get invasive carcinoma
Histo: Koilocytes (HPV infected cells) - raisin nuclei, perinuclear halo
Mild: dysplastic cells in lower 1/3 epithelium (high N:C, dark chromatin, mitosis)
Moderate: dysplastic cells in middle 1/3 epithelium
Severe: dysplastic cells in upper 1/3 epithelium
HPV
- what do its viral proteins do
How do you screen for a dysplastic lesion?
E6 = targets p53 degradation = no apoptosis, more DNA damage, more cell division
E7 = binds Rb and frees E2F = promote cell division
- removes negative fb on p16 = accumulation of p16 (IHC STAIN FOR DYSPLASIA)
PAP SMEAR: ID dysplastic lesions before they progress to carcinoma
Condyloma Acuminatum
- what is it
- cause
- malignancy risk
- path
Condyloma Acuminata
Multiple genital warts due to HPV 6,11
- not premalignant
Path: koilocytes, papillae with fibrovascular core, epithelial thickening (acanthosis = squamous hyperplasia)
Lichen Sclerosus
- what is it
- demographics
- cause
- malignancy risk
Thinning (atrophy) of epithelium with stromal hyalinization (dense fibrotic stoma)
demo: older pts with white scaly plaques
Cause: autoimmune or low E (post-mp women)
CAN LEAD TO INVASIVE SCC (neoplastic!)
Lichen Simplex Chronicus
- what is it
- cause
- malignancy risk
AKA squamous cell hyperplasia
anywhere on skin; caused by chronic irritation (itching) induced hyperplasia (thickened epidermis) and hyperkeratosis
BENIGN lesion
Vulvar SCC
- pathways/pgen
- demographics of each pathway
- histo
Type 1: USUAL - HPV driven (LSIL > HSIL) = 30%
- younger women
Type 2: DIFFERENTIATED - assoc with p53 mutations or LICHEN SCLEROSIS = 70%
- older women
- parakeratosis: nuclei within keratin layer
Histo: infiltrating squamous cell nests
Vulvar Paget Disease
- what is it
- malignancy risk
- path
Crusted red vulvar/perianal lesion
SIGN OF CANCER SPREAD
can spread from neoplasm of sweat glands or skin adnexae; or represent internal malignancy (colon, urothelial ca)
Path: neoplastic glandular cells proliferate thru epidermis (Pagetoid pattern - spread without invasion)
HSV-2 vs. Syphilis
- CP
- Path
HSV-2
- painful palpable vesicles > ulcer, may be recurrent
- Path: Multinucleated cells, Molding nuclei, Margination (chromatin pushed to edge by viral proteins), Cowdry bodies (pink nuclear inclusions)
Syphilis
- Primary: painless chancre, numerous perivascular plasma cells
- Secondary: highest bacteremia, condyloma lata (plaques/papules on genitalia, palms, soles, vaginal/oral mucosa), rash, perivascular plasma cell infiltrate
- Tertiary: aortitis, CNS, gummas (necrotic center surrounded by histiocytes - granulomatous rxn)
