Pathology of the Uterus, Vagina, and Vulva Flashcards
1
Q
Dx?
A
- HSV 1/2
- Painful red lesions 3-7 days after exposure. HSV-2 is >70% , causes eosinophilic intranuclear inclusions
2
Q
Dx?
A
- Molluscum Contagiosum
- In adults, usually genital.
- Common in children sharing towels, found on extremities.
- Flesh colored, pearly skin lesions.
- 1-5 mm, painless.
- Shows endophytic growth with eosinophilic inclusion bodies.
3
Q
Dx?
A
- Condyloma Acuminatum
- sexually transmitted (HPV), benign lesions that have a distinct verrucous gross appearance.
- may be solitary, they are more frequently multifoca
- may involve vulvar, perineal, and perianal regions
- ess commonly cervix
- The lesions are identical to those on penis/anus males.
- Shows hyperkeratosis and perakeratosis, especially in papillae tips.
4
Q
Common infections of vulva/vagina
A
- Trichomonas
- flagellated protozoan
- “stawberry cervix” on colposcopy
- Candida
- overgrown in DM, abx, pregnancy
- curdlike, pruritis
- Actinomyces
- “sulfur granule” + club-liek projections
- non-copper IUD
5
Q
Dx?
A
- Bartholin cyst
- relatively common, occur at all ages, and result from obstruction of the duct by an inflammatory process (often infection)
- The resulting cysts are lined by the ductal squamous metaplastic and/or epithelium.
- They may become large, up to 3 to 5 cm in diameter, and produce pain and local discomfort.
- Bartholin duct cysts are either excised or opened permanently.
6
Q
Dx?
A
- Classic VIN is characterized by nuclear atypia of the squamous cells, ↑ mitoses, lack of cellular maturation.
- Reproductive-aged women
- Same risk factors as those for cervical squamous intraepithelial lesions
- Most VIN: HPV 16+, less frequently HPV 18+ or 31+.
- Discrete white (hyperkeratotic), flesh colored or pigmented, slightly raised lesions
- Classic precursor of SCC
7
Q
Dx?
A
- Lichen sclerosis
- thinning of the epidermis
- disappearance of rete pegs, hydropic degeneration of the basal cells
- superficial hyperkeratosis, and dermal fibrosis
- scant perivascular mononuclear inflammatory cell infiltrate.
- It occurs in all age groups but is most common in postmenopausal women.
- Possible autoimmune involvement
8
Q
Characteristics of HPV-associated SCC
A
- Basaloid cells (dark staining, poorly differentiated cells) are in the infiltrating cords and nests.
- Characterized by increased mitoses, loss of maturity in the full thickness of the epithelium and infiltrating nests/cords of malignant cells which elicit a desmoplastic stroma response.
- These tumors often grow upwards from the cervix.
9
Q
Characteristics of non-HPV related/inflammatory-associated SCC
A
- Keratizing squamous cell carcinomas often arise in patients with long standing lichen sclerosus (precursor lesion)
- This present in older woman, avg age 76
- It is characterized by atypia of the basal cell layer, but with normal appearing epithelial maturation and differentiation, keratin pearls and lots of pink cytoplasm.
10
Q
Dx?
A
- Endocervical polyps are benign exophytic growths that occur in 2% to 5% of adult women.
- polyps ==> irregular vaginal “spotting” or bleeding that arouses suspicion of some more ominous lesion.
- Most polyps arise within the endocervical canal and vary from small and sessile to large, 5 cm masses that may protrude through the cervical os.
- All are soft, almost mucoid, lesions composed of a loose fibromyxomatous stroma harboring dilated, mucus secreting endocervical glands, often accompanied by inflammation.
- Simple curettage or surgical excision effects a cure. Have to check them out to make sure they are benign.
11
Q
Characteristics of adenocarcinoma in situ
A
Hyperchromasia, mucin depletion, luminal mitoses, high N:C ratio, precursor to malignant cervical adenocarcinoma
12
Q
Pathogenesis of dysplasia/carcinoma in vulva, vagina, cervix
A
- Most dysplasia in lower genital tract is HPV related and can progress to cancer.
- Infection with HPV 16 and 18 are high risk factors.
- Viral E6 and E7 ==> oncogenic effects of HPV
- promote cell cycle by binding to RB and up-regulation of cyclin E (E7);
- interrupt cell death pathways by binding to p53 (E6)
- induce centrosome duplication and genomic instability (E6, E7); and prevent replicative senescence by up-regulation of telomerase (E6).
13
Q
Mechanism of HPV E6 & E7 ==> carcinoma
A
- HPV E6 induces rapid degradation of p53 via ubiquitin-dependent proteolysis, reducing p53 levels by two- to three-fold.
- E7 complexes with the hypophosphorylated (active) form of RB, promoting its proteolysis via the proteosome pathway
- hypophosphorylated RB normally inhibits S-phase entry via binding to the E2F transcription factor
- the two viral oncogenes cooperate to promote DNA synthesis while interrupting p53-mediated growth arrest and apoptosis of genetically altered cells.
14
Q
5 most common epithelial and mesenchymal lesions of the uterine corpus
A
- Endometrial polyps
- Endometritis
- Adenomyosis
- Leiomyoma
- Leiomyosarcoma
15
Q
Clinical significance of endometrial polyps
A
- proliferation of glands and stroma
- Cause irregular bleeding and spotting
16
Q
Clinical significance of endometritis
A
- looks like PID clinically. Can be acute or chronic.
- Acute: ↑ PMN in stroma and glands,
- Curettage is curative
- Chronic: Plasma cells and Infertility
- Caused by IUD (chronic) as a method of preventing pregnancy
- Both can cause abnormal bleeding
17
Q
Clinical significance of Adenomyosis/Endometriosis
A
- Adenomyosis (within myometrium of uterus) /Endometriosis (extrauterine)
- Endometrial glands and stroma in abnormal location
- Leads to infertility and dysmenorrhea
- Activated inflammatory cascade
18
Q
Clinical significance of leiomyoma
A
- Leiomyoma (fibroids)
- Gross: single or multiple, spherical, firm, “white and whorled”, well circumscribed
- Infertility, dysmenorrhea, abnormal bleeding
- Often asymptomatic, totally benign
- Treat with surgery, embolization, nothing
19
Q
Characteristics of leiomyosarcoma
A
- Leiomyosarcoma
- Malignant smooth muscle tumor
- Infiltrating, polypoid mass, hemorrhage, necrosis
- Most common uterine sarcoma, esp in women 40-60 (but still quite rare)
- Really bad. Difficult to treat - doesn’t respond well to chemo or radiation and recur after surgical removal.
- > 50% metastasize.
- 5yr survival: ~40%, but only 10-15% for anaplastic lesions
20
Q
Type I endometrial carcinoma: clinical setting, morphology, precursor
A
- Clinical setting
- Unopposed Estrogen
- Obesity
- Hypertension
- Diabetes
- Morphology
- Endometroid appearance of malignant glands = crowded, irregularly-shaped
- Hyperplasia
21
Q
Type I endometrial carcinoma: molecular genetics
A
- PTEN - tumor suppressor gene
- PIK3CA
- KRAS
- Microsatellite instability
- β-catenin
- p53
22
Q
Type I endometrial carcinoma: behavior, tx, other, sx
A
- Behavior
- Indolent,
- Spreads via lymphatics
- Other facts
- More common
- Peak incidence in 5th/6th decade
- Good prognosis
- Tx
- Hormonal, curretage, surgery
- Sx
- Abnormal uterine bleeding postmenopausal, or asymptomatic
23
Q
Type II endometrial carcinoma: behavior, tx, other, sx
A
- Behavior
- Aggressive
- Intraperitoneal and lypmhatic spread
- Other facts
- Post menopausal
- Older women → 65-75 yrs
- Poor prognosis
- Tx
- Surgery, Chemotherapy, Radiation
- Sx
- Post menopausal bleeding, shortness of breath if already metastasized
24
Q
Type II endometrial carcinoma: clinical setting, morphology, precursor, molecular genetics
A
- Clinical setting
- Post-menopausal
- Atrophy
- Thin physique
- Morphology
- Serous - (pic) prototypical type 2 tumor
- Clear cell, Mixed mullerian tumor
- Poorly differentiated
- Worse histologic changes
- Precursor
- Endometrial intraepithelial carcinoma
- Genetics
- p53 - guardian of the genome
- Aneuploidy
- PIK3CA
25
Q
Type I endometrial carcinoma progression
A
26
Q
Type II endometrial carcinoma progression
A
