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
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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.
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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.
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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
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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.
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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
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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
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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.
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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.
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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.
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11
Q

Characteristics of adenocarcinoma in situ

A

Hyperchromasia, mucin depletion, luminal mitoses, high N:C ratio, precursor to malignant cervical adenocarcinoma

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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).
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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.
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14
Q

5 most common epithelial and mesenchymal lesions of the uterine corpus

A
  • Endometrial polyps
  • Endometritis
  • Adenomyosis
  • Leiomyoma
  • Leiomyosarcoma
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15
Q

Clinical significance of endometrial polyps

A
  • proliferation of glands and stroma
  • Cause irregular bleeding and spotting
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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