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Life Cycles Unit 1 > Pathology of the uterus, vulva, and vagina > Flashcards

Pathology of the uterus, vulva, and vagina Flashcards

(52 cards)

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1
Q

endophytic

A

enDophytic = DOWN into the tissue

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2
Q

exophytic

A

OUT from the surface

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3
Q

Pagetoid

A

Single cells/clusters PERCOLATING through the epithelium

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4
Q

Molluscum Contagiosum

A

In adults, usually genital Common in children on extremities via sharing of towels Flesh colored, pearly skin lesions 1-5 mm, PAINLESS Endophytic growth with eosinophilic inclusion bodie

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5
Q

Condyloma Acuminatum

A

HPV 6 and 11 Hyperkeratosis and parakeratosis Especially papillae tips Hypergranulosis and elongated rete ridges Koilocytes

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6
Q

Koilocytes

A

Raisonoid nuclei Perinuclear clearing HPV!!

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7
Q

Trichomonas

A

flagellated protozoan; frothy yellow d/c, dysuria, dyspareunia; “strawberry cervix” on colposcopy

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8
Q

Candida

A

normal vaginal flora, but can overgrow (DM, Abx, pregnancy); curdlike d/c and pruritis

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9
Q

Actinomyces

A

“sulfur granule” with clublike projection non-copper IUD non-pathogenic

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10
Q

Vulvar Intraepithelial Neoplasia

A

Nuclear atypia (koilocytic) and lack of maturation= DYSPLASIA HPV 16, 18, other high-risk

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11
Q

VIN III / SCCIS

A

Increased mitoses, full thickness dysmaturity (cells at the surface look the same as those near the base)

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12
Q

HPV-associated SCC

A

♀

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13
Q

Inflammatory-associated SCC

A

♀ > 70 years HPV NEGATIVE Lichen sclerosus/d-VIN Prominent keratin “pearls” in well-differentiated carcinoma Increased mitoses, pink cytoplasm

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14
Q

Lichen Sclerosus

A

Smooth white plaques/papules, resembles parchment Dermal fibrosis with perivascular mononuclear infiltrate Thinned epidermis w loss of rete pegs, hydropic degeneration of basal cells & superficial hyperkeratosis

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15
Q

Extramammary Paget Disease

A

Adenocarcinoma variant Make sure it’s not melanoma Red, crusted sharply demarcated map-like area Marked hyperkeratosis and “pale” basal epidermis Tumor cells with “halo” lie singly or in clusters (with occasional gland formation *) in epidermis NOT usually associated with underlying invasive carcinoma

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16
Q

Malignant Melanoma

A
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17
Q

Embryonal Rhabdomyosarcoma

A

Cambium layer: Dense zone of rhabdomyoblast present beneath the surface epithelium Grossly: Polypoid, rounded, bulky masses which fills and protrude from vagina, resembling GRAPE-LIKE clusters (sarcoma botryoides)

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18
Q

Adenosis

A

Glandular tissue in vagina +/- DES exposure Present in 35-90% of exposed women Mucinous epithelium Can progress to clear cell carcinoma

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19
Q

DES-associated: Clear Cell Carcinoma

A

Tubulocystic pattern of growth with dense hyaline stroma; clear cytoplasm with bland nuclei “kissing lesion”: Anterior upper 1/3 of vagina, often w discontinuous areas

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20
Q

Endocervical Polyps

A

2-5% adult women Can cause “spotting” Curettage curative Dilated glands, dense eosinophilic stroma

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21
Q

Squamous Cell Carcinoma

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A

Increased mitoses, full thickness dysmaturity Infiltrating irregular nests of malignant squamous cells, eliciting a desmoplastic stromal response

22
Q

How is the staging of cervical cancer done?

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A

Unlike endometrial cancers, the STAGING of cervical cancers is based on clinical factors

23
Q

Adenocarcinoma in situ (AIS)

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A

Hyperchromasia Mucin Depletion Luminal Mitoses High N:C ratio Almost always HPV-related

24
Q

Proliferative phase of menstrual cycle

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A

Estrogen as mitogen Histology Straight tubular glands Mitoses (*) Nuclear stratification

25
Secretory Phase of menstrual cycle
↑ Progesterone, E2 falling Histology “S-shaped” tortuous, coiling glands, secretory activity Subnuclear vacuoles “piano keys”
26
Menstrual Phase
↓↓ E2 and Progesterone Histology Stromal/glandular breakdown Inflammation Intravascular fibrin
27
Exogenous Hormone Effect
Hypersecretory glands (short-term) Decidualized stromal cells Inactive glands (chronic)
28
Pregnancy
Hormones: Progesterone, hCG Histology: Stromal decidualization Arias-Stella Reaction Hypersecretory glands w architectural complexity, nuclear enlargement, no mitoses
29
Menopause
\>6 months without menstruation Thin endometrium w/o mitoses ↓ Cervical mucous and glycogenation Cystic atrophy
30
Abnormal Uterine Bleeding
Irregularity in menstrual cycle Amenorrhea- lack of menstruation Menorrhagia- heavy or prolonged Metrorrhagia- irregular Dysfunctional: no pathologic cause identified
31
Endometrial Polyps
Dense pink stroma, haphazardly arranged glands Cystic dilatation, hormonally unresponsive
32
Endometritis
Clinically PID Acute ↑ polys in stroma & glands (top) Curettage curative Chronic Plasma cells (bottom) Infertility
33
Adenomyosis/Endometriosis
Endometrial glands and stroma in abnormal location Infertility, dysmenorrhea In uterine wall = adenomyosis Extrauterine = endometriosis Activated inflammatory cascade
34
Leiomyoma
Gross: Single or multiple Spherical, Firm “White, Whorled” Well circumscribed Most common uterine tumor Menometrorrhagia, infertility, mass Whorled bundles of bland smooth muscle cells Hormonally responsive Treatment: Surgery Embolization GnRH agonist Nothing
35
Leiomyosarcoma
Malignant smooth muscle tumor Infiltrating, polypoid mass HIGH GRADE BY DEFINITION Hemorrhage, necrosis Most common uterine sarcoma 40-60 years Behavior: Rapid increase in size Metastasizes to lungs 5-year survival: 15-40%
36
Type I Endometrial Cancer
Pre-menopausal Risk factors: Unopposed estrogen, Genetics Background hyperplasia Minimal invasion/spread ER/PR positive
37
HNPCC
Mutated mismatch repair genes: Microsatellite instability 4 genes: MLH1, PMS2, MSH2, MSH6 Heterodimers with dominant & “recessive” element ♂ present w colon cancer; ♀ w endometrial cancer Women: 25-50% lifetime risk colorectal CA, 25-70% LR endometrial, 10% LR ovarian or stomach
38
Endometrial Hyperplasia
Physiologic response to unopposed estrogen: polyclonal process or EIN: clonal proliferation (PTEN mutation) AUB or asymptomatic Treatment: Hormonal Curettage Surgery
39
Simple Hyperplasia
Increased gland to stroma ratio Rarely progresses to cancer Treated with progestins Crowded, hyperchromatic glands Thickened, “fluffy” endometrium
40
Complex Hyperplasia
+/- Atypia Glandular crowding and architectural complexity 5-30% progress to cancer Diffuse involvement of endometrial cavity
41
Endometrial Carcinoma
Usually PMB, but many asymptomatic Peak in 5th and 6th decades 85% endometrioid Resembles endometrial glands Exophytic (protruding) mass of tightly packed glands without intervening stroma
42
Prognosis of endometrial carcinoma
Depends on stage and spread
43
Treatment of endometrial carcinoma
Surgery Radiation Vaginal brachy Whole pelvis Chemotherapy
44
Type II Endometrial Cancer
Post-menopausal Aggressive 10-20% endometrial cancers p53 mutation
45
Serous Carcinoma
Type II cancer Papillary growth, atypia Disseminated at presentation
46
Malignant Mixed Müllerian Tumor (Carcinosarcoma)
Biphasic tumor Homologous (left) vs Heterologous (right)
47
What are the most important lesions to remember in a patient with abnormal uterine bleeding?
polyps, adenomyosis, leiomyomas, hyperplasia and carcinoma But most cases aren't due to lesions
48
Grade vs stage
GRADE is the degree of differentiation STAGE is the extent of spread
49
Difference between type I and type II endometrial cancers
Type I endometrial cancers occur in younger women and are estrogen-dependent with a generally good prognosis Type II endometrial cancers occur in older women, have higher grade histology and poorer prognosis
50
What gene(s) is (are) mutated in type II endometial cancers usually?
p53
51
What gene(s) is (are) mutated in type I endometial cancers usually?
BRAF, mismatch repair proteins (MLH-1), β-catenin
52
What is this?
Lichen sclerosis

Life Cycles Unit 1 (17 decks)

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