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

Pathology of the uterus, vulva, and vagina Flashcards

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

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?

A

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

23
Q

Adenocarcinoma in situ (AIS)

A

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

24
Q

Proliferative phase of menstrual cycle

A

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

25
Q

Secretory Phase of menstrual cycle

A

↑ Progesterone, E2 falling Histology “S-shaped” tortuous, coiling glands, secretory activity Subnuclear vacuoles “piano keys”

26
Q

Menstrual Phase

A

↓↓ E2 and Progesterone Histology Stromal/glandular breakdown Inflammation Intravascular fibrin

27
Q

Exogenous Hormone Effect

A

Hypersecretory glands (short-term) Decidualized stromal cells Inactive glands (chronic)

28
Q

Pregnancy

A

Hormones: Progesterone, hCG Histology: Stromal decidualization Arias-Stella Reaction Hypersecretory glands w architectural complexity, nuclear enlargement, no mitoses

29
Q

Menopause

A

>6 months without menstruation Thin endometrium w/o mitoses ↓ Cervical mucous and glycogenation Cystic atrophy

30
Q

Abnormal Uterine Bleeding

A

Irregularity in menstrual cycle Amenorrhea- lack of menstruation Menorrhagia- heavy or prolonged Metrorrhagia- irregular Dysfunctional: no pathologic cause identified

31
Q

Endometrial Polyps

A

Dense pink stroma, haphazardly arranged glands Cystic dilatation, hormonally unresponsive

32
Q

Endometritis

A

Clinically PID Acute ↑ polys in stroma & glands (top) Curettage curative Chronic Plasma cells (bottom) Infertility

33
Q

Adenomyosis/Endometriosis

A

Endometrial glands and stroma in abnormal location Infertility, dysmenorrhea In uterine wall = adenomyosis Extrauterine = endometriosis Activated inflammatory cascade

34
Q

Leiomyoma

A

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
Q

Leiomyosarcoma

A

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
Q

Type I Endometrial Cancer

A

Pre-menopausal Risk factors: Unopposed estrogen, Genetics Background hyperplasia Minimal invasion/spread ER/PR positive

37
Q

HNPCC

A

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
Q

Endometrial Hyperplasia

A

Physiologic response to unopposed estrogen: polyclonal process or EIN: clonal proliferation (PTEN mutation) AUB or asymptomatic Treatment: Hormonal Curettage Surgery

39
Q

Simple Hyperplasia

A

Increased gland to stroma ratio Rarely progresses to cancer Treated with progestins Crowded, hyperchromatic glands Thickened, “fluffy” endometrium

40
Q

Complex Hyperplasia

A

+/- Atypia Glandular crowding and architectural complexity 5-30% progress to cancer Diffuse involvement of endometrial cavity

41
Q

Endometrial Carcinoma

A

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
Q

Prognosis of endometrial carcinoma

A

Depends on stage and spread

43
Q

Treatment of endometrial carcinoma

A

Surgery Radiation Vaginal brachy Whole pelvis Chemotherapy

44
Q

Type II Endometrial Cancer

A

Post-menopausal Aggressive 10-20% endometrial cancers p53 mutation

45
Q

Serous Carcinoma

A

Type II cancer Papillary growth, atypia Disseminated at presentation

46
Q

Malignant Mixed Müllerian Tumor (Carcinosarcoma)

A

Biphasic tumor Homologous (left) vs Heterologous (right)

47
Q

What are the most important lesions to remember in a patient with abnormal uterine bleeding?

A

polyps, adenomyosis, leiomyomas, hyperplasia and carcinoma But most cases aren’t due to lesions

48
Q

Grade vs stage

A

GRADE is the degree of differentiation STAGE is the extent of spread

49
Q

Difference between type I and type II endometrial cancers

A

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
Q

What gene(s) is (are) mutated in type II endometial cancers usually?

A

p53

51
Q

What gene(s) is (are) mutated in type I endometial cancers usually?

A

BRAF, mismatch repair proteins (MLH-1), β-catenin

52
Q

What is this?

A

Lichen sclerosis

Life Cycles Unit 1 (17 decks)

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