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GU / GYN & Renal > Overview: GYN Pathology > Flashcards

Overview: GYN Pathology Flashcards

1
Q

Vulva

  • Raised, wart-like growths
  • Infectious etiology or reactive conditions of unknown etiology
    • Conditions with unknown etiology:
      • Fibroepithelial polyps (skin tags)
      • Vulvar squamous papillomas
    • Conditions with sexual transmission:
      • Condyloma acuminatum (HPV)
      • Condyloma larum (syphilis)
A

Benign exophytic lesions

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2
Q

Vulva

  • Benign genital warts caused by HPV infection
    • Low oncogenic risk HPV –> types 6 & 11
  • Sexually transmitted
  • Occur in vulva, perineum, perianal region & anus, vagina, and cervix (less commonly)
    • Penile, urethral, and perianal condylomata in men
  • Usually multiple lesions (may be solitary)
A

Condyloma acuminata (genital wart)

Benign exophytic lesion

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3
Q

Vulva

  • Architecture: papillary, exophytic
    • Tree-like FV cores of stroma covered by thickened squamous epithelium
  • Epithelium: koilocytic atypia
    • Nuclear enlargement
    • Nuclear hyperchromasia
    • Multinucleation
    • Perinuclear cytoplasmic vacuolization (halo)

Histology

A

Condylomata acuminata

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4
Q
  • Rare malignant neoplasm: 3% of genital cancers in females
  • 30% associated with high-risk HPV (type 16)
    • Classic VIN
    • Develops from in situ lesion
  • 70% not related to HPV
    • Differentiated VIN
    • Develops from premalignant lesion

Epidemiology

VIN = vulvar intraepithelial neoplasia

A

Vulvar carcinoma

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5
Q

Vulva

  • Younger age
  • Multifocal lesions
  • A/w CIN and/or VAIN
  • Hx: STD, smoking, immunodeficiency
  • Precursor to basaloid & warty carcinomas
A

Classic VIN

VIN, HPV positive (16) type

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6
Q

Vulva

  • Older age
  • Unifocal lesions
  • A/w inflammation, lichen sclerosus por squamos cell hyperplasia
  • p53 mutation
  • Precursor to keratinized squamous carcinomas
A

Differentiated VIN (VIN simplex)

VIN, HPV negative type

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7
Q

Vulva

  • In situ lesion
  • Epidermal thickening
  • Nuclear atypia & enlargement
  • Hyperchromasia
  • Increased mitoses & lack of cell maturation w/ small basaloid cells extending to surface
    • Basaloid = blue cells with high N:C ratio
    • Basaloid cells span entire epithelium

Histology

A

Classic VIN

VIN, HPV-pos

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8
Q

Vulva

  • Invasive lesion
  • Nests & cords of small, immature basaloid cells
    • Immature cells resembling basal layer of normal epithelium
  • Invasive tumor w/ central necrosis

Histology

A

Basaloid vulvar carcinoma

VIN, HPV-pos; basaloid & warty carcinoma

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9
Q

Vulva

  • In situ lesion
  • Mature superficial layers & atypia of basal layer
    • Basal cells at basal layer
    • Differentiated cells towards surface
  • Hyperkeratosis

Histology

A

Differentiated VIN

VIN, HPV-neg

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10
Q

Vulva

  • Invasive lesion
  • Nests & cords of malignant squamous epithelium with keratin pearls

Histology

A

Well-differentiated vulvar SCC

HPV-neg; keratinized squamous carcinoma

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11
Q

Vulva

  • Pruritis
  • Pain
  • Discharge
  • Bleeding

Clinical Presentation

A

Vulvar SCC

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12
Q

Vulva

  • Usually solitary lesion
  • Exophytic mass +/1 ulceration
  • Ulcerated tumors may mimic STD

Histology

A

Vulvar SCC

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13
Q

Vulva

  • Spread: direct extension to adjacent structures
    • Urethra, bladder, vagina, anus, rectum
  • Metastases: femoral & inguinal lymph nodes
    • Distant metastases may occur (e.g., bone)
  • Recurrence: usually local
A

Vulvar SCC

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14
Q

Vagina

Normal pre-menopausal vaginal mucosa

Histology

A
  • Stratified squamous epithelium
  • Non-keratinized
  • Rich in glycogen, driven by estrogen
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15
Q

Vagina

Normal post-menopausal vaginal mucosa

Histology

A
  • Stratified squamous epithelium
  • Non-keratinized
  • Atrophic
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16
Q

Vagina

Normal stratified squamous epithelium

Histology

A
  • Basal cells
    • Small undifferentiated cells that resemble histiocytes
    • Seldom seen in pap smear –> sometimes w/ atrophy
  • Parabasal cells
    • 1st to acquire squamous features
      • Dense cytoplasm / cell borders
    • Moderate cytoplasm & nuclei (50 um)
    • Cytoplasm = abundant, thin, blue, transparent
  • Intermediate cells
    • Key reference for nuclear size
      • Nucleus = RBC (35 um)
    • Chromatin = fine texture; normochromatic
    • Slightly larger than parabasal cells
  • Superficial cells
    • Final surface cell type
    • Similar to intermediate cells except pyknotic nuclei (India ink dot-like)
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17
Q

Vagina

  1. HPV infection
  2. VIN / CIN or vulvar / cervical SCC
  3. Immunosuppression
  4. Prior pelvic irradiation for benign or malignant disease

Risk Factors

A

Vaginal cancer

Both VAIN & vaginal SCC

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18
Q

Tumor associated with in utero / prenatal exposure to diethylstilbestrol (DES)

A

Vaginal clear cell carcinoma

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19
Q

Vagina

Most common primary malignant vaginal neoplasm in adults

A

Vaginal SCC

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20
Q

Vagina

  • Rare tumor: 0.6/100,000 women/year
  • Secondary carcinoma more common than primary
    • Direct extension or metastasis via lymphatics / blood vessels
    • Especially from cervical SCC
  • Most patients are post-menopausal

Epidemiology

A

Vaginal SCC

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21
Q

Vagina

  • Painless vaginal bleeding / discharge
  • Dysuria
  • Urinary frequency

Clinical Presentation

A

Vaginal SCC

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22
Q

Vagina

  • Tumors range from microscopic to large
  • May be indurated, ulcerated, or exophytic

Gross Appearance

A

Vaginal SCC

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23
Q

Vagina

  • Spread: direct extension to mucosa of bladder or rectum
  • Metastases: inguinal or pelvic lymph nodes
    • Distant metastases may occur (e.g., pulmonary)
  • Recurrence: usually local
A

Vaginal SCC

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24
Q

Vagina

Greatest risk factor for vaginal SCC

Risk Factors

A

Previous carcinoma of cervix / vulva

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25
Q

Cervix

Ectocervix vs. Endocervix

Histology

A
  • Ectocervix: mature stratified squamous epithelium; outside external os
  • Endocervix: columnar, mucus-secreting epithelium; between internal os & external os
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26
Q

Cervix

Region of cervix susceptible to HPV infections

A

Transformation zone

Columnar epithelium abuts squamous epithelium; immature squamous cells

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27
Q
  • Approx. 90% of deaths occur in low- & middle-income countries
  • Highest incidence: Latin America, the Caribbean, Africa, and South & Southeast Asia

Epidemiology

A

Cervical cancer

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28
Q

Infections

  • Common cause of STD in US & worldwide
  • Can progress to CIN & invasive SCC
A

HPV

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29
Q

HPV

HPV types 6 & 11

Genotypes

A
  • Low-risk oncogenes
  • Benign cervical changes
  • Progress to genital warts
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30
Q

HPV

HPV types 16 & 18

Genotypes

A
  • High-risk oncogenes
  • Premalignant cervical changes
  • Progress to cervical cancer, anal & other cancers
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31
Q

HPV

Natural history of HPV infection

A
  • Within 1 year: initial HPV infection –>
    • Cleared HPV infection
    • CIN 1 –> cleared HPV infection
    • CIN 1 –> persistent infection
    • Persistent infection
  • 1-5 years: persistent infection –>
    • CIN 2/3
    • CIN 2/3 –> cleared HPV infection
  • Decades: CIN 2/3
    • Cervical cancer
  • HPV infection is cleared in 6-12 mos in 70% of women, <24 mos in 90% of women
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32
Q

Cervix

  • Mild cervical dysplasia (CIN 1)
  • Clinical & morphological manifestation of productive HPV infection
  • Most common & benign form of CIN
  • Usually resolves spontaenously within 2 years
  • Low-risk of concurrent or future cancer

Bethesda System

A

LSIL

LSIL = low-grade squamous intraepithelial lesion

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33
Q

Cervix

  • Moderate & severe dysplasia (CIN 2/3)
  • CIS (CIN 3)
  • Significant risk of progressing to invasive cancer if untreated

Categories of squamous cell abnormalities

A

HSIL

HSIL = high-grade squamous intraepithelial lesion

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34
Q

Cervix

Squamous Intraepithelial Lesions

A
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35
Q

Cervix

  • Proliferation of basal / parabasal cels with abnormal nuclear features
  • Little cytoplasmic maturation in lower third but maturation begins in middle third & is relatively normal in upper third
    • Mitotic figures limited to lower third of epithelium
  • Diagnostic HPV cytopathic effect = koilocytes:
    • Multinucleation
    • Nuclear enlargement & pleomorphism
    • Nuclear hyperchromasia
    • Nuclear membrane irregularities
    • Perinuclear halos

Histology

A

LSIL

Previously CIN 1

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36
Q

Cervix

  • Abnormal nuclear features:
    • Increased nuclear size & N:C ratios
    • Irregular nuclear membranes
  • Little / no cytoplasmic differentiation in middle & upper thirds of epithelium
    • Mitotic figures may be found in middle and/or upper thirds of epithelium

Histology

A

HSIL

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37
Q

Cervix

Spectrum of CIN

Classification

A
  1. Normal: normal squamous epithelium
  2. LSIL (CIN 1): koilocytic atypia
  3. HSIL (CIN 2): progressive atypia & expansion of immature basal cells above lower 1/3 of epithelium
  4. HSIL (CIN 3): diffuse atypia; loss of maturation & expansion of immature basal cells to epithelial surface
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38
Q

Cervix

  1. Average age: 40-50 yo
  2. High-risk HPV exposure: early age at 1st intercourse, multiple sexual partneres
  3. Smoking
  4. Immunodeficiency

Risk Factors

A

Invasive cervical SCC

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39
Q

Cervix

  • Vaginal bleeding (especially post-coital)
  • Cervical discharge
  • Dyspareunia (painful intercourse)
  • Dysuria

Clinical Presentation

A

Invasive cervical SCC

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40
Q

Cervix

Invasive cervical SCC

Treatment

A

Surgical
* Small tumors: cone biopsy
* Large tumors: hysterectomy & LN dissection

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41
Q

Cervix

  • Endocervical glands lined by crowded, atypical epithelial cells
  • Hyperchromatic nuclei containing coarse or granular chromatin
  • Increased N/C ratio
  • Mitotic figures common

Histology

A

Cervical adenocarcinoma in situ (AIS)

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42
Q

Cervix

Most common histologic type of cervical adenocarcinoma

A

Usual type
* Glands exhibit a hybrid of endocervical & endometrioid differentiatiom

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43
Q

Cervix

  • Patients are usually asymptomatic
  • Symptomatic patients present with abnormal vaginal bleeding

Clinical Presentation

A

Cervical AIS

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44
Q

Cervix

Cervical AIS

Epidemiology

A
  • Less common than CIN (SIL)
  • Associated with high-risk HPV (most frequently type 18)
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45
Q

Cervix

Cervical AIS

Approach to Diagnosis

A
  • Incidental finding in cervical biopsy done for CIN
  • Abnormal glandular cells detected on Pap smear
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46
Q

Menstrual Cycle

Days 0 - 14

A
  • LH & FSH: peak before ovulation
    • LH surge at ~Day 14 triggers ovulation
  • Estrogen: peaks before ovulation
    • Secreted by follicle
  • Progesterone: low
  • Ovary: follicular phase; ends with ovulation
    • Ovum is ejected from follicle
    • Remaining follicle becomes corpus lutem
  • Endometrium: proliferative phase
    • Driven by estrogen
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47
Q

Menstrual Cycle

  • Tubular shaped glands
  • Pseudostratified nuclei
  • Mitotic figures present

Histology

A

Proliferative endometrium

Cycle day 1-15

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48
Q

Menstrual Cycle

Days 15 - 28

A
  • LH & FSH: low
  • Estrogen: low
  • Progesterone: high
    • Secreted by corpus luteum in ovary
  • Ovary: luteal phase
  • Endometrium: secretory phase
    • Driven by progesterone
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49
Q

Uterus

Increased proliferation of the endometrial glands relative to the stroma, resulting in crowded glands
* Tends to be diffuse but may occasionally be focal

Pathophysiology

A

Endometrial hyperplasia

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50
Q

Uterus

  • Increased gland/stroma ratio compared to normal proliferative endometrium
  • Glands with abnormal shapes, irregular sizes

Histology

A

Endometrial hyperplasia

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51
Q

Uterus

Prolonged estrogen stimulation of endometrium

Etiology

A

Endometrial hyperplasia

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52
Q

Uterus

Endometrial hyperplasia

Potential complications

A
  • Important cause of abnormal bleeding
  • Malignant potential: continued prolfieration of glandular lesions may culminate in carcinoma
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53
Q

Uterus

Associated with mutation in PTEN tumor suppressor gene

Etiology

A

Endometrial hyperplasia

PTEN is mutated in ~20% of endometrial hyperplasias

`

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54
Q

Uterus

Associated with mutation in PTEN tumor suppressor gene

Etiology

A

Endometrial hyperplasia

PTEN is mutated in ~20% of endometrial hyperplasias

`

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55
Q

Uterus

Types of endometrial hyperplasia

Histology

A
  • Simple hyperplasia
  • Complex hyperplasia
  • Atypical hyperplasia
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56
Q

Uterus

  • Mild crowding of glands
  • “Swiss cheese” appearance
  • No cytologic atypia
    • Nuclei are correctly polarized, with cell’s long axis perpendicular to gland luminal plane
    • Absence of eosinophilic macronucleoli

Histology

A

Simple endometrial hyperplasia

Cystic dilation of glands: lumens resembles holes in swiss cheese

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57
Q

Uterus

  • Moderate-to-severe glandular crowding
  • Irregular / branched glands
  • No cytologic atypia: no loss of polarity; no macronucleoli

Histology

A

Complex endometrial hyperplasia

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58
Q

Uterus

  • Severe glandular crowding
  • Irregular / round glands
  • Nuclear atypia
    • Stratification & loss of polarity
    • Vesicualr chromatin & nucleoli

Histology

A

Atypical endometrial hyperplasia

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59
Q

Uterus

Most common invasive cancer of the female genital tract

A

Endometrial carcinoma

Accounts for 7% of all invasive cancers in women

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60
Q

Uterus

  • Increased life expectancy
  • Tamoxifen use
  • Obesity

Risk Factors

A

Endometrial carcinoma

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61
Q

Uterus

Types of endometrial carcinoma

Histology

A
  • Type 1: estrogen-dependent adenocarcioma w/ endometroid morphology
  • Type 2: non-estrogen dependent adenocarcinoma
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62
Q

Uterus

Age: 55-65 yrs

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 1

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63
Q

Uterus

Clinical setting
* Unopposed estrogen
* Obesity
* Hypertension
* Diabetes

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 1

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64
Q

Uterus

Morphology: endometrioid

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 1

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65
Q

Uterus

Precursor: atypical endometrial hyperplasia

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 1

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66
Q

Uterus

Genetic abnormalities
* Mutations in MMR genes
* Mutations in PTEN tumor suppressor gene

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 1

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67
Q

Uterus

Behavior: indolent; spreads via lymphatics

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 1

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68
Q

Uterus

Most common type of endometrial carcinoma

A

Endometrial carcinoma, type 1

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69
Q

Uterus

Age: 65-75 yrs

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 2

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70
Q

Uterus

Clinical setting:
* Endometrial atrophy
* Thin physique

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 2

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71
Q

Uterus

Morphology: serous; clear cell; mixed mullerian tumor

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 2

72
Q

Uterus

Precursor: serous endometrial intraepithelial carcinoma

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 2

73
Q

Uterus

Genetic abnormalities:
* Mutations in TP53 TSG

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 2

Mutations in DNA MMR genes & PTEN are rare

74
Q

Uterus

Behavior: aggressive; intraperitoneal & lymphatic spread

Characteristics of Endometrial Carcinoma

A

Endometrial carcinoma, type 2

75
Q

Uterus

Presents as a fungating mass in the uterus

Gross Appearance

A

Endometrial carcinoma, type 1

76
Q

Uterus

Endometrioid adenocarcinoma w/ preserved glandular architecture but lack of intervening stroma
* Less than 5% solid growth

Histology

A

Well-differentiated (grade 1) endometrial carcinoma, type 1

Lack of intervening stroma distinguishes carcinoma from hyperplasia

77
Q

Uterus

Endometrioid adenocarcinoma w/ glandular architecture admixed with solid areas
* Less than 50% solid growth

Histology

A

Moderately differentiated (grade 2) endometrial carcinoma, type 1

78
Q

Uterus

Endometrioid carcinoma w/ predominantly solid growth
* Greater than 50% solid growth

Histology

A

Poorly differentiated (grade 3) endometrial carcinoma, type 1

79
Q

Uterus

Subtypes of type 2 endometrial carcinoma

Histology

A
  1. Serous endometrial carcinoma
  2. Clear cell endometrial carcinoma
80
Q

Uterus

Most common subtype of endometrial carcinoma, type 2

A

Serous endometrial carcinoma

81
Q

Uterus

Nuclei are oval, mildly enlarged, and have evenly dispersed chromatin

Endometrial Carcinoma: Nuclear Grading

A

Grade 1

82
Q

Uterus

Nuclei are markedly enlarged & pleomorphic, with irregular coarse chromatin, and prominent eosinophilic nucleoli

Endometrial Carcinoma: Nuclear Grading

A

Grade 3

83
Q

Uterus

Nuclei have features intermediate to grades 1 & 3

Endometrial Carcinoma: Nuclear Grading

A

Grade 2

84
Q

Uterus

<5% of tumor composed of solid masses

Endometrial Carcinoma: Architectural Grading

A

Grade 1

85
Q

Uterus

<50% of tumor composed of solid masses

Endometrial Carcinoma: Architectural Grading

A

Grade 2

86
Q

Uterus

> 50% of tumor composed of solid masses

Endometrial Carcinoma: Architectural Grading

A

Grade 3

87
Q

Endometrial Carcinoma: Architectural Grading

Carcinoma confined to corpus uteri itself

Endometrial Carcinoma: Staging

A

Stage I

88
Q

Uterus

Carcinoma involves corpus & cervix

Endometrial Carcinoma: Staging

A

Stage II

89
Q

Uterus

Carcinoma extends outside uterus but not outside pelvis

Endometrial Carcinoma: Staging

A

Stage III

90
Q

Uterus

Carcinoma extends outside pelvis or involves mucosa of bladder or rectum

Endometrial Carcinoma: Staging

A

Stage IV

91
Q

Ovary

Originate from unruptured graafian follicles or from follicles that rupture & seal
* Develop subadjacent to ovarian serosa

Pathology

A

Follicular & luteal cysts

92
Q

Ovary

  • Typically small (1-1.5 cm) lesions
  • Filled with clear serous fluid
  • Lined by granulosa cells (as fluid accumulates pressure leads to atrophy of these cells)

Presentation

A

Follicular & luteal cysts

93
Q

Ovary

  • Occassionally become large (4-5 cm) & produces palpable masses & pelvic pain
  • Can rupture causing intraperitoneal bleeding & peritoneal symptoms (acute abdomen)

Potential Complications

A

Follicular & luteal cysts

94
Q

Ovary

Types of ovarian tumors

Histology

A

Classification of tumors is based on origin
1. Surface epithelial tumors: 65-70%
3. Germ cell tumors: 15-20%
4. Sex cord-stromal tumors: 5-10%
5. Metastasis

95
Q

Ovary

Most common type of ovarian tumor

A

Surface epithelial tumor

65-70% of cases

96
Q

Ovary

2nd most common type of ovarian tumor

A

GCT

15-20% of cases

97
Q

Ovary

Types of superficial epithelial tumors

Histology

A
  1. Serous tumors
  2. Mucinous tumors
  3. Endometrioid tumors
  4. Brenner tumors
98
Q

Ovary

Types of GCT

Histology

A
  1. Teratoma
  2. Dysgerminoma
  3. Endodermal sinus tumor
  4. Choriocarcinoma
  5. Embryonal carcinoma
99
Q

Ovary

Most common GCT in females

A

Teratoma

100
Q

Ovary

Most common malignant GCT in females

A

Dysgerminoma

101
Q

Ovary

Most common GCT in children

A

Endodermal sinus tumor

102
Q

Ovary

Types of sex-cord stromal tumors

Histology

A
  1. Fibroma
  2. Granulosa-theca cell tumor
  3. Sertoli-Leydig cell tumor
103
Q

Ovary

  • 25% of gynecologic malignancies
  • 90% of cases are sporadic; 10% inherited
  • Highest mortality due to a pelvic malignancy
  • General population lifetime risk: 1.5%
  • 80% diagnosed in Stages III/IV; dismal survival
  • 92% survival if diagnosed in Stage I

Epidemiology

A

Ovarian carcinoma

104
Q

Ovary

  • Increased risk:
    • Age
    • Nulliparity
    • Late menopause
    • Incessant ovulation
  • Decreased risk:
    • Pregnancy
    • Lactation
    • Oral contraception

Risk Factors

A

Ovarian carcinoma

105
Q

Ovary

Progression from benign tumors through borderline tumors that may give rise to low-grade carcinoma
* Slow growth; rarely progress to high-grade carcinomas

Pathogenesis

A

Type I ovarian carcinoma

106
Q

Ovary

Type I ovarian carcinoma

Precursor

A

Cystadenoma

107
Q

Ovary

Type I ovarian carcinoma

Prototype

A

Low-grade serous carcinoma
* Also mucinous and endometrioid carcinomas

108
Q

Ovary

Associated with mutations in KRAS, BRAF

Etiology

A

Type I ovarian carcinoma

109
Q

Ovary

Arise from inclusion cysts / fallopian tube epithlelium via intraepithial precursors that are often not identified
* Often demonstrate high-grade features and are most commonly of serous histology
* Highly aggressive; rapid progression

Pathogenesis

A

Type II ovarian carcinoma

110
Q

Ovary

Type II ovarian carcinoma

Precursor

A

Serous tubal intraepithelial carcinoma (STIC)

Same p53 mutation

111
Q

Ovary

Type II ovarian carcinoma

Prototype

A

High-grade serous carcinoma

112
Q

Ovary

Associated with p53 mutation

Etiology

A

Type II ovarian carcinoma

113
Q

Ovary

  • 30% of all ovarian tumors
  • 50% of ovarian epithelial tumors
  • 70% are benign or borderline; 30% are malignant
    • Benign & borderline tumors are most common between ages 20-45

Epidemiology

A

Ovarian serous tumors

114
Q

Ovary

Cystic neoplasms lined by tall, columnar, ciliated & non-ciliated epithelial cells and filled with clear watery fluid

Histology

A

Ovarian serous tumors

115
Q

Ovary

Types of ovarian serous tumors

Histology

A
  • Benign: serous cystadenoma
  • Borderline: serous borderline tumor
  • Malignant: serous cystadenocarcinoma
116
Q

Ovary

  • Most common malignant ovarian tumor
  • Most common ovarian epithelial tumor
  • ~75% of cases are detected in Stage III
  • More common in postmenopausal women
    • Earlier onset in familial cases (BRCA1)
  • Mostly bilateral (70% of cases)
  • Widespread peritoneal involvement

Epidemiology

A

Ovarian serous carcinoma

117
Q

Ovary

  • Papillary structures
  • Psamomma bodies

Histology

A

Ovarian serous carcinoma

118
Q

Ovary

  • Architecture: micropapillae
  • Nuclear features:
    • Mostly uniform round/oval shape
    • Evenly distributed chromatin
    • +/- conspicuous nucleoli

Histology

A

Low-grade ovarian serous carcinoma

119
Q

Ovary

  • Architecture:
    • Large, complex papillae/glands/solid areas
  • Nuclear features:
    • Variation in size, shape
    • Irregular chromatin
    • +/- macronucleoli
    • Multinucleated tumor giant cells

Histology

A

High-grade ovarian serous carcinoma

120
Q

Ovary

  • Mainly occur in middle adult life
    • Rare before puberty / after menopause
  • 30% of all ovarian tumors
  • 80% are benign or borderline; 15% are malignant

Epidemiology

A

Ovarian mucinous tumors

Primary ovarian mucinous carcinomas are rare (<5% of ovarian cancers)

121
Q

Ovary

  • Variable size cysts: large cystic masses (up to 25 kg)
  • Smooth external surface
  • Multilobulated
  • Filled w/ sticky, gelatinous fluid: glycoprotein rich

Gross Appearance

A
122
Q

Ovary

Types of ovarian mucinous tumors

Histology

A
  • Benign: mucinous cystadenoma
  • Borderline: mucinous borderline tumor
  • Malignant: mucinous cystadenocarcinoma
123
Q

Ovary

  • Uncommon primary ovarian tumor
  • Typically metastatic from appendiceal tumor
    • Associated w/ pseudomyxoma peritonei
  • Unilateral, stage I, infiltrative stromal invasion

Presentation

A

Ovarian mucinous cystadenocarcinoma

124
Q

Ovary

Implantation of mucinous tumor in the peritoneum with excessive mucin production

Pathology

A

Pseudomyxoma peritonei

125
Q

Ovary

Ovarian mucinous cystadenocarcinoma

Approach to Diagnosis

A

IHC: CK7+/CK20-

126
Q

Ovary

  • Represents 10-15% of ovarian carcinomas
  • Typically unilateral (13% bilateral)
  • Associated endometrial carcionoma: 15% of cases
  • Associated endometriosis: 10-20% of cases
    • More common in younger patients

Epidemiology

A

Ovarian endometrioid carcinoma

127
Q

Ovary

  • Nuclei are cleared out & pleomorphic
  • Distinct glandular spaces
    • Occassional “gland-in-gland” organization
  • Central necrosis within some glands

Histology

A

Ovarian endometrioid carcinoma

Resembles uterine endometrioid carcinoma

128
Q

Ovary

  • 6% of ovarian carcinomas
  • Often associated with endometrioid carcinoma & endometriotic cysts
  • Highest association with ovarian & pelvic endometriosis and paraendocrine hypercalcemia
  • Often unilateral & low-grade malignancy

Epidemiology

A

Ovarian clear cell carcinoma

129
Q

Ovary

  • Polyhedral cells with abundant clear and/or eosinophilic granular cytoplasm
  • Hobnail cells w/ scant cytoplasm & enlarged, bulbous nuclei protruding into cystic lumens
    • Glycogen-rich & PAS-pos cytoplasm

Histology

A

Ovarian clear cell carcinoma

130
Q

Ovary

Ovarian clear cell carcinoma

Approach to Diagnosis

A
  • Histology: hobnail cells (hallmark)
  • IHC: cytokeratin+, EMA+
    • Most exhibit CK7+/CK20- profile
131
Q

Ovary

Types of Ovarian GCT

Histogenesis

A
  • Undifferntiated –> dysgerminoma (oocytes)
  • Differentiated
    • Embryonal
      • Embryonal carcinoma (fetal tissue)
      • Teratoma (fetal tissue)
    • Extraembryonal
      • Endodermal sinus tumor (yolk sac)
      • Choriocarcinoma (placental tissue)
132
Q

Ovary

  • Most common malignant GCT in females
  • Most often seen in patients age < 30
    • Seen in pregnant patients (age-related)
  • Associated with gonadal anomaly: 5-10% of cases
  • Analogous to seminoma of testis
  • Can be pure form or associated with other GCT

Epidemiology

A

Dysgerminoma

133
Q

Ovary

Unilateral, solid, gray, soft encapsulated tumors; rapid destructive growth

Presentation

A

Ovarian dysgerminoma

134
Q

Ovary

  • Large tumor cells of undifferentiated germ cell origin arranged in sheets, nests, trabeculae
    • Clear cytoplasm
    • Central nuclei
  • Fibrous septae infiltrated by lymphocytes & plasma cells; often granulomas with giant cells

Histology

A

Ovarian dysgerminoma

135
Q

Ovary

Ovarian dysgerminoma

Approach to Therapy

A

Radiotherapy, CTX

136
Q

Ovary

  • 15-20% of ovarian tumors
  • 90% benign; rare malignant variant

Epidemiology

A

Teratomas

137
Q

Ovary

Most common type of teratoma

A

Benign mature cystic teratoma

>90% of teratomas; immature, malignant variant is rare

138
Q

Ovary

Most common type of teratoma

A

Benign mature cystic teratoma

>90% of teratomas; immature, malignant variant is rare

139
Q

Ovary

  • Size: ~10 cm
  • May contain sebaceous secretions, hair, teeth, etc.

Gross Appearance

A

Teratoma

140
Q

Ovary

  • 90% are unilateral; R. side more common
  • Most discovered in young women as ovarian masses or found incidentally on abdominal scans
  • Malignant transformation: usually SCC; rare (1%)

Epidemiology

A

Mature cystic teratoma (dermoid cyst)

141
Q

Ovary

Rare tumors composed of tissues that resemble embryona & immature fetal tissue
* Typically occur in prepubertal / young women
* Rapid growth; frequent invasion of capsule
* Local or distant spread
* Stage I tumors: excellent prognosis
* Most recurrences within first 2 yrs
* Absence after 2 yrs: great chance of cure

Pathology

A

Immature malignant teratomas

142
Q

Ovary

  • Bulky & smooth external surface
  • Solid / predominantly solid structure
  • +/- hair, sebaceous material, cartilage, bone, Ca2+

Gross Appearance

A

Immature malignant teratomas

143
Q

Ovary

  • Islands of immature tissue: usually neuroepithelium
    • Can be cartilage, muscle, bone, etc.
  • Invasion of capsule

Histology

A

Immature malignant teratomas

144
Q

Ovary

Immature malignant teratomas

Approach to Therapy

A

Prophylactic CTX

145
Q

Ovary

Specialized ovarian teratomas

Histology

A

Monodermal teratomas
* Only thyroid elements (follicles & colloid): struma ovari
* Pts present w/ hyperthyroidism
* Only carcinoid elements: neuroendocrine tumor
* Pts present w/ unilateral mass / carcinoid syndrome
* Thyroid & carcinoid elements: strumal carcinoid

146
Q

Ovary

  • Most common between 20s-30s
  • Origin: primitive embryonal cell
  • Can be pure form or component of mixed GCT
    • Sometimes contralateral to dermoid cyst

Epidemiology

A

Ovarian embryonal carcinoma

147
Q

Ovary

Rapidly growing, large, soft, necrotic & hemorrhagic tumor mass

Gross Appearance

A

Ovarian embryonal carcinoma

148
Q

Ovary

Ovarian embryonal carcinoma

Approach to Diagnosis

A

Labs: elevated AFP
IHC: Cytokeratin+, CD30+, OCT3/4+, NANOG+, SALL4+, SOX2+

149
Q

Ovary

  • Histological patterns resemble yolk salk development
    • Reticular, myxoid, glandular, polyvesicualr patterns
  • Schiller-Duval bodies: papillations w/ central blood vessels

Histology

A

Endodermal sinus tumor

Schiller-Duval bodies = histological hallmark

150
Q

Ovary

Endodermal sinus tumor

Approach to Diagnosis

A

Histology: Schiller-Duval bodies; eosinophilic hyalin globules
IHC: AFP+, glypican3+, SALL4+, cytokeratin+

151
Q

Ovary

Uncommon tumors with potential hormonal activity composed of stroma & sex cord elements

Pathology

A

Sex cord-stromal tumors

152
Q

Ovary

Types of sex cord-stromal tumors

Histology

A
  1. Fibroma, fibrothecoma
  2. Granulosa cell tumor
  3. Sertoli & Sertoli-Leydig cell tumors
  4. Steroid (lipid) cell tumors
153
Q

Ovary

Benign fibroblast tumor
* A/w nevoid BCC (Gorlin’s syndrome)

Pathology

A

Ovarian fibroma

154
Q

Ovary

Firm, well-circumscribed white whorled masses with smooth surface

Gross Appearance

A

Ovarian fibroma

155
Q

Ovary

Short fascicles of closely packed bland spindle cells with a storiform arrangement

Histology

A

Ovarian fibroma

“Storiform”: fascicles intertwine in pattern resembling cartwheel

156
Q

Ovary

Ovarian fibroma

Potential Complications

A

Meig’s syndrome: ascites, right hydrothorax
* Syndrome resolves with removal of tumor

157
Q

Ovary

Benign theca cell tumor
* Estrogenic

Pathology

A

Thecoma

158
Q

Ovary

Yellow, lipid-rich masses

Gross Appearance

A

Thecoma

159
Q

Ovary

Fascicles of spindle cells w/ central nuclei & moderate pale cytoplasm
* IHC: inhibin+

Histology

A

Thecoma

160
Q

Ovary

Thecoma

Potential Complications

A

Estrogenic - may cause endometrial hyperplasia / carcinoma

161
Q

Ovary

  • Only 2% of all ovarian tumors
  • 2 types:
    • Adult: 95%
    • Juvenile: 5%
  • Hormonally active: mostly estrogenic
    • Rarely androgenic
  • Most are unilateral & diagnoed in early stages

Epidemiology

A

Granulosa cell tumor

162
Q

Ovary

Solid, cystic, soft, hemorrhagic masses

Gross Appearance

A

Granulosa cell tumor

163
Q

Ovary

  • Uniform cells w/ grooved nuclei, C-Ex bodies
  • Patterns: microfollicular, macrofollicular, insular, trabecular, diffuse

Histology

A

Granulosa

Carl-Exner (C-Ex) bodies = histological hallmark

163
Q

Ovary

  • Uniform cells w/ grooved nuclei, C-Ex bodies
  • Patterns: microfollicular, macrofollicular, insular, trabecular, diffuse

Histology

A

Granulosa

Carl-Exner (C-Ex) bodies = histological hallmark

164
Q

Ovary

  • Prepubertal: precocious puberty
  • Post-menopausal: endometrial hyperplasia

Clinical Presentation

A

Granulosa cell tumor

165
Q

Ovary

Granulosa cell tumor

Potential Complications

A

Estrogenic - may result in endometrial carcinoma or fibrocystic change in breast

166
Q

Ovary

Granulosa cell tumor

Approach to Diagnosis

A

Elevated inhibit: tissue & serum levels
* Used to identify & monitor granulosa cell tumors

Strong IHC positivity with anti-inhibin AB = characteristic

167
Q

Ovary

  • Average age: 30 yrs
  • Unilateral
  • Mostly diagnosed in Stage 1: good prognosis

Epidemiology

A

Ovarian Sertoli cell tumors

168
Q

Ovary

Firm, solid, yellow-brown masses

Gross Appearance

A

Ovarian Sertoli cell tumors

169
Q

Ovary

Hollow or solid tubules lined by cuboidal cells with vacuolated cytoplasm

Histology

A

Ovarian Sertoli cell tumors

170
Q

Ovary

  • Rare; average age: 25 yrs
  • Androgenic tumors

Epidemiology

A

Sertoli-Leydig cell tumors

171
Q

Ovary

Solid, cystic yellow masses with necrosis & hemorrhage

Gross Appearance

A

Sertoli-Leydig cell tumors

172
Q

Ovary

Tubules lined by Sertoli-like cells separated by variable numbers of round, eosinophilic Leydig-like cells

Histology

A

Sertoli-Leydig cell tumors

173
Q

Ovary

  • About 70% bilateral
  • Presence of multiple nodules or tumors on surface
  • Solid & cystic

Presentation

A

Metastatic ovarian cancer

Consider mets when tumor is bilateral & multifocal on exterior

174
Q

Ovary

Origins of metastatic ovarian cancer

Pathology

A
  • Gastric origin: Krukenberg tumors
  • Intestinal origin: mostly colonic
  • Breast carcinoma
  • Other origins: endometrial, tubal, lymphoma etc.

GU / GYN & Renal (23 decks)

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