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ENRP Exam 1 > Female Reproductive Tract Pathology Dr. Hillard > Flashcards

Female Reproductive Tract Pathology Dr. Hillard Flashcards

1
Q

The skene glands and the bartholin glands

A

Skene = adjacent to urethra
Bartholian = posterior to vaginal orifice
(Secrete sexual fluids)

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2
Q

Cervix transformaion zone

A

Squamous mucosa to columnar mucosa

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3
Q

Germ cells forming uterus

A

Migrate from yolk sac to genital ridge = gonads

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4
Q

Gonads (2 ducts that are made?) become male or female how

A

Mullerian (paramesonephric) ——> MALE from SRY gene
Wolffian Duct (Mesonephric) ——> FEMALE from estogen
= no SRY gene —-> Ovary from the gonads
= Estrogen —-> female reproductive tract

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5
Q

Urogenital sinus becomes

A

Lower part of vagina close to cervix

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6
Q

Uterine Didelphys is what and casued by, assoicated with

A

2 uterus and 2 cervix made, 2 vagina cavities (septum)
= X fusion of mullarian ducts during development
= associated with kidney problems also

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7
Q

Mayer Rokitnsky Kuster Hauser Syndrome is what and cuased by
SX

A

= NO uterus and NO vagina
= Mullerian agenesis
= amenorrhea, normal breasts, normal pubic hair, normal vulvar development

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8
Q

Mullerian duct makes up

A

Fallopian tube, uterus, upper 1/3 vagina

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9
Q

Bartholin cyst

A

From obstruction of duct
= Cyst is nontender, unilateral**, soft mass, posterior to vaginal opening
= When infected —-> warm, tender, pussy, Cellulitis around

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10
Q

Lichen Sclerosis
Is caused by and who
Sx
Risk of what

A

Activated T-cell inflammation disorder, (effects vulva and genital skin)
= post-menopause usually
= Pruritis, dyspareunia, dysuria, White Plaques*
= TP53 keratinizing SSC

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11
Q

Lichen Sclerosis Histology

A

Thinning atrophy, edematous band lymphocytic infiltrate, hyperkeratosis

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12
Q

Lichen Simplex Chronicus

  1. Is what
  2. Cuased by
  3. SX + location
  4. Associated with 3 things
A
  1. Squamous cell Hyperplasia
  2. Chronic rubbin or scratiching
  3. Thickened (acanthosis), reddened surface —> can whiten over time + on vulva
  4. Dermatitis, psoriasis, lichen sclerosis, SCC
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13
Q

Histology of Condylomata Acuminata

A

HPV warts on genitals and anus
= Papillary projections
= superficial parakeratosis
= Koilocyte nuclei with Halo (from HPV proteins)

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14
Q

Vulvar Carcinoma

  1. Most common type , age
  2. 2 categories and comes from
A
  1. SCC , after 60yo
  2. Basaliod/warty SCC, Keratinizing SCC (both from precursor lesion Vulvar Intraepithelial Neoplasia (VIN) = immune system tried to keep it from becoming invasive
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15
Q

Basaloid / Warty SCC

  1. Age
  2. Precursor lesion
  3. Risk
A
  1. 60yo
  2. Classic VIN (vulvar High squamous intraepithelial lesion)
  3. High risk HPV (16, 18)
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16
Q

Keratinizing SCC

  1. Age
  2. Precursor lesion
  3. Risk
A
  1. 75yo
  2. Differentiated VIN
  3. Chronic irritation (long standing) Lichen Sclerosis or Squamous Cell Hyperplasia
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17
Q

SCC associated with what 2 things

A
  1. P53

2. Chronic itching and irritation

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18
Q

Histology of classic VIN

A

Full thickness atypia with clear mito tic figures, progressing to invasive basoloid SCC or invasive warty SCC

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19
Q

Differentiated VIN histology

A

Basal and parabasal atypia, ancanthosis, can lead do Keratinizing SCC

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20
Q

Papillary Hidradenoma

  1. What is it
  2. Histo
  3. Arise from
A

Benign

  1. Solid, dermal or subQ nodule
  2. Columnar myoepithelial + apocrine (sweat glands)
  3. Mammary type glands on the primitive milk line
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21
Q

Papillary Hidradenoma of the breast is called

A

Intraductal papilloma

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22
Q

Extramammary Pagets Disease (EMPD)

  1. Is what
  2. Histo
  3. SX
  4. Risk of
A
  1. Intraepithelial adenocarcinoma (vulvar and Ano/genital region)
  2. Sweat glands (apocrine + eccrine) + Keratinocytes,
  3. Pruritic, red/white crusted lesions, ill defined
  4. Synchronous noncontiguous carcinoma (can take long time)
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23
Q

Gartner duct cysts are from what and who , location , sx

A

= Wolffian (Mesonephric) remanants (cuboidal to low columnar)
= Reproductive age women
= Anterior lateral wall of vagina (can protrude out)
= asymptomatic (painful intercourses or vaginal pressure)

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24
Q

Mullerian Cysts are from what, who, location, sx

A

= Mullerian (paramesonephric) remanants (any epithelium, endocervial usually)
= Reproductive age women
= Anterior lateral wall of vagina (can protrude out)
= asymptomatic (painful intercourses or vaginal pressure)

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25
Q

Diethylstilbestrol (DES) Exposure

A

Disrupts vaginal epithelium causing clear cell adenocarcinoma = vaginal adenosis (glandular change) (transoplacental carcinogen affecting the daughters of pregnant women taking this)

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26
Q

Vaginal Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)

  1. Who
  2. Looks like
  3. Complication
  4. Histo cell
A
  1. young to infant F, under 5yo
  2. Protruding bulky polypoid, grape like mass, bloody discharge
  3. Invasion causing death = bladder obstruction / peritoneal cavity invasion
  4. Embryonal rhabdomyoblasts (Cambium layer)(elongated eosinophilic cells**)
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27
Q

Vaginal SCC is similar to what other SCC

  1. Starts how
  2. From what
  3. Spreads to what
A
  1. Premalignant lesion vaginal intraepithelial neoplasm (VAIN)
  2. HPV type 16, 18
  3. (Lower 2/3 vagina = inguinal and femoral LNs), (Upper 1/3 vagina = iliac LNs —-> periaortic LNs)
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28
Q

High risk HPV types and does what

A

16 MOST , and 18, causes almost ALL of cervical + vaginal carcinomas

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29
Q

How does HPV cause carcinoma

A

Enters body making E6 = INCREASE telomerase, degrade p53
+ E7 = drives proliferation INactivating p21 and RB binding —-> E2F into cell cycle

Telomerase increased —> immortality

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30
Q

Mild dysplasia
Moderate dysplasia
Severe dysplasia
Carcinoma in situ

(SIL grade and CIN type)

A
  1. Mild dysplasia = LSIL (low grade squamous Intraepithelial lesion)
  2. Moderate dysplasia = HSIL (high grade squamous Intraepithelial lesion)
  3. Severe dysplasia = HSIL
  4. Carcinoma in situ = HSIL
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31
Q

HSIL and LSIL tx

A 
LSIL = observe and monitor
HSIL = Excise
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32
Q
  1. HSIL and LSIL that are HPV +

2. HSILs progression to carcinoma

A
  1. 80% LSILs + all HSILs

2. 10% progress (LSILs 60% regression , 10% progression to HSIL)

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33
Q

Ectocervical

Endocervical mucosa cell type

A

Ectocervical = stratified squamous mucosa
Endocervical = cuboidal mucosa
(Transition zone between them)

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34
Q

HPV happens in what layer of the cervix

A

Basal layer

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35
Q

LSILs histology looks like

A

Lower part of epithelium layer is not maturing normally

Upper part has koilocytes

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36
Q

CIN 2 histology HSIL

CIN 3 histology HSIL

A
  1. Middle 3rd of epithelium layer shows atypia

2. Entire epithelium is atypical , identifiable mitosis figures

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37
Q

Pap smear does what

A

Gets cells from top layer of epithelium
LSIL = see koilocytes
HSILs = dysplastic cells + basal cells

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38
Q

PAP test guidelines

A

21- 29yo, every 3 years if no abnormality

30-65yo, every 5 years + molecular testing if normal

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39
Q

Pap test after 65 is not needed when

A

If - test past 3 times (15 years) and - molecular test past 10 years

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40
Q

Colposcopy is done how and for what

A

Biopsy taken of lesion
1. Acetic acid applied (precipitation/ coagulation of proteins)
2. Turns white if dysplasia (acetowhite) CIN2,CIN3 = coarse punctation
CIN1 = faint punctation
3. TYPICAL BVs can be seen in acetowhite areas

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41
Q

HSILS TX how

A
  1. Cervical conization ( cutting cone shaped cervix off)

2. LEEP (Loop electro surgical excision) (electric current in wire cuts tissue)

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42
Q

HPV dysplasia if not TX becomes

A
  1. SCC ** (transition zone) 80%
  2. Or invasive adenocarcinoma in situ —-> cervical adenocarcinoma (if effecting cervical endocervical mucosa) atypical glandular cells, 15%
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43
Q
  1. Cervical carcinoma age average
  2. Age to take Gardasil (which protects from what strains)
  3. Males take it to protect from
A
  1. 45-50yo
  2. 11-12yo, low and high risk strains
  3. Penile, anal, oral pharyngeal carcinoma
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44
Q

Endocervical Polyps

  1. Are what and what age
  2. Sx
  3. Tx
  4. Histology
A
  1. Benign lesions during reproductive years after 40yo
  2. Spotting or bleeding
  3. Polypectomy = curative
  4. Endocervial glands , fibrovsuclar core,
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45
Q

Right after menses what causes estrogen to increase

A

FSH

46
Q

After ovulation what happens

A

Corpus luteum forms = releasing progesterone
= secratory phase = prepare endometrium for fertilization (LUTEAL)
Then corpus albicans = no P no E = menses

47
Q

Proliferative phase endometrium HISTOLOGY

A
  1. Cellular Blue stroma , many round and tubular glands (pseudostratified + mitotic figures on cross section of tubular glands)
48
Q

Secretory Phase Endometrium HISTOLOGY

A

= tortuous and serrated glands , PIANO KEY VACUOLES (subliminal, early secretory)
= subnuclear vacuoles move adjacent to lumen ——> luminal secretions (PINK eosinophilia stroma, PREDECIDUALIZED STROMA + spiral As)

49
Q

Menstrual Phase Endometrium HISTOLOGY

A
  1. Spiral As constrict = tight blue clusters of stromal cells
  2. Ischemia of endometrium, superficial endometrium sloughs off + hemorrhage
50
Q
  1. Most common cause of abnormal uterine bleeding
  2. What is dysfunctional uterine bleeding
  3. Adolescents cause vs perimenopausal cause
A
  1. DYSFUNCTIONAL UTERINE BLEEDING Due to hormonal imbalance
  2. Not bleeding , anovulatory cycle
  3. Adolescents = due to H-P-ovarian cycle immaturity or low functionality, Perimenopausal = menopausal hormonal imbalance
51
Q

Anatomical lesions leading to abnormal uterine bleeding adolescents vs perimenopausal

A 
Adolescents = benign
Postmenopausal = need to screen for endometrial carcinoma if any bleeding
52
Q

Dysfunction uterine bleeding : most common causes of hormonal imbalance causes (3)

A
  1. PCOS : polycystic ovarian syndrome , ovarian tumor
  2. Metabolic disorder (obesity, malnutrition, chronic system disease)
  3. Endocrine disorders (thyroid, adrenal, pituitary disease)
53
Q

Acute endometritis

  1. Is what and usually when
  2. Sx
  3. Histo
A
  1. Infection GROUP A STREP, or staph, after delivery OR also seen in PID (pelvic infl dz of chlamydia)
  2. Post-party fever, uterine tenderness, ABDpain
  3. Microabscesses , NEUTROPHILS
54
Q

Chronic Endometritis

  1. Histo
  2. From what
  3. Sx
A
  1. Plasma cells**, perinuclear hof around cells
  2. Products of conception remain, Chronic PID, IUD (actinomyces infection from an IUD)
  3. Asymptomatic (can cause bleeding)
55
Q 
Endometriosis 
1. Definition 
2. Effects what tissues
3. SX
4, risk
A
  1. Ectopic endometrial tissue outside the uterus (reacting to same stimuli going through cycle)
  2. Ovaries, pelvic tissues, (many other places)
  3. Severe dysmenorrhea (painful menses, pelvic pain), Ovarian mass, Dyspareunia (sex pain),
  4. infertility
56
Q

Endometriosis is thought to be caused by what theories + what things in detail cause it to maintain its survival outside the uterus

A
  1. (Regurgitation theory) flow of endometrial tissue, tissue spread through Lymph(benign metastases theory), embryonic remnants(metaplastic theory), from BM (extrauterine Stem cell theory)
  2. inflammatory factors, Metalloproteases, VEGF, increased AROMATASE = estrogen, mutations**
57
Q

Endometriosis

  1. looks like
  2. histology 3 things you see
A
  1. red-brown, blue-black lesions (POWDER BURN), if involving the ovary (blood filled cyst =CHOCOLATE CYST)
  2. 2/3 need : endometrial glands, endometrial stroma, hemorrhage (Hemosiderin laden M seen*)
58
Q

Adenomyosis

  1. definition
  2. SX
A
  1. endometrial tissue in muscle of uterus (myometrium)
  2. similar to endometriosis (dysmenorrhea, dyspareunia, infertility)
  3. hemorrhages seen inside the uterine myometrium + endometrial stroma/glands
59
Q

Endometrial Polyps

  1. are what
  2. histology
  3. causes + who
  4. risk increased from what
A
  1. exophytic (protrude into uterine cavity) benign** hyperplastic neoplastic mass
  2. stroma + glands cysts
  3. MOST common cause of bleeding in perimenopause and postmenopause
  4. Tamoxifen (decrease E in breast, increase in endometrium) + other proESTROGEN factors, obesity, oral contraception
60
Q

Endometrial Hyperplasia

  1. definition
  2. 2 main types + histo of them
  3. risk of carcinoma
A
  1. increase endometrial glands > stroma (premalignant condition to endometrial carcinoma)
  2. Typical hyperplasia : glandular crowing
    ATYPICAL hyperplasia : atypia, complex glandular proliferation/extreme crowding
  3. high risk in atypical esp atypical complex
61
Q

risk of hyperplasia and endometrial carcinoma

A
  1. UNOPPOSED ESTROGEN** (no preg, early starting period + menopause late) prog has not opposed E for a long time
    = obesity
    = PCOS
    = estrogen oral contraceptive
    = Tamoxifen
    = tumors : Granulosa cell tumor + ovarian thecoma making E
62
Q

how obesity increased E + tumors increasing E

A
  1. has aromatase = androgens —-> Estrogen

2. Grandular cell tumor + Ovarian Thecoma

63
Q

Endometrial cancer must know SX and who and what do I do

A

postmenopausal bleeding** (sometimes pelvic pain + watery discharge, WL)

==== Biopsy + dilation and curettage for DX

64
Q

most common type of endometrial cancer, and characteristics, and what factors CAUSES this cancer to happen + age

A

endometrial endometrioid carcinoma = mimic normal endometrium, slow (glands crowed so there in NO stroma inbetween)
* typical hyperplasia (PTEN) —-> Atypical hyperplasia (KRAS)

= 55yo-65yo

65
Q

Serous Carcinoma or Uterus

  1. who
  2. histo
  3. factor causing this
  4. characteristic of this tumor
A
  1. older 65-75yo postmenopause, AA*
  2. Papillary growth pattern, cytologic atypia
  3. TP53
  4. Atrophic non-cycling endometrium —-> aggressive high grade serous carcinoma ***** (always high grade)
66
Q

Malignant Mixed Mullarian Tumor (MMMT)

  1. type of cancer
  2. who
  3. histo
  4. characteristic
A
  1. Carcinosarcoma
  2. older 65-75yo postmenopausal, AA**
  3. malignant glands + stroma
  4. atrophic endometrium—-> aggressive (esp if heterologous component present)**
67
Q

MMMT with heterogenous component means what

A
  1. stroma becomes a sarcomatous element (chondrosarcoma or rhabdomyosarcoma) = poor prognosis
68
Q

MMMT glands can looks like

A

either endometrioid carcinoma or serous high grade uterine carcinoma

69
Q

Lynch Syndrome in Women

  1. inheritance, how
  2. risk of causing
A
  1. AD, MLH1 or MLH2 (mismatch repair gene mutations) —-> MSI (microsatellite instability
  2. colorectal carcinoma , endometrial + ovarian cancer (endometrioid carcinoma)

can effect stomach also

70
Q

Type 1 endometrial Carcinoma SUMMARY**

  1. what
  2. caused by
  3. risks
  4. mutations
  5. prognosis + who
A
  1. Endometrial Endometrioid carcinoma
  2. Unopposed Estrogen
  3. Obesity, DM
  4. PTEN —> PI3K/AKT pathway + MSI (lynch syndrome)
  5. slow, favorable prognosis, 55yo-65yo
71
Q

Type 2 endometrial Carcinoma SUMMARY**

  1. what
  2. caused by
  3. risks
  4. mutations
  5. prognosis
A
  1. Serous carcinoma, MMMT (malignant mixed Mullerian tumor)
  2. atrophy postmenopausal
  3. age
  4. P53
  5. aggressive high grade (esp heterogenous condition of MMMT) 65yo-75yo, AA
72
Q

Adenosarcoma

  1. what
  2. histo
A
  1. stromal low grade sarcoma = (benign glands tumor + malignant stroma tumor)
73
Q
  1. benign glands proliferating + normal stroma =
  2. benign glands proliferating + stromal malignancy =
  3. malignant glands + normal stroma =
  4. malignant glands + malignant stroma =
A
  1. endometrial polyp
  2. adenosarcoma
  3. endometrioid carcinoma
  4. MMMT
74
Q

Low Grade Endometrial Stromal Sarcoma

  1. what
  2. invades
  3. sx
  4. factors causing it
A
  1. malignant tumor = endometrial stroma (small blue cells)
  2. myometrium +LN +BV ** invasion is dx
  3. bleeding, abd pain
  4. JAZF1** gene translocation = fusion of SUZ12 (good prognosis)
75
Q

Leiomyoma (fibroid)

  1. is what and location
  2. looks like
  3. sx
  4. mutation commonly
A
  1. benign very common SM tumor in myometrium
  2. white-tan/white nodules
  3. (uterine bleeding, infertilit)**, higher urination due to bladder compression
  4. MED12 mutation
76
Q

Leiomyoma histology and fact

A
  1. benign spindle SM cells with CIGAR shaped nuclei, NO atypia
  2. most common gynecologic tumor (check in females having hard time getting pregnant)
77
Q

Leiomyosarcoma

  1. what
  2. characteristic
  3. looks like
A
  1. uncommon malignant SM tumor
  2. aggressive , 50% metastasize (lung, bone, brain)
  3. fleshy, bulky mass
78
Q

Leiomyosarcoma histology + mutation

A

atypia, mitotic figures, tumor necrosis are all seen
+ MED12 mutation present
(how this is separated from Leiomyoma when DX it)

79
Q

Paratubal Cysts if the Fallopian Tube

  1. are what
  2. comes from what
  3. sx
A
  1. benign cysts, incidental
  2. from mullerian duct or wolffian duct remnants, or from oeritoneal meothelium
  3. sx only if rupture or torsion
80
Q

Hydatid Cyst of Morgagni

  1. is what
  2. located
  3. comes from
A
  1. and paratubal cyst type that is larger (some cm)
  2. towards the fimbriated end of Fallopian tube
  3. from mullarian duct remnants
81
Q

Benign Cysts of the Ovary 2 types

  • DX criteria
  • sx and imaging
A
  1. follicular (from ovarian follicle)
  2. Luteal (corpus luteum of ovary fails to regress)
    * has to be over 3cm
    * pelvic exam or US, no sx usually
82
Q

cells seen in follicular cyst

cells seen in luteal cyst

A
  1. granulosa cells and follicular cells

2. granulosa cells + theca cells

83
Q

Adenomatoid Tumor

  1. is what
  2. location
  3. sx
A
  1. mesothelial origin benign tumor, most common in fallopian tube
  2. fallopian tube
  3. none usually found during surgery
84
Q

Adenomatoid Tumor :

  1. looks like
  2. male locations
  3. histology
A
  1. grey, white, yellow color
  2. epididymis and testis
  3. Sieve like appearance with many spaces in it
85
Q

PCOS is characterized by what 4 things that it causes in the syndrome

A
  1. Hyperandrogenism (high testosterone, male patterns/chracteristics) = HAIR GROWTH on face, balding
  2. Hormonal imbalance (chronic anovulaiton, low fertility, high estrogen)
  3. insulin resistance (obesity, DM)
  4. Polycystic ovaries
86
Q

PCOS is in risk of what

A

Endometrial hyperplasia —-> endometrial carcinoma

87
Q

Stromal Hyperthecosis

  1. is what
  2. in who
  3. looks like
A
  1. severe hyperandrogenism + insulin resistance
  2. post-menopausal
  3. ovarian enlargement, HIGH luteinized stromal cells (has yellow/white center)
88
Q

Theca Lutein Hyperplasia of Pregnancy

  1. is what
  2. what happens
A
  1. response to Gonadotropins (hCG) in pregnancy

2. ovarian enlargement = stromal hyperplasia –> increases androgens (mild)

89
Q

4 types of ovarian tumors (age, most common one)

A
  1. Epithelial Tumor : most common, 20+yo = from mullerian epithelium
  2. Germ Cell Tumor : 0-25yo
  3. Sex Cord Stromal Tumors : all ages
  4. Metastasis to ovaries : variable age, least common
90
Q

Epithelial ovarian tumor 5 types

A
  1. serous
  2. endometrioid
  3. clear cell
  4. transitional cell (Brenner tumors)
  5. mucinous
91
Q

4 types of germ cell tumors in ovary

A
  1. yolk sac tumor
  2. immature cystic teratoma, mature cystic teratoma, monodermal teratoma
  3. dysgerminoma
  4. ovarian choriocarcinoma
92
Q

Ovarian sex cord stromal tumors 3 types

A
  1. granulosa cell tumor
  2. fibroma/thecoma
  3. Sertoli-Leydig cell tumors
93
Q

Metastatic ovaian tumors 2 types

A
  1. Krukenberg tumor

2. pseudomyxoma Peritonei

94
Q
  1. most common malignant primary ovarian tumor

2. malignant tumors in ovary are what

A
  1. Serous Carcinoma

2. bilateral (except for mucinous tumor is unilateral)

95
Q

sx ovarian tumors

A
  1. asymptomatic* (until very large or late stage)
  2. adnexal mass palpation
  3. abd pain, vaginal bleeding
  4. WL, ascities
96
Q

EPITHELIAL TUMORS can be named how based on cystic and fibrous components
+ benign vs borderline appearance

A
  1. cystadenoma (cystic), Cystadenofibroma (cystic + fibrous), adenofibroma (fibrous)
  2. benign = smooth surface, borderline = rough nudular, peritoneal implants noninvasive
97
Q

Type 1 ovarian tumors

A

begin as benign precursor lesion–> borderline –> low grade carcinoma

  1. serous low grade
  2. mucinous
  3. endometrial
  4. clear cell
  5. transitional (Brenner)
98
Q

Type 2 ovarian tumors

A

derived from tubal or ovarian surface epithelial abnormality —-> high grade aggressive carcinoma
1. High grade serous carcinoma (from fallopian tube precursor = Serous Tubal Intraepithelial Carcinoma STIC)

99
Q

low grade serous tumor

  1. histology
  2. types
A
  1. cystic tumor with tubal like epithelium , papillary growth pattern
  2. benign, borderline, malignant
100
Q

high grade serous tumor

  1. histology
  2. what factors cause this
A
  1. solid tumor, atypia

2. from STIC, p53 mutation, or BRCA1 or BRCA 2 mutation(both breast carcinoma and high grade ovarian serous carcinoma)

101
Q

Ovarian Mucinous Tumor

  1. histology
  2. 2 types
  3. factor causing this
  4. special feature of this tumor type
A
  1. columnar epithelium tumor
  2. Intestinal (gastric / GI) + Mullerian (endocerival)
  3. KRAS mutation
  4. unilateral + large (multilocular cystic lesions filled with mucinous fluid)
102
Q

Ovarian Endometrioid Tumor

  1. most common type, age
  2. histology
  3. comes from what
A
  1. most are carcinomas, younger age
  2. very similar to endomertrial endometrioid carcinoma
  3. endometriosis of ovary can be a precursor lesion
103
Q

Clear Cell Tumor of Ovary

  1. what type
  2. histology
A
  1. most are carcinomas malignant

2. variant of endometrioid carcinoma, Large epithelial cells with clear cytoplasms

104
Q

Brenner Tumor (Ovarian Transitional Cell Tumor)

  1. histology
  2. type it usually it
  3. presents how
A
  1. urothelial type transitional epithelium** (metaplasia from simple squamous ovarian epithelium)
  2. typically benign
  3. unilateral (since not malignant)
105
Q

Mature Cystic Teratoma (Dermoid Cyst)

  1. type
  2. ul or bl
A
  1. Benign germ cell tumor

2. unilateral, most common germ cell tumor

106
Q

Immature Malignant Teratoma

  1. who
  2. type and histology
A
  1. prepubertal adolescent females young women

2. malignant immature neuroepithelium (degree of this = grading and prognosis)

107
Q

Monodermal (Specialized) Teratoma

  1. what is this
  2. Struma ovarii sx
  3. Carcinoid Tumor sx
A
  1. teratoma with predominantly 1 tissue type
  2. mature thyroid tissue on ovary = htn, heat intolerance, tremor, low TSH)
  3. Carcinoid syndrome = flushing, D, hypotension (even in absence of hepatic metastasis, 5-hydroxyptamine)
108
Q

Dysgerminoma

  1. what
  2. factor causing it
  3. associated with
  4. most common
A
  1. ovarian counterpart of testicular seminoma (polygonal, eosinophillic, lymphocytes)
  2. KIT mutation
  3. gonadal dysgenesis
  4. most common malignant* germ cell tumor
109
Q

Yolk Sac Tumor

  1. what is it, common type of
  2. tumor cells make
  3. histology
A
  1. 2nd most common malignant germ cell tumor, from yolk sac (endodermal sinus tumor)
  2. AFP (alpha-fetoprotein)
  3. Schiller Duval body (Vein surrounded by glomerulus like cells) + Hyaline bodies **
110
Q

Ovarian Choriocarcinoma

  1. type + what
  2. tumor cells make
  3. can resemble
A
  1. aggressive, malignant germ cell tumor + placental trophoblastic differentiation
  2. B-hCG high levels
  3. ectopic pregnancy**, dysgerminoma, embryonal carcinoma = all also secrete hCG

ENRP Exam 1 (13 decks)

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