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Path 22a

1.

A patient has pelvic pain and purulent-appearing discharge. Most likely pathogen?
A. HSV-1
B. VZV
C. HSV-2
D. CMV

C. HSV-2

2.

During active genital HSV, latency is established in:
A. Lumbosacral nerve ganglia
B. Dorsal root ganglia (cervical)
C. Trigeminal ganglion
D. Enteric plexuses

A. Lumbosacral nerve ganglia

3.

Pregnant patient with primary active genital HSV at delivery. Best management?
A. Vaginal delivery, observe lesions
B. Vacuum-assisted vaginal delivery
C. Forceps-assisted vaginal delivery
D. Cesarean section

D. Cesarean section

4.

Molluscum contagiosum is caused by a:
A. Herpesvirus
B. Poxvirus
C. Papillomavirus
D. Adenovirus

B. Poxvirus

5.

MCV-2 is most commonly transmitted via:
A. Sexual contact
B. Fomites
C. Respiratory droplets
D. Insect vectors

A. Sexual contact

6.

Pearly dome-shaped papules with central dimple suggest:
A. Condyloma acuminatum
B. Genital herpes
C. Molluscum contagiosum
D. Syphilitic chancre

C. Molluscum contagiosum

7.

Molluscum viral inclusions are located in the:
A. Nucleolus
B. Cytoplasm
C. Mitochondria
D. ER lumen

B. Cytoplasm

8.

Thick vulvovaginal erythema and swelling with “curd-like” discharge is most associated with:
A. Trichomonas vaginalis
B. HSV-2
C. Molluscum contagiosum
D. Candida

D. Candida

9.

The discharge classically described for Candida is:
A. Curd-like discharge
B. Thin gray discharge
C. Frothy green discharge
D. Bloody mucoid discharge

A. Curd-like discharge

10.

Trichomonas vaginalis is best described as a:
A. Encapsulated yeast
B. Gram-negative diplococcus
C. Flagellated protozoan
D. Obligate intracellular bacterium

C. Flagellated protozoan

11.

Post–spontaneous/induced abortion infections that can cause PID are often:
A. Chlamydial infections
B. Puerperal infections
C. Viral infections
D. Mycobacterial infections

B. Puerperal infections

12.

Puerperal infections spread upward via:
A. Direct arterial spread
B. Perineural spread
C. Lymphatic and venous channels
D. Transplacental spread

C. Lymphatic and venous channels

13.

Compared with gonococcal PID, puerperal infections tend to inflame:
A. Deeper organ layers
B. Superficial mucosa
C. Cervical epithelium
D. Serosal surfaces

A. Deeper organ layers

14.

Smooth white vulvar plaques that enlarge/coalesce suggest:
A. Vulvar papillomatosis
B. Lichen sclerosus
C. Squamous papilloma
D. Trichomoniasis

B. Lichen sclerosus

15.

Advanced lichen sclerosus can lead to:
A. Labial hypertrophy
B. Cervical dilation
C. Endometrial hypertrophy
D. Constricted vaginal orifice

D. Constricted vaginal orifice

16.

Key histologic feature of lichen sclerosus is:
A. Epidermal thinning
B. Epidermal acanthosis
C. Full-thickness atypia
D. Koilocytosis

A. Epidermal thinning

17.

Squamous cell hyperplasia (lichen simplex chronicus) is driven by:
A. HPV integration
B. Chronic scratching/rubbing
C. Estrogen deficiency
D. Acute gonococcal infection

B. Chronic scratching/rubbing

18.

Squamous cell hyperplasia is characterized by:
A. Dermal mucin deposition
B. Epidermal thinning
C. Loss of rete ridges
D. Epidermal thickening

D. Epidermal thickening

19.

Both lichen sclerosus and squamous hyperplasia often show:
A. Koilocytosis
B. Full-thickness dysplasia
C. Hyperkeratosis
D. Caseating granulomas

C. Hyperkeratosis

20.

Vulvar squamous papillomas are best described as:
A. Malignant ulcerative tumors
B. Benign exophytic papilloma
C. Pigmented melanocytic lesions
D. Deep infiltrative nodules

B. Benign exophytic papilloma

21.

Most common histologic type of vulvar cancer is:
A. Basal cell carcinoma
B. Adenocarcinoma
C. Squamous cell carcinoma
D. Melanoma

C. Squamous cell carcinoma

22.

Basaloid and warty vulvar carcinomas arise from:
A. Differentiated VIN
B. Lichen sclerosus
C. Squamous papillomatosis
D. Classic VIN

D. Classic VIN

23.

Keratinizing vulvar SCC most often arises from:
A. Classic VIN
B. Squamous papilloma
C. Papillary hidradenoma
D. Differentiated VIN

D. Differentiated VIN

24.

Differentiated VIN is most associated with a history of:
A. Recurrent trichomoniasis
B. Chronic lichen sclerosus
C. Primary HSV infection
D. Molluscum contagiosum

B. Chronic lichen sclerosus

25.

A sharply circumscribed nodule on labia majora/interlabial fold suggests:
A. Bartholin cyst
B. VIN lesion
C. Papillary hidradenoma
D. Condyloma lata

C. Papillary hidradenoma

26.

Papillary hidradenoma histology shows:
A. Sheets of atypical keratinocytes
B. Koilocytes with perinuclear halos
C. Granulomatous inflammation
D. Two-layer glandular lining

D. Two-layer glandular lining

27.

Basaloid and warty vulvar carcinomas are:
A. Unrelated to HPV
B. HPV-related
C. Always estrogen-driven
D. Always postmenopausal only

B. HPV-related

28.

Basaloid and warty vulvar carcinomas typically occur:
A. At younger ages
B. Only after menopause
C. Only during pregnancy
D. Only in adolescence

A. At younger ages

29.

A vulvar carcinoma subtype is not HPV-related. Which is it?
A. Basaloid squamous carcinoma
B. Warty squamous carcinoma
C. Keratinizing squamous carcinoma
D. Clear cell carcinoma

C. Keratinizing squamous carcinoma

30.

Keratinizing vulvar SCC occurs most often in:
A. Older women
B. Teenagers
C. Children
D. Pregnant patients

A. Older women

31.

Keratinizing vulvar SCC is best described as:
A. Rare, younger onset
B. Equal to warty types
C. Less common than basaloid
D. More common than warty

D. More common than warty

32.

Pruritic red, crusted, maplike vulvar lesion suggests:
A. Lichen sclerosus
B. Extramammary Paget disease
C. Squamous papilloma
D. Condyloma lata

B. Extramammary Paget disease

33.

Extramammary Paget disease is usually on the:
A. Labia majora
B. Cervix
C. Endocervix
D. Vaginal fornix

A. Labia majora

34.

A lateral vaginal wall cyst from duct rests is:
A. Müllerian cyst
B. Gartner duct cyst
C. Bartholin cyst
D. Nabothian cyst

B. Gartner duct cyst

35.

Gartner duct cysts are most often found on the:
A. Posterior vaginal wall
B. Cervical os
C. Labia minora
D. Lateral vaginal walls

D. Lateral vaginal walls

36.

Gartner duct cysts are typically:
A. Submucosal, fluid-filled cysts
B. Solid ulcerated plaques
C. Keratin-filled epidermoid cysts
D. Deep infiltrative masses

A. Submucosal, fluid-filled cysts

37.

Virtually all primary vaginal cancers are:
A. Adenocarcinoma
B. Melanoma
C. Squamous cell carcinoma
D. Leiomyosarcoma

C. Squamous cell carcinoma

38.

Primary vaginal SCC is strongly associated with:
A. Low-risk HPV
B. EBV infection
C. HSV infection
D. High-risk HPV

D. High-risk HPV

39.

Vaginal SCC often arises from a premalignant:
A. CIN
B. VAIN
C. VIN
D. AIS

B. VAIN

40.

The cervical site most susceptible to HPV is:
A. Mature ectocervix
B. Endocervical glands
C. Immature metaplastic cells
D. Myometrial smooth muscle

C. Immature metaplastic cells

41.

HPV primarily infects which epithelial cells?
A. Immature basal cells
B. Mature superficial cells
C. Keratinized surface cells
D. Columnar ciliated cells

A. Immature basal cells

42.

HPV cannot infect directly the:
A. Basal squamous cells
B. Mature superficial squamous cells
C. Immature metaplastic cells
D. Parabasal squamous cells

B. Mature superficial squamous cells

43.

HPV infection of vagina/vulva usually requires:
A. Intact epithelium
B. High progesterone
C. High estrogen
D. Surface epithelial damage

D. Surface epithelial damage

44.

Low-risk HPV dysregulates growth via:
A. Wnt pathway
B. Notch pathway
C. Hedgehog pathway
D. TGF-β pathway

B. Notch pathway

45.

LSIL typically shows HPV replication that is:
A. Absent
B. Low
C. High
D. Integrated only

C. High

46.

Most LSIL lesions:
A. Regress spontaneously
B. Metastasize early
C. Require hysterectomy
D. Progress rapidly

A. Regress spontaneously

47.

In HSIL, HPV replication tends to be:
A. Very high
B. Unchanged
C. Variable
D. Low

D. Low

48.

HSIL most characteristically shows:
A. Normal maturation
B. Increased maturation
C. Arrested epithelial maturation
D. Keratin pearl formation

C. Arrested epithelial maturation

49.

HSIL carries a:
A. Negligible cancer risk
B. High cancer progression risk
C. Risk only in pregnancy
D. Risk only postmenopause

B. High cancer progression risk

50.

A benign exophytic lesion causing spotting arises in the:
A. Ectocervix surface
B. Vaginal introitus
C. Labia majora
D. Endocervical canal

D. Endocervical canal

51.

Endocervical polyps contain:
A. Dense collagen stroma
B. Caseating granulomas
C. Loose fibromyxoid stroma
D. Solid atypical nests

C. Loose fibromyxoid stroma

52.

Endocervical polyps commonly present with:
A. Thick curd discharge
B. Irregular bleeding/spotting
C. Frothy green discharge
D. Vesicular vulvar pain

B. Irregular bleeding/spotting

53.

Endocervical polyps are lined by:
A. Mucus-secreting endocervical glands
B. Keratinized squamous epithelium
C. Transitional urothelium
D. Ciliated tubal epithelium

A. Mucus-secreting endocervical glands

54.

HPV reaches target cells mainly through:
A. Hematogenous spread
B. Lymphatic invasion
C. Epithelial breaks at SCJ
D. Transplacental passage

C. Epithelial breaks at SCJ

55.

HSIL reflects progressive cell-cycle deregulation by:
A. Candida
B. HPV
C. HSV
D. MCV

B. HPV

56.

Gartner duct cysts derive from:
A. Müllerian duct
B. Urogenital sinus
C. Cloacal membrane
D. Wolffian duct

D. Wolffian duct

57.

Which IHC pair is most associated with HPV-related SIL?
A. ER and PR
B. CD3 and CD20
C. Ki-67 and p16
D. PAS and mucicarmine

C. Ki-67 and p16

58.

Why can Ki-67 appear in upper epithelium in HPV lesions?
A. E6/E7 block cell-cycle arrest
B. p53 hyperactivation halts mitosis
C. Estrogen withdrawal accelerates turnover
D. Hypoxia induces senescence pathways

A. E6/E7 block cell-cycle arrest

59.

Most common HPV type in both LSIL/HSIL?
A. HPV-6
B. HPV-11
C. HPV-18
D. HPV-16

D. HPV-16

60.

About what fraction of LSIL is HPV-associated?
A. About 20%
B. About 80%
C. About 40%
D. About 60%

B. About 80%

61.

About what fraction of HSIL is HPV-associated?
A. Nearly 100%
B. About 80%
C. About 60%
D. About 40%

A. Nearly 100%

62.

Most common histologic subtype of cervical cancer?
A. Small cell carcinoma
B. Adenosquamous carcinoma
C. Squamous cell carcinoma
D. Clear cell carcinoma

C. Squamous cell carcinoma

63.

Second most common cervical cancer type is:
A. Neuroendocrine carcinoma
B. Adenocarcinoma
C. Squamous cell carcinoma
D. Sarcoma botryoides

B. Adenocarcinoma

64.

Precursor lesion for cervical adenocarcinoma?
A. CIN III
B. Classic VIN
C. Differentiated VIN
D. Adenocarcinoma in situ

D. Adenocarcinoma in situ

65.

Tumor with malignant glandular + squamous cells?
A. Adenosquamous carcinoma
B. Adenocarcinoma
C. Squamous carcinoma
D. Neuroendocrine carcinoma

A. Adenosquamous carcinoma

66.

Which category tends to progress faster and worse?
A. Keratinizing squamous carcinomas
B. Classic VIN lesions
C. Adenocarcinoma and neuroendocrine
D. Endocervical polyps

C. Adenocarcinoma and neuroendocrine

67.

Advanced cervical carcinoma spreads mainly by:
A. Hematogenous dissemination
B. Direct extension
C. Transcoelomic seeding
D. Perineural invasion

B. Direct extension

68.

Cervical cancer confined to cervix is stage:
A. Stage II
B. Stage III
C. Stage I
D. Stage IV

C. Stage I

69.

Carcinoma in situ (CIN III/HSIL) is stage:
A. Stage 0
B. Stage I
C. Stage II
D. Stage III

A. Stage 0

70.

Beyond cervix, not pelvic wall; vagina not lower third:
A. Stage III
B. Stage II
C. Stage IV
D. Stage I

B. Stage II

71.

Pelvic wall involvement and lower third vagina:
A. Stage I
B. Stage II
C. Stage IV
D. Stage III

D. Stage III

72.

Beyond true pelvis or bladder/rectum mucosa:
A. Stage IV
B. Stage III
C. Stage II
D. Stage I

A. Stage IV

73.

Rectal exam shows no tumor-free space. Stage?
A. Stage II
B. Stage IV
C. Stage III
D. Stage I

C. Stage III

74.

Hydronephrosis in cervical cancer suggests extension to:
A. Paracervical soft tissue
B. Ureters
C. Vagina
D. Rectum

B. Ureters

75.

HPV vaccination is routinely recommended for:
A. Girls only
B. Boys only
C. Pregnant patients only
D. Girls and boys

D. Girls and boys

76.

Anovulatory cycles cause endometrium exposure to:
A. Excess progesterone
B. Excess androgens
C. Unopposed estrogens
D. Unopposed inhibin

C. Unopposed estrogens

77.

Anovulatory endometrium typically lacks:
A. Glandular secretory changes
B. Squamous metaplasia
C. Koilocytosis
D. Viral inclusions

A. Glandular secretory changes

78.

Another progesterone-dependent feature absent in anovulation:
A. Increased mitoses only
B. Basal vacuolization only
C. Keratin pearl formation
D. Stromal predecidualization

D. Stromal predecidualization

79.

Progesterone is absent in anovulation because:
A. Placenta fails to form
B. No corpus luteum forms
C. Theca cells stop aromatase
D. Pituitary secretes excess prolactin

B. No corpus luteum forms

80.

Postpartum fever with uterine tenderness most suggests:
A. Chronic endometritis
B. Endometriosis
C. Cervical ectropion
D. Acute endometritis

D. Acute endometritis

81.

Acute endometritis is most linked to infections after:

A. Ovulation
B. Delivery or miscarriage
C. Menopause
D. HPV vaccination

B. Delivery or miscarriage

82.

Endometriosis is best defined as:
A. Ectopic endometrial tissue outside uterus
B. Endometrial atrophy in uterus
C. Tubal squamous metaplasia
D. Cervical gland hyperplasia

A. Ectopic endometrial tissue outside uterus

83.

Most common site for endometriosis is:
A. Myometrium
B. Cervix
C. Ovaries
D. Liver capsule

C. Ovaries

84.

A common endometriosis location is the:
A. Fallopian fimbriae
B. Rectovaginal septum
C. Urinary bladder mucosa
D. Ovarian medulla

B. Rectovaginal septum

85.

In HPV-related SIL, Ki-67 staining often extends into:
A. Basal layer
B. Stromal fibroblasts
C. Glandular lumen
D. Upper epithelial layers

D. Upper epithelial layers

86.

Strong p16 staining most supports:
A. Candida infection
B. HSV infection
C. High-risk HPV infection
D. Trichomonas infection

C. High-risk HPV infection

87.

Roughly what percent of cervical cancers are SCC?
A. About 80%
B. About 15%
C. About 5%
D. About 40%

A. About 80%

88.

Endometriotic stromal cells generate excess estrogen due to increased:
A. 5α-reductase activity
B. Sulfatase activity
C. Aromatase expression
D. COMT activity

C. Aromatase expression

89.

Endometriosis has been reported in men treated for prostate cancer with:
A. High-dose estrogens
B. High-dose androgens
C. Radiation alone
D. GnRH agonists only

A. High-dose estrogens

90.

A medication class beneficial in endometriosis targets which enzyme?
A. COX-1
B. 5α-reductase
C. Desmolase
D. Aromatase

D. Aromatase

91.

Which hormone most directly enhances persistence of endometriotic tissue?
A. Progesterone
B. Estrogen
C. Inhibin
D. Prolactin

B. Estrogen

92.

A woman with endometriosis has higher risk for certain ovarian cancers. The underlying condition is:
A. Endometriosis
B. Adenomyosis
C. Endometritis
D. PCOS

A. Endometriosis

93.

Likely precursor to endometriosis-related ovarian carcinoma:
A. Adenomyosis
B. Endometrial polyp
C. Atypical endometriosis
D. Non-atypical hyperplasia

C. Atypical endometriosis

94.

Adenomyosis is defined as endometrial tissue within the:
A. Serosa
B. Myometrium
C. Endocervix
D. Vagina

B. Myometrium

95.

Microscopy shows irregular stromal nests ± glands within uterine wall. Diagnosis?
A. Endometrial polyp
B. Endometrial hyperplasia
C. Endometriosis
D. Adenomyosis

D. Adenomyosis

96.

Endometrial polyps can come from using:
A. Letrozole
B. Leuprolide
C. Tamoxifen
D. Clomiphene

C. Tamoxifen

97.

Tamoxifen’s tissue-selective action is best described as:
A. Agonist breast, antagonist endometrium
B. Antagonist breast, agonist endometrium
C. Antagonist breast, antagonist endometrium
D. Agonist breast, agonist endometrium

B. Antagonist breast, agonist endometrium

98.

A common cause of abnormal uterine bleeding and frequent precursor to carcinoma:
A. Adenomyosis
B. Endometriosis
C. Cervicitis
D. Endometrial hyperplasia

D. Endometrial hyperplasia

99.

Endometrial hyperplasia is most strongly linked to:
A. Prolonged estrogenic stimulation
B. Chronic progesterone exposure
C. High prolactin states
D. Acute bacterial infection

A. Prolonged estrogenic stimulation

100.

The estrogen source driving hyperplasia may be:
A. Only ovarian
B. Endogenous or exogenous
C. Only exogenous
D. Only adrenal

B. Endogenous or exogenous

101.

Common genetic alteration in hyperplasia and endometrial carcinoma:
A. APC loss
B. BRCA1 loss
C. RB1 loss
D. PTEN inactivation

D. PTEN inactivation

102.

PTEN loss most directly overactivates which pathway?
A. PI3K/AKT pathway
B. JAK/STAT pathway
C. Notch pathway
D. Hedgehog pathway

A. PI3K/AKT pathway

103.

Germline PTEN mutations causing high endometrial cancer risk:
A. Lynch syndrome
B. Li-Fraumeni syndrome
C. Cowden syndrome
D. Peutz-Jeghers syndrome

C. Cowden syndrome

104.

Cowden syndrome is strongly associated with increased:
A. Colon and gastric cancers
B. Ovarian and pancreatic cancers
C. Liver and lung cancers
D. Breast and endometrial cancers

D. Breast and endometrial cancers

105.

Endometrial hyperplasia is classified as:
A. Non-atypical or atypical
B. Serous or mucinous
C. Diffuse or nodular
D. Simple or cystic

A. Non-atypical or atypical

106.

Atypical endometrial hyperplasia is also called:
A. VIN
B. VAIN
C. Endometrial intraepithelial neoplasia
D. Adenocarcinoma in situ

C. Endometrial intraepithelial neoplasia

107.

Cardinal feature of non-atypical hyperplasia:
A. Stromal invasion
B. Increased gland-to-stroma ratio
C. Koilocytosis
D. Caseating granulomas

B. Increased gland-to-stroma ratio

108.

Atypical hyperplasia is best described as:
A. Complex glands with nuclear atypia
B. Simple glands without atypia
C. Pure stromal overgrowth
D. Surface ulceration only

A. Complex glands with nuclear atypia

109.

Most common type of endometrial carcinoma:
A. Type II carcinoma
B. Clear cell carcinoma
C. Serous carcinoma
D. Type I carcinoma

D. Type I carcinoma

110.

Enzyme high in endometriotic stroma but absent in normal endometrial stroma:
A. 5α-reductase
B. Aromatase
C. DNMT1
D. Myeloperoxidase

B. Aromatase

111.

Endometriosis increases risk of which ovarian cancer subtypes?
A. Serous and mucinous
B. Dysgerminoma and yolk sac
C. Endometrioid and clear cell
D. Granulosa and thecoma

C. Endometrioid and clear cell

112.

Estrogen’s main effect in endometriosis is to:
A. Induce rapid tissue necrosis
B. Enhance tissue survival
C. Block aromatase transcription
D. Prevent stromal proliferation

B. Enhance tissue survival

113.

A uterine wall lesion containing endometrial stroma ± glands is located in the:
A. Endometrium
B. Cervical stroma
C. Myometrium
D. Vaginal submucosa

C. Myometrium

114.

Tamoxifen-associated endometrial polyps best reflect tamoxifen acting as:
A. Weak endometrial estrogen agonist
B. Pure endometrial estrogen antagonist
C. Pure progesterone agonist
D. Aromatase inhibitor

A. Weak endometrial estrogen agonist

115.

Complex gland crowding with nuclear atypia is:
A. Atypical hyperplasia
B. Non-atypical hyperplasia
C. Endometrial polyp
D. Adenomyosis

A. Atypical hyperplasia

116.

Type I endometrial carcinomas are also called:
A. Serous carcinomas
B. Clear cell carcinomas
C. Endometrioid carcinomas
D. Mixed Müllerian tumors

C. Endometrioid carcinomas

117.

Type I endometrioid carcinoma typically arises in the setting of:
A. Endometrial atrophy
B. Endometrial hyperplasia
C. Cervical dysplasia
D. Myometrial fibrosis

B. Endometrial hyperplasia

118.

Type I tumors share risk factors with hyperplasia, including:
A. Obesity and diabetes
B. Smoking and HPV
C. Early menopause only
D. Hyperprolactinemia

A. Obesity and diabetes

119.

Atypical hyperplasia and endometrial carcinoma commonly share mutations in:
A. TP53
B. PTEN
C. RB1
D. APC

B. PTEN

120.

This supports atypical hyperplasia as a:
A. Late metastasis marker
B. Precursor to carcinoma
C. Non-neoplastic change
D. Treatment complication

B. Precursor to carcinoma

121.

Common mutations in type I endometrioid carcinomas increase signaling through:
A. MAPK/ERK
B. JAK/STAT
C. PI3K/AKT
D. Notch

C. PI3K/AKT

122.

PI3K/AKT signaling in endometrial cells tends to augment:
A. Androgen receptor targets
B. Estrogen receptor targets
C. Progesterone receptor targets
D. p53-dependent targets

B. Estrogen receptor targets

123.

Endometrioid carcinoma gross pattern can be:
A. Only diffuse infiltrative
B. Only polypoid
C. Ulcerative
D. Local polypoid or diffuse

D. Local polypoid or diffuse

124.

Typical spread for endometrioid carcinoma occurs via:
A. Lymphatics invasion then extension
B. Hematogenous invasion then extension
C. Myometrial invasion then extension
D. Transcoelomic invasion then extension

C. Myometrial invasion then extension

125.

Endometrioid adenocarcinomas are characterized by glands resembling:
A. Tubal epithelium
B. Normal endometrial epithelium
C. Squamous epithelium
D. Cervical mucus glands

B. Normal endometrial epithelium

126.

Type II endometrial carcinomas most often arise in:
A. Hyperplasia
B. Endometrial atrophy
C. Pregnancy
D. Endometritis

B. Endometrial atrophy

127.

Type II (serous) carcinomas are by definition:
A. Well differentiated
B. Poorly differentiated
C. Low grade
D. Benign

B. Poorly differentiated

128.

Most common subtype of type II endometrial carcinoma:
A. Endometrioid
B. Mucinous
C. Serous carcinoma
D. Adenosquamous

C. Serous carcinoma

129.

Tumor suppressor mutated in ≥90% of serous carcinomas:
A. PTEN
B. BRCA1
C. TP53
D. MLH1

C. TP53

130.

Precursor lesion of serous endometrial carcinoma:
A. EIN
B. Endometrial intraepithelial carcinoma
C. CIN III
D. VAIN

B. Endometrial intraepithelial carcinoma

131.

Endometrial intraepithelial carcinoma consists of:
A. Cells identical to serous carcinoma
B. Benign glands only
C. Stromal invasion present
D. Squamous metaplasia only

A. Cells identical to serous carcinoma

132.

Serous carcinomas often arise in:
A. Enlarged gravid uteri
B. Small atrophic uteri
C. Hypertrophic uteri
D. Adolescent uteri

B. Small atrophic uteri

133.

Serous carcinomas are often:
A. Tiny and superficial
B. Bulky or deeply invasive
C. Always polypoid only
D. Always mucinous

B. Bulky or deeply invasive

134.

Incidence of endometrial carcinoma peaks in:
A. Teen years
B. 20–30
C. 35–45
D. Postmenopausal 55–65

D. Postmenopausal 55–65

135.

Serous carcinoma occurs more frequently in women of:
A. Asian descent
B. African American descent
C. Native American descent
D. Hispanic descent

B. African American descent

136.

Serous carcinoma contributes to mortality in African American women being:
A. 2-fold higher
B. 10-fold higher
C. Equal to Caucasian women
D. Lower than Caucasian women

A. 2-fold higher

137.

Typical presenting symptom aiding early detection for Serous carcinoma:
A. Purulent cervical discharge
B. Postmenopausal vaginal bleeding
C. Cyclic pelvic pain only
D. Urinary retention

B. Postmenopausal vaginal bleeding

138.

For Serous carcinoma, Postmenopausal bleeding may occur with:
A. Excess leukorrhea
B. Frothy green discharge
C. Curdy discharge
D. Vesicular lesions

A. Excess leukorrhea

139.

Malignant mixed Müllerian tumors are typically:
A. Small and cystic
B. Bulky/polypoid
C. Flat plaques
D. Papillary fronds only

B. Bulky/polypoid

140.

Histology of malignant mixed Müllerian tumor shows:
A. Pure adenocarcinoma only
B. Adenocarcinoma + malignant mesenchyme
C. Pure sarcoma only
D. Pure squamous nests

B. Adenocarcinoma + malignant mesenchyme

141.

Malignant mixed Müllerian tumors most often occur in:
A. Premenopausal teens
B. Postmenopausal women
C. Pregnant women
D. Men

B. Postmenopausal women

142.

Typical presentation of malignant mixed Müllerian tumors:
A. Vaginal bleeding
B. Painless vulvar papules
C. Amenorrhea only
D. Galactorrhea

A. Vaginal bleeding

143.

Diagnosis of adenosarcoma requires:
A. Malignant glands, benign stroma
B. Malignant stroma, benign abnormal glands
C. Benign glands, benign stroma
D. Malignant glands, malignant stroma

B. Malignant stroma, benign abnormal glands

144.

Adenosarcomas are commonly seen in:
A. 4th–5th decade
B. 1st–2nd decade
C. 7th–8th decade
D. Childhood only

A. 4th–5th decade

145.

Adenosarcomas are generally:
A. High grade aggressive
B. Low grade malignancy
C. Always metastatic
D. Always benign

B. Low grade malignancy

146.

Type I endometrioid tumors are associated with unopposed:
A. Estrogen stimulation
B. Progesterone stimulation
C. Inhibin stimulation
D. Oxytocin stimulation

A. Estrogen stimulation

147.

Oophorectomy benefits endometrial stromal adenosarcoma because of:
A. Progesterone replacement effect
B. HPV eradication mechanism
C. Estrogen withdrawal effect
D. Iron chelation effect

C. Estrogen withdrawal effect

148.

Low-grade endometrial stromal sarcoma commonly shows:
A. JAZF1–SUZ12 fusion
B. PTEN–TP53 fusion
C. MED12–RB1 fusion
D. KRAS–APC fusion

A. JAZF1–SUZ12 fusion

149.

JAZF1 most directly encodes a:
A. Histone acetyltransferase
B. Cell-surface receptor
C. Spindle checkpoint kinase
D. Transcriptional repressor

D. Transcriptional repressor

150.

SUZ12 is best linked to:
A. Microtubule polymerization
B. Repressive histone marks
C. Steroid hormone cleavage
D. Viral capsid assembly

B. Repressive histone marks

151.

MED12 mutations occur in ~70% of uterine:
A. Endometrial polyps
B. Leiomyomas
C. Granulosa tumors
D. Stromal sarcomas

B. Leiomyomas

152.

MED12 mutations are virtually unique to:
A. Müllerian epithelial tumors
B. Germ cell tumors
C. Sex cord tumors
D. Uterine smooth muscle tumors

D. Uterine smooth muscle tumors

153.

MED12 mutations are seen in:
A. Leiomyomas and leiomyosarcomas
B. Adenomatoid tumors only
C. Paratubal cysts only
D. Serous carcinomas only

A. Leiomyomas and leiomyosarcomas

154.

A uterine leiomyosarcoma most often metastasizes by:
A. Perineural spread
B. Transcoelomic seeding
C. Hematogenous spread
D. Direct extension only

C. Hematogenous spread

155.

Most typical distant metastasis site for leiomyosarcoma:
A. Thyroid
B. Lungs
C. Spleen
D. Pancreas

B. Lungs

156.

Distant spread pattern most consistent with leiomyosarcoma:
A. Omentum, peritoneum, ovaries
B. Pelvic nodes, inguinal nodes
C. Skin, liver, adrenal
D. Lung, bone, brain

D. Lung, bone, brain

157.

Regurgitation theory of endometriosis proposes ectopic implants via:
A. Direct cervical invasion
B. Sexual transmission
C. Retrograde menstrual flow
D. Hematogenous emboli only

C. Retrograde menstrual flow

158.

“Benign metastases” theory proposes endometriosis spreads via:
A. Blood and lymphatics
B. Retrograde flow only
C. Surface inoculation only
D. Ovulation-related rupture

A. Blood and lymphatics

159.

Most common primary fallopian tube lesion:
A. Serous carcinoma
B. Salpingitis nodosa
C. Endometriosis plaque
D. Paratubal cysts

D. Paratubal cysts

160.

Paratubal cysts are typically:
A. Solid nodules, hemorrhagic
B. Translucent cysts, clear fluid
C. Papillary masses, mucin-filled
D. Ulcerated plaques, crusted

B. Translucent cysts, clear fluid

161.

Benign fallopian tube tumor is usually:
A. Adenomatoid tumor
B. Dysgerminoma
C. Brenner tumor
D. Choriocarcinoma

A. Adenomatoid tumor

162.

Tubal adenomatoid tumors often occur:
A. Intramucosal only
B. Endometrial stroma only
C. Subserosal or mesosalpinx
D. Cervical transformation zone

C. Subserosal or mesosalpinx

163.

Tubal adenomatoid tumor counterpart occurs in:
A. Endocervix
B. Breast ducts
C. Bartholin gland
D. Testis or epididymis

D. Testis or epididymis

164.

PCOS is best defined by:
A. Hyperandrogenism with chronic anovulation
B. Hypoandrogenism with ovulation
C. Progesterone excess only
D. Estrogen deficiency only

A. Hyperandrogenism with chronic anovulation

165.

PCOS reflects dysregulation of enzymes in:
A. Collagen synthesis
B. Androgen biosynthesis
C. Heme synthesis
D. Bile acid synthesis

B. Androgen biosynthesis

166.

PCOS increases endometrial risk via increased free:
A. Progesterone
B. Testosterone
C. Estrone
D. Inhibin

C. Estrone

167.

In PCOS, increased free estrone raises risk of:
A. Cervical dysplasia
B. Ovarian torsion
C. Vaginal SCC
D. Endometrial hyperplasia/carcinoma

D. Endometrial hyperplasia/carcinoma

168.

Stromal hyperthecosis is seen most often in:
A. Adolescents
B. Postmenopausal women
C. Pregnancy
D. Prepubertal girls

B. Postmenopausal women

169.

Stromal hyperthecosis classically shows:
A. Bilateral uniform ovarian enlargement
B. Unilateral ovarian atrophy
C. Small ovaries with fibrosis
D. Calcified cortical plaques

A. Bilateral uniform ovarian enlargement

170.

Microscopy in stromal hyperthecosis shows:
A. Koilocytosis with halos
B. Caseating granulomas
C. Hypercellular stroma, luteinization
D. Glands invading myometrium

C. Hypercellular stroma, luteinization

171.

Virilization in stromal hyperthecosis is:
A. Less than PCOS
B. More striking than PCOS
C. Absent versus PCOS
D. Identical to PCOS

B. More striking than PCOS

172.

Cystic ovarian follicles can arise from:
A. Luteal cyst rupture
B. Teratoma degeneration
C. Tubal epithelial rests
D. Unruptured Graafian follicles

D. Unruptured Graafian follicles

173.

Cystic follicles can also form when follicles:
A. Rupture then immediately seal
B. Never reach antral stage
C. Implant in myometrium
D. Become malignant rapidly

A. Rupture then immediately seal

174.

Most primary ovarian neoplasms derive from:
A. Germ cell lineage
B. Müllerian epithelium
C. Smooth muscle lineage
D. Neural crest lineage

B. Müllerian epithelium

175.

Benign ovarian tumor with cystic areas:
A. Adenofibroma
B. Cystadenofibroma
C. Cystadenoma
D. Borderline serous tumor

C. Cystadenoma

176.

Benign ovarian tumor with mainly fibrous areas:
A. Adenofibroma
B. Cystadenoma
C. Mature teratoma
D. Fibrosarcoma

A. Adenofibroma

177.

Benign ovarian tumor with cystic and fibrous areas:
A. Cystadenoma
B. Adenofibroma
C. Dysgerminoma
D. Cystadenofibroma

D. Cystadenofibroma

178.

Stromal hyperthecosis is also called:
A. Endosalpingiosis
B. Adenomyosis
C. Cortical stromal hyperplasia
D. Endometrial atrophy

C. Cortical stromal hyperplasia

179.

An ovarian tumor described as borderline/malignant with a cystic component is:
A. Adenofibroma
B. Cystadenocarcinoma
C. Cystadenoma
D. Fibroma

B. Cystadenocarcinoma

180.

Benign ovarian tumors are more common in:
A. Women age 20–45
B. Women age 45–65
C. Postmenopausal women only
D. Prepubertal girls only

A. Women age 20–45

181.

Malignant ovarian tumors are more common in:
A. Women age 20–45
B. Adolescents
C. Women age 45–65
D. Children

C. Women age 45–65

182.

Type I ovarian carcinomas are typically:
A. Low-grade tumors
B. High-grade serous tumors
C. Always mucinous tumors
D. Always germ cell tumors

A. Low-grade tumors

183.

Type I ovarian carcinomas often arise with:
A. Endometriosis or borderline tumors
B. STIC lesions only
C. HPV-associated lesions
D. Leiomyomas

A. Endometriosis or borderline tumors

184.

Type II ovarian carcinomas are best described as:
A. Low-grade endometrioid tumors
B. High-grade serous carcinomas
C. Benign cystic neoplasms
D. Borderline mucinous tumors

B. High-grade serous carcinomas

185.

Type II ovarian carcinomas arise from:
A. Endometriosis implants
B. Serous borderline tumors
C. Serous intraepithelial carcinoma
D. Granulosa cell tumors

C. Serous intraepithelial carcinoma

186.

Most common malignant ovarian tumor type:
A. Serous tumors
B. Mucinous tumors
C. Clear cell tumors
D. Brenner tumors

A. Serous tumors

187.

Serous tumors are typically:
A. Solid-only neoplasms
B. Cystic neoplasms
C. Purely stromal tumors
D. Always bilateral fibromas

B. Cystic neoplasms

188.

Germline mutations increasing ovarian cancer risk include:
A. PTEN and TP53
B. KRAS and BRAF
C. MLH1 and MSH2
D. BRCA1 and BRCA2

D. BRCA1 and BRCA2

189.

Low-grade serous carcinomas often arise with:
A. Serous borderline tumors
B. STIC lesions
C. Endometriosis only
D. Vaginal SCC

A. Serous borderline tumors

190.

High-grade serous carcinomas often arise from:
A. Serous borderline tumors
B. In situ lesions in fimbriae
C. Ovarian fibromas
D. Cervical HSIL

B. In situ lesions in fimbriae

191.

Serous tubal intraepithelial carcinoma (STIC) is associated with sporadic:
A. Low-grade mucinous cancers
B. High-grade serous ovarian cancers
C. Endometrioid hyperplasia
D. Leiomyosarcoma

B. High-grade serous ovarian cancers

192.

Women with BRCA mutation and strong family history may undergo:
A. Prophylactic hysterectomy only
B. Prophylactic salpingo-oophorectomy
C. Cervical conization
D. Endometrial ablation

B. Prophylactic salpingo-oophorectomy

193.

High-grade serous tumors commonly show mutations in:
A. KRAS
B. BRAF
C. TP53
D. ERBB2

C. TP53

194.

Low-grade serous tumors more often show mutations in:
A. KRAS/BRAF/ERBB2
B. TP53
C. PTEN
D. APC

KRAS/BRAF/ERBB2

195.

STIC lesions are identical to high-grade serous carcinoma except they lack:
A. Necrosis
B. Papillary architecture
C. Pleomorphism
D. Invasion

D. Invasion

196.

Mucinous tumors occur most frequently in:
A. Childhood
B. Middle adult life
C. After menopause
D. Before puberty

B. Middle adult life

197.

Mucinous tumors rarely occur:
A. In middle adult life
B. In adolescence only
C. Before puberty or after menopause
D. In reproductive years

C. Before puberty or after menopause

198.

Mucinous tumors are:
A. Benign only
B. Borderline mostly
C. Benign mostly
D. Borderline only

C. Benign mostly

199.

A large unilateral ovarian mass shows mucinous epithelium. Which mutation is most consistent?
A. TP53 mutation
B. KRAS mutation
C. FOXL2 mutation
D. PTEN mutation

A. TP53 mutation

200.

Which feature best fits mucinous ovarian tumors?
A. Surface commonly involved
B. Usually bilateral disease
C. Diffuse peritoneal implants
D. Surface rarely involved

D. Surface rarely involved

201.

Histology shows tubular glands resembling endometrium. Tumor type?
A. Endometrioid ovarian tumor
B. Serous cystadenocarcinoma
C. Mucinous cystadenoma
D. Dysgerminoma

A. Endometrioid ovarian tumor

202.

Endometrioid ovarian carcinomas may coexist with:
A. PCOS
B. Salpingitis
C. Endometriosis
D. Leiomyomas

C. Endometriosis

203.

Endometrioid carcinoma + endometriosis often share mutations affecting:
A. Hedgehog and Wnt
B. PI3K/AKT and mismatch repair
C. JAK/STAT and p53
D. EGFR and ALK

B. PI3K/AKT and mismatch repair

204.

Endometrioid ovarian carcinomas are usually:
A. High-grade tumors
B. Borderline only
C. Always metastatic
D. Low-grade tumors

D. Low-grade tumors

205.

Large epithelial cells with clear cytoplasm suggest:
A. Serous carcinoma
B. Mucinous carcinoma
C. Clear cell carcinoma
D. Transitional cell tumor

C. Clear cell carcinoma

206.

Transitional cell tumors of the ovary are usually:
A. Benign
B. Highly malignant
C. Always bilateral
D. Always functional

A. Benign

207.

Ovarian carcinoma seeds peritoneum via capsule. Expected finding?
A. Hyperandrogenism
B. Chylous pleural effusion
C. Pelvic inflammatory disease
D. Massive ascites

D. Massive ascites

208.

Most ovarian carcinomas present with:
A. Cyclic bleeding only
B. Lower abdominal pain, enlargement
C. Postcoital spotting only
D. Acute fever and discharge

B. Lower abdominal pain, enlargement

209.

Benign ovarian teratomas are commonly called:
A. Dermoid cysts
B. Serous cysts
C. Brenner tumors
D. Krukenberg tumors

A. Dermoid cysts

210.

Mature (benign) teratoma is occasionally linked to:
A. Lambert-Eaton syndrome
B. Hashimoto encephalopathy
C. Inflammatory limbic encephalitis
D. Guillain-Barré syndrome

C. Inflammatory limbic encephalitis

211.

A teratoma causes flushing and wheeze. Most likely syndrome?
A. Cushing syndrome
B. Carcinoid syndrome
C. Turner syndrome
D. Conn syndrome

B. Carcinoid syndrome

212.

An 18-year-old has malignant ovarian teratoma. Type?
A. Immature teratoma
B. Mature teratoma
C. Struma ovarii
D. Dermoid cyst

A. Immature teratoma

213.

Most dysgerminomas are:
A. Bilateral tumors
B. Multifocal tumors
C. Capsular-seeding tumors
D. Unilateral tumors

D. Unilateral tumors

214.

Rapidly growing pelvic mass in a child suggests:
A. Brenner tumor
B. Thecoma
C. Yolk sac tumor
D. Endometrioma

C. Yolk sac tumor

215.

Ovarian choriocarcinoma (nongestational) is typically:
A. Chemo-sensitive, favorable outcome
B. Chemo-resistant, often fatal
C. Slow-growing, indolent course
D. Benign, hormonally silent

B. Chemo-resistant, often fatal

216.

Granulosa cell tumors are usually:
A. Benign, potentially malignant
B. Bilateral, potentially malignant
C. Nonfunctional, potentially malignant
D. Unilateral, potentially malignant

D. Unilateral, potentially malignant

217.

FOXL2 mutations are common in:
A. Adult granulosa tumors
B. Yolk sac tumors
C. Mucinous carcinomas
D. Dysgerminomas

A. Adult granulosa tumors

218.

Tumors composed predominantly of theca cells are:
A. Usually malignant
B. Usually borderline
C. Almost always benign
D. Always metastatic

C. Almost always benign

219.

Plump spindle stromal cells with lipid droplets indicates:
A. Fibroma
B. Thecoma
C. Dysgerminoma
D. Brenner tumor

B. Thecoma

220.

Most fibromas, fibrothecomas, and thecomas are:
A. Benign
B. Highly malignant
C. Always bilateral
D. Often metastatic

A. Benign

221.

Over half of Sertoli-Leydig tumors show mutation in:
A. KRAS
B. TP53
C. FOXL2
D. DICER1

D. DICER1

222.

DICER1 mutations primarily disrupt:
A. DNA mismatch repair
B. Steroid receptor binding
C. microRNA regulation
D. Collagen cross-linking

C. microRNA regulation

223.

A pregnancy-associated ovarian mass mimics corpus luteum. Diagnosis?
A. Pregnancy luteoma
B. Krukenberg tumor
C. STIC lesion
D. Endometrioma

A. Pregnancy luteoma

224.

Pregnancy luteoma may cause:
A. Maternal hypocalcemia
B. Virilization in female infants
C. Severe hyperprolactinemia
D. Autoimmune oophoritis

B. Virilization in female infants

225.

Metastatic GI carcinoma to ovaries is termed:
A. Brenner tumor
B. Dermoid cyst
C. Krukenberg tumor
D. Thecoma

C. Krukenberg tumor

226.

Krukenberg tumor is classically:
A. Unilateral, serous papillary
B. Pure squamous morphology
C. Clear-cell, endometrial-type
D. Bilateral mucin signet-ring cells

D. Bilateral mucin signet-ring cells

227.

In mucinous ovarian tumors, laterality is most often:
A. Unilateral
B. Bilateral
C. Diffusely multifocal
D. Always midline

A. Unilateral

228.

Clear cell ovarian carcinoma most resembles:
A. Secretory-phase normal endometrium
B. Hypersecretory gestation endometrium
C. Atrophic endometrium
D. Proliferative-phase endometrium

B. Hypersecretory gestation endometrium