Robbins Flashcards

(125 cards)

1
Q

gives rise to the epithelium and stroma of the ovary

A

mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

these mature into the fallopian tubes

A

unfused upper portions of the müllerian ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

these develop into the uterus, cervix, and upper vagina

A

fused lower portion of the müllerian ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

forms the lower part of the vagina and the vestibule of the external genitalia

A

urogenital sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

in embryology, which of the ducts regress in the female?

A

mesonephric ducts (wolffian ducts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In females, remnants of the mesonephric ducts may persist into adult life as epithelial inclusions adjacent to the ovaries, tubes, and uterus called

A

Gartner duct cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

infection shows characteristic colposcopic appearance of strawberry cervix.

A

Trichomonas vaginalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the most serious complication of gonorrhea in women

A

Pelvic inflammatory disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

tubal plicae, denuded of epithelium, adhere to one another and slowly fuse in a reparative, scarring process that forms glandlike spaces and blind pouches, referred to as

A

chronic salpingitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

marked thinning of the epidermis, degeneration of the basal epithelial cells, excessive keratinization (hyperkeratosis), sclerotic changes of the superficial dermis, and a bandlike lymphocytic infiltrate in the underlying dermis

A

Lichen sclerosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinically it presents as leukoplakia, and histologic examination reveals thickening of the epidermis (acanthosis) and hyperkeratosis. Lymphocytic infiltration of the dermis is sometimes present. The hyperplastic epithelium may show mitotic activity but lacks cellular atypia

A

squamous cell hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

___ are benign genital warts caused by low-risk HPV, mainly types __ and __

A

Condyloma acuminata, 6 and 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

characteristic viral cytopathic changes seen in condyloma acuminata which manifest as nuclear enlargement, hyperchromasia, and a cytoplasmic perinuclear halo

A

koilocytic atypia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F Condylomata acuminata are precancerous lesions

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

most common histologic type of vulvar cancer

A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

This vulvar squamous cell carcinoma subtype is related to infection with high-risk HPVs, most commonly HPV-16. These are less common (30% of cases) and occur in younger women (average 60 years of age)

A

Basaloid and warty carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

This vulvar squamous cell carcinoma subtype is unrelated to HPV infection. These are more common (70% of cases) and occur in older women (average 75 years of age)

A

Keratinizing squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

precursor lesion of vulvar Basaloid and warty carcinomas

A

classic vulvar intraepithelial neoplasia (VIN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

risk of progression to invasive carcinoma of vulvar intraepithelial neoplasia (VIN) is higher in women who are older than ___ years of age or who are_______.

A

45, immunosuppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

precursor lesion of vular Keratinizing squamous cell carcinoma

A

differentiated vulvar intraepithelial neoplasia (differentiated VIN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Vulvar Keratinizing squamous cell carcinoma occurs most often in individuals with

A

long-standing lichen sclerosus or squamous cell hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

sometimes found to be mutated in VIN

A

TP53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

this vulvar precursor lesion is microscopically characterized by epidermal thickening, nuclear atypia, increased mitoses, and lack of cellular maturation, features analogous to those seen in cervical squamous intraepithelial lesions

A

Classic VIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

this vulvar precursor lesion is microscopically characterized by marked atypia of the basal layer of the squamous epithelium and normal-appearing differentiation of the more superficial layers

A

Differentiated VIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
sharply circumscribed nodule, most commonly on the labia majora or interlabial folds, it consists of papillary projections covered by two cell layers, an upper layer of columnar secretory cells and a deeper layer of flattened myoepithelial cells
Papillary hidradenoma
26
T/F Vulvar Paget like it’s counterpart in the nipple, is typically associated with underlying cancer
False
27
a failure of müllerian duct fusion and is accompanied by a double uterus
uterus didelphys
28
Vaginal adenosis is found in only a small percentage of adult women, but has been reported in 35% to 90% of women exposed to
diethylstilbestrol (DES)
29
most common and 2nd most common malignant tumors to involve the vagina are
carcinoma spreading from the cervix, followed by primary squamous cell carcinoma of the vagina
30
Virtually all primary carcinomas of the vagina are squamous cell carcinomas associated with infection with
high-risk HPV infection
31
Squamous cell carcinoma of the vagina arises from a premalignant lesion called
vaginal intraepithelial neoplasia
32
found in infants and children younger than 5 years of age. These tumors tend to grow as polypoid, rounded, bulky masses that have the appearance and consistency of grapelike clusters
Embryonal Rhabdomyosarcoma (sarcoma botryoides)
33
HPV- susceptible cells in the cervix
immature basal squamous cells and endocervical glandular cells
34
most susceptible to HPV infection in the cervix
Immature squamous cells
35
stimulates maturation of the cervical and vaginal squamous mucosa and formation of intracellular glycogen vacuoles in the squamous cells
production of estrogens by the ovary
36
dominant microbial species in the normal vagina
Lactobacilli
37
Lactobacilli produce lactic acid, which maintains the vaginal pH at _____
below 4.5
38
fourth most common cancer in women
cervical cancer
39
this infection is most important factor in the development of cervical cancer
High-risk HPV infection
40
This high-risk HPV subtype alone accounts for almost 60% of cervical cancer cases
HPV-16
41
This high-risk HPV subtype alone accounts for another 10% of cervical cancer cases
HPV-18
42
50% of HPV infections are cleared within
8 months
43
90% of HPV infections are cleared within
2 years
44
The ability of HPV to act as a carcinogen depends on these viral proteins (2)
viral E6 and E7 proteins
45
viral protein E6 interferes with____ and E7 with____
p53, RB
46
How does the viral E7 protein of high-risk HPV promote cancer?
It binds the hypophosphorylated (active) form of RB and promotes its degradation via the proteasome pathway and also binds and inhibits p21 and p27
47
How does the viral E6 protein of high-risk HPV promote cancer?
it binds p53 and promote its degradation by the proteasome and upregulates the expression of telomerase
48
represents a productive HPV infection in which there is a high level of viral replication
LSIL
49
represents an HPV infection in which there is a low level of viral replication
HSIL
50
At an ultrastructural level, these “halos” consist of perinuclear vacuoles, a cytopathic change created in part by an HPV-encoded protein
E5
51
T/F The progression time from in situ to invasive adenosquamous and neuroendocrine carcinomas is shorter than in squamous cell carcinoma
TRUE
52
most common cause of dysfunctional uterine bleeding which results in excessive endometrial stimulation by estrogens that is unopposed by progesterone
Failure of ovulation/ anovulation
53
diagnosis of chronic endometritis rests on the identification of _______ in the stroma
plasma cells
54
likely precursor to endometriosis-related ovarian carcinoma
Atypical endometriosis
55
defined as the presence of endometrial tissue within the uterine wall (myometrium)
adenomyosis
56
It is defined as an abnormal proliferation of the endometrial glands relative to the stroma, resulting in an increased gland-to-stroma ratio when compared with normal proliferative endometrium.
Endometrial hyperplasia
57
Inactivation of the this tumor suppressor gene is a common genetic alteration in both endometrial hyperplasias and endometrioid endometrial carcinoma
PTEN
58
increased gland-to- stroma ratio. The glands show variation in size and shape and may be dilated. Although there may be back-to-back glands focally, some intervening stroma is usually retained
Typical hyperplasia
59
composed of complex patterns of proliferating glands displaying nuclear atypia.The glands are commonly back- to-back and often have complex outlines due to branching structures. Individual cells are rounded and lose the normal perpendicular orientation to the basement membrane. In addition, the nuclei have open (vesicular) chromatin and conspicuous nucleoli.
atypical hyperplasia
60
Endometrial hyperplasia is most commonly caused by
unopposed estrogen stimulation
61
most common invasive cancer of the female genital tract
Endometrial carcinoma
62
When PTEN function is lost, the _______ pathways becomes overactive
phosphatidylinositol 3-kinase (PI3K)/AKT pathway
63
Endometrial carcinoma molecular subtype that has an exceptionally high burden of somatic mutations
Ultramutated/POLE tumors
64
Endometrial carcinoma molecular subtype defined by mutations in or epigenetic silencing of mismatch repair genes, also leading to genomic instability and a high burden of somatic mutations
Hypermutated/MSI (microsatellite instability) tumors
65
Endometrial carcinoma molecular subtype associated with endometrioid morphology that is frequently associated with mutations that upregulate signaling through the PI3K/AKT pathway
Copy number low/MSS (microsatellite stable) tumors
66
Endometrial carcinoma molecular subtype with aggressive tumors with serous or high-grade endometrioid morphology that are often associated with TP53 mutations and numerous genomic copy number variants
Copy number high/ serous-like tumors
67
most common type of endometrial carcinoma
Endometrioid Endometrial Carcinoma
68
Endometrioid Endometrial Carcinoma falls under what type category?
type 1
69
hallmark of the endometrioid endometrial carcinoma tumor type is that the most common mutations present act to increase signaling through what pathway?
PI3K/AKT pathway
70
this signaling pathway augments expression of estrogen receptor–dependent target genes in endometrial cells
PI3K/AKT pathway
71
mutations that impact the PI3K/AKT pathway in endometrial carcinomas are (4)
PTEN PIK3CA KRAS ARID1A
72
mutations in endometrioid carcinoma disrupt genes that are required for the maintenance of genomic stability (3)
MMR (MSH1, MLH2) POLE TP53
73
Tumors with these mutations or defects are frequently associated with large numbers of infiltrating T cells (2)
POLE and MMR
74
Serous Endometrial Carcinoma falls under what type category?
type 2
75
All serous carcinomas belong to which molecular category?
copy number high / serous-like
76
Serous endometrial carcinoma is highly associated with disruptive mutations in what gene?
TP53
77
precursor lesion of Serous endometrial carcinoma
serous endometrial intraepithelial carcinoma
78
T/F All of the tumors in the category of Serous endometrial caracinoma are classified as grade 3 irrespective of architectural pattern
True
79
T/F Carcinosarcoma (Malignant Mixed Müllerian Tumors) are carcinomas that have acquired the capacity for mesenchymal differentiation
True
80
Usual mutations found in carcinosarcomas (malignant mixed mullerian tumos) (3)
PTEN, PT53, PIK3CA
81
endometrial stromal tumor which presents as a large broad-based polypoid growth that has malignant-appearing stroma, which coexists with benign but abnormally shaped endometrial glands
adenosarcoma
82
Endometrial stromal neoplasms are divided into two categories which are
benign stromal nodules and endometrial stromal sarcoma
83
fusion gene usually found in Low-grade endometrial stromal sarcoma
JAZF1-SUZ12 fusion
84
mutation that occurs in roughly 70% of uterine leiomyomas that appears to be virtually unique to uterine smooth muscle tumors
MED12
85
well circumscribed monotonous proliferation of bland endometrial stromal cells with expansive growth pattern at the margins but not infiltrating. If protrusions present must be <3mm and <3 protrusions
Endometrial stromal nodule
86
mutation in endometrial stromal nodule
JAZF1-SUZ12
87
Distinction between leiomyomas and leiomyosarcomas are based on (3)
Nuclear atypia, mitotic index, and tumor necrosis
88
cystic follicle size
>/= 2 cm
89
follicle cyst size
>2cm
90
ovarian cyst lined by a rim of bright yellow tissue containing luteinized granulosa cells and are prone to rupture
luteal cyst / corpus luteum
91
Most primary ovarian neoplasms arise from
müllerian epithelium
92
three major ovarian tumor histologic types based on the differentiation of the neoplastic epithelium
serous, mucinous, and endometrioid tumors
93
inherited germline mutations in both these 2 genes increase susceptibility to both ovarian cancer and breast cancer
BRCA1 and BRCA2
94
recently thought to be the precursor lesion for sporadic high-grade serous ovarian cancers
serous tubal intraepithelial carcinoma (STIC)
95
What is the origin of high-grade serous carcinomas that involve the ovary, without concomitant involvement of the fallopian tube?
cortical inclusion cysts or implantation of detached fallopian tube epithelium at ovary
96
Low-grade ovarian tumors arising in serous borderline tumors have mutations in ___________(3) and usually have ____ type Tp53 genes
KRAS, BRAF, or ERBB2 oncogenes, and usually have wild-type TP53 genes
97
High-grade ovarian serous tumors have a high frequency of what mutation?
TP53
98
Almost all ovarian carcinomas arising in women with BRCA1 or BRCA2 mutations are
high-grade serous carcinomas with TP53 mutations
99
In serous, mucinous, or seroumucinous ovarian tumors, if intracystic epithelial proliferation accounts for < 10% of the tumour, the neoplasm should be classified as
cystadenoma with focal epithelial proliferation
100
T/F Bilaterality is an uncommon finding in, benign serous cystadenomas, serous borderline tumors, serous carcinomas.
False. Bilaterality is common, occurring in 20% of benign serous cystadenomas, 30% of serous borderline tumors, and approximately 66% of serous carcinomas.
101
Stromal microinvasion in ovarian serous tumors is defined as
invasion < 5 mm in greatest dimension in any single focus
102
The term “implant” is used in the context of extraovarian disease associated with SBT of the ovary. Implants of serous borderline are, by definition,_______; if there is invasion, a diagnosis of ______should be made
non-invasive, LOW GRADE SEROUS CARCINOMA
103
precursor to low-grade ovarian serous carcinoma
micropapillary carcinoma
104
ovarian serous tumor subtype that has elongated micropapillae without stromal cores (at least 5 times longer than wide) that directly emanate from large papillae (the so-called Medusa head appearance) and/or small punched-out cribriform spaces. An area of pure growth measuring > 5 mm is required for the tumour to be classified as the this subtype
micropapillary/cribriform
105
a consistent genetic alteration in mucinous tumors of the ovary, including the majority of benign mucinous cystadenomas (58%), mucinous borderline tumors (75% to 86%), and ovarian mucinous carcinomas (85%)
KRAS
106
T/F In ovarian mucinous tumors, the surface of the ovary is rarely involved, and only 5% of primary mucinous cystadenomas and mucinous carcinomas are bilateral
T
107
is marked by mucinous ascites, cystic epithelial implants on the peritoneal surfaces, adhesions, and frequent involvement of the ovaries, if extensive, may result in intestinal obstruction and death.
pseudomyxoma peritonei
108
T/F Because the majority of primary mucinous ovarian tumors are unilateral, bilateral presentation of mucinous tumors always requires exclusion of metastasis from a non-ovarian primary tumor.
True
109
sometimes a precursor lesion to ovarian endometrioid carcinoma
ovarian endometriosis
110
Molecular studies have found similarities of ovarian endometrioid carcinoma to endometrial endometrioid carcinoma; shared features include mutations in _____ pathway and _____
mutations that increase PI3K/AKT pathway (PTEN, PIK3CA, ARID1A, and KRAS) and MMR
111
an uncommon variant ovarian tumor in which there is pronounced proliferation of the fibrous stroma that underlies the columnar lining epithelium, usually small and multilocular and have simple papillary processes that are not as complicated and branching as those found in the ordinary cystadenoma
Cystadenofibroma
112
contain neoplastic epithelial cells resembling urothelium and are usually benign
Transitional cell tumors / Brenner tumors
113
karyotype of almost all benign ovarian teratomas is
46,XX
114
teratoma composed entirely of mature thyroid tissue, which may be functional and cause hyperthyroidism
Struma ovarii
115
how do you deyermine the histologic grading (I to III) of an ovarian immature malignant teratoma
116
yolk sac tumor is also known as
endodermal sinus tumor
117
characteristic histologic feature of yolk sac tumor
Schiller-Duval body
118
undifferentiated gonadal mesenchyme eventually produces specific types of cells in male (___________) and female (_________)
Sertoli and Leydig granulosa and theca
119
small, distinctive, glandlike structures filled with an acidophilic material recall immature follicles in Granulosa cell tumors
Call-Exner bodies
120
The most common driver mutation found in granulosa cell tumors
FOXL2 gene
121
syndrome with these combination of findings: ovarian tumor, hydrothorax, and ascites
Meigs syndrome
122
3 Tumors arising in the ovarian stroma
Fibromas,Thecomas, and Fibrothecomas
123
in one-half of cases, Sertoli-Leydig Cell Tumors have mutations in
DICER1
124
metastatic gastrointestinal carcinoma involving the ovaries characterized by bilateral metastases composed of mucin- producing cancer cells with a “signet-ring” appearance, most often of gastric origin
Krukenberg tumor
125