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Block 10 Week 3 > GYN Path - Fung > Flashcards

GYN Path - Fung Flashcards

1
Q

most disorders of the vulva are inflammatory and similar to skin path, such as what three things?

A

conact dermatitis
eczematous dermatitis
infectious

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2
Q

what are the three M’s used to describe HSV infections histologically?

A

molding
margination
multinucleation

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3
Q

Lichen sclerosis is characterized by thinning of the (blank) and sclerosis of the (blank) of the vulva

A

thinning of the epidermis

sclerosis of the dermis

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4
Q

Describe the general appearance grossly of lichen sclerosis?

A

leukoplakia with parchment-like vulvar skin

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5
Q

t/f: leukoplakia can be neoplastic or non-neoplastic

A

true

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6
Q

what is the only way to tell if leukoplakia is neoplastic?

A

biopsy

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7
Q

is lichen sclerosis benign/

A

yes, but has a slight chance of going to squamous cell carcinoma

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8
Q

in lichen simplex chronicus, you get hyperplasia of what cell type and hyperkeratosis

A

hyperplasia of the squamous cell epithelium

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9
Q

describe the gross appearance of lichen simplex chronicus/

A

white patch over thick, leathery skin

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10
Q

Lichen simplex chronicus is associated with what behavior?

A

chronic itching and scratching; pruritis

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11
Q

Condyloma is most commonly due to what two strains of HPV?

A

6 and 11

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12
Q

HPV-associated condylomas have what HPV hallmark histologically?

A

koilocytic changes (raisin-like nucleus)

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13
Q

t/f: condylomas often progress to carcinoma

A

false; rarely; low risk strains of HPV

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14
Q

vulvar intraepithelial neoplasa (VIN) is ascc’d with what strains of HPV

A

16
18
31
33

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15
Q

How does VIN initially present?

A

also as leukoplakia; need biopsy to distinguish from lichen sclerosis

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16
Q

t/f: non-HPV etiology of VIN is long standing lichen sclerosis

A

true

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17
Q

describe the grading system for VIN

A

I: less than 1/3 of the thickness of the epi
II: less than 2/3 of the epi
III: almost all of the epi
Carcinoma in situ: entire thickness of the epi

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18
Q

What causes “orange skinning” of the breast?

A

Paget’s dz of the breast

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19
Q

What is the underyling cause of the orange skinning in Paget’s dz of the breast?

A

carcinoma

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20
Q

Is there underlying carcinoma in Paget’s of the vulva?

A

nope!

it is carcinoma in situ with no underlying carcinoma

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21
Q

From what type of cancer must you distinguish Paget’s of the vulva?

A

melanoma

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22
Q

describe the physical findings that suggest melanoma and not Paget’s vulva

A

superficial spreading
not as cohesive of a lesion
produces pigment

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23
Q

Describe the following markers for Paget cells:
PAS
Keratin
S100

A

PAS +
Keratin +
S100 -

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24
Q

Describe the folloing markers for melanoma:
PAS
Keratin
S100

A

PAS -
Keratin -
S100 +

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25
Q

which biomarker stains for mucin?

A

PAS

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26
Q

Histologically, how do the malignant cells in Paget’s vulva stand out to you?

A

They are large with cleared out cytoplasm

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27
Q

Clear cell adenocarcinoma is a complication of use of what drug?

A

DES; use was stopped in the 70’s

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28
Q

What type of cell lines the vagina?

A

non keratinized squamous epithelium

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29
Q

At what point in the female tract do you get glandular epithelium?

A

endocervical canal

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30
Q

what was the complication of the female fetuses whose mothers were given DES?

A

Adenosis; persistence of columnar epithelium in the upper vagina

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31
Q

Adenosis has an increased risk of developing what type of cancer?

A

Clear cell adenocarcinoma

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32
Q

What part of the cervix does HPV like to infect?

A

transformation zone where the squamous of the ectocervix meets the columnar of the endocervix

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33
Q

Why does the glandular epithelium undergo metaplasia in the transformation zone?

A

the pH of the vagina is acidic an the glandular epi is not hardy, so it mutates

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34
Q

what type of virus is HPV?

A

dsDNA

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35
Q

> 80% of carcinomas are caused by what type of HPV?

A

16

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36
Q

Type 18 HPV is known to cause what type of cancer?

A

adenocarcinoma

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37
Q

which HPV gene inhibits p53?

A

E6

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38
Q

which HPV gene inhibits Rb?

A

E7

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39
Q

which two HPV genes are the most important in carcinogenesis?

A

E6 and E7

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40
Q

What gene in HPV controls maintanence and replication of the viral genome?

A

E1

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41
Q

What gene in HPV controls transformation?

A

E5

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42
Q

What gene in HPV controls DNA binding proteins that regulate viral replication?

A

E2

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43
Q

What gene in HPV controls binding and disrupts cytokeratin?

A

E4

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44
Q

What gene in HPV controls the major capsid protein?

A

L1

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45
Q

What gene in HPV controls the minor capsid protein?

A

L2

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46
Q

Describe the difference in DNA rep between high risk and low risk HPV

A

high risk: DNA integrates into host DNA

low risk: replication in the cytoplasm

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47
Q

What is the hallmark of the changes to cell shape and size that indicate dysplasia?

A

high nucleus to cytoplasm (N:C) ratio

hyperchromaticity

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48
Q

What percent of low grade squamous intraepithelial lesions (LSIL) regress?

A

60%

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49
Q

Of the cases of LSIL that progress, what do they progress to?

A

HSIL

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50
Q

Of the cases of HSIL (high grade squamous intraepithelial lesion), what percent PERSIST?

A

60%

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51
Q

Of the cases of HSIL that progress, what do they progress to?

A

carcinoma

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52
Q

should we screen younger than 21 for cervical cancer?

A

no

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53
Q

How often should we screen 21-29 year olds for cervical cancer?

A

cytology alone every 3 years

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54
Q

How often should we screen 30-65 year olds for cervical cancer?

A

HPV and cytology cotesting every 5 years

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55
Q

How often do we screen >65 year olds for cervical cancer?

A

we don’t if there is adequate negative prior screening

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56
Q

which HPV vaccine is given to males and females? What strains does it cover?

A

Gardasil

6, 11, 16, 18

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57
Q

Which HPV vaccine is given to females only? what strains does it cover?

A

Cervarix

16 and 18

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58
Q

what hormone does the corpus luteum produce?

A

progesterone

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59
Q

the prolierative phase of the endometrium is driven by…

A

estrogen

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60
Q

the secretory phase of the endometrium is driven by….

A

progesterone

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61
Q

Shedding (bleeding) ocurrs with the loss of what hormone?

A

progesterone

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62
Q

acute endometritis is due to what?

A

bacterial infection or retained products of conception

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63
Q

how does acute endometritis usually present?

A

fever, abnl uterine bleeding, pelvic pain

64
Q

what types of cells are seen in the infiltrate in chronic endometritis?

A

plasma cells and lymphocytes

65
Q

what cell MUST be seen in the infiltrate to make the Dx of chronic endometritis?

A

plasma cells

66
Q

What are some of the causes of chronic endometritis?

A
  1. retained products of conception
  2. chronic PID d/t chlamydia
  3. IUD
  4. TB; WILL SEE GRANULOMAS on histo
67
Q

What is endometriosis?

A

endometrial glands and stroma outside of the uterine lining

68
Q

What are the theories of the development of endometriosis?

A
  1. lymphatic dissemination
  2. venous dissemination
  3. retrograde menstruation with implantation at an ectopic site
69
Q

what is the most common site for endometriosis? how does this present?

A

Ovary; chocolate cyst

70
Q

Endometriosis in the fallopian tube increases the risk for…

A

ectopic pregnancy

71
Q

Involvement of the uterine myometrium in endometriosis is known as…

A

adenomyosis

72
Q

What are some causes of abnormal bleeding from the uterus?

A

anovulatory cycles
polyps
hyperplasia
carcinoma

73
Q

what is an anovulatory cycle?

A

Estrogen-estrogen cycles without the progesterone phase; so you get uterine bleeding

74
Q

Endometrial hyperplasia results as a consequence to unapposed….

A

estrogen

75
Q

what drug is a risk factor for developing endometrial polyps?

A

tamoxifen

76
Q

How does endometrial hyperplasia usually present?

A

post menopausal uterine bleeding

77
Q

What are the histologic changes seen in simple endometrial hyperplasia?

A

cystic dilations

corkscrewing of the glands

78
Q

What is the most important predictor of whether endometrial hyperplasia progresses to carcinoma?

A

presence of cellular atypia

79
Q

what are the histologic changes seen in complex endometrial hyperplasia?

A

increased spacing of endometrial glands
cystic dilations
cellular crowding

80
Q

What are the histologic changes seen in complex endometrial hyperplasia WITH cellular atypia?

A

not stratified

no stroma between glands

81
Q

what two mutation are implicated in endometrIOID carcinoma?

A

PTEN and DNA mismatch repair

82
Q

What is the classic patient who has endometrioid carcinoma?

A

obese female with PCOS

83
Q

what system is used to grade endometrioid carcinoma?

A

FIGO

84
Q

t/f: serous hyperplasia of the endometrium is a result of hyperplasia

A

false; unrelated

85
Q

Where in the female tract does serous carcinoma occur?

A

fallopian tube and ovary

86
Q

what gene mutatoin is implicated in serous carcinoma?

A

p53

87
Q

what is the fancy name for uterine fibroids?

A

leiomyoma

88
Q

what tissue makes up leiomyoma?

A

smooth muscle; its from the myometrium!

89
Q

leiomyoma presents with (single/multiple) lesions

A

multiple

90
Q

what does leiomyoma look like grossly?

A

multiple white whorled masses

91
Q

leiomyoma is related to (blank) exposure

A

estrogen

92
Q

leiomyosarcoma presents as (single/multiple) lesions

A

single lesions

93
Q

Gross exam of leiomyosarcoma shows what?

A

necrosis and hemorrhage

94
Q

What are the histologic features of leiomyosarcoma?

A

necrosis, mitotic activity, and cellular atypia, hyperchromasia

95
Q

t/f: leiomyoma can progress to leiomyosarcoma

A

FALSE

96
Q

what race has a predisposition to leiomyoma?

A

blacks

97
Q

where does fertilization occur?

A

fallopian toob

98
Q

What are three causes of salpingitis

A

chlamydia
gonorrhea
PID

99
Q

Recurrent episodes of salpingitis can lead to (blank) as a result of scar tissue build

A

infertility

100
Q

what is the most common cause of salpingitis?

A

gonorrhea

101
Q

what is the major risk factor for ectopic pregnancy?

A

scarring of the fallopian tube 2ry to PID or endometriosis

102
Q

what is the most common location for ectopic pregnancy?

A

lumen of the fallopian tube

103
Q

what are the three tissues from which ovarian tumors may arise?

A

surface epithelium
germ cells
sex cord stroma

104
Q

what is the most common ovarian tissue that forms tumors?

A

surface (germinal) epithelium

105
Q

what are the two subtypes of surface epithelial ovarian tumors?

A

mucinous and serous

106
Q

surface epi ovarian tumors are usually (blank) grossly

A

cystic

107
Q

what are the three levels of malignancy that mucinous, serous, and endometrioid tumors may all show?

A

adenoma (benign), borderline, or carcinoma (malignant)

108
Q

Describe the histology of cystadenomas?

A

SINGLE cyst with simple, flat lining

109
Q

Describe the histology of cystadenocarcinomas?

A

COMPLEX cysts with thick, shaggy lining

110
Q

Describe the malignant potential and histology of borderline tumors?

A

features inbetween the benign and malignant but still carry malignant potential

111
Q

are endometrioid tumors usually benign or malignant?

A

malignant

112
Q

what cells are endometrioid tumors made of/

A

endometrial like glands; usu arise from endometriosis

113
Q

what type of tumor are composed of urothelium and are benign?

A

Brenner tumors

114
Q

BRCA1 mutations carry an increased risk for what type of female tract cancer?

A

serous carcinoma of the ovary and fallopian tube

115
Q

what cell type of ovarian tumors affects women 0-25?

A

germ cell

116
Q

what is the most common type of ovarian tumor?

A

serous surface epi tumor

117
Q

mucinous mets to the ovary tend to come from which organ? What is the name of this tumor?

A

GI tract; Krukenberg tumor

118
Q

serous tumors of the ovary have what characteristic structure on histology?

A

papillary stuctures

119
Q

(blank) tumors of the ovary show some arborization with papillae, atypia, but no invasion

A

borderline serous tumors

120
Q

(blank) tumors tend to be friable, discohesive, with high grade nuclei

A

serous carcinoma

121
Q

t/f: borderline tumors don’t invade but still show some level of atypia

A

true

122
Q

Granulosa cell tumors and fibromas of the ovary tend to present in pts with what characteristic physical finding?

A

hirsutism

123
Q

Mature teratomas are always (blank) while immature teratomas are always (blank)

A

mature: benign
immature: malignant

124
Q

What are the four tumors that arise from germ cells?

A
  1. teratoma
  2. dysgerminoma
  3. endodermal sinus tumor
  4. choriocarcinoma
125
Q

teratomas arise from what tissue type produced from germ cells?

A

fetal tissue

126
Q

dysgerminomas arise from what tissue type produced from germ cells?

A

oocytes (dysGERMinoma aka germ cells)

127
Q

endodermal sinus tumors arise from what tissue type produced from germ cells?

A

yolk sac

128
Q

choriocarcinoma arise from what tissue type produced from germ cells?

A

placental tissue

129
Q

what is the most common germ cell tumor in females?

A

teratomas

130
Q

Struma ovarii is a teratoma composed of primarily….

A

thyroid tissue, can cause hyperthyroidism

131
Q

what is the most common malignant germ cell tumor?

A

dysgerminoma

132
Q

what is the testicular counterpart to dysgerminoma?

A

seminoma

133
Q

serum LDH may be elevated in which germ cell tumor?

A

dysgerminoma

134
Q

This tumor is composed of large cells with clear cytoplasm and central nuclei that resemble oocytes

A

dysgerminoma

135
Q

What is the most common germ cell tumor in kids?

A

endodermal sinus tumor (think yolk sac so development so kids)

136
Q

what is the glomerulus-like structure seen in endodermal sinus tumors?

A

Schiller-Duval bodies

137
Q

in what germ cell tumor is serum AFP elevated?

A

endodermal sinus tumor (yolk sac aka fetus aka AFP!)

138
Q

choriocarcinoma is a malignant tumor composed of what two cell types?

A

cytotrophoblasts

syncytiotrophoblasts

139
Q

choriocarcinoma mimics placental tissue but what structure is absent/

A

villi

140
Q

Because cytotrophoblasts/ syncytiotrophoblasts, choriocarcinoma will begin as a small hemorrhagic tumor with early (blank) spread

A

hematogenous

141
Q

in what germ cell tumor is b-HCG elevated/

A

choriocarcinoma (mimics placenta therefore pregnant therefore b-HCG)

142
Q

granulosa-theca cell tumors present with what hormone excess?

A

estrogen

143
Q

What are the signs of estrogen excess with regard to age?

A

beofre puberty: precocious puberty
reproductive age: menorrhagia / metrorrhagia
postmenopause: not common

144
Q

t/f: sertoli-leydig tumors can form in the ovary

A

true

145
Q

what characteristic crystal is found in sertoli-leydig tumors?

A

Reinke crystals

146
Q

what type of sex cord stromal tumor presents with hirsutism and virilization?

A

sertoli-leydig; may produce androgens (think about the one that comes from men)

147
Q

mucinous carcinoma of the ovary is usually bilateral, while (blank) is usually bilateral

A

Krukenberg tumors from the GI tract

148
Q

what is real name for jelly belly?

A

Pseudomyxoma peritonei

149
Q

Where does the tumor arise from in pseudomyxoma peritonei?

A

mucinous tumor of appendix; goes to ovary

150
Q

monoamnion twins are (fraternal/identical)

A

identical

151
Q

what is the most common amnion arrangement for twins?

A

monochorionic monoamnionic

152
Q

t/f: monochorionic twins are identical

A

true

153
Q

What is a complete mole?

A

two sperms joined with one ovum

154
Q

t/f: in incomplete mole there is no genetic material in the ovum

A

false; complete

155
Q

what is the chromosome number of incomplete moles?

A

triploid; 69 XXY; two sperms in the ovum

156
Q

Complete moles can be invasive and cause rupture of the (blank) arteries and hemorrhage

A

endoemtrial

157
Q

Moles can develop choriocarcinoma becuase they contain what two cell types?

A

CT and ST

Block 10 Week 3 (7 decks)

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