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Pathology > Uterus, placenta > Flashcards

Uterus, placenta Flashcards

0
Q

normal weight of uterus

A

50g

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1
Q

uterus division

A

corpus uteri with myometrium and endometrium
lower uterine segment
cervix

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2
Q

normal size of uterus

A

8x6x3 cm

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3
Q

two major components of the uterus

A

myometrium

endometrium

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4
Q

endometrium- functionalis

A

horomone responsive upper zone

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5
Q

how much is shed in the functionalis at the start of the cycle?

A

upper half to 2/3

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6
Q

surface epithelium covering the endometrial mucosa

A

compacta layer

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7
Q

most hormonaly sensitive layer of the functionalis

A

spongiosa layer

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8
Q

hormonally sensitive endometrial layer

A

basalis layer

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9
Q

most common disorders of the uterus result from

A

endocrine imbalances
complication in pregnancy
neoplastic proliferation

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10
Q

clinical usefulness of endometrial dating

A

assess hormonal status
document ovulation
determine cause of endometrial bleeding- most important indication
for infertility workup

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11
Q

1st half of the endometrial cycle is characterized by

A

proliferation of both endometrial glands and stroma to build up then shedding from previous menstruation

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12
Q

which part of the endometrial cycle is variable among women?

A

1st half of the cycle

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13
Q

the 2nd half of the endometrial cycle aka

A

post ovulatory phase or secretory phase

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14
Q

2nd half of the cycle is controlled by

A

progesterone

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15
Q

clinical significance of post ovulatory or secretory phase

A

14day period: can be used to date the endometrium for monitoring of abnormal bleeding and part of infertility work up

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16
Q

granulosa cells produce estrogen effect on basalis layer

A

proliferation: extremely rapid growth of both glands and stroma

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17
Q

proliferative phase is at

A

day 1-14

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18
Q

proliferative phase histo features

A

straight, tubular glands
pseudostratified columnar, nonvacuolated lining epithelia
pencil like nucleus- elongated and slender
mitotic figures
increase in number of cells
compact spindly stroma

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19
Q

proliferative is dictated by

A

FSH

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20
Q

proliferative phase is interrupted by

A

ovulation ➡️rupture of Graafian follicle

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21
Q

if no fertilization, Graafian follicle becomes

A

corpus luteum

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22
Q

early secretory phase histo features

A

subnuclear or supranuclear vacuoles in the lining cells of the gland
luminal position of the nuclei
cease of mitotic activity

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23
Q

during early secretory phase, the corpus luteum produces

A

progesterone

estrogen

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24
Q

when basal vacuoles becomes prominent

A

3rd week of the menstrual cycle

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25
Q

midsecretory histo features

A

accumulation of intraluminal secretions within the lumen of the glands
loosed stroma due to edema
glands tortuous and coiled

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26
Q

secretions are discharged into the gland lumens by the

A

4th week

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27
Q

late secretory phase histo features

A

pre decidual stroma
round and plump stromal cells
serrated saw tooth appearance

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28
Q

days 21-22 of the endometrial cycle

A

development of spiral arterioles

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29
Q

days 23-24 of the endometrial cycle

A

increase in ground substance and edema
accumulation of cytoplasmic eosinophilia
mitoses

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30
Q

days 24-28 of the endometrial cycle

A

neutrophils and lymphocytes

disintegration of the functionalis layer

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31
Q

signaling by estrogen and progesterone on local production of molecules

A

autocrin

paracrine

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32
Q

much of the effect of estrogen in glandular proliferation occurs via

A

stromal cells

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33
Q

estrogen on stromal cells cause production of

A

ILGF-1

EGF

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34
Q

progesterone in the secretory phase

A

inhibits proliferation in both the glands and stroma
promotes differentiation of the glands
cause profound alteration of the stroma

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35
Q

disintegration, fissuring of the functional layer leads to

A

menstrual shedding

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36
Q

menstrual shedding (day24-28) begins with

A

dissolution of the corpus luteum

sudden withdrawal of estrogen and progesterone

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37
Q

characterized by short or long menstrual period or period of bleeding in between the normal cycle

A

abnormal uterine bleeding

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38
Q

most common clinical presentation of different diseases of endometrium

A

bleeding

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39
Q

dysfunctional in DUB means

A

not associated with pathologic condition of the uterus

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40
Q

50% with DUB are

A

> 45

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41
Q

30% of DUB px are

A

in reproductive years

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42
Q

20% of DUB px are

A

adolescents

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43
Q

DUB cause in prepuberty

A

precocious puberty

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44
Q

DUB cause in adolescence

A

anovulatory cycle

coagulation disorder

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45
Q

DUB cause in reproductive age

A

pregnancy complication
organic lesions
ovulatory dysfunction

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46
Q

DUB cause in perimenopausal age group

A

anovulatory cycle
irregular shedding
organic lesion

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47
Q

DUB cause in postmenopausal age group

A

organic lesions

endometrial atrophy

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48
Q

most common form of DUB dt hormonal imbalance

A

anovulatory bleeding or cycle

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49
Q

hormonal imbalance in anovulatory bleeding is due to

A

excess estrogen production

prolinged estrogen stimulation without ovulation

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50
Q

two possible mechanisms of anovulatory bleeding

A
  1. unopposed estrogen stimulation due to persistence of follicles without ovulation
  2. sudden regress of follicles causing reduction of estrogen production➡️withdrawal bleeding or estrogen breakthrough bleeding
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51
Q

hallmark of anovulatory bleeding

A

no ovulation and unopposed, prolonged estrogenic stimulation

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52
Q

endocrine disorders causing anovulatory bleeding or cycle

A

thyroid, adrenal disease

pituitary tumors

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53
Q

primary ovarian lesions causing anovulatory bleeding or cycle

A

granuloma-theca tumors

polycystic ovaries

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54
Q

generalized metabolic problem causing anovulatory bleeding or cycle

A

obesity
severe malnutrition
chronic systemic disease

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55
Q

anovulatory bleeding histo

A

cystic, irregular glandular architecture

stromal breakdown

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56
Q

morphologic patterns of anovulatory bleeding

A 
normal proliferative
weakly proliferative
disordered proliferative
glandulostromal breakdown
***hyperplasia
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57
Q

hyperplasia in Anovulatory bleeding

A

not a morphological pattern

due to prolonged estrogen stimulation

can lead to endometrial cancer in 20% cases

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58
Q

deficient progesterone secretion by corpus luteum either because of failure to develop normally or premature regression

A

Luteal Phase defect

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59
Q

clinical significance of luteal phase defect

A

menstrual abnormality
infertility
habitual 1st trimester abortion

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60
Q

diagnosis of luteal phase defect

A

at least 2 consecutive cycles

at least 2 biopsies showing delay in development of secretory changes

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61
Q

biopsy in mid secretory phase of px with luteal phase defect

A

normal looking glands

early secretory features: supra or subnuclear vacuoles, luminal nuclei

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62
Q

biopsy in secretory phase in px with luteal phase defect

A

normal glands

mid secretory feature: maximal stromal edema

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63
Q

inadequate luteal phase histo feature

A

normal secretory but out of date
lack of gland tortuosity
disassociation between glands of stromal development

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64
Q

rare cause of DUB

caused by persistence of corpus luteum function

A

irregular shedding syndrome

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65
Q

clinical features of irregular shedding syndrome

A

> 2 weeks bleeding

occurence in every menstruation

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66
Q

irregular shedding syndrome histo

A

star shaped secretory glands admixed with early proliferative glands
arias-stella
fibrin thrombi
glandular and stromal breakdown

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67
Q

which syndrome of luteal phase defect is due to increased progesterone?

A

irregular shedding syndrome

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68
Q

pill endometrium histo

A

small and inactive glands

poor stromal development

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69
Q

causes of inflammatory disease of the uterus

A 
abortion
retained products of conception
ascending infection from cervix
IUD
systemic spread to uterus
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70
Q

nonspecific inflammatory response limited to the interstitium usually associated with pregnancy, abortion, miscarriage, perineal or cervial lacerations during delivery, instrumentation

A

acute endometritis

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71
Q

common causative agents of acute endometritis

A

strep
staph
clostridium

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72
Q

chronic endometritis hallmark

A

plasma cells

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73
Q

IUD associated with chronic endometritis is caused by

A

mycoplasma
chlamydia
actinomycosis

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74
Q

bacteria common in both acute and chronic endometritis

A

chlamydia

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75
Q

rare and usually a result of extension of tuberculous lesion in the uterine tubes

A

tuberculous endometritis

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76
Q

tuberculous endometritis generally found in

A

reproductive women

  • infertile
  • pelvic mass
  • lower ab pain
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77
Q

tuberculousendometritis diagnosis

A

curettage sample during the late secretory or menstrual phase showing caseation necrosis

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78
Q

single and multiple exophytic mass
sessile
0.5 to 3 cm in diameter
large and pedunculated

A

endometrial polyp

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79
Q

breast cancer hormonal treatment causing endometrial polyp

A

tamoxifen

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80
Q

stromal cells in endometrial polyps contain

A

chromosome 6p21 rearrangements involving HMGIY gene

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81
Q

endometrial polyp is mostly encountered in

A

perimenopausal

menopausal women

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82
Q

occurence of carcinoma in endometrial polyps is

A

rare

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83
Q

most common clinical presentation of endometrial polyp

A

abnormal bleeding

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84
Q

endometrial polyp histo

A 
covered on 3 sides by surface endometrium
cystic glands
estatic, thick-walled blood vessels
fibrous stroma (*edematous in endocervical)
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85
Q

most commonly the glands of endometrial polyps are

A

atrophic or hyperplastic

86
Q

endometrial polyp gland that demonstrate secretory changes

A

functional polyp

87
Q

endometrial polyp that develop in association with generalized endometrial hyperplasia
responsive to estrogen
little or no progesterone response

A

hyperplastic polyp

88
Q

presence of ectopic endometrial glands and stroma in the myometrium

A

adenomyosis

89
Q

criteria for adenomyosis diagnosis

A

one low power field or more below the endomypmetrial junction

glands accompanied by stroma, no cyclical bleeding

90
Q

etiology of adenomyosis

A

unknown

91
Q

clinical features of adenomyosis

A

menorrhagea
dysmenorrhea
dyspareunia
pelvic pain during menstrual period

92
Q

adenomyosis gross

A

globular thickend uterine wall
cigarette burnlike lesions
not well circumscribed unlike leiomyoma

93
Q

precursor lesion to endometrial carcinoma

A

endometrial hyperplasia

94
Q

endometrial hyperplasia histo

A

increased gland to stroma ratio
haphazard distribution
epithelium abnormalities
true stratification of lining

95
Q

etiology of endometrial hyperplasia

A

increased and unopposed estrogen stimulation with decreased progesterone activity

96
Q

conditions promoting endometrial hyperplasia

A 
menopause
PCOS
granulosa cell tumor
HRT
obesity
Stein-leventhal  syndrome
97
Q

common genetic alteration in hyperplasia and endometrial carcinomas is

A

inactivation of PTEN suppressor gene located on chromosome 10q23.3

98
Q

simple hyperplasia without atypia

A

cystically dilated glands, focally crowded

pseudo stratified columnar with amphophilic cytoplasm
mitotic figures

abundant, cellular, spindles enlarged nuclei, indistinct cytoplasm, increase in mitosis

99
Q

endometrial hyperplasia progression to ca

A 
simple, -atypia 1%
simple, +atypia 8% 
complex, -atypia 3%
complex, +atypia 23-48%
atypical hyperplasia VERY POOR PROGNOSIS
100
Q

when estrogen stimulation is withdrawn, simple hyperplasia with atypia may evolve into

A

cystic atrophy

101
Q

cheeselike appearance, fingerglovee, and adenomatous budding is seen in

A

simple hyperplasia without atypia

102
Q

is simple hyperplasia with atypia common?

A

NOOOO

103
Q

simple hyperplasia with atypia morphology

A

loss of polarity
vesicular nuclei with open chromatin pattern
prominent nucleoli
round cells
lost normal perpendicular orientation to BM

104
Q

complex hyperplasia without atypia or adenomatous hyperplasia histo

A 
increase in number
crowded 
back to back
complex budding
dense stroma with lipid laden cells
105
Q

morphologic overlap with well differentiated endometrioid adenocarcinoma and an accurate distinction may not be possible without hysterectomy

A

complex hyperplasia with atypia

106
Q

complex hyperplasia with atypia management

A

hysterectomy

progestin therapy in young women

107
Q

atypical hyperplasia

A 
round nuclei
nucleoli starts to appear
irregular thickening of nuclear membrane
chromatin clumping
loss of polarity 
more eosinophilic cytoplasm
108
Q

most common cancer of the female genital tract replacing cancer of the cervix

A

endometrial carcinoma

109
Q

accounts for 7% of all cancer in the female

A

endometrial carcinoma

110
Q

peak incidence of endometrial cancer

A

55-65

usual in post and perimenopausals

111
Q

endometrial cancer risk factor

A 
advancing age
obesity
HPN 
DM
infertility
nulliparity
hyperestrogenism
112
Q

most common clinical presentation of endometrial cancer

A

painless vaginal bleeding

113
Q

more common histo classification of endometrial carcinoma

A

type 1 favorable

114
Q

type 1 endometrial ca histo

A

low grade, better differentiated
minimal or no myometrial invasion
endometrioid adenoca

115
Q

type 1 endometrial ca is common in

A

perimenopausal women

116
Q

type 1 endometrial ca genetic factor

A

PTEN mutation

117
Q

G1 endometrial ca

A

well differentiate

<5% solid growth pattern tumor

118
Q

G2 endometrial ca

A

moderately differentiated

<50% solid tumor growth

119
Q

G3 endometrial ca

A

poorly differentiated

>50% solid growth

120
Q

endometrial cancer squamous differentitaion

A

toward malignancy ➡️adenosquamous

121
Q

PIK3CA is RARE in complex hyperplasia with atypia and they play a role in

A

invasion

122
Q

molecular changes in type 1 endometrial ca

A

PIK3CA mutation
KRAS mutation
Beta-catenin mutation

123
Q

aside from type 1 endometrial ca, which has also mutation in KRAS?

A

complex atypical hyperplasia

124
Q

sporadic endometrioid ca molecular change

A

promoter hypermethylation of one of the DNA mismatch repair genes

125
Q

type 1 and type 2 share this mutation

A

p53

126
Q

p53 unlike KRAS is not found in

A

complex atypical hyperplasia

127
Q

grading of type 2 endometrial ca

A

3

128
Q

most common type 2 subtype of endometrial ca

A

serous carcinoma

129
Q

90% of serous endometrial ca have this mutation

A

p53

130
Q

must know features of type 2 endometrial ca

A 
rarely associated with hyperplasia and estrogen
arise from EIN or endometrial atrophy
serous
fingerlike lined by cuboidal cells 
endometrioid tubular pattern
131
Q

all of nonendometrioid carcinoma are graded

A

3

132
Q

only endometrial ca graded with 1-3

A

endometrioid ca

133
Q

histo type of endometrial ca with 70% frequency

A

adeno or endometrioid

134
Q

endometrial adenoca with benign sq component

A

adenocanthoma

135
Q

stage 1 endometrial CA

A

ca is confined to corpus uteri

136
Q

stage2 endometrial ca

A

corpus

cervix

137
Q

stage 3 endometrial ca

A

outside uterus but not outside of true pelvis

138
Q

stage 4 endometrial ca

A

outside pelvis

extended to mucosa of bladder or rectum

139
Q

diagnosis of endometrial dse

A

transvaginal ultrasonography
endometrial biopsy
d and C
MR imaging

140
Q

preferred methods for diagnosis of endometrial dse

A

biopsy and D&c

141
Q

also know as carcinosarcomas

A

malignant mixed mullerian tumor or MMMT

142
Q

differentiation in MMMT

A

presence of muscle, cartilage, osteoid

143
Q

most common tumor in women

A

leiomyomas or fibrinoids

144
Q

genes that regulate chromatin structure that is involved in leiomyomas

A

HMGIC

HMGIY

145
Q

molecular change in leiomyomas

A

12q14

6p

146
Q

leiomyomas are common in

A

reproductive age women

147
Q

hormones thataffect leiomyomas

A

progesterone

estrogen

148
Q

symptoms of leiomyoma (uncommon)

A 
pain
infertility
abnormal uterine bleeding
frequent urination
UTI
149
Q

type of leiomyoma located at outside the surface

A

serosal

150
Q

type of leiomyoma located within uterine cavity

A

submucosal

151
Q

degenerative changes in leiomyoma

A 
hyaline degeneration 60%
edema
cystic degeneration
calcification 4%
myxomatous
infarcted 10%
152
Q

malignant transformation of myoma to malignancy is

A

rare

153
Q

leiomyoma gross

A 
sharply circumscribed
round
firm
gray white
sometimes nodules to massive to fill the pelvis
154
Q

leiomyoma rarely found in

A

myometrium of corpus
uterine ligaments
cervix

155
Q

leiomyoma in the myometrium

A

intramural

156
Q

leiomyoma just beneath the endometrium

A

submucosal

157
Q

leiomyoma beneath the serosa

A

subserosal

158
Q

red degeneration in leiomyoma shows

A

yellow-brown to red softening

159
Q

leiomyoma histo

A

oval nucleus

long slender bipolar cytoplasmic processes

160
Q

extremely rare variant of leiomyoma that extends into vessels and migrates to other sites

A

benign metastasizing leiomyoma

161
Q

presents as multiple small nodules on the peritoneum

A

leiomyomatosis

162
Q

leiomyomatosis and benign metastasizing leiomyoma are considered

A

benign

163
Q

not to be considered in differentiating leiomyoma and leiomyosarcoma

A

increased cellularity
size
hemorrhage

164
Q

malignancy histo important determinant in leiomyoma

A

10 or more per 10 high power fields

165
Q

leiomyosarcoma gross

A

bulky, fleshy or polypoid masses

166
Q

leiomyosarcoma histo

A

wide range atypia

167
Q

determining factors of malignancy of the smooth muscle of the endometrium

A

mitosis>zona necrosis>nuclear atypia

168
Q

in these groups, mitotically active leiomyosarcoma may mimic histo of leiomyosarcoma

A

young or pregnant

169
Q

normal umbilical cord insertion

A

paracentral

170
Q

umbilical cord features gross

A

straight

shiny smooth outer surface

171
Q

cotyledon features

A

reddish brown
nodular
meaty

172
Q

lining of villi in placenta

A

syncitiotrophoblast

173
Q

chorionic villi are a little bit large enclosed by

A

nonproliferating trophoblast cells

174
Q

stroma of placental is

A

loose

vascular

175
Q

mature placenta at

A

20th week of pregnancy

176
Q

syncitiotrophoblast secretes

A

hCG

177
Q

aggregation of syncitiotrophoblast on maturation with no clinical significance

A

knotting

178
Q

presence of intervillous fibrin is

A

normal or physiologic feature in mature placenta

179
Q

abnormal adherence of the placenta to the uterine wall ➡️inadequate separation after delivery

A

placenta accreta

180
Q

placenta accreta cause

A

partial or complete absence of the decidua with adherence of the placental villous tissue directly to the myometrium

failure of placental separation

181
Q

normally the placenta is attached at the uterine plate at the

A

basalis or decidual plate

182
Q

incomplete attachment of the placenta up to myometrium

A

placenta increta

183
Q

placenta invaded the full thickness of myometrium

A

placenta percreta

184
Q

abnormal implantation or location of the placental at cervical os

A

placenta previa

185
Q

usual manifestation of placenta previa

A

serious 3rd trimester bleeding

186
Q

systemic syndrome characterized by widespread maternal endothelial dysfunction

A

preeclampsia

187
Q

preecclampsia prevalence

A

6% in women

last trimester and primiparas

188
Q

eclampsia is associated with

A

convulsion

DIC

189
Q

pathogenesis of preeclampsia

A

abnormality of placentations ➡️placental ischemia➡️ decresse uteroplacental perfusion➡️stimulation of vasoconstrictors and inh of vasodilators

190
Q

mature placenta normally has infarctions ar

A

periphery

191
Q

manifestation of preeclampsia

A

HPN
edema
proteinuria

192
Q

hydatidiform moles and choriocarcinoma are both associated with

A

increased or persistent levels of hCG

193
Q

hydatidiform moles is also known as

A

non invasive mole

194
Q

H.mole classic manifestations

A

discordant size of the abdomen with the gestational age
high hCG titer
gelatinous discharge

195
Q

h mole gross

A

delicate, friable mass of thinwalled, translucent, cystic, grapelike structures of swollen villi

196
Q

h mole histo

A

cystic swelling of chroionic villi

variable trophoblastic proliferation

197
Q

complete mole karyotype

A

diploid 46,XX (46 XY)

198
Q

partial mole karyotype

A

triploid

199
Q

results from fertilization of an egg that has lost its chromosomes
genetic material is paternally derived

A

complete mole

200
Q

results from fertilization of egg with two sperm

A

partial mole

201
Q

complete mole microscopy

A

enlarged, edematous villi

diffuse trophoblast hyperplasia

202
Q

partial mole histo

A

edematous villi, some with only minor changes

focal less marked trophoblastic proliferation

203
Q

atypia is present in this HMole

A

complete hmole

204
Q

hmole with 2% risk of choriocarcinoma

A

complete hmole

205
Q

most aggressive form of GTD with 1:40 chance following complete hmole

A

choriocarcinoma

206
Q

choriocarcinoma preceded by

A

complete hmole
abortion
ectopic pregnancy
term pregnancy

207
Q

choriocarcinoma morphology

A

dimorphic
well circumscribed dark red hemorrhagic necrotic mass
no chorionic villi

208
Q

chorioca from placenta

A

gestational trophoblast disease

209
Q

chorioca from ovary

A

nongestational CA

210
Q

choriocarcinoma response to chemotherapy

A

good

211
Q

syncitiotrophoblast normally has

A

big multinucleate cells

212
Q

cytotrophoblast normally has

A

polygonal with round central nucleus

Pathology (5 decks)

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