path of uterus 12/10 Flashcards

1
Q

during proliferative phase

A

see increased mitotic figures in endometrium

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2
Q

after ovulation

A

See subnuclear vacuoles in ednometrium

also called piano keys

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3
Q

Day 21 of cycle

A

see increased stromal edema and secretions in glands

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4
Q

Day 23 (pre-implantation)

A

see pre-decidua around vessels

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5
Q

Day 26

A

entire stroma is decidualized

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6
Q

changes in usterus during the cycle

A
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7
Q

anovulatory bleeding

A

most common cause of DUB

excess estrogen and no progesterone–> endometrial hyperplasia and cells grow out of their blood supply and bleed

most are due to subtle hormonal changes

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8
Q

additional causes od DUB

A

inadequate luteal phase: inadequate progesterone from corpus luteum–> menstruation 6-9 days after LH surge

irregular shedding: heavy bleeding due to extended secretion of progesterone, see proliferative and secretory phases together

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9
Q

congenital usterus anomalies

A

septate: wedges of fibrous tissue dividing uterine cavity

asherman’s syndrome: adhesions (band-like) formations crossing the lining of uterus

bicornuate: incomplete uniting of uterus

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10
Q

leiomyoma

A

submucosal ones are most responsible for abnormal bleeding and infertility

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11
Q

histology of leiomyoma

A

whorled bundles of smooth muscle cells that resemble uninvolved myometrium

cells uniform in size and shape and have characteristic oval nucleus and long, slender ‘cigar-shaped’ cytoplasm

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12
Q

benign metastasizing leiomyoma

A

extend into vessels and migrate to other sites, most commonly lungs (benign)

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13
Q

disseminated peritoneal leiomyomatosis

A

multiple small nodules on peritoneum (benign)

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14
Q

endometrial hyperplasia

A

also endometrial intraepithelial neoplasia (EIN)

can cause abnormal bleeding

can progress from simple–>atypical–>carcinoma

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15
Q

conditions promoting EIN

A

menopause

PCOS

functioning granulosa cell tumors of ovary

excessive cortical function

estrogen replacement therapy

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16
Q

high grade or atypical EIN

A

from inactivation of PTEN tumor suppressor gene through deletion or inactivation

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17
Q

simple hyperplasia without atypia

A

lowest grade out of 4

increase in glands:stroma

rarely malignant

caused by persistent estrogen stimulation and usually becomes cystic atrophy if estrogen is withdrawn

18
Q

simple hyperplasia with atypia

A

uncommon

cells of glands are rounded and lose their perpendicular orientation to BM

8% progresses to CA

19
Q

complex hyperplasia without atypia

A

increase in number and size of glands

glands crowded and show branching:back-to-back with little stroma and lots of mitotic figure

epithelial cells normal

20
Q

complex hyperplasia with atypia

A

hard to distinguish from well-differentiated endometroid adenocarcinoma

35% of pts have CA of uterus

can treat with progestin if keeping uterus is important

21
Q

endometrial hyperplasia with squamous metaplasia

A

less easily classified

22
Q

endometrial adenocarcinoma

A

most common invasive CA of femal genital tract

mainly in post-menopausal as abnormal bleeding

23
Q

risk factors for endometrial adenocarcinoma

A

obesity

diabetes

HTN

infertility (anovulatory cycles)

24
Q

2 pathogenetic groups of endometrial CA

A

type I: in background of estrogen stimulation and endometrial hyperplasia

type II: sporadic

25
type I endo. adenocarcinoma
estrogen-dependent: ovarian estrogen-secreting tumor increases risk estrogen replacement therapy tend to be well-differentiated and endometroid more favorable prognosis
26
grading of endometroid tumors
grade1: well-differentiated grade2: moderately differentiated,well-formed glands mixed with solid sheets of malignant cells grade3: poorly diff.,solid sheets of cells with few glands,more nuclear atypia with mitotic figures
27
type2 endometrial adenocarcinoma
less estrogen-dependent and less often preceded by hyperplasia pts are older and tumors more poorly differentiated resemble serous carcinoma of ovaries
28
why type2 have poor prognosis
tend to exfoliate,undergo tubal spread,and implant on peritoneal surfaces like their ovarian counterparts
29
all non-endometriod carcinoma
classified as grade3
30
staging of endometrial adenocarcinoma
1) confined to corpus uteri 2) involved corpus and cervix 3) outside uterus but not outside pelvis 4) outside of pelvis involving rectum or bladder
31
malignant mixed muellerian tumors MMMT
endometrial adenocarcinoma that undergo stromal differentiation
32
MMMT(carcinosarcoma)
bulky,polypoid tumors that can protrude through cervical os adenocarcinoma mixed with stromal elements(muscle,fat,cartilage) outcome depends on stage and grade of adenocarcinoma see it in post-menopasual women and those with preveious radiation therapy
33
adenosarcoma
large broad-based endometrial polypoid growths and may prolapse through cervical os diagnosis based on malignant appearing stroma with benign but abnormally shaped glands seen in women 4th-5th decades and is considered low grade confined to pelvis abnormal bleeding
34
stromal nodule
well-circumscribed aggregate of endometrial stromal cells in myometrium. mean age is 47 abnormal bleeding
35
stromal sarcoma
neoplastic endometrial stroma lying between muscle bundles of myometrium can infiltrate myometrium OR goes to lymph--\>mets
36
leimyosarcoma
cells are spindled main criterion for diagnosis is increased mitotic figures,need 10 mitoses/10 HPF don't originate from leiomyoma
37
sites for endometriosis
ovary\>uterine ligaments\>rectovaginal septum\>pelvic peritoneum\>laporatomy scars\>umbilicus,vulva,intestines
38
diagnosis of endometriosis
see hemosideren-laden MQ plus correct clinical presentation--\> presumptive endometriosis
39
by 27th day of menstrual cycle
stroma is infiltrated by neutrophils and so-called stromal granulocytes
40
Arias-Stella reaction
when nuclei of endometrial glands protrude beyond cytoplasmic limits and appear in lumen due to high mitotic activity during the secrtetory phase dont confuse with adenocarcinoma
41
enometrial polyps will appear in curretage as
polypoid-shaped fragments of tissue with epithelium on 3 sides