uterine disorders Flashcards

1
Q

what are the 2 divisions of the endometrium

A

Functional endometrium: hormonally responsive

Basal endometrium: remaining 1/3rd which undergoes rapid growth in proliferative phase.

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2
Q

what are characteristic of endometrial cells in proliferative phase

A

mitosis

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3
Q

what are characteristic of endometrial cells in early secretory phase

A

vacuoles

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4
Q

what are characteristic of endometrial cells in late secretory phase

A

predecidual changes

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5
Q

what are characteristic of endometrial cells in menstrual endometrium

A

stromal breakdown with blood vessle rupture

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6
Q

what is polymenorrhea

A

cycles <3wks

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7
Q

what is oligomennorrhea

A

cycles >6-7wks

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8
Q

what is hypermenorrhea

A

excessive flow

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9
Q

what is menorrhagia

A

inc amt and duration of flow

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10
Q

what is menometrorrhagia

A

prolonged flow with irregular intermittent spotting bt bleeding episodes

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11
Q

what is DUB

A

uterine bleeding not caused by any underlying organic (structural) abnormality

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12
Q

what are prepuberty causes of abn uterine bleeding

A

hypothalamic, pit, or ovarian origin

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13
Q

what are adolescence causes of abn uterine bleeding

A

anovulatory cycle, coag disorders

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14
Q

what are repro age causes of abn uterine bleeding

A
preg complications
organic lesion
hyperplasia, carcinoma
DUB
dysfunctional bleeding= inadequate luteal phase
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15
Q

what are prepuberty causes of abn uterine bleeding

A

dysfunctional uterine bleeding

organic lesions

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16
Q

what are prepuberty causes of abn uterine bleeding

A

endometrial atrophy

organic lesions

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17
Q

what are causes of DUB

A

Anovulatory cycle (80%)

Inadequate luteal phase (~20%)

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18
Q

how does thyroid fxn affect menses

A

hypothyroid= heavy and frequent menses bc dec protein in blood. steroids are protein bound= inc free estrogen/prog effect

hyperthyroid= light and infrequent

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19
Q

what is the likely cause of DUB from anovulatory cycle

A

Excessive, prolonged estrogenic stimulation

No counteractive progesterone phase

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20
Q

what are Less likely causes of DUB from anovulatory cycle

A
Endocrine disorder (thyroid disease, adrenal disease, or pituitary tumors)
Primary lesion of the ovary:
Metabolic disturbance:
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21
Q

what is the pathology of anovulatory cycle caused by excessive endometrial stimulation by estrogens

A

Endometrial glands undergo architectural changes with cystic dilation

Endometrium attains abnormal height with increasing hypervascularity but without intervening stromal support matrix

Unopposed estrogen induces proliferation, hyperplasia and adenomatous hyperplasia

Usually self limited by the occurrence of next ovulatory cycle.

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22
Q

what do you need to r/o to dx DUB? what labs would you check?

A
R/O 
Hypothalamic dysfunction
Perimenopause
Thyroid disorders
Hyperprolactinemia

check FSH, LH, TSH, Prolactin

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23
Q

what are the treatment options for DUB

A
Progesterone
High dose estrogen & high dose progesterone
Prostaglandin synthetase inhibitors:  
Desmopressin: esp with vWF dz
Ablation
Hysterectomy
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24
Q

what causes inadequate corpus luteum to cause DUB

A

Corpus luteum develops improperly or regresses prematurely= Decreased progesterone

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25
what does inadequate corpus luteum manifest with
Infertility(inadequate endometrium) with increased bleeding or amenorrhea Early menses
26
what would Endometrial biopsy at estimated postovulatory date show with inadequate corpus luteum
Shows secretory endometrium which lags behind expected date
27
how can oral contraceptives cause endometrial changes
endometrim becomes atrophic and ulceratived bc of lack of E and Prog spiral arteries do not develope properly if not enough E Prog only BC can lead freq break through bleeding
28
what is the major diff bt acute and chronic endometritis
acute presents with fever and chronic typically does not
29
what is the pathology of acute endometritis
inflamm limited to interstitum
30
what type of cells are found within the endometrial glands for acute/ chronic endometritis
``` acute= neutrophils chronic= lymphocytes and macrophages ```
31
how is chronic endometritis diagnosed and treated
If abnormal vaginal bleeding: endometrial biopsy is done Lymphocytes and plasma cells within stroma treatment is specific to cause
32
what is endometriosis
presence of endometrial tissue outside of the uterus - Consists of endometrial glands and stroma - Rarely only endometrial stroma
33
what is endometriosis dependent on
Estrogen-dependent disorder
34
what is the metastatic theory of endometriosis
Theory(appearance of endometrial tissue in extrauterine locations) Retrograde menstruation through fallopian tube Local spread Distant spread through lymphatics and hematologic
35
according to the metastatic theory of endometriosis what may facilitate its development
Altered immune response may facilitate the development
36
what is the metaplastic theory of endometriosis
Endometrium arise directly from coelomic epithelium from which the endometirum itself originate during embryonic development Undifferentiated cells differentiate to endometrial tissue
37
how is the immune system related to endometriosis
Activation of Inflammatory cascade in endometriosis High levels of PGE2, IL-1beta, TNF, IL-6 -Explains why COX inhibitors are beneficial
38
how do endometriotic stromal cells cause endometriosis
They upregulate estrogen production due to high levels of aromatase. Estrogen enhances survival of endometrial tissue. Aromatase is absent in normal endometrium
39
what is letrozole
aromatase inhibitor- can be used to tx endometriosis
40
how are genetic alterations involved in endometriosis
Changes in key genes encoding two nuclear receptors -Steroidogenic factor-1 -Estrogen receptor-Beta Decreased methylation of promoters of these genes causing overexpression -Favors overproduction of estrogen and -prostaglandin Resistance to progesterone action.
41
what are the diff stages of endometriosis
``` Stage I (minimal): Isolated implants; no significant adhesions Stage II (mild): Superficial implants -<5cm in aggregate, scattered on peritoneum and ovaries -No significant adhesions Stage III (moderate) -Multiple implants=Superficial and invasive -Adhesions may be evident=Peritubal and periovarian Stage IV (severe) -Multiple implants=Superficial and deep -Including large ovarian -Firm dense adhesions ```
42
what are the consequences of endometriosis
Infertility Dysmenorrhea Pelvic pain
43
what are the 3 ways adenomyosis can form
Invagination of endometrium De novo from mullerian rests Hormonal driven - Estrogen produced in adenomyotic tissue - Increased aromatase
44
what are characteristics of endometrial polyps
usually sessile
45
are endometrial polyps responsive to hormones
Responsive to estrogen but little or no progesterone response
46
what is the malignant risk with endometrial polyps
Rarely transform to adenocarcinoma
47
what is the pathogenesis of endometrial polyps
Stromal cells contain chromosome (6p21) rearrangements Involve HMGI Y gene which cause benign mesenchymal tumors. A mutation activates C-MYC which is a transcription factor for replication
48
what is endometrial hyperplasia? what is it related to?
Increased proliferation of the endometrial glands relative to the stroma Increased gland to stroma ratio Related to endometrial carcinoma
49
what is the pathogenesis of endometrial hyperplasia
estrogen without unopposed progesterone)
50
what is Endometriod hyperplasia (Type I)
- associated with unopposed estrogen= more glandular - PTEN mutation=phosphatase and tensin homologue making PTEN a inactive "brake"= activation of AKT and uncontrolled proliferation
51
what is Nonendometriod hyperplasia(Type II)
more stromal tissue and less glandular - p53 mutations - not assoc with inc estrogen
52
how does the WHO classify endometrial hyperplasia
WHO classification based on 2 factors 1.Glandular/Stromal architectural pattern(simple/complex hyperplasia) 2.Presence or absence of nuclear atypia
53
what is simple hyperplasia without atypia
Glands: various size and irregular shape Mild increase in gland: stroma ratio Epithelial growth similar to proliferative endometrium
54
what is simple hyperplasia with atypia
Appearance of simple hyperplasia Atypia: loss of polarity, vesicular nuclei, prominent nucleoli 8% progress to CA
55
what is complex hyperplasia without atypia
Increase number and size of glands, gland crowding Abundant mitotic figures Cytology: cells normal 3% progress to CA
56
what is complex hyperplasia with atypia
23 to 48% to CA)
57
what are type 1 and 2 carcinoma of the endometrium precursors
from type 1(PTEN, K-ras mutations) or 2(p53) endo hyperplasia
58
what are the majority of type 1 carcinomas
Majority are endometrioid carcinoma: well differentiated and look like proliferative endometrial glands
59
what are the different endometriod grading for type 1 endometrial carcinoma
Grade 1: Well differentiated adenocarcinoma-50% solid)
60
what are the different endometriod staging
Stage I: Carcinoma confined to corpus uteri itself Stage II: Carcinoma has involved the corpus and the cervix Stage III: Carcinoma has extended outside uterus but not outside the true pelvis Stage IV: Carcinoma has extended outside true pelvis or involved mucosa of bladder or rectum
61
what are malignant mixed mullerian tumors
Endometrial adenocarcinomas with malignant changes in the stroma( may protrude through cervical os) Stroma differentiate into variety of malignant mesodermal components -muscle -cartilage -osteoid
62
what is the prognosis of malignant mixed mullerian tumors
Prognosis influenced by grade and type Highly malignant Same staging as Type 1 endometrial carcinoma 5 year survival rate: 25-30%
63
what is characteristic of adenosarcomas
``` Prolapse through the cervical os Malignant appearing stroma coexisting with benign but abnormally shaped endometrial glands Incidence: 4th to 5th decade of life Low-grade malignancy *Reoccurrence: 25% Usually confined to pelvic ```
64
what are the 2 categories of stromal tumors
Benign stromal nodules(aggregate of endometrial stromal cells) -Does not penetrate the myometrium -Little consequences Endometrial stromal sarcomas -Lies between muscle bundles of the myometrium -Diffuse infiltration (not nodular)
65
what is the pathogenesis of endometrial stromal sarcomas
Chromosomal translocation (JJAZ1 )=anti-apoptotic properties
66
are leiomyomas hormonally responsive
yes, Regress in menopause Expand in pregnancy
67
what is the pathology of leiomyomas
Sharply circumscribed, discrete, round, firm, gray white tumors Vary in size Located within the myometrium just beneath the endometrium Malignant transformation is rare Low mitotic index
68
what are the growth patterns of leiomyosarcomas
2 growth patterns Bulky fleshy masses invading uterine wall Polypoid masses that project into the uterine lumen
69
what is the difference between leiomyomas and leiomyosarcomas
Degree of nuclear atypia Mitotic index Zonal necrosis