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Pathophys > uterine disorders > Flashcards

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
Q

what does inadequate corpus luteum manifest with

A

Infertility(inadequate endometrium) with increased bleeding or amenorrhea
Early menses

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26
Q

what would Endometrial biopsy at estimated postovulatory date show with inadequate corpus luteum

A

Shows secretory endometrium which lags behind expected date

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27
Q

how can oral contraceptives cause endometrial changes

A

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

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28
Q

what is the major diff bt acute and chronic endometritis

A

acute presents with fever and chronic typically does not

29
Q

what is the pathology of acute endometritis

A

inflamm limited to interstitum

30
Q

what type of cells are found within the endometrial glands for acute/ chronic endometritis

A 
acute= neutrophils
chronic= lymphocytes and macrophages
31
Q

how is chronic endometritis diagnosed and treated

A

If abnormal vaginal bleeding: endometrial biopsy is done
Lymphocytes and plasma cells within stroma

treatment is specific to cause

32
Q

what is endometriosis

A

presence of endometrial tissue outside of the uterus

  • Consists of endometrial glands and stroma
  • Rarely only endometrial stroma
33
Q

what is endometriosis dependent on

A

Estrogen-dependent disorder

34
Q

what is the metastatic theory of endometriosis

A

Theory(appearance of endometrial tissue in extrauterine locations)

Retrograde menstruation through fallopian tube
Local spread
Distant spread through lymphatics and hematologic

35
Q

according to the metastatic theory of endometriosis what may facilitate its development

A

Altered immune response may facilitate the development

36
Q

what is the metaplastic theory of endometriosis

A

Endometrium arise directly from coelomic epithelium from which the endometirum itself originate during embryonic development
Undifferentiated cells differentiate to endometrial tissue

37
Q

how is the immune system related to endometriosis

A

Activation of Inflammatory cascade in endometriosis
High levels of PGE2, IL-1beta, TNF, IL-6
-Explains why COX inhibitors are beneficial

38
Q

how do endometriotic stromal cells cause endometriosis

A

They upregulate estrogen production due to high levels of aromatase. Estrogen enhances survival of endometrial tissue. Aromatase is absent in normal endometrium

39
Q

what is letrozole

A

aromatase inhibitor- can be used to tx endometriosis

40
Q

how are genetic alterations involved in endometriosis

A

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
Q

what are the diff stages of endometriosis

A 
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
Q

what are the consequences of endometriosis

A

Infertility
Dysmenorrhea
Pelvic pain

43
Q

what are the 3 ways adenomyosis can form

A

Invagination of endometrium

De novo from mullerian rests

Hormonal driven

  • Estrogen produced in adenomyotic tissue
  • Increased aromatase
44
Q

what are characteristics of endometrial polyps

A

usually sessile

45
Q

are endometrial polyps responsive to hormones

A

Responsive to estrogen but little or no progesterone response

46
Q

what is the malignant risk with endometrial polyps

A

Rarely transform to adenocarcinoma

47
Q

what is the pathogenesis of endometrial polyps

A

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
Q

what is endometrial hyperplasia? what is it related to?

A

Increased proliferation of the endometrial glands relative to the stroma
Increased gland to stroma ratio
Related to endometrial carcinoma

49
Q

what is the pathogenesis of endometrial hyperplasia

A

estrogen without unopposed progesterone)

50
Q

what is Endometriod hyperplasia (Type I)

A
  • associated with unopposed estrogen= more glandular
  • PTEN mutation=phosphatase and tensin homologue making PTEN a inactive “brake”= activation of AKT and uncontrolled proliferation
51
Q

what is Nonendometriod hyperplasia(Type II)

A

more stromal tissue and less glandular

  • p53 mutations
  • not assoc with inc estrogen
52
Q

how does the WHO classify endometrial hyperplasia

A

WHO classification based on 2 factors 1.Glandular/Stromal architectural pattern(simple/complex hyperplasia)
2.Presence or absence of nuclear atypia

53
Q

what is simple hyperplasia without atypia

A

Glands: various size and irregular shape
Mild increase in gland: stroma ratio
Epithelial growth similar to proliferative endometrium

54
Q

what is simple hyperplasia with atypia

A

Appearance of simple hyperplasia
Atypia: loss of polarity, vesicular nuclei, prominent nucleoli
8% progress to CA

55
Q

what is complex hyperplasia without atypia

A

Increase number and size of glands, gland crowding
Abundant mitotic figures
Cytology: cells normal
3% progress to CA

56
Q

what is complex hyperplasia with atypia

A

23 to 48% to CA)

57
Q

what are type 1 and 2 carcinoma of the endometrium precursors

A

from type 1(PTEN, K-ras mutations) or 2(p53) endo hyperplasia

58
Q

what are the majority of type 1 carcinomas

A

Majority are endometrioid carcinoma: well differentiated and look like proliferative endometrial glands

59
Q

what are the different endometriod grading for type 1 endometrial carcinoma

A

Grade 1: Well differentiated adenocarcinoma-50% solid)

60
Q

what are the different endometriod staging

A

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
Q

what are malignant mixed mullerian tumors

A

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
Q

what is the prognosis of malignant mixed mullerian tumors

A

Prognosis influenced by grade and type
Highly malignant
Same staging as Type 1 endometrial carcinoma
5 year survival rate: 25-30%

63
Q

what is characteristic of adenosarcomas

A 
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
Q

what are the 2 categories of stromal tumors

A

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
Q

what is the pathogenesis of endometrial stromal sarcomas

A

Chromosomal translocation (JJAZ1 )=anti-apoptotic properties

66
Q

are leiomyomas hormonally responsive

A

yes,
Regress in menopause
Expand in pregnancy

67
Q

what is the pathology of leiomyomas

A

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
Q

what are the growth patterns of leiomyosarcomas

A

2 growth patterns
Bulky fleshy masses invading uterine wall
Polypoid masses that project into the uterine lumen

69
Q

what is the difference between leiomyomas and leiomyosarcomas

A

Degree of nuclear atypia
Mitotic index
Zonal necrosis

Pathophys (15 decks)

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