L40- Female GUT Pathology I (uterus) Flashcards

1
Q

list the endometrium phases

A

(Menstrual Cycle)
Day 1-13: proliferation, estrogen (days 1-4 = menstruation)

Day 14: ovulation

Day 15-28: secretory, progesterone

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2
Q

describe the key feature of the endometrium during:

  • (1) proliferative phase
  • (2) early secretory phase
  • (3) late secretory phase
  • (4) menstration
A

1- mitoses, straight glands, single/double layer of cuboidal to tall cells (pseudostratification), dense stroma, compact cells, round glands

(coiled glands / single layer tall cells with vacuoles, edematous stroma, plump cells, conspicuous arterioles)
2- subnuclear (clear mucinous) vacuoles, inc vascularization
3- pre-decidual changes, apical vaculoes, serrated glands, inc vascularization

4- stromal breakdown, blood

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3
Q

list the many Uterus Sxs

A
  • Amenorrhea- primary or secondary
  • Menorrhagia: excess bleeding (cyclical)
  • Metrorrhagia (epimenorrhea)- irregular non-cyclical bleeding

Dysmenorrhea (pain with menses):

  • primary at menarche (nerve/muscle activity abnormality)
  • secondary after menarche

Infertility- congenital anomalies, neoplasms, endometrial disease

Mass- palpable when large

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4
Q

Amenorrhea:

  • (1) definition
  • (2) primary causes
  • (3) secondary causes
A

1- absence of menstruation

2- (never menarche) hypoplastic uterus, imperforate hymen, endocrine problems

3- (after menarche) pregnancy, lactation, endocrine problems, stress

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5
Q

list the uterine / cervical disease evaluation techniques

A

Pelvic Exam: speculum, colposcopy, US, CT scan

Pap smear: infection, CIN, neoplasia

Biopsy- cervix, endometrium

D&C- dilatation and curettage

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6
Q

DUB = (1):

-(2) describe cycle / hormone status that may cause DUB

A

1- dysfunctional uterine bleeding (abnormal endometrial cycle)

2:

  • unopposed estrogen effect
  • exogenous progesterone effect
  • inadequate luteal phase
  • persistent luteal phase
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7
Q

Unopposed Estrogen: list causes of anovulatory cycles

A
  • extremes of reproductive life (most common)
  • PCOD (Stein-Leventhal Syndrome)
  • endocrine disorders (thyroid, adrenal)
  • Obesity, emotional stress
  • excess physical activty
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8
Q

Unopposed Estrogen in abnormal endometrial cycle may develop from (1) disease and has the (2) as net effects

A

1- estrogen producing neoplasms: granulosa cell tumor in ovary, adrenal cortcal adenoma (glomerulosa)

2- persistent proliferation –> irregular bleeding breakdown (DUB), endometrial hyperplasia, endometrial carcinoma

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9
Q

Exogenous Progesterone Effect:

  • (1) is the primary cause
  • (2) is the descriptive result with (3) as features
A

1- contraceptive pills with progesterone

2- ‘Pill endometrium’

3:

  • abundant stroma, plump cells (pseudodecidualized), edema
  • small atrophic glands (lack of priming by estrogen)
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10
Q

Inadequate Luteal Phase:

  • (1) common cause
  • (2) net effects
  • (3) labs
A

1- inadequate corpus luteum function (dec progesterone)

2:

  • irregular ripening
  • irregular breakdown (DUB)
  • poorly developed secretory endometrium, lacks secondary characteristics

3- low progesterone, low FSH, low LH

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11
Q

Persistent Luteal Phase:

  • (1) perpetuates normal menstruation
  • (2) is the abnormality of (1) here
  • (3) is the main change via (2)
  • (4) is evident on biopsy
A

1- abrupt cessation of progesterone secretion of corpus luteum

2- continued corpus luteum secretion of low levels of progesterone

3- regular periods, but excess bleeding and prolonged (10-14 days)

4- persistent secretory appearance 5 days post-menstruation

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12
Q

Endometriosis:

  • (1) definition and (2) locations
  • (3) is endometrial tissue w/in uterine wall
  • (4) Sxs
A

1- endometrial tissue outside of uterus

2- ovaries, uterine ligaments, rectovaginal septum, cul-de-sac / pouches, GIT, appendix, laparotomy scars

3- adenomyosis, 20% uteri

4- pelvic pain, dysmenorrhea, infertility

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13
Q

list the 2 theorized pathogenic mechanisms of endometriosis

A
  • metastatic pathogenesis, metaplasia of coelomic epithelium

- inflammatory cascade- PGs, estrogen

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14
Q

list the changes seen in endometriosis (3 main ones)

A

Endometrium: glands and stroma undergo cyclical bleeding, hemosiderin deposition, fibrosis, adhesions

Ovary- chocolate cysts

Fallopian Tubes: tubal Scars –> infertility

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15
Q

Endometriosis:

  • (1) time of occurrence
  • (2) is the common presentation, (3) is seen at higher disease progression
  • (4) when regression may occur
A

1- reproductive phase of life

2- asymptomatic

3- dysmenorrhea, menorrhagia, infertility

4- after pregnancy, oral contraceptives

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16
Q

Endometriosis:

  • cyclical bleeding is observed in (1)
  • fibrosis may lead to the following- (2)
A

1- urinary tract, rectum, umbilicus, surgical scars

2:

  • infertility (tubes), risk of tubal pregnancy
  • urinary obstruction
  • intestinal obstruction
17
Q

Acute Endometritis definition and causes

A

-active inflammation

Postpartum: offensive lochia (puerperal sepsis, Strep/Staph spp.)

Ascending gonococcal / chlamydia

Pyometrium- os obstruction by neoplasm, fibrosis

18
Q

Chronic Endometritis causes

A

(15% nonspecific)

  • chronic PID
  • postpartum / post-abortion (retained products)
  • IUDs
  • TB
  • chlamydia
19
Q

Endometrial Polyp:

  • (1) size
  • (2) developmental association
  • (3) presentation
  • (4) possible complication
A

1- 0.5-3 cm
2- certain drugs- Tamoxifen
3- asymptomatic or metrorrhagia
4- malignant transformation

20
Q

Endometrial Hyperplasia:

  • (1) and (2) are main causes
  • (3) are other causes
  • (4) is genetic association
  • (5) Tx
A

1- excess unopposed estrogen effect
2- perimenopausal metrorrhagia
3- obesity, PCOD, menopause, estrogen replacement therapy, estrogen tumor (granulosa tumor), adrenal disorder

4- PTEN, tumor suppressor
5- hysterectomy, progesterone therapy (small number of patients)

21
Q

list the forms of endometrial hyperplasia and the risks for carcinoma development

A

Simple hyperplasia:

  • w/o atypia –> 1%
  • w/ atypia –> 8%

Complex hyperplasia:

  • w/o atypia –> 3%
  • w/ atypia –> 24-48%
22
Q

name the genetic changes related to the following:

  • (1) development into non-atypical endometrial hyperplasia
  • (2) change while in non-atypical hyperplasia
  • (3) progression from non-atypical to atypical
  • (4) progression from atypical to grade I carcinoma
A

1- PTEN (tumor suppressor)

2- MLH1

3- KRAS, MSI

4- ARID1A, PIK3CA, CTNNB1, FGFR2

23
Q

list the criteria needed to consider endometrial hyperplasia as atypical

A
  • nuclear enlargement (x2-3 bigger than RBC)
  • pleomorphisms
  • vesicular change
  • chromatin irregularity
  • loss of polarity
  • prominent nucleoli
  • cellular stratification
24
Q

______ is the most common invasive carcinoma of female genital tract

A

endometrial carcinoma: type I > type II

-biopsy needed for Dx

25
Q

Type I endometrial CA:

  • (more/less) prevalent than type II
  • (2) age group
  • (3) key clinical history feature
  • (4) risk factors
  • (5) genetic associations
  • (6) types
  • (fast/slow)
  • (8) precursor
A
1- more
2- 55-65 y/o
3- nulliparous
4- unopposed estrogen, obesity, DM, HTN
5- PTEN, KRAS, MSI
6- endometrioid (only)
7- slow, indolent
8- complex hyperplasia with atypia (endometrium)
26
Q

Type II endometrial CA:

  • (more/less) prevalent than type I
  • (2) age group
  • (3) key clinical history feature
  • (4) risk factors
  • (5) genetic associations
  • (6) types
  • (fast/slow)
  • (8) precursor
A
1- less
2- 65-75 y/o
3- thin physique
4- endometrial atrophy (age)
5- p53
6- serous, clear cell, malignant mixed mullerian tumor
7- rapid / aggressive
8- endometrial intraepithelial carcinoma
27
Q

Endometrial CA:

  • (1) mass description
  • (2) describe metastasis
A

1) polyploid fungating mass in cavity, asymmetric enlargement of the uterus, back-to-back glands

2)

  • local: myometrium, cervix, vagina, rectum
  • peritoneum
  • lymphatics: iliac, para-aortic
  • blood: lung, liver
28
Q

briefly describe Endometrial CA grading

A

I- confined to uterus (corpus)
II- involves uterine corpus and cervix
III- outside uterus, still w/in pelvis
IV- outside pelvis, involves rectum, bladder

29
Q

Malignant Mixed Mullerian tumor, aka (1):

  • (2) age group
  • (3) origin –> prefixes
  • (4) aggressiveness / prognosis
  • (5) gross appearance
A

1- mixed mesodermal tumor / carcinosarcoma

2- >55 y/o

3- epithelial, mesenchymal origin ==> leio-, rhabdo-, chondro-, osteo-

4- high grade, metastasis depends on epithelial component, poor prognosis

5- large, fleshy mass, hemorrhage, necrosis

30
Q

Leiomyoma:

  • (1) prevalence and definition
  • (2) age group
  • (3) key property, in relation to growth
  • (high/low) malignant potential
A

1- 25% of women, benign smooth muscle tumor

2- 20-40 y/o

3- estrogen dependent growth (regression with menopause)

4- NO potential

31
Q

Leiomyoma:

  • (single/multiple) in (2) location related to layers of uterus
  • (3) nodule description
A

1- multiple

2- subserosal, intramural, submucosal

3- circumscribed whorled nodules, resembles normal smooth muscle with fibrosis

32
Q

Leiomyoma:

  • (1) Sxs
  • (2) Tx
A

1:

  • asymptomatic
  • menorrhagia, metrorrhagia, infertility
  • mass effects (compression)
  • acute pain –> red degeneration, especially in pregnancy

2: laproscopic resection, hysterectomy

33
Q

list leiomyoma variants

A
  • atypical / symplastic
  • cellular
  • benign metastasizing leiomyoma
  • disseminated peritoneal leiomyomatosis
34
Q

describe the aspects of smooth muscle tumors of the uterus that are evaluated upon investigation / biopsy and how they influence DDx and further investigation

A

1) nuclear atypia

2) tumor necrosis
i) absent –> **leiomyoma (skip 3)
ii) present –> step 3

3) mitotic count > 10 –> **leiomyosarcoma

35
Q

(T/F) leiomyosarcomas result from malignant transformations of leiomyomas

A

F- de novo derivation

-leiomyomas have NO malignant potential

36
Q

Leiomyosarcoma:

  • (1) age group
  • (2) gross appearance
  • (3) microscopic appearance
  • (good/poor) prognosis
A

1- 40-60 y/o, post-menopausal bleeding

2- large, bulky, hemorrhage, necrosis

3- hypercellular with atypia, >10 mitoses, coagulative necrosis

4- poor, 5yr ~40%

37
Q

Endometrial tumors with stromal differentiation:

  • aka (1)
  • resembles (2) tumor
  • (3) age group
  • (high/low) malignancy
  • (5) genetic association
A

1- adenosarcoma (benign epithelium + malignant stroma)

2- phyllodes tumor in breast

3- 30s-40s

4- low grade malignancy (decades for metastasis), but local recurrence [15% cases are fatal]

5- t(7;17) –> fusion of JAZF1 and JJAZ1

38
Q

briefly describe the types of Endometrial tumors with stromal differentiation

A

(stromal tumors)
i) benign stromal nodule- endometrial stromal cells, well circumscribed

ii) endometrial stromal sarcoma- low grade (infiltrative edge + lymphovascular invasion) or high grade

39
Q

In the ovarian follicle, (1) produces the androgens and (2) converts it to estrogens

A

1- theca cells

2- granulosa cells