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RGU Exam 1 > Pathology Of Uterus > Flashcards

Pathology Of Uterus Flashcards

1
Q

Dysfunctional uterine bleeding

A
  • The most common form of vaginal bleeding in women
  • Abnormal bleeding in the absence of a well defined organic lesion
  • Endometrium goes thru a proliferative phase w/o a secretory phase eventually collapses and bleeds
  • Common at both ends of reproductive life
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2
Q

Dysfunctional uterine bleeding causes

A
  • Most common cause: Anovulatory cycle: excess of estrogen relative to progesterone
  • Any dysfunction of hypothalamus, pituitary gland, thyroid
  • Ovarian lesion, malnutrition, obesity stress
  • Inadequate luteal phase

*corpus luteum fails to mature or may regress prematurely leading to a relative lack of progesterone

*endometrium has a delay in development

  • Contraceptive induced bleeding
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3
Q
A
  • Anovulatory bleeding
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4
Q

Endometritis

A
  • Part of pelvic inflammatory disease
  • Endometrium is inflammed
  • May be assoc. w/ retained POC (products of conception; like placenta) or FB (foreign bodies) such as IUD
  • Acute and chronic forms
  • Chronic forms have plasma cells
  • Infection
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5
Q

Endometritis Symptoms

A
  • Fever, pain, ectopic pregnancy, menstrual irregularities
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6
Q

Chronic Endometritis Histology

A
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7
Q

Endometrial Polyps

A
  • Sessile lesions, 0.5-3cm in diameter
  • Covered w/ columnar cells, adenomatous stroma
  • More common around menopause
  • May produce abnormal uterine bleeding
  • Foci of adenocarcinoma are rarely present
  • Stromal cells have a cytogenetic arrangement of 6P21
  • Has been assoc. w/ the use of Tamoxifen
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8
Q

Adenomyosis

A
  • Growth of endometrial basal layer into the myometrium

*benign growth

  • Uterine wall is thickened
  • Cyclic bleeding can occur but is unusual
  • May produce menorrhagia, dysmenorrhea and pelvic pain
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9
Q

Adenomyosis Histology

A
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10
Q

Endometriosis

A
  • Endometrial tissue outside the uterus
  • Benign tissue but can cause complications from bleeding
  • Common locations: ovaries, pouch of Douglas, uterine ligaments, tubes, rectovaginal septum
  • Uncommonly: LN, lungs, heart
  • Endometrial foci often undergoes cyclic bleeding
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11
Q

Endometriosis Complications

A
  • Can lead to Infertility
  • Can cause Dysmenorrhea
  • Can cause Pelvic pain
  • Seen during active reproductive life
  • Affects approx. 10% of women often in 20-30’s
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12
Q

Endometriosis Four Major Theories

A
  • The regurgitation theory
  • Metaplastic theory
  • The benign metastasis theory
  • The extra uterine stem/progenitor cell theory
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13
Q

Endometriosis-regurgitation theory

A
  • Endometrial tissue implanted at abnormal locations
  • Retrograde menstruation thru fallopian tubes could mediate spread of endometrial tissue to the peritoneal cavity
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14
Q

Endometriosis-metaplastic theory

A
  • Endometrium arising directly from coelomic epithelium which is mesothelium of the pelvis
  • Mullerian ducts and endometrium originates from this during embryonic development
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15
Q

The benign metastases theory

A
  • Endometrial foci pass thru the lymphatic and hematogenous system
  • Can reach distant sites such as the lung, bone and brain
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16
Q

The extrauterine stem/progenitor cell theory

A
  • Proposes that stem/progenitor cells from the bone marrow differentiate into endometrial tissue
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17
Q

Endometriotic tissue characteristics

A
  • There are specific abnormalities that distinguish normal endometrium from endometriotic tissue
  • Activation of the inflammatory cascade: high lvls of prostaglandin E2, interleukin-1 beta, tumor necrosis factor and interleukin-6
  • Upregulation of estrogen production by stromal cells due to high lvls of steroidogenic enzyme aromatase which is absent in normal endometrial stroma
  • Epigenetic changes in genes that encode 2 nuclear receptors: steroidogenic factor 1 and estrogen receptor beta
  • This results in overexpression causing a cascade leading to overproduction of estrogen and prostaglandin and resistance to progesterone action
  • Produces nodules w/ a red-blue to yellow-brown appearance (due to early hemoglobin appearing red-blue and then as it breaks down to hemosiderin you get the yellow-brown)
  • Hemorrhage may cause xtensive fibrous adhesions b/w tubes, ovaries and other structures
  • Chocalate cysts
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18
Q

Endometriosis Diagnosis

A
  • Histologic diagnosis of endometriosis requires the presence of both endometrial glands and stroma
19
Q

Chocalate Cysts

A
  • Cystic masses in the ovaries filled w/ brown fluid resulting from previous hemorrhage
20
Q

Endometriosis Clincal Features

A
  • Severe dysmenorrhea
  • Dyspareunia
  • Pelvic pain
  • Occasional pain on defecation
  • Menstrual irregularities
  • Infertility
21
Q

Atypical endometriosis

A
  • Possible precursor to endometriosis related ovarian carcinoma
  • Has 2 morphologic appearances
    1) cytologic atypia of the epithelium lining the endometriotic cyst w/o major architectural changes
    2) marked glandular crowding from epithelial proliferation often w/ cytologic atypia
22
Q

Endometrios Diagnosis Histology Slide

A
23
Q

Endometrial hyperplasia

A
  • An important cause of endometrial bleeding
  • Defined as an increase proliferation of the endometrial glands relative to the stroma
  • Results in an increased gland to stroma ratio when compared w/ normal proliferative endometrium
  • Malignant potential
  • Assoc. w/ prolonged estrogen stimulation of the endometrium
24
Q

Endometrial hyperplasia associated diseases

A
  • Obesity, menopause, PCOS, functioning granulosa cell tumors of the ovary, excessive cortical function, and prolonged administration of estrogenic substances such as estrogen replacement therapy
25
Q

PTEN Gene

A
  • Tumor suppressor gene
  • Common genetic alteration found in hyperplasias and related endometrial carcinomas
  • Encodes a dual specificity phosphatase capable of disphosphorylating both lipid and protein molecules
  • It dephosphorylates lipid molecule phosphatidylinositol triphosphate which blocks the phosphorylation of AKT a central factor in the phosphatidylinositol 3 kinase growth regulatory pathway
  • When PTEN is inactive AKT phosphorylation is enhanced, stimulating protein synthesis and cell proliferation while inhibiting apoptosis
  • Loss of PTEN may activate pathways normally activated by estrogen
26
Q

Simple hyperplasia without atypia

A
  • Glands of various sizes and irregular shapes w/ cystic dilation
  • Milde increase in the gland to stroma ratio
  • Epithelial growth pattern and cytology are similar to proliferative endometrium w/ less prominent mitoses
  • Uncommonly progress to adenocarcinoma
27
Q

Simple hyperplasia with atypia

A
  • Simple hyperplasia w/ cytologic atypia within the glandular epithelial cells
  • Loss of polarity
  • Vesicular nuclei and prominent nucleoli
  • Cells become rounded and lose the normal perpendicular orientation to the basement membrane
  • Approx. 8% progress to carcinoma
28
Q

Complex hyperplasia without atypia

A
  • Characterized by increased number and size of endometrial glands
  • Marked gland crowding
  • Branching of glands
  • Crowded glands w/ abundant mitotic figures
  • The glands remain distinct and the epithelial cells are cytologically normal
  • 3% progress to carcinoma
29
Q

Complex hyperplasia with atypia

A
  • Can overlap w/ well-differentiated endometrioid adenocarcinom
  • Architectural features are similar to complex hyperplasia w/o atypia but the cytologic features have changed
  • Cells show atypia w/ rounded vesicular nuclei and prominent nucleoli
30
Q

Carcinoma of the endometrium

A
  • Most common invasive cancer of the female genital tract
  • Arise mainly in postmenopausal women and presents w/ abnormal postmenopausal bleeding
  • Uncommon in women younger than 40
  • Incidence is in 55-65
  • Clinicopathologic studies and molecular analysis divide endometrial carcinoma into two broad categories
31
Q

Carcinoma of the endometrium type I

A
  • Most common type accounting for greater than 80% of cases
  • Majority are well differentiated and mimic proliferative endometrial glands
  • Referred to as endometrioid carcinoma
  • Typically arise in the setting of endometrial hyperplasia
  • Contributing factors: obesity, diabetes, hypertension, infertility and unopposed estrogen stimulation
32
Q

Carcinoma of the endometrium type I genetic mutations

A
  • PTEN tumor suppressor gene has been identified in 30-80%
  • PIK3CA mutations have been reported and endometrial carcinomas
  • PIK3CA is the catalytic subunit of PI3K, a lipid kinase that phosphorylates PIP2 to PIP3, directly antagonizing the action of PTEN
  • Microsatellite instability and mutations in the K-ras and beta catenin oncogenes can also be present
  • Mutations in p53
33
Q

Carcinoma of the endometrium appearance

A
  • Can be either a localized polypoid tumor or a diffuse tumor involving the endometrial surface
  • Direct myometrial invasion and eventual extension to the periuterine structures
  • Dissemination to the regional lymph nodes, lungs, liver and other organs can occur
34
Q

Carcinoma of the endometrium type I gradings

A
  • Most are endometrioid adenocarcinomas w/ gland patterns resembling normal endometrial epithelium
  • 3 step grading system; G1, G2, G3 (as move up in grade, the more solid the tumor becomes)
35
Q

Carcinoma of the endometrium type I

A
  • Up to 20% of endometrioid carcinomas contain foci of squamous differentiation

- The squamous elements are generally benign appearing

  • Occasionally moderately to poorly differentiated endometrioid carcinomas have malignant squamous elements
36
Q

Carcinoma of the endometrium type II

A
  • Generally occur in women a decade later than type I
  • Usually arises in the setting of endometrial atrophy
  • They are by definition poorly differentiated grade 3 tumors
  • The most common cell type is serous carcinoma b/c it resembles ovarian serous carcinoma
37
Q

Carcinoma of the endometrium type II genetic mutations

A
  • Most common genetic alteration is a mutation in the p53 tumor suppressor gene
38
Q

Carcinoma of the endometrium type II appearance

A
  • Tumors are often large bulky or deeply invasive into the myometrium
  • Endometrial intraepithelial carcinoma: malignant cells in the gland surface w/o stromal invasion
  • Invasive lesions: may have a papillary growth pattern
39
Q

Carcinoma of the endometrium Symptoms

A
  • May be asymptomatic for a period of time
  • Usually presents w/ irregular postmenopausal vaginal bleeding or leukorrhea
  • Prognosis depends on stage and histologic grade and type
40
Q

Malignant mixed mullerian tumor

A
  • AKA carcinosarcoma
  • Usually seen in post menopausal pts
  • Uterine bleeding and enlargement
  • Large soft, polypoid growths
  • Admixture of carcinomatous and sarcoma-like elements
  • Highly aggressive
41
Q

Leiomyoma

A
  • Benign tumors from smooth muscle cells
  • AKA fibroids (is NOT fibrotic tissue)
  • Most common benign tumor in females
  • Estrogens stimulate their growth
  • Many have MED 12 gene mutations
  • MED 12 stimulates gene expression
42
Q

Leiomyoma appearance

A
  • Well circumscribed, gray white masses
  • Small to very large, may be multiple
  • May become hemorrhagic or calcifie
  • Whorling bundles of smooth muscle
  • May be asymptomatic or present w/ menorrhagia
43
Q

Leiomyosarcomas

A
  • Do NOT arise from preexisting leiomyomas
  • Usually solitary
  • May be infiltrating, polypoid or discrete tumors
  • Frequent mitoses, cellular atypia, coagulative necrosis
  • Can be difficult to distinguish from leiomyoma
  • Recurrence is common, may metastasize widely

RGU Exam 1 (14 decks)

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