Uterus Flashcards
What are the two parts of the endometrium?
What is the function of each?
1. Functionalis - near the lumen, hormonally responsive
During the proliferative phase/follicular phase, the secretion of estrogen through the grwoing ovarian follicle is responsible for the proliferation of the endometrium/intensive mitosis in the glandualr epithelium and in the stroma. Sheds at the start of the proliferative phase
During the secretory phase/luteal phase, endometrium differentiates itself due to the influence of progesterone (from the corpus luteum) and attains its full maturity - glands and arteries begin to entwine, connetive tissue stroma becomes the place of edematous change
2. Basalis - produces new cells to replace endometrium that was she during menstruation
How does the endometrium change post-menopause?
–> atrophic endometrium
- Glands diminish*
- Epithelium thins*
Stroma contains abundant collagen
What is the pathology behind endometritis?
How can you distinguish between acute vs chronic endometritis?
Endometritis = inflammed endometrium
Acute - abnormal presence of neutrophils
note: neutrophils are normally present during menstruation
Chronic - INCREASED numbers of lymphocytes (present normally in endometrium) and plasma cells are diagnostic of chronic endometritis
Endometritis:
Etiologies (3)
Presentation (3)
Long-term complications (2)
Endometritis:
Etiologies: Ascending infection (STDs, PID, delivery, med instrumentation ), intrauterine device (IUD), retained products of conception post delivery (stormy onset)
Presentation: Fever, abdominal pain, menstrual abnormalities
Long-term complications: infertility, ectopic pregnancy (if ascneding to fallopian tube –> scarring –> could prevent the ovuum from getting through)
Pelvic inflammatory disease (PID)
Pathogenesis:
Major infectious agents (3):
Symptoms and physical exam findings (6):
Long-term consequences (2):
Pelvic inflammatory disease (PID)
Pathogenesis: ASCENDING INFECTION. acute inflammatory process - cervicitis, endometritis, salpingitis, tuoovarian abscess
Major infectious agents (3): chlamydia trachomatis, neisseria gonorrhoeae, polymicrobial
Symptoms and physical exam findings (6): purulent cervical discharge (thick green/yello secretions, cervical motion tenderness (pain with bimanual exam/tenderness), systemically - fever, N/V, abdominal pain and anorexia
Long-term consequences: fallopian tubes distored –> fimbriated ends adherent and serosa hyperemic, exudate –> infertility, ectopic pregnancy
What is endometriosis?
Where is endometriosis most commonly found (5) and other less frequent locations?
Symptoms (6):
Endometriosis = presence of endometrial glands and stroma OUTSIDE of the endometrium
Normally, it could be found: ovaries, uterine ligaments, fallopian tubes, pouch of Douglas, rectovaginal septum and less frequently, peritoneal cavity, periumbilical tissue and even less commonly lungs, heart, lymph nodes
Symptoms are dependent on the site of implants (endometriosis tissue/implants is also active during the women’s regular menstrual cycle)
Severe dysmenorrhea
Infertility (50% of infertile women! result of scarring - ectopic pregnancy or complete infertility)
Intrapelvic bleeding
Pelvic pain
Pain with defecation
Pain with urination
What are the three theories behind endometriosis?
1. Regurgitation: favored - menstrual backflow/retrograde through fallopian tubes leads to implantation/refluxed endometrial framents adhere to and invade the peritoneal mesothelium, develop a blood supply –> implant, survival and growth
2. Metaplastic: endometrial differntiation of multipotential coelomic epithelium; metaplasic change of peritoneal mesothelial cells into endometrial glandular cells
3. Vascular or lymphatic dissemination: explains extrapelvic, intranodal implants [lungs, lymph nodes…]
Pathogenesis: How does endometrial tissue survive elsewhere? (4)
INC inflammatory mediators - esp prostaglandin E2
INC estrogen production due to high aromatase activity of stromal cells
Macrophages contribute to establishment and maintenance
DEC immune clearance
Mileu: aromatase, VEGF, PGE1, MMPs TIMPs, IL1, IL8, IL6, TNFalpha, NGF
What is adenomyosis?
What causes adenomyosis?
What are the clinical and gross presentations?
Treatment?
Adenomyosis = presence of endometrial glands and stroma within the myometrium
UNKNOWN cause
Presentation: uterus may enlarge as a result of myometrial hypertropy
SX varies- asymptomatic –> irregular bleeding –> pelvic pain
Treatment: generally no treatment unless severe pain/discomfort
What is the criteria for endometriosis?
2 of 3 must be present:
Endometrial glands
Endometrial stroma
Hemosiderin pigment
What is endometrial hyperplasia?
What causes endometiral hyperplasia?
Possible risk factors? (4)
Clinical presentation (2):
Endometrial hyperplasia: exaggerated endometrial proliferation (glands > stromal hyperplasia)
What causes endometiral hyperplasia? EXCESS ESTROGEN
Possible risk factors? exogenous estrogen, estrogen producing ovarian lesions (PCOS, granulosa-theca cell tumor), obesity (aromatase), failure of ovulation (perimenopause)
Clinical presentation: postmenopausal uterine bleeding OR heavy bleeding menses
What is the histology associated with endometrial hyperplasia?
What are the two types of endometrial hyperplasia histology? What is the difference between each..
Which, if any, has an increased risk for endometrial cancer?
Histo: cytologic atypia of gland cells - too many glands/stroma
[note: in a normal cycle it is okay, but when there is excess it throws balance off, especially due to menopause]
- Non-atypical = short term risk of endometrial cancer low risk
Glandular crowding but overall “normal epithelium” lining the glands [normal cubodial, small nucleli, lined up normally around gland]
- Atypical = endometrial intraepithelial hyperplasia
MARKED INC RISK for endometrial cancer
glandular crowding AND abnormal cells [higher N:C ratio, cytologically atypical rounded, vesicular nuclei with prominent nucleoli]
What contributes to the carcinogenicity of atypical endometrial hyperplasia?
2-hit: hyperplastic glands + PTEN tumor suppressor gene mutations
PTEN tumor suppressor gene mutations
Phosphatase protein product involved in the regulation of the cell cycle = mutation turns off the tumor suppressor capability–> hyperplastic glands can autonomously proliferiate –> neoplasia
–> Endometrial intraepithelial neoplasia (EIN) = neoplastic growth genetically altered cells with greatly increased risk of becoming endometrioid type of endometrial carcinoma
Endometrial CA:
Presentation:
Histologic types (2):
Overall course (3):
Presentation: Postmenopausal bleeding
**cancer until proven otherwise, R/O endometrial CA!**
Type histologic types:
Endometrioid (80%)
Serous (15%) more frequent extrauterine extension at dx, worst prognosis
other rare types
General course: stage major determinant of survival
INVADES myometrium, uterus may affix to surrounding structures
Invades vascular spaces
METASTASIZE to regional lymph nodes – distant sites
Endometrioid type endometrial CA:
Where does it arise from?
Risk factors?
Presentation?
Histology:
Endometrioid type endometrial CA:
Where does it arise from: endometrial hyperplasia (atypical)
Risk factors: UNOPPOSED ESTROGEN (obesity, esogenous, early menarche, late menopause) DM, HTN, infertility with anovulatory cycles, PTEN mutations (most frequently altered gene in endometrioid CA - early inactivation of DNA mismatch repair genes)
Presentation: ~ 60 y/o
Histology: appears reminiscent of “normal” endometrium
