Flashcards in Female Genital Tract 2 Deck (25):
What are the two layers of the uterus?
-lined by columnar epithelium and deep to that endometrial glands (glads change depending phase) and stroma
-normally some lymphocytes
A. functionalis-near the lumen, hormonally responsive
B. basalis-produces new cells to replace endometrium that was shed during menstruation
-smooth muscle layer
What does normal postmenopausal endometrium look like?
-glands diminished in number, thin epithelium
-stroma abundant collagen
Acute vs Chronic
-abnormal presence of neutrophils
-neutrophils normally present during menstruation
-plasma cells diagnostic
-lymphocytes present in normal endometrium
What are causes of endometritis? What is the presentation? What are the long term complications?
1. Ascending infection from cervix
-std, pelvic inflammatory disease
-abortion, delivery, medical instrumentation
3. Retained products of conception post delivery
-fever, abdominal pain, menstrual abnormalities
Long term complications
-ectopic pregnancy-if ascending to fallopian tube-scarring
What can cause PID? How does it present and look? What can it lead to?
Cervicitis--Endometritis---Salpingitis--Tubo Ovarian abscess
-purulent cervical discharge, cervical motion tenderness
Fallopian tubes distorted
Fimbriated ends adherent
--infertility and ectopic pregnancy
Presence of endometrial glands and stroma outside the endometrium
-ovaries, uterine ligaments, fallopian tubes, pouch of douglas, rectovaginal septum
-less frequently peritoneal cavity, periumbilical tissues
-uncommonly lungs, heart, lymph nodes
What are the three theories of endometriosis?
1. Regurgitation (favored)
-menstrual flow back through fallopian tubes leads to implantation
-endometrial differentiation of multipotential coelomic epithelium
3. Vascular or Lymphatic dissemination
-explains extrapelvic intranodal implants
What is the pathogenesis of endometriosis?
1. Increased inflammatory mediators
2. High aromatase activity of stromal cells, increasing estrogen production
3. Activated macrophages contribute to establishment, maintenance
4. Decreased immune clearance
What must be present histologically for endometriosis?
1. Endometrial glands
2. Endometrial stroma
3. Hemosiderin pigment
Chocolate cyst ovary
What are the symptoms of endometriosis, which affects 10% of women?
1. infertility ~50%
Depends on site of implants
1. severe dysmenorrhea--intrapelvic bleeding
2. pelvic pain, increased risk of ectopic pregnancy, infertility--result of scarring
3. pain with defecation
4. pain with urination
Presence of endometrial glands and stroma within the myometrium
-uterus may enlarge-result of myometrial hypertrophy
-clinically asymptomatic to irregular bleeding to pelvic pain
What is endometrial hyperplasia and what causes it? HOw does it present?
Exaggerated endometrial proliferation
Result of ESTROGEN EXCESS
-estrogen producing ovarian lesions
Granulosa theca cell tumor
-failure of ovulation
-postmenopausal uterine bleeding
How does non atypical vs atypical hyperplasia affect the risk of endometrial cancer?
-short term risk of endometrial cancer is LOW
-marked increased risk of endometrial cancer
Atypical Hyperplasia Histology
Low power: glandular crowding
High power: cytologically atypical rounded, vesicular nuclei with prominent nucleoli
What causes atypical endometrial hyperplasia?
PTEN tumor suppressor gene mutation
-phosphatase protein product involved in the regulation of the cell cycle
-hyperplastic glands may ultimately proliferate autonomously
Endometrial Intraepithelial Neoplasm= neoplastic growth genetically altered cells with greatly increased risk o becoming endometrioid type of endometrial carcinoma
What are the two types of endometrial cancer? What is the presentation?
Post menopausal bleeding
2. serous type
What is the difference between endometrioid and serous endometrial carcinoma?
Endometrioid: from endometrial hyperplasia
Serous: sporadic- no defined precursor lesion-arises from atrophic endometrium
2. Risk factors
Endometrioid: Obesity, exogenous estrogen, early menarche, late menopause, DM, HTN, infertility with anovulatory cycles
Serous: 70 yrs
Endometrioid: appears reminiscent of "normal" endometrium
Serous: papillary structures
Endometrioid: PTEN, early inactivation of DNA mismatch repair genes
Serous: p53 mutations
Serous: aggressive behavior
What happens with endometrial carcinoma?
1. invade myometrium, uterus may affix to surrounding structures
2. Invade vascular spaces
3. Metastasize to regional lymph nodes, distant sites
Usually in fundus
Monoclonal stromal cells + endometrial glands
-association with tamoxifen
most common benign tumor females
-arise from myometrial smooth muscle cells
2. Chromosomal abnormalities
-6, 12 rearrangements
3. almost never transform to malignancy
What causes Leiomyomas? What is the presentation?
Estrogens stimulate growth
-common in premenopausal women
-growth in pregnancy
-arise de novo from mesenchymal cells of myometrium
-do NOT arise from benign leiomyomas
2. Postmenopausal women
3. Clinical Course:
-recur after removal
-metastasize-often to lungs
4. 5 Year survival 40%
2. cytologic atypia
What causes abnormal uterine bleeding for each age group?
-Complications of pregnancy, proliferations (leiomyoma, adenomyosis, polyps)
-Anovulatory cycle proliferation (polyps, hyperplasia, carcinoma)
-Carcinoma, hyperplasia, polyps
Failure of ovulation- anovulatory cycle- what happens?
-endometrium does not progress to normal progesterone driven secretory phase
-endometrium prone to breakdown--abnormal bleeding
-lack of progesterone leads to abnormal development of endometrial arteries