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MHD > Female Genital Tract 2 > Flashcards

Female Genital Tract 2 Flashcards

1
Q

What are the two layers of the uterus?

A
  1. endometrium
    -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
  2. myometrium
    - smooth muscle layer
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2
Q

What does normal postmenopausal endometrium look like?

A

atrophic endometrium

  • glands diminished in number, thin epithelium
  • stroma abundant collagen
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3
Q

Endometritis

Acute vs Chronic

A

Acute
-abnormal presence of neutrophils
-neutrophils normally present during menstruation
Chronic
-plasma cells diagnostic
-lymphocytes present in normal endometrium

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4
Q

What are causes of endometritis? What is the presentation? What are the long term complications?

A

Causes
1. Ascending infection from cervix
-std, pelvic inflammatory disease
-abortion, delivery, medical instrumentation
2. IUDs
3. Retained products of conception post delivery
Presentation
-fever, abdominal pain, menstrual abnormalities
Long term complications
-infertility
-ectopic pregnancy-if ascending to fallopian tube-scarring

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5
Q

What can cause PID? How does it present and look? What can it lead to?

A

STD

  • chlamydia trachomatis
  • neisseria gonorrhoea
  • polymicrobial

Ascending infection
Cervicitis–Endometritis—Salpingitis–Tubo Ovarian abscess

present
-purulent cervical discharge, cervical motion tenderness

Fallopian tubes distorted
Fimbriated ends adherent
Serosa hyperemic
Exudate

–infertility and ectopic pregnancy

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6
Q

Endometriosis?

A

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
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7
Q

What are the three theories of endometriosis?

A
  1. Regurgitation (favored)
    - menstrual flow back through fallopian tubes leads to implantation
  2. Metaplastic
    - endometrial differentiation of multipotential coelomic epithelium
  3. Vascular or Lymphatic dissemination
    - explains extrapelvic intranodal implants
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8
Q

What is the pathogenesis of endometriosis?

A
  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
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9
Q

What must be present histologically for endometriosis?

A
  1. Endometrial glands
  2. Endometrial stroma
  3. Hemosiderin pigment

Chocolate cyst ovary

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10
Q

What are the symptoms of endometriosis, which affects 10% of women?

A
  1. infertility ~50%
    Depends on site of implants
  2. severe dysmenorrhea–intrapelvic bleeding
  3. pelvic pain, increased risk of ectopic pregnancy, infertility–result of scarring
  4. pain with defecation
  5. pain with urination
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11
Q

Adenomyosis

A

Presence of endometrial glands and stroma within the myometrium

  • cause unknown
  • uterus may enlarge-result of myometrial hypertrophy
  • clinically asymptomatic to irregular bleeding to pelvic pain
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12
Q

What is endometrial hyperplasia and what causes it? HOw does it present?

A

Exaggerated endometrial proliferation
glands>stromal hyperplasia

Result of ESTROGEN EXCESS
-exogenous estrogen
-estrogen producing ovarian lesions
PCOS
Granulosa theca cell tumor
-obesity
-failure of ovulation
Perimenopause

Presents
-postmenopausal uterine bleeding

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13
Q

How does non atypical vs atypical hyperplasia affect the risk of endometrial cancer?

A

Non atypical
-short term risk of endometrial cancer is LOW

Atypical
-marked increased risk of endometrial cancer

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14
Q

Atypical Hyperplasia Histology

A

Low power: glandular crowding

High power: cytologically atypical rounded, vesicular nuclei with prominent nucleoli

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15
Q

What causes atypical endometrial hyperplasia?

A

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

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16
Q

What are the two types of endometrial cancer? What is the presentation?

A

Postmenopausal women
Post menopausal bleeding
1. endometrioid
2. serous type

17
Q

What is the difference between endometrioid and serous endometrial carcinoma?

A
  1. Arise
    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
  3. Presentation
    Endometrioid: 60yrs
    Serous: 70 yrs
  4. Histology
    Endometrioid: appears reminiscent of “normal” endometrium
    Serous: papillary structures
  5. Mutations
    Endometrioid: PTEN, early inactivation of DNA mismatch repair genes
    Serous: p53 mutations
  6. Behavior
    Serous: aggressive behavior
18
Q

What happens with endometrial carcinoma?

A
  1. invade myometrium, uterus may affix to surrounding structures
  2. Invade vascular spaces
  3. Metastasize to regional lymph nodes, distant sites
19
Q

Endometrial polyp

A 
Usually in fundus
Monoclonal stromal cells + endometrial glands 
-perimenopause
-bleeding
-association with tamoxifen
20
Q

Leiomyoma “fibroids”

A

most common benign tumor females

  • arise from myometrial smooth muscle cells
  • whorled appearance
  1. Monoclonal
  2. Chromosomal abnormalities
    - 6, 12 rearrangements
    - others
  3. almost never transform to malignancy
21
Q

What causes Leiomyomas? What is the presentation?

A

Estrogens stimulate growth

  • common in premenopausal women
  • growth in pregnancy
  • shrink postmenopausal

30-50% women
blacks> whites

Presentation :

  • asymptomatic
  • abnormal bleeding
  • pelvic mass
  • pain
  • infertility
22
Q

Leiomyosarcoma

A
  1. malignant
    - 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%

Histology

  1. necrosis
  2. cytologic atypia
  3. mitosis
23
Q

What causes abnormal uterine bleeding for each age group?

A

Prepuberty
-Precocious puberty

Adolescence
-Anovulatory Cycle

Reproductive Age
-Complications of pregnancy, proliferations (leiomyoma, adenomyosis, polyps)

Peri menopause
-Anovulatory cycle proliferation (polyps, hyperplasia, carcinoma)

Postmenopause
-Carcinoma, hyperplasia, polyps

24
Q

Failure of ovulation- anovulatory cycle- what happens?

A
  • 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
25
Q

Abnormal uterine bleeding can be caused by uterine organic lesions, systemic abnormalities or absence of distance uterine lesion, what are some examples of these things?

A 
Uterine organic lesion
-polyp
Systemic abnormalities
-exogenous hormones, coagulopathies, thyroid disorders
Absence of distinct uterine lesion
-dysfunctional uterine bleeding

MHD (81 decks)

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