Module 3: Genitals: Endometrium Flashcards Preview

Pathology Post Midterm > Module 3: Genitals: Endometrium > Flashcards

Flashcards in Module 3: Genitals: Endometrium Deck (39):

Now moving onto Endometrial Female Reproductive Pathology. When is the normal physiological endometrium?

Proliferative Endometrium
--day 1-13
--Estrogen Dominant
--Follicular Phase in Ovary
(remember Polycystic ovarian disease trapped in this stage)
Ovulation day 14
Secretory Endometrium
--day 15-28
---progesterone dominant
--more torturous glands
--luteal phase in ovary
--decidua in prego
(remember women who dont ovulate are stuck in this phase)
Shedding of Endometrium due to loss of progesterone = menstruation


Explain the endometrium proliferative and secretory in terms of histology, slide 1a and 1b

Proliferative and Secretory:
--gland to stroma ratio does not change unless there is a pathology
Architecture Changes!
**proliferative: straight glands, cuboidal to tall epithelium with single to double layer and stroma is dense
***Secretory: coiled glands, tall with vacuoles single layer epithelium, edematous stroma with plump cells and conspicous arterioles


Abnormal Endometrial Cycle is termed Dysfunctional Uterine Bleeding (DUB). There are four types, each card will go through the types of DUB. 1. Unopposed Estrogen Effect

1. Unopposed Estrogen Effect:
---Anovulatory cycles: proliferative epithelium (due to excessive estrogen stimulation)
**leads to polycystic ovaries (Again because excess estrogen)
---Estrogen producing neoplasms: granulosa cell tumor & adrenal cortical adenoma
--Endometrial hyperplasia and Endometrial Carcinoma
--Effect: persistent proliferation: irregular bleeding (DUB)


The next type of DUB is Exogenous Progesterone Effect. What are some features?

2. Exogenous Progesterone Effect
--Contraceptive Pills with progesterone
--abundant stroma with plump cells (pseudodecidualized) and edema
--glands small and atrophic (lined by single inactive epithelium) due to lack of priming by estrogen therefore no proliferative changes.


The third type of DUB is Inadequate luteal phase. What are some features?

3. Inadequate Luteal Phase (ovary)
--Inadequate corpus luteum function due to poor immune secretory glands
--low progesterone, FSH and LH
--irregular ripening


The fourth type of DUB is Persistent luteal phase. What are some features?

4. Menstruation occurs with abrupt cessation of progesterone secretion
--if corpus luteum continues to secrete low levels of progesterone --- excessive and prolonged bleeding (aka protracted and irregular shedding)
--regular periods just long periods
--histology would show persistent secretory phase even after 5 days of menstruation


Now moving on to Endometriosis. What is it? pathogenesis?

Endometrosis = endometrial tissue outside of the lining of the uterus.
Pathogensis: metaplasia of celomic epithelium and inflammatory cascade (prostaglandins, estrogen) (another theory is retrograde flow through the fallopian tubes)


What are the symptoms in a patient with Endometriosis?



What are some complications of endometriosis?

Risk of tubal pregnancy
Rectal bleeding during menstruation if extrauterine site is the colon


Regression can happen with the help of what in endometriosis patients?

Oral contraceptives


Next condition is endometritis, what is it?

Cyclical shedding of endometrium


Explain acute endometritis

Acute (Active inflammation)
--can happen postpartum (puerperal sepsis)
--Can happen with ascending gonococal/chlamydia infection from lower genital tract (foul smelling vaginal discharge, tenderness in suprapubic area and cervical motion tenderness)


Explain Chronic Endometritis

Chronic (chronic inflammation): of the uterine cavity
--plasma cells in stroma (normal stroma does not contain plasma cells)
--risk factors: chronic PID, postpartum/postabortion, IUCD, TB, and Chlamydia


Next topic is endometrial hyperplasia. Who is this seen in? Etiology?

Menopausal Women
Pathological because no progesterone
Etiology: Unopposed Estrogen -- nulliparty, obesity, granulosa theca tumor, polycystic ovarian disease, HRT in postmenopausal women and Tamoxifen (agonist of the estrogen receptor causing endometrial hyperplasia but antagonist in the breast) and adrenal cortical adenoma from zone reticulosis (This is the one they will put on the test)


What are the two types of endometrial hyperplasia?

Simple Cyst
--with or without atypia
--less glands thats why its "Simple"
--with or without atypia
--more glands that why its "complex" (more back to back glands changes the architecture of the glands as well)


What is the presentation for a patient with endometrial hyperplasia?

Menopausal women
Random vaginal bleeding (perimenopausal metrorrhagia)


Hysteroscopy and biopsy are the most accurate tests for endometrial hyperplasia, what is seen?

Proliferating glands
--complex has many more glands (alteration of the gland to stromal ratio --- increased proliferation of glands and less stroma -- over population of glands)


What are the complications to endometrial hyperplasia?

Can undergo atypica
--chance of malignant transformation
--atypical endometrial hyperplasia is premalignant lesion of endometrial carcinoma
--FCC and breast cancer from the high estrogen


What is the treatment for endometrial hyperplasia?

Hysterectomy (if older patients)
Progesterone treatment (cyclic progestin therapy)


In general what is the criteria for atypica?

Nuclear Enlargement (2-3 times RBC)
Vesicular Change
Chromatin Irregularity
Loss of Polarity
Prominent Nucleoli
Cellular Stratification


Moving on to polyps, there are endometrial and endocervical polyps. First what are endometrial polyps?

--perimenopausal women
---associated with Tamoxifen (used to treat breast cancer)
--Asymptomatic or metrorrhagia
--Malignant transformation is rare


What are endocervical polyps?

--pre-menopausal women
--vaginal spotting
--dilated endocervical glands, vascularity, edema and inflammation
--no malignant potential


Moving onto the next topic of the endometrial pathologies is endometrial carcinoma. What is the precursor lesion and etiology?

Precursor Lesion: Atypical Endometrial Hyperplasia
Dysplastic glands invading the myometrium
Etiology: Anything that causes excess estrogen (obesity being key and PCOS)
--remember in ovaries Granulosa Theca cell tumor and in breast FCC are all unopposed estrogen


What is presentation of a patient with endometrial carcinoma?

Post menopausal vaginal bleeding is the most common symptom
Leukoria: white vaginal discharge


What is seen on gross and histology of a patient with endometrial carcinoma?

Gross: polypoid fungating mass in the cavity, enlarged uterus with back to back glands
Histology: no stroma with back to back glands and invasion of the myometrium


There are two types of endometrial carcinoma based on the mass itself. The first is type I Endometrioid. what are some features?

Endometrioid Adenocarcinoma:
--early postmenopausal women in 50-60s
--more common overall
--lots of glands
--P10 mutation (cowden's family history)
-Associations: endometrial hyperplasia
--less than 5% solid (mostly cystic)


The second type of endometrial carcinoma is type II Serous Adenocarcinoma. What are some features?

Serous Adenocarcinoma:
--late postmenopausal women in 70-80s
--Papillary projections with psammona bodies
--P53 mutation (Li Fraumeni family history)
--Association: endometrial atrophy


What are the complications of a patient with endometrial carcinoma?

Regular Metastasis
Invasion: bladder (hydronephrosis), rectum, cervix and vagina


Very briefly, what is a malignant mixed mullerian tumor? (mixed mesodermal tumor/carinosarcoma)?

Women aged over 55 years old
High Grade: large, hemorrhagic and necrotic
Epithelial (defines metastasis and behavior) and mesenchymal components
Poor Prognosis
histology: spindle with whirling cells both sarcoma and glandular components


Next for the uterus pathology is Uterine Fibroids (Leiomyoma). What is the gross and histology? Slide 4

Gross: Benign Smooth Muscle Tumors on the Uterus
--without necrosis or hemorrhage ; clear demarcation, localized and pseudocapsule
Histology: whorls of well differentiated spindle shaped smooth muscle cells


What is the etiology and pathogenesis for uterine fibroids?

Etiology: Unknown
Pathogenesis: Grow bigger in the presence of estrogen (so smaller in menopause and bigger in pregnancy)
--similar to fibroadenoma in that it grows bigger in the presence of estrogen


What population are uterine fibroids seen in?

Most common in nulliparous African American Women


What are complications of uterine fibroids?

2. If fibroids become too big for their blood supply, they undergo coagulative necrosis and then a red infarct
3. Uterus grows bigger and presses on rectum (Constipation) and bladder (hydronephrosis) -- mass effect
4. Heavy Periods (menorrhagia) -- iron deficiency anemia --- left ventricular hypertrophy -- left ventricular failure -- pulmonary edema --- @ 2 weeks hemosiderin laden macrophages in alveolar space


Finally the last pathology of the uterus is Leiomyosarcoma. What are some features?

Arrive De Novo (do not arise from leiomyoma)
--rare and in older women (40-60s), post menopausal
--large, hemorrhagic and necrotic
--hypercellular with atypica, coagulative necrosis
--poor prognosis


What is the criteria for SM tumors?

1.Nuclear Atypica
2. Tumor Necrosis
3. Mitotic Index over 10


in regards to the two different types of endometrial hyperplasia, list in order of greatest to least chance of becoming malignant

Complex with atypia
Simple with atypia
Complex without atypia
Simple without atypia


When does red degeneration of fibroids occur?

During pregnancy (growing so big they are outgrowing their blood supply)


Another condition they may compare to uterine fibroids is adenomyosis, what is this?

Normal looking glands but in the myometrium its a type of endometrosis.
--tender and super painful
--soft in the uterus
--globular enlargement of the uterus (bilateral)


In fibroids is there enlargement of the uterus?

Yes, unilateral

Decks in Pathology Post Midterm Class (50):