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Reproductive Pathology > Endometrium > Flashcards

Endometrium Flashcards

1
Q

Compare and contrast the two layers of the endometrium with regard to:

  • hormonal responsiveness
  • shedding
A

Functional Layer
- responds to hormonal stimulation

Basal Layer
- is never shed it just maintains the foundation on whcih the functional layer develops

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2
Q

Compare the histology that you would see in the following phases of the menstrual cycle.

  • Proliferative
  • Early Secretory
  • Late Secretory
  • Menses

**In what cell layer are these changes occuring?

A

Proliferative:
- Round Glands that are fairly straight with Mitotic Figures

Secretory:
- Corkscrew Glands with no mitotic Figures

  • *Early** - Glands are empty with vacuoles on the basal side
  • *Late** - Gland are filled with fluid (not blood) and vacuoles are on the apical side

Menses:
- blood and hemorrhage coming off in clumps

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3
Q

What is Dysfunctional Uterine Bleeding?
* most common cause?
* pathophysiology of that cause?

A

Bleeding that lacks any underlying anatomical explanation, most often due to **hormonal abnormalities

Dysfunctional Uterine Bleeding**
is commonly due to anovulatory cycles caused by unopposed estrogen that leads to tissue proliferation and eventual shedding

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4
Q

What would you see on an endometrial biopsy of a woman with dysfunctional uterine bleeding/anovulatory cycles?

A

Biopsy shows disorded proliferative pattern with glands shooting off in many directions

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5
Q

When are anovulatory cycles most likely to occur?
*cause?

A

Hormonal Imbalances in general

  • *Menarche** - HPO axis hasn’t gotten in rhythm yet
  • *Perimenopausa**l - Follicles are taking longer to meet the estrogen theshold of to induce postive estrogen feedback on LH in the anterior pituitary
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6
Q

Other than normal hormone imbalances in women around menarche and menopause, what causes Anovulatory Cycles?

A

Endocrine Disorders - e.g. Hypothyroidism => increased TRH => increased TSH and Prolactin Secretion => Prolactin inhibits GnRH release and FSH and LH decrease

Ovarian Lesions - Polycystic Ovaries and Functional Ovarian Tumors

Generalized Disturbances - Obesity, Malnutrition, other Chronic Diseases (all could lead to hyperestrogen or hypo-hormone states)

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7
Q

A woman presents with a pedunculated, localized overgrowth of endometrial GLAND and STROMA in the uterine cavity.

  • What is this lesion?
  • Likely cause?
  • Symptoms?
A
  • *Endometrial Polyp**
  • likely causesd by a hyperplastic response of endometrial tissue to estrogen (most not functional)

Symptoms:
May be an incidental finding (most often) or may present with abnormal bleeding

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8
Q

What do you need to rule out before calling something an endometrial polyp?

A

Cancer

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9
Q

Endometrial Polyp

  • what do you expect the tissue to look like on gross examination?
  • Histologically?
A

Very Red Polyp - from unopposed estrogen and vessel proliferation and WHITE areas of hyperplastic stroma (often have cystic change)

Histologically this will resemble normal endometrial glandular tissue, cystic changes will show up as gaps in the cells with a fibrous stroma and thickened vessel walls

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10
Q

3 common sources of unopposed estrogen leading to endometrial polyps.

A
  • *1. Tamoxifen** (anti-estrogen in breast, pro-estrogen in endometrium)
  • *2. Obesity
    3. Estrogen Therapy**
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11
Q

What is Ashermann Syndrome?
- what causes it?

A

**lack of ovulation secondary to LOSS OF THE BASALIS and scarring

Often due to OVERAGGRESIVE dilation and CURETTAGE**

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12
Q

Acute Endometritis

  • How does this present?
  • What causes it?
A

Presentation:
- Fever, abdominal pain, Uterine Bleeding, Pelvic Pain

Cause:
- Often from retained products of conception - these serve as a nidus for infection

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13
Q

Acute Endometritis
- Treatment?

A

Remove the retained products of conception that probably caused the acute episode in the first place

Give Abx

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14
Q

Chronic Endometritis

  • what 4 potential causes should you have in your differential?
  • what are you looking for on histology?
A
  • *1. Pelvic Inflammatory Disease** (Gonorrhea, Chlamydia)
  • *2.** Retained Gestational tissue (post-pardum, post-abortion)
  • *3.** Intrauterine Contraceptives
    4. TB

Histology Should Show PLASMA CELLS (lymphocytes aren’t good enough because they’re there all the time)

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15
Q

Ectopic Endometrial tissue is found the pouch of Douglas and is thought to the etiology or your patients recurrent pain with bowel movements.

  • What is this called?
  • What might it look like on histo?
A

Endometriosis - while it is ectopic it still has the appearance of normal endometrial tissue with BOTH Glands and Stroma

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16
Q

What can severe endometriosis in the ovary cause?
- what risk is associated with endometriosis in the fallopian tube?

A

Chocolate Cyst

Fallopian Tube endometriosis puts the patient at a high risk of endometriosis

17
Q

What is endometriosis in the myometrium called?

A

Adenomyosis

18
Q

Note: endometriosis may be referred to as having a gun powder appearance due to hemosiderin that has resided in the tissue has it has cycled with the rest of the endometrial tissue, but had nowhere to dump the blood.

A
19
Q

Endometriosis
Typical Presentation

A
  • *Pelvic Pain** and Pain during Menses in a woman between 25 and 30 years old
  • *Infertility** may also bring this to attention
20
Q

Who typically presents with ENDOMETRIAL HYPERPLASIA?
- risk factors for getting this disease?

A

Endometrial Hyperplasia:
Should be suspected in a postmenopausal woman with uterine bleeding (note: this is hyperplasia so it is a precursor to endometrial carcinoma)

Risks (all have to do with HYPERESTROGENIC STATES):

  • **Granulosa cell tumor
  • Obesity
  • Polycystic Ovarian Disease
  • Estrogen Therapy**
21
Q

Endometrial Hyperplasia

  • what do you expect to see histologically?
  • what gene is associated with this disease (gain of function or loss of function)?
  • what is the most important predictor of whether it will progress to cancer?
A

Histologically:
Persistent Estogen stimulation leads to and increased ratio of glands to stroma

Gene - PTEN - tumor suppressor gene also implicated frequently in endometrial carcinoma

CELLULAR ATYPIA IS THE MOST IMPORTANT PREDICTOR OF WHETHER THESE LESIONS WILL PROGRESS TO CANCER

22
Q

What are the 3 categories of Endometrial Hyperplasia?

A

Hyperplasia without Atypia
Endometrial Intraepithelial Neoplasia
Endometrial Carcinoma

**I think this is more of a progression than distinct categories

23
Q

What is the difference between simple and complex variants of Endometrial Hyperplasia?

A

Complex has glands that are increased to the point of there being very little stroma in between them and glands are back to back

**This is a prognostic indicator but is not nearly as important as atypia

24
Q

Hyperplasia without Atypia
- Histology?

A 
NL glands, there are just more of them 
Nuclear Polarity (towards the bottom of the cell) is maintained
25
Q
  • *Endometrial Intraepithelial Neoplasia**
  • Chances of progressing to invasive carcinoma?
  • Histology?
A

25-50% of these patients ALREADY have carcinoma when they are diagnosed with a biopsy showing this

Histology:

  • *- High N/C ratio
  • Chromatin is more irregular
  • Loss of nuclear polarity**
26
Q

T or F: Endometrial Carcinoma is the most common invasive cancer of the female genital tract

A

True.

27
Q

What Familial Disease should you associated with Invasive Endometrial Carcinoma?
- What does the gene product do?

A

People with LYNCH SYNDROME (familial nonpolyposis colorectal carcinoam) (Autosomal Dominant) have loss of a gene that functions in DNA mismatch repair leading to MICROSATELLITE INSTABILTY

28
Q

Compare the age groups in which we see types I and II endometrial carcinoma?
- which is more common?

A

Type I (75% of cases) => women 55-65
Type II => women 65-75

29
Q

Type I endometrial Carcinoma

  • who is this typically seen in?
  • Risk factors?
  • Morphology?
  • Associated Genes?
A

Type I Endometrial Carcinoma
WHO:
- Women 55-65

Risk Factors:

  • *- Unopposed Estrogen/Obesity
  • HTN
  • Diabetes**

Morphology: Endometriod

Associated Gene:

  • *- PTEN
  • MSI** (microsatellite instability) - Lynch Syndrome
30
Q

Type I Endometrial Cancer

  • How does it like to spread?
  • Prognosis?
  • Histology?
A

Type I Endometrial Carcinoma
Spread/Prognosis:
- This is a pretty Indolent cancer and tends to spread through Lymphatic (its a carcinoma)

Histology:
- Looks like Hyperplastic Endometrium (no stroma) as glandular structure is lost and a more sheetlike morphology is taken on the cancer becomes higher grade.

31
Q

Type II Endometrial Carcinomas

  • Age?
  • Risk factors?
  • Subtypes?
  • Associated mutations?
A

Type II endometrial Carcinoma
Age:
women 65-75

Risk Factors:
Atrophy

Subtypes:
- Serous, Clear Cell, MMT (mixed Mullerian tumor)

Mutations:
TP53 (Li-fraumeni)

32
Q

Type II endometrial Carcinoma

  • Method of Spread/Prognosis?
  • Histology?
A

Spread/Px:
Type II endometrial carcinoma is aggressive and spreads via lymphatics and intraperitoneal spread

Histology:
Histology shows Psammona Bodes, and a Medussa head appearance
**P53 staining will be NEGATIVE
**Regardless of histologic pattern this cancer starts off at grade 3.

33
Q

Malignant Mixed Mullerian Tumors

  • Derived from which cell type?
  • Prognostic Indicators?
  • Histology?
A

MMTs
Composition:
Composed of BOTH epithelial and stromal components that may metastasize SEPARATELY

Prognosis:
Prognosis is POOR, presence of heterologous elements like bone or cartilage makes Px even worse.

Histology:
TONS of mitotic figures, epithelial and stromal components

34
Q

Leimyomas

  • Symptoms
  • Reasons for Changes in Size
  • Gross Appearance
A

Symptoms:
- Most commonly asymptomatic, but can be associated with mild abdominal discomfort and pain on defication

Reasons for Size Change:
- May Enlarge During pregnancy and shrink after shrink after menopause

Gross Appearance:
- Well-defined, white, whorled masses

35
Q
A

Reproductive Pathology (6 decks)

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