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Pathology Pt. 4 > Female Genital and Breast 1 > Flashcards

Female Genital and Breast 1 Flashcards

1
Q

What is vulvitis? What two general things often cause it?

A

Inflammation of the vulva (external female genitalia).

Often caused by STDs (chlamydia is most common STD in North America!) or contact dermatitis (irritant or allergic).

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2
Q

What is a Bartholin cyst? What causes it? At what ages does it occur? What are complications and treatments?

A

Bartholin duct obstruction –> gland inflammation and cyst formation. Gonorrhea, staph, chlamydia and anaerobes are often involved.

Common in all ages.

Can lead to abscess.

Tx includes incision, drainage, marsupialization, and antibiotics.

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3
Q

What is lichen sclerosus of the vulva?

A

It is an non-neoplastic inflammatory disease of the epithelium of the vulva, often associated with autoimmune diseases.

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4
Q

What gross (3) and microscopic changes (5) are seen in lichen sclerosus of the vulva?

A

Gross:

  1. Looks like leukoplakia.
  2. Skin is atrophic.
  3. Parchment-like or crinkled appearance.

Microscopic:

  1. Thinning of the epidermis.
  2. Disappearance of rete pegs (the epithelial papilla).
  3. Hydropic degeneration of the basal cells.
  4. Superficial hyperkeratosis and dermal fibrosis.
  5. Not much inflammatory infiltrate but sometimes a bandlike lymphocytic infiltrate is seen.
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5
Q

What are three clinical features of lichen sclerosus of the vulva?

A
  1. Can be seen in all ages but most common in post-menopausal women.
  2. Pruritus/itching (most common).
  3. Dyspareunia (pain during sex)
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6
Q

Is lichen sclerosis of the vulva cancerous? Can it lead to cancer?

A

It is non-neoplastic but 1-5% develop keratinizing squamous cell carcinoma of the vulva. Biopsy is needed to differentiate from other premalignant or malignant lesions.

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7
Q

What is condyloma acuminatum and what causes it?

A

Anogenital warts caused by HPV 6, 11, and sometimes 16 and 18.

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8
Q

What is a koilocyte?

A

A cell that is observed to have undergone changes as a result of HPV infection:

  1. Nuclear enlargement (two to three times normal size).
  2. Irregularity of the nuclear membrane contour.
  3. Hyperchromasia.
  4. A clear area around the nucleus, known as a perinuclear halo.
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9
Q

What microscopic changes are seen in condyloma acuminatum?

A
  1. Branching, villous, papillary CT stroma covered by epithelium with hyperkeratosis and a thickened epidermis.
  2. Epithelial maturation is preserved.
  3. Presence of koilocytes.
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10
Q

Does condyloma acuminatum often progress to carcinoma in situ or cancer?

A

No, only rarely.

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11
Q

90% of vulva carcinomas are _______ ______ carcinomas, and the rest are adenomas, melanomas, or basal cell carcinomas.

A

most are squamous cell carcinomas

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12
Q

What are basaloid and warty carcinomas?

A

A type of squamous cell carcinoma associated with HPV 16 and 18 that develops from vulvar intraepithelial neoplasia (VIN).

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13
Q

What is the precursor condition of basaloid and warty carcinomas?

A

A precancerous in situ lesion called vulvar intraepithelial neoplasia (VIN).

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14
Q

What three cellular changes are seen in basaloid and warty carcinomas (a type of squamous cell carcinoma)? What change is specifically characteristic of a warty carcinoma?

A
  1. Nests and cords of small, tightly packed malignant squamous cells lacking maturation.
  2. May have foci of central necrosis.
  3. VIN shows nuclear atypia, increased mitosis, LACK OF CELLULAR MATURATION (vs. condylomas or keratinizing carcinomas - where there IS maturation).

Warty carcinoma is characterized by exophytic papilla and prominent koilocytic changes.

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15
Q

Name two squamous cell carcinomas that ARE associated with HPV and one that is NOT associated with HPV.

A

Basaloid and warty carcinomas are associated with HPV.

Keratinizing squamous cell carcinomas are NOT associated with HPV.

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16
Q

What two long-standing conditions may result in the development of keratinizing squamous cell carcinoma of the vulva? At what age is keratinizing squamous cell carcinoma of the vulva seen?

A

These arise in people with long-standing lichen sclerosus or squamous cell hyperplasia and arise directly from differentiated vulvar intraepithelial neoplasia (VIN).

Mean age in 76 years old

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17
Q

What microscopic morphologic changes are seen as a VIN develops into a keratinizing squamous cell carcinoma of the vulva?

A

VIN is characterized by basal layer atypia and NORMAL maturation/differentiation of superficial layers.

Keratinizing squamous cell carcinoma will have nests and tongues of malignant squamous epithelium with prominent central KERATIN PEARLS.

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18
Q

What are the major symptoms of keratinizing squamous cell carcinoma of the vulva?

A
  1. Long-standing pruritus/itching.

2. Ulceration, bleeding, and secondary infection may develop.

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19
Q

How do keratinizing squamous cell carcinomas of the vulva metastasize?

A

Lymphatic: superficial inguinal nodes –> deep inguinal nodes –> femoral and pelvic nodes.

Lympho-hematogenous spread to the lungs, liver, and other organs can happen.

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20
Q

What is the prognosis for keratinizing squamous cell carcinoma of the vulva?

A

Lesions less than 2 cm in diameter: 60-80% 5-year survival after treatment with vulvectomy and lymphadenectomy.

Larger lesions with lymph node involvement have a 5-year survival rate of less than 10%.

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21
Q

Most tumors of the cervix are of ________ origin and are associated with _____.

A

epithelial origin, associated with HPV (oncogenic strains)

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22
Q

What is cervical intraepithelial neoplasia (CIN)?

A

Same thing as dysplasia or SIL (squamous intraepithelial lesion); a benign precursor to cervical squamous cell carcinomas. Not all progress to malignant cancer.

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23
Q

What four microscopic changes are characteristic of cervical intraepithelial neoplasia (CIN) and how is it graded?

A
  1. Nuclear atypia and heterogeneity with nuclear enlargement.
  2. Hyperchromasia.
  3. Presence of coarse chromatin granules.
  4. Koilocytes present.

Grading:
Low (CIN grade I) or high SIL (CIN grade II or III). Low means the weird cells are confined to the lower third of the epithelium. High means that the cells have expanded to 2/3 of the epithelial thickness.

24
Q

State how a CIN with the following characteristics should be classified:

  1. Progressive deregulation of the cell cycle by HPV.
  2. Increased cellular proliferation, decreased or arrested epithelial maturation, lower rate of viral replication.
  3. 10% will progress to carcinoma, usually within 2-10 years.
A

CIN II or III (same as high-grade squamous intraepithelial lesion)

25
Q

What percentage of low grade SILs and high grade SILs are associated with oncogenic HPV strains, respectively?

A

80% of LSILs and 100% of HSILs

26
Q

What other factors are involved with cervical cancer development from HPV? Do most women with HPV have cervical cancer?

A

Other factors include immune status, environmental factors. The majority of women with HPV do not have cancer.

27
Q

Vaccines presently being used for HPV 6, 11, 16, and 18 are not as effective amongst which population?

A

Black women

28
Q

Is the timeline for development of cervical intraepithelial neoplasia –> cervical cancer highly variable?

A

Yeah

29
Q

Most (75%) of the cancers of the cervix are ______ ______ carcinomas, and the rest are adenocarcinomas or mixed adenosquamous carcinomas (20%) and misc. (5%), all of which are associated with _____.

A

squamous cell carcinomas.

All associated with high risk HPV

30
Q

Are squamous cell carcinomas of the cervix keratinizing, or non-keratinizing?

A

Can be either!

Remember that keratinizing squamous cell carcinomas of the VULVA are NOT associated with HPV.

31
Q

What three microscopic morphological changes are seen in an adenocarcinoma of the cervix?

A
  1. Glandular cell proliferation
  2. Large, hyperchromatic nuclei
  3. Mucin-depleted cytoplasm –> dark appearance of the glands.
32
Q

What are some treatments for cervical cancer? What is the prognosis?

A

Tx includes electrocautery, conization (cone biopsy), cryosurgery, hysterectomy, lymph node dissection, irradiation.

Prognosis depends on the stage (and to a lesser degree the grade) at the time of detection.

33
Q

What is endometriosis and how common is it?

A

The presence of benign but ABNORMAL endometrial tissue (glands AND stroma) outside the uterus (most often in the ovary). Seen in 5-10% of women in reproductive age.

34
Q

In what way is endometriotic tissue abnormal?

A

The tissue exhibits a number of changes which enhance survival and persistence of the tissue within a foreign location.

35
Q

Describe the three theories for how endometrial tissue gets outside the uterus.

A

Regurgitation theory: menstrual endometrial fragments are refluxed through the fallopian tubes into the abdominal cavity.

Metaplastic theory: endometrial tissue arises directly from coelomic epithelium (the epithelium that lines the surface of the body wall and abdominal organs).

Vascular/lymphatic dissemination theory.

Multiple mechanisms may be at play at once.

36
Q

What are the morphologic changes associated with endometriosis (5)?

A
  1. Color is variable; yellow-red staining = blood product breakdown.
  2. Early disease: red lesions.
  3. Repeated hemorrhage and tissue repair –> fibrosis with brown discoloration.
  4. Extensive fibrosis in extensive cases.
  5. Chocolate cysts in the ovary from repeated hemorrhage.
37
Q

What are the clinical features of endometriosis (3)?

A
  1. Dysmenorrhea
  2. Dyspareunia (pain during sex)
  3. Pelvic pain due to intrapelvic bleeding.
38
Q

What complications may arise from endometriosis (3)?

A
  1. Malignancy occurs in 1-2% of cases.
  2. Adhesions –> infertility in 30-40% of cases.
  3. Ectopic pregnancy.
39
Q

What is the most frequent cancer occurring in the female genital tract?

A

Endometrial carcinoma

40
Q

What is the difference between endometrioid cancers (type 1 carcinoma) and non-endometrioid cancers (type 2 carcinoma)?

A

Endometrioid cancers (type 1 carcinomas) are associated with endometrial intraepithelial neoplasia and respond to estrogen, while non-endometrioid cancers (type 2 carcinomas) are not associated with estrogen and emerge without warning (higher fatality rates).

41
Q

Endometrioid adenocarcinomas are a major form of endometrial cancer, making up ____% of cases. They are linked to…..(3)? The precursor lesion is….?

A

80% of cases.

Linked to
1) prolonged estrogen stimulation of the endometrium, 2) obesity, hypertension, diabetes, 3) mismatch repair gene and PTEN tumor suppressor mutations (30-80% of cases).

Precursor lesion is complex endometrial hyperplasia with atypia.

42
Q

How are endometrioid adenocarcinomas (type 1 carcinomas) graded?

A

Based on level of differentiation of the tumor cells:

Grade 1 = well differentiated
Grade 2 = moderately differentiated
Grade 3 = poorly differentiated; barely recognizable as glandular tissue, lots of nuclear atypia and mitotic activity.

43
Q

Do type 2 (non-endometrioid) adenocarcinomas usually occur later, or earlier in life than type 1 endometrioid adenocarcinomas? Name three other characteristics of type 2 adenocarcinomas.

A

They usually occur a decade later than type 1 adenocarcinomas.

  1. Associated with endometrial atrophy.
  2. Not associated with estrogen.
  3. Poorly differentiated.
44
Q

What type of adenocarcinomas are serous carcinomas of the endometrium? (type 1 or 2). Name two morphological changes seen in these. What genetic mutation is associated with it?

A

Serous carcinomas of the endometrium are Type 2 (non-endometrioid - don’t respond to estrogen).

Changes: poorly differentiated, cytologic atypia is seen.

Mutation in p53 seen in 90% of cases.

45
Q

How are type 2 endometrial adenocarcinomas graded?

A

They are always classified as grade 3 no matter what.

46
Q

Prognosis of endometrial adenocarcinomas depend on the clinical _____ of the disease at the time of discovery. Further, tumors that have high levels of ______ and _______ receptors (as the case in endometrioid type 1) correlate with a better prognosis.

A

prognosis depends on stage.

high levels of estrogen and progesterone receptors = better prognosis

47
Q

To which lymph nodes do endometrial adenocarcinomas spread?

A

para-aortic lymph nodes

48
Q

What is a leiomyoma and how common are they?

A

Benign tumor of the smooth muscle in the uterus (myometrium). Seen in 30-50% of females during reproductive life.

49
Q

________ is known to promote the growth of leiomyomas, but it does not initate their growth. Therefore, these tumors will ________ in post-menopausal life.

A

Estrogen promotes growth, so they shrink after menopause

50
Q

In the case of multiple leiomyomas, each tumor is _________ and nonrandom _________ abnormalities are seen in 40% of the tumors.

A

each tumor is monoclonal and nonrandom chromosomal abnormalities are seen

51
Q

What morphological changes are seen in a leiomyoma (5)?

A
  1. Firm, well-circumscribed, not encapsulated.
  2. WHORLED bundles of smooth muscle cells.
  3. 1mm-30cm in diameter
  4. Can be intramural, submucosal, or subserosal.
  5. Foci of fibrosis, calcification, ischemic necrosis, cystic degeneration, and hemorrhage my be present.
52
Q

What are the clinical features of leiomyoma (3)? Do they often become cancerous?

A
  1. Can be silent
  2. Menorrhagia (heavy menstrual bleeding) is the most common symptom.
  3. Metrorrhagia (irregular, acyclic bleeding between periods).

They rarely transform into sarcomas.

53
Q

Do leiomyosacromas arise from leiomyomas?

A

No! They arise de novo from mesenchymal cells.

54
Q

How common are leiomyosarcomas and in what population are they seen?

A

Not common (2% of uterine malignancies). They appear later than leiomyomas (>50 y.o.)

55
Q

Leiomyosarcomas are usually ________ (bigger or smaller) than leiomyomas and are also usually ________.

A

usually bigger (10-15cm) and solitary

56
Q

What morphological changes are sen in leiomyosarcomas? What criteria are used for diagnosing it?

A
  1. Morphology is variable from bulky to polyploid lesions projecting into the cavity to structures that look like leiomyomas.
  2. Soft, hemorrhagic, necrotic.
  3. Differentiation is highly variable.

Diagnostic criteria: mitotic activity, cellular atypia, extent of necrosis.

57
Q

Do leiomyosarcomas often recur after removal? Do they metastasize? What is the prognosis?

A

Recurrence is common. Metastasis to lungs is common. 5-year survival rate is 40%.

Pathology Pt. 4 (10 decks)

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