Pathology of the female genital system

Question 1

Causes of vulvitis (5)

Answer 1

1. HPV
2. HSV-2: papules –> vesicles –> coalescent ulcers
3. Syphilis: caused by Treponema pallidum
4. Candida albicans
5. Gonorrhea

Question 2

Lichen sclerosus

Answer 2

Characterized by thinning of skin and appearance of white plaques. Pathogenesis is uncertain, but may be autoimmune. Usually seen in post-menopausal women.

Question 3

Lichen simplex chronicus

Answer 3

End stage of many inflammatory dermatoses.

Features:

• Epidermal thickening
• Leukoplakia - white, depigmented lesions

Question 4

Types of condylomas and their features

Answer 4

Condyloma lata

• Flat
• Occur in the 2nd phase of syphilis

Condyloma acuminata

• Perinuclear cytoplasmic vacuolization
• Nuclear angular pleomorphism
• Koilocytosis
• Caused by HPV of low malignant potential

Question 5

Differences between HPV and non-HPV associated vulvar cancer

Answer 5

HPV

• In younger people; better prognosis
• Basoidal or warty
• Multifocal

Non-HPV

• Preceded by years of non-neoplastic epithelial changes
• Unifocal

Question 6

Extramammary Paget disease

Answer 6

• Type of intraepithelial form of carcinoma

- Presents as red, scaly, crusted plaque

Question 7

(2) Most common pathogens causing vaginitis

Answer 7

C. albicans
- Causes vulvovaginitis and white discharge

Trichomonas vaginalis
- Causes purulent discharge and “strawberry cervix”

Question 8

CIN grading

Answer 8

CIN I: mild dysplasia with koilocyte atypia in the superficial layers of the epithelium

CIN II: moderate dysplasia with progressive atypia into the middle third of the epithelium

CIN III: severe dysplasia throughout the entire thickness of the epithelium; carcinoma in situ

Question 9

Low-risk HPV subtypes

Answer 9

6, 11, 42, 44

Question 10

High-risk HPV subtypes

Answer 10

16, 18, 31, 33, 35

Question 11

Most common cervical carcinomas (3)

Answer 11

1. Squamous cell cc (75%)
2. Adenocarcinomas (20%)
3. Small-cell neuroendocrine carcinomas

Question 12

Acute vs. chronic endometritis

Answer 12

Acute: characterized by presence of neutrophils within the endometrial glands

Chronic: characterized by presence of plasma cells and lymphoid cells within the endometrial stroma

Question 13

Etiology of endometrial hyperplasia

Answer 13

There’s an excess of estrogen relative to progesterone. I.e. caused by failure of ovulation, administration of estrogenic steroids or estrogen-producing ovarian tumors.

Question 14

Endometriosis: pathogenesis (3 theories)

Answer 14

1. Regurgitation theory: menstrual backflow through the fallopian tubes causes implantation
2. Metaplastic theory: endometrial differentiation of coelomic epithelium
3. Vascular or lymphatic dissemination

Question 15

Clinical patterns of endometrial carcinomas (2)

Answer 15

1. Endometroid type: seen in postmenopausal women with estrogen excess; often arises from endometrial hyperplasia
2. Serous type: arises on the background of atrophy; seen in the setting of an endometrial polyp

Question 16

Salpingitis: etiology and clinical features

Answer 16

Almost always part of PID and of microbial origin (Gonorrhea, Chlamydia, Mycoplasma hominis).

Produces fever, lower abdominal or pelvic pain and pelvic masses.

Adherence to nearby structures can cause formation of tubo-ovarian abscesses.

Question 17

Symptoms and etiology of polycystic ovary disease

Answer 17

• Oligomenorrhea
• Hirutism
• Infertility
• Obesity

Related to increased production of estrogen and androgens.

Question 18

Classification of ovarian tumors

Answer 18

1. Surface epithelial
2. Germ cell
3. Sex-cord stroma
4. Metastases

Question 19

Surface epithelial tumors of the ovaries (4)

Answer 19

1. Serous
2. Mucinous
3. Endometroid
4. Brenner

Question 20

What are Psammoma bodies and where are they seen?

Answer 20

Round collection of calcium with concentric laminations.

Seen in:

• Serous cystadenocarcinomas
• Papillary thyroid cc
• Papillary renal cell cc
• Meningiomas
• Mesotheliomas

Question 21

Classification of teratomas

Answer 21

• Benign (mature) cystic teratoma: produces a dermoid cyst

- Immature malignant teratomas: bulky, solid and puncuated by areas of necrosis

Question 22

Classification of gestational trophoblastic disease

Answer 22

1. Hyaditiform mole
2. 1 Complete: empty egg is fertilized by two spermatozoa or diploid sperm, yielding a diploid karyotype
3. 2 Partial: normal egg is fertilized by two spermatozoa or diploid sperm, yielding a triploid karyotype
4. Invasive mole: complete mole that is locally invasive
5. Choriocarcinoma

Question 23

Choriocarcinoma

Answer 23

Aggressive malignant tumor arising from either gestational chorionic epithelium or (less frequently) totipotential cells.

Usually arise from complete hyaditiform moles.

Widespread dissemination via blood to the lungs, vagina, brain, liver and kidneys.

Question 24

Preeclampsia vs. eclampsia

Answer 24

Preeclampsia: development of HTN accompanied by proteinuria and edema in the third trimester

Eclampsia: preeclampsia + convulsive seizures; can lead to DIC

Question 25

Consequences of preeclampsia and eclampsia

Answer 25

- Placental hypoperfusion -> infarction - Trophoblasts release less vasodilators--> HTN - Ischemic placenta produces trophoblastic substances -> DIC

Question 26

Inflammatory lesions of the breast (3)

Answer 26

1. Acute mastitis: inflammation of breast tissue; bacteria (S. aureus) gains access to the breast tissue via the ducts 2. Mammary duct ectasia: nonbacterial chronic inflammation; thickening of breast secretions 3. Traumatic fat necrosis

Question 27

Nonproliferative vs. proliferative patterns of fibrocystic changes of the breast

Answer 27

- Nonproliferative: cysts and fibrosis, characterized by increase in fibrous stroma associated with dilation of ducts and cyst formation Proliferative: - Epithelial hyperplasia: more atypical hyperplasias can have malignant potential - Sclerosing adenitis: intralobular fibrosis and proliferation of small ductules and acini

Question 28

Relationship between fibrocystic changes of the breast and risk for developing breast carcinoma

Answer 28

Minimal/no increased risk: - Fibrosis, cystic changes, apocrine metaplasia and fibroadenoma Slightly increased risk: - Moderate hyperplasia, sclerosing adenitis Greatly increased risk: - Atypical hyperplasia, ductular or lobular

Question 29

Tumors of the breast (4)

Answer 29

1. Fibroadenoma 2. Phyllodes tumor 3. Intraductal papilloma 4. Carcinoma

Question 30

Breast carcinoma: risk factors

Answer 30

- Higher incidence in USA and northern Europa - Increased risk after age 30 - Genetic factors: mutations in BRCA 1 or 2 - Obesity and high fat diets - Benign breast diseases

Question 31

Breast carcinoma: genetic changes

Answer 31

Several mutations can co-exist: - Overexpression of HER2/NEU proto-oncogene - Amplification of RAS and MYC genes - Mutations in RB and p53

Question 32

Breast cc: metastasis

Answer 32

- LN metastasis to axillary nodes or nodes along the internal mammary arteries - Hematogenous spread to especially lungs, skeleton, liver and adrenals

Question 33

Non-invasive breast cc

Answer 33

- Ductal cc in situ (DCIS; intraductal cc) | - Lobular cc in situ (LCIS): dyscohesive cells that lack E-cadherin

Question 34

Invasive breast cc

Answer 34

Invasive lobular cc: - Cells grow in a single-file patterns - Lack of E-cadherin prevents cells from sticking together Invasive ductal cc has the following subtypes: - Medullary cc: high grade malignant cells and lymphocytes; associated with BRCA1 mutation - Colloid cc (mucinous): malignant cells in pools of mucous; good prognosis - Tubular cc: cancer produces tubules that resemble normal breast; good prognosis