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Pathology > Pathology of the female genital system > Flashcards

Pathology of the female genital system Flashcards

1
Q

Causes of vulvitis (5)

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

Lichen sclerosus

A

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

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3
Q

Lichen simplex chronicus

A

End stage of many inflammatory dermatoses.

Features:

  • Epidermal thickening
  • Leukoplakia - white, depigmented lesions
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4
Q

Types of condylomas and their features

A

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
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5
Q

Differences between HPV and non-HPV associated vulvar cancer

A

HPV

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

Non-HPV

  • Preceded by years of non-neoplastic epithelial changes
  • Unifocal
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6
Q

Extramammary Paget disease

A
  • Type of intraepithelial form of carcinoma

- Presents as red, scaly, crusted plaque

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7
Q

(2) Most common pathogens causing vaginitis

A

C. albicans
- Causes vulvovaginitis and white discharge

Trichomonas vaginalis
- Causes purulent discharge and “strawberry cervix”

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8
Q

CIN grading

A

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

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9
Q

Low-risk HPV subtypes

A

6, 11, 42, 44

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10
Q

High-risk HPV subtypes

A

16, 18, 31, 33, 35

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11
Q

Most common cervical carcinomas (3)

A
  1. Squamous cell cc (75%)
  2. Adenocarcinomas (20%)
  3. Small-cell neuroendocrine carcinomas
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12
Q

Acute vs. chronic endometritis

A

Acute: characterized by presence of neutrophils within the endometrial glands

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

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13
Q

Etiology of endometrial hyperplasia

A

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.

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14
Q

Endometriosis: pathogenesis (3 theories)

A
  1. Regurgitation theory: menstrual backflow through the fallopian tubes causes implantation
  2. Metaplastic theory: endometrial differentiation of coelomic epithelium
  3. Vascular or lymphatic dissemination
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15
Q

Clinical patterns of endometrial carcinomas (2)

A
  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
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16
Q

Salpingitis: etiology and clinical features

A

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.

17
Q

Symptoms and etiology of polycystic ovary disease

A
  • Oligomenorrhea
  • Hirutism
  • Infertility
  • Obesity

Related to increased production of estrogen and androgens.

18
Q

Classification of ovarian tumors

A
  1. Surface epithelial
  2. Germ cell
  3. Sex-cord stroma
  4. Metastases
19
Q

Surface epithelial tumors of the ovaries (4)

A
  1. Serous
  2. Mucinous
  3. Endometroid
  4. Brenner
20
Q

What are Psammoma bodies and where are they seen?

A

Round collection of calcium with concentric laminations.

Seen in:

  • Serous cystadenocarcinomas
  • Papillary thyroid cc
  • Papillary renal cell cc
  • Meningiomas
  • Mesotheliomas
21
Q

Classification of teratomas

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

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

22
Q

Classification of gestational trophoblastic disease

A
  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
23
Q

Choriocarcinoma

A

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.

24
Q

Preeclampsia vs. eclampsia

A

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

Eclampsia: preeclampsia + convulsive seizures; can lead to DIC

25
Q

Consequences of preeclampsia and eclampsia

A
  • Placental hypoperfusion -> infarction
  • Trophoblasts release less vasodilators–> HTN
  • Ischemic placenta produces trophoblastic substances -> DIC
26
Q

Inflammatory lesions of the breast (3)

A
  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
27
Q

Nonproliferative vs. proliferative patterns of fibrocystic changes of the breast

A
  • 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
28
Q

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

A

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

29
Q

Tumors of the breast (4)

A
  1. Fibroadenoma
  2. Phyllodes tumor
  3. Intraductal papilloma
  4. Carcinoma
30
Q

Breast carcinoma: risk factors

A
  • 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
31
Q

Breast carcinoma: genetic changes

A

Several mutations can co-exist:

  • Overexpression of HER2/NEU proto-oncogene
  • Amplification of RAS and MYC genes
  • Mutations in RB and p53
32
Q

Breast cc: metastasis

A
  • LN metastasis to axillary nodes or nodes along the internal mammary arteries
  • Hematogenous spread to especially lungs, skeleton, liver and adrenals
33
Q

Non-invasive breast cc

A
  • Ductal cc in situ (DCIS; intraductal cc)

- Lobular cc in situ (LCIS): dyscohesive cells that lack E-cadherin

34
Q

Invasive breast cc

A

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

Pathology (14 decks)

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