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Pathophysiology > Gynecologic Pathophysiology > Flashcards

Gynecologic Pathophysiology Flashcards

1
Q

Describe the presentation of contact dermatitis of the vulva.

A

Scratching-induced trauma secondary to associated pruritus often exacerbates the primary condition.

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2
Q

What is the difference between irritant and allergic causes of contact dermatitis of the vulva?

A

CONTACT IRRITANT

  • reaction to urine, soap, detergents, antiseptics, deodorant, alcohol
  • well-defined erythematous weeping/crusting papules and plaques

ALLERGIC

  • allergy to perfume, creams, lotions, soaps, chemical in clothing and antigens
  • similar appearance with irritant dermatitis.
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3
Q

What is the infectious agents that can cause non-contact vulvitis?

A 
HPV
HSV-1 / HSV-2
N. gonorrhoeae
Treponema pallidum
Candida
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4
Q

Describe the following for LICHEN SCLEROSUS:

  • etiology
  • epidemiology
  • gross morphology
  • predisposition to carcinoma

as opposed to lichen simplex chronicus

A

ETIOLOGY

  • THINNING of epidermis
  • activated T- cells in subepithelial inflammatory infiltrate and increase frequency of autoimmune disorders

EPIDEMIOLOGY

  • Postmenopausal and prepubertal
  • but can include all age groups

GROSS MORPHOLOGY

  • smooth, white plaques (leukoplakia)
  • labia can become atrophic and stiffen constricting vaginal orifice

PREDISPOSITION TO CARCINOMA
- benign but 1-5% can lead to HPV-negaitve SCC of vulva.

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5
Q

Describe the following for LICHEN SIMPLEX CHRONICUS:

  • etiology
  • gross morphology
  • predisposition to carcinoma

as opposed to lichen sclerosus

A

ETIOLOGY

  • THICKENING of epithelium (hyperkeratosis) w/o atypia
  • increased mitotic activity in basal and suprabasal layer

GROSS MORPHOLOGY

  • leukocytic infiltration of dermis, appears leukoplakia; sometimes pronounced
  • d/t chronic irritation

PREDISPOSITION TO CARCINOMA
- none but can be found in margins of vulvar cancer

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6
Q

What are the causative agents for condylomata lata v. condylomata acuminata?

A

Condylomata LATA
- secondary syphilis

Condylomata ACUMINATA
- HPV 6 and 11

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7
Q

What is the clinical morphology and anatomical locations of condylomata acuminata?

A

Clinical morphology:

  • genital warts
  • papillary, flat-to-elevated, rugose
  • koilocytosis

Anatomical locations

  • anywhere on anogenital surface
  • vulva lesions; red-brown, few mm to cm
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8
Q

What are the two types of squamous cell carcinoma (SCC) of the vulva?

A
  1. Carcinoma in-situ

2. Well-differentiated, keratinizing

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9
Q

What are the following for SCC of the vulva carcinoma in-situ?

  • risk factors
  • precursor lesions
  • presentations
A

RISK FACTORS

  • high risk HPV strain (HPV 16)
  • middle-aged women
  • smokers
  • immunodeficiency

PRECURSOR LESIONS

  • vulvular intraepithelia neoplasia (VIN)
  • large degrees of atypia

PRESENTATIONS

  • leukoplakia
  • multifocal, warty
  • HPV-positive
  • poorly differentiated
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10
Q

What are the following for well-differentiated, keratizing SCC of the vulva?

  • risk factors
  • precursor lesions
  • presentations
A

RISK FACTORS

  • older women
  • history of epithelia changes (i.e. lichen sclerosus)

PRECURSOR LESIONS

  • differentiated vulvar intraepithelial neoplasia (dVIN)
  • atypia of basal layer, kertinization

PRESENTATIONS

  • leukoplakia
  • well-differentiated
  • HPV-negative
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11
Q

What are the two types of carcinomas of the vagina? Differentiate between their risk factors, causative agents and precursor lesions.

A

Squamous cell carcinoma (SCC) and Clear cell adenocarcinoma (CCA)

SCC

  • RISK: > 60 y/o, early age of 1st intercourse, multiplesex partners, persistent infections
  • AGENT: HPV infection
  • LESION: Vaginal intraepithelial neoplasia (VAIN)

CCA

  • RISK: ?
  • AGENT: DES (diethylstilbestrol)
  • LESION: vaginal adenosis (red, granular foci lined by mucus-secreting or ciliated columnar cells)
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12
Q

Where does most invasive cervical cancer occur?

A

Transition zone between squamous cell epithelium (outside) to the columnar epithelium (inside)

Originate in the epithelium of the endocervix where it joins the squamous epithelial covering of the exocervix at the cervical os.

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13
Q

What is the risk factors for developing high-grade cervical lesions and squamous cell carcinoma of cervix?

A

Cigarette smoking

HIV

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14
Q

What is the causative agent of cervical neoplasia and the high-risk strain use to induce the disease?

A

HPV (16, 18, 31, 33)

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15
Q

Describe the Squamous Intraepithelial Lesion (SIL) / Cervical Intraepithelial Neoplasia (CIN) grading system for cervical dysplasia.

A

LSIL / CIN I
HSIL / CIN II –> CIN III

Regress-Persist-Progress
LSIL: 60-30-10%
HSIL: 30-60-10%

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16
Q

Describe the following for endometritis:

  • etiologies
  • clinical presentation
  • long term risks (2)
A

ETIOLOGIES
- N. gonorrhoeae, C. trachomitis infeciton

CLINICAL PRESENTATION
- fever, abdominal pain, menstrual abnormalities

LONG-TERM RISKS

  • infertility
  • ectopic pregnancy
17
Q

What is adenomyosis and the typical clinical findings and presentation?

A

ADENOMYOSIS
- presence endometrial tissue in myometrium leading to hypertrophy resulting in enlarged, globular uterus

Findings/Presentation

  • Menorrhagia, dysmenorrhea, pelvic pain
  • can coexist with endometriosis
18
Q

Define endometriosis and the hypotheses (4) of the origin of the lesions.

A

ENDOMETRIOSIS
- endometrial glands and stroma in location outside the uterus

1) Regurgitation theory
- – menstrual backflow into fallopian tubes
2) Benign metastasis theory
- – spread via blood and lymphatics
3) Metaplastic theory
- – endometrial differentiation of coelomic epithelium
4) Extrauterine stem/progenitor cell theory
- – circulating stem/progenitor cells from bone marrow differentiate into endometrial tissue

19
Q

What is endometrial hyperplasia and the underlying hormonal basis as well as the possible precursor lesions?

A

ENDOMETRIAL HYPERPLASIA
- excess of estrogen relative to progestin; induces exaggerated endometrial growth

UNDERLYING BASIS/RISKS

  • obesity
  • failure of ovulation
  • prolonged administration of estrogenic steroids
  • estrogen producing ovarian lesions
20
Q

For endometrial hyperplasia, what are the risk of malignancy based on presence or absence of atypia?

A

Hyperplasia WITH atypia: high risk (20-50%)

Hyperplasia WITHOUT atypia: low risk (1-3%)

21
Q

Describe the following for ENDOMETROID CARCINOMA.

  • precursor lesions
  • risk factors
  • epidemiology

as compared to serous endometrial carcinoma

A

PRECURSOR LESIONS
- endometrial hyperplasia in d/t estrogen excess

RISK FACTORS
- obesity, diabetes, hypertension, infertility, exposure to estrogen

EPIDEMIOLOGY
- 80% of cases of carcinoma, women of color

22
Q

Describe the following for SEROUS ENDOMETRIAL CARCINOMA.

  • precursor lesions
  • risk factors
  • epidemiology

as compared to endometroid carcinoma

A

PRECURSOR LESIONS

  • endometrial atrophy
  • preceded by serous endometrial intraepithelial carcinoma

RISK FACTORS

  • TP53 mutations
  • postmenopausal women

EPIDEMIOLOGY
- 15% of cases, women of color

23
Q

Define leiomyoma.
Identify which cell line they originate from.
List the common presenting signs.

A

Fibroids, tumors of myometrium.
Benign masses of uterine smooth muscle cells.
Usually asymptomatic but can present with heavy menstrual bleeding.

24
Q

Describe the relationship between primary adenocarcinoma of the fallopian tube and high-grade serous carcinoma of the ovary.

A

Primary adenocarcinomas of fallopian tube may be site of origin for high-grade serous carcinomas

Both have TP53 mutations.

Found after prophylactic removal of fallopian tubes of patients with BRCA1 / BRCA2.

25
Q

List the risk factors for ovarian cancers.

A

Nulliparity
Family history
Germline mutations in tumor suppressor genes

Oral contraceptives decrease risk.

26
Q

What are the microscopic findings in benign (mature) v. malignant teratomas?

A

Benign (mature)

  • mature tissues derived from all 3 germ layers
  • sebaceous secretion and matted hair
  • teeth, hair, cartilage, other tissues

Malignant

  • immature elements, minimally differentiated cartilage, bone, nerve, other tissues
  • bulky, solid, areas of necrosis
27
Q

What is gestational trophoblastic disease? What are the two categories?

A

GESTATIONAL TROPHOBLASTIC DISEASE
- abnormal proliferation of fetal trophoblast cells.

1) Molar lesions: further divided into partial, complete and invasive hydatidifrom moles
2) Nonmolar lesions: choriocarcinoma and other uncommon trophoblast-malignancies

28
Q

What are the following for complete moles?

  • karyotype
  • risk of carcinoma
  • presence/absence of fetal parts

as compared to partial moles

A

Karyotype

  • diploid, all paternal chromosomes
  • 46 XX (46XY)
  • egg w/o DNA is fertilized

Risk of carcinoma
- 2%

Presence/Absence of fetal parts:
- Rare

29
Q

What are the following for partial moles?

  • karyotype
  • risk of carcinoma
  • presence/absence of fetal parts

as compared to complete moles

A

Karyotype

  • triploid
  • fetal issue
  • some normal chorionic villi

Risk of carcinoma
- rare

Presence/Absence of fetal parts
- Present

30
Q

Define invasive moles.

A

Complete moles that are locally invasive but does not metastasize easily.

Retains hydropic villi penetrating uterine wall deeply possibly causing rupture and life-threatening metastasis.

31
Q

Describe the following for choriocarcinoma.

  • malignant potential
  • predisposing conditions
  • common sites of metastasis
A

Malignant potential
- very aggressive (but responsive to chemo)

Predisposing conditions
- hydatidiform moles, post-abortion, pregnancy

Metastatic sites:
- lungs > vagina> brain, liver, kidneys

Pathophysiology (9 decks)

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